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Carbapenems | O=C1N2C(=CCC2C1)C(=O)O | During this study period, the institution's microbiology laboratory utilized the Brucker MALDI Biotyper for the identification of bacteria and yeast.This system uses mass spectrometry to determine the proteomic fingerprints of microorganisms and compares these to the research-use-only database for microbial identification.The BD Phoenix™ automated system was used as a backup method for identification, and was the primary system used for antimicrobial susceptibility testing.The identification of microbes was based on the results of 45 chromogenic and fluorogenic substrates.ESBL production identified in isolates of E. coli, K. pneumoniae, and K. oxytoca was based on differential responses to third-generation cephalosporins in the presence and absence of the beta-lactamase inhibitor clavulanic acid.Carbapenem resistance for other organisms was determined by resistance to either meropenem or ertapenem, which were the representative O=C1N2C(=CCC2C1)C(=O)O on the antimicrobial susceptibility testing panel.The BD Phoenix system uses a Carbapenemaseproducing Organism Detect Panel.Specific genetic testing for resistance at our institution requires samples to be sent out to consulting laboratories, and must be requested.The rules for antibiotic reporting and interpretation for MIC values from the BD Phoenix™ system were based on United States Food and Drug Administration-cleared interpretations built within the automated system.Additional or reflex-sensitivity testing that may have been reported was done iteratively or collaboratively according to intramural antimicrobial stewardship guidance and adhered to Clinical & Laboratory Standards Institute breakpoints using the Kirby-Bauer disk diffusion method.Disk diffusion was rare and utilized only in cases of ceftazidime-avibactam, meropenem-vaborbactam, or ceftolozane-tazobactam susceptibilities for multidrug-resistant Acinetobacter spp., Enterobacterales spp., or Pseudomonas spp.Quality control for Phoenix identification and MICs followed the package insert for the Phoenix products.Kirby-Bauer interpretation, reporting and quality control followed CLSI recommendations. | 271556193 |
Ceftolozane-tazobactam | C1C(N2[C@@H]1S(=O)(=O)[C@@](CN1C=CN=N1)([C@@H]2C(=O)O)C)=O.O=C(/C(=N/OC(C)(C(O)=O)C)C1=NSC(=N1)N)N[C@H]1[C@H]2SCC(=C(C([O-])=O)N2C1=O)C[N+]1N(C)C(=C(C=1)NC(=O)NCCN)N.OS(=O)(=O)O | During this study period, the institution's microbiology laboratory utilized the Brucker MALDI Biotyper for the identification of bacteria and yeast.This system uses mass spectrometry to determine the proteomic fingerprints of microorganisms and compares these to the research-use-only database for microbial identification.The BD Phoenix™ automated system was used as a backup method for identification, and was the primary system used for antimicrobial susceptibility testing.The identification of microbes was based on the results of 45 chromogenic and fluorogenic substrates.ESBL production identified in isolates of E. coli, K. pneumoniae, and K. oxytoca was based on differential responses to third-generation cephalosporins in the presence and absence of the beta-lactamase inhibitor clavulanic acid.Carbapenem resistance for other organisms was determined by resistance to either meropenem or ertapenem, which were the representative carbapenems on the antimicrobial susceptibility testing panel.The BD Phoenix system uses a Carbapenemaseproducing Organism Detect Panel.Specific genetic testing for resistance at our institution requires samples to be sent out to consulting laboratories, and must be requested.The rules for antibiotic reporting and interpretation for MIC values from the BD Phoenix™ system were based on United States Food and Drug Administration-cleared interpretations built within the automated system.Additional or reflex-sensitivity testing that may have been reported was done iteratively or collaboratively according to intramural antimicrobial stewardship guidance and adhered to Clinical & Laboratory Standards Institute breakpoints using the Kirby-Bauer disk diffusion method.Disk diffusion was rare and utilized only in cases of ceftazidime-avibactam, meropenem-vaborbactam, or C1C(N2[C@@H]1S(=O)(=O)[C@@](CN1C=CN=N1)([C@@H]2C(=O)O)C)=O.O=C(/C(=N/OC(C)(C(O)=O)C)C1=NSC(=N1)N)N[C@H]1[C@H]2SCC(=C(C([O-])=O)N2C1=O)C[N+]1N(C)C(=C(C=1)NC(=O)NCCN)N.OS(=O)(=O)O susceptibilities for multidrug-resistant Acinetobacter spp., Enterobacterales spp., or Pseudomonas spp.Quality control for Phoenix identification and MICs followed the package insert for the Phoenix products.Kirby-Bauer interpretation, reporting and quality control followed CLSI recommendations. | 271556193 |
Nystatin | [C@H]1(O)[C@@H]([C@H](O)[C@@H](O[C@@H]1C)O[C@@H]1C[C@@H]2O[C@](C[C@H](O)[C@H](O)CC[C@@H](C[C@H](O)C[C@@H](CC(=O)O[C@H]([C@H]([C@H](O)[C@@H](C)C=CC=CCCC=CC=C/C=C\C=C/1)C)C)O)O)(C[C@@H]([C@H]2C(O)=O)O)O)N | A total of 376 pathogens were isolated from the 65 patients in the cohort.No significant differences were observed in culture source between those who grew DTp and non-DTp (p = 0.99).Pathogens were most commonly isolated from wounds (50.5%), followed by blood (23.9%) and the lungs (22.8%).Pathogens were isolated from other sources 2.7% of the time, most often from the urine, though this source was rarely cultured in our study.Here, 57% of pathogens isolated in our cohort were classified as DTp, with the other 43% were classified as non-DTp.Resistance patterns are illustrated in Figure 2. Of the 213 pathogens classified as DTp, 153 (71.8%) of organisms were considered to be MDR, and 46 (21.5%) were classified as XDR.Of DTp, 107 (50.2%) were known or presumed ESBL-producers and 106 (49.8%) were known or presumed AmpC-producers.We observed an overall ESBL and AmpC rate of 28.4% and 28.2%, respectively.Carbapenem-resistance was fairly common, with 17.3% of isolated pathogens exhibiting resistance to these agents.Distributions of organism-specific DTp can also be seen in Figure 2. Of DTp, 62 (29%) were MRSA, 12 (5.6%)difficult-to-treat resistance Pseudomonas spp., 9 Topical and systemic antimicrobials are commonly utilized in burn patients.Figure 3 illustrates the association between topical exposure and DTp development.We found that 354 (94.1%) of the isolated pathogens were exposed to a topical antimicrobial agent prior to their development and this exposure was associated with a statistically significant increase in DTp development (p = 0.0002).Exposures to many topical antimicrobials were found to be statistically significant predictors of DTp development, including bacitracin (p < 0.001), Dakins (p = 0.003), silver nitrate solution (p < 0.001), hypochlorous acid (p < 0.001), and other topicals (p = 0.0005), largely composed of antifungal agents including [C@H]1(O)[C@@H]([C@H](O)[C@@H](O[C@@H]1C)O[C@@H]1C[C@@H]2O[C@](C[C@H](O)[C@H](O)CC[C@@H](C[C@H](O)C[C@@H](CC(=O)O[C@H]([C@H]([C@H](O)[C@@H](C)C=CC=CCCC=CC=C/C=C\C=C/1)C)C)O)O)(C[C@@H]([C@H]2C(O)=O)O)O)N and clotrimazole.Mafenide, silver sulfadiazine (SSD), and mupirocin were not found to be statistically significant predictors of DTp development, though mafenide (i.e., ears) and mupirocin (i.e., most use was a state-mandated routine nasal decolonization before a switch to ethanol-based prophylaxis) are not rarely prescribed in our center.Nasal decolonization with either ethanol-based solutions or mupirocin was not significantly associated with DTp development in either direction (p = 0.62).Interestingly, solid silver dressings were found to be associated with a significant decrease in DTp development (p = 0.002).During the study period, the only solid silver dressing in use was a nanocrystalline dressing. | 271556193 |
Clotrimazole | Clc1ccccc1C(c1ccccc1)(n1ccnc1)c1ccccc1 | A total of 376 pathogens were isolated from the 65 patients in the cohort.No significant differences were observed in culture source between those who grew DTp and non-DTp (p = 0.99).Pathogens were most commonly isolated from wounds (50.5%), followed by blood (23.9%) and the lungs (22.8%).Pathogens were isolated from other sources 2.7% of the time, most often from the urine, though this source was rarely cultured in our study.Here, 57% of pathogens isolated in our cohort were classified as DTp, with the other 43% were classified as non-DTp.Resistance patterns are illustrated in Figure 2. Of the 213 pathogens classified as DTp, 153 (71.8%) of organisms were considered to be MDR, and 46 (21.5%) were classified as XDR.Of DTp, 107 (50.2%) were known or presumed ESBL-producers and 106 (49.8%) were known or presumed AmpC-producers.We observed an overall ESBL and AmpC rate of 28.4% and 28.2%, respectively.Carbapenem-resistance was fairly common, with 17.3% of isolated pathogens exhibiting resistance to these agents.Distributions of organism-specific DTp can also be seen in Figure 2. Of DTp, 62 (29%) were MRSA, 12 (5.6%)difficult-to-treat resistance Pseudomonas spp., 9 Topical and systemic antimicrobials are commonly utilized in burn patients.Figure 3 illustrates the association between topical exposure and DTp development.We found that 354 (94.1%) of the isolated pathogens were exposed to a topical antimicrobial agent prior to their development and this exposure was associated with a statistically significant increase in DTp development (p = 0.0002).Exposures to many topical antimicrobials were found to be statistically significant predictors of DTp development, including bacitracin (p < 0.001), Dakins (p = 0.003), silver nitrate solution (p < 0.001), hypochlorous acid (p < 0.001), and other topicals (p = 0.0005), largely composed of antifungal agents including nystatin and Clc1ccccc1C(c1ccccc1)(n1ccnc1)c1ccccc1.Mafenide, silver sulfadiazine (SSD), and mupirocin were not found to be statistically significant predictors of DTp development, though mafenide (i.e., ears) and mupirocin (i.e., most use was a state-mandated routine nasal decolonization before a switch to ethanol-based prophylaxis) are not rarely prescribed in our center.Nasal decolonization with either ethanol-based solutions or mupirocin was not significantly associated with DTp development in either direction (p = 0.62).Interestingly, solid silver dressings were found to be associated with a significant decrease in DTp development (p = 0.002).During the study period, the only solid silver dressing in use was a nanocrystalline dressing. | 271556193 |
Mafenide | C(c1ccc(cc1)S(=O)(=O)N)N | A total of 376 pathogens were isolated from the 65 patients in the cohort.No significant differences were observed in culture source between those who grew DTp and non-DTp (p = 0.99).Pathogens were most commonly isolated from wounds (50.5%), followed by blood (23.9%) and the lungs (22.8%).Pathogens were isolated from other sources 2.7% of the time, most often from the urine, though this source was rarely cultured in our study.Here, 57% of pathogens isolated in our cohort were classified as DTp, with the other 43% were classified as non-DTp.Resistance patterns are illustrated in Figure 2. Of the 213 pathogens classified as DTp, 153 (71.8%) of organisms were considered to be MDR, and 46 (21.5%) were classified as XDR.Of DTp, 107 (50.2%) were known or presumed ESBL-producers and 106 (49.8%) were known or presumed AmpC-producers.We observed an overall ESBL and AmpC rate of 28.4% and 28.2%, respectively.Carbapenem-resistance was fairly common, with 17.3% of isolated pathogens exhibiting resistance to these agents.Distributions of organism-specific DTp can also be seen in Figure 2. Of DTp, 62 (29%) were MRSA, 12 (5.6%)difficult-to-treat resistance Pseudomonas spp., 9 Topical and systemic antimicrobials are commonly utilized in burn patients.Figure 3 illustrates the association between topical exposure and DTp development.We found that 354 (94.1%) of the isolated pathogens were exposed to a topical antimicrobial agent prior to their development and this exposure was associated with a statistically significant increase in DTp development (p = 0.0002).Exposures to many topical antimicrobials were found to be statistically significant predictors of DTp development, including bacitracin (p < 0.001), Dakins (p = 0.003), silver nitrate solution (p < 0.001), hypochlorous acid (p < 0.001), and other topicals (p = 0.0005), largely composed of antifungal agents including nystatin and clotrimazole.C(c1ccc(cc1)S(=O)(=O)N)N, silver sulfadiazine (SSD), and mupirocin were not found to be statistically significant predictors of DTp development, though C(c1ccc(cc1)S(=O)(=O)N)N (i.e., ears) and mupirocin (i.e., most use was a state-mandated routine nasal decolonization before a switch to ethanol-based prophylaxis) are not rarely prescribed in our center.Nasal decolonization with either ethanol-based solutions or mupirocin was not significantly associated with DTp development in either direction (p = 0.62).Interestingly, solid silver dressings were found to be associated with a significant decrease in DTp development (p = 0.002).During the study period, the only solid silver dressing in use was a nanocrystalline dressing. | 271556193 |
Silver sulfadiazine | [N-](S(C1=CC=C(N)C=C1)(=O)=O)C1=NC=CC=N1.[Ag+] | A total of 376 pathogens were isolated from the 65 patients in the cohort.No significant differences were observed in culture source between those who grew DTp and non-DTp (p = 0.99).Pathogens were most commonly isolated from wounds (50.5%), followed by blood (23.9%) and the lungs (22.8%).Pathogens were isolated from other sources 2.7% of the time, most often from the urine, though this source was rarely cultured in our study.Here, 57% of pathogens isolated in our cohort were classified as DTp, with the other 43% were classified as non-DTp.Resistance patterns are illustrated in Figure 2. Of the 213 pathogens classified as DTp, 153 (71.8%) of organisms were considered to be MDR, and 46 (21.5%) were classified as XDR.Of DTp, 107 (50.2%) were known or presumed ESBL-producers and 106 (49.8%) were known or presumed AmpC-producers.We observed an overall ESBL and AmpC rate of 28.4% and 28.2%, respectively.Carbapenem-resistance was fairly common, with 17.3% of isolated pathogens exhibiting resistance to these agents.Distributions of organism-specific DTp can also be seen in Figure 2. Of DTp, 62 (29%) were MRSA, 12 (5.6%)difficult-to-treat resistance Pseudomonas spp., 9 Topical and systemic antimicrobials are commonly utilized in burn patients.Figure 3 illustrates the association between topical exposure and DTp development.We found that 354 (94.1%) of the isolated pathogens were exposed to a topical antimicrobial agent prior to their development and this exposure was associated with a statistically significant increase in DTp development (p = 0.0002).Exposures to many topical antimicrobials were found to be statistically significant predictors of DTp development, including bacitracin (p < 0.001), Dakins (p = 0.003), silver nitrate solution (p < 0.001), hypochlorous acid (p < 0.001), and other topicals (p = 0.0005), largely composed of antifungal agents including nystatin and clotrimazole.Mafenide, [N-](S(C1=CC=C(N)C=C1)(=O)=O)C1=NC=CC=N1.[Ag+] (SSD), and mupirocin were not found to be statistically significant predictors of DTp development, though mafenide (i.e., ears) and mupirocin (i.e., most use was a state-mandated routine nasal decolonization before a switch to ethanol-based prophylaxis) are not rarely prescribed in our center.Nasal decolonization with either ethanol-based solutions or mupirocin was not significantly associated with DTp development in either direction (p = 0.62).Interestingly, solid silver dressings were found to be associated with a significant decrease in DTp development (p = 0.002).During the study period, the only solid silver dressing in use was a nanocrystalline dressing. | 271556193 |
Sulfadiazine | O=S(Nc1ncccn1)(c1ccc(cc1)N)=O | A total of 376 pathogens were isolated from the 65 patients in the cohort.No significant differences were observed in culture source between those who grew DTp and non-DTp (p = 0.99).Pathogens were most commonly isolated from wounds (50.5%), followed by blood (23.9%) and the lungs (22.8%).Pathogens were isolated from other sources 2.7% of the time, most often from the urine, though this source was rarely cultured in our study.Here, 57% of pathogens isolated in our cohort were classified as DTp, with the other 43% were classified as non-DTp.Resistance patterns are illustrated in Figure 2. Of the 213 pathogens classified as DTp, 153 (71.8%) of organisms were considered to be MDR, and 46 (21.5%) were classified as XDR.Of DTp, 107 (50.2%) were known or presumed ESBL-producers and 106 (49.8%) were known or presumed AmpC-producers.We observed an overall ESBL and AmpC rate of 28.4% and 28.2%, respectively.Carbapenem-resistance was fairly common, with 17.3% of isolated pathogens exhibiting resistance to these agents.Distributions of organism-specific DTp can also be seen in Figure 2. Of DTp, 62 (29%) were MRSA, 12 (5.6%)difficult-to-treat resistance Pseudomonas spp., 9 Topical and systemic antimicrobials are commonly utilized in burn patients.Figure 3 illustrates the association between topical exposure and DTp development.We found that 354 (94.1%) of the isolated pathogens were exposed to a topical antimicrobial agent prior to their development and this exposure was associated with a statistically significant increase in DTp development (p = 0.0002).Exposures to many topical antimicrobials were found to be statistically significant predictors of DTp development, including bacitracin (p < 0.001), Dakins (p = 0.003), silver nitrate solution (p < 0.001), hypochlorous acid (p < 0.001), and other topicals (p = 0.0005), largely composed of antifungal agents including nystatin and clotrimazole.Mafenide, silver O=S(Nc1ncccn1)(c1ccc(cc1)N)=O (SSD), and mupirocin were not found to be statistically significant predictors of DTp development, though mafenide (i.e., ears) and mupirocin (i.e., most use was a state-mandated routine nasal decolonization before a switch to ethanol-based prophylaxis) are not rarely prescribed in our center.Nasal decolonization with either ethanol-based solutions or mupirocin was not significantly associated with DTp development in either direction (p = 0.62).Interestingly, solid silver dressings were found to be associated with a significant decrease in DTp development (p = 0.002).During the study period, the only solid silver dressing in use was a nanocrystalline dressing. | 271556193 |
Mupirocin | O[C@H]1[C@@H](OC[C@@H]([C@H]1O)C[C@@H]1O[C@H]1[C@H]([C@H](C)O)C)C/C(=C/C(OCCCCCCCCC(O)=O)=O)C | A total of 376 pathogens were isolated from the 65 patients in the cohort.No significant differences were observed in culture source between those who grew DTp and non-DTp (p = 0.99).Pathogens were most commonly isolated from wounds (50.5%), followed by blood (23.9%) and the lungs (22.8%).Pathogens were isolated from other sources 2.7% of the time, most often from the urine, though this source was rarely cultured in our study.Here, 57% of pathogens isolated in our cohort were classified as DTp, with the other 43% were classified as non-DTp.Resistance patterns are illustrated in Figure 2. Of the 213 pathogens classified as DTp, 153 (71.8%) of organisms were considered to be MDR, and 46 (21.5%) were classified as XDR.Of DTp, 107 (50.2%) were known or presumed ESBL-producers and 106 (49.8%) were known or presumed AmpC-producers.We observed an overall ESBL and AmpC rate of 28.4% and 28.2%, respectively.Carbapenem-resistance was fairly common, with 17.3% of isolated pathogens exhibiting resistance to these agents.Distributions of organism-specific DTp can also be seen in Figure 2. Of DTp, 62 (29%) were MRSA, 12 (5.6%)difficult-to-treat resistance Pseudomonas spp., 9 Topical and systemic antimicrobials are commonly utilized in burn patients.Figure 3 illustrates the association between topical exposure and DTp development.We found that 354 (94.1%) of the isolated pathogens were exposed to a topical antimicrobial agent prior to their development and this exposure was associated with a statistically significant increase in DTp development (p = 0.0002).Exposures to many topical antimicrobials were found to be statistically significant predictors of DTp development, including bacitracin (p < 0.001), Dakins (p = 0.003), silver nitrate solution (p < 0.001), hypochlorous acid (p < 0.001), and other topicals (p = 0.0005), largely composed of antifungal agents including nystatin and clotrimazole.Mafenide, silver sulfadiazine (SSD), and O[C@H]1[C@@H](OC[C@@H]([C@H]1O)C[C@@H]1O[C@H]1[C@H]([C@H](C)O)C)C/C(=C/C(OCCCCCCCCC(O)=O)=O)C were not found to be statistically significant predictors of DTp development, though mafenide (i.e., ears) and O[C@H]1[C@@H](OC[C@@H]([C@H]1O)C[C@@H]1O[C@H]1[C@H]([C@H](C)O)C)C/C(=C/C(OCCCCCCCCC(O)=O)=O)C (i.e., most use was a state-mandated routine nasal decolonization before a switch to ethanol-based prophylaxis) are not rarely prescribed in our center.Nasal decolonization with either ethanol-based solutions or O[C@H]1[C@@H](OC[C@@H]([C@H]1O)C[C@@H]1O[C@H]1[C@H]([C@H](C)O)C)C/C(=C/C(OCCCCCCCCC(O)=O)=O)C was not significantly associated with DTp development in either direction (p = 0.62).Interestingly, solid silver dressings were found to be associated with a significant decrease in DTp development (p = 0.002).During the study period, the only solid silver dressing in use was a nanocrystalline dressing. | 271556193 |
Nystatin | O[C@@H]1[C@@H](CC[C@@H](C[C@@H](C[C@@H](CC(O[C@@H](C)[C@H]([C@H](O)[C@@H](C)C=CC=CCCC=CC=C/C=C\C=C/[C@@H](C[C@H]2[C@@H]([C@H](C[C@](O)(O2)C1)O)C(=O)O)O[C@@H]1O[C@@H]([C@@H](O)[C@@H]([C@@H]1O)N)C)C)=O)O)O)O)O | 3 illustrates the association between topical exposure and DTp development.We found that 354 (94.1%) of the isolated pathogens were exposed to a topical antimicrobial agent prior to their development and this exposure was associated with a statistically significant increase in DTp development (p = 0.0002).Exposures to many topical antimicrobials were found to be statistically significant predictors of DTp development, including bacitracin (p < 0.001), Dakins (p = 0.003), silver nitrate solution (p < 0.001), hypochlorous acid (p < 0.001), and other topicals (p = 0.0005), largely composed of antifungal agents including O[C@@H]1[C@@H](CC[C@@H](C[C@@H](C[C@@H](CC(O[C@@H](C)[C@H]([C@H](O)[C@@H](C)C=CC=CCCC=CC=C/C=C\C=C/[C@@H](C[C@H]2[C@@H]([C@H](C[C@](O)(O2)C1)O)C(=O)O)O[C@@H]1O[C@@H]([C@@H](O)[C@@H]([C@@H]1O)N)C)C)=O)O)O)O)O and clotrimazole.Mafenide, silver sulfadiazine (SSD), and mupirocin were not found to be statistically significant predictors of DTp development, though mafenide (i.e., ears) and mupirocin (i.e., most use was a state-mandated routine nasal decolonization before a switch to ethanol-based prophylaxis) are not rarely prescribed in our center.Nasal decolonization with either ethanol-based solutions or mupirocin was not significantly associated with DTp development in either direction (p = 0.62).Interestingly, solid silver dressings were found to be associated with a significant decrease in DTp development (p = 0.002).During the study period, the only solid silver dressing in use was a nanocrystalline dressing. | 271556193 |
Clotrimazole | C1=CC=C(Cl)C(=C1)C(C1=CC=CC=C1)(C1=CC=CC=C1)N1C=NC=C1 | 3 illustrates the association between topical exposure and DTp development.We found that 354 (94.1%) of the isolated pathogens were exposed to a topical antimicrobial agent prior to their development and this exposure was associated with a statistically significant increase in DTp development (p = 0.0002).Exposures to many topical antimicrobials were found to be statistically significant predictors of DTp development, including bacitracin (p < 0.001), Dakins (p = 0.003), silver nitrate solution (p < 0.001), hypochlorous acid (p < 0.001), and other topicals (p = 0.0005), largely composed of antifungal agents including nystatin and C1=CC=C(Cl)C(=C1)C(C1=CC=CC=C1)(C1=CC=CC=C1)N1C=NC=C1.Mafenide, silver sulfadiazine (SSD), and mupirocin were not found to be statistically significant predictors of DTp development, though mafenide (i.e., ears) and mupirocin (i.e., most use was a state-mandated routine nasal decolonization before a switch to ethanol-based prophylaxis) are not rarely prescribed in our center.Nasal decolonization with either ethanol-based solutions or mupirocin was not significantly associated with DTp development in either direction (p = 0.62).Interestingly, solid silver dressings were found to be associated with a significant decrease in DTp development (p = 0.002).During the study period, the only solid silver dressing in use was a nanocrystalline dressing. | 271556193 |
Mafenide | O=S(N)(c1ccc(cc1)CN)=O | 3 illustrates the association between topical exposure and DTp development.We found that 354 (94.1%) of the isolated pathogens were exposed to a topical antimicrobial agent prior to their development and this exposure was associated with a statistically significant increase in DTp development (p = 0.0002).Exposures to many topical antimicrobials were found to be statistically significant predictors of DTp development, including bacitracin (p < 0.001), Dakins (p = 0.003), silver nitrate solution (p < 0.001), hypochlorous acid (p < 0.001), and other topicals (p = 0.0005), largely composed of antifungal agents including nystatin and clotrimazole.O=S(N)(c1ccc(cc1)CN)=O, silver sulfadiazine (SSD), and mupirocin were not found to be statistically significant predictors of DTp development, though O=S(N)(c1ccc(cc1)CN)=O (i.e., ears) and mupirocin (i.e., most use was a state-mandated routine nasal decolonization before a switch to ethanol-based prophylaxis) are not rarely prescribed in our center.Nasal decolonization with either ethanol-based solutions or mupirocin was not significantly associated with DTp development in either direction (p = 0.62).Interestingly, solid silver dressings were found to be associated with a significant decrease in DTp development (p = 0.002).During the study period, the only solid silver dressing in use was a nanocrystalline dressing. | 271556193 |
Silver sulfadiazine | n1cccnc1[N-]S(c1ccc(cc1)N)(=O)=O.[Ag+] | 3 illustrates the association between topical exposure and DTp development.We found that 354 (94.1%) of the isolated pathogens were exposed to a topical antimicrobial agent prior to their development and this exposure was associated with a statistically significant increase in DTp development (p = 0.0002).Exposures to many topical antimicrobials were found to be statistically significant predictors of DTp development, including bacitracin (p < 0.001), Dakins (p = 0.003), silver nitrate solution (p < 0.001), hypochlorous acid (p < 0.001), and other topicals (p = 0.0005), largely composed of antifungal agents including nystatin and clotrimazole.Mafenide, n1cccnc1[N-]S(c1ccc(cc1)N)(=O)=O.[Ag+] (SSD), and mupirocin were not found to be statistically significant predictors of DTp development, though mafenide (i.e., ears) and mupirocin (i.e., most use was a state-mandated routine nasal decolonization before a switch to ethanol-based prophylaxis) are not rarely prescribed in our center.Nasal decolonization with either ethanol-based solutions or mupirocin was not significantly associated with DTp development in either direction (p = 0.62).Interestingly, solid silver dressings were found to be associated with a significant decrease in DTp development (p = 0.002).During the study period, the only solid silver dressing in use was a nanocrystalline dressing. | 271556193 |
Sulfadiazine | c1c(ccc(c1)N)S(Nc1ncccn1)(=O)=O | 3 illustrates the association between topical exposure and DTp development.We found that 354 (94.1%) of the isolated pathogens were exposed to a topical antimicrobial agent prior to their development and this exposure was associated with a statistically significant increase in DTp development (p = 0.0002).Exposures to many topical antimicrobials were found to be statistically significant predictors of DTp development, including bacitracin (p < 0.001), Dakins (p = 0.003), silver nitrate solution (p < 0.001), hypochlorous acid (p < 0.001), and other topicals (p = 0.0005), largely composed of antifungal agents including nystatin and clotrimazole.Mafenide, silver c1c(ccc(c1)N)S(Nc1ncccn1)(=O)=O (SSD), and mupirocin were not found to be statistically significant predictors of DTp development, though mafenide (i.e., ears) and mupirocin (i.e., most use was a state-mandated routine nasal decolonization before a switch to ethanol-based prophylaxis) are not rarely prescribed in our center.Nasal decolonization with either ethanol-based solutions or mupirocin was not significantly associated with DTp development in either direction (p = 0.62).Interestingly, solid silver dressings were found to be associated with a significant decrease in DTp development (p = 0.002).During the study period, the only solid silver dressing in use was a nanocrystalline dressing. | 271556193 |
Mupirocin | O1C[C@@H]([C@H]([C@H]([C@@H]1C/C(C)=C/C(=O)OCCCCCCCCC(=O)O)O)O)C[C@@H]1O[C@H]1[C@@H](C)[C@H](C)O | 3 illustrates the association between topical exposure and DTp development.We found that 354 (94.1%) of the isolated pathogens were exposed to a topical antimicrobial agent prior to their development and this exposure was associated with a statistically significant increase in DTp development (p = 0.0002).Exposures to many topical antimicrobials were found to be statistically significant predictors of DTp development, including bacitracin (p < 0.001), Dakins (p = 0.003), silver nitrate solution (p < 0.001), hypochlorous acid (p < 0.001), and other topicals (p = 0.0005), largely composed of antifungal agents including nystatin and clotrimazole.Mafenide, silver sulfadiazine (SSD), and O1C[C@@H]([C@H]([C@H]([C@@H]1C/C(C)=C/C(=O)OCCCCCCCCC(=O)O)O)O)C[C@@H]1O[C@H]1[C@@H](C)[C@H](C)O were not found to be statistically significant predictors of DTp development, though mafenide (i.e., ears) and O1C[C@@H]([C@H]([C@H]([C@@H]1C/C(C)=C/C(=O)OCCCCCCCCC(=O)O)O)O)C[C@@H]1O[C@H]1[C@@H](C)[C@H](C)O (i.e., most use was a state-mandated routine nasal decolonization before a switch to ethanol-based prophylaxis) are not rarely prescribed in our center.Nasal decolonization with either ethanol-based solutions or O1C[C@@H]([C@H]([C@H]([C@@H]1C/C(C)=C/C(=O)OCCCCCCCCC(=O)O)O)O)C[C@@H]1O[C@H]1[C@@H](C)[C@H](C)O was not significantly associated with DTp development in either direction (p = 0.62).Interestingly, solid silver dressings were found to be associated with a significant decrease in DTp development (p = 0.002).During the study period, the only solid silver dressing in use was a nanocrystalline dressing. | 271556193 |
Cefazolin | n1(CC(=O)N[C@H]2[C@@H]3N(C2=O)C(C(=O)O)=C(CS3)CSc2nnc(C)s2)nnnc1 | As seen in Figure 4, exposures to many of the tested systemic antimicrobials prior to culture obtainment were also associated with an increased incidence of DTp.In this unadjusted analysis, exposures to non-pseudomonal beta-lactams (e.g., n1(CC(=O)N[C@H]2[C@@H]3N(C2=O)C(C(=O)O)=C(CS3)CSc2nnc(C)s2)nnnc1, ceftriaxone, or ampicillin-sulbactam) and metronidazole were not found to be associated with DTp development (p = 0.95 and 0.66, respectively).In contrast, exposure to all other tested antimicrobials was associated with an increased incidence of DTp development, including: anti-pseudomonal (e.g., cefepime or piperacillin-tazobactam) beta-lactams (p < 0.0001), extended-spectrum (e.g., ceftazidime-avibactam, ceftolozane-tazobactam, or | 271556193 |
Ceftriaxone | C(C1=C(C(=O)O)N2C(=O)[C@@H](NC(=O)/C(=N/OC)C3=CSC(N)=N3)C2SC1)SC1N(C)NC(C(N=1)=O)=O | As seen in Figure 4, exposures to many of the tested systemic antimicrobials prior to culture obtainment were also associated with an increased incidence of DTp.In this unadjusted analysis, exposures to non-pseudomonal beta-lactams (e.g., cefazolin, C(C1=C(C(=O)O)N2C(=O)[C@@H](NC(=O)/C(=N/OC)C3=CSC(N)=N3)C2SC1)SC1N(C)NC(C(N=1)=O)=O, or ampicillin-sulbactam) and metronidazole were not found to be associated with DTp development (p = 0.95 and 0.66, respectively).In contrast, exposure to all other tested antimicrobials was associated with an increased incidence of DTp development, including: anti-pseudomonal (e.g., cefepime or piperacillin-tazobactam) beta-lactams (p < 0.0001), extended-spectrum (e.g., ceftazidime-avibactam, ceftolozane-tazobactam, or | 271556193 |
Ampicillin-sulbactam | C1(S(C2CC(C2C1C(=O)O)=O)(=O)=O)(C)C.C1(C(C2SC(C(C(O)=O)N12)(C)C)NC(C(c1ccccc1)N)=O)=O | As seen in Figure 4, exposures to many of the tested systemic antimicrobials prior to culture obtainment were also associated with an increased incidence of DTp.In this unadjusted analysis, exposures to non-pseudomonal beta-lactams (e.g., cefazolin, ceftriaxone, or C1(S(C2CC(C2C1C(=O)O)=O)(=O)=O)(C)C.C1(C(C2SC(C(C(O)=O)N12)(C)C)NC(C(c1ccccc1)N)=O)=O) and metronidazole were not found to be associated with DTp development (p = 0.95 and 0.66, respectively).In contrast, exposure to all other tested antimicrobials was associated with an increased incidence of DTp development, including: anti-pseudomonal (e.g., cefepime or piperacillin-tazobactam) beta-lactams (p < 0.0001), extended-spectrum (e.g., ceftazidime-avibactam, ceftolozane-tazobactam, or | 271556193 |
Metronidazole | N1=C(N(C(=C1)[N+]([O-])=O)CCO)C | As seen in Figure 4, exposures to many of the tested systemic antimicrobials prior to culture obtainment were also associated with an increased incidence of DTp.In this unadjusted analysis, exposures to non-pseudomonal beta-lactams (e.g., cefazolin, ceftriaxone, or ampicillin-sulbactam) and N1=C(N(C(=C1)[N+]([O-])=O)CCO)C were not found to be associated with DTp development (p = 0.95 and 0.66, respectively).In contrast, exposure to all other tested antimicrobials was associated with an increased incidence of DTp development, including: anti-pseudomonal (e.g., cefepime or piperacillin-tazobactam) beta-lactams (p < 0.0001), extended-spectrum (e.g., ceftazidime-avibactam, ceftolozane-tazobactam, or | 271556193 |
Cefepime | C(=O)(N[C@@H]1C(N2C(=C(CSC21)C[N+]1(CCCC1)C)C([O-])=O)=O)/C(=N/OC)C1=CSC(=N1)N | As seen in Figure 4, exposures to many of the tested systemic antimicrobials prior to culture obtainment were also associated with an increased incidence of DTp.In this unadjusted analysis, exposures to non-pseudomonal beta-lactams (e.g., cefazolin, ceftriaxone, or ampicillin-sulbactam) and metronidazole were not found to be associated with DTp development (p = 0.95 and 0.66, respectively).In contrast, exposure to all other tested antimicrobials was associated with an increased incidence of DTp development, including: anti-pseudomonal (e.g., C(=O)(N[C@@H]1C(N2C(=C(CSC21)C[N+]1(CCCC1)C)C([O-])=O)=O)/C(=N/OC)C1=CSC(=N1)N or piperacillin-tazobactam) beta-lactams (p < 0.0001), extended-spectrum (e.g., ceftazidime-avibactam, ceftolozane-tazobactam, or | 271556193 |
Piperacillin-tazobactam | [C@@H]1(C([O-])=O)N2[C@@H]([C@@H](C2=O)NC(=O)[C@H](C2=CC=CC=C2)NC(=O)N2CCN(C(C2=O)=O)CC)SC1(C)C.N1C=CN(N=1)C[C@]1([C@@H](N2[C@@H](CC2=O)S1(=O)=O)C(O)=O)C.[Na+] | As seen in Figure 4, exposures to many of the tested systemic antimicrobials prior to culture obtainment were also associated with an increased incidence of DTp.In this unadjusted analysis, exposures to non-pseudomonal beta-lactams (e.g., cefazolin, ceftriaxone, or ampicillin-sulbactam) and metronidazole were not found to be associated with DTp development (p = 0.95 and 0.66, respectively).In contrast, exposure to all other tested antimicrobials was associated with an increased incidence of DTp development, including: anti-pseudomonal (e.g., cefepime or [C@@H]1(C([O-])=O)N2[C@@H]([C@@H](C2=O)NC(=O)[C@H](C2=CC=CC=C2)NC(=O)N2CCN(C(C2=O)=O)CC)SC1(C)C.N1C=CN(N=1)C[C@]1([C@@H](N2[C@@H](CC2=O)S1(=O)=O)C(O)=O)C.[Na+]) beta-lactams (p < 0.0001), extended-spectrum (e.g., ceftazidime-avibactam, ceftolozane-tazobactam, or | 271556193 |
Ceftolozane-tazobactam | n1(ccnn1)C[C@]1(C)S([C@H]2N(C(=O)C2)[C@H]1C(O)=O)(=O)=O.C1S[C@@H]2[C@@H](C(N2C(C(=O)[O-])=C1C[n+]1cc(c(n1C)N)NC(=O)NCCN)=O)NC(/C(=N/OC(C)(C(O)=O)C)c1nc(sn1)N)=O.O=S(O)(O)=O | As seen in Figure 4, exposures to many of the tested systemic antimicrobials prior to culture obtainment were also associated with an increased incidence of DTp.In this unadjusted analysis, exposures to non-pseudomonal beta-lactams (e.g., cefazolin, ceftriaxone, or ampicillin-sulbactam) and metronidazole were not found to be associated with DTp development (p = 0.95 and 0.66, respectively).In contrast, exposure to all other tested antimicrobials was associated with an increased incidence of DTp development, including: anti-pseudomonal (e.g., cefepime or piperacillin-tazobactam) beta-lactams (p < 0.0001), extended-spectrum (e.g., ceftazidime-avibactam, n1(ccnn1)C[C@]1(C)S([C@H]2N(C(=O)C2)[C@H]1C(O)=O)(=O)=O.C1S[C@@H]2[C@@H](C(N2C(C(=O)[O-])=C1C[n+]1cc(c(n1C)N)NC(=O)NCCN)=O)NC(/C(=N/OC(C)(C(O)=O)C)c1nc(sn1)N)=O.O=S(O)(O)=O, or | 271556193 |
Cefazolin | O=C(O)C1=C(CSc2sc(nn2)C)CS[C@H]2N1C(=O)[C@H]2NC(Cn1nnnc1)=O | As seen in Figure 4, exposures to many of the tested systemic antimicrobials prior to culture obtainment were also associated with an increased incidence of DTp.In this unadjusted analysis, exposures to non-pseudomonal beta-lactams (e.g., O=C(O)C1=C(CSc2sc(nn2)C)CS[C@H]2N1C(=O)[C@H]2NC(Cn1nnnc1)=O, ceftriaxone, or ampicillin-sulbactam) and metronidazole were not found to be associated with DTp development (p = 0.95 and 0.66, respectively).In contrast, exposure to all other tested antimicrobials was associated with an increased incidence of DTp development, including: anti-pseudomonal (e.g., cefepime or piperacillin-tazobactam) beta-lactams (p < 0.0001), extended-spectrum (e.g., ceftazidime-avibactam, ceftolozane-tazobactam, or meropenemvaborbactam) beta-lactam beta-lactamase inhibitors (p < 0.001), fluoroquinolones (p < 0.001), aminoglycosides (p < 0.001), antifungal agents (p = 0.03), sulfamethoxazole-trimethoprim (p < 0.001), carbapenems (p < 0.001), and tetracyclines (p = 0.01). | 271556193 |
Ceftriaxone | C1(N=C(N(NC1=O)C)SCC1CSC2N(C([C@H]2NC(=O)/C(C2=CSC(N)=N2)=N/OC)=O)C=1C(=O)O)=O | As seen in Figure 4, exposures to many of the tested systemic antimicrobials prior to culture obtainment were also associated with an increased incidence of DTp.In this unadjusted analysis, exposures to non-pseudomonal beta-lactams (e.g., cefazolin, C1(N=C(N(NC1=O)C)SCC1CSC2N(C([C@H]2NC(=O)/C(C2=CSC(N)=N2)=N/OC)=O)C=1C(=O)O)=O, or ampicillin-sulbactam) and metronidazole were not found to be associated with DTp development (p = 0.95 and 0.66, respectively).In contrast, exposure to all other tested antimicrobials was associated with an increased incidence of DTp development, including: anti-pseudomonal (e.g., cefepime or piperacillin-tazobactam) beta-lactams (p < 0.0001), extended-spectrum (e.g., ceftazidime-avibactam, ceftolozane-tazobactam, or meropenemvaborbactam) beta-lactam beta-lactamase inhibitors (p < 0.001), fluoroquinolones (p < 0.001), aminoglycosides (p < 0.001), antifungal agents (p = 0.03), sulfamethoxazole-trimethoprim (p < 0.001), carbapenems (p < 0.001), and tetracyclines (p = 0.01). | 271556193 |
Ampicillin-sulbactam | C(O)(=O)C1C(C)(S(C2C1C(C2)=O)(=O)=O)C.C1(C(O)=O)N2C(SC1(C)C)C(NC(=O)C(N)c1ccccc1)C2=O | As seen in Figure 4, exposures to many of the tested systemic antimicrobials prior to culture obtainment were also associated with an increased incidence of DTp.In this unadjusted analysis, exposures to non-pseudomonal beta-lactams (e.g., cefazolin, ceftriaxone, or C(O)(=O)C1C(C)(S(C2C1C(C2)=O)(=O)=O)C.C1(C(O)=O)N2C(SC1(C)C)C(NC(=O)C(N)c1ccccc1)C2=O) and metronidazole were not found to be associated with DTp development (p = 0.95 and 0.66, respectively).In contrast, exposure to all other tested antimicrobials was associated with an increased incidence of DTp development, including: anti-pseudomonal (e.g., cefepime or piperacillin-tazobactam) beta-lactams (p < 0.0001), extended-spectrum (e.g., ceftazidime-avibactam, ceftolozane-tazobactam, or meropenemvaborbactam) beta-lactam beta-lactamase inhibitors (p < 0.001), fluoroquinolones (p < 0.001), aminoglycosides (p < 0.001), antifungal agents (p = 0.03), sulfamethoxazole-trimethoprim (p < 0.001), carbapenems (p < 0.001), and tetracyclines (p = 0.01). | 271556193 |
Metronidazole | C1(=CN=C(N1CCO)C)[N+]([O-])=O | As seen in Figure 4, exposures to many of the tested systemic antimicrobials prior to culture obtainment were also associated with an increased incidence of DTp.In this unadjusted analysis, exposures to non-pseudomonal beta-lactams (e.g., cefazolin, ceftriaxone, or ampicillin-sulbactam) and C1(=CN=C(N1CCO)C)[N+]([O-])=O were not found to be associated with DTp development (p = 0.95 and 0.66, respectively).In contrast, exposure to all other tested antimicrobials was associated with an increased incidence of DTp development, including: anti-pseudomonal (e.g., cefepime or piperacillin-tazobactam) beta-lactams (p < 0.0001), extended-spectrum (e.g., ceftazidime-avibactam, ceftolozane-tazobactam, or meropenemvaborbactam) beta-lactam beta-lactamase inhibitors (p < 0.001), fluoroquinolones (p < 0.001), aminoglycosides (p < 0.001), antifungal agents (p = 0.03), sulfamethoxazole-trimethoprim (p < 0.001), carbapenems (p < 0.001), and tetracyclines (p = 0.01). | 271556193 |
Cefepime | C1[N+](C)(CCC1)CC1=C(N2C(SC1)[C@@H](C2=O)NC(/C(c1nc(sc1)N)=N/OC)=O)C(=O)[O-] | As seen in Figure 4, exposures to many of the tested systemic antimicrobials prior to culture obtainment were also associated with an increased incidence of DTp.In this unadjusted analysis, exposures to non-pseudomonal beta-lactams (e.g., cefazolin, ceftriaxone, or ampicillin-sulbactam) and metronidazole were not found to be associated with DTp development (p = 0.95 and 0.66, respectively).In contrast, exposure to all other tested antimicrobials was associated with an increased incidence of DTp development, including: anti-pseudomonal (e.g., C1[N+](C)(CCC1)CC1=C(N2C(SC1)[C@@H](C2=O)NC(/C(c1nc(sc1)N)=N/OC)=O)C(=O)[O-] or piperacillin-tazobactam) beta-lactams (p < 0.0001), extended-spectrum (e.g., ceftazidime-avibactam, ceftolozane-tazobactam, or meropenemvaborbactam) beta-lactam beta-lactamase inhibitors (p < 0.001), fluoroquinolones (p < 0.001), aminoglycosides (p < 0.001), antifungal agents (p = 0.03), sulfamethoxazole-trimethoprim (p < 0.001), carbapenems (p < 0.001), and tetracyclines (p = 0.01). | 271556193 |
Piperacillin-tazobactam | c1cc(ccc1)[C@H](NC(N1C(=O)C(N(CC)CC1)=O)=O)C(=O)N[C@H]1[C@H]2SC([C@H](C(=O)[O-])N2C1=O)(C)C.C1C(=O)N2[C@@H]1S(=O)([C@](Cn1ccnn1)(C)[C@@H]2C(O)=O)=O.[Na+] | As seen in Figure 4, exposures to many of the tested systemic antimicrobials prior to culture obtainment were also associated with an increased incidence of DTp.In this unadjusted analysis, exposures to non-pseudomonal beta-lactams (e.g., cefazolin, ceftriaxone, or ampicillin-sulbactam) and metronidazole were not found to be associated with DTp development (p = 0.95 and 0.66, respectively).In contrast, exposure to all other tested antimicrobials was associated with an increased incidence of DTp development, including: anti-pseudomonal (e.g., cefepime or c1cc(ccc1)[C@H](NC(N1C(=O)C(N(CC)CC1)=O)=O)C(=O)N[C@H]1[C@H]2SC([C@H](C(=O)[O-])N2C1=O)(C)C.C1C(=O)N2[C@@H]1S(=O)([C@](Cn1ccnn1)(C)[C@@H]2C(O)=O)=O.[Na+]) beta-lactams (p < 0.0001), extended-spectrum (e.g., ceftazidime-avibactam, ceftolozane-tazobactam, or meropenemvaborbactam) beta-lactam beta-lactamase inhibitors (p < 0.001), fluoroquinolones (p < 0.001), aminoglycosides (p < 0.001), antifungal agents (p = 0.03), sulfamethoxazole-trimethoprim (p < 0.001), carbapenems (p < 0.001), and tetracyclines (p = 0.01). | 271556193 |
Ceftolozane-tazobactam | c1cn(nn1)C[C@@]1(C)[C@@H](N2[C@@H](CC2=O)S1(=O)=O)C(O)=O.OC(=O)C(C)(C)O/N=C(\c1nc(N)sn1)C(=O)N[C@@H]1C(N2[C@@H]1SCC(C[n+]1n(c(N)c(NC(NCCN)=O)c1)C)=C2C([O-])=O)=O.O=S(O)(O)=O | As seen in Figure 4, exposures to many of the tested systemic antimicrobials prior to culture obtainment were also associated with an increased incidence of DTp.In this unadjusted analysis, exposures to non-pseudomonal beta-lactams (e.g., cefazolin, ceftriaxone, or ampicillin-sulbactam) and metronidazole were not found to be associated with DTp development (p = 0.95 and 0.66, respectively).In contrast, exposure to all other tested antimicrobials was associated with an increased incidence of DTp development, including: anti-pseudomonal (e.g., cefepime or piperacillin-tazobactam) beta-lactams (p < 0.0001), extended-spectrum (e.g., ceftazidime-avibactam, c1cn(nn1)C[C@@]1(C)[C@@H](N2[C@@H](CC2=O)S1(=O)=O)C(O)=O.OC(=O)C(C)(C)O/N=C(\c1nc(N)sn1)C(=O)N[C@@H]1C(N2[C@@H]1SCC(C[n+]1n(c(N)c(NC(NCCN)=O)c1)C)=C2C([O-])=O)=O.O=S(O)(O)=O, or meropenemvaborbactam) beta-lactam beta-lactamase inhibitors (p < 0.001), fluoroquinolones (p < 0.001), aminoglycosides (p < 0.001), antifungal agents (p = 0.03), sulfamethoxazole-trimethoprim (p < 0.001), carbapenems (p < 0.001), and tetracyclines (p = 0.01). | 271556193 |
Sulfamethoxazole-trimethoprim | C1C=C(N)C=CC=1S(=O)(=O)NC1=NOC(C)=C1.C1=C(CC2=CC(OC)=C(OC)C(OC)=C2)C(=NC(N)=N1)N | As seen in Figure 4, exposures to many of the tested systemic antimicrobials prior to culture obtainment were also associated with an increased incidence of DTp.In this unadjusted analysis, exposures to non-pseudomonal beta-lactams (e.g., cefazolin, ceftriaxone, or ampicillin-sulbactam) and metronidazole were not found to be associated with DTp development (p = 0.95 and 0.66, respectively).In contrast, exposure to all other tested antimicrobials was associated with an increased incidence of DTp development, including: anti-pseudomonal (e.g., cefepime or piperacillin-tazobactam) beta-lactams (p < 0.0001), extended-spectrum (e.g., ceftazidime-avibactam, ceftolozane-tazobactam, or meropenemvaborbactam) beta-lactam beta-lactamase inhibitors (p < 0.001), fluoroquinolones (p < 0.001), aminoglycosides (p < 0.001), antifungal agents (p = 0.03), C1C=C(N)C=CC=1S(=O)(=O)NC1=NOC(C)=C1.C1=C(CC2=CC(OC)=C(OC)C(OC)=C2)C(=NC(N)=N1)N (p < 0.001), carbapenems (p < 0.001), and tetracyclines (p = 0.01). | 271556193 |
Carbapenems | C(=O)(O)C1=CCC2N1C(=O)C2 | As seen in Figure 4, exposures to many of the tested systemic antimicrobials prior to culture obtainment were also associated with an increased incidence of DTp.In this unadjusted analysis, exposures to non-pseudomonal beta-lactams (e.g., cefazolin, ceftriaxone, or ampicillin-sulbactam) and metronidazole were not found to be associated with DTp development (p = 0.95 and 0.66, respectively).In contrast, exposure to all other tested antimicrobials was associated with an increased incidence of DTp development, including: anti-pseudomonal (e.g., cefepime or piperacillin-tazobactam) beta-lactams (p < 0.0001), extended-spectrum (e.g., ceftazidime-avibactam, ceftolozane-tazobactam, or meropenemvaborbactam) beta-lactam beta-lactamase inhibitors (p < 0.001), fluoroquinolones (p < 0.001), aminoglycosides (p < 0.001), antifungal agents (p = 0.03), sulfamethoxazole-trimethoprim (p < 0.001), C(=O)(O)C1=CCC2N1C(=O)C2 (p < 0.001), and tetracyclines (p = 0.01). | 271556193 |
Silver sulfadiazine | c1ccnc([N-]S(=O)(c2ccc(N)cc2)=O)n1.[Ag+] | \nFigure 3 .\n3\nFigure 3. Impact of exposure to topical antimicrobials prior to culture obtainment on DTp development.* denotes p < 0.05.SSD, c1ccnc([N-]S(=O)(c2ccc(N)cc2)=O)n1.[Ag+]; CHG, chlorohexidine gluconate. | 271556193 |
Sulfadiazine | C1C=C(C=CC=1S(NC1N=CC=CN=1)(=O)=O)N | \nFigure 3 .\n3\nFigure 3. Impact of exposure to topical antimicrobials prior to culture obtainment on DTp development.* denotes p < 0.05.SSD, silver C1C=C(C=CC=1S(NC1N=CC=CN=1)(=O)=O)N; CHG, chlorohexidine gluconate. | 271556193 |
Chlorohexidine | N(=C(/N=C(/Nc1ccc(Cl)cc1)N)N)CCCCCCN=C(N)/N=C(\N)Nc1ccc(cc1)Cl | \nFigure 3 .\n3\nFigure 3. Impact of exposure to topical antimicrobials prior to culture obtainment on DTp development.* denotes p < 0.05.SSD, silver sulfadiazine; CHG, N(=C(/N=C(/Nc1ccc(Cl)cc1)N)N)CCCCCCN=C(N)/N=C(\N)Nc1ccc(cc1)Cl gluconate. | 271556193 |
Gluconate | C(=O)([C@H](O)[C@@H](O)[C@@H]([C@H](O)CO)O)[O-] | \nFigure 3 .\n3\nFigure 3. Impact of exposure to topical antimicrobials prior to culture obtainment on DTp development.* denotes p < 0.05.SSD, silver sulfadiazine; CHG, chlorohexidine C(=O)([C@H](O)[C@@H](O)[C@@H]([C@H](O)CO)O)[O-]. | 271556193 |
Silver sulfadiazine | n1cccnc1[N-]S(c1ccc(N)cc1)(=O)=O.[Ag+] | \nFigure 3 .\n3\nFigure 3. Impact of to topical antimicrobials prior to culture obtainment on DTp development.* denotes p < 0.05.SSD, n1cccnc1[N-]S(c1ccc(N)cc1)(=O)=O.[Ag+]; CHG, chlorohexidine gluconate. | 271556193 |
Sulfadiazine | C1=CC(=CC=C1S(NC1=NC=CC=N1)(=O)=O)N | \nFigure 3 .\n3\nFigure 3. Impact of to topical antimicrobials prior to culture obtainment on DTp development.* denotes p < 0.05.SSD, silver C1=CC(=CC=C1S(NC1=NC=CC=N1)(=O)=O)N; CHG, chlorohexidine gluconate. | 271556193 |
Chlorohexidine | C(/N=C(\N)Nc1ccc(Cl)cc1)(=NCCCCCCN=C(/N=C(/Nc1ccc(Cl)cc1)N)N)N | \nFigure 3 .\n3\nFigure 3. Impact of to topical antimicrobials prior to culture obtainment on DTp development.* denotes p < 0.05.SSD, silver sulfadiazine; CHG, C(/N=C(\N)Nc1ccc(Cl)cc1)(=NCCCCCCN=C(/N=C(/Nc1ccc(Cl)cc1)N)N)N gluconate. | 271556193 |
Gluconate | [C@@H](O)([C@H]([C@H](O)[C@H](O)CO)O)C(=O)[O-] | \nFigure 3 .\n3\nFigure 3. Impact of to topical antimicrobials prior to culture obtainment on DTp development.* denotes p < 0.05.SSD, silver sulfadiazine; CHG, chlorohexidine [C@@H](O)([C@H]([C@H](O)[C@H](O)CO)O)C(=O)[O-]. | 271556193 |
Sulfamethoxazole-trimethoprim | N(S(=O)(C1=CC=C(N)C=C1)=O)C1=NOC(C)=C1.C1C(CC2=CN=C(N)N=C2N)=CC(=C(C=1OC)OC)OC | \nFigure 4 .\n4\nFigure 4. Impact of exposure to systemic antimicrobials prior to culture obtainment on DTp development.* Denotes p < 0.05.Non-Pse BL, non-pseudomonal beta-lactam; Anti-Pse BL, anti-pseudomonal beta-lactam; Ext Spec BLI, extended-spectrum beta-lactam beta-lactamase inhibitor; FQ, fluoroquinolone; MRSA, methicillin-resistant Staphylococcus aureus; AMG, aminoglycoside; Sulfa/Trim, N(S(=O)(C1=CC=C(N)C=C1)=O)C1=NOC(C)=C1.C1C(CC2=CN=C(N)N=C2N)=CC(=C(C=1OC)OC)OC; TCN, tetracycline. | 271556193 |
Tetracycline | CN([C@H]1[C@@H]2C[C@H]3C(C(=O)[C@@]2(C(=C(C1=O)C(=O)N)O)O)=C(O)C1=C(C=CC=C1O)[C@@]3(C)O)C | \nFigure 4 .\n4\nFigure 4. Impact of exposure to systemic antimicrobials prior to culture obtainment on DTp development.* Denotes p < 0.05.Non-Pse BL, non-pseudomonal beta-lactam; Anti-Pse BL, anti-pseudomonal beta-lactam; Ext Spec BLI, extended-spectrum beta-lactam beta-lactamase inhibitor; FQ, fluoroquinolone; MRSA, methicillin-resistant Staphylococcus aureus; AMG, aminoglycoside; Sulfa/Trim, sulfamethoxazole-trimethoprim; TCN, CN([C@H]1[C@@H]2C[C@H]3C(C(=O)[C@@]2(C(=C(C1=O)C(=O)N)O)O)=C(O)C1=C(C=CC=C1O)[C@@]3(C)O)C. | 271556193 |
Sulfamethoxazole-trimethoprim | C1C(=CC=C(C=1)S(=O)(=O)NC1C=C(ON=1)C)N.C1(OC)=CC(CC2=CN=C(N)N=C2N)=CC(=C1OC)OC | \nFigure 4 .\n4\nFigure 4. Impact of exposure to systemic antimicrobials prior to culture obtainment on DTp development.* Denotes p < 0.05.Non-Pse BL, non-pseudomonal beta-lactam; Anti-Pse BL, anti-pseudomonal beta-lactam; Ext Spec BLI, extended-spectrum beta-lactam beta-lactamase inhibitor; FQ, fluoroquinolone; MRSA, methicillin-resistant Staphylococcus aureus; AMG, aminoglycoside; Sulfa/Trim, C1C(=CC=C(C=1)S(=O)(=O)NC1C=C(ON=1)C)N.C1(OC)=CC(CC2=CN=C(N)N=C2N)=CC(=C1OC)OC; TCN, tetracycline. | 271556193 |
Tetracycline | c1cc(c2C(=C3[C@@H]([C@@](O)(C)c2c1)C[C@@H]1[C@@](O)(C(=C(C(=O)N)C(=O)[C@H]1N(C)C)O)C3=O)O)O | \nFigure 4 .\n4\nFigure 4. Impact of exposure to systemic antimicrobials prior to culture obtainment on DTp development.* Denotes p < 0.05.Non-Pse BL, non-pseudomonal beta-lactam; Anti-Pse BL, anti-pseudomonal beta-lactam; Ext Spec BLI, extended-spectrum beta-lactam beta-lactamase inhibitor; FQ, fluoroquinolone; MRSA, methicillin-resistant Staphylococcus aureus; AMG, aminoglycoside; Sulfa/Trim, sulfamethoxazole-trimethoprim; TCN, c1cc(c2C(=C3[C@@H]([C@@](O)(C)c2c1)C[C@@H]1[C@@](O)(C(=C(C(=O)N)C(=O)[C@H]1N(C)C)O)C3=O)O)O. | 271556193 |
Sulfamethoxazole-trimethoprim | C1(=NOC(=C1)C)NS(=O)(=O)C1C=CC(=CC=1)N.N1=C(N)C(=CN=C1N)CC1=CC(OC)=C(OC)C(=C1)OC | \nfold increased risk of DTp development [OR 3.45 (95% C.I. 1.82, 6.53)], while exposure to anti-pseudomonal beta-lactams [OR 2.91 (95% C.I. 1.67, 5.06)], MRSA agents [OR 2.73 (95% C.I. 1.58, 4.68)], extended-spectrum beta-lactam beta-lactamase inhibitors [OR 2.25 (95% C.I. 1.26, 4.03)], and C1(=NOC(=C1)C)NS(=O)(=O)C1C=CC(=CC=1)N.N1=C(N)C(=CN=C1N)CC1=CC(OC)=C(OC)C(=C1)OC [OR 2.14 (95% C.I. 1.21, 3.79)] were associated with a 2-3-times increased risk of DTp development.Exposure to nonpseudomonal beta-lactams gained significance after controlling for TBSA and flame injury [OR 1.67 (95% C.I. 1.04, 2.69)].Exposure to antifungal agents was not found to be associated with DTp development after controlling for TBSA and flame, though antifungal agents were uncommon. | 271556193 |
Carbapenem | O=C1N2C=CC[C@@H]2C1 | \n(4.2%) CRAB, and 26 (12.2%) were Stenotrophomonas maltophilia.No vancomycin-resistance was observed in this cohort.The median time to DTp development was found to be 19 (10, 164) days.Infections with MRSA developed most rapidly with a median of 16 (8, 164) days, while DTR-Pseudomonas spp.took the longest to develop with a median of 52 (17.75, 88) days.Organisms producing ESBLs or AmpCs, or exhibiting O=C1N2C=CC[C@@H]2C1 resistance, all had a median time to development of 22 days.\nDays to first BWE b Days to final graft b2 (1, 3) 20 (7, 34)2 (1, 4) 7 (4, 13)0.84 0.003BWE, burn wound excision; a n (%), b median (25th, 75th percentile). | 271556193 |
Carbapenem | C1[C@@H]2CC(=O)N2C=C1 | (4.2%) CRAB, and 26 (12.2%) were Stenotrophomonas maltophilia.No vancomycin-resistance was observed in this cohort.The median time to DTp development was found to be 19 (10, 164) days.Infections with MRSA developed most rapidly with a median of 16 (8, 164) days, while DTR-Pseudomonas spp.took the longest to develop with a median of 52 (17.75, 88) days.Organisms producing ESBLs or AmpCs, or exhibiting C1[C@@H]2CC(=O)N2C=C1 resistance, all had a median time to development of 22 days. | 271556193 |
Carbapenems | C1C2N(C1=O)C(=CC2)C(=O)O | \n., this analysis identified bacitracin exposure prior to culture obtainment [OR 2.7 (95% C.I. 1.57, 4.65)], silver nitrate solution exposure prior to culture obtainment [OR 1.89 (95% C.I. 1.1, 3.26)], and exposure to anti-pseudomonal beta-lactams prior to culture obtainment [OR 2.6 (95% C.I. 1.46, 4.61)] as the most significant predictors of DTp development.\nPathogens 2024, 13, x FOR PEER REVIEW9 of 16Pathogens 2024, 13, 628meropenem-vaborbactam) beta-lactam beta-lactamase inhibitors (p < 0.001), fluoroquin-9 of 16 olones (p < 0.001), aminoglycosides (p < 0.001), antifungal agents (p = 0.03), sulfamethoxa-zole-trimethoprim (p < 0.001), C1C2N(C1=O)C(=CC2)C(=O)O (p < 0.001), and tetracyclines (p = 0.01). | 271556193 |
Chlorohexidine | C(CN=C(/N=C(\N)NC1C=CC(Cl)=CC=1)N)CCCCN=C(N)/N=C(/NC1=CC=C(Cl)C=C1)N | \nTable 5 .\n5\nResults of the individual multivariable logistic regressions for topical exposures found to be statistically significant.\nExposureOR95% CIBacitracin3.161.88, 5.32Flame5.001.84, 13.54TBSA1.021, 1.03Silver nitrate solution2.581.54, 4.32Flame4.291.6, 11.5TBSA1.011, 1.03Hypochlorous acid2.441.45, 4.11Flame4.151.55, 11.08TBSA1.021, 1.03Other topical1.991.14, 3.46Flame3.161.19, 8.38TBSA1.021.01, 1.04Solid silver dressing0.420.24, 0.72Flame3.881.46, 10.28TBSA1.021.01, 1.04CHG bathing1.811.1, 2.97Flame3.561.35, 9.4TBSA1.021, 1.03\nCHG, C(CN=C(/N=C(\N)NC1C=CC(Cl)=CC=1)N)CCCCN=C(N)/N=C(/NC1=CC=C(Cl)C=C1)N gluconate; CI, confidence interval; OR, odds ratio; TBSA, total body surface area. | 271556193 |
Gluconate | [O-]C([C@@H]([C@@H](O)[C@H](O)[C@@H](CO)O)O)=O | \nTable 5 .\n5\nResults of the individual multivariable logistic regressions for topical exposures found to be statistically significant.\nExposureOR95% CIBacitracin3.161.88, 5.32Flame5.001.84, 13.54TBSA1.021, 1.03Silver nitrate solution2.581.54, 4.32Flame4.291.6, 11.5TBSA1.011, 1.03Hypochlorous acid2.441.45, 4.11Flame4.151.55, 11.08TBSA1.021, 1.03Other topical1.991.14, 3.46Flame3.161.19, 8.38TBSA1.021.01, 1.04Solid silver dressing0.420.24, 0.72Flame3.881.46, 10.28TBSA1.021.01, 1.04CHG bathing1.811.1, 2.97Flame3.561.35, 9.4TBSA1.021, 1.03\nCHG, chlorohexidine [O-]C([C@@H]([C@@H](O)[C@H](O)[C@@H](CO)O)O)=O; CI, confidence interval; OR, odds ratio; TBSA, total body surface area. | 271556193 |
Not specified | C1C[C@H]([C@@H]2N(S(=O)(O1)=O)C(=O)O[C@@H]2CCC1=CC=CC=C1)O[Si](C)(C)C(C)(C)C | \n-face parent and teacher groups (community) Parents' knowledge and skills Children's behaviour and discipline C1C[C@H]([C@@H]2N(S(=O)(O1)=O)C(=O)O[C@@H]2CCC1=CC=CC=C1)O[Si](C)(C)C(C)(C)C Kurani et al. (2009) Face-to-face parent groups (home and school) Parents' knowledge and skills Children's social/emotional support Academic performance -face parent and teacher groups (home and school) Parents' knowledge, skills, and confidence Children'Hampshire et al. (2016) Face-to-face parent and teacher groups (home) Academic performance and attainment C1C[C@H]([C@@H]2N(S(=O)(O1)=O)C(=O)O[C@@H]2CCC1=CC=CC=C1)O[Si](C)(C)C(C)(C)C (Continued) | 261595698 |
Percoll | N(C(C(=Cc1ccc(N(CCC)CCC)cc1)C#N)=O)CC(CO)C.C(#N)C(S(=O)(NCC(CO)C)=O)=Cc1ccc2c(c1)ccc(N(CCC)CCC)c2.c1(C=C(C(NCC(C)CO)=O)C#N)ccc(cc1)N(CC)CC.C(C)N(CC)c1cc2c(cc(cc2)C=C(S(=O)(NCC(C)CO)=O)C#N)cc1.C(C(=Cc1ccc(cc1)N(C)C)C(=O)NCC(CO)C)#N.N(S(=O)(=O)C(=Cc1cc2c(cc(NCCN3CCOCC3)cc2)cc1)C#N)CC(CO)C.C1CCCCN1c1cc2c(cc1)cc(C=C(C#N)S(=O)(NCC(C)CO)=O)cc2.C(C(CNS(=O)(C(C#N)=Cc1ccc2cc(ccc2c1)N1CCN(C)CC1)=O)C)O.CC(CNS(=O)(C(C#N)=Cc1ccc2cc(ccc2c1)N1CCOCC1)=O)CO | Natural killer (NK) 1 cells are a heterogeneous population of lymphoid cells from an unimmunized host that are able to lyse certain tumor cells and virally infected cells through a mechanism unrestricted by the major histocompatibility complex (MHC). Human lymphocytes with NK activity can be highly enriched in the low density fractions of discontinuous N(C(C(=Cc1ccc(N(CCC)CCC)cc1)C#N)=O)CC(CO)C.C(#N)C(S(=O)(NCC(CO)C)=O)=Cc1ccc2c(c1)ccc(N(CCC)CCC)c2.c1(C=C(C(NCC(C)CO)=O)C#N)ccc(cc1)N(CC)CC.C(C)N(CC)c1cc2c(cc(cc2)C=C(S(=O)(NCC(C)CO)=O)C#N)cc1.C(C(=Cc1ccc(cc1)N(C)C)C(=O)NCC(CO)C)#N.N(S(=O)(=O)C(=Cc1cc2c(cc(NCCN3CCOCC3)cc2)cc1)C#N)CC(CO)C.C1CCCCN1c1cc2c(cc1)cc(C=C(C#N)S(=O)(NCC(C)CO)=O)cc2.C(C(CNS(=O)(C(C#N)=Cc1ccc2cc(ccc2c1)N1CCN(C)CC1)=O)C)O.CC(CNS(=O)(C(C#N)=Cc1ccc2cc(ccc2c1)N1CCOCC1)=O)CO gradients (1). Morphological examination of this low density population demonstrates that the majority of these cells are large granular ]ymphocytes (LGL) (1). Recently (2)(3)(4)(5), several murine monoclonal antibodies, including anti-Leu-11, B73.1, 3G8, and VEP 13, have been produced that react with essentially all human NK cells, but not T cells, B cells, or monocytes. Anti-Leu-11 and related mAb react with an antigen associated with the Fc receptor for IgG present on NK cells and neutrophils, and can specifically inhibit Fc receptor-mediated functions (2,3,5). | 5903544 |
Mitomycin | O=C1C2[C@@H](COC(=O)N)[C@@]3(OC)[C@@H]4[C@H](CN3C=2C(=O)C(C)=C1N)N4 | In the present experiments, we have questioned whether NK cells can be activated by direct stimulation with the NK-sensitive tumor cell line, K562. Using highly purified populations of NK (Leu-11 +) and T (Leu-11-) lymphocytes, we observed that Leu-11 + cells were activated when cocultured with O=C1C2[C@@H](COC(=O)N)[C@@]3(OC)[C@@H]4[C@H](CN3C=2C(=O)C(C)=C1N)N4 Ctreated K562 cells. This activation process resulted in proliferation, enhanced cytotoxic activity, and expression of activation antigens, such as transferrin receptor and class II MHC antigens. The activation was a direct consequence of interactions between Leu-ll + cells and K562. Exogenous growth factors or accessory cells were not required. Previously (2), we demonstrated that Leu-11 + lymphocytes could be divided into discrete subpopulations on the basis of Leu-7 antigen expression. We now report that expression of the Leu-7 antigen can be induced in the Leu-7+l 1 + subset by activation with K562. In contrast, stimulation of the Leu-7+l 1 + cells with K562 did not affect the antigenic phenotype. These data establish a developmental relationship between the Leu-7-11 ÷ and Leu-7+11 + cells and are consistent with the possibility that Leu-7 is a differentiation antigen that appears late in the development of NK cells. | 5903544 |
Percoll | c1c(N(CCC)CCC)ccc(c1)C=C(C#N)C(=O)NCC(CO)C.c1c(ccc2cc(N(CCC)CCC)ccc21)C=C(C#N)S(=O)(NCC(CO)C)=O.c1(C=C(C(NCC(C)CO)=O)C#N)ccc(N(CC)CC)cc1.C(=C(S(=O)(=O)NCC(C)CO)C#N)c1ccc2c(ccc(c2)N(CC)CC)c1.c1cc(N(C)C)ccc1C=C(C(NCC(C)CO)=O)C#N.c1c2ccc(cc2ccc1C=C(S(=O)(NCC(C)CO)=O)C#N)NCCN1CCOCC1.C(O)C(CNS(C(=Cc1cc2ccc(N3CCCCC3)cc2cc1)C#N)(=O)=O)C.C(C(S(=O)(NCC(C)CO)=O)=Cc1cc2ccc(cc2cc1)N1CCN(CC1)C)#N.O=S(C(C#N)=Cc1ccc2c(ccc(N3CCOCC3)c2)c1)(=O)NCC(C)CO | Enrichment of LGL. Monocytes were depleted from the peripheral blood mononuclear cells by adherence to plastic tissue culture flasks (26). B lymphocytes and residual adherent cells were removed by passing the cells through nylon wool (26). Nylon wool-nonadherent cells were layered onto a cushion of 43.5% c1c(N(CCC)CCC)ccc(c1)C=C(C#N)C(=O)NCC(CO)C.c1c(ccc2cc(N(CCC)CCC)ccc21)C=C(C#N)S(=O)(NCC(CO)C)=O.c1(C=C(C(NCC(C)CO)=O)C#N)ccc(N(CC)CC)cc1.C(=C(S(=O)(=O)NCC(C)CO)C#N)c1ccc2c(ccc(c2)N(CC)CC)c1.c1cc(N(C)C)ccc1C=C(C(NCC(C)CO)=O)C#N.c1c2ccc(cc2ccc1C=C(S(=O)(NCC(C)CO)=O)C#N)NCCN1CCOCC1.C(O)C(CNS(C(=Cc1cc2ccc(N3CCCCC3)cc2cc1)C#N)(=O)=O)C.C(C(S(=O)(NCC(C)CO)=O)=Cc1cc2ccc(cc2cc1)N1CCN(CC1)C)#N.O=S(C(C#N)=Cc1ccc2c(ccc(N3CCOCC3)c2)c1)(=O)NCC(C)CO, centrifuged for 50 min at 300 g, and the low density fraction was harvested from the gradient interface. We have demonstrated (26), using this procedure, that essentially all lymphocytes with NK activity are contained in the low density fraction. Typically, ~30-60% of the low density lymphocytes expressed the NK cell-associated antigen, Leu-11, whereas ~40-70% expressed the pan T cell antigen, CD3, depending on the individual donor. Monoclonal Antibodies. All antibodies were prepared by the Becton Dickinson Monoclonal Center, Inc. Anti-Tac (IL-2 receptor) mAb was generously provided by Dr. T. Waldmann, National Institutes of Health (27). Anti-Leu-4 mAb recognizes the pan T cell antigen CD3. Anti-Leu-11 reacts with an antigen (CD 16) associated with the Fc receptor for IgG present on essentially all NK cells and neutrophils (2,5). Anti-Leu-2a and anti-Leu-3a react with the CD8 and CD4 antigens, respectively. Anti-Leu-7 reacts with a subset of NK cells (2,28). Anti-Leu-15 reacts with an antigen associated with the complement receptor type 3 (CRy) (L. Lanier and G. Ross, unpublished observation). Anti-Leu-M3 reacts with an antigen exclusively present on monocytes. The CD nomenclature for human differentiation antigens, proposed by the International Workshop on Human Leukocyte Differentiation Antigens (29) and approved by the World Health Organization, will be used to describe the T cell differentiation antigens discussed in this paper. Immunofluorescence and Flow Cytometry. Immunofluorescent staining procedures have been described previously (2,30). Fluorochrome-conjugated, isotype-matched mAb that did not specifically react with human cells were used to control for nonspecific binding. Immunofluorescence was measured using a fluorescence-activated cell sorter (FACS) (FACS 440; Becton Dickinson Immunocytometry Systems, Mountain View, CA). Methods of flow cytometry have been described in detail elsewhere (2,30). Tumor Cells. All tumor cell lines were obtained from the American Type Culture Collection, Rockville, MD and were tested monthly to ensure against mycoplasma contamination. | 5903544 |
Mitomycin | C1(C(=C(C)C(=O)C2N3[C@](OC)([C@@H]4[C@H](C3)N4)[C@@H](C1=2)COC(=O)N)N)=O | In Vitro Stimulation of Lymphocytes Subsets. Lymphocytes were cocultured with C1(C(=C(C)C(=O)C2N3[C@](OC)([C@@H]4[C@H](C3)N4)[C@@H](C1=2)COC(=O)N)N)=O C-treated (80 ~g/ml, 1 h) tumor cells in RPMI 1640 (Irvine Scientific, Santa Ana, CA) supplemented with 5% heat-inactivated horse serum (JR Scientific, Woodland, CA), 1 mM glutamine (Gibco Laboratories, Grand Island, NY), and antibiotics (complete culture medium). Responder cells in complete culture medium (0.5-5 × 106/ml) were mixed with stimulator cells (0.1-1.0 × 106/ml) to achieve a ratio of 5:1. Cells were placed into 96well round-bottom or 24-well plastic tissue culture plates (Falcon Plastics, Oxnard, CA). Lymphocytes (1 × 106/ml) in complete culture medium were stimulated with phytohemagglutinin (PHA-M) (Gibco Laboratories) at a concentration of 2% (wt/vol). Lymphocyte proliferation was measured by incorporation of [~H]thymidine. Cultures were pulsed overnight with 1 uCi [gH]thymidine (Amersham Corp., Arlington Heights, IL), and the cells harvested using a PHD Celt Harvester (Cambridge Technology, Inc., Cambridge, MA). Samples were placed in vials containing Complete Counting Cocktail 3a20 (Research Products International Corp., Mt. Prospect, IL) and the radioactivity determined using an LS 7800 liquid scintillation counter (Beckman Instruments, Inc., Fullerton, CA). The mean of triplicate samples was used for all statistical evaluation. | 5903544 |
Glutamine | C(=O)(O)[C@@H](N)CCC(N)=O | In Vitro Stimulation of Lymphocytes Subsets. Lymphocytes were cocultured with mitomycin C-treated (80 ~g/ml, 1 h) tumor cells in RPMI 1640 (Irvine Scientific, Santa Ana, CA) supplemented with 5% heat-inactivated horse serum (JR Scientific, Woodland, CA), 1 mM C(=O)(O)[C@@H](N)CCC(N)=O (Gibco Laboratories, Grand Island, NY), and antibiotics (complete culture medium). Responder cells in complete culture medium (0.5-5 × 106/ml) were mixed with stimulator cells (0.1-1.0 × 106/ml) to achieve a ratio of 5:1. Cells were placed into 96well round-bottom or 24-well plastic tissue culture plates (Falcon Plastics, Oxnard, CA). Lymphocytes (1 × 106/ml) in complete culture medium were stimulated with phytohemagglutinin (PHA-M) (Gibco Laboratories) at a concentration of 2% (wt/vol). Lymphocyte proliferation was measured by incorporation of [~H]thymidine. Cultures were pulsed overnight with 1 uCi [gH]thymidine (Amersham Corp., Arlington Heights, IL), and the cells harvested using a PHD Celt Harvester (Cambridge Technology, Inc., Cambridge, MA). Samples were placed in vials containing Complete Counting Cocktail 3a20 (Research Products International Corp., Mt. Prospect, IL) and the radioactivity determined using an LS 7800 liquid scintillation counter (Beckman Instruments, Inc., Fullerton, CA). The mean of triplicate samples was used for all statistical evaluation. | 5903544 |
Thymidine | N1C(C(=CN(C1=O)[C@@H]1O[C@H](CO)[C@@H](O)C1)C)=O | In Vitro Stimulation of Lymphocytes Subsets. Lymphocytes were cocultured with mitomycin C-treated (80 ~g/ml, 1 h) tumor cells in RPMI 1640 (Irvine Scientific, Santa Ana, CA) supplemented with 5% heat-inactivated horse serum (JR Scientific, Woodland, CA), 1 mM glutamine (Gibco Laboratories, Grand Island, NY), and antibiotics (complete culture medium). Responder cells in complete culture medium (0.5-5 × 106/ml) were mixed with stimulator cells (0.1-1.0 × 106/ml) to achieve a ratio of 5:1. Cells were placed into 96well round-bottom or 24-well plastic tissue culture plates (Falcon Plastics, Oxnard, CA). Lymphocytes (1 × 106/ml) in complete culture medium were stimulated with phytohemagglutinin (PHA-M) (Gibco Laboratories) at a concentration of 2% (wt/vol). Lymphocyte proliferation was measured by incorporation of [~H]N1C(C(=CN(C1=O)[C@@H]1O[C@H](CO)[C@@H](O)C1)C)=O. Cultures were pulsed overnight with 1 uCi [gH]N1C(C(=CN(C1=O)[C@@H]1O[C@H](CO)[C@@H](O)C1)C)=O (Amersham Corp., Arlington Heights, IL), and the cells harvested using a PHD Celt Harvester (Cambridge Technology, Inc., Cambridge, MA). Samples were placed in vials containing Complete Counting Cocktail 3a20 (Research Products International Corp., Mt. Prospect, IL) and the radioactivity determined using an LS 7800 liquid scintillation counter (Beckman Instruments, Inc., Fullerton, CA). The mean of triplicate samples was used for all statistical evaluation. | 5903544 |
Methanol | OC | Morphology. Cells were cytocentrifuged onto ethanol-cleaned glass slides. The specimens were fixed in absolute OC for 10 min, air dried, stained in a 10% aqueous solution of Giemsa for 10 min, and washed in distilled water. | 5903544 |
Distilled water | O | Morphology. Cells were cytocentrifuged onto ethanol-cleaned glass slides. The specimens were fixed in absolute methanol for 10 min, air dried, stained in a 10% aqueous solution of Giemsa for 10 min, and washed in O. | 5903544 |
Fluorescein | c1cc2C3(c4ccc(O)cc4Oc2cc1O)OC(c1c3cccc1)=O | Stimulation of Leu-l l-and Leu-l l + Lymphocytes With K562. Peripheral blood lymphocytes from randomly selected normal individuals, depleted of monocytes by adherence, were stained with c1cc2C3(c4ccc(O)cc4Oc2cc1O)OC(c1c3cccc1)=O isothiocyanate (FITC)-conjugated anti-Leu-11 a mAb. ~ 10-20% of the lymphocytes were antigen positive, depending on the donor. Lymphocytes were sorted into Leu-11-and Leu-11 ÷ fractions using a FACS. The isolated subpopulations, >90% pure as determined by reanalysis, were cocultured with an NK-sensitive tumor cell line, K562, or a relatively NK-insensitive B cell line, CCRF-SB. The stimulator cell lines were treated with mitomycin C to prevent cell division. Proliferation by the responder cells was measured on day 6 by [3H]thymidine incorporation. Leu-ll + cells significantly proliferated in response to coculture with K562, but usually not CCRF-SB (Table I). In contrast, Leu-11-lymphocytes strongly proliferated in response to the B cell line CCRF-SB, but reacted only weakly against K562. This preferential activation of Leu-1 ! + cells against K562 was observed in all donors, although the magnitude of the response varied (Table I). Kinetic studies revealed that the proliferative response of both the T lymphocytes against CCRF-SB and the NK cells against K562 peaked on day 5 of culture ( Fig. 1). | 5903544 |
Mitomycin | O=C1C2=C(C(=O)C(C)=C1N)N1[C@@]([C@@H]3[C@@H](N3)C1)(OC)[C@@H]2COC(N)=O | Stimulation of Leu-l l-and Leu-l l + Lymphocytes With K562. Peripheral blood lymphocytes from randomly selected normal individuals, depleted of monocytes by adherence, were stained with fluorescein isothiocyanate (FITC)-conjugated anti-Leu-11 a mAb. ~ 10-20% of the lymphocytes were antigen positive, depending on the donor. Lymphocytes were sorted into Leu-11-and Leu-11 ÷ fractions using a FACS. The isolated subpopulations, >90% pure as determined by reanalysis, were cocultured with an NK-sensitive tumor cell line, K562, or a relatively NK-insensitive B cell line, CCRF-SB. The stimulator cell lines were treated with O=C1C2=C(C(=O)C(C)=C1N)N1[C@@]([C@@H]3[C@@H](N3)C1)(OC)[C@@H]2COC(N)=O C to prevent cell division. Proliferation by the responder cells was measured on day 6 by [3H]thymidine incorporation. Leu-ll + cells significantly proliferated in response to coculture with K562, but usually not CCRF-SB (Table I). In contrast, Leu-11-lymphocytes strongly proliferated in response to the B cell line CCRF-SB, but reacted only weakly against K562. This preferential activation of Leu-1 ! + cells against K562 was observed in all donors, although the magnitude of the response varied (Table I). Kinetic studies revealed that the proliferative response of both the T lymphocytes against CCRF-SB and the NK cells against K562 peaked on day 5 of culture ( Fig. 1). | 5903544 |
Thymidine | c1(=O)[nH]c(c(cn1[C@H]1C[C@H](O)[C@H](O1)CO)C)=O | Stimulation of Leu-l l-and Leu-l l + Lymphocytes With K562. Peripheral blood lymphocytes from randomly selected normal individuals, depleted of monocytes by adherence, were stained with fluorescein isothiocyanate (FITC)-conjugated anti-Leu-11 a mAb. ~ 10-20% of the lymphocytes were antigen positive, depending on the donor. Lymphocytes were sorted into Leu-11-and Leu-11 ÷ fractions using a FACS. The isolated subpopulations, >90% pure as determined by reanalysis, were cocultured with an NK-sensitive tumor cell line, K562, or a relatively NK-insensitive B cell line, CCRF-SB. The stimulator cell lines were treated with mitomycin C to prevent cell division. Proliferation by the responder cells was measured on day 6 by [3H]c1(=O)[nH]c(c(cn1[C@H]1C[C@H](O)[C@H](O1)CO)C)=O incorporation. Leu-ll + cells significantly proliferated in response to coculture with K562, but usually not CCRF-SB (Table I). In contrast, Leu-11-lymphocytes strongly proliferated in response to the B cell line CCRF-SB, but reacted only weakly against K562. This preferential activation of Leu-1 ! + cells against K562 was observed in all donors, although the magnitude of the response varied (Table I). Kinetic studies revealed that the proliferative response of both the T lymphocytes against CCRF-SB and the NK cells against K562 peaked on day 5 of culture ( Fig. 1). | 5903544 |
Mitomycin | NC1C(C2=C(N3[C@]([C@@H]4[C@H](C3)N4)([C@@H]2COC(N)=O)OC)C(=O)C=1C)=O | Peripheral blood mononuclear celts were stained with F1TC anti-Leu-1 la mAb, then separated into Leu-11-and Leu-11 ÷ lymphocyte subpopulations using a FACS. Reanalysis of the sorted cells indicated >95% purity. Lymphocytes were cocultured with or without NC1C(C2=C(N3[C@]([C@@H]4[C@H](C3)N4)([C@@H]2COC(N)=O)OC)C(=O)C=1C)=O C-treated K562 or CCRF-SB tumor cells, as indicated. The culture wells were pulses overnight with 1 gCi [~H]thymidine and harvested after 6 d culture. * Background thymidine incorporation by the NC1C(C2=C(N3[C@]([C@@H]4[C@H](C3)N4)([C@@H]2COC(N)=O)OC)C(=O)C=1C)=O C-treated K562 or CCRF-SB tumor cells (tumor inactivation control) was subtracted from the raw counts to determine the specific incorporation by the effector cell population. Stimulation index: (cpm with stimulator)/(cpm without stimulator). . Blastogenesis and expression of activation antigens on lymphocyte subsets cocultured with K562. Peripheral blood mononuclear cells were stained with FITC anti-Leu-1 la mAb and separated into Leu-11-and Leu-11 + lymphocyte subpopulations using a FACS. Reanalysis indicated >90% purity. >99% of the sorted cells were lymphocytes by morphological criteria. Leu-11-(left) and Leu-11 + (right) lymphocytes were cocuhured with NC1C(C2=C(N3[C@]([C@@H]4[C@H](C3)N4)([C@@H]2COC(N)=O)OC)C(=O)C=1C)=O Ctreated K562 in 24-well culture plates. After 6 d, cells were harvested and stained with: FITC IgG and PE IgG control antibodies; FITC anti-Leu-1 la and PE anti-Tac; or FITC anti-Leu-1 la and PE anti-HLA-DR. In the upper panels, histograms displaying the forward angle light scatter are presented (x axis, 256 channels, linear scale; y axis, relative number of cells). Forward angle light scatter measurements essentially reflect cell size for lymphoid cells (31). | 5903544 |
Thymidine | c1(C)c([nH]c(n([C@@H]2O[C@H](CO)[C@H](C2)O)c1)=O)=O | Peripheral blood mononuclear celts were stained with F1TC anti-Leu-1 la mAb, then separated into Leu-11-and Leu-11 ÷ lymphocyte subpopulations using a FACS. Reanalysis of the sorted cells indicated >95% purity. Lymphocytes were cocultured with or without mitomycin C-treated K562 or CCRF-SB tumor cells, as indicated. The culture wells were pulses overnight with 1 gCi [~H]c1(C)c([nH]c(n([C@@H]2O[C@H](CO)[C@H](C2)O)c1)=O)=O and harvested after 6 d culture. * Background c1(C)c([nH]c(n([C@@H]2O[C@H](CO)[C@H](C2)O)c1)=O)=O incorporation by the mitomycin C-treated K562 or CCRF-SB tumor cells (tumor inactivation control) was subtracted from the raw counts to determine the specific incorporation by the effector cell population. Stimulation index: (cpm with stimulator)/(cpm without stimulator). . Blastogenesis and expression of activation antigens on lymphocyte subsets cocultured with K562. Peripheral blood mononuclear cells were stained with FITC anti-Leu-1 la mAb and separated into Leu-11-and Leu-11 + lymphocyte subpopulations using a FACS. Reanalysis indicated >90% purity. >99% of the sorted cells were lymphocytes by morphological criteria. Leu-11-(left) and Leu-11 + (right) lymphocytes were cocuhured with mitomycin Ctreated K562 in 24-well culture plates. After 6 d, cells were harvested and stained with: FITC IgG and PE IgG control antibodies; FITC anti-Leu-1 la and PE anti-Tac; or FITC anti-Leu-1 la and PE anti-HLA-DR. In the upper panels, histograms displaying the forward angle light scatter are presented (x axis, 256 channels, linear scale; y axis, relative number of cells). Forward angle light scatter measurements essentially reflect cell size for lymphoid cells (31). | 5903544 |
Mitomycin | C1[C@@H]2N[C@@H]2[C@@]2([C@H](COC(N)=O)C3=C(N12)C(=O)C(=C(N)C3=O)C)OC | lymphocytes that lacked Leu-11 antigen before coculture with K562 were Leu-11-after 6 d. Thus, there was no evidence for acquisition or loss of this antigen as a consequence of stimulation with K562. A proportion of the Leu-11 + cells coexpressed HLA-DR antigen (25% in Fig. 2) and transferrin receptor (not shown) after coculture with K562. Before culture, <1% of Leu-11 ÷ cells coexpressed HLA-DR or transferrin receptor, indicating that class II MHC antigens and transferrin receptor were induced as a consequence of activation. Further evidence for activation of the Leu-11 + cells was obtained by examining the forward angle light scatter properties of these cells. For lymphoid cells, light scatter is essentially proportional to cell size (31). In contrast to the Leu-11-cells that proliferated only weakly in response to coculture with K562, a majority of the Leu-11 + cells demonstrated light scatter characteristics similar to mitogenactivated lymphoblasts (Fig. 2). This was confirmed by microscopic examination. A majority of the K562-activated Leu-11 + cells were lymphoblasts with abundant cytoplasm and azurophilic granules (not shown). IL-2 receptor-associated antigen, Tac, was not detected on these Leu-11 ÷ lymphoblasts (Fig. 2). Similar results were obtained in three independent experiments. A more extensive antigenic profile of the K562-activated Leu-11 + lymphoblasts is presented in Fig. 3. A proportion of the Leu-11 + lymphoblasts coexpressed . Antigenic pbenotype of Leu-I 1 + lymphocytes after coculture with K562. Purified Leu-1 l + lymphocytes were cocultured with C1[C@@H]2N[C@@H]2[C@@]2([C@H](COC(N)=O)C3=C(N12)C(=O)C(=C(N)C3=O)C)OC C-treated K562 cells, as described in Fig. 2 After 6 d, viable cells were recovered and stained with: FITC IgG and PE IgG control antibodies; FITC anti-Leu-7 and PE anti-Leu-1 lc; FITC anti-Leu-1 la and PE anti-Leu-2; FITC anti-Leu-1 la and PE anti-Leu-4; FITC anti-Leu-I la and PE anti-CR3(Leu-15); and FITC anti-Leu-1 la and PE anti-Leu-M3. Data are presented as described in Fig. 3. Quantitation of the results revealed: 43.7% Leu-ll+7+; 43.3% Leu-1 I+7-; <5% Leu-ll-7 +. 26.3% Leu-ll+2+; 56.8% Leu-11+2-; 8.6% Leu-11-2 + . <5% Leu-ll+4+; 83.5% Leu-11+4-; <5% Leu-11-4 +. 17.5% Leu-11+CRs+; 67.6% Leu-11+CR3-; 6.3% Leu-11-CRs +. <5% Leu-1 l+M3+; 85.3% Leu-1 l+M3-; <5% Leu-1 l-M3 +. >95% of the cells in the IgG control sample were unstained (quadrant lII). | 5903544 |
Mitomycin | C1(N)=C(C)C(=O)C2=C(C1=O)[C@H]([C@]1(OC)N2C[C@H]2[C@@H]1N2)COC(=O)N | Leu-2 (CD8), Leu-7, and Leu-15 (CR3 associated) antigens. These antigens are expressed on subpopulations of resting Leu-! 1 + ceils isolated from fresh blood (2, 32). The only notable difference between the freshly isolated Leu-11 + cells and the activated Leu-11 + lymphoblasts was that the cell surface density of Leu-15 apparently decreases during culture. Similarly, we observed that the density of Leu-11 antigen decreases after activation. Leu-M3, an antigen expressed on most monocytes, and Leu-4 (CD3), an antigen associated with the T cell antigen receptor complex, were not detected on the K562-activated Leu-11 + lymphoblasts (Fig. 3). The cytotoxic activity of the Leu-11-and Leu-11 + cells was determined after coculture with or without C1(N)=C(C)C(=O)C2=C(C1=O)[C@H]([C@]1(OC)N2C[C@H]2[C@@H]1N2)COC(=O)N C-treated K562 cells for 6 d. Leu-11lymphocytes cocultured with K562 usually demonstrated minimal cytotoxicity against K562 (Fig. 4), although low levels of cytotoxicity were occasionally observed in some individuals. Lymphoblasts derived from cocultures of Leu-11 + lymphocytes and K562 were significantly more cytotoxic against K562 than Leu-11 + cells cultured for 6 d without K562 (Fig. 4). Moreover, the K562-activated Leu-I 1 + lymphoblasts were highly cytotoxic at low effector-to-target (E/T) ratios for a broad range of tumor cell targets, including U937, CEM, HSB-2, CCRF-SB, HUT-78, and K562. (Fig. 5). FIGURE 5. Cytotoxicity of activated Leu-] 1 + lymphocytes. Leu-11 ÷ lymphocytes were cocultured with C1(N)=C(C)C(=O)C2=C(C1=O)[C@H]([C@]1(OC)N2C[C@H]2[C@@H]1N2)COC(=O)N C-treated K562 cells for 6 d, as described in Fig. 2. Viable cells were isolated and tested for cytotoxic activity against K562, CCRF-SB, U937, CEM, HUT-78, and HSB-2 tumor cell targets in a 4 h radioisotope release assay. Unstimulated Leu-11 + lymphocytes and Leu-I 1-lymphocytes did not lyse (<5%) any of these targets at comparable E/T ratios (not shown). Proliferation of lymphocytes expressing the Leu-7 and/or Leu-11 antigens cocultured with K562. Nylon wool-nonadherent peripheral blood lymphocytes, enriched for NK cells using Percoll (Materials and Methods), were stained with FITC anti-Leu-1 la and PEavidin/biotin antiLeu-7. The resulting four subsets were separated by two-color FACS sorting. Reanalysis of the isolated populations indicated that all subsets were >95% pure. The cells were cocuhured with or without C1(N)=C(C)C(=O)C2=C(C1=O)[C@H]([C@]1(OC)N2C[C@H]2[C@@H]1N2)COC(=O)N C-treated K562 cells in 96-well round-bottom plates for 6 d. Cultures were pulsed overnight with 1 #Ci [SHlthymidine and harvested. | 5903544 |
Percoll | C(C(=CC1C=CC(N(CCC)CCC)=CC=1)C#N)(NCC(C)CO)=O.C12C=CC(=CC=1C=CC(=C2)C=C(C#N)S(=O)(NCC(CO)C)=O)N(CCC)CCC.C(N(CC)C1C=CC(C=C(C(NCC(CO)C)=O)C#N)=CC=1)C.C1(N(CC)CC)=CC2C=CC(C=C(S(NCC(C)CO)(=O)=O)C#N)=CC=2C=C1.OCC(CNC(=O)C(C#N)=CC1=CC=C(N(C)C)C=C1)C.C1COCCN1CCNC1C=CC2C=C(C=CC=2C=1)C=C(C#N)S(=O)(=O)NCC(C)CO.N(CC(CO)C)S(C(C#N)=CC1=CC2C=CC(N3CCCCC3)=CC=2C=C1)(=O)=O.C1=C(N2CCN(CC2)C)C=CC2=C1C=CC(=C2)C=C(S(=O)(=O)NCC(C)CO)C#N.O=S(=O)(NCC(C)CO)C(C#N)=CC1C=CC2C=C(C=CC=2C=1)N1CCOCC1 | Leu-2 (CD8), Leu-7, and Leu-15 (CR3 associated) antigens. These antigens are expressed on subpopulations of resting Leu-! 1 + ceils isolated from fresh blood (2, 32). The only notable difference between the freshly isolated Leu-11 + cells and the activated Leu-11 + lymphoblasts was that the cell surface density of Leu-15 apparently decreases during culture. Similarly, we observed that the density of Leu-11 antigen decreases after activation. Leu-M3, an antigen expressed on most monocytes, and Leu-4 (CD3), an antigen associated with the T cell antigen receptor complex, were not detected on the K562-activated Leu-11 + lymphoblasts (Fig. 3). The cytotoxic activity of the Leu-11-and Leu-11 + cells was determined after coculture with or without mitomycin C-treated K562 cells for 6 d. Leu-11lymphocytes cocultured with K562 usually demonstrated minimal cytotoxicity against K562 (Fig. 4), although low levels of cytotoxicity were occasionally observed in some individuals. Lymphoblasts derived from cocultures of Leu-11 + lymphocytes and K562 were significantly more cytotoxic against K562 than Leu-11 + cells cultured for 6 d without K562 (Fig. 4). Moreover, the K562-activated Leu-I 1 + lymphoblasts were highly cytotoxic at low effector-to-target (E/T) ratios for a broad range of tumor cell targets, including U937, CEM, HSB-2, CCRF-SB, HUT-78, and K562. (Fig. 5). FIGURE 5. Cytotoxicity of activated Leu-] 1 + lymphocytes. Leu-11 ÷ lymphocytes were cocultured with mitomycin C-treated K562 cells for 6 d, as described in Fig. 2. Viable cells were isolated and tested for cytotoxic activity against K562, CCRF-SB, U937, CEM, HUT-78, and HSB-2 tumor cell targets in a 4 h radioisotope release assay. Unstimulated Leu-11 + lymphocytes and Leu-I 1-lymphocytes did not lyse (<5%) any of these targets at comparable E/T ratios (not shown). Proliferation of lymphocytes expressing the Leu-7 and/or Leu-11 antigens cocultured with K562. Nylon wool-nonadherent peripheral blood lymphocytes, enriched for NK cells using C(C(=CC1C=CC(N(CCC)CCC)=CC=1)C#N)(NCC(C)CO)=O.C12C=CC(=CC=1C=CC(=C2)C=C(C#N)S(=O)(NCC(CO)C)=O)N(CCC)CCC.C(N(CC)C1C=CC(C=C(C(NCC(CO)C)=O)C#N)=CC=1)C.C1(N(CC)CC)=CC2C=CC(C=C(S(NCC(C)CO)(=O)=O)C#N)=CC=2C=C1.OCC(CNC(=O)C(C#N)=CC1=CC=C(N(C)C)C=C1)C.C1COCCN1CCNC1C=CC2C=C(C=CC=2C=1)C=C(C#N)S(=O)(=O)NCC(C)CO.N(CC(CO)C)S(C(C#N)=CC1=CC2C=CC(N3CCCCC3)=CC=2C=C1)(=O)=O.C1=C(N2CCN(CC2)C)C=CC2=C1C=CC(=C2)C=C(S(=O)(=O)NCC(C)CO)C#N.O=S(=O)(NCC(C)CO)C(C#N)=CC1C=CC2C=C(C=CC=2C=1)N1CCOCC1 (Materials and Methods), were stained with FITC anti-Leu-1 la and PEavidin/biotin antiLeu-7. The resulting four subsets were separated by two-color FACS sorting. Reanalysis of the isolated populations indicated that all subsets were >95% pure. The cells were cocuhured with or without mitomycin C-treated K562 cells in 96-well round-bottom plates for 6 d. Cultures were pulsed overnight with 1 #Ci [SHlthymidine and harvested. | 5903544 |
Thymidine | C1(C)C(=O)NC(N([C@H]2C[C@@H]([C@@H](CO)O2)O)C=1)=O | with mitornycin C-treated K562 cells. After 6 d of culture, proliferation was measured by [3H]C1(C)C(=O)NC(N([C@H]2C[C@@H]([C@@H](CO)O2)O)C=1)=O incorporation (Fig. 6). Both the Leu-7+l 1 + and Leu-7-1 1 + proliferated in response to K562, with the latter population consistently demonstrating significantly higher levels of proliferation (2-10-fold higher in three experiments, depending on the donor). The Leu-7+l 1-and Leu-7-11lymphocytes were weakly stimulated by K562, although significant proliferation was observed in some donors (e.g., Table II, experiment 2). The anti-Leu-7 and anti-Leu-11 antibodies were not mitogenic for these cell populations, as demonstrated by the lack of proliferation in the cultures without K562 (Fig. 6). Furthermore, when Percoll gradient-enriched LGL were stained with anti-Leu-7 and anti-Leu-11 antibodies before cocuhured with mitomycin C-treated K562 cells, the stimulation index was essentially identical to the response of LGL not stained with these antibodies. Therefore, it is unlikely that using these mAb for isolation of these subpopulations significantly influenced their response. | 5903544 |
Percoll | CCCN(CCC)c1ccc(C=C(C#N)C(NCC(CO)C)=O)cc1.C(CO)(C)CNS(=O)(C(C#N)=Cc1cc2c(cc(cc2)N(CCC)CCC)cc1)=O.C(C(NCC(CO)C)=O)(=Cc1ccc(cc1)N(CC)CC)C#N.O=S(NCC(C)CO)(C(C#N)=Cc1cc2c(cc(cc2)N(CC)CC)cc1)=O.N(C)(C)c1ccc(cc1)C=C(C#N)C(NCC(CO)C)=O.C(CN1CCOCC1)Nc1cc2ccc(C=C(S(=O)(=O)NCC(CO)C)C#N)cc2cc1.C(C(=Cc1ccc2cc(ccc2c1)N1CCCCC1)S(NCC(C)CO)(=O)=O)#N.OCC(CNS(C(C#N)=Cc1ccc2c(c1)ccc(N1CCN(C)CC1)c2)(=O)=O)C.CC(CO)CNS(=O)(=O)C(=Cc1ccc2cc(N3CCOCC3)ccc2c1)C#N | with mitornycin C-treated K562 cells. After 6 d of culture, proliferation was measured by [3H]thymidine incorporation (Fig. 6). Both the Leu-7+l 1 + and Leu-7-1 1 + proliferated in response to K562, with the latter population consistently demonstrating significantly higher levels of proliferation (2-10-fold higher in three experiments, depending on the donor). The Leu-7+l 1-and Leu-7-11lymphocytes were weakly stimulated by K562, although significant proliferation was observed in some donors (e.g., Table II, experiment 2). The anti-Leu-7 and anti-Leu-11 antibodies were not mitogenic for these cell populations, as demonstrated by the lack of proliferation in the cultures without K562 (Fig. 6). Furthermore, when CCCN(CCC)c1ccc(C=C(C#N)C(NCC(CO)C)=O)cc1.C(CO)(C)CNS(=O)(C(C#N)=Cc1cc2c(cc(cc2)N(CCC)CCC)cc1)=O.C(C(NCC(CO)C)=O)(=Cc1ccc(cc1)N(CC)CC)C#N.O=S(NCC(C)CO)(C(C#N)=Cc1cc2c(cc(cc2)N(CC)CC)cc1)=O.N(C)(C)c1ccc(cc1)C=C(C#N)C(NCC(CO)C)=O.C(CN1CCOCC1)Nc1cc2ccc(C=C(S(=O)(=O)NCC(CO)C)C#N)cc2cc1.C(C(=Cc1ccc2cc(ccc2c1)N1CCCCC1)S(NCC(C)CO)(=O)=O)#N.OCC(CNS(C(C#N)=Cc1ccc2c(c1)ccc(N1CCN(C)CC1)c2)(=O)=O)C.CC(CO)CNS(=O)(=O)C(=Cc1ccc2cc(N3CCOCC3)ccc2c1)C#N gradient-enriched LGL were stained with anti-Leu-7 and anti-Leu-11 antibodies before cocuhured with mitomycin C-treated K562 cells, the stimulation index was essentially identical to the response of LGL not stained with these antibodies. Therefore, it is unlikely that using these mAb for isolation of these subpopulations significantly influenced their response. | 5903544 |
Mitomycin | C([C@@H]1C2C(C(=C(C)C(=O)C=2N2C[C@@H]3N[C@@H]3[C@@]21OC)N)=O)OC(N)=O | with mitornycin C-treated K562 cells. After 6 d of culture, proliferation was measured by [3H]thymidine incorporation (Fig. 6). Both the Leu-7+l 1 + and Leu-7-1 1 + proliferated in response to K562, with the latter population consistently demonstrating significantly higher levels of proliferation (2-10-fold higher in three experiments, depending on the donor). The Leu-7+l 1-and Leu-7-11lymphocytes were weakly stimulated by K562, although significant proliferation was observed in some donors (e.g., Table II, experiment 2). The anti-Leu-7 and anti-Leu-11 antibodies were not mitogenic for these cell populations, as demonstrated by the lack of proliferation in the cultures without K562 (Fig. 6). Furthermore, when Percoll gradient-enriched LGL were stained with anti-Leu-7 and anti-Leu-11 antibodies before cocuhured with C([C@@H]1C2C(C(=C(C)C(=O)C=2N2C[C@@H]3N[C@@H]3[C@@]21OC)N)=O)OC(N)=O C-treated K562 cells, the stimulation index was essentially identical to the response of LGL not stained with these antibodies. Therefore, it is unlikely that using these mAb for isolation of these subpopulations significantly influenced their response. | 5903544 |
Mitomycin | [C@]12([C@H]3N[C@H]3CN2C2C(=O)C(C)=C(C(C=2[C@H]1COC(=O)N)=O)N)OC | With respect to antigenic phenotype, we consistently observed that a significant proportion (20-40% in three independent experiments, depending on the donor; 37.7% in Fig. 8) of the Leu-7-11 + cells acquired expression of Leu-7 antigen after stimulation with K562 (Fig. 8). It is unlikely that the appearance of the Leu-7+l 1 + cells in the Leu-7-11 ÷ population after stimulation with K562 resulted Effector to Target Ratio FIGURE 7. Cytotoxic activity of lymphocytes expressing the Leu-7 and/or Leu-11 antigens cocuhured with K562. Lymphocyte subsets expressing the Leu-7 and/or Leu-11 antigens were isolated by two-color FACS sorting and cocuhured with [C@]12([C@H]3N[C@H]3CN2C2C(=O)C(C)=C(C(C=2[C@H]1COC(=O)N)=O)N)OC C-treated K562 cells, as described in Fig. 6. After 6 d, the viable cells were harvested and tested for cytotoxic activity against K562 and CCRF-SB using a 4 h radioisotope release assay. with [C@]12([C@H]3N[C@H]3CN2C2C(=O)C(C)=C(C(C=2[C@H]1COC(=O)N)=O)N)OC C-treated K562. After 6 d, the viable cells were recovered and stained with FITC anti-Leu-I la and PE-avidin/biotin anti-Leu-7. Data are presented as described in Fig. 2. <5% of the cells in the Leu-7-11-population expressed the Leu-7 and/or Leu-I 1 antigen after coculture with K562.95% of the Leu-7+l 1 + cells coexpressed both antigens before and after stimulation with K562. In contrast, 37.7 % of the Leu-7-11 + cells demonstrated expression of Leu-7 after stimulation with K562. The small proportion of Leu-7-11-cells (14.9%) shown in the Leu-7+l 1-population after coculture with K562 was not observed in three subsequent experiments, and was likely explained by expansion or preferential survival of the 5% contamination of this population with Leu-7-11-cells during the sort. | 5903544 |
Mitomycin | C(N)(OC[C@H]1[C@@]2(N(C3C(C(C)=C(N)C(C=31)=O)=O)C[C@@H]1N[C@@H]12)OC)=O | To determine the role of IL-2 receptors in the activation of granular lymphocytes by K562, anti-Tac (IL-2) receptor mAb or an isotype-matched nonreactive control IgG antibody were added to cocultures of C(N)(OC[C@H]1[C@@]2(N(C3C(C(C)=C(N)C(C=31)=O)=O)C[C@@H]1N[C@@H]12)OC)=O C-treated K562 and lymphocyte subpopulations, isolated by twocolor cell sorting with FITC anti-Leu-lla and PE-avidin/biotin anti-Leu-7. Results from two independent donors are presented in Table II. The proliferative response of the Leu-7-11 + against K562 was minimally inhibited (9%, Exp. 1; 6%, Exp. 2), whereas the response of the Leu-7+l 1 + was partially inhibited (17%, Exp. 1; 18%, Exp. 2) by anti-Tac. In contrast, the mitogenic response of the T lymphocytes (Leu-7-11-) from both donors was completely inhibited (98%) by anti-Tac. Furthermore, the proliferation in the Leu-7-11-and Leu-7+l 1-cells against K562 in Exp. 2 also was completely inhibited by anti-Tac, suggesting that a different mechanism may be involved in the response of Leu-11-and Leu-11 + FIGURE 9. Morphology of lymphocytes expressing the Leu-7 and/or Leu-11 antigens after coculture with K562. Lymphocytes subsets expressing the Leu-7 and/or Leu-11 antigens were isolated to >95% purity by two-color FACS cell sorting. Immediately after sorting (A, C, E, and G) or after 6 d of coculture with C(N)(OC[C@H]1[C@@]2(N(C3C(C(C)=C(N)C(C=31)=O)=O)C[C@@H]1N[C@@H]12)OC)=O C-treated K562 (B, D, F, and H), Leu-7-11 + (A, B), Leu-7÷l 1 + (C, D), Leu-7+l 1-(E, F), and Leu-7-11-(G, H) were stained with Giemsa and examined by light microscopy, x 4,500. Leu-7 and Leu-11 subpopulations isolated by FACS sorting, as described in Fig. 6, were stimulated by coculture with K562 or PHA. Anti-Tac antibody and nonreactive IgG control antibodies were added to the cultures at a final concentration of 150 #g/ml. Cultures were pulsed overnight with 1 #Ci [3H]thymidine and were harvested on day 6. The stimulation index is defined in Table I. * Background thymidine incorporation by the C(N)(OC[C@H]1[C@@]2(N(C3C(C(C)=C(N)C(C=31)=O)=O)C[C@@H]1N[C@@H]12)OC)=O C-treated K562 or CCRF-SB tumor cells (tumor inactivation control) was subtracted from the raw counts to determine the specific incorporation by the effector cell population. Percent inhibition is defined as: 100 × [(cpm with K562 and control IgG -cpm without stimulator and antibody) -(cpm with K562 and anti-Tac -cpm without stimulator or antibody)/(cpm with K562 and control IgG -cpm without stimulator or antibody)]. | 5903544 |
Thymidine | C1(C(=CN(C(N1)=O)[C@H]1C[C@H](O)[C@H](O1)CO)C)=O | To determine the role of IL-2 receptors in the activation of granular lymphocytes by K562, anti-Tac (IL-2) receptor mAb or an isotype-matched nonreactive control IgG antibody were added to cocultures of mitomycin C-treated K562 and lymphocyte subpopulations, isolated by twocolor cell sorting with FITC anti-Leu-lla and PE-avidin/biotin anti-Leu-7. Results from two independent donors are presented in Table II. The proliferative response of the Leu-7-11 + against K562 was minimally inhibited (9%, Exp. 1; 6%, Exp. 2), whereas the response of the Leu-7+l 1 + was partially inhibited (17%, Exp. 1; 18%, Exp. 2) by anti-Tac. In contrast, the mitogenic response of the T lymphocytes (Leu-7-11-) from both donors was completely inhibited (98%) by anti-Tac. Furthermore, the proliferation in the Leu-7-11-and Leu-7+l 1-cells against K562 in Exp. 2 also was completely inhibited by anti-Tac, suggesting that a different mechanism may be involved in the response of Leu-11-and Leu-11 + FIGURE 9. Morphology of lymphocytes expressing the Leu-7 and/or Leu-11 antigens after coculture with K562. Lymphocytes subsets expressing the Leu-7 and/or Leu-11 antigens were isolated to >95% purity by two-color FACS cell sorting. Immediately after sorting (A, C, E, and G) or after 6 d of coculture with mitomycin C-treated K562 (B, D, F, and H), Leu-7-11 + (A, B), Leu-7÷l 1 + (C, D), Leu-7+l 1-(E, F), and Leu-7-11-(G, H) were stained with Giemsa and examined by light microscopy, x 4,500. Leu-7 and Leu-11 subpopulations isolated by FACS sorting, as described in Fig. 6, were stimulated by coculture with K562 or PHA. Anti-Tac antibody and nonreactive IgG control antibodies were added to the cultures at a final concentration of 150 #g/ml. Cultures were pulsed overnight with 1 #Ci [3H]C1(C(=CN(C(N1)=O)[C@H]1C[C@H](O)[C@H](O1)CO)C)=O and were harvested on day 6. The stimulation index is defined in Table I. * Background C1(C(=CN(C(N1)=O)[C@H]1C[C@H](O)[C@H](O1)CO)C)=O incorporation by the mitomycin C-treated K562 or CCRF-SB tumor cells (tumor inactivation control) was subtracted from the raw counts to determine the specific incorporation by the effector cell population. Percent inhibition is defined as: 100 × [(cpm with K562 and control IgG -cpm without stimulator and antibody) -(cpm with K562 and anti-Tac -cpm without stimulator or antibody)/(cpm with K562 and control IgG -cpm without stimulator or antibody)]. | 5903544 |
Mitomycin | C1N2C3=C([C@@H](COC(=O)N)[C@]2([C@H]2N[C@H]21)OC)C(=O)C(N)=C(C)C3=O | Discussion Leu-11 + lymphoblasts (6) were a minor population in MLTR cultures using an allogeneic B cell line as the stimulator. In general, allogeneic B cell lines are relatively insensitive to NK-mediated cytotoxicity. We questioned whether Leu-11 + cells could be preferentially stimulated if an NK-sensitive tumor cell line was used as the stimulator in an MLTR culture. Poros and Klein (33) have reported that coculture of peripheral blood mononuclear cells with an NK-sensitive tumor cell, K562, results in the preferential activation of lymphoblasts that express Fc receptors and are highly cytotoxic for K562. In contrast (33), stimulation with allogeneic peripheral blood lymphocytes preferentially stimulates typical E rosette-positive lymphoblasts that lack Fc receptor expression. We have confirmed these observations (34). Coculture of C1N2C3=C([C@@H](COC(=O)N)[C@]2([C@H]2N[C@H]21)OC)C(=O)C(N)=C(C)C3=O C-treated K562 with either unseparated peripheral blood lymphocytes or Percoll gradient-enriched low density lymphocytes results in proliferation and activation of cells expressing the Leu-11 antigen, but usually lacking pan T cell antigens (34). Depletion studies (34) with antibody and complement show that the peripheral blood precursor of the activated Leu-11 + cell expresses the Leu-11 antigen. The structure on K562 responsible for activation of NK cells is unknown, but it is important to note that K562 lacks expression of both class I and II MHC antigens on the cell surface. We do not know if K562 cells stimulate NK cells through release of a soluble product, but are exploring this possibility. | 5903544 |
Percoll | C(CC)N(c1ccc(cc1)C=C(C(NCC(C)CO)=O)C#N)CCC.c12ccc(C=C(S(=O)(=O)NCC(C)CO)C#N)cc2ccc(N(CCC)CCC)c1.N(C(C(=Cc1ccc(cc1)N(CC)CC)C#N)=O)CC(CO)C.c1c(cc2ccc(N(CC)CC)cc2c1)C=C(S(=O)(=O)NCC(C)CO)C#N.N(C(C(=Cc1ccc(cc1)N(C)C)C#N)=O)CC(CO)C.C(Nc1cc2c(cc1)cc(cc2)C=C(S(=O)(=O)NCC(C)CO)C#N)CN1CCOCC1.O=S(=O)(C(C#N)=Cc1cc2ccc(cc2cc1)N1CCCCC1)NCC(C)CO.C(=Cc1ccc2cc(N3CCN(C)CC3)ccc2c1)(C#N)S(=O)(NCC(CO)C)=O.C(NS(=O)(C(=Cc1ccc2cc(N3CCOCC3)ccc2c1)C#N)=O)C(C)CO | Discussion Leu-11 + lymphoblasts (6) were a minor population in MLTR cultures using an allogeneic B cell line as the stimulator. In general, allogeneic B cell lines are relatively insensitive to NK-mediated cytotoxicity. We questioned whether Leu-11 + cells could be preferentially stimulated if an NK-sensitive tumor cell line was used as the stimulator in an MLTR culture. Poros and Klein (33) have reported that coculture of peripheral blood mononuclear cells with an NK-sensitive tumor cell, K562, results in the preferential activation of lymphoblasts that express Fc receptors and are highly cytotoxic for K562. In contrast (33), stimulation with allogeneic peripheral blood lymphocytes preferentially stimulates typical E rosette-positive lymphoblasts that lack Fc receptor expression. We have confirmed these observations (34). Coculture of mitomycin C-treated K562 with either unseparated peripheral blood lymphocytes or C(CC)N(c1ccc(cc1)C=C(C(NCC(C)CO)=O)C#N)CCC.c12ccc(C=C(S(=O)(=O)NCC(C)CO)C#N)cc2ccc(N(CCC)CCC)c1.N(C(C(=Cc1ccc(cc1)N(CC)CC)C#N)=O)CC(CO)C.c1c(cc2ccc(N(CC)CC)cc2c1)C=C(S(=O)(=O)NCC(C)CO)C#N.N(C(C(=Cc1ccc(cc1)N(C)C)C#N)=O)CC(CO)C.C(Nc1cc2c(cc1)cc(cc2)C=C(S(=O)(=O)NCC(C)CO)C#N)CN1CCOCC1.O=S(=O)(C(C#N)=Cc1cc2ccc(cc2cc1)N1CCCCC1)NCC(C)CO.C(=Cc1ccc2cc(N3CCN(C)CC3)ccc2c1)(C#N)S(=O)(NCC(CO)C)=O.C(NS(=O)(C(=Cc1ccc2cc(N3CCOCC3)ccc2c1)C#N)=O)C(C)CO gradient-enriched low density lymphocytes results in proliferation and activation of cells expressing the Leu-11 antigen, but usually lacking pan T cell antigens (34). Depletion studies (34) with antibody and complement show that the peripheral blood precursor of the activated Leu-11 + cell expresses the Leu-11 antigen. The structure on K562 responsible for activation of NK cells is unknown, but it is important to note that K562 lacks expression of both class I and II MHC antigens on the cell surface. We do not know if K562 cells stimulate NK cells through release of a soluble product, but are exploring this possibility. | 5903544 |
Jalan | C(N1CCCCCC1)(SCC)=O | Dr. Gunasekaran Venugopal, Advanced Nanomaterials and System Lab, Department of Materials Science, School of Technology, Central University of Tamil Nadu, Thiruvarur -610005, Tamil Nadu, India. Email: [email protected] : [email protected] Dr. Vanitha Mariappan, Center for Toxicology and Health Risk Studies, Faculty of Health Sciences, Universiti Kebangsaan Malaysia, C(N1CCCCCC1)(SCC)=O Raja Muda Abdul Aziz, Kuala Lumpur 50300, Malaysia Email: [email protected] | 252787029 |
Antioxidant | C(CC(OCCNC(=O)C(NCCOC(=O)CCc1cc(C(C)(C)C)c(O)c(C(C)(C)C)c1)=O)=O)c1cc(C(C)(C)C)c(c(c1)C(C)(C)C)O | Citrus essential oils (EOs) have several applications in cosmetics, the food industry, and the flavor and fragrance industry. They are also utilized as natural preservatives because of their wide range of biological activities, which include C(CC(OCCNC(=O)C(NCCOC(=O)CCc1cc(C(C)(C)C)c(O)c(C(C)(C)C)c1)=O)=O)c1cc(C(C)(C)C)c(c(c1)C(C)(C)C)O and antimicrobial actions [1]. These strong biological activities are attributed to the presence of terpenes, flavonoids, carotenes, and coumarins [2]. Several studies have investigated the volatile makeup of various parts of Citrus species due to their significant economic importance. All cold-pressed Citrus oils contain a portion of non-volatiles fundamentally made of simple coumarins, psoralens, and methoxy-flavones [3]. Coumarins (1,2-benzopyrones) are a huge family of naturally occurring secondary metabolites. Psoralens, also known as furanocoumarins (FCs), are a large family of compounds commonly found in Rutaceae, Apiaceae, and Fabaceae, with Rutaceae containing the highest concentrations [4,5]. FCs contain a furan ring fused to a coumarin core [6]. The fusion helps separate the FCs into linear or angular structural forms. FCs have shown a potential to elicit variable degrees of phototoxic skin reactions. In comparison to angular FCs, linear FCs have often been proven to cause phototoxic responses at lower doses [7]. | 252558909 |
Flavonoids | C1(C(=O)C2C(OC=1C1=CC=CC=C1)=CC=CC=2)O | Citrus essential oils (EOs) have several applications in cosmetics, the food industry, and the flavor and fragrance industry. They are also utilized as natural preservatives because of their wide range of biological activities, which include antioxidant and antimicrobial actions [1]. These strong biological activities are attributed to the presence of terpenes, C1(C(=O)C2C(OC=1C1=CC=CC=C1)=CC=CC=2)O, carotenes, and coumarins [2]. Several studies have investigated the volatile makeup of various parts of Citrus species due to their significant economic importance. All cold-pressed Citrus oils contain a portion of non-volatiles fundamentally made of simple coumarins, psoralens, and methoxy-flavones [3]. Coumarins (1,2-benzopyrones) are a huge family of naturally occurring secondary metabolites. Psoralens, also known as furanocoumarins (FCs), are a large family of compounds commonly found in Rutaceae, Apiaceae, and Fabaceae, with Rutaceae containing the highest concentrations [4,5]. FCs contain a furan ring fused to a coumarin core [6]. The fusion helps separate the FCs into linear or angular structural forms. FCs have shown a potential to elicit variable degrees of phototoxic skin reactions. In comparison to angular FCs, linear FCs have often been proven to cause phototoxic responses at lower doses [7]. | 252558909 |
Coumarins | O=C1C(C(CC(=O)C)C2C=CC=CC=2)=C(C2C(=CC=CC=2)O1)O | Citrus essential oils (EOs) have several applications in cosmetics, the food industry, and the flavor and fragrance industry. They are also utilized as natural preservatives because of their wide range of biological activities, which include antioxidant and antimicrobial actions [1]. These strong biological activities are attributed to the presence of terpenes, flavonoids, carotenes, and O=C1C(C(CC(=O)C)C2C=CC=CC=2)=C(C2C(=CC=CC=2)O1)O [2]. Several studies have investigated the volatile makeup of various parts of Citrus species due to their significant economic importance. All cold-pressed Citrus oils contain a portion of non-volatiles fundamentally made of simple O=C1C(C(CC(=O)C)C2C=CC=CC=2)=C(C2C(=CC=CC=2)O1)O, psoralens, and methoxy-flavones [3]. O=C1C(C(CC(=O)C)C2C=CC=CC=2)=C(C2C(=CC=CC=2)O1)O (1,2-benzopyrones) are a huge family of naturally occurring secondary metabolites. Psoralens, also known as furanoO=C1C(C(CC(=O)C)C2C=CC=CC=2)=C(C2C(=CC=CC=2)O1)O (FCs), are a large family of compounds commonly found in Rutaceae, Apiaceae, and Fabaceae, with Rutaceae containing the highest concentrations [4,5]. FCs contain a furan ring fused to a coumarin core [6]. The fusion helps separate the FCs into linear or angular structural forms. FCs have shown a potential to elicit variable degrees of phototoxic skin reactions. In comparison to angular FCs, linear FCs have often been proven to cause phototoxic responses at lower doses [7]. | 252558909 |
A coumarin | C12C(=CC=CC=1)OC(=O)C=C2 | Citrus essential oils (EOs) have several applications in cosmetics, the food industry, and the flavor and fragrance industry. They are also utilized as natural preservatives because of their wide range of biological activities, which include antioxidant and antimicrobial actions [1]. These strong biological activities are attributed to the presence of terpenes, flavonoids, carotenes, and coumarins [2]. Several studies have investigated the volatile makeup of various parts of Citrus species due to their significant economic importance. All cold-pressed Citrus oils contain a portion of non-volatiles fundamentally made of simple coumarins, psoralens, and methoxy-flavones [3]. Coumarins (1,2-benzopyrones) are a huge family of naturally occurring secondary metabolites. Psoralens, also known as furanocoumarins (FCs), are a large family of compounds commonly found in Rutaceae, Apiaceae, and Fabaceae, with Rutaceae containing the highest concentrations [4,5]. FCs contain a furan ring fused to C12C(=CC=CC=1)OC(=O)C=C2 core [6]. The fusion helps separate the FCs into linear or angular structural forms. FCs have shown a potential to elicit variable degrees of phototoxic skin reactions. In comparison to angular FCs, linear FCs have often been proven to cause phototoxic responses at lower doses [7]. | 252558909 |
Coumarin | c1cc2c(cc1)ccc(=O)o2 | Citrus essential oils (EOs) have several applications in cosmetics, the food industry, and the flavor and fragrance industry. They are also utilized as natural preservatives because of their wide range of biological activities, which include antioxidant and antimicrobial actions [1]. These strong biological activities are attributed to the presence of terpenes, flavonoids, carotenes, and c1cc2c(cc1)ccc(=O)o2s [2]. Several studies have investigated the volatile makeup of various parts of Citrus species due to their significant economic importance. All cold-pressed Citrus oils contain a portion of non-volatiles fundamentally made of simple c1cc2c(cc1)ccc(=O)o2s, psoralens, and methoxy-flavones [3]. c1cc2c(cc1)ccc(=O)o2s (1,2-benzopyrones) are a huge family of naturally occurring secondary metabolites. Psoralens, also known as furanoc1cc2c(cc1)ccc(=O)o2s (FCs), are a large family of compounds commonly found in Rutaceae, Apiaceae, and Fabaceae, with Rutaceae containing the highest concentrations [4,5]. FCs contain a furan ring fused to a c1cc2c(cc1)ccc(=O)o2 core [6]. The fusion helps separate the FCs into linear or angular structural forms. FCs have shown a potential to elicit variable degrees of phototoxic skin reactions. In comparison to angular FCs, linear FCs have often been proven to cause phototoxic responses at lower doses [7]. | 252558909 |
Coumarins | C1(O)C2=CC=CC=C2OC(=O)C=1C(C1C=CC=CC=1)CC(C)=O | While studying the volatile composition of Citrus oils, the nonvolatile fractions are hard to detect under standard gas chromatography conditions because of their limited volatilities, relatively polar or heat-liable nature. These nonvolatile ingredients may hold the secret to constructing a perfect analytical strategy for interspecies adulteration detection. the secret to constructing a perfect analytical strategy for interspecies adulteration detection. This essential fraction of the cold-pressed oil can be used to identify speciesspecific patterns and establish Citrus species fingerprinting. For instance, creating synthetic bergamot oils or adulterating bergamot oils with similar Citrus oils like bitter orange are simple strategies to boost profits. Both strategies make it essentially impossible for consumers to detect the difference. The non-volatile fraction contributes very little to the Citrus oils' aroma, but because of its high complexity, commercial unavailability, or extremely high cost in comparison to the Citrus oils themselves, it is more difficult to manipulate. Previous studies report the separation and identification of C1(O)C2=CC=CC=C2OC(=O)C=1C(C1C=CC=CC=1)CC(C)=O and FCs in Citrus peel extracts and oils using gas chromatography-mass spectroscopy (GC-MS) after derivatization [8], high-performance liquid chromatography (HPLC) [8], enzyme-linked immunosorbent assay (ELISA) [9], reversed-phase (RP)-HPLC [10,11], HPLC-diode array detector (DAD) [12], HPLC-nuclear magnetic resonance (NMR) [13], ultra-performance liquid chromatography coupled with mass spectrometry (UPLC-MS) [14,15], LC-MS [16], and HPLC-UV-MS [17]. | 252558909 |
Coumarins | c1(O)c2ccccc2oc(c1C(CC(=O)C)c1ccccc1)=O | The objective of the present study was to develop a sensitive UPLC-MS/MS method to quantify 14 selected c1(O)c2ccccc2oc(c1C(CC(=O)C)c1ccccc1)=O and FCs (Figure 1). This validated method was then applied to the cold-pressed essential oils of bergamot (Citrus bergamia Risso & Poit), bitter orange (C. aurantium L.), calamansi (C. × microcarpa (Bunge) Wijnands), clementine (C. clementina Hort. ex Tanaka), grapefruit (C. × paradisi Macfady), kumquat (C. japonica Thunb.), lemon (C. limon Osbeck), lime (C. aurantifolia (Christm.) Swingle), mandarin (C. reticulata Blanco), sweet orange (C. sinensis L.), tangerine (C. tangerina Hort. ex Tanaka), and yuzu (C. junos Sieb. ex Tanaka) as well as petitgrain EO. Figure 1. Chemical structure of key non-volatile components in expressed Citrus essential oils. | 252558909 |
Aurantium | C1=CC=C(C(=C1)N=CCC(C)CCCC(C)(O)C)C(OC)=O | The objective of the present study was to develop a sensitive UPLC-MS/MS method to quantify 14 selected coumarins and FCs (Figure 1). This validated method was then applied to the cold-pressed essential oils of bergamot (Citrus bergamia Risso & Poit), bitter orange (C. C1=CC=C(C(=C1)N=CCC(C)CCCC(C)(O)C)C(OC)=O L.), calamansi (C. × microcarpa (Bunge) Wijnands), clementine (C. clementina Hort. ex Tanaka), grapefruit (C. × paradisi Macfady), kumquat (C. japonica Thunb.), lemon (C. limon Osbeck), lime (C. aurantifolia (Christm.) Swingle), mandarin (C. reticulata Blanco), sweet orange (C. sinensis L.), tangerine (C. tangerina Hort. ex Tanaka), and yuzu (C. junos Sieb. ex Tanaka) as well as petitgrain EO. Figure 1. Chemical structure of key non-volatile components in expressed Citrus essential oils. | 252558909 |
Coumarins | c1(C(c2c(c3c(oc2=O)cccc3)O)CC(=O)C)ccccc1 | The LC-MS/MS chromatogram of 14 c1(C(c2c(c3c(oc2=O)cccc3)O)CC(=O)C)ccccc1 using the MRM acquisition mode is shown in Figure 2. Specificity, precision, accuracy, linearity, intermediate precision, and LOQ results are summarized in Table 1. The method proved specific to the target compounds since no interferences were found in any of the processed blanks. All com- The LC-MS/MS chromatogram of 14 c1(C(c2c(c3c(oc2=O)cccc3)O)CC(=O)C)ccccc1 using the MRM acquisition mode is shown in Figure 2. Specificity, precision, accuracy, linearity, intermediate precision, and LOQ results are summarized in Table 1. The method proved specific to the target compounds since no interferences were found in any of the processed blanks. All compounds met the acceptance criterion of RSD% ≤ 10 based on the precision and intermediate precision results. Compound recovery percentages ranged from 94.07 to 114.53% of the expected value. The linearity of the calibration curve of the 14 compounds was well correlated (r ≥ 0.98) within a range of 0.00010.1 ppm. The LOQ values ranged from 0.0001 to 0.005 ppm. These findings demonstrate that the developed method is suitable for analyzing the 14 targeted compounds in EOs. (Table 3). The non-volatile components are far more species-specific than the volatile components, which have comparable patterns in different Citrus oils. We found patterns in FC profiles that correspond with published differences among the Citrus ancestral taxa [15,18]. Our findings are in line with previous reports that found a mixture of FCs from the bergapten, xanthotoxin, and isopimpinellin clusters in EOs derived from the citron (C. medica) and papeda (C. micrantha) ancestral taxa [15]. In this study, EOs derived from fruits of the mandarin taxa (mandarin, clementine, and tangerine) showed low total coumarin (2.44-149.45 ppm) and FC levels (2.44-149.45 ppm), not aligning with a previous report that this taxon is nearly devoid of FCs [14,15]. Interestingly, trioxsalen and toncarine were not detected in any of the Citrus EOs. Epoxybegamottin was absent from calamansi, clementine, mandarin, kaffir lime, and petitgrain oils. The content of psoralen was almost negligible in most of the Citrus EOs but was relatively high in white grapefruit EO (82.65 ± 0.76 ppm). Furthermore, large amounts of xanthotoxin were detected in bergamot and lime EOs. Previous reports indicate that xanthotoxin is absent from sweet orange (C. sinensis, pummelo taxon) and the mandarin taxa [14,15] while we found 4.85 ± 0.32 ppm in sweet orange EO and 0.33-15.24 ppm xanthotoxin in the mandarin taxa EOs. Bergamottin and 5-geranyloxy-7-methoxycoumarin were reported in mandarin, lemon, and lime oils but not in orange oil [17]. The differences between our findings and previous studies could be due to genetic and/or environmental impacts on FC biosynthesis [19]. Our LOQ, however, may be lower than that of other reports because it was based on the weight of EO rather than the weight of fresh fruit peel. Alternative explanations for the differences in our findings include genetic admixture in Citrus varieties or contamination during processing and handling. | 252558909 |
Bergapten | C1(C2C=COC=2C=C2C=1C=CC(O2)=O)OC | The LC-MS/MS chromatogram of 14 coumarins using the MRM acquisition mode is shown in Figure 2. Specificity, precision, accuracy, linearity, intermediate precision, and LOQ results are summarized in Table 1. The method proved specific to the target compounds since no interferences were found in any of the processed blanks. All com- The LC-MS/MS chromatogram of 14 coumarins using the MRM acquisition mode is shown in Figure 2. Specificity, precision, accuracy, linearity, intermediate precision, and LOQ results are summarized in Table 1. The method proved specific to the target compounds since no interferences were found in any of the processed blanks. All compounds met the acceptance criterion of RSD% ≤ 10 based on the precision and intermediate precision results. Compound recovery percentages ranged from 94.07 to 114.53% of the expected value. The linearity of the calibration curve of the 14 compounds was well correlated (r ≥ 0.98) within a range of 0.00010.1 ppm. The LOQ values ranged from 0.0001 to 0.005 ppm. These findings demonstrate that the developed method is suitable for analyzing the 14 targeted compounds in EOs. (Table 3). The non-volatile components are far more species-specific than the volatile components, which have comparable patterns in different Citrus oils. We found patterns in FC profiles that correspond with published differences among the Citrus ancestral taxa [15,18]. Our findings are in line with previous reports that found a mixture of FCs from the C1(C2C=COC=2C=C2C=1C=CC(O2)=O)OC, xanthotoxin, and isopimpinellin clusters in EOs derived from the citron (C. medica) and papeda (C. micrantha) ancestral taxa [15]. In this study, EOs derived from fruits of the mandarin taxa (mandarin, clementine, and tangerine) showed low total coumarin (2.44-149.45 ppm) and FC levels (2.44-149.45 ppm), not aligning with a previous report that this taxon is nearly devoid of FCs [14,15]. Interestingly, trioxsalen and toncarine were not detected in any of the Citrus EOs. Epoxybegamottin was absent from calamansi, clementine, mandarin, kaffir lime, and petitgrain oils. The content of psoralen was almost negligible in most of the Citrus EOs but was relatively high in white grapefruit EO (82.65 ± 0.76 ppm). Furthermore, large amounts of xanthotoxin were detected in bergamot and lime EOs. Previous reports indicate that xanthotoxin is absent from sweet orange (C. sinensis, pummelo taxon) and the mandarin taxa [14,15] while we found 4.85 ± 0.32 ppm in sweet orange EO and 0.33-15.24 ppm xanthotoxin in the mandarin taxa EOs. Bergamottin and 5-geranyloxy-7-methoxycoumarin were reported in mandarin, lemon, and lime oils but not in orange oil [17]. The differences between our findings and previous studies could be due to genetic and/or environmental impacts on FC biosynthesis [19]. Our LOQ, however, may be lower than that of other reports because it was based on the weight of EO rather than the weight of fresh fruit peel. Alternative explanations for the differences in our findings include genetic admixture in Citrus varieties or contamination during processing and handling. | 252558909 |
Isopimpinellin | O(C1C2=C(C(=C3C=1OC=C3)OC)C=CC(=O)O2)C | The LC-MS/MS chromatogram of 14 coumarins using the MRM acquisition mode is shown in Figure 2. Specificity, precision, accuracy, linearity, intermediate precision, and LOQ results are summarized in Table 1. The method proved specific to the target compounds since no interferences were found in any of the processed blanks. All com- The LC-MS/MS chromatogram of 14 coumarins using the MRM acquisition mode is shown in Figure 2. Specificity, precision, accuracy, linearity, intermediate precision, and LOQ results are summarized in Table 1. The method proved specific to the target compounds since no interferences were found in any of the processed blanks. All compounds met the acceptance criterion of RSD% ≤ 10 based on the precision and intermediate precision results. Compound recovery percentages ranged from 94.07 to 114.53% of the expected value. The linearity of the calibration curve of the 14 compounds was well correlated (r ≥ 0.98) within a range of 0.00010.1 ppm. The LOQ values ranged from 0.0001 to 0.005 ppm. These findings demonstrate that the developed method is suitable for analyzing the 14 targeted compounds in EOs. (Table 3). The non-volatile components are far more species-specific than the volatile components, which have comparable patterns in different Citrus oils. We found patterns in FC profiles that correspond with published differences among the Citrus ancestral taxa [15,18]. Our findings are in line with previous reports that found a mixture of FCs from the bergapten, xanthotoxin, and O(C1C2=C(C(=C3C=1OC=C3)OC)C=CC(=O)O2)C clusters in EOs derived from the citron (C. medica) and papeda (C. micrantha) ancestral taxa [15]. In this study, EOs derived from fruits of the mandarin taxa (mandarin, clementine, and tangerine) showed low total coumarin (2.44-149.45 ppm) and FC levels (2.44-149.45 ppm), not aligning with a previous report that this taxon is nearly devoid of FCs [14,15]. Interestingly, trioxsalen and toncarine were not detected in any of the Citrus EOs. Epoxybegamottin was absent from calamansi, clementine, mandarin, kaffir lime, and petitgrain oils. The content of psoralen was almost negligible in most of the Citrus EOs but was relatively high in white grapefruit EO (82.65 ± 0.76 ppm). Furthermore, large amounts of xanthotoxin were detected in bergamot and lime EOs. Previous reports indicate that xanthotoxin is absent from sweet orange (C. sinensis, pummelo taxon) and the mandarin taxa [14,15] while we found 4.85 ± 0.32 ppm in sweet orange EO and 0.33-15.24 ppm xanthotoxin in the mandarin taxa EOs. Bergamottin and 5-geranyloxy-7-methoxycoumarin were reported in mandarin, lemon, and lime oils but not in orange oil [17]. The differences between our findings and previous studies could be due to genetic and/or environmental impacts on FC biosynthesis [19]. Our LOQ, however, may be lower than that of other reports because it was based on the weight of EO rather than the weight of fresh fruit peel. Alternative explanations for the differences in our findings include genetic admixture in Citrus varieties or contamination during processing and handling. | 252558909 |
Coumarin | C12=CC=CC=C2C=CC(O1)=O | The LC-MS/MS chromatogram of 14 C12=CC=CC=C2C=CC(O1)=Os using the MRM acquisition mode is shown in Figure 2. Specificity, precision, accuracy, linearity, intermediate precision, and LOQ results are summarized in Table 1. The method proved specific to the target compounds since no interferences were found in any of the processed blanks. All com- The LC-MS/MS chromatogram of 14 C12=CC=CC=C2C=CC(O1)=Os using the MRM acquisition mode is shown in Figure 2. Specificity, precision, accuracy, linearity, intermediate precision, and LOQ results are summarized in Table 1. The method proved specific to the target compounds since no interferences were found in any of the processed blanks. All compounds met the acceptance criterion of RSD% ≤ 10 based on the precision and intermediate precision results. Compound recovery percentages ranged from 94.07 to 114.53% of the expected value. The linearity of the calibration curve of the 14 compounds was well correlated (r ≥ 0.98) within a range of 0.00010.1 ppm. The LOQ values ranged from 0.0001 to 0.005 ppm. These findings demonstrate that the developed method is suitable for analyzing the 14 targeted compounds in EOs. (Table 3). The non-volatile components are far more species-specific than the volatile components, which have comparable patterns in different Citrus oils. We found patterns in FC profiles that correspond with published differences among the Citrus ancestral taxa [15,18]. Our findings are in line with previous reports that found a mixture of FCs from the bergapten, xanthotoxin, and isopimpinellin clusters in EOs derived from the citron (C. medica) and papeda (C. micrantha) ancestral taxa [15]. In this study, EOs derived from fruits of the mandarin taxa (mandarin, clementine, and tangerine) showed low total C12=CC=CC=C2C=CC(O1)=O (2.44-149.45 ppm) and FC levels (2.44-149.45 ppm), not aligning with a previous report that this taxon is nearly devoid of FCs [14,15]. Interestingly, trioxsalen and toncarine were not detected in any of the Citrus EOs. Epoxybegamottin was absent from calamansi, clementine, mandarin, kaffir lime, and petitgrain oils. The content of psoralen was almost negligible in most of the Citrus EOs but was relatively high in white grapefruit EO (82.65 ± 0.76 ppm). Furthermore, large amounts of xanthotoxin were detected in bergamot and lime EOs. Previous reports indicate that xanthotoxin is absent from sweet orange (C. sinensis, pummelo taxon) and the mandarin taxa [14,15] while we found 4.85 ± 0.32 ppm in sweet orange EO and 0.33-15.24 ppm xanthotoxin in the mandarin taxa EOs. Bergamottin and 5-geranyloxy-7-methoxyC12=CC=CC=C2C=CC(O1)=O were reported in mandarin, lemon, and lime oils but not in orange oil [17]. The differences between our findings and previous studies could be due to genetic and/or environmental impacts on FC biosynthesis [19]. Our LOQ, however, may be lower than that of other reports because it was based on the weight of EO rather than the weight of fresh fruit peel. Alternative explanations for the differences in our findings include genetic admixture in Citrus varieties or contamination during processing and handling. | 252558909 |
Trioxsalen | c12c(c3oc(cc(c3cc1cc(o2)C)C)=O)C | The LC-MS/MS chromatogram of 14 coumarins using the MRM acquisition mode is shown in Figure 2. Specificity, precision, accuracy, linearity, intermediate precision, and LOQ results are summarized in Table 1. The method proved specific to the target compounds since no interferences were found in any of the processed blanks. All com- The LC-MS/MS chromatogram of 14 coumarins using the MRM acquisition mode is shown in Figure 2. Specificity, precision, accuracy, linearity, intermediate precision, and LOQ results are summarized in Table 1. The method proved specific to the target compounds since no interferences were found in any of the processed blanks. All compounds met the acceptance criterion of RSD% ≤ 10 based on the precision and intermediate precision results. Compound recovery percentages ranged from 94.07 to 114.53% of the expected value. The linearity of the calibration curve of the 14 compounds was well correlated (r ≥ 0.98) within a range of 0.00010.1 ppm. The LOQ values ranged from 0.0001 to 0.005 ppm. These findings demonstrate that the developed method is suitable for analyzing the 14 targeted compounds in EOs. (Table 3). The non-volatile components are far more species-specific than the volatile components, which have comparable patterns in different Citrus oils. We found patterns in FC profiles that correspond with published differences among the Citrus ancestral taxa [15,18]. Our findings are in line with previous reports that found a mixture of FCs from the bergapten, xanthotoxin, and isopimpinellin clusters in EOs derived from the citron (C. medica) and papeda (C. micrantha) ancestral taxa [15]. In this study, EOs derived from fruits of the mandarin taxa (mandarin, clementine, and tangerine) showed low total coumarin (2.44-149.45 ppm) and FC levels (2.44-149.45 ppm), not aligning with a previous report that this taxon is nearly devoid of FCs [14,15]. Interestingly, c12c(c3oc(cc(c3cc1cc(o2)C)C)=O)C and toncarine were not detected in any of the Citrus EOs. Epoxybegamottin was absent from calamansi, clementine, mandarin, kaffir lime, and petitgrain oils. The content of psoralen was almost negligible in most of the Citrus EOs but was relatively high in white grapefruit EO (82.65 ± 0.76 ppm). Furthermore, large amounts of xanthotoxin were detected in bergamot and lime EOs. Previous reports indicate that xanthotoxin is absent from sweet orange (C. sinensis, pummelo taxon) and the mandarin taxa [14,15] while we found 4.85 ± 0.32 ppm in sweet orange EO and 0.33-15.24 ppm xanthotoxin in the mandarin taxa EOs. Bergamottin and 5-geranyloxy-7-methoxycoumarin were reported in mandarin, lemon, and lime oils but not in orange oil [17]. The differences between our findings and previous studies could be due to genetic and/or environmental impacts on FC biosynthesis [19]. Our LOQ, however, may be lower than that of other reports because it was based on the weight of EO rather than the weight of fresh fruit peel. Alternative explanations for the differences in our findings include genetic admixture in Citrus varieties or contamination during processing and handling. | 252558909 |
Toncarine | C1(C=CC2OC(C=CC=2C=1)=O)C | The LC-MS/MS chromatogram of 14 coumarins using the MRM acquisition mode is shown in Figure 2. Specificity, precision, accuracy, linearity, intermediate precision, and LOQ results are summarized in Table 1. The method proved specific to the target compounds since no interferences were found in any of the processed blanks. All com- The LC-MS/MS chromatogram of 14 coumarins using the MRM acquisition mode is shown in Figure 2. Specificity, precision, accuracy, linearity, intermediate precision, and LOQ results are summarized in Table 1. The method proved specific to the target compounds since no interferences were found in any of the processed blanks. All compounds met the acceptance criterion of RSD% ≤ 10 based on the precision and intermediate precision results. Compound recovery percentages ranged from 94.07 to 114.53% of the expected value. The linearity of the calibration curve of the 14 compounds was well correlated (r ≥ 0.98) within a range of 0.00010.1 ppm. The LOQ values ranged from 0.0001 to 0.005 ppm. These findings demonstrate that the developed method is suitable for analyzing the 14 targeted compounds in EOs. (Table 3). The non-volatile components are far more species-specific than the volatile components, which have comparable patterns in different Citrus oils. We found patterns in FC profiles that correspond with published differences among the Citrus ancestral taxa [15,18]. Our findings are in line with previous reports that found a mixture of FCs from the bergapten, xanthotoxin, and isopimpinellin clusters in EOs derived from the citron (C. medica) and papeda (C. micrantha) ancestral taxa [15]. In this study, EOs derived from fruits of the mandarin taxa (mandarin, clementine, and tangerine) showed low total coumarin (2.44-149.45 ppm) and FC levels (2.44-149.45 ppm), not aligning with a previous report that this taxon is nearly devoid of FCs [14,15]. Interestingly, trioxsalen and C1(C=CC2OC(C=CC=2C=1)=O)C were not detected in any of the Citrus EOs. Epoxybegamottin was absent from calamansi, clementine, mandarin, kaffir lime, and petitgrain oils. The content of psoralen was almost negligible in most of the Citrus EOs but was relatively high in white grapefruit EO (82.65 ± 0.76 ppm). Furthermore, large amounts of xanthotoxin were detected in bergamot and lime EOs. Previous reports indicate that xanthotoxin is absent from sweet orange (C. sinensis, pummelo taxon) and the mandarin taxa [14,15] while we found 4.85 ± 0.32 ppm in sweet orange EO and 0.33-15.24 ppm xanthotoxin in the mandarin taxa EOs. Bergamottin and 5-geranyloxy-7-methoxycoumarin were reported in mandarin, lemon, and lime oils but not in orange oil [17]. The differences between our findings and previous studies could be due to genetic and/or environmental impacts on FC biosynthesis [19]. Our LOQ, however, may be lower than that of other reports because it was based on the weight of EO rather than the weight of fresh fruit peel. Alternative explanations for the differences in our findings include genetic admixture in Citrus varieties or contamination during processing and handling. | 252558909 |
Psoralen | O=c1ccc2c(o1)cc1occc1c2 | The LC-MS/MS chromatogram of 14 coumarins using the MRM acquisition mode is shown in Figure 2. Specificity, precision, accuracy, linearity, intermediate precision, and LOQ results are summarized in Table 1. The method proved specific to the target compounds since no interferences were found in any of the processed blanks. All com- The LC-MS/MS chromatogram of 14 coumarins using the MRM acquisition mode is shown in Figure 2. Specificity, precision, accuracy, linearity, intermediate precision, and LOQ results are summarized in Table 1. The method proved specific to the target compounds since no interferences were found in any of the processed blanks. All compounds met the acceptance criterion of RSD% ≤ 10 based on the precision and intermediate precision results. Compound recovery percentages ranged from 94.07 to 114.53% of the expected value. The linearity of the calibration curve of the 14 compounds was well correlated (r ≥ 0.98) within a range of 0.00010.1 ppm. The LOQ values ranged from 0.0001 to 0.005 ppm. These findings demonstrate that the developed method is suitable for analyzing the 14 targeted compounds in EOs. (Table 3). The non-volatile components are far more species-specific than the volatile components, which have comparable patterns in different Citrus oils. We found patterns in FC profiles that correspond with published differences among the Citrus ancestral taxa [15,18]. Our findings are in line with previous reports that found a mixture of FCs from the bergapten, xanthotoxin, and isopimpinellin clusters in EOs derived from the citron (C. medica) and papeda (C. micrantha) ancestral taxa [15]. In this study, EOs derived from fruits of the mandarin taxa (mandarin, clementine, and tangerine) showed low total coumarin (2.44-149.45 ppm) and FC levels (2.44-149.45 ppm), not aligning with a previous report that this taxon is nearly devoid of FCs [14,15]. Interestingly, trioxsalen and toncarine were not detected in any of the Citrus EOs. Epoxybegamottin was absent from calamansi, clementine, mandarin, kaffir lime, and petitgrain oils. The content of O=c1ccc2c(o1)cc1occc1c2 was almost negligible in most of the Citrus EOs but was relatively high in white grapefruit EO (82.65 ± 0.76 ppm). Furthermore, large amounts of xanthotoxin were detected in bergamot and lime EOs. Previous reports indicate that xanthotoxin is absent from sweet orange (C. sinensis, pummelo taxon) and the mandarin taxa [14,15] while we found 4.85 ± 0.32 ppm in sweet orange EO and 0.33-15.24 ppm xanthotoxin in the mandarin taxa EOs. Bergamottin and 5-geranyloxy-7-methoxycoumarin were reported in mandarin, lemon, and lime oils but not in orange oil [17]. The differences between our findings and previous studies could be due to genetic and/or environmental impacts on FC biosynthesis [19]. Our LOQ, however, may be lower than that of other reports because it was based on the weight of EO rather than the weight of fresh fruit peel. Alternative explanations for the differences in our findings include genetic admixture in Citrus varieties or contamination during processing and handling. | 252558909 |
Bergamottin | C(CC=C(C)C)/C(=C/COc1c2c(cc3occc31)oc(=O)cc2)C | The LC-MS/MS chromatogram of 14 coumarins using the MRM acquisition mode is shown in Figure 2. Specificity, precision, accuracy, linearity, intermediate precision, and LOQ results are summarized in Table 1. The method proved specific to the target compounds since no interferences were found in any of the processed blanks. All com- The LC-MS/MS chromatogram of 14 coumarins using the MRM acquisition mode is shown in Figure 2. Specificity, precision, accuracy, linearity, intermediate precision, and LOQ results are summarized in Table 1. The method proved specific to the target compounds since no interferences were found in any of the processed blanks. All compounds met the acceptance criterion of RSD% ≤ 10 based on the precision and intermediate precision results. Compound recovery percentages ranged from 94.07 to 114.53% of the expected value. The linearity of the calibration curve of the 14 compounds was well correlated (r ≥ 0.98) within a range of 0.00010.1 ppm. The LOQ values ranged from 0.0001 to 0.005 ppm. These findings demonstrate that the developed method is suitable for analyzing the 14 targeted compounds in EOs. (Table 3). The non-volatile components are far more species-specific than the volatile components, which have comparable patterns in different Citrus oils. We found patterns in FC profiles that correspond with published differences among the Citrus ancestral taxa [15,18]. Our findings are in line with previous reports that found a mixture of FCs from the bergapten, xanthotoxin, and isopimpinellin clusters in EOs derived from the citron (C. medica) and papeda (C. micrantha) ancestral taxa [15]. In this study, EOs derived from fruits of the mandarin taxa (mandarin, clementine, and tangerine) showed low total coumarin (2.44-149.45 ppm) and FC levels (2.44-149.45 ppm), not aligning with a previous report that this taxon is nearly devoid of FCs [14,15]. Interestingly, trioxsalen and toncarine were not detected in any of the Citrus EOs. Epoxybegamottin was absent from calamansi, clementine, mandarin, kaffir lime, and petitgrain oils. The content of psoralen was almost negligible in most of the Citrus EOs but was relatively high in white grapefruit EO (82.65 ± 0.76 ppm). Furthermore, large amounts of xanthotoxin were detected in bergamot and lime EOs. Previous reports indicate that xanthotoxin is absent from sweet orange (C. sinensis, pummelo taxon) and the mandarin taxa [14,15] while we found 4.85 ± 0.32 ppm in sweet orange EO and 0.33-15.24 ppm xanthotoxin in the mandarin taxa EOs. C(CC=C(C)C)/C(=C/COc1c2c(cc3occc31)oc(=O)cc2)C and 5-geranyloxy-7-methoxycoumarin were reported in mandarin, lemon, and lime oils but not in orange oil [17]. The differences between our findings and previous studies could be due to genetic and/or environmental impacts on FC biosynthesis [19]. Our LOQ, however, may be lower than that of other reports because it was based on the weight of EO rather than the weight of fresh fruit peel. Alternative explanations for the differences in our findings include genetic admixture in Citrus varieties or contamination during processing and handling. | 252558909 |
5-geranyloxy-7-methoxycoumarin | C(CC/C(=C/COC1C2C=CC(OC=2C=C(OC)C=1)=O)C)=C(C)C | The LC-MS/MS chromatogram of 14 coumarins using the MRM acquisition mode is shown in Figure 2. Specificity, precision, accuracy, linearity, intermediate precision, and LOQ results are summarized in Table 1. The method proved specific to the target compounds since no interferences were found in any of the processed blanks. All com- The LC-MS/MS chromatogram of 14 coumarins using the MRM acquisition mode is shown in Figure 2. Specificity, precision, accuracy, linearity, intermediate precision, and LOQ results are summarized in Table 1. The method proved specific to the target compounds since no interferences were found in any of the processed blanks. All compounds met the acceptance criterion of RSD% ≤ 10 based on the precision and intermediate precision results. Compound recovery percentages ranged from 94.07 to 114.53% of the expected value. The linearity of the calibration curve of the 14 compounds was well correlated (r ≥ 0.98) within a range of 0.00010.1 ppm. The LOQ values ranged from 0.0001 to 0.005 ppm. These findings demonstrate that the developed method is suitable for analyzing the 14 targeted compounds in EOs. (Table 3). The non-volatile components are far more species-specific than the volatile components, which have comparable patterns in different Citrus oils. We found patterns in FC profiles that correspond with published differences among the Citrus ancestral taxa [15,18]. Our findings are in line with previous reports that found a mixture of FCs from the bergapten, xanthotoxin, and isopimpinellin clusters in EOs derived from the citron (C. medica) and papeda (C. micrantha) ancestral taxa [15]. In this study, EOs derived from fruits of the mandarin taxa (mandarin, clementine, and tangerine) showed low total coumarin (2.44-149.45 ppm) and FC levels (2.44-149.45 ppm), not aligning with a previous report that this taxon is nearly devoid of FCs [14,15]. Interestingly, trioxsalen and toncarine were not detected in any of the Citrus EOs. Epoxybegamottin was absent from calamansi, clementine, mandarin, kaffir lime, and petitgrain oils. The content of psoralen was almost negligible in most of the Citrus EOs but was relatively high in white grapefruit EO (82.65 ± 0.76 ppm). Furthermore, large amounts of xanthotoxin were detected in bergamot and lime EOs. Previous reports indicate that xanthotoxin is absent from sweet orange (C. sinensis, pummelo taxon) and the mandarin taxa [14,15] while we found 4.85 ± 0.32 ppm in sweet orange EO and 0.33-15.24 ppm xanthotoxin in the mandarin taxa EOs. Bergamottin and C(CC/C(=C/COC1C2C=CC(OC=2C=C(OC)C=1)=O)C)=C(C)C were reported in mandarin, lemon, and lime oils but not in orange oil [17]. The differences between our findings and previous studies could be due to genetic and/or environmental impacts on FC biosynthesis [19]. Our LOQ, however, may be lower than that of other reports because it was based on the weight of EO rather than the weight of fresh fruit peel. Alternative explanations for the differences in our findings include genetic admixture in Citrus varieties or contamination during processing and handling. | 252558909 |
Coumarin | c1cccc2oc(=O)ccc21 | In order to examine the similarities and relationships between the c1cccc2oc(=O)ccc21 compositions and the Citrus essential oils, AHC and PCA were carried out based on a data matrix comprised of 28 Citrus \types\" and 12 c1cccc2oc(=O)ccc21 components. Based on > 25% similarity | 252558909 |
Bergamottin | c12c(c(OC/C=C(/CCC=C(C)C)C)c3c(c1)occ3)ccc(=O)o2 | In order to examine the similarities and relationships between the coumarin compositions and the Citrus essential oils, AHC and PCA were carried out based on a data matrix comprised of 28 Citrus \types\" and 12 coumarin components. Based on > 25% similarity | 252558909 |
Bergapten | c1oc2c(c(OC)c3ccc(=O)oc3c2)c1 | In order to examine the similarities and relationships between the coumarin compositions and the Citrus essential oils, AHC and PCA were carried out based on a data matrix comprised of 28 Citrus \types\" and 12 coumarin components. Based on > 25% similarity | 252558909 |
Oxypeucedanin | C1=CC2=C(C3C=COC=3C=C2OC1=O)OCC1OC1(C)C | In order to examine the similarities and relationships between the coumarin compositions and the Citrus essential oils, AHC and PCA were carried out based on a data matrix comprised of 28 Citrus \types\" and 12 coumarin components. Based on > 25% similarity | 252558909 |
Citropten | COC1C2C=CC(OC=2C=C(OC)C=1)=O | In order to examine the similarities and relationships between the coumarin compositions and the Citrus essential oils, AHC and PCA were carried out based on a data matrix comprised of 28 Citrus \types\" and 12 coumarin components. Based on > 25% similarity | 252558909 |
5-geranyloxy-7-methoxycoumarin | C(C)(C)=CCC/C(C)=C/COC1=CC(OC)=CC2OC(C=CC1=2)=O | In order to examine the similarities and relationships between the coumarin compositions and the Citrus essential oils, AHC and PCA were carried out based on a data matrix comprised of 28 Citrus \types\" and 12 coumarin components. Based on > 25% similarity | 252558909 |
Psoralen | c1(=O)oc2c(cc1)cc1ccoc1c2 | In order to examine the similarities and relationships between the coumarin compositions and the Citrus essential oils, AHC and PCA were carried out based on a data matrix comprised of 28 Citrus \types\" and 12 coumarin components. Based on > 25% similarity | 252558909 |
Coumarins | C(C)(CC(c1ccccc1)c1c(c2ccccc2oc1=O)O)=O | In order to examine the similarities and relationships between the coumarin compositions and the Citrus essential oils, AHC and PCA were carried out based on a data matrix comprised of 28 Citrus \types\" and 12 coumarin components. Based on > 25% similarity | 252558909 |
Herniarin | C1=CC2C=CC(=CC=2OC1=O)OC | Xanthotoxin, C1=CC2C=CC(=CC=2OC1=O)OC, toncarine, bergamottin, oxypeucedanin, biacangelicol, psoralen, isopimpinellin, bergapten, and imperatorin (purity ≥ 98%) were purchased from Chengdu Alfa Biotechnology (Chengdu, China). 5-Geranyloxy-7-methoxycoumarin (purity ≥ 99%) was bought from Extrasynthese (Genay, France). Trioxsalen and 6′,7′epoxybergamottin (purity ≥ 98%) were obtained from Cayman Chemical Company (Michigan, USA). Citropten (purity ≥ 99%) was purchased from Sigma-Aldrich (St. Louis, MO, USA). LCMS-grade methanol, LCMS-grade water, and HPLC-formic acid were purchased from Sigma-Aldrich (St. Louis, MO, USA). Stock solutions of each standard at a concentration of 10 ppm were prepared by diluting the powder in methanol. | 252558909 |
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