Oligotypes from only 10 Brazilian human fecal samples collected from individuals in a rural village encompassed 97% of all Blautia oligotypes found in a Brazilian sewage sample from a
city of three million people. selleck compound Further, 75% of the oligotypes in Brazilian human fecal samples matched those in US sewage samples, implying that a universal set of Blautia strains may be shared among culturally and geographically distinct human populations. Such strains can serve as universal markers to assess human fecal contamination in environmental samples. Our results indicate that host-specificity and host-preference patterns of organisms within this genus are driven by host physiology more than dietary habits.”
“Accumulating in vitro and in vivo studies have proposed a role for mast cells in the pathogenesis of atherosclerosis. Here, we studied the role of mast cells in lipoprotein metabolism, a key element in the atherosclerotic disease. Male mice deficient in low-density lipoprotein receptors and mast cells on a Western diet for 26 weeks had significantly BMS-345541 clinical trial less atherosclerotic changes both in aortic sinus (55%, P = 0.0009) and in aorta (31%, P=0.049), as compared to mast cell-competent littermates. Mast cell-deficient female mice had significantly
less atherosclerotic changes in aortic sinus (43%, P=0.011). Furthermore, we found a significant positive correlation between the extent or atherosclerosis and the number of adventitial/perivascular mast cells in aortic sinus of mast cell-competent mice (r=0.615, P=0.015). Serum cholesterol and triglyceride levels were significantly lower in both male (63%, P=0.0005 and 57%, P=0.004) and female (73%, P=0.00009 and 54%, P=0.007) mast cell-deficient mice, with a concomitant decrease in atherogenic apoB-containing particles and serum prep-high-density lipoprotein and phospholipid transfer protein activity in both male (69% and 24%) and female (74% and 54%) mast cell-deficient mice. Serum soluble intercellular
adhesion molecule was decreased in both male (32%, Duvelisib P=0.004) and female (28%, P=0.003) roast cell-deficient mice, whereas serum amyloid A was similar between mast cell-deficient and competent mice. In conclusion, mast cells participate in the pathogenesis of atherosclerosis in ldlr(-/-) mice by inducing both an atherogenic lipid profile and vascular inflammation. J. Cell. Biochem. 109: 615-623, 2010. (C) 2009 Wiley-Liss, Inc.”
“The BH3-only protein Bad is a proapoptotic Bcl-2 family member that acts as a sensitizer in intrinsic apoptosis by inactivating antiapoptotic members through heterodimer formation. Bad has been shown to contribute to tumorigenesis, including lymphoma formation in humans and mice, through alteration in expression or functional status. Here, its immunohistochemical expression was analyzed in canine nonneoplastic and lymphoma tissues using tissue microarrays.