Definition of temperature in nonequilibrium processes

Temperature of classical thermodynamics in nonequilibrium processe

A direct method for calculation of the flow about an axisymmetric blunt body at angle of attack

Direct calculation method for supersonic inviscid flow around axisymmetric blunt body with conically reentrant afterbody flying at large angle of attac

Catalysis of hydrogen-atom recombination in rocket nozzles

Oxygen and oxygen-nitrogen mixtures as catalysts for hydrogen atom recombination in rocket nozzle

Estimates of nonequilibrium ionization phenomena in the inviscid Apollo plasma sheath

Nonequilibrium ionization in asymmetric plasma sheath determined for Apollo spacecraft at superorbital velocity reentr

Molecular-beam epitaxy of p-type m-plane GaN

We report on the plasma-assisted molecular-beam epitaxy of Mg-doped (10 (1) over bar0) GaN on (10 (1) over bar0) 6H-SiC. Secondary ion mass spectroscopy measurements show the incorporation of Mg into the GaN films with an enhanced Mg incorporation under N-rich conditions relative to Ga-rich growth. Transport measurements of Mg-doped layers grown under Ga-rich conditions show hole concentrations in the range of p=1x10(18) to p=7x10(18) cm(-3) and a dependence between hole concentration and Mg beam equivalent pressure. An anisotropy in in-plane hole mobilities was observed, with the hole mobility parallel to [11 (2) over bar0] being higher than that parallel to [0001] for the same hole concentration. Mobilities parallel to [11 (2) over bar0] were as high as similar to 11.5 cm(2)/Vs (at p similar to 1.8 x 10(18) cm(-3)). (c) 2005 American Institute of Physics

Lack of Matrilin-2 Favors Liver Tumor Development via Erk1/2 and GSK-3 beta Pathways In Vivo

Matrilin-2 (Matn2) is a multidomain adaptor protein which plays a role in the assembly of extracellular matrix (ECM). It is produced by oval cells during stem cell-driven liver regeneration. In our study, the impact of Matn2 on hepatocarcinogenesis was investigated in Matn2(-/-) mice comparing them with wild-type (WT) mice in a diethylnitrosamine (DEN) model. The liver tissue was analyzed macroscopically, histologically and immunohistochemically, at protein level by Proteome Profiler Arrays and Western blot analysis. Matn2(-/-) mice exhibited higher susceptibility to hepatocarcinogenesis compared to wild-type mice. In the liver of Matn2(-/-) mice, spontaneous microscopic tumor foci were detected without DEN treatment. After 15 mu g/g body weight DEN treatment, the liver of Matn2(-/-) mice contained macroscopic tumors of both larger number and size than the WT liver. In contrast with the WT liver, spontaneous phosphorylation of EGFR, Erk1/2 GSK-3 alpha/beta and retinoblastoma protein (p-Rb), decrease in p21/CIP1 level, and increase in beta-Catenin protein expression were detected in Matn2(-/-) livers. Focal Ki-67 positivity of these samples provided additional support to our presumption that the lack of Matn2 drives the liver into a pro-proliferatory state, making it prone to tumor development. This enhanced proliferative capacity was further increased in the tumor nodules of DEN-treated Matn2(-/-) livers. Our study suggests that Matn2 functions as a tumor suppressor in hepatocarcinogenesis, and in this process activation of EGFR together with that of Erk1/2, as well as inactivation of GSK-3 beta, play strategic roles

Von Hippel-Lindau (VHL) inactivation in sporadic clear cell renal cancer: Associations with germline VHL polymorphisms and etiologic risk factors

Renal tumor heterogeneity studies have utilized the von Hippel-Lindau VHL gene to classify disease into molecularly defined subtypes to examine associations with etiologic risk factors and prognosis. The aim of this study was to provide a comprehensive analysis of VHL inactivation in clear cell renal tumors (ccRCC) and to evaluate relationships between VHL inactivation subgroups with renal cancer risk factors and VHL germline single nucleotide polymorphisms (SNPs). VHL genetic and epigenetic inactivation was examined among 507 sporadic RCC/470 ccRCC cases using endonuclease scanning and using bisulfite treatment and Sanger sequencing across 11 CpG sites within the VHL promoter. Case-only multivariate analyses were conducted to identify associations between alteration subtypes and risk factors. VHL inactivation, either through sequence alterations or promoter methylation in tumor DNA, was observed among 86.6% of ccRCC cases. Germline VHL SNPs and a haplotype were associated with promoter hypermethylation in tumor tissue (OR = 6.10; 95% CI: 2.28-16.35, p = 3.76E-4, p-global = 8E-5). Risk of having genetic VHL inactivation was inversely associated with smoking due to a higher proportion of wild-type ccRCC tumors [former: OR = 0.70 (0.20-1.31) and current: OR = 0.56 (0.32-0.99); P-trend = 0.04]. Alteration prevalence did not differ by histopathologic characteristics or occupational exposure to trichloroethylene. ccRCC cases with particular VHL germline polymorphisms were more likely to have VHL inactivation through promoter hypermethylation than through sequence alterations in tumor DNA, suggesting that the presence of these SNPs may represent an example of facilitated epigenetic variation (an inherited propensity towards epigenetic variation) in renal tissue. A proportion of tumors from current smokers lacked VHL alterations and may represent a biologically distinct clinical entity from inactivated cases