Methods: Toxigenic stool culture was used in this study. Diarrhoeal stool specimens were cultured for C. difficile, followed by direct immunoassay on colonies of positive cultures with significant growth to detect toxins A or B. Results: C. difficile was detected in 8.6% (n=23) of the 268 diarrhoeal stool specimens. All C. difficile isolates were susceptible to find protocol metronidazole,

vancomycin, chloramphenicol and doxycyline, and resistant to clindamycin, ciprofloxacin, gentamicin and cefotaxime. About 70% of the isolates were resistant to co-trimoxazole. Conclusions: C. difficile was observed to be an important diarrhoeal pathogen and metronidazole was effective in treating diarrhoea caused by the bacterium. Co-trimoxazole, which is widely used as prophylaxis against opportunistic infections in HIV/AIDS patients, was not very effective in preventing diarrhoea caused by C. difficile.”
“Biodegradation of polycyclic aromatic hydrocarbons (PAHs) in soils has been linked to history of exposure to PAHs and prevailing

environmental conditions. This work assessed the capacity of indigenous microorganisms in soils collected in Livingstone Island (South Shetlands Islands, Antarctica) with no history of pollution (?PAHs: 0.141.47 similar to ng similar to g-1 dw) to degrade XMU-MP-1 ic50 14C-phenanhthrene at 4, 12 and 22 similar to circle C. The study provides evidence of the presence of phenanthrene-degrading microorganisms in all studied soils. Generally, the percentage of 14C-phenanhthrene mineralized increased with increasing temperature. The highest extent of 14C-phenanhthrene mineralization (47.93%) was observed in the slurried RSL3 system at 22 similar to degrees C. This work supports findings of the presence of PAH-degrading microorganisms in uncontaminated soils and suggests the case is the same for uncontaminated Antarctic remote soils.”
“By mimicking sympathetic

stimulation in vivo, we previously reported that mice globally lacking serotonin 5-HT(2B) receptors did not develop isoproterenol-induced left ventricular hypertrophy. However, the exact cardiac cell type(s) expressing 5-HT(2B) receptors (cardiomyocytes versus noncardiomyocytes) involved in pathological heart hypertrophy was never addressed in vivo. We report here that mice expressing the 5-HT(2B) receptor solely in cardiomyocytes, like global 5-HT(2B) receptor-null mice, are resistant to isoproterenol-induced cardiac hypertrophy and dysfunction, as well as to isoproterenol-induced increases in cytokine plasma-levels. These data reveal a key role of noncardiomyocytes in isoproterenol-induced hypertrophy in vivo.