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21167931
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{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nLymphocytes in neuroprotection, cognition and emotion: is intolerance really the answer? Clinical, epidemiological and therapeutic studies indicate that some human depression is associated with proinflammatory cytokines, chronic inflammatory disorders, and inflammation-inducing lifestyle factors. Moreover depression can be induced by administration of proinflammatory cytokines, including IL-2 or IFN-α. However, recent studies in specific pathogen-free (SPF) rodents suggest a different--and potentially contradictory--relationship between immune processes and mental health. These studies suggest that effector T cells specific for central nervous system (CNS) antigens can assist recovery from an array of environmental insults ranging from nerve injury to psychological stress, while in contrast, regulatory T cells (Treg) oppose such recovery. Indeed, some reported effects of this so-called \"protective autoimmunity\" seem of direct relevance to depressive disorders. These findings pose a dilemma for those intending to manipulate inflammatory pathways as a treatment for depression. Should we administer anti-inflammatory treatments, or should we induce self-reactive T cells? We re-examine the rodent findings and outline immunological peculiarities of SPF rodents, the abnormal properties of their regulatory T cells, and the impact of gut microbiota. We find that \"protective autoimmunity\" is likely to be relevant only to very clean SPF animals that lack normal levels of activated T cells, CNS T cell traffic and mature Treg. The data indicate that even in SPF models the effectors of beneficial effects are not the proinflammatory autoimmune cells themselves, but rather unidentified regulatory cells. This reinterpretation of findings relevant to \"protective autoimmunity\" suggests that ongoing, and planned, clinical trials of anti-inflammatory strategies to treat depressive disorders are justified.",
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"content": "Lymphocytes in neuroprotection, cognition and emotion: is <DDF>intolerance</DDF> really the answer? Clinical, epidemiological and therapeutic studies indicate that some <DDF>human depression</DDF> is associated with <chemical>proinflammatory cytokines</chemical>, <DDF>chronic inflammatory disorders</DDF>, and inflammation-inducing lifestyle factors. Moreover <DDF>depression</DDF> can be induced by administration of <chemical>proinflammatory cytokines</chemical>, including <chemical>IL-2</chemical> or <chemical>IFN-α</chemical>. However, recent studies in <animal>specific pathogen-free (SPF) rodents</animal> suggest a different--and potentially contradictory--relationship between immune processes and mental health. These studies suggest that effector T cells specific for <chemical>central nervous system (CNS) antigens</chemical> can assist recovery from an array of environmental insults ranging from <DDF>nerve injury</DDF> to <DDF>psychological stress</DDF>, while in contrast, regulatory T cells (Treg) oppose such recovery. Indeed, some reported effects of this so-called \"protective autoimmunity\" seem of direct relevance to <DDF>depressive disorders</DDF>. These findings pose a dilemma for those intending to manipulate inflammatory pathways as a treatment for <DDF>depression</DDF>. Should we administer anti-inflammatory treatments, or should we induce self-reactive T cells? We re-examine the rodent findings and outline immunological peculiarities of <animal>SPF rodents</animal>, the abnormal properties of their regulatory T cells, and the impact of <microbiome>gut microbiota</microbiome>. We find that \"protective autoimmunity\" is likely to be relevant only to very clean <animal>SPF animals</animal> that lack normal levels of activated T cells, CNS T cell traffic and mature Treg. The data indicate that even in SPF models the effectors of beneficial effects are not the proinflammatory autoimmune cells themselves, but rather unidentified regulatory cells. This reinterpretation of findings relevant to \"protective autoimmunity\" suggests that ongoing, and planned, clinical trials of anti-inflammatory strategies to treat <DDF>depressive disorders</DDF> are justified.",
"role": "assistant"
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24103493
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nExcess body weight during pregnancy and offspring obesity: potential mechanisms. The rates of child and adult obesity have increased in most developed countries over the past several decades. The health consequences of obesity affect both physical and mental health, and the excess body weight can be linked to an elevated risk for developing type 2 diabetes, cardiovascular problems, and depression. Among the factors that can influence the development of obesity are higher infant weights and increased weight gain, which are associated with higher risk for excess body weight later in life. In turn, mother's excess body weight during and after pregnancy can be linked to the risk for offspring overweight and obesity through dietary habits, mode of delivery and feeding, breast milk composition, and through the influence on infant gut microbiota. This review considers current knowledge of these potential mechanisms that threaten to create an intergenerational cycle of obesity.",
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"content": "<DDF>Excess body weight during pregnancy</DDF> and <DDF>offspring obesity</DDF>: potential mechanisms. The rates of <DDF>child and adult obesity</DDF> have increased in most developed countries over the past several decades. The health consequences of <DDF>obesity</DDF> affect both physical and mental health, and the <DDF>excess body weight</DDF> can be linked to an elevated risk for developing <DDF>type 2 diabetes</DDF>, <DDF>cardiovascular problems</DDF>, and <DDF>depression</DDF>. Among the factors that can influence the development of <DDF>obesity</DDF> are higher infant weights and increased weight gain, which are associated with higher risk for <DDF>excess body weight</DDF> later in life. In turn, mother's <DDF>excess body weight during and after pregnancy</DDF> can be linked to the risk for <DDF>offspring overweight</DDF> and <DDF>obesity</DDF> through dietary habits, mode of delivery and feeding, breast milk composition, and through the influence on <microbiome>infant gut microbiota</microbiome>. This review considers current knowledge of these potential mechanisms that threaten to create an intergenerational cycle of <DDF>obesity</DDF>.",
"role": "assistant"
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24798884
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nPriming for health: gut microbiota acquired in early life regulates physiology, brain and behaviour. The infant gut microbiome is dynamic, and radical shifts in composition occur during the first 3 years of life. Disruption of these developmental patterns, and the impact of the microbial composition of our gut on brain and behaviour, has attracted much recent attention. Integrating these observations is an important new research frontier. Early-life perturbations of the developing gut microbiota can impact on the central nervous system and potentially lead to adverse mental health outcomes.",
"role": "user"
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{
"content": "Priming for health: <microbiome>gut microbiota</microbiome> acquired in early life regulates physiology, <anatomical location>brain</anatomical location> and behaviour. The <microbiome>infant gut microbiome</microbiome> is dynamic, and radical shifts in composition occur during the first 3 years of life. Disruption of these developmental patterns, and the impact of the microbial composition of our <anatomical location>gut</anatomical location> on <anatomical location>brain</anatomical location> and behaviour, has attracted much recent attention. Integrating these observations is an important new research frontier. Early-life perturbations of the <microbiome>developing gut microbiota</microbiome> can impact on the central nervous system and potentially lead to adverse mental health outcomes.",
"role": "assistant"
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24956966
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nMicrobiota and neurodevelopmental windows: implications for brain disorders. Gut microbiota is essential to human health, playing a major role in the bidirectional communication between the gastrointestinal tract and the central nervous system. The microbiota undergoes a vigorous process of development throughout the lifespan and establishes its symbiotic rapport with the host early in life. Early life perturbations of the developing gut microbiota can impact neurodevelopment and potentially lead to adverse mental health outcomes later in life. This review compares the parallel early development of the intestinal microbiota and the nervous system. The concept of parallel and interacting microbial-neural critical windows opens new avenues for developing novel microbiota-modulating based therapeutic interventions in early life to combat neurodevelopmental deficits and brain disorders.",
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"content": "Microbiota and neurodevelopmental windows: implications for <DDF>brain disorders</DDF>. <microbiome>Gut microbiota</microbiome> is essential to human health, playing a major role in the bidirectional communication between the <anatomical location>gastrointestinal tract</anatomical location> and the central nervous system. The microbiota undergoes a vigorous process of development throughout the lifespan and establishes its symbiotic rapport with the host early in life. Early life perturbations of the developing <microbiome>gut microbiota</microbiome> can impact neurodevelopment and potentially lead to adverse <DDF>mental health outcomes</DDF> later in life. This review compares the parallel early development of the <microbiome>intestinal microbiota</microbiome> and the nervous system. The concept of parallel and interacting microbial-neural critical windows opens new avenues for developing novel microbiota-modulating based therapeutic interventions in early life to combat <DDF>neurodevelopmental deficits</DDF> and <DDF>brain disorders</DDF>.",
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25173628
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nObese-type gut microbiota induce neurobehavioral changes in the absence of obesity. The prevalence of mental illness, particularly depression and dementia, is increased by obesity. Here, we test the hypothesis that obesity-associated changes in gut microbiota are intrinsically able to impair neurocognitive behavior in mice. Conventionally housed, nonobese, adult male C57BL/6 mice maintained on a normal chow diet were subjected to a microbiome depletion/transplantation paradigm using microbiota isolated from donors on either a high-fat diet (HFD) or control diet. Following re-colonization, mice were subjected to comprehensive behavioral and biochemical analyses. The mice given HFD microbiota had significant and selective disruptions in exploratory, cognitive, and stereotypical behavior compared with mice with control diet microbiota in the absence of significant differences in body weight. Sequencing-based phylogenetic analysis confirmed the presence of distinct core microbiota between groups, with alterations in α- and β-diversity, modulation in taxonomic distribution, and statistically significant alterations to metabolically active taxa. HFD microbiota also disrupted markers of intestinal barrier function, increased circulating endotoxin, and increased lymphocyte expression of ionized calcium-binding adapter molecule 1, toll-like receptor 2, and toll-like receptor 4. Finally, evaluation of brain homogenates revealed that HFD-shaped microbiota increased neuroinflammation and disrupted cerebrovascular homeostasis. Collectively, these data reinforce the link between gut dysbiosis and neurologic dysfunction and suggest that dietary and/or pharmacologic manipulation of gut microbiota could attenuate the neurologic complications of obesity.",
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"content": "<microbiome>Obese-type gut microbiota</microbiome> induce <DDF>neurobehavioral changes</DDF> in the absence of <DDF>obesity</DDF>. The prevalence of <DDF>mental illness</DDF>, particularly <DDF>depression</DDF> and <DDF>dementia</DDF>, is increased by <DDF>obesity</DDF>. Here, we test the hypothesis that obesity-associated changes in <microbiome>gut microbiota</microbiome> are intrinsically able to impair neurocognitive behavior in <animal>mice</animal>. <animal>Conventionally housed, nonobese, adult male C57BL/6 mice</animal> maintained on a normal chow diet were subjected to a microbiome depletion/transplantation paradigm using microbiota isolated from <animal>donors</animal> on either a high-fat diet (HFD) or control diet. Following re-colonization, <animal>mice</animal> were subjected to comprehensive <biomedical technique>behavioral and biochemical analyses</biomedical technique>. The <animal>mice</animal> given <microbiome>HFD microbiota</microbiome> had significant and selective disruptions in <DDF>exploratory, cognitive, and stereotypical behavior</DDF> compared with <animal>mice</animal> with <microbiome>control diet microbiota</microbiome> in the absence of significant differences in body weight. <biomedical technique>Sequencing-based phylogenetic analysis</biomedical technique> confirmed the presence of distinct <microbiome>core microbiota</microbiome> between groups, with alterations in α- and β-diversity, modulation in taxonomic distribution, and statistically significant alterations to metabolically active taxa. <microbiome>HFD microbiota</microbiome> also disrupted markers of intestinal barrier function, increased <chemical>circulating endotoxin</chemical>, and increased lymphocyte expression of <gene>ionized calcium-binding adapter molecule 1</gene>, <gene>toll-like receptor 2</gene>, and <gene>toll-like receptor 4</gene>. Finally, evaluation of brain homogenates revealed that <microbiome>HFD-shaped microbiota</microbiome> increased <DDF>neuroinflammation</DDF> and disrupted cerebrovascular homeostasis. Collectively, these data reinforce the link between <DDF>gut dysbiosis</DDF> and <DDF>neurologic dysfunction</DDF> and suggest that dietary and/or pharmacologic manipulation of <microbiome>gut microbiota</microbiome> could attenuate the neurologic complications of <DDF>obesity</DDF>.",
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25231862
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nArtificial sweeteners induce glucose intolerance by altering the gut microbiota. Non-caloric artificial sweeteners (NAS) are among the most widely used food additives worldwide, regularly consumed by lean and obese individuals alike. NAS consumption is considered safe and beneficial owing to their low caloric content, yet supporting scientific data remain sparse and controversial. Here we demonstrate that consumption of commonly used NAS formulations drives the development of glucose intolerance through induction of compositional and functional alterations to the intestinal microbiota. These NAS-mediated deleterious metabolic effects are abrogated by antibiotic treatment, and are fully transferrable to germ-free mice upon faecal transplantation of microbiota configurations from NAS-consuming mice, or of microbiota anaerobically incubated in the presence of NAS. We identify NAS-altered microbial metabolic pathways that are linked to host susceptibility to metabolic disease, and demonstrate similar NAS-induced dysbiosis and glucose intolerance in healthy human subjects. Collectively, our results link NAS consumption, dysbiosis and metabolic abnormalities, thereby calling for a reassessment of massive NAS usage.",
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"content": "<dietary supplement>Artificial sweeteners</dietary supplement> induce <DDF>glucose intolerance</DDF> by altering the <microbiome>gut microbiota</microbiome>. <dietary supplement>Non-caloric artificial sweeteners</dietary supplement> (<dietary supplement>NAS</dietary supplement>) are among the most widely used food additives worldwide, regularly consumed by <human>lean and obese individuals</human> alike. NAS consumption is considered safe and beneficial owing to their low caloric content, yet supporting scientific data remain sparse and controversial. Here we demonstrate that consumption of commonly used NAS formulations drives the development of <DDF>glucose intolerance</DDF> through induction of compositional and functional alterations to the <microbiome>intestinal microbiota</microbiome>. These <DDF>NAS-mediated deleterious metabolic effects</DDF> are abrogated by <drug>antibiotic treatment</drug>, and are fully transferrable to <animal>germ-free mice</animal> upon faecal transplantation of microbiota configurations from <animal>NAS-consuming mice</animal>, or of microbiota anaerobically incubated in the presence of <dietary supplement>NAS</dietary supplement>. We identify NAS-altered microbial metabolic pathways that are linked to host susceptibility to <DDF>metabolic disease</DDF>, and demonstrate similar <DDF>NAS-induced dysbiosis</DDF> and <DDF>glucose intolerance</DDF> in <human>healthy human subjects</human>. Collectively, our results link NAS consumption, <DDF>dysbiosis</DDF> and <DDF>metabolic abnormalities</DDF>, thereby calling for a reassessment of massive NAS usage.",
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26129950
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nAntibiotic-induced imbalances in gut microbiota aggravates cholesterol accumulation and liver injuries in rats fed a high-cholesterol diet. Increasing evidence suggests that maintenance of homeostasis between gut microbiota and host plays an important role in human health. Many diseases, such as those affecting the liver, have been linked to imbalances in gut microbial communities. However, it is not clear whether an imbalance in gut microbiota promotes the onset of liver injury or if the imbalance results from the pathological state. In the current study, antibiotics were used to disturb the gut microbiota of both rats fed a high-cholesterol diet and rats fed a normal diet (controls). The prevalence of Bacteroidetes and Firmicutes were reduced, and Proteobacteria was greatly increased in the guts of rats after antibiotic treatment. The antibiotic-induced perturbation of gut microbiota aggravated cholesterol accumulation and liver injury in rats fed a high-cholesterol diet. This may have been due to an increase in intestinal permeability and plasma lipopolysaccharide (LPS), which lead to an increase in LPS absorption and activation of TLR4 signaling, resulting in the synthesis of pro-inflammatory cytokines and chemokines in liver tissues. This study suggests that imbalances in gut microbiota may be a predisposing factor for the onset of metabolic diseases and liver injuries related to cholesterol and high-cholesterol diets. Modulation of gut microbiota could be a novel target for preventing cholesterol-related metabolic disorders.",
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"content": "<DDF>Antibiotic-induced imbalances</DDF> in <microbiome>gut microbiota</microbiome> aggravates <DDF>cholesterol accumulation</DDF> and <DDF>liver injuries</DDF> in <animal>rats</animal> fed a <food>high-cholesterol diet</food>. Increasing evidence suggests that maintenance of homeostasis between <microbiome>gut microbiota</microbiome> and host plays an important role in human health. Many diseases, such as those affecting the <anatomical location>liver</anatomical location>, have been linked to imbalances in gut microbial communities. However, it is not clear whether an imbalance in <microbiome>gut microbiota</microbiome> promotes the onset of <DDF>liver injury</DDF> or if the imbalance results from the pathological state. In the current study, <drug>antibiotics</drug> were used to disturb the <microbiome>gut microbiota</microbiome> of both <animal>rats</animal> fed a <food>high-cholesterol diet</food> and <animal>rats</animal> fed a <food>normal diet</food> (controls). The prevalence of <bacteria>Bacteroidetes</bacteria> and <bacteria>Firmicutes</bacteria> were reduced, and <bacteria>Proteobacteria</bacteria> was greatly increased in the <anatomical location>guts</anatomical location> of <animal>rats</animal> after antibiotic treatment. The antibiotic-induced perturbation of <microbiome>gut microbiota</microbiome> aggravated <DDF>cholesterol accumulation</DDF> and <DDF>liver injury</DDF> in <animal>rats</animal> fed a <food>high-cholesterol diet</food>. This may have been due to an increase in intestinal permeability and <chemical>plasma lipopolysaccharide</chemical> (<chemical>LPS</chemical>), which lead to an increase in LPS absorption and activation of TLR4 signaling, resulting in the synthesis of <chemical>pro-inflammatory cytokines</chemical> and <chemical>chemokines</chemical> in <anatomical location>liver tissues</anatomical location>. This study suggests that imbalances in <microbiome>gut microbiota</microbiome> may be a predisposing factor for the onset of <DDF>metabolic diseases</DDF> and <DDF>liver injuries</DDF> related to <chemical>cholesterol</chemical> and <food>high-cholesterol diets</food>. Modulation of <microbiome>gut microbiota</microbiome> could be a novel target for preventing <DDF>cholesterol-related metabolic disorders</DDF>.",
"role": "assistant"
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26190966
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nRole of neuroinflammation in the emotional and cognitive alterations displayed by animal models of obesity. Obesity is associated with a high prevalence of mood disorders and cognitive dysfunctions in addition to being a significant risk factor for important health complications such as cardiovascular diseases and type 2 diabetes. Identifying the pathophysiological mechanisms underlying these health issues is a major public health challenge. Based on recent findings, from studies conducted on animal models of obesity, it has been proposed that inflammatory processes may participate in both the peripheral and brain disorders associated with the obesity condition including the development of emotional and cognitive alterations. This is supported by the fact that obesity is characterized by peripheral low-grade inflammation, originating from increased adipose tissue mass and/or dysbiosis (changes in gut microbiota environment), both of which contribute to increased susceptibility to immune-mediated diseases. In this review, we provide converging evidence showing that obesity is associated with exacerbated neuroinflammation leading to dysfunction in vulnerable brain regions associated with mood regulation, learning, and memory such as the hippocampus. These findings give new insights to the pathophysiological mechanisms contributing to the development of brain disorders in the context of obesity and provide valuable data for introducing new therapeutic strategies for the treatment of neuropsychiatric complications often reported in obese patients.",
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"content": "Role of <DDF>neuroinflammation</DDF> in the emotional and cognitive alterations displayed by animal models of <DDF>obesity</DDF>. <DDF>Obesity</DDF> is associated with a high prevalence of <DDF>mood disorders</DDF> and <DDF>cognitive dysfunctions</DDF> in addition to being a significant risk factor for important health complications such as <DDF>cardiovascular diseases</DDF> and <DDF>type 2 diabetes</DDF>. Identifying the pathophysiological mechanisms underlying these health issues is a major public health challenge. Based on recent findings, from studies conducted on animal models of <DDF>obesity</DDF>, it has been proposed that inflammatory processes may participate in both the <DDF>peripheral and brain disorders</DDF> associated with the <DDF>obesity</DDF> condition including the development of <DDF>emotional and cognitive alterations</DDF>. This is supported by the fact that <DDF>obesity</DDF> is characterized by <DDF>peripheral low-grade inflammation</DDF>, originating from increased adipose tissue mass and/or <DDF>dysbiosis</DDF> (changes in gut microbiota environment), both of which contribute to increased susceptibility to <DDF>immune-mediated diseases</DDF>. In this review, we provide converging evidence showing that <DDF>obesity</DDF> is associated with exacerbated <DDF>neuroinflammation</DDF> leading to <DDF>dysfunction</DDF> in <anatomical location>vulnerable brain regions</anatomical location> associated with mood regulation, learning, and memory such as the <anatomical location>hippocampus</anatomical location>. These findings give new insights to the pathophysiological mechanisms contributing to the development of <DDF>brain disorders</DDF> in the context of <DDF>obesity</DDF> and provide valuable data for introducing new therapeutic strategies for the treatment of <DDF>neuropsychiatric complications</DDF> often reported in <human>obese patients</human>.",
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26408987
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nAdministration of Lactobacillus helveticus NS8 improves behavioral, cognitive, and biochemical aberrations caused by chronic restraint stress. Increasing numbers of studies have suggested that the gut microbiota is involved in the pathophysiology of stress-related disorders. Chronic stress can cause behavioral, cognitive, biochemical, and gut microbiota aberrations. Gut bacteria can communicate with the host through the microbiota-gut-brain axis (which mainly includes the immune, neuroendocrine, and neural pathways) to influence brain and behavior. It is hypothesized that administration of probiotics can improve chronic-stress-induced depression. In order to examine this hypothesis, the chronic restraint stress depression model was established in this study. Adult specific pathogen free (SPF) Sprague-Dawley rats were subjected to 21 days of restraint stress followed by behavioral testing (including the sucrose preference test (SPT), elevated-plus maze test, open-field test (OFT), object recognition test (ORT), and object placement test (OPT)) and biochemical analysis. Supplemental Lactobacillus helveticus NS8 was provided every day during stress until the end of experiment, and selective serotonin reuptake inhibitor (SSRI) citalopram (CIT) served as a positive control. Results showed that L. helveticus NS8 improved chronic restraint stress-induced behavioral (anxiety and depression) and cognitive dysfunction, showing an effect similar to and better than that of CIT. L. helveticus NS8 also resulted in lower plasma corticosterone (CORT) and adrenocorticotropic hormone (ACTH) levels, higher plasma interleukin-10 (IL-10) levels, restored hippocampal serotonin (5-HT) and norepinephrine (NE) levels, and more hippocampal brain-derived neurotrophic factor (BDNF) mRNA expression than in chronic stress rats. Taken together, these results indicate an anti-depressant effect of L. helveticus NS8 in rats subjected to chronic restraint stress depression and that this effect could be due to the microbiota-gut-brain axis. They also suggest the therapeutic potential of L. helveticus NS8 in stress-related and possibly other kinds of depression.",
"role": "user"
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"content": "Administration of <bacteria>Lactobacillus helveticus NS8</bacteria> improves <DDF>behavioral, cognitive, and biochemical aberrations</DDF> caused by <DDF>chronic restraint stress</DDF>. Increasing numbers of studies have suggested that the <microbiome>gut microbiota</microbiome> is involved in the pathophysiology of <DDF>stress-related disorders</DDF>. <DDF>Chronic stress</DDF> can cause <DDF>behavioral, cognitive, biochemical, and gut microbiota aberrations</DDF>. Gut bacteria can communicate with the host through the microbiota-gut-brain axis (which mainly includes the immune, neuroendocrine, and neural pathways) to influence <anatomical location>brain</anatomical location> and behavior. It is hypothesized that administration of <dietary supplement>probiotics</dietary supplement> can improve <DDF>chronic-stress-induced depression</DDF>. In order to examine this hypothesis, the chronic restraint stress depression model was established in this study. <animal>Adult specific pathogen free (SPF) Sprague-Dawley rats</animal> were subjected to 21 days of <DDF>restraint stress</DDF> followed by behavioral testing (including the <biomedical technique>sucrose preference test</biomedical technique> (<biomedical technique>SPT</biomedical technique>), <biomedical technique>elevated-plus maze test</biomedical technique>, <biomedical technique>open-field test</biomedical technique> (<biomedical technique>OFT</biomedical technique>), <biomedical technique>object recognition test</biomedical technique> (<biomedical technique>ORT</biomedical technique>), and <biomedical technique>object placement test</biomedical technique> (<biomedical technique>OPT</biomedical technique>)) and <biomedical technique>biochemical analysis</biomedical technique>. <dietary supplement>Supplemental Lactobacillus helveticus NS8</dietary supplement> was provided every day during <DDF>stress</DDF> until the end of experiment, and <drug>selective serotonin reuptake inhibitor (SSRI) citalopram</drug> (<drug>CIT</drug>) served as a positive control. Results showed that <dietary supplement>L. helveticus NS8</dietary supplement> improved <DDF>chronic restraint stress-induced behavioral</DDF> (<DDF>anxiety</DDF> and <DDF>depression</DDF>) and <DDF>cognitive dysfunction</DDF>, showing an effect similar to and better than that of <drug>CIT</drug>. <dietary supplement>L. helveticus NS8</dietary supplement> also resulted in lower plasma corticosterone (CORT) and adrenocorticotropic hormone (ACTH) levels, higher plasma <chemical>interleukin-10</chemical> (IL-10) levels, restored <chemical>hippocampal serotonin</chemical> (<chemical>5-HT</chemical>) and <chemical>norepinephrine</chemical> (<chemical>NE</chemical>) levels, and more hippocampal brain-derived neurotrophic factor (BDNF) mRNA expression than in <animal>chronic stress rats</animal>. Taken together, these results indicate an anti-depressant effect of <dietary supplement>L. helveticus NS8</dietary supplement> in <animal>rats</animal> subjected to <DDF>chronic restraint stress depression</DDF> and that this effect could be due to the microbiota-gut-brain axis. They also suggest the therapeutic potential of <dietary supplement>L. helveticus NS8</dietary supplement> in stress-related and possibly other kinds of <DDF>depression</DDF>.",
"role": "assistant"
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26426677
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nNeuroimmune pharmacological approaches. Intestinal inflammation is a major health problem which impairs the quality of life, impacts mental health and is exacerbated by stress and psychiatric disturbances which, in turn, can affect disease prognosis and response to treatment. Accumulating evidence indicates that the immune system is an important interface between intestinal inflammation and the enteric, sensory, central and autonomic nervous systems. In addition, the neuroimmune interactions originating from the gastrointestinal tract are orchestrated by the gut microbiota. This article reviews some major insights into this complex homeostatic network that have been achieved during the past two years and attempts to put these advances into perspective with novel opportunities of pharmacological intervention.",
"role": "user"
},
{
"content": "Neuroimmune pharmacological approaches. <DDF>Intestinal inflammation</DDF> is a major health problem which impairs the quality of life, impacts mental health and is exacerbated by <DDF>stress</DDF> and <DDF>psychiatric disturbances</DDF> which, in turn, can affect disease prognosis and response to treatment. Accumulating evidence indicates that the immune system is an important interface between <DDF>intestinal inflammation</DDF> and the enteric, sensory, central and autonomic nervous systems. In addition, the neuroimmune interactions originating from the <anatomical location>gastrointestinal tract</anatomical location> are orchestrated by the <microbiome>gut microbiota</microbiome>. This article reviews some major insights into this complex homeostatic network that have been achieved during the past two years and attempts to put these advances into perspective with novel opportunities of <drug>pharmacological intervention</drug>.",
"role": "assistant"
}
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26627987
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nGut microbiome in health and disease: Linking the microbiome-gut-brain axis and environmental factors in the pathogenesis of systemic and neurodegenerative diseases. The gut microbiome comprises the collective genome of the trillions of microorganisms residing in our gastrointestinal ecosystem. The interaction between the host and its gut microbiome is a complex relationship whose manipulation could prove critical to preventing or treating not only various gut disorders, like irritable bowel syndrome (IBS) and ulcerative colitis (UC), but also central nervous system (CNS) disorders, such as Alzheimer's and Parkinson's diseases. The purpose of this review is to summarize what is known about the gut microbiome, how it is connected to the development of disease and to identify the bacterial and biochemical targets that should be the focus of future research. Understanding the mechanisms behind the activity and proliferation of the gut microbiome will provide us new insights that may pave the way for novel therapeutic strategies.",
"role": "user"
},
{
"content": "<microbiome>Gut microbiome</microbiome> in health and disease: Linking the microbiome-gut-brain axis and environmental factors in the pathogenesis of <DDF>systemic and neurodegenerative diseases</DDF>. The <microbiome>gut microbiome</microbiome> comprises the collective genome of the trillions of microorganisms residing in our gastrointestinal ecosystem. The interaction between the host and its <microbiome>gut microbiome</microbiome> is a complex relationship whose manipulation could prove critical to preventing or treating not only various <DDF>gut disorders</DDF>, like <DDF>irritable bowel syndrome</DDF> (<DDF>IBS</DDF>) and <DDF>ulcerative colitis</DDF> (<DDF>UC</DDF>), but also <DDF>central nervous system (CNS) disorders</DDF>, such as <DDF>Alzheimer's and Parkinson's diseases</DDF>. The purpose of this review is to summarize what is known about the <microbiome>gut microbiome</microbiome>, how it is connected to the development of disease and to identify the bacterial and biochemical targets that should be the focus of future research. Understanding the mechanisms behind the activity and proliferation of the <microbiome>gut microbiome</microbiome> will provide us new insights that may pave the way for novel therapeutic strategies.",
"role": "assistant"
}
] |
27319972
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nMicrobes, Immunity, and Behavior: Psychoneuroimmunology Meets the Microbiome. There is now a large volume of evidence to support the view that the immune system is a key communication pathway between the gut and brain, which plays an important role in stress-related psychopathologies and thus provides a potentially fruitful target for psychotropic intervention. The gut microbiota is a complex ecosystem with a diverse range of organisms and a sophisticated genomic structure. Bacteria within the gut are estimated to weigh in excess of 1 kg in the adult human and the microbes within not only produce antimicrobial peptides, short chain fatty acids, and vitamins, but also most of the common neurotransmitters found in the human brain. That the microbial content of the gut plays a key role in immune development is now beyond doubt. Early disruption of the host-microbe interplay can have lifelong consequences, not just in terms of intestinal function but in distal organs including the brain. It is clear that the immune system and nervous system are in continuous communication in order to maintain a state of homeostasis. Significant gaps in knowledge remain about the effect of the gut microbiota in coordinating the immune-nervous systems dialogue. However, studies using germ-free animals, infective models, prebiotics, probiotics, and antibiotics have increased our understanding of the interplay. Early life stress can have a lifelong impact on the microbial content of the intestine and permanently alter immune functioning. That early life stress can also impact adult psychopathology has long been appreciated in psychiatry. The challenge now is to fully decipher the molecular mechanisms that link the gut microbiota, immune, and central nervous systems in a network of communication that impacts behavior patterns and psychopathology, to eventually translate these findings to the human situation both in health and disease. Even at this juncture, there is evidence to pinpoint key sites of communication where gut microbial interventions either with drugs or diet or perhaps fecal microbiota transplantation may positively impact mental health.",
"role": "user"
},
{
"content": "Microbes, Immunity, and Behavior: Psychoneuroimmunology Meets the Microbiome. There is now a large volume of evidence to support the view that the immune system is a key communication pathway between the <anatomical location>gut</anatomical location> and <anatomical location>brain</anatomical location>, which plays an important role in <DDF>stress-related psychopathologies</DDF> and thus provides a potentially fruitful target for psychotropic intervention. The <microbiome>gut microbiota</microbiome> is a complex ecosystem with a diverse range of organisms and a sophisticated genomic structure. Bacteria within the <anatomical location>gut</anatomical location> are estimated to weigh in excess of 1 kg in the <human>adult human</human> and the microbes within not only produce <chemical>antimicrobial peptides</chemical>, <chemical>short chain fatty acids</chemical>, and <chemical>vitamins</chemical>, but also most of the common neurotransmitters found in the <anatomical location>human brain</anatomical location>. That the microbial content of the <anatomical location>gut</anatomical location> plays a key role in immune development is now beyond doubt. Early disruption of the host-microbe interplay can have lifelong consequences, not just in terms of intestinal function but in distal organs including the <anatomical location>brain</anatomical location>. It is clear that the immune system and nervous system are in continuous communication in order to maintain a state of homeostasis. Significant gaps in knowledge remain about the effect of the <microbiome>gut microbiota</microbiome> in coordinating the immune-nervous systems dialogue. However, studies using <animal>germ-free animals</animal>, infective models, <dietary supplement>prebiotics</dietary supplement>, <dietary supplement>probiotics</dietary supplement>, and <drug>antibiotics</drug> have increased our understanding of the interplay. <DDF>Early life stress</DDF> can have a lifelong impact on the microbial content of the <anatomical location>intestine</anatomical location> and permanently alter immune functioning. That <DDF>early life stress</DDF> can also impact <DDF>adult psychopathology</DDF> has long been appreciated in psychiatry. The challenge now is to fully decipher the molecular mechanisms that link the <microbiome>gut microbiota</microbiome>, immune, and central nervous systems in a network of communication that impacts behavior patterns and psychopathology, to eventually translate these findings to the human situation both in health and disease. Even at this juncture, there is evidence to pinpoint key sites of communication where gut microbial interventions either with drugs or diet or perhaps fecal microbiota transplantation may positively impact mental health.",
"role": "assistant"
}
] |
27566465
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nAlzheimer's disease and gut microbiota. Alzheimer's disease (AD) is a most common neurodegenerative disorder, which associates with impaired cognition. Gut microbiota can modulate host brain function and behavior via microbiota-gut-brain axis, including cognitive behavior. Germ-free animals, antibiotics, probiotics intervention and diet can induce alterations of gut microbiota and gut physiology and also host cognitive behavior, increasing or decreasing risks of AD. The increased permeability of intestine and blood-brain barrier induced by gut microbiota disturbance will increase the incidence of neurodegeneration disorders. Gut microbial metabolites and their effects on host neurochemical changes may increase or decrease the risk of AD. Pathogenic microbes infection will also increase the risk of AD, and meanwhile, the onset of AD support the \"hygiene hypothesis\". All the results suggest that AD may begin in the gut, and is closely related to the imbalance of gut microbiota. Modulation of gut microbiota through personalized diet or beneficial microbiota intervention will probably become a new treatment for AD.",
"role": "user"
},
{
"content": "<DDF>Alzheimer's disease</DDF> and <microbiome>gut microbiota</microbiome>. <DDF>Alzheimer's disease</DDF> (<DDF>AD</DDF>) is a most common <DDF>neurodegenerative disorder</DDF>, which associates with <DDF>impaired cognition</DDF>. <microbiome>Gut microbiota</microbiome> can modulate host brain function and behavior via microbiota-gut-brain axis, including cognitive behavior. <animal>Germ-free animals</animal>, <drug>antibiotics</drug>, <dietary supplement>probiotics</dietary supplement> intervention and diet can induce alterations of <microbiome>gut microbiota</microbiome> and gut physiology and also host cognitive behavior, increasing or decreasing risks of <DDF>AD</DDF>. The increased permeability of <anatomical location>intestine</anatomical location> and blood-brain barrier induced by <microbiome>gut microbiota</microbiome> disturbance will increase the incidence of <DDF>neurodegeneration disorders</DDF>. <chemical>Gut microbial metabolites</chemical> and their effects on host neurochemical changes may increase or decrease the risk of <DDF>AD</DDF>. <DDF>Pathogenic microbes infection</DDF> will also increase the risk of <DDF>AD</DDF>, and meanwhile, the onset of <DDF>AD</DDF> support the \"hygiene hypothesis\". All the results suggest that <DDF>AD</DDF> may begin in the <anatomical location>gut</anatomical location>, and is closely related to the imbalance of <microbiome>gut microbiota</microbiome>. Modulation of <microbiome>gut microbiota</microbiome> through personalized diet or beneficial microbiota intervention will probably become a new treatment for <DDF>AD</DDF>.",
"role": "assistant"
}
] |
27698624
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nIntegrative Therapies in Anxiety Treatment with Special Emphasis on the Gut Microbiome. Over the past decade, research has shown that diet and gut health affects symptoms expressed in stress related disorders, depression, and anxiety through changes in the gut microbiota. Psycho-behavioral function and somatic health interaction have often been ignored in health care with resulting deficits in treatment quality and outcomes. While mental health care requires the professional training in counseling, psychotherapy and psychiatry, complimentary therapeutic strategies, such as attention to a nutritional and diverse diet and supplementation of probiotic foods, may be integrated alongside psychotherapy treatment models. Development of these alternative strategies is predicated on experimental evidence and diligent research on the biology of stress, fear, anxiety-related behaviors, and the gut-brain connection. This article provides a brief overview on biological markers of anxiety and the expanding nutritional literature relating to brain health and mental disorders. A case study demonstrates an example of a biopsychosocial approach integrating cognitive psychotherapy, dietary changes, and mindfulness activities, in treating symptoms of anxiety. This case study shows a possible treatment protocol to explore the efficacy of targeting the gut-brain-axis that may be used as an impetus for future controlled studies.",
"role": "user"
},
{
"content": "Integrative Therapies in <DDF>Anxiety</DDF> Treatment with Special Emphasis on the <microbiome>Gut Microbiome</microbiome>. Over the past decade, research has shown that diet and gut health affects symptoms expressed in <DDF>stress related disorders</DDF>, <DDF>depression</DDF>, and <DDF>anxiety</DDF> through changes in the <microbiome>gut microbiota</microbiome>. Psycho-behavioral function and somatic health interaction have often been ignored in health care with resulting deficits in treatment quality and outcomes. While mental health care requires the professional training in counseling, psychotherapy and psychiatry, complimentary therapeutic strategies, such as attention to a nutritional and diverse diet and supplementation of <dietary supplement>probiotic foods</dietary supplement>, may be integrated alongside psychotherapy treatment models. Development of these alternative strategies is predicated on experimental evidence and diligent research on the biology of <DDF>stress</DDF>, <DDF>fear</DDF>, <DDF>anxiety-related behaviors</DDF>, and the gut-brain connection. This article provides a brief overview on biological markers of <DDF>anxiety</DDF> and the expanding nutritional literature relating to brain health and <DDF>mental disorders</DDF>. A case study demonstrates an example of a biopsychosocial approach integrating cognitive psychotherapy, dietary changes, and mindfulness activities, in treating symptoms of <DDF>anxiety</DDF>. This case study shows a possible treatment protocol to explore the efficacy of targeting the gut-brain-axis that may be used as an impetus for future controlled studies.",
"role": "assistant"
}
] |
27763700
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nEarly life diets with prebiotics and bioactive milk fractions attenuate the impact of stress on learned helplessness behaviours and alter gene expression within neural circuits important for stress resistance. Manipulating gut microbes may improve mental health. Prebiotics are indigestible compounds that increase the growth and activity of health-promoting microorganisms, yet few studies have examined how prebiotics affect CNS function. Using an acute inescapable stressor known to produce learned helplessness behaviours such as failure to escape and exaggerated fear, we tested whether early life supplementation of a blend of two prebiotics, galactooligosaccharide (GOS) and polydextrose (PDX), and the glycoprotein lactoferrin (LAC) would attenuate behavioural and biological responses to stress later in life. Juvenile, male F344 rats were fed diets containing either GOS and PDX alone, LAC alone, or GOS, PDX and LAC. All diets altered gut bacteria, while diets containing GOS and PDX increased Lactobacillus spp. After 4 weeks, rats were exposed to inescapable stress, and either immediately killed for blood and tissues, or assessed for learned helplessness 24 h later. Diets did not attenuate stress effects on spleen weight, corticosterone and blood glucose; however, all diets differentially attenuated stress-induced learned helplessness. Notably, in situ hybridization revealed that all diets reduced stress-evoked cfos mRNA in the dorsal raphe nucleus (DRN), a structure important for learned helplessness behaviours. In addition, GOS, PDX and LAC diet attenuated stress-evoked decreases in mRNA for the 5-HT<sub>1A</sub> autoreceptor in the DRN and increased basal BDNF mRNA within the prefrontal cortex. These data suggest early life diets containing prebiotics and/or LAC promote behavioural stress resistance and uniquely modulate gene expression in corresponding circuits.",
"role": "user"
},
{
"content": "Early life diets with <dietary supplement>prebiotics</dietary supplement> and <dietary supplement>bioactive milk fractions</dietary supplement> attenuate the impact of <DDF>stress</DDF> on <DDF>learned helplessness behaviours</DDF> and alter gene expression within neural circuits important for stress resistance. Manipulating <microbiome>gut microbes</microbiome> may improve mental health. <dietary supplement>Prebiotics</dietary supplement> are indigestible compounds that increase the growth and activity of health-promoting microorganisms, yet few studies have examined how <dietary supplement>prebiotics</dietary supplement> affect CNS function. Using an acute inescapable stressor known to produce <DDF>learned helplessness behaviours</DDF> such as <DDF>failure to escape</DDF> and <DDF>exaggerated fear</DDF>, we tested whether early life supplementation of a blend of two <dietary supplement>prebiotics</dietary supplement>, <dietary supplement>galactooligosaccharide</dietary supplement> (<dietary supplement>GOS</dietary supplement>) and <dietary supplement>polydextrose</dietary supplement> (<dietary supplement>PDX</dietary supplement>), and the glycoprotein <chemical>lactoferrin</chemical> (<chemical>LAC</chemical>) would attenuate behavioural and biological responses to <DDF>stress</DDF> later in life. <animal>Juvenile, male F344 rats</animal> were fed diets containing either <dietary supplement>GOS</dietary supplement> and <dietary supplement>PDX</dietary supplement> alone, <chemical>LAC</chemical> alone, or <dietary supplement>GOS</dietary supplement>, <dietary supplement>PDX</dietary supplement> and <chemical>LAC</chemical>. All diets altered <bacteria>gut bacteria</bacteria>, while diets containing <dietary supplement>GOS</dietary supplement> and <dietary supplement>PDX</dietary supplement> increased <bacteria>Lactobacillus spp.</bacteria> After 4 weeks, <animal>rats</animal> were exposed to <DDF>inescapable stress</DDF>, and either immediately killed for blood and tissues, or assessed for learned helplessness 24 h later. Diets did not attenuate stress effects on spleen weight, <chemical>corticosterone</chemical> and <chemical>blood glucose</chemical>; however, all diets differentially attenuated <DDF>stress-induced learned helplessness</DDF>. Notably, <biomedical technique>in situ hybridization</biomedical technique> revealed that all diets reduced <gene>stress-evoked cfos mRNA</gene> in the dorsal raphe nucleus (DRN), a structure important for <DDF>learned helplessness behaviours</DDF>. In addition, <dietary supplement>GOS</dietary supplement>, <dietary supplement>PDX</dietary supplement> and <chemical>LAC</chemical> diet attenuated <DDF>stress-evoked decreases in mRNA</DDF> for the <chemical>5-HT<sub>1A</sub> autoreceptor</chemical> in the DRN and increased <gene>basal BDNF mRNA</gene> within the <anatomical location>prefrontal cortex</anatomical location>. These data suggest early life diets containing <dietary supplement>prebiotics</dietary supplement> and/or LAC promote behavioural <DDF>stress resistance</DDF> and uniquely modulate gene expression in corresponding circuits.",
"role": "assistant"
}
] |
27793225
|
[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nThe Importance of Diet and Gut Health to the Treatment and Prevention of Mental Disorders. The departure from traditional lifestyles and the rising disease burden of mental disorders are increasing global health concerns. Changes in diet around the world mean that populations are now increasingly reliant on highly processed, poor quality foods, which have been linked to increased risk for mental disorder. Conversely, a nutrient-rich diet is understood to be protective of mental health, and researchers are now aiming to understand the biological underpinnings of this relationship. The gut microbiota has been proposed as a key mediator of this link, given its association with both diet and mental health. Importantly, several critical \"windows of opportunity\" for prevention and intervention have been identified, particularly early life and adolescence; these are periods of rapid development and transition that provide a foundation for future health. Strategies that promote overall diet quality, high in fiber and nutrients, have been linked to increased microbial diversity and gut health. Improving diet quality and subsequent gut health may have benefits for individuals' mental health, as well as the mental health of future generations. Here we discuss specific, targeted dietary and gut focused strategies for the prevention and treatment of mental disorder.",
"role": "user"
},
{
"content": "The Importance of Diet and Gut Health to the Treatment and Prevention of <DDF>Mental Disorders</DDF>. The departure from traditional lifestyles and the rising disease burden of <DDF>mental disorders</DDF> are increasing global health concerns. Changes in diet around the world mean that <human>populations</human> are now increasingly reliant on <food>highly processed, poor quality foods</food>, which have been linked to increased risk for <DDF>mental disorder</DDF>. Conversely, a <food>nutrient-rich diet</food> is understood to be protective of mental health, and researchers are now aiming to understand the biological underpinnings of this relationship. The <microbiome>gut microbiota</microbiome> has been proposed as a key mediator of this link, given its association with both diet and mental health. Importantly, several critical \"windows of opportunity\" for prevention and intervention have been identified, particularly early life and adolescence; these are periods of rapid development and transition that provide a foundation for future health. Strategies that promote overall diet quality, high in <dietary supplement>fiber</dietary supplement> and <food>nutrients</food>, have been linked to increased microbial diversity and gut health. Improving diet quality and subsequent gut health may have benefits for individuals' mental health, as well as the mental health of future generations. Here we discuss specific, targeted dietary and gut focused strategies for the prevention and treatment of <DDF>mental disorder</DDF>.",
"role": "assistant"
}
] |
27900676
|
[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nFunctional Implications of the IL-23/IL-17 Immune Axis in Schizophrenia. The aetiology of schizophrenia seems to stem from complex interactions amongst environmental, genetic, metabolic, immunologic and oxidative components. Chronic low-grade inflammation has been persistently linked to schizophrenia, and this has primarily been based on the findings derived from Th1/Th2 cytokine balance. While the IL-23/IL-17 axis plays crucial role in the pathogenesis of several immune-mediated disorders, it has remained relatively unexplored in neuropsychiatric disorders. Altered levels of cytokines related to IL-23/IL-17 axis have been observed in schizophrenia patients in a few studies. In addition, other indirect factors known to confer schizophrenia risk like complement activation and altered gut microbiota are shown to modulate the IL-23/IL-17 axis. These preliminary observations provide crucial clues about the functional implications of IL-23/IL-17 axis in schizophrenia. In this review, an attempt has been made to highlight the biology of IL-23/IL-17 axis and its relevance to schizophrenia risk and pathogenesis. Given the pathogenic potential of the IL-23/IL-17 axis, therapeutic targeting of this axis may be a promising approach to benefit patients suffering from this devastating disorder.",
"role": "user"
},
{
"content": "Functional Implications of the IL-23/IL-17 Immune Axis in <DDF>Schizophrenia</DDF>. The aetiology of <DDF>schizophrenia</DDF> seems to stem from complex interactions amongst environmental, genetic, metabolic, immunologic and oxidative components. <DDF>Chronic low-grade inflammation</DDF> has been persistently linked to <DDF>schizophrenia</DDF>, and this has primarily been based on the findings derived from Th1/Th2 cytokine balance. While the IL-23/IL-17 axis plays crucial role in the pathogenesis of several <DDF>immune-mediated disorders</DDF>, it has remained relatively unexplored in <DDF>neuropsychiatric disorders</DDF>. Altered levels of <chemical>cytokines</chemical> related to IL-23/IL-17 axis have been observed in <human>schizophrenia patients</human> in a few studies. In addition, other indirect factors known to confer schizophrenia risk like complement activation and altered <microbiome>gut microbiota</microbiome> are shown to modulate the IL-23/IL-17 axis. These preliminary observations provide crucial clues about the functional implications of IL-23/IL-17 axis in <DDF>schizophrenia</DDF>. In this review, an attempt has been made to highlight the biology of IL-23/IL-17 axis and its relevance to schizophrenia risk and pathogenesis. Given the pathogenic potential of the IL-23/IL-17 axis, therapeutic targeting of this axis may be a promising approach to benefit <human>patients</human> suffering from this devastating disorder.",
"role": "assistant"
}
] |
27930574
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nA MeSH-based text mining method for identifying novel prebiotics. Prebiotics contribute to the well-being of their host by altering the composition of the gut microbiota. Discovering new prebiotics is a challenging and arduous task due to strict inclusion criteria; thus, highly limited numbers of prebiotic candidates have been identified. Notably, the large numbers of published studies may contain substantial information attached to various features of known prebiotics that can be used to predict new candidates. In this paper, we propose a medical subject headings (MeSH)-based text mining method for identifying new prebiotics with structured texts obtained from PubMed. We defined an optimal feature set for prebiotics prediction using a systematic feature-ranking algorithm with which a variety of carbohydrates can be accurately classified into different clusters in accordance with their chemical and biological attributes. The optimal feature set was used to separate positive prebiotics from other carbohydrates, and a cross-validation procedure was employed to assess the prediction accuracy of the model. Our method achieved a specificity of 0.876 and a sensitivity of 0.838. Finally, we identified a high-confidence list of candidates of prebiotics that are strongly supported by the literature. Our study demonstrates that text mining from high-volume biomedical literature is a promising approach in searching for new prebiotics.",
"role": "user"
},
{
"content": "A <statistical technique>MeSH-based text mining method</statistical technique> for identifying <dietary supplement>novel prebiotics</dietary supplement>. <dietary supplement>Prebiotics</dietary supplement> contribute to the well-being of their host by altering the composition of the <microbiome>gut microbiota</microbiome>. Discovering new <dietary supplement>prebiotics</dietary supplement> is a challenging and arduous task due to strict inclusion criteria; thus, highly limited numbers of prebiotic candidates have been identified. Notably, the large numbers of published studies may contain substantial information attached to various features of known <dietary supplement>prebiotics</dietary supplement> that can be used to predict new candidates. In this paper, we propose a <statistical technique>medical subject headings (MeSH)-based text mining method</statistical technique> for identifying new <dietary supplement>prebiotics</dietary supplement> with structured texts obtained from PubMed. We defined an optimal feature set for prebiotics prediction using a <statistical technique>systematic feature-ranking algorithm</statistical technique> with which a variety of <chemical>carbohydrates</chemical> can be accurately classified into different clusters in accordance with their chemical and biological attributes. The optimal feature set was used to separate positive <dietary supplement>prebiotics</dietary supplement> from other <chemical>carbohydrates</chemical>, and a <statistical technique>cross-validation procedure</statistical technique> was employed to assess the prediction accuracy of the model. Our method achieved a specificity of 0.876 and a sensitivity of 0.838. Finally, we identified a high-confidence list of candidates of <dietary supplement>prebiotics</dietary supplement> that are strongly supported by the literature. Our study demonstrates that <statistical technique>text mining from high-volume biomedical literature</statistical technique> is a promising approach in searching for new <dietary supplement>prebiotics</dietary supplement>.",
"role": "assistant"
}
] |
28073356
|
[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nGut microbiota disturbance during helminth infection: can it affect cognition and behaviour of children? Bidirectional signalling between the brain and the gastrointestinal tract is regulated at neural, hormonal, and immunological levels. Recent studies have shown that helminth infections can alter the normal gut microbiota. Studies have also shown that the gut microbiota is instrumental in the normal development, maturation and function of the brain. The pathophysiological pathways by which helminth infections contribute to altered cognitive function remain poorly understood. We put forward the hypothesis that gastrointestinal infections with parasitic worms, such as helminths, induce an imbalance of the gut-brain axis, which, in turn, can detrimentally manifest in brain development. Factors supporting this hypothesis are: 1) research focusing on intelligence and school performance in school-aged children has shown helminth infections to be associated with cognitive impairment, 2) disturbances in gut microbiota have been shown to be associated with important cognitive developmental effects, and 3) helminth infections have been shown to alter the gut microbiota structure. Evidence on the complex interactions between extrinsic (parasite) and intrinsic (host-derived) factors has been synthesised and discussed. While evidence in favour of the helminth-gut microbiota-central nervous system hypothesis is circumstantial, it would be unwise to rule it out as a possible mechanism by which gastrointestinal helminth infections induce childhood cognitive morbidity. Further empirical studies are necessary to test an indirect effect of helminth infections on the modulation of mood and behaviour through its effects on the gut microbiota.",
"role": "user"
},
{
"content": "<DDF>Gut microbiota disturbance</DDF> during <DDF>helminth infection</DDF>: can it affect cognition and behaviour of <human>children</human>? Bidirectional signalling between the <anatomical location>brain</anatomical location> and the <anatomical location>gastrointestinal tract</anatomical location> is regulated at neural, hormonal, and immunological levels. Recent studies have shown that <DDF>helminth infections</DDF> can alter the normal <microbiome>gut microbiota</microbiome>. Studies have also shown that the <microbiome>gut microbiota</microbiome> is instrumental in the normal development, maturation and function of the <anatomical location>brain</anatomical location>. The pathophysiological pathways by which <DDF>helminth infections</DDF> contribute to altered cognitive function remain poorly understood. We put forward the hypothesis that <DDF>gastrointestinal infections</DDF> with <animal>parasitic worms</animal>, such as <animal>helminths</animal>, induce an imbalance of the gut-brain axis, which, in turn, can detrimentally manifest in brain development. Factors supporting this hypothesis are: 1) research focusing on intelligence and school performance in <human>school-aged children</human> has shown <DDF>helminth infections</DDF> to be associated with <DDF>cognitive impairment</DDF>, 2) disturbances in <microbiome>gut microbiota</microbiome> have been shown to be associated with important cognitive developmental effects, and 3) <DDF>helminth infections</DDF> have been shown to alter the gut microbiota structure. Evidence on the complex interactions between extrinsic (parasite) and intrinsic (host-derived) factors has been synthesised and discussed. While evidence in favour of the helminth-gut microbiota-central nervous system hypothesis is circumstantial, it would be unwise to rule it out as a possible mechanism by which <DDF>gastrointestinal helminth infections</DDF> induce <DDF>childhood cognitive morbidity</DDF>. Further empirical studies are necessary to test an indirect effect of <DDF>helminth infections</DDF> on the modulation of mood and behaviour through its effects on the <microbiome>gut microbiota</microbiome>.",
"role": "assistant"
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28399458
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nThe role of maternal anxiety and depressive disorders prior to and during pregnancy and perinatal psychopathological symptoms for early infant diseases and drug administration. Maternal mental health prior to and during pregnancy has been shown to be associated with inflammatory diseases and gastrointestinal complaints in the offspring. Unfortunately, many studies merely focused on perinatal distress without consideration of lifetime anxiety and depressive disorders. To prospectively investigate associations of anxiety and depressive disorders prior to and during pregnancy as well as perinatal distress with infants' inflammatory diseases, gastrointestinal complaints and corresponding drug administration. Prospective-longitudinal study initiated in 2009/2010. N=306 (expectant) mothers with and without DSM-IV lifetime anxiety and depressive disorders (Composite International Diagnostic Interview for Women) and low vs. high severity of psychopathological symptoms during pregnancy (Brief Symptom Inventory) enrolled in early pregnancy and repeatedly assessed during peripartum period. Infant inflammatory diseases, gastrointestinal complaints and drug administration assessed via questionnaire (maternal report) at four months postpartum (n=279). Severe psychopathological symptoms during pregnancy were associated with inflammatory diseases and anti-infective medication, whereas anxiety and depressive disorders prior to and during pregnancy were related to gastrointestinal complaints (diarrhea, colic complaints) and corresponding medication. These results have to be discussed with caution, because information on infants' diseases were based exclusively on maternal self-reports. However, they suggest promising directions regarding our current knowledge about the relevance of maternal perinatal distress for infant inflammatory diseases (e.g. fetal programming). Moreover, the association between maternal anxiety and depressive disorders and infant gastrointestinal complaints may be explained by an anxious misinterpretation of 'normal' infant signals or a transmission of adverse gut microbiota, respectively.",
"role": "user"
},
{
"content": "The role of <DDF>maternal anxiety</DDF> and <DDF>depressive disorders</DDF> prior to and during pregnancy and <DDF>perinatal psychopathological symptoms</DDF> for <DDF>early infant diseases</DDF> and drug administration. Maternal mental health prior to and during pregnancy has been shown to be associated with <DDF>inflammatory diseases</DDF> and <DDF>gastrointestinal complaints</DDF> in the <human>offspring</human>. Unfortunately, many studies merely focused on <DDF>perinatal distress</DDF> without consideration of <DDF>lifetime anxiety</DDF> and <DDF>depressive disorders</DDF>. To prospectively investigate associations of <DDF>anxiety</DDF> and <DDF>depressive disorders</DDF> prior to and during pregnancy as well as <DDF>perinatal distress</DDF> with <DDF>infants' inflammatory diseases</DDF>, <DDF>gastrointestinal complaints</DDF> and corresponding drug administration. Prospective-longitudinal study initiated in 2009/2010. N=306 <human>(expectant) mothers</human> with and without <DDF>DSM-IV lifetime anxiety and depressive disorders</DDF> (<biomedical technique>Composite International Diagnostic Interview for Women</biomedical technique>) and low vs. high severity of psychopathological symptoms during pregnancy (<biomedical technique>Brief Symptom Inventory</biomedical technique>) enrolled in early pregnancy and repeatedly assessed during peripartum period. <DDF>Infant inflammatory diseases</DDF>, <DDF>gastrointestinal complaints</DDF> and drug administration assessed via questionnaire (maternal report) at four months postpartum (n=279). Severe <DDF>psychopathological symptoms</DDF> during pregnancy were associated with <DDF>inflammatory diseases</DDF> and <drug>anti-infective medication</drug>, whereas <DDF>anxiety</DDF> and <DDF>depressive disorders</DDF> prior to and during pregnancy were related to <DDF>gastrointestinal complaints</DDF> (<DDF>diarrhea</DDF>, <DDF>colic complaints</DDF>) and corresponding medication. These results have to be discussed with caution, because information on <DDF>infants' diseases</DDF> were based exclusively on maternal self-reports. However, they suggest promising directions regarding our current knowledge about the relevance of <DDF>maternal perinatal distress</DDF> for <DDF>infant inflammatory diseases</DDF> (e.g. fetal programming). Moreover, the association between <DDF>maternal anxiety</DDF> and <DDF>depressive disorders</DDF> and <DDF>infant gastrointestinal complaints</DDF> may be explained by an anxious misinterpretation of 'normal' infant signals or a transmission of adverse <microbiome>gut microbiota</microbiome>, respectively.",
"role": "assistant"
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28442250
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nAnalysis of microbiota in first episode psychosis identifies preliminary associations with symptom severity and treatment response. The effects of gut microbiota on the central nervous system, along its possible role in mental disorders, have received increasing attention. Here we investigated differences in fecal microbiota between 28 patients with first-episode psychosis (FEP) and 16 healthy matched controls and explored whether such differences were associated with response after up to 12months of treatment. Numbers of Lactobacillus group bacteria were elevated in FEP-patients and significantly correlated with severity along different symptom domains. A subgroup of FEP patients with the strongest microbiota differences also showed poorer response after up to 12months of treatment. The present findings support the involvement of microbiota alterations in psychotic illness and may provide the basis for exploring the benefit of their modulation on treatment response and remission.",
"role": "user"
},
{
"content": "Analysis of microbiota in <DDF>first episode psychosis</DDF> identifies preliminary associations with symptom severity and treatment response. The effects of <microbiome>gut microbiota</microbiome> on the central nervous system, along its possible role in <DDF>mental disorders</DDF>, have received increasing attention. Here we investigated differences in <microbiome>fecal microbiota</microbiome> between 28 <human>patients</human> with <DDF>first-episode psychosis</DDF> (<DDF>FEP</DDF>) and 16 <human>healthy matched controls</human> and explored whether such differences were associated with response after up to 12months of treatment. Numbers of <bacteria>Lactobacillus group bacteria</bacteria> were elevated in <human>FEP-patients</human> and significantly correlated with severity along different symptom domains. A subgroup of <human>FEP patients</human> with the strongest microbiota differences also showed poorer response after up to 12months of treatment. The present findings support the involvement of <DDF>microbiota alterations</DDF> in <DDF>psychotic illness</DDF> and may provide the basis for exploring the benefit of their modulation on treatment response and remission.",
"role": "assistant"
}
] |
28629758
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nImplications of the gut microbiota in vulnerability to the social avoidance effects of chronic social defeat in male mice. Appreciable evidence suggests that perturbations within the gut microbiome and the immune system may play a key role in the pathogenesis of depression stemming from earlier stressful experiences. In the present investigation we examined whether microbial changes in cecum contents were associated with social avoidance behaviors, a feature of depression, and pro-inflammatory variations among socially stressed mice. Male C57BL/6 mice experienced social defeat or a control condition once a day for 10 consecutive days. Social avoidance behaviors were examined three weeks after the last defeat or control episode and blood, brain, and cecum contents were collected 24h afterward for the determination of corticosterone, pro-inflammatory cytokines, and microbial populations. Mice that were most susceptible to the behavioral effects of chronic social defeat (reflected by severe social avoidance behaviors) displayed the greatest changes within particular sets of bacteria at the phylum and genus taxonomic ranks. Although plasma and brain cytokines were not significantly altered in socially defeated mice, changes in the mRNA expression of interleukin (IL)-1β and IL-6 within the prefrontal cortex were associated with elevated abundance of Flavobacterium spp. and reduced abundance of Turicibacter spp., which were also strongly correlated to social avoidance severity. Although at this time a causal connection cannot be inferred, these results point to the possibility that specific clusters of bacterial communities in cecum contents may be linked to vulnerability to social deficits stemming from prolonged social stressor experiences.",
"role": "user"
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{
"content": "Implications of the <microbiome>gut microbiota</microbiome> in vulnerability to the <DDF>social avoidance effects</DDF> of <DDF>chronic social defeat</DDF> in <animal>male mice</animal>. Appreciable evidence suggests that perturbations within the <microbiome>gut microbiome</microbiome> and the immune system may play a key role in the pathogenesis of <DDF>depression</DDF> stemming from earlier stressful experiences. In the present investigation we examined whether microbial changes in cecum contents were associated with <DDF>social avoidance behaviors</DDF>, a feature of <DDF>depression</DDF>, and <DDF>pro-inflammatory variations</DDF> among <animal>socially stressed mice</animal>. <animal>Male C57BL/6 mice</animal> experienced social defeat or a control condition once a day for 10 consecutive days. <DDF>Social avoidance behaviors</DDF> were examined three weeks after the last defeat or control episode and blood, brain, and cecum contents were collected 24h afterward for the determination of <chemical>corticosterone</chemical>, <chemical>pro-inflammatory cytokines</chemical>, and microbial populations. <animal>Mice</animal> that were most susceptible to the behavioral effects of <DDF>chronic social defeat</DDF> (reflected by <DDF>severe social avoidance behaviors</DDF>) displayed the greatest changes within particular sets of bacteria at the phylum and genus taxonomic ranks. Although <chemical>plasma and brain cytokines</chemical> were not significantly altered in <animal>socially defeated mice</animal>, changes in the mRNA expression of <chemical>interleukin (IL)-1β</chemical> and <chemical>IL-6</chemical> within the <anatomical location>prefrontal cortex</anatomical location> were associated with elevated abundance of <bacteria>Flavobacterium spp.</bacteria> and reduced abundance of <bacteria>Turicibacter spp.</bacteria>, which were also strongly correlated to social avoidance severity. Although at this time a causal connection cannot be inferred, these results point to the possibility that specific clusters of bacterial communities in cecum contents may be linked to vulnerability to <DDF>social deficits</DDF> stemming from prolonged social stressor experiences.",
"role": "assistant"
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28816544
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nAnimal inflammation-based models of depression and their application to drug discovery. Depression, anxiety and other affective disorders are globally widespread and severely debilitating human brain diseases. Despite their high prevalence and mental health impact, affective pathogenesis is poorly understood, and often remains recurrent and resistant to treatment. The lack of efficient antidepressants and presently limited conceptual innovation necessitate novel approaches and new drug targets in the field of antidepressant therapy. Areas covered: Herein, the authors discuss the emerging role of neuro-immune interactions in affective pathogenesis, which can become useful targets for CNS drug discovery, including modulating neuroinflammatory pathways to alleviate affective pathogenesis. Expert opinion: Mounting evidence implicates microglia, polyunsaturated fatty acids (PUFAs), glucocorticoids and gut microbiota in both inflammation and depression. It is suggested that novel antidepressants can be developed based on targeting microglia-, PUFAs-, glucocorticoid- and gut microbiota-mediated cellular pathways. In addition, the authors call for a wider application of novel model organisms, such as zebrafish, in studying shared, evolutionarily conserved (and therefore, core) neuro-immune mechanisms of depression.",
"role": "user"
},
{
"content": "Animal inflammation-based models of <DDF>depression</DDF> and their application to drug discovery. <DDF>Depression</DDF>, <DDF>anxiety</DDF> and other <DDF>affective disorders</DDF> are globally widespread and severely debilitating <DDF>human brain diseases</DDF>. Despite their high prevalence and mental health impact, affective pathogenesis is poorly understood, and often remains recurrent and resistant to treatment. The lack of efficient <drug>antidepressants</drug> and presently limited conceptual innovation necessitate novel approaches and new drug targets in the field of antidepressant therapy. Areas covered: Herein, the authors discuss the emerging role of neuro-immune interactions in affective pathogenesis, which can become useful targets for CNS drug discovery, including modulating neuroinflammatory pathways to alleviate <DDF>affective pathogenesis</DDF>. Expert opinion: Mounting evidence implicates microglia, <chemical>polyunsaturated fatty acids</chemical> (<chemical>PUFAs</chemical>), <chemical>glucocorticoids</chemical> and <microbiome>gut microbiota</microbiome> in both <DDF>inflammation</DDF> and <DDF>depression</DDF>. It is suggested that novel <drug>antidepressants</drug> can be developed based on targeting microglia-, PUFAs-, glucocorticoid- and gut microbiota-mediated cellular pathways. In addition, the authors call for a wider application of novel model organisms, such as <animal>zebrafish</animal>, in studying shared, evolutionarily conserved (and therefore, core) neuro-immune mechanisms of <DDF>depression</DDF>.",
"role": "assistant"
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28843021
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nThe nasal and gut microbiome in Parkinson's disease and idiopathic rapid eye movement sleep behavior disorder. Increasing evidence connects the gut microbiota and the onset and/or phenotype of Parkinson's disease (PD). Differences in the abundances of specific bacterial taxa have been reported in PD patients. It is, however, unknown whether these differences can be observed in individuals at high risk, for example, with idiopathic rapid eye movement sleep behavior disorder, a prodromal condition of α-synuclein aggregation disorders including PD. To compare microbiota in carefully preserved nasal wash and stool samples of subjects with idiopathic rapid eye movement sleep behavior disorder, manifest PD, and healthy individuals. Microbiota of flash-frozen stool and nasal wash samples from 76 PD patients, 21 idiopathic rapid eye movement sleep behavior disorder patients, and 78 healthy controls were assessed by 16S and 18S ribosomal RNA amplicon sequencing. Seventy variables, related to demographics, clinical parameters including nonmotor symptoms, and sample processing, were analyzed in relation to microbiome variability and controlled differential analyses were performed. Differentially abundant gut microbes, such as Akkermansia, were observed in PD, but no strong differences in nasal microbiota. Eighty percent of the differential gut microbes in PD versus healthy controls showed similar trends in idiopathic rapid eye movement sleep behavior disorder, for example, Anaerotruncus and several Bacteroides spp., and correlated with nonmotor symptoms. Metagenomic sequencing of select samples enabled the reconstruction of genomes of so far uncharacterized differentially abundant organisms. Our study reveals differential abundances of gut microbial taxa in PD and its prodrome idiopathic rapid eye movement sleep behavior disorder in comparison to the healthy controls, and highlights the potential of metagenomics to identify and characterize microbial taxa, which are enriched or depleted in PD and/or idiopathic rapid eye movement sleep behavior disorder. © 2017 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.",
"role": "user"
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{
"content": "The <microbiome>nasal and gut microbiome</microbiome> in <DDF>Parkinson's disease</DDF> and <DDF>idiopathic rapid eye movement sleep behavior disorder</DDF>. Increasing evidence connects the <microbiome>gut microbiota</microbiome> and the onset and/or phenotype of <DDF>Parkinson's disease</DDF> (<DDF>PD</DDF>). Differences in the abundances of specific bacterial taxa have been reported in <human>PD patients</human>. It is, however, unknown whether these differences can be observed in individuals at high risk, for example, with <DDF>idiopathic rapid eye movement sleep behavior disorder</DDF>, a prodromal condition of <DDF>α-synuclein aggregation disorders</DDF> including <DDF>PD</DDF>. To compare microbiota in carefully preserved nasal wash and stool samples of subjects with <DDF>idiopathic rapid eye movement sleep behavior disorder</DDF>, <DDF>manifest PD</DDF>, and <human>healthy individuals</human>. Microbiota of flash-frozen stool and nasal wash samples from 76 <human>PD patients</human>, 21 <human>idiopathic rapid eye movement sleep behavior disorder patients</human>, and 78 <human>healthy controls</human> were assessed by <biomedical technique>16S and 18S ribosomal RNA amplicon sequencing</biomedical technique>. Seventy variables, related to demographics, clinical parameters including <DDF>nonmotor symptoms</DDF>, and sample processing, were analyzed in relation to microbiome variability and controlled differential analyses were performed. Differentially abundant <bacteria>gut microbes</bacteria>, such as <bacteria>Akkermansia</bacteria>, were observed in <DDF>PD</DDF>, but no strong differences in <microbiome>nasal microbiota</microbiome>. Eighty percent of the differential <bacteria>gut microbes</bacteria> in <human>PD</human> versus <human>healthy controls</human> showed similar trends in <DDF>idiopathic rapid eye movement sleep behavior disorder</DDF>, for example, <bacteria>Anaerotruncus</bacteria> and several <bacteria>Bacteroides spp.</bacteria>, and correlated with <DDF>nonmotor symptoms</DDF>. <biomedical technique>Metagenomic sequencing</biomedical technique> of select samples enabled the reconstruction of genomes of so far uncharacterized differentially abundant organisms. Our study reveals differential abundances of gut microbial taxa in <DDF>PD</DDF> and its <DDF>prodrome idiopathic rapid eye movement sleep behavior disorder</DDF> in comparison to the <human>healthy controls</human>, and highlights the potential of <biomedical technique>metagenomics</biomedical technique> to identify and characterize microbial taxa, which are enriched or depleted in <DDF>PD</DDF> and/or <DDF>idiopathic rapid eye movement sleep behavior disorder</DDF>. © 2017 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.",
"role": "assistant"
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28852308
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nInfluence of gut microbiota on neuropsychiatric disorders. The last decade has witnessed a growing appreciation of the fundamental role played by an early assembly of a diverse and balanced gut microbiota and its subsequent maintenance for future health of the host. Gut microbiota is currently viewed as a key regulator of a fluent bidirectional dialogue between the gut and the brain (gut-brain axis). A number of preclinical studies have suggested that the microbiota and its genome (microbiome) may play a key role in neurodevelopmental and neurodegenerative disorders. Furthermore, alterations in the gut microbiota composition in humans have also been linked to a variety of neuropsychiatric conditions, including depression, autism and Parkinson's disease. However, it is not yet clear whether these changes in the microbiome are causally related to such diseases or are secondary effects thereof. In this respect, recent studies in animals have indicated that gut microbiota transplantation can transfer a behavioral phenotype, suggesting that the gut microbiota may be a modifiable factor modulating the development or pathogenesis of neuropsychiatric conditions. Further studies are warranted to establish whether or not the findings of preclinical animal experiments can be generalized to humans. Moreover, although different communication routes between the microbiota and brain have been identified, further studies must elucidate all the underlying mechanisms involved. Such research is expected to contribute to the design of strategies to modulate the gut microbiota and its functions with a view to improving mental health, and thus provide opportunities to improve the management of psychiatric diseases. Here, we review the evidence supporting a role of the gut microbiota in neuropsychiatric disorders and the state of the art regarding the mechanisms underlying its contribution to mental illness and health. We also consider the stages of life where the gut microbiota is more susceptible to the effects of environmental stressors, and the possible microbiota-targeted intervention strategies that could improve health status and prevent psychiatric disorders in the near future.",
"role": "user"
},
{
"content": "Influence of <microbiome>gut microbiota</microbiome> on <DDF>neuropsychiatric disorders</DDF>. The last decade has witnessed a growing appreciation of the fundamental role played by an early assembly of a diverse and balanced <microbiome>gut microbiota</microbiome> and its subsequent maintenance for future health of the host. <microbiome>Gut microbiota</microbiome> is currently viewed as a key regulator of a fluent bidirectional dialogue between the <anatomical location>gut</anatomical location> and the <anatomical location>brain</anatomical location> (gut-brain axis). A number of preclinical studies have suggested that the microbiota and its genome (microbiome) may play a key role in <DDF>neurodevelopmental and neurodegenerative disorders</DDF>. Furthermore, alterations in the gut microbiota composition in <human>humans</human> have also been linked to a variety of <DDF>neuropsychiatric conditions</DDF>, including <DDF>depression</DDF>, <DDF>autism</DDF> and <DDF>Parkinson's disease</DDF>. However, it is not yet clear whether these changes in the microbiome are causally related to such diseases or are secondary effects thereof. In this respect, recent studies in <animal>animals</animal> have indicated that gut microbiota transplantation can transfer a behavioral phenotype, suggesting that the <microbiome>gut microbiota</microbiome> may be a modifiable factor modulating the development or pathogenesis of <DDF>neuropsychiatric conditions</DDF>. Further studies are warranted to establish whether or not the findings of preclinical animal experiments can be generalized to <human>humans</human>. Moreover, although different communication routes between the <microbiome>microbiota</microbiome> and <anatomical location>brain</anatomical location> have been identified, further studies must elucidate all the underlying mechanisms involved. Such research is expected to contribute to the design of strategies to modulate the <microbiome>gut microbiota</microbiome> and its functions with a view to improving mental health, and thus provide opportunities to improve the management of <DDF>psychiatric diseases</DDF>. Here, we review the evidence supporting a role of the <microbiome>gut microbiota</microbiome> in <DDF>neuropsychiatric disorders</DDF> and the state of the art regarding the mechanisms underlying its contribution to <DDF>mental illness</DDF> and health. We also consider the stages of life where the <microbiome>gut microbiota</microbiome> is more susceptible to the effects of environmental stressors, and the possible microbiota-targeted intervention strategies that could improve health status and prevent <DDF>psychiatric disorders</DDF> in the near future.",
"role": "assistant"
}
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29249803
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nPossible role of the gut microbiota-brain axis in the antidepressant effects of (R)-ketamine in a social defeat stress model. Accumulating evidence suggests that the gut microbiota-brain axis plays a role in the pathogenesis of depression, thereby contributing to the antidepressant actions of certain compounds. (R)-ketamine has a greater potency and longer-lasting antidepressant effects than (S)-ketamine. Here, we investigated whether the gut microbiota plays a role in the antidepressant effects of these two ketamine enantiomers. The role of the gut microbiota in the antidepressant effects of ketamine enantiomers in a chronic social defeat stress (CSDS) model of depression was examined using 16S ribosomal RNA gene sequencing of fecal samples. At the phylum level, CSDS-susceptible mice showed alterations in the levels of Tenericutes and Actinobacteria; however, neither ketamine enantiomers influenced these alterations. At the class level, both ketamine enantiomers significantly attenuated the increase in the levels of Deltaproteobacteria in the susceptible mice after CSDS. Furthermore, (R)-ketamine, but not (S)-ketamine, significantly attenuated the reduction in the levels of Mollicutes in the susceptible mice. At the genus level, both ketamine enantiomers significantly attenuated the decrease in the levels of Butyricimonas in the susceptible mice. Notably, (R)-ketamine was more potent than (S)-ketamine at reducing the levels of Butyricimonas in the susceptible mice. In conclusion, this study suggests that the antidepressant effects of two enantiomers of ketamine in CSDS model may be partly mediated by the restoration of the gut microbiota. Furthermore, the specific effect of (R)-ketamine on the levels of Mollicutes and Butyricimonas may explain its robust antidepressant action.",
"role": "user"
},
{
"content": "Possible role of the gut microbiota-brain axis in the antidepressant effects of <drug>(R)-ketamine</drug> in a social defeat stress model. Accumulating evidence suggests that the gut microbiota-brain axis plays a role in the pathogenesis of <DDF>depression</DDF>, thereby contributing to the antidepressant actions of certain compounds. <drug>(R)-ketamine</drug> has a greater potency and longer-lasting antidepressant effects than <drug>(S)-ketamine</drug>. Here, we investigated whether the <microbiome>gut microbiota</microbiome> plays a role in the antidepressant effects of these two <drug>ketamine enantiomers</drug>. The role of the <microbiome>gut microbiota</microbiome> in the antidepressant effects of <drug>ketamine enantiomers</drug> in a chronic social defeat stress (CSDS) model of <DDF>depression</DDF> was examined using <biomedical technique>16S ribosomal RNA gene sequencing</biomedical technique> of fecal samples. At the phylum level, <animal>CSDS-susceptible mice</animal> showed alterations in the levels of <bacteria>Tenericutes</bacteria> and <bacteria>Actinobacteria</bacteria>; however, neither <drug>ketamine enantiomers</drug> influenced these alterations. At the class level, both <drug>ketamine enantiomers</drug> significantly attenuated the increase in the levels of <bacteria>Deltaproteobacteria</bacteria> in the <animal>susceptible mice</animal> after CSDS. Furthermore, <drug>(R)-ketamine</drug>, but not <drug>(S)-ketamine</drug>, significantly attenuated the reduction in the levels of <bacteria>Mollicutes</bacteria> in the <animal>susceptible mice</animal>. At the genus level, both <drug>ketamine enantiomers</drug> significantly attenuated the decrease in the levels of <bacteria>Butyricimonas</bacteria> in the <animal>susceptible mice</animal>. Notably, <drug>(R)-ketamine</drug> was more potent than <drug>(S)-ketamine</drug> at reducing the levels of <bacteria>Butyricimonas</bacteria> in the <animal>susceptible mice</animal>. In conclusion, this study suggests that the antidepressant effects of two enantiomers of <drug>ketamine</drug> in CSDS model may be partly mediated by the restoration of the <microbiome>gut microbiota</microbiome>. Furthermore, the specific effect of <drug>(R)-ketamine</drug> on the levels of <bacteria>Mollicutes</bacteria> and <bacteria>Butyricimonas</bacteria> may explain its robust antidepressant action.",
"role": "assistant"
}
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29955222
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nAncient <i>Thali</i> Diet: Gut Microbiota, Immunity, and Health. Diet provides macronutrients (carbohydrates, proteins, and fats), micronutrients (vitamins and minerals), and phytochemicals (non-nutrient bioactive compounds). Emerging evidence suggests that above dietary components can directly impact the composition and metabolic activity of the mammalian gut microbiota and in turn, affect both physical and mental health. There is a growing recognition that rise in chronic disease burden in Western countries may due to progressive loss of beneficial bacteria and microbial diversity. This perspective explores the possibility of using Indian <i>thali</i>, an ancient approach to diet that provides both fiber and different phytochemicals by incorporating a variety of plant foods in different colors. This variety helps to restore diversity in the gut bacteria and may potentially prevent or reverse chronic disease, such as colon cancer or type 2 diabetes.",
"role": "user"
},
{
"content": "Ancient <i>Thali</i> Diet: <microbiome>Gut Microbiota</microbiome>, Immunity, and Health. Diet provides <chemical>macronutrients</chemical> (<chemical>carbohydrates</chemical>, <chemical>proteins</chemical>, and <chemical>fats</chemical>), <chemical>micronutrients</chemical> (<chemical>vitamins</chemical> and <chemical>minerals</chemical>), and <chemical>phytochemicals</chemical> (<chemical>non-nutrient bioactive compounds</chemical>). Emerging evidence suggests that above dietary components can directly impact the composition and metabolic activity of the <microbiome>mammalian gut microbiota</microbiome> and in turn, affect both physical and mental health. There is a growing recognition that rise in chronic disease burden in Western countries may due to progressive loss of beneficial bacteria and microbial diversity. This perspective explores the possibility of using Indian <i>thali</i>, an ancient approach to diet that provides both <chemical>fiber</chemical> and different <chemical>phytochemicals</chemical> by incorporating a variety of <food>plant foods</food> in different colors. This variety helps to restore diversity in the <bacteria>gut bacteria</bacteria> and may potentially prevent or reverse <DDF>chronic disease</DDF>, such as <DDF>colon cancer</DDF> or <DDF>type 2 diabetes</DDF>.",
"role": "assistant"
}
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30033172
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nTowards microbiome-informed dietary recommendations for promoting metabolic and mental health: Opinion papers of the MyNewGut project. The gut microbiota coexists in partnership with the human host through adaptations to environmental and physiological changes that help maintain dynamic homeostatic healthy states. Break-down of this delicate balance under sustained exposure to stressors (e.g. unhealthy diets) can, however, contribute to the onset of disease. Diet is a key modifiable environmental factor that modulates the gut microbiota and its metabolic capacities that, in turn, could impact human physiology. On this basis, the diet and the gut microbiota could act as synergistic forces that provide resilience against disease or that speed the progress from health to disease states. Associations between unhealthy dietary patterns, non-communicable diseases and intestinal dysbiosis can be explained by this hypothesis. Translational studies showing that dietary-induced alterations in microbial communities recapitulate some of the pathological features of the original host further support this notion. In this introductory paper by the European project MyNewGut, we briefly summarize the investigations conducted to better understand the role of dietary patterns and food components in metabolic and mental health and the specificities of the microbiome-mediating mechanisms. We also discuss how advances in the understanding of the microbiome's role in dietary health effects can help to provide acceptable scientific grounds on which to base dietary advice for promoting healthy living.",
"role": "user"
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{
"content": "Towards microbiome-informed dietary recommendations for promoting metabolic and mental health: Opinion papers of the MyNewGut project. The <microbiome>gut microbiota</microbiome> coexists in partnership with the <human>human host</human> through adaptations to environmental and physiological changes that help maintain dynamic homeostatic healthy states. Break-down of this delicate balance under sustained exposure to stressors (e.g. unhealthy diets) can, however, contribute to the onset of disease. Diet is a key modifiable environmental factor that modulates the <microbiome>gut microbiota</microbiome> and its metabolic capacities that, in turn, could impact human physiology. On this basis, the diet and the <microbiome>gut microbiota</microbiome> could act as synergistic forces that provide resilience against disease or that speed the progress from health to disease states. Associations between unhealthy dietary patterns, <DDF>non-communicable diseases</DDF> and <DDF>intestinal dysbiosis</DDF> can be explained by this hypothesis. Translational studies showing that <DDF>dietary-induced alterations</DDF> in microbial communities recapitulate some of the pathological features of the original host further support this notion. In this introductory paper by the European project MyNewGut, we briefly summarize the investigations conducted to better understand the role of dietary patterns and food components in metabolic and mental health and the specificities of the microbiome-mediating mechanisms. We also discuss how advances in the understanding of the microbiome's role in dietary health effects can help to provide acceptable scientific grounds on which to base dietary advice for promoting healthy living.",
"role": "assistant"
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30072879
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nEffects of Sub-Chronic MPTP Exposure on Behavioral and Cognitive Performance and the Microbiome of Wild-Type and mGlu8 Knockout Female and Male Mice. Motor dysfunction is a hallmark of Parkinson's disease (PD); however, non-motor symptoms such as gastrointestinal dysfunction often arise prior to motor symptoms. Alterations in the gut microbiome have been proposed as the earliest event in PD pathogenesis. PD symptoms often demonstrate sex differences. Glutamatergic neurotransmission has long been linked to PD pathology. Metabotropic glutamate receptors (mGlu), a family of G protein-coupled receptors, are divided into three groups, with group III mGlu receptors mainly localized presynaptically where they can inhibit glutamate release in the CNS as well as in the gut. Additionally, the gut microbiome can communicate with the CNS via the gut-brain axis. Here, we assessed whether deficiency of metabotropic glutamate receptor 8 (mGlu8), group III mGlu, modulates the effects of the neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), on behavioral and cognitive performance in female and male mice. We studied whether these effects are associated with changes in striatal tyrosine hydroxylase (TH) levels and the gut microbiome. Two-week sub-chronic MPTP increased activity of female and male wild-type (WT) and mGlu8 knockout (KO) mice in the open field. MPTP also showed genotype- and sex-dependent effects. MPTP increased the time WT, but not KO, females and males spent exploring objects. In WT mice, MPTP improved sensorimotor function in males but impaired it in females. Further, MPTP impaired cued fear memory in WT, but not KO, male mice. MPTP reduced striatal TH levels in WT and KO mice but these effects were only pronounced in males. MPTP treatment and genotype affected the diversity of the gut microbiome. In addition, there were significant associations between microbiome α-diversity and sensorimotor performance, as well as microbiome composition and fear learning. These results indicate that specific taxa may directly affect motor and fear learning or that the same physiological effects that enhance both forms of learning also alter diversity of the gut microbiome. MPTP's effect on motor and cognitive performance may then be, at least in part, be mediated by the gut microbiome. These data also support mGlu8 as a novel therapeutic target for PD and highlight the importance of including both sexes in preclinical studies.",
"role": "user"
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{
"content": "Effects of Sub-Chronic MPTP Exposure on Behavioral and Cognitive Performance and the Microbiome of <animal>Wild-Type and mGlu8 Knockout Female and Male Mice</animal>. <DDF>Motor dysfunction</DDF> is a hallmark of <DDF>Parkinson's disease</DDF> (<DDF>PD</DDF>); however, non-motor symptoms such as <DDF>gastrointestinal dysfunction</DDF> often arise prior to motor symptoms. Alterations in the <microbiome>gut microbiome</microbiome> have been proposed as the earliest event in <DDF>PD pathogenesis</DDF>. PD symptoms often demonstrate sex differences. Glutamatergic neurotransmission has long been linked to <DDF>PD pathology</DDF>. <chemical>Metabotropic glutamate receptors</chemical> (<chemical>mGlu</chemical>), a family of <chemical>G protein-coupled receptors</chemical>, are divided into three groups, with <chemical>group III mGlu receptors</chemical> mainly localized presynaptically where they can inhibit glutamate release in the <anatomical location>CNS</anatomical location> as well as in the <anatomical location>gut</anatomical location>. Additionally, the <microbiome>gut microbiome</microbiome> can communicate with the <anatomical location>CNS</anatomical location> via the gut-brain axis. Here, we assessed whether deficiency of <chemical>metabotropic glutamate receptor 8</chemical> (<chemical>mGlu8</chemical>), <chemical>group III mGlu</chemical>, modulates the effects of the neurotoxin, <chemical>1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine</chemical> (<chemical>MPTP</chemical>), on behavioral and cognitive performance in <animal>female and male mice</animal>. We studied whether these effects are associated with changes in <gene>striatal tyrosine hydroxylase</gene> (<gene>TH</gene>) levels and the <microbiome>gut microbiome</microbiome>. Two-week sub-chronic MPTP increased activity of <animal>female and male wild-type (WT) and mGlu8 knockout (KO) mice</animal> in the open field. <chemical>MPTP</chemical> also showed genotype- and sex-dependent effects. <chemical>MPTP</chemical> increased the time <animal>WT</animal>, but not <animal>KO</animal>, females and males spent exploring objects. In <animal>WT mice</animal>, <chemical>MPTP</chemical> improved sensorimotor function in <animal>males</animal> but impaired it in <animal>females</animal>. Further, <chemical>MPTP</chemical> impaired cued fear memory in <animal>WT</animal>, but not <animal>KO</animal>, male mice. <chemical>MPTP</chemical> reduced striatal TH levels in <animal>WT and KO mice</animal> but these effects were only pronounced in <animal>males</animal>. MPTP treatment and genotype affected the diversity of the <microbiome>gut microbiome</microbiome>. In addition, there were significant associations between microbiome α-diversity and sensorimotor performance, as well as microbiome composition and fear learning. These results indicate that specific taxa may directly affect motor and fear learning or that the same physiological effects that enhance both forms of learning also alter diversity of the <microbiome>gut microbiome</microbiome>. MPTP's effect on motor and cognitive performance may then be, at least in part, be mediated by the <microbiome>gut microbiome</microbiome>. These data also support <chemical>mGlu8</chemical> as a novel therapeutic target for <DDF>PD</DDF> and highlight the importance of including both sexes in preclinical studies.",
"role": "assistant"
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30258234
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nMicroglia in neurodegeneration. The neuroimmune system is involved in development, normal functioning, aging, and injury of the central nervous system. Microglia, first described a century ago, are the main neuroimmune cells and have three essential functions: a sentinel function involved in constant sensing of changes in their environment, a housekeeping function that promotes neuronal well-being and normal operation, and a defense function necessary for responding to such changes and providing neuroprotection. Microglia use a defined armamentarium of genes to perform these tasks. In response to specific stimuli, or with neuroinflammation, microglia also have the capacity to damage and kill neurons. Injury to neurons in Alzheimer's, Parkinson's, Huntington's, and prion diseases, as well as in amyotrophic lateral sclerosis, frontotemporal dementia, and chronic traumatic encephalopathy, results from disruption of the sentinel or housekeeping functions and dysregulation of the defense function and neuroinflammation. Pathways associated with such injury include several sensing and housekeeping pathways, such as the Trem2, Cx3cr1 and progranulin pathways, which act as immune checkpoints to keep the microglial inflammatory response under control, and the scavenger receptor pathways, which promote clearance of injurious stimuli. Peripheral interference from systemic inflammation or the gut microbiome can also alter progression of such injury. Initiation or exacerbation of neurodegeneration results from an imbalance between these microglial functions; correcting such imbalance may be a potential mode for therapy.",
"role": "user"
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{
"content": "Microglia in <DDF>neurodegeneration</DDF>. The neuroimmune system is involved in development, normal functioning, aging, and injury of the central nervous system. Microglia, first described a century ago, are the main neuroimmune cells and have three essential functions: a sentinel function involved in constant sensing of changes in their environment, a housekeeping function that promotes neuronal well-being and normal operation, and a defense function necessary for responding to such changes and providing neuroprotection. Microglia use a defined armamentarium of genes to perform these tasks. In response to specific stimuli, or with <DDF>neuroinflammation</DDF>, microglia also have the capacity to damage and kill neurons. <DDF>Injury to neurons</DDF> in <DDF>Alzheimer's</DDF>, <DDF>Parkinson's</DDF>, <DDF>Huntington's</DDF>, and prion diseases, as well as in <DDF>amyotrophic lateral sclerosis</DDF>, <DDF>frontotemporal dementia</DDF>, and <DDF>chronic traumatic encephalopathy</DDF>, results from <DDF>disruption of the sentinel or housekeeping functions</DDF> and <DDF>dysregulation of the defense function</DDF> and <DDF>neuroinflammation</DDF>. Pathways associated with such injury include several sensing and housekeeping pathways, such as the <gene>Trem2</gene>, <gene>Cx3cr1</gene> and progranulin pathways, which act as immune checkpoints to keep the <DDF>microglial inflammatory response</DDF> under control, and the scavenger receptor pathways, which promote clearance of injurious stimuli. Peripheral interference from <DDF>systemic inflammation</DDF> or the <microbiome>gut microbiome</microbiome> can also alter progression of such injury. Initiation or exacerbation of <DDF>neurodegeneration</DDF> results from an imbalance between these microglial functions; correcting such imbalance may be a potential mode for therapy.",
"role": "assistant"
}
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30317530
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nAn insight into gut microbiota and its functionalities. Gut microbiota has evolved along with their hosts and is an integral part of the human body. Microbiota acquired at birth develops in parallel as the host develops and maintains its temporal stability and diversity through adulthood until death. Recent developments in genome sequencing technologies, bioinformatics and culturomics have enabled researchers to explore the microbiota and in particular their functions at more detailed level than before. The accumulated evidences suggest that though a part of the microbiota is conserved, the dynamic members vary along the gastrointestinal tract, from infants to elderly, primitive tribes to modern societies and in different health conditions. Though the gut microbiota is dynamic, it performs some basic functions in the immunological, metabolic, structural and neurological landscapes of the human body. Gut microbiota also exerts significant influence on both physical and mental health of an individual. An in-depth understanding of the functioning of gut microbiota has led to some very exciting developments in therapeutics, such as prebiotics, probiotics, drugs and faecal transplantation leading to improved health.",
"role": "user"
},
{
"content": "An insight into <microbiome>gut microbiota</microbiome> and its functionalities. <microbiome>Gut microbiota</microbiome> has evolved along with their hosts and is an integral part of the <anatomical location>human body</anatomical location>. Microbiota acquired at birth develops in parallel as the host develops and maintains its temporal stability and diversity through adulthood until death. Recent developments in <biomedical technique>genome sequencing technologies</biomedical technique>, <biomedical technique>bioinformatics</biomedical technique> and <biomedical technique>culturomics</biomedical technique> have enabled researchers to explore the <microbiome>microbiota</microbiome> and in particular their functions at more detailed level than before. The accumulated evidences suggest that though a part of the <microbiome>microbiota</microbiome> is conserved, the dynamic members vary along the <anatomical location>gastrointestinal tract</anatomical location>, from <human>infants</human> to <human>elderly</human>, primitive tribes to modern societies and in different health conditions. Though the <microbiome>gut microbiota</microbiome> is dynamic, it performs some basic functions in the immunological, metabolic, structural and neurological landscapes of the <anatomical location>human body</anatomical location>. <microbiome>Gut microbiota</microbiome> also exerts significant influence on both physical and mental health of an <human>individual</human>. An in-depth understanding of the functioning of <microbiome>gut microbiota</microbiome> has led to some very exciting developments in therapeutics, such as <dietary supplement>prebiotics</dietary supplement>, <dietary supplement>probiotics</dietary supplement>, <drug>drugs</drug> and faecal transplantation leading to improved health.",
"role": "assistant"
}
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30518033
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nDifferences in Anxiety Levels of Various Murine Models in Relation to the Gut Microbiota Composition. Psychobiotics are probiotic strains that confer mental health benefits to the host through the modulation of the gut microbial population. Mounting evidence shows that the gut microbiota play an important role in communication within the gut⁻brain axis. However, the relationship between the host genetics and the gut microbiota and their influence on anxiety are still not fully understood. Hence, in our research, we attempted to draw a connection between host genetics, microbiota composition, and anxiety by performing an elevated plus maze (EPM) test on four genetically different mice. Four different breeds of 5-week-old mice were used in this experiment: Balb/c, Orient C57BL/6N, Taconic C57BL/6N, and Taconic C57BL/6J. After 1 week of adaptation, their initial anxiety level was monitored using the EPM test via an EthoVision XT, a standardized software used for behavorial testing. Significant differences in the initial anxiety level and microbial composition were detected. Subsequently, the microbiota of each group was modulated by the administration of either a probiotic, fecal microbiota transplantation, or antibiotics. Changes were observed in host anxiety levels in correlation to the shift of the gut microbiota. Our results suggest that the microbiota, host genetics, and psychological symptoms are strongly related, yet the deeper mechanistic links need further exploration.",
"role": "user"
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{
"content": "Differences in <DDF>Anxiety Levels</DDF> of Various Murine Models in Relation to the <microbiome>Gut Microbiota Composition</microbiome>. <dietary supplement>Psychobiotics</dietary supplement> are <dietary supplement>probiotic strains</dietary supplement> that confer mental health benefits to the host through the modulation of the gut microbial population. Mounting evidence shows that the <microbiome>gut microbiota</microbiome> play an important role in communication within the gut⁻brain axis. However, the relationship between the host genetics and the <microbiome>gut microbiota</microbiome> and their influence on <DDF>anxiety</DDF> are still not fully understood. Hence, in our research, we attempted to draw a connection between host genetics, microbiota composition, and <DDF>anxiety</DDF> by performing an <biomedical technique>elevated plus maze (EPM) test</biomedical technique> on four genetically different <animal>mice</animal>. Four different breeds of <animal>5-week-old mice</animal> were used in this experiment: <animal>Balb/c</animal>, <animal>Orient C57BL/6N</animal>, <animal>Taconic C57BL/6N</animal>, and <animal>Taconic C57BL/6J</animal>. After 1 week of adaptation, their initial <DDF>anxiety level</DDF> was monitored using the <biomedical technique>EPM test</biomedical technique> via an EthoVision XT, a standardized software used for <biomedical technique>behavorial testing</biomedical technique>. Significant differences in the initial <DDF>anxiety</DDF> level and microbial composition were detected. Subsequently, the microbiota of each group was modulated by the administration of either a <dietary supplement>probiotic</dietary supplement>, fecal microbiota transplantation, or <drug>antibiotics</drug>. Changes were observed in <DDF>host anxiety levels</DDF> in correlation to the shift of the <microbiome>gut microbiota</microbiome>. Our results suggest that the microbiota, host genetics, and <DDF>psychological symptoms</DDF> are strongly related, yet the deeper mechanistic links need further exploration.",
"role": "assistant"
}
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30528936
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nRole of Actinobacteria and Coriobacteriia in the antidepressant effects of ketamine in an inflammation model of depression. Ketamine, an N-methyl-d-aspartic acid receptor (NMDAR) antagonist, elicits rapid-acting and sustained antidepressant effects in treatment-resistant depressed patients. Accumulating evidence suggests that gut microbiota via the gut-brain axis play a role in the pathogenesis of depression, thereby contributing to the antidepressant actions of certain compounds. Here we investigated the role of gut microbiota in the antidepressant effects of ketamine in lipopolysaccharide (LPS)-induced inflammation model of depression. Ketamine (10 mg/kg) significantly attenuated the increased immobility time in forced swimming test (FST), which was associated with the improvements in α-diversity, consisting of Shannon, Simpson and Chao 1 indices. In addition to α-diversity, β-diversity, such as principal coordinates analysis (PCoA), and linear discriminant analysis (LDA) coupled with effect size measurements (LEfSe), showed a differential profile after ketamine treatment. Furthermore, a total of 30 bacteria were significantly altered in the LPS + saline treated mice and LPS + ketamine treated mice. Interestingly, two bacteria, including the phylum Actinobacteria and the class Coriobacteriia were significantly correlated with the immobility time of FST. Importantly, the receiver operating characteristic (ROC) curves demonstrated that the phylum Actinobacteria and the class Coriobacteriia were potential biomarker for the antidepressant effects of ketamine in an inflammation model. These findings suggest that antidepressant effects of ketamine might be related to the regulation of abnormal composition of gut microbiota, and that the phylum Actinobacteria and the class Coriobacteriia might be potential biomarkers for ketamine's antidepressant efficacy.",
"role": "user"
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{
"content": "Role of <bacteria>Actinobacteria</bacteria> and <bacteria>Coriobacteriia</bacteria> in the antidepressant effects of <drug>ketamine</drug> in an inflammation model of <DDF>depression</DDF>. <drug>Ketamine</drug>, an <chemical>N-methyl-d-aspartic acid receptor</chemical> (<chemical>NMDAR</chemical>) antagonist, elicits rapid-acting and sustained antidepressant effects in <human>treatment-resistant depressed patients</human>. Accumulating evidence suggests that <microbiome>gut microbiota</microbiome> via the gut-brain axis play a role in the pathogenesis of <DDF>depression</DDF>, thereby contributing to the antidepressant actions of certain compounds. Here we investigated the role of <microbiome>gut microbiota</microbiome> in the antidepressant effects of <drug>ketamine</drug> in <DDF>lipopolysaccharide (LPS)-induced inflammation</DDF> model of <DDF>depression</DDF>. <drug>Ketamine</drug> (10 mg/kg) significantly attenuated the increased <DDF>immobility time</DDF> in <biomedical technique>forced swimming test</biomedical technique> (<biomedical technique>FST</biomedical technique>), which was associated with the improvements in α-diversity, consisting of <statistical technique>Shannon, Simpson and Chao 1 indices</statistical technique>. In addition to α-diversity, β-diversity, such as <statistical technique>principal coordinates analysis</statistical technique> (<statistical technique>PCoA</statistical technique>), and <statistical technique>linear discriminant analysis</statistical technique> (<statistical technique>LDA</statistical technique>) coupled with <statistical technique>effect size measurements</statistical technique> (<statistical technique>LEfSe</statistical technique>), showed a differential profile after <drug>ketamine</drug> treatment. Furthermore, a total of 30 bacteria were significantly altered in the <animal>LPS + saline treated mice</animal> and <animal>LPS + ketamine treated mice</animal>. Interestingly, two bacteria, including the phylum <bacteria>Actinobacteria</bacteria> and the class <bacteria>Coriobacteriia</bacteria> were significantly correlated with the <DDF>immobility</DDF> time of <biomedical technique>FST</biomedical technique>. Importantly, the <statistical technique>receiver operating characteristic (ROC) curves</statistical technique> demonstrated that the phylum <bacteria>Actinobacteria</bacteria> and the class <bacteria>Coriobacteriia</bacteria> were potential biomarker for the antidepressant effects of <drug>ketamine</drug> in an inflammation model. These findings suggest that antidepressant effects of <drug>ketamine</drug> might be related to the regulation of abnormal composition of <microbiome>gut microbiota</microbiome>, and that the phylum <bacteria>Actinobacteria</bacteria> and the class <bacteria>Coriobacteriia</bacteria> might be potential biomarkers for <drug>ketamine</drug>'s antidepressant efficacy.",
"role": "assistant"
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30659564
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nCan microbiology affect psychiatry? A link between gut microbiota and psychiatric disorders. Every single human consists of thousands of genes, billions of neurons and trillions of bacteria. There is a rapidly growing number of data that links the gut microbiome to the development and functioning of the central nervous system, which is a currently proposed paradigm shift in neuroscience. Knowledge on the relationship between gut microbiota and mental disorders is constantly increasing. This phenomenon is known as \"gut-brain axis\". The strongest evidence for the role of microbes in the gut-brain axis comes from animal studies. Nevertheless, the gutbrain crosstalk is a bidirectional communication system that not only provides gastrointestinal homeostasis, but can also affect motivation as well as higher cognitive functions. Moreover, gut microbiome can be associated with obesity and inflammatory gastrointestinal disorders. According to the recent studies, there is a link between the composition of gut microbiota and mental disorders in animals (response to depression and chronic stress). This subject requires further examination, especially taking into consideration potential therapeutic options.",
"role": "user"
},
{
"content": "Can microbiology affect psychiatry? A link between <microbiome>gut microbiota</microbiome> and <DDF>psychiatric disorders</DDF>. Every single human consists of thousands of genes, billions of neurons and trillions of bacteria. There is a rapidly growing number of data that links the <microbiome>gut microbiome</microbiome> to the development and functioning of the central nervous system, which is a currently proposed paradigm shift in neuroscience. Knowledge on the relationship between <microbiome>gut microbiota</microbiome> and <DDF>mental disorders</DDF> is constantly increasing. This phenomenon is known as \"gut-brain axis\". The strongest evidence for the role of microbes in the gut-brain axis comes from animal studies. Nevertheless, the gutbrain crosstalk is a bidirectional communication system that not only provides gastrointestinal homeostasis, but can also affect motivation as well as higher cognitive functions. Moreover, <microbiome>gut microbiome</microbiome> can be associated with <DDF>obesity</DDF> and <DDF>inflammatory gastrointestinal disorders</DDF>. According to the recent studies, there is a link between the composition of <microbiome>gut microbiota</microbiome> and <DDF>mental disorders</DDF> in animals (response to <DDF>depression</DDF> and <DDF>chronic stress</DDF>). This subject requires further examination, especially taking into consideration potential therapeutic options.",
"role": "assistant"
}
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30701194
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nAlterations in Gut Glutamate Metabolism Associated with Changes in Gut Microbiota Composition in Children with Autism Spectrum Disorder. Changes in the gut microenvironment may influence the pathogenesis of autism spectrum disorders (ASD). Here, we investigated the composition of the gut microbiota and metabolites in children with ASD. Ninety-two children with ASD and 42 age-matched children exhibiting typical development (TD) were enrolled in the two-stage study. In the discovery stage, shotgun metagenomic sequencing and liquid chromatography-mass spectrometry (LC-MS) were performed simultaneously on fecal samples obtained from 43 children in the ASD group and 31 children in the TD group. Systematic bioinformatic analyses were performed to identify gut metabolites associated with altered gut microbiota composition. At the validation stage, differential metabolites were tested using LC-MS with an additional 49 and 11 children in the ASD and TD groups, respectively. Altered glutamate metabolites were found in the ASD group, along with a decline in 2-keto-glutaramic acid and an abundance of microbiota associated with glutamate metabolism. These changes in glutamate metabolism were correlated with lower levels of the highly abundant bacteria Bacteroides vulgatus and higher levels of the potentially harmful Eggerthella lenta and Clostridium botulinum. Lower gut cortisol levels have also been identified in the ASD group and associated with changes in gut microbiota glutamate metabolism. Finally, gut 2-keto-glutaramic acid was validated as a potential biomarker for ASD. The significant changes in the gut microenvironment in children with ASD may provide new insight into the cause of ASD and aid in the search for diagnostic and therapeutic approaches. <b>IMPORTANCE</b> Multiple lines of evidence suggest that the gut microbiota may play an important role in the pathogenesis of ASD, but the specific mechanism is still unclear. Through a comprehensive gut metagenomic and metabolome study of children with ASD, alterations in gut metabolite composition were found in children with ASD, and these alterations were linked to changes in gut microbiota composition. This may give us a deeper understanding of the role of gut microbiota in the pathogenesis of ASD.",
"role": "user"
},
{
"content": "Alterations in Gut Glutamate Metabolism Associated with Changes in Gut Microbiota Composition in <human>Children</human> with <DDF>Autism Spectrum Disorder</DDF>. Changes in the gut microenvironment may influence the pathogenesis of <DDF>autism spectrum disorders</DDF> (<DDF>ASD</DDF>). Here, we investigated the composition of the <microbiome>gut microbiota</microbiome> and metabolites in <human>children</human> with <DDF>ASD</DDF>. Ninety-two <human>children</human> with <DDF>ASD</DDF> and 42 <human>age-matched children</human> exhibiting <DDF>typical development</DDF> (<DDF>TD</DDF>) were enrolled in the two-stage study. In the discovery stage, <biomedical technique>shotgun metagenomic sequencing</biomedical technique> and <biomedical technique>liquid chromatography-mass spectrometry</biomedical technique> (<biomedical technique>LC-MS</biomedical technique>) were performed simultaneously on fecal samples obtained from 43 <human>children</human> in the <human>ASD group</human> and 31 <human>children</human> in the <human>TD group</human>. Systematic <biomedical technique>bioinformatic analyses</biomedical technique> were performed to identify <chemical>gut metabolites</chemical> associated with altered gut microbiota composition. At the validation stage, differential metabolites were tested using <biomedical technique>LC-MS</biomedical technique> with an additional 49 and 11 <human>children</human> in the <human>ASD and TD groups</human>, respectively. Altered <chemical>glutamate metabolites</chemical> were found in the <human>ASD group</human>, along with a decline in <chemical>2-keto-glutaramic acid</chemical> and an abundance of microbiota associated with glutamate metabolism. These changes in glutamate metabolism were correlated with lower levels of the highly abundant bacteria <bacteria>Bacteroides vulgatus</bacteria> and higher levels of the potentially harmful <bacteria>Eggerthella lenta</bacteria> and <bacteria>Clostridium botulinum</bacteria>. Lower gut cortisol levels have also been identified in the <human>ASD group</human> and associated with changes in gut microbiota glutamate metabolism. Finally, <chemical>gut 2-keto-glutaramic acid</chemical> was validated as a potential biomarker for <DDF>ASD</DDF>. The significant changes in the gut microenvironment in <human>children</human> with <DDF>ASD</DDF> may provide new insight into the cause of <DDF>ASD</DDF> and aid in the search for diagnostic and therapeutic approaches. <b>IMPORTANCE</b> Multiple lines of evidence suggest that the <microbiome>gut microbiota</microbiome> may play an important role in the pathogenesis of <DDF>ASD</DDF>, but the specific mechanism is still unclear. Through a comprehensive <biomedical technique>gut metagenomic and metabolome study</biomedical technique> of <human>children</human> with <DDF>ASD</DDF>, alterations in gut metabolite composition were found in <human>children</human> with <DDF>ASD</DDF>, and these alterations were linked to changes in gut microbiota composition. This may give us a deeper understanding of the role of <microbiome>gut microbiota</microbiome> in the pathogenesis of <DDF>ASD</DDF>.",
"role": "assistant"
}
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30826885
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nThe Relationship Between Perinatal Mental Health and Stress: a Review of the Microbiome. Our current understanding of the underlying mechanisms and etiologies of perinatal mood and anxiety disorders (PMADs) is not clearly identified. The relationship of stress-induced adaptations (i.e., the hypothalamic-pituitary-adrenal (HPA) axis, the autonomic nervous system (ANS), the immune system) and the microbiota are potential contributors to psychopathology exhibited in women during pregnancy and postpartum and should be investigated. The stress response activates the HPA axis and dysregulates the ANS, leading to the inhibition of the parasympathetic system. Sustained high levels of cortisol, reduced heart variability, and modulated immune responses increase the vulnerability to PMAD. Bidirectional communication between the nervous system and the microbiota is an important factor to alter host homeostasis and development of PMAD. Future research in the relationship between the psychoneuroimmune system, the gut microbiota, and PMAD has the potential to be integrated in clinical practice to improve screening, diagnosis, and treatment.",
"role": "user"
},
{
"content": "The Relationship Between Perinatal Mental Health and <DDF>Stress</DDF>: a Review of the Microbiome. Our current understanding of the underlying mechanisms and etiologies of <DDF>perinatal mood and anxiety disorders</DDF> (<DDF>PMADs</DDF>) is not clearly identified. The relationship of stress-induced adaptations (i.e., the hypothalamic-pituitary-adrenal (HPA) axis, the autonomic nervous system (ANS), the immune system) and the microbiota are potential contributors to <DDF>psychopathology</DDF> exhibited in <human>women during pregnancy and postpartum</human> and should be investigated. The stress response activates the HPA axis and dysregulates the ANS, leading to the inhibition of the parasympathetic system. Sustained high levels of <chemical>cortisol</chemical>, reduced heart variability, and modulated immune responses increase the vulnerability to <DDF>PMAD</DDF>. Bidirectional communication between the nervous system and the microbiota is an important factor to alter host homeostasis and development of <DDF>PMAD</DDF>. Future research in the relationship between the psychoneuroimmune system, the <microbiome>gut microbiota</microbiome>, and <DDF>PMAD</DDF> has the potential to be integrated in clinical practice to improve screening, diagnosis, and treatment.",
"role": "assistant"
}
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30828318
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nDisentangling What We Know About Microbes and Mental Health. Much has been written in recent years about the gut-brain axis. Exciting pilot studies suggest probiotic applications to the gut can reduce anxiety and depression via the vagus nerve. But not to diminish such findings, much still needs to be considered, including the fact that the vagus nerve links to many other body sites that also host a microbiome. Questions remain that touch the core of being human: (i) Do our microbes influence happiness and to what extent? (ii) What components of the gut microbiota and their function, including as it relates to mental health, are critical and how do they differ between agile, fit hunter gatherers and obese westerners or Danes described as the happiest people on the planet? (iii) What role do environmental pollutants play in this microbes-host ecosystem? While approaching life from a reductionist perspective has a long history in science, we need to try to interrogate these health and disease issues from a wider perspective. For verification of a link between the gut microbiota and brain, and to test new therapies, human studies are needed, and are long overdue.",
"role": "user"
},
{
"content": "Disentangling What We Know About Microbes and Mental Health. Much has been written in recent years about the gut-brain axis. Exciting pilot studies suggest <dietary supplement>probiotic applications</dietary supplement> to the <anatomical location>gut</anatomical location> can reduce <DDF>anxiety</DDF> and <DDF>depression</DDF> via the <anatomical location>vagus nerve</anatomical location>. But not to diminish such findings, much still needs to be considered, including the fact that the <anatomical location>vagus nerve</anatomical location> links to many other body sites that also host a microbiome. Questions remain that touch the core of being human: (i) Do our microbes influence happiness and to what extent? (ii) What components of the <microbiome>gut microbiota</microbiome> and their function, including as it relates to mental health, are critical and how do they differ between <human>agile, fit hunter gatherers</human> and <human>obese westerners</human> or <human>Danes</human> described as the <human>happiest people</human> on the planet? (iii) What role do <chemical>environmental pollutants</chemical> play in this microbes-host ecosystem? While approaching life from a reductionist perspective has a long history in science, we need to try to interrogate these health and disease issues from a wider perspective. For verification of a link between the <microbiome>gut microbiota</microbiome> and <anatomical location>brain</anatomical location>, and to test new therapies, human studies are needed, and are long overdue.",
"role": "assistant"
}
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31132457
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nGut microbiota composition is associated with temperament traits in infants. One of the key behavioral phenotypes in infancy are different temperament traits, and certain early life temperament traits have been shown to precede later mental health problems. Differences in the gut microbiota composition (GMC) have been suggested to link with neurodevelopment. For example, toddler temperament traits have been found to associate with differences in GMC; however, studies in infants are lacking although infancy is a rapid period of neurodevelopment as well as GM development. Thus, we aimed to investigate association between infant GMC and temperament. The study population (n = 301, 53% boys) was drawn from the FinnBrain Birth Cohort Study. Stool samples were collected from the 2.5-month-old infants and sequenced with 16S Illumina MiSeq platform. GMC taxonomic composition (at Genus and OTU level), observed sample clusters, diversity and richness were investigated in relation to the maternal reports of Infant Behavior Questionnaire -Revised (IBQ-R) at the age of 6 months. Three sample clusters (Bifidobacterium/Enterobacteriaceae, Bacteroides, V. Dispar) based on GMC were identified, of which Bifidobacterium/Enterobacteriaceae-cluster presented with higher scores on the IBQ-R main dimension regulation and its subscale duration of orienting compared to Bacteroides-cluster. The clusters associated with temperament in a sex-dependent manner. The IBQ-R main dimension surgency (positive emotionality) was associated positively both with genus Bifidobacterium and Streptococcus. Alpha diversity had a negative association with negative emotionality and fear reactivity. This is the first study demonstrating associations, but not causal connections, between GMC and temperament in young infants in a prospective design.",
"role": "user"
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{
"content": "<microbiome>Gut microbiota composition</microbiome> is associated with temperament traits in <human>infants</human>. One of the key behavioral phenotypes in infancy are different temperament traits, and certain early life temperament traits have been shown to precede later <DDF>mental health problems</DDF>. Differences in the <microbiome>gut microbiota composition</microbiome> (<microbiome>GMC</microbiome>) have been suggested to link with neurodevelopment. For example, <human>toddler</human> temperament traits have been found to associate with differences in <microbiome>GMC</microbiome>; however, studies in <human>infants</human> are lacking although infancy is a rapid period of neurodevelopment as well as GM development. Thus, we aimed to investigate association between <microbiome>infant GMC</microbiome> and temperament. The study population (n = 301, 53% <human>boys</human>) was drawn from the FinnBrain Birth Cohort Study. Stool samples were collected from the <human>2.5-month-old infants</human> and sequenced with 16S Illumina MiSeq platform. <microbiome>GMC</microbiome> taxonomic composition (at Genus and OTU level), observed sample clusters, diversity and richness were investigated in relation to the maternal reports of <biomedical technique>Infant Behavior Questionnaire -Revised</biomedical technique> (<biomedical technique>IBQ-R</biomedical technique>) at the age of 6 months. Three sample clusters (<bacteria>Bifidobacterium/Enterobacteriaceae</bacteria>, <bacteria>Bacteroides</bacteria>, <bacteria>V. Dispar</bacteria>) based on <microbiome>GMC</microbiome> were identified, of which Bifidobacterium/Enterobacteriaceae-cluster presented with higher scores on the <biomedical technique>IBQ-R</biomedical technique> main dimension regulation and its subscale duration of orienting compared to Bacteroides-cluster. The clusters associated with temperament in a sex-dependent manner. The <biomedical technique>IBQ-R</biomedical technique> main dimension surgency (positive emotionality) was associated positively both with genus <bacteria>Bifidobacterium</bacteria> and <bacteria>Streptococcus</bacteria>. Alpha diversity had a negative association with negative emotionality and fear reactivity. This is the first study demonstrating associations, but not causal connections, between <microbiome>GMC</microbiome> and temperament in <human>young infants</human> in a prospective design.",
"role": "assistant"
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31148353
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nGutting the brain of inflammation: A key role of gut microbiome in human umbilical cord blood plasma therapy in Parkinson's disease model. Current therapies for Parkinson's disease (PD), including L-3,4-dihydroxyphenylalanine (L-DOPA), and clinical trials investigating dopaminergic cell transplants, have generated mixed results with the eventual induction of dyskinetic side effects. Although human umbilical cord blood (hUCB) stem/progenitor cells present with no or minimal capacity of differentiation into mature dopaminergic neurons, their transplantation significantly attenuates parkinsonian symptoms likely via bystander effects, specifically stem cell graft-mediated secretion of growth factors, anti-inflammatory cytokines, or synaptic function altogether promoting brain repair. Recognizing this non-cell replacement mechanism, we examined here the effects of intravenously transplanted combination of hUCB-derived plasma into the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced rat model of PD. Animals received repeated dosing of either hUCB-derived plasma or vehicle at 3, 5 and 10 days after induction into MPTP lesion, then behaviourally and immunohistochemically evaluated over 56 days post-lesion. Compared to vehicle treatment, transplantation with hUCB-derived plasma significantly improved motor function, gut motility and dopaminergic neuronal survival in the substantia nigra pars compacta (SNpc), which coincided with reduced pro-inflammatory cytokines in both the SNpc and the intestinal mucosa and dampened inflammation-associated gut microbiota. These novel data directly implicate a key pathological crosstalk between gut and brain ushering a new avenue of therapeutically targeting the gut microbiome with hUCB-derived stem cells and plasma for PD.",
"role": "user"
},
{
"content": "Gutting the <anatomical location>brain</anatomical location> of <DDF>inflammation</DDF>: A key role of <microbiome>gut microbiome</microbiome> in human umbilical cord blood plasma therapy in Parkinson's disease model. Current therapies for <DDF>Parkinson's disease</DDF> (<DDF>PD</DDF>), including <drug>L-3,4-dihydroxyphenylalanine (L-DOPA)</drug>, and clinical trials investigating dopaminergic cell transplants, have generated mixed results with the eventual induction of <DDF>dyskinetic side effects</DDF>. Although human umbilical cord blood (hUCB) stem/progenitor cells present with no or minimal capacity of differentiation into mature dopaminergic neurons, their transplantation significantly attenuates <DDF>parkinsonian symptoms</DDF> likely via bystander effects, specifically stem cell graft-mediated secretion of growth factors, <chemical>anti-inflammatory cytokines</chemical>, or synaptic function altogether promoting brain repair. Recognizing this non-cell replacement mechanism, we examined here the effects of intravenously transplanted combination of hUCB-derived plasma into the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced rat model of <DDF>PD</DDF>. Animals received repeated dosing of either <chemical>hUCB-derived plasma</chemical> or vehicle at 3, 5 and 10 days after induction into <DDF>MPTP lesion</DDF>, then behaviourally and immunohistochemically evaluated over 56 days post-lesion. Compared to vehicle treatment, transplantation with <chemical>hUCB-derived plasma</chemical> significantly improved motor function, gut motility and dopaminergic neuronal survival in the <anatomical location>substantia nigra pars compacta</anatomical location> (<anatomical location>SNpc</anatomical location>), which coincided with reduced <chemical>pro-inflammatory cytokines</chemical> in both the <anatomical location>SNpc</anatomical location> and the intestinal mucosa and dampened <microbiome>inflammation-associated gut microbiota</microbiome>. These novel data directly implicate a key pathological crosstalk between <anatomical location>gut</anatomical location> and <anatomical location>brain</anatomical location> ushering a new avenue of therapeutically targeting the <microbiome>gut microbiome</microbiome> with hUCB-derived stem cells and plasma for <DDF>PD</DDF>.",
"role": "assistant"
}
] |
31154909
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nUnravelled facets of milk derived opioid peptides: a focus on gut physiology, fractures and obesity. Beyond being a source of key nutrients, bovine milk influences physiological functions by synthesising bioactive peptides during the process of digestion. Some of the claimed negative health outcomes associated with milk consumption, such as cardiovascular diseases and type 1 diabetes may be attributed to an opioid peptide, beta-casomorphin-7 (BCM-7), derived from A1 beta-casein. BCM-7 exerts its function by binding to the μ-opioid receptors in the body. It is hypothesised that activation of the μ-opioid receptors in the gut can alter gut microbial composition, impair gut barrier integrity and bile acid metabolism, in addition to increasing gastrointestinal transit time and gut inflammation. Further, it is hypothesised that BCM-7 may influence fractures and obesity via μ-opioid receptor pathways. In conclusion, it appears that BCM-7 might have multiple functions pertinent to human health; however, the evidence is limited and warrants further pre-clinical and clinical studies for hypothesis confirmation.",
"role": "user"
},
{
"content": "Unravelled facets of <chemical>milk derived opioid peptides</chemical>: a focus on gut physiology, <DDF>fractures</DDF> and <DDF>obesity</DDF>. Beyond being a source of key nutrients, <food>bovine milk</food> influences physiological functions by synthesising <chemical>bioactive peptides</chemical> during the process of digestion. Some of the claimed negative health outcomes associated with milk consumption, such as <DDF>cardiovascular diseases</DDF> and <DDF>type 1 diabetes</DDF> may be attributed to an <chemical>opioid peptide</chemical>, <chemical>beta-casomorphin-7</chemical> (<chemical>BCM-7</chemical>), derived from <chemical>A1 beta-casein</chemical>. <chemical>BCM-7</chemical> exerts its function by binding to the <chemical>μ-opioid receptors</chemical> in the body. It is hypothesised that activation of the <chemical>μ-opioid receptors</chemical> in the <anatomical location>gut</anatomical location> can alter gut microbial composition, impair gut barrier integrity and bile acid metabolism, in addition to increasing gastrointestinal transit time and <DDF>gut inflammation</DDF>. Further, it is hypothesised that <chemical>BCM-7</chemical> may influence <DDF>fractures</DDF> and <DDF>obesity</DDF> via μ-opioid receptor pathways. In conclusion, it appears that <chemical>BCM-7</chemical> might have multiple functions pertinent to human health; however, the evidence is limited and warrants further pre-clinical and clinical studies for hypothesis confirmation.",
"role": "assistant"
}
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31218116
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nA 12-Week Pilot Exercise Program for Inactive Adults With Celiac Disease: Study Protocol. Individuals with celiac disease must follow a strict gluten-free diet (GFD) in order to avoid negative short- and long-term health consequences. Unfortunately, many people with celiac disease report poor quality of life (QoL) despite following a strict GFD, and up to 30% still report negative symptoms (eg, gastrointestinal upset). The purpose of the MOVE-C (understanding the relationship between the <i>M</i>icrobi<i>O</i>me, <i>V</i>itality, and <i>E</i>xercise in <i>C</i>eliac disease) pilot study is to explore the effects of a 12-week supervised progressive high-intensity interval training (HIIT) and lifestyle intervention on physiological, behavioral, and psychosocial outcomes among inactive adults with celiac disease.<b>Methods/Design:</b> Sixty inactive adults diagnosed with celiac disease will be randomized to HIIT+ or waitlist control (WLC). Participants in the HIIT+ will engage in a 12-week HIIT + lifestyle education program. HIIT sessions will be comprised of 2 workouts per week, working up to 14 × 30-second intervals at 90% maximal heart rate (HRmax) followed by 2 minutes recovery at 50% HRmax. The 6 biweekly lifestyle sessions will involve education on the promotion of a whole foods GFD, sleep hygiene, psychosocial coping skills (eg, self-compassion), and self-regulatory skills to master changes in behaviors. Assessments will occur at pre and post 12-week intervention and 3-month follow-up. WLC participants will be offered a 12-week HIIT program + online lifestyle education sessions after completing the final assessment. The primary outcomes are QoL and gut microbiota composition assessed with 16S rRNA sequencing. The secondary outcomes are markers of metabolic syndrome (waist circumference, fasting glucose, serum lipids, blood pressure, and body composition), gastrointestinal symptoms, sleep quality, adherence to a GFD, exercise behavior, self-regulatory efficacy, and self-compassion. It is hypothesized that participants in the HIIT+ will experience improvements in all outcomes when compared to those in the WLC. These improvements are expected to be maintained at the 3-month follow-up. The findings from this study will advance the knowledge regarding the effects of HIIT and lifestyle education on key outcomes for an at-risk chronic disease population. Furthermore, the findings can be used to inform future programs to improve fitness and physical and mental health outcomes for people with celiac disease.",
"role": "user"
},
{
"content": "A 12-Week Pilot Exercise Program for <human>Inactive Adults</human> With <DDF>Celiac Disease</DDF>: Study Protocol. <human>Individuals</human> with <DDF>celiac disease</DDF> must follow a strict gluten-free diet (GFD) in order to avoid negative short- and long-term health consequences. Unfortunately, many <human>people</human> with <DDF>celiac disease</DDF> report poor quality of life (QoL) despite following a strict GFD, and up to 30% still report negative symptoms (eg, <DDF>gastrointestinal upset</DDF>). The purpose of the MOVE-C (understanding the relationship between the <i>M</i>icrobi<i>O</i>me, <i>V</i>itality, and <i>E</i>xercise in <DDF><i>C</i>eliac disease</DDF>) pilot study is to explore the effects of a 12-week supervised progressive high-intensity interval training (HIIT) and lifestyle intervention on physiological, behavioral, and psychosocial outcomes among <human>inactive adults</human> with <DDF>celiac disease</DDF>.<b>Methods/Design:</b> Sixty <human>inactive adults</human> diagnosed with <DDF>celiac disease</DDF> will be randomized to HIIT+ or waitlist control (WLC). Participants in the HIIT+ will engage in a 12-week HIIT + lifestyle education program. HIIT sessions will be comprised of 2 workouts per week, working up to 14 × 30-second intervals at 90% maximal heart rate (HRmax) followed by 2 minutes recovery at 50% HRmax. The 6 biweekly lifestyle sessions will involve education on the promotion of a whole foods GFD, sleep hygiene, psychosocial coping skills (eg, self-compassion), and self-regulatory skills to master changes in behaviors. Assessments will occur at pre and post 12-week intervention and 3-month follow-up. WLC participants will be offered a 12-week HIIT program + online lifestyle education sessions after completing the final assessment. The primary outcomes are QoL and gut microbiota composition assessed with <biomedical technique>16S rRNA sequencing</biomedical technique>. The secondary outcomes are markers of <DDF>metabolic syndrome</DDF> (waist circumference, fasting glucose, <chemical>serum lipids</chemical>, blood pressure, and body composition), <DDF>gastrointestinal symptoms</DDF>, sleep quality, adherence to a GFD, exercise behavior, self-regulatory efficacy, and self-compassion. It is hypothesized that <human>participants</human> in the HIIT+ will experience improvements in all outcomes when compared to those in the WLC. These improvements are expected to be maintained at the 3-month follow-up. The findings from this study will advance the knowledge regarding the effects of HIIT and lifestyle education on key outcomes for an at-risk chronic disease population. Furthermore, the findings can be used to inform future programs to improve fitness and physical and mental health outcomes for <human>people</human> with <DDF>celiac disease</DDF>.",
"role": "assistant"
}
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31255682
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nAltered gut microbiota and mucosal immunity in patients with schizophrenia. Evidence shows that gut microbiota may play important roles in schizophrenia pathogenesis via the \"gut-brain\" axis, but the mechanisms remain unclear. Here, eighty-four patients with schizophrenia and 84 sex- and age-matched healthy controls were enrolled. Shotgun metagenomic sequencing and 16S rRNA sequencing were performed, and the gut microbiota-associated epitopes (MEs) were predicted, which, together with IgA content, were used to determine the gut microbiota composition associated with gut immune status. Patients with schizophrenia had significantly reduced gut microbiota richnesses compared with those of the healthy controls, and the gut microbiota compositions clearly distinguished the patients with schizophrenia from the healthy controls. Based on two-stage metagenomic-wide association studies, nineteen gut microbiota taxonomies were associated with schizophrenia, and the microbial dysbiosis (MD) index was calculated based on the abundance of differential taxonomies. We found that MD index was positively correlated with MEs diversity and gut IgA levels, and negatively correlated with gut microbiota richness. Glutamate synthase (GOGAT) was more active in the guts of patients with schizophrenia than in those of healthy controls, and high GOGAT activity was associated with altered gut microbiota taxonomies associated with gut IgA levels. Our results may imply a role of the microbiome in the etiology of schizophrenia and contribute to the development of microbiome targeted interventions for schizophrenia.",
"role": "user"
},
{
"content": "<microbiome>Altered gut microbiota</microbiome> and <DDF>mucosal immunity</DDF> in <human>patients</human> with <DDF>schizophrenia</DDF>. Evidence shows that <microbiome>gut microbiota</microbiome> may play important roles in schizophrenia pathogenesis via the \"gut-brain\" axis, but the mechanisms remain unclear. Here, eighty-four <human>patients</human> with <DDF>schizophrenia</DDF> and 84 <human>sex- and age-matched healthy controls</human> were enrolled. <biomedical technique>Shotgun metagenomic sequencing</biomedical technique> and <biomedical technique>16S rRNA sequencing</biomedical technique> were performed, and the gut microbiota-associated epitopes (MEs) were predicted, which, together with IgA content, were used to determine the gut microbiota composition associated with gut immune status. <human>Patients</human> with <DDF>schizophrenia</DDF> had significantly reduced gut microbiota richnesses compared with those of the <human>healthy controls</human>, and the gut microbiota compositions clearly distinguished the <human>patients</human> with <DDF>schizophrenia</DDF> from the <human>healthy controls</human>. Based on <biomedical technique>two-stage metagenomic-wide association studies</biomedical technique>, nineteen gut microbiota taxonomies were associated with <DDF>schizophrenia</DDF>, and the microbial dysbiosis (MD) index was calculated based on the abundance of differential taxonomies. We found that MD index was positively correlated with MEs diversity and gut IgA levels, and negatively correlated with gut microbiota richness. <gene>Glutamate synthase</gene> (<gene>GOGAT</gene>) was more active in the <anatomical location>guts</anatomical location> of <human>patients</human> with <DDF>schizophrenia</DDF> than in those of <human>healthy controls</human>, and <DDF>high GOGAT activity</DDF> was associated with altered gut microbiota taxonomies associated with gut IgA levels. Our results may imply a role of the microbiome in the etiology of <DDF>schizophrenia</DDF> and contribute to the development of microbiome targeted interventions for <DDF>schizophrenia</DDF>.",
"role": "assistant"
}
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31260640
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nMicrobiota-gut brain axis involvement in neuropsychiatric disorders. <b>Introduction</b>: The microbiota-gut brain (MGB) axis is the bidirectional communication between the intestinal microbiota and the brain. An increasing body of preclinical and clinical evidence has revealed that the gut microbial ecosystem can affect neuropsychiatric health. However, there is still a need of further studies to elucidate the complex gene-environment interactions and the role of the MGB axis in neuropsychiatric diseases, with the aim of identifying biomarkers and new therapeutic targets, to allow early diagnosis and improving treatments. <b>Areas covered</b>: To review the role of MGB axis in neuropsychiatric disorders, prediction and prevention of disease through exploitation, integration, and combination of data from existing gut microbiome/microbiota projects and appropriate other International '-Omics' studies. The authors also evaluated the new technological advances to investigate and modulate, through nutritional and other interventions, the gut microbiota. <b>Expert opinion</b>: The clinical studies have documented an association between alterations in gut microbiota composition and/or function, whereas the preclinical studies support a role for the gut microbiota in impacting behaviors which are of relevance to psychiatry and other central nervous system (CNS) disorders. Targeting MGB axis could be an additional approach for treating CNS disorders and all conditions in which alterations of the gut microbiota are involved.",
"role": "user"
},
{
"content": "Microbiota-gut brain axis involvement in <DDF>neuropsychiatric disorders</DDF>. <b>Introduction</b>: The microbiota-gut brain (MGB) axis is the bidirectional communication between the <microbiome>intestinal microbiota</microbiome> and the <anatomical location>brain</anatomical location>. An increasing body of preclinical and clinical evidence has revealed that the <microbiome>gut microbial ecosystem</microbiome> can affect neuropsychiatric health. However, there is still a need of further studies to elucidate the complex gene-environment interactions and the role of the MGB axis in <DDF>neuropsychiatric diseases</DDF>, with the aim of identifying biomarkers and new therapeutic targets, to allow early diagnosis and improving treatments. <b>Areas covered</b>: To review the role of MGB axis in <DDF>neuropsychiatric disorders</DDF>, prediction and prevention of disease through exploitation, integration, and combination of data from existing gut microbiome/microbiota projects and appropriate other International '-Omics' studies. The authors also evaluated the new technological advances to investigate and modulate, through nutritional and other interventions, the <microbiome>gut microbiota</microbiome>. <b>Expert opinion</b>: The clinical studies have documented an association between alterations in gut microbiota composition and/or function, whereas the preclinical studies support a role for the <microbiome>gut microbiota</microbiome> in impacting behaviors which are of relevance to <DDF>psychiatry and other central nervous system (CNS) disorders</DDF>. Targeting MGB axis could be an additional approach for treating <DDF>CNS disorders</DDF> and all conditions in which alterations of the <DDF>gut microbiota</DDF> are involved.",
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31302116
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nStress-induced disturbances along the gut microbiota-immune-brain axis and implications for mental health: Does sex matter? Women are roughly twice as likely as men to suffer from stress-related disorders, especially major depression and generalized anxiety. Accumulating evidence suggest that microbes inhabiting the gastrointestinal tract (the gut microbiota) interact with the host brain and may play a key role in the pathogenesis of mental illnesses. Here, the possibility that sexually dimorphic alterations along the gut microbiota-immune-brain axis could play a role in promoting this female bias of mood and anxiety disorders will be discussed. This review will also analyze the idea that gut microbes and sex hormones influence each other, and that this reciprocal crosstalk may come to modulate inflammatory players along the gut microbiota-immune-brain axis and influence behavior in a sex-dependent way.",
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"content": "<DDF>Stress-induced disturbances</DDF> along the gut microbiota-immune-brain axis and implications for mental health: Does sex matter? <human>Women</human> are roughly twice as likely as <human>men</human> to suffer from <DDF>stress-related disorders</DDF>, especially <DDF>major depression</DDF> and <DDF>generalized anxiety</DDF>. Accumulating evidence suggest that microbes inhabiting the <anatomical location>gastrointestinal tract</anatomical location> (the <microbiome>gut microbiota</microbiome>) interact with the <anatomical location>host brain</anatomical location> and may play a key role in the pathogenesis of <DDF>mental illnesses</DDF>. Here, the possibility that sexually dimorphic alterations along the gut microbiota-immune-brain axis could play a role in promoting this female bias of <DDF>mood and anxiety disorders</DDF> will be discussed. This review will also analyze the idea that <microbiome>gut microbes</microbiome> and <chemical>sex hormones</chemical> influence each other, and that this reciprocal crosstalk may come to modulate inflammatory players along the gut microbiota-immune-brain axis and influence behavior in a sex-dependent way.",
"role": "assistant"
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31330299
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nMonocyte mobilisation, microbiota & mental illness. The gastrointestinal microbiome has emerged as a key player in regulating brain and behaviour. This has led to the strategy of targeting the gut microbiota to ameliorate disorders of the central nervous system. Understanding the underlying signalling pathways in which the microbiota impacts these disorders is crucial for the development of future therapeutics for improving CNS functionality. One of the major pathways through which the microbiota influences the brain is the immune system, where there is an increasing appreciation for the role of monocyte trafficking in regulating brain homeostasis. In this review, we will shed light on the role of monocyte trafficking as a relay of microbiota signals in conditions where the central nervous system is in disorder, such as stress, peripheral inflammation, ageing, traumatic brain injury, stroke, multiple sclerosis, Alzheimer's disease and Parkinson's disease. We also cover how the gastrointestinal microbiota is implicated in these mental illnesses. In addition, we aim to discuss how the monocyte system can be modulated by the gut microbiota to mitigate disorders of the central nervous system, which will lead to novel microbiota-targeted strategies.",
"role": "user"
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{
"content": "Monocyte mobilisation, microbiota & <DDF>mental illness</DDF>. The <microbiome>gastrointestinal microbiome</microbiome> has emerged as a key player in regulating <anatomical location>brain</anatomical location> and behaviour. This has led to the strategy of targeting the <microbiome>gut microbiota</microbiome> to ameliorate <DDF>disorders of the central nervous system</DDF>. Understanding the underlying signalling pathways in which the microbiota impacts these disorders is crucial for the development of future therapeutics for improving CNS functionality. One of the major pathways through which the microbiota influences the <anatomical location>brain</anatomical location> is the immune system, where there is an increasing appreciation for the role of monocyte trafficking in regulating brain homeostasis. In this review, we will shed light on the role of monocyte trafficking as a relay of microbiota signals in conditions where the central nervous system is in disorder, such as <DDF>stress</DDF>, <DDF>peripheral inflammation</DDF>, ageing, <DDF>traumatic brain injury</DDF>, <DDF>stroke</DDF>, <DDF>multiple sclerosis</DDF>, <DDF>Alzheimer's disease</DDF> and <DDF>Parkinson's disease</DDF>. We also cover how the <microbiome>gastrointestinal microbiota</microbiome> is implicated in these <DDF>mental illnesses</DDF>. In addition, we aim to discuss how the monocyte system can be modulated by the <microbiome>gut microbiota</microbiome> to mitigate disorders of the central nervous system, which will lead to novel microbiota-targeted strategies.",
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31377712
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nBiopsychosocial model of resilience in young adults with multiple sclerosis (BPS-ARMS): an observational study protocol exploring psychological reactions early after diagnosis. Multiple sclerosis (MS), the most common neurological disease causing disability in young adults, is widely recognised as a major stress factor. Studies have shown that the first years after the diagnosis are distressing in terms of adjustment to the disease and that MS negatively affects patients' psychological well-being, quality of life (QoL) and social functioning. However, the links between disease-specific variables at diagnosis, resilience and psychological adjustment of patients with MS remain largely unexplored, especially in adolescents and young adults. This observational study aims to fill the gap of knowledge on <u>b</u>io<u>p</u>sycho<u>s</u>ocial characteristics and <u>r</u>esilience of young <u>a</u>dults with MS to evaluate the relationship among these variables and to develop a biopsychosocial model of resilience. Biological and clinical characteristics of young adults newly diagnosed with MS will be investigated by collecting clinical information, performing neurological examinations, MRI and analysing cerebrospinal fluid and blood biomarkers (eg, measures of inflammation), body composition, gut microbiota and movement/perceptual markers. Psychosocial characteristics (eg, psychological distress, coping strategies), QoL, psychological well-being and resilience will be assessed by self-report questionnaires. Comparative statistics (ie, analysis of variance or unpaired samples t-test, correlation and regression analyses) will be applied to evaluate the relationship among biological, psychological and social factors. The results are expected to allow a comprehensive understanding of the determinants of resilience in young patients with MS and to inform resilience interventions, tailored to young patients' specific needs, aiming to reduce the risk of maladaptive reactions to the disease and to improve psychological well-being and QoL. The study has been approved by the Verona University Hospital Ethics Committee (approval number: 2029CESC). The findings will be disseminated through scientific publications in peer-reviewed journals, conference presentations, social media and specific websites. ClinicalTrials.gov (NCT03825055).",
"role": "user"
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"content": "Biopsychosocial model of resilience in <human>young adults</human> with <DDF>multiple sclerosis</DDF> (BPS-ARMS): an observational study protocol exploring psychological reactions early after diagnosis. <DDF>Multiple sclerosis</DDF> (<DDF>MS</DDF>), the most common <DDF>neurological disease</DDF> causing <DDF>disability</DDF> in <human>young adults</human>, is widely recognised as a major stress factor. Studies have shown that the first years after the diagnosis are distressing in terms of adjustment to the disease and that <DDF>MS</DDF> negatively affects patients' psychological well-being, quality of life (QoL) and social functioning. However, the links between disease-specific variables at diagnosis, resilience and psychological adjustment of <human>patients</human> with <DDF>MS</DDF> remain largely unexplored, especially in <human>adolescents</human> and <human>young adults</human>. This observational study aims to fill the gap of knowledge on <u>b</u>io<u>p</u>sycho<u>s</u>ocial characteristics and <u>r</u>esilience of <human>young <u>a</u>dults</human> with <DDF>MS</DDF> to evaluate the relationship among these variables and to develop a biopsychosocial model of resilience. Biological and clinical characteristics of <human>young adults</human> newly diagnosed with <DDF>MS</DDF> will be investigated by collecting clinical information, performing <biomedical technique>neurological examinations</biomedical technique>, <biomedical technique>MRI</biomedical technique> and analysing <biomedical technique>cerebrospinal fluid and blood biomarkers</biomedical technique> (eg, measures of <DDF>inflammation</DDF>), body composition, <microbiome>gut microbiota</microbiome> and movement/perceptual markers. Psychosocial characteristics (eg, psychological distress, coping strategies), QoL, psychological well-being and resilience will be assessed by <biomedical technique>self-report questionnaires</biomedical technique>. <statistical technique>Comparative statistics</statistical technique> (ie, <statistical technique>analysis of variance</statistical technique> or <statistical technique>unpaired samples t-test</statistical technique>, <statistical technique>correlation and regression analyses</statistical technique>) will be applied to evaluate the relationship among biological, psychological and social factors. The results are expected to allow a comprehensive understanding of the determinants of resilience in <human>young patients</human> with <DDF>MS</DDF> and to inform resilience interventions, tailored to young patients' specific needs, aiming to reduce the risk of maladaptive reactions to the disease and to improve psychological well-being and QoL. The study has been approved by the Verona University Hospital Ethics Committee (approval number: 2029CESC). The findings will be disseminated through scientific publications in peer-reviewed journals, conference presentations, social media and specific websites. ClinicalTrials.gov (NCT03825055).",
"role": "assistant"
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31383280
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nImproving Mental Health for the Mother-Infant Dyad by Nutrition and the Maternal Gut Microbiome. Perinatal mood and anxiety disorders (PMAD) have significant negative impacts on mother and child, yet treatments are limited. Adequate nutrition during the perinatal period is essential to maternal and infant health, including maternal mental health and the child's neurologic and neuropsychiatric development. Nutrition holds promise to improve prevention and treatment of PMAD. The ability to manipulate the gut microbiota composition and structure through host nutrition and to harness the gut microbes for improved individualized nutrition may be an important new direction for prevention and treatment of PMAD, thus improving the mental health of mother and child.",
"role": "user"
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{
"content": "Improving Mental Health for the <human>Mother-Infant Dyad</human> by Nutrition and the <microbiome>Maternal Gut Microbiome</microbiome>. <DDF>Perinatal mood and anxiety disorders</DDF> (<DDF>PMAD</DDF>) have significant negative impacts on <human>mother</human> and <human>child</human>, yet treatments are limited. Adequate nutrition during the perinatal period is essential to maternal and infant health, including maternal mental health and the child's neurologic and neuropsychiatric development. Nutrition holds promise to improve prevention and treatment of <DDF>PMAD</DDF>. The ability to manipulate the gut microbiota composition and structure through host nutrition and to harness the gut microbes for improved individualized nutrition may be an important new direction for prevention and treatment of <DDF>PMAD</DDF>, thus improving the mental health of <human>mother</human> and <human>child</human>.",
"role": "assistant"
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31488882
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nSodium oligomannate therapeutically remodels gut microbiota and suppresses gut bacterial amino acids-shaped neuroinflammation to inhibit Alzheimer's disease progression. Recently, increasing evidence has suggested the association between gut dysbiosis and Alzheimer's disease (AD) progression, yet the role of gut microbiota in AD pathogenesis remains obscure. Herein, we provide a potential mechanistic link between gut microbiota dysbiosis and neuroinflammation in AD progression. Using AD mouse models, we discovered that, during AD progression, the alteration of gut microbiota composition leads to the peripheral accumulation of phenylalanine and isoleucine, which stimulates the differentiation and proliferation of pro-inflammatory T helper 1 (Th1) cells. The brain-infiltrated peripheral Th1 immune cells are associated with the M1 microglia activation, contributing to AD-associated neuroinflammation. Importantly, the elevation of phenylalanine and isoleucine concentrations and the increase of Th1 cell frequency in the blood were also observed in two small independent cohorts of patients with mild cognitive impairment (MCI) due to AD. Furthermore, GV-971, a sodium oligomannate that has demonstrated solid and consistent cognition improvement in a phase 3 clinical trial in China, suppresses gut dysbiosis and the associated phenylalanine/isoleucine accumulation, harnesses neuroinflammation and reverses the cognition impairment. Together, our findings highlight the role of gut dysbiosis-promoted neuroinflammation in AD progression and suggest a novel strategy for AD therapy by remodelling the gut microbiota.",
"role": "user"
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{
"content": "<dietary supplement>Sodium oligomannate</dietary supplement> therapeutically remodels <microbiome>gut microbiota</microbiome> and suppresses <DDF>gut bacterial amino acids-shaped neuroinflammation</DDF> to inhibit <DDF>Alzheimer's disease progression</DDF>. Recently, increasing evidence has suggested the association between <DDF>gut dysbiosis</DDF> and <DDF>Alzheimer's disease</DDF> (<DDF>AD</DDF>) progression, yet the role of <microbiome>gut microbiota</microbiome> in AD pathogenesis remains obscure. Herein, we provide a potential mechanistic link between <DDF>gut microbiota dysbiosis</DDF> and <DDF>neuroinflammation</DDF> in <DDF>AD progression</DDF>. Using AD mouse models, we discovered that, during <DDF>AD progression</DDF>, the alteration of <microbiome>gut microbiota</microbiome> composition leads to the peripheral accumulation of <chemical>phenylalanine</chemical> and <chemical>isoleucine</chemical>, which stimulates the differentiation and proliferation of pro-inflammatory T helper 1 (Th1) cells. The brain-infiltrated peripheral Th1 immune cells are associated with the M1 microglia activation, contributing to <DDF>AD-associated neuroinflammation</DDF>. Importantly, the elevation of <chemical>phenylalanine</chemical> and <chemical>isoleucine</chemical> concentrations and the increase of Th1 cell frequency in the blood were also observed in two small independent cohorts of <human>patients</human> with <DDF>mild cognitive impairment</DDF> (<DDF>MCI</DDF>) due to <DDF>AD</DDF>. Furthermore, <drug>GV-971</drug>, a <drug>sodium oligomannate</drug> that has demonstrated solid and consistent cognition improvement in a phase 3 clinical trial in China, suppresses <DDF>gut dysbiosis</DDF> and the associated <chemical>phenylalanine</chemical>/<chemical>isoleucine</chemical> accumulation, harnesses <DDF>neuroinflammation</DDF> and reverses the <DDF>cognition impairment</DDF>. Together, our findings highlight the role of <DDF>gut dysbiosis-promoted neuroinflammation</DDF> in AD progression and suggest a novel strategy for AD therapy by remodelling the <microbiome>gut microbiota</microbiome>.",
"role": "assistant"
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