In this study, we evaluated the therapeutic role of BM-MSC transplantation in lipopolysaccharide (LPS)- induced ALI and assessed the importance of HIMF in MSC transplantation. MSCs were isolated and identified, and untransduced MSCs, MSCs transduced with null vector or MSCs transduced with a vector encoding HIMF were transplanted into mice with LPS-induced ALI. Histopathological changes, cytokine expression and indices of lung inflammation and lung injury were

assessed in the various experimental groups. Lentiviral transduction did not influence the biological features of MSCs. In addition, transplantation of BM-MSCs alone had significant therapeutic effects on LPS-induced ALI, although BM-MSCs expressing HIMF failed to PSI-7977 improve the histopathological changes observed with lung injury. Unexpectedly, tumour necrosis factor a levels in lung tissues, lung oedema and leucocyte infiltration into lungs were even higher after the transplantation of MSCs expressing HIMF,

followed by a significant increase in lung hydroxyproline content and SRT1720 in vitro a-smooth muscle actin expression on day 14, as compared to treatment with untransduced MSCs. BM-MSC transplantation improved LPS-induced lung injury independent of HIMF.”
“Background. The adverse effects of smoking on wound healing of the skin are known clinically. Recently, an endogenous cholinergic pathway for angiogenesis mediated by endothelial nicotinic acetylcholine receptors was discovered. The objective of

this study was to investigate the appropriate concentration of nicotine at which angiogenesis and wound healing are accelerated in a murine excisional wound model.\n\nMaterials and methods. Full-thickness skin defects (8 mm) were created on the dorsum of C57BL mice and a silicone sheet (8 mm) was sutured. PF-562271 Angiogenesis inhibitor PBS (10 mu L), bFGF (1 mu g), nicotine (10(-1) M, 10(-3) M, 10(-4) M, 10(-7) M, and 10(-10)M), and both bFGF and 10(-4) M nicotine were topically injected for 7 days. Mice were sacrificed on day 8, and the wound area, the neoepithelium length, and the area of newly formed capillaries were assessed.\n\nResults. The wound area was significantly decreased in the wound treated with bFGF, with 10(-4) M nicotine, and with both bFGF and 10(-4) M nicotine. The length of the epithelium was significantly longer and the area of capillaries was also increased significantly in these three groups. The wound area, the length of the epithelium, and the area of capillaries in the group treated with both bFGF and 10 (-4) M nicotine were significantly different from those in the 10(-4) M nicotine-treated group.\n\nConclusions. In this study, nicotine at a low concentration accelerated angiogenesis and promoted wound healing; these effects of nicotine were synergistic with bFGF. (C) 2008 Elsevier Inc. All rights reserved.”
“P>Disseminated adenoviral infection is a serious problem, especially in an immunocompromised host.