Cardiac output did not change (P = .238). Lung attenuation and subjective score assignment for GGO were significantly correlated with Ppa and Pc’ (P < .001 to .002).
Conclusion: Acute PE induces GGO in unobstructed lung zones. Given constant cardiac output, GGO is likely to be related
to redistribution of blood flow from obstructed to unobstructed BMN 673 cell line lung zones and occurs at a pressure consistent with pulmonary edema. (c) RSNA, 2009″
“An analytic model of deposition is applied on reactive ion beam sputtering to optimize the properties of iron oxide thin films. This model will be able to predict deposition rate and phase contents. Among its hypotheses, we assume oxygen adsorption at the surface of the target to explain variations of deposition rate for oxygen flow. This hypothesis is validated by chemical analyses on iron targets. An ellipsoidal distribution of probability is introduced to model sputtered matter distribution from iron target and to calculate sputtering yield. Comparison between experimental and calculated deposition rates validates previously assumed hypotheses. (C) 2010 American Institute of Physics. PS 341 [doi: 10.1063/1.3327431]“
“Background: Glycolic acid (GA) is the most commonly
used alpha-hydroxy acid (AHA) for dermatologic applications, and is considered as a versatile superficial peeling agent for facial rejuvenation. Its therapeutic effect includes acceleration of epidermal turnover without apparent inflammation,
and its action is pH-dependent. However, little is known about the molecular mechanism of GA-induced peeling.
Objective: To investigate the effects of topical application of GA on cell proliferation using a skin equivalent model and to examine the molecular mechanisms of GA-induced peeling.
Methods: GA solution was applied on the Surface Of a skin equivalent model, and cell proliferation was measured by means of BrdU-incorporation and immunohistochemical methods. Release of chemical mediators Such as ATP into the medium was examined. The effects of antagonists of ion channels were also analyzed.
Results: Sapitinib molecular weight At 24 h after GA application, BrdU-incorporation into basal keratinocytes was significantly increased. Induction of keratinocyte proliferation was pH-dependent, and was inhibited by antagonists of TRPV1, an acid-sensitive ion channel. Furthermore, transient ATP release was detected in the Culture medium after GA stimulation, and this was also suppressed by TRPV1 antagonists.
Conclusion: These results suggest that one of the mechanisms of GA-induced epidermal proliferation is a growth response of basal keratinocytes to the local elevation of H(+)-ion concentration by infiltrated GA. This response is mediated by TRPV1 activation and ATP release. Activation of P2 receptors by the released ATP may also be involved. (C) 2009 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.