Phase Stability and Oxidation Behavior of an Alumina Scale-Forming NiCrAlY Alloy

The phase constitution and associated oxidation behavior were determined for an alloy of composition (in wt%) Ni–31.5Cr–11.5Al–0.61Y. The identity, relative amount, and approximate composition of each phase were determined after equilibration at 700, 900, and 1100°C using SEM/EDS, XRD, and image analysis. The CALPHAD method was used to predict the phase equilibria in this system, and the results showed good agreement with experiment. Cyclic oxidation behavior at 900, 1050, and 1100°C in air was determined and assessment of the results was aided by CALPHAD predictions in conjunction with dilatometric measurements.     

Compositional effects on the Type I hot corrosion of β-NiAl alloys

Cast alloys of nominal compositions Ni-36Al, Ni-36Al-5Co, Ni-36Al-5Pt, Ni-36Al-5Co-5Pt, and Ni-36Al-5Cr (at.%) were tested under Type I (900 °C) hot corrosion conditions in order to determine the influence of various elements commonly found in diffusion aluminide coatings on the resistance to this mode of attack. Chromium was found to be the most effective element in conferring hot corrosion resistance, but improvements in performance were also found with the addition of Co and/or Pt. Experimental evidence is presented which suggests that each of these elements increase the hot corrosion resistance of β-NiAl alloys primarily by increasing their ability to rapidly form a thermally grown Al₂O₃ scale and to heal this scale in the event of damage. Potential explanations for this enhanced scale formation and healing capability are discussed.     

Increased activation of protein kinase A type I contributes to the T cell deficiency in common variable immunodeficiency

The molecular mechanisms underlying the T cell dysfunction often present in common variable immunodeficiency (CVI) are not established. cAMP-dependent protein kinase A type I (PKAI) is an important inhibitor of T cell proliferation after Ag stimulation. We therefore investigated the possibility that activation of PKAI may be involved in the development of T cell dysfunction in CVI. An exogenously added PKAI-selective antagonist (Rp-8-Br-cAMPS) induced a significant increase in anti-CD3-stimulated PBMC proliferation in 20 CVI patients compared with no effect in 15 controls. Purified T cells from 7 CVI patients with strictly defined T cell deficiency had elevated endogenous cAMP levels compared with controls. Treatment of T cells from these CVI patients with Rp-8-bromo-cAMP-phosphorothioate markedly improved anti-CD3-stimulated proliferation (up to 3.7-fold), particularly in CD4+ lymphocytes, reaching proliferation levels comparable to control values. No effect of cAMP antagonist on T cell proliferation was seen in controls. In these CVI patients, cAMP antagonist also increased IL-2 production in anti-CD3-stimulated T cells. However, exogenously added IL-2 at concentrations comparable to the achieved increase in IL-2 levels after addition of cAMP antagonist had no effect on T cell proliferation. Furthermore, the stimulatory effects of exogenously added IL-2 at higher concentrations and cAMP antagonist on T cell proliferation were additive. Our findings indicate that increased PKAI activation may be an important molecular basis for the T cell defect in CVI and suggest that the cAMP/PKAI system may be a potential molecular target for immunomodulating therapy in these patients.     

Selective activation of cAMP-dependent protein kinase type I inhibits rat natural killer cell cytotoxicity

The present study examines the expression and involvement of cAMP-dependent protein kinase (PKA) isozymes in cAMP-induced inhibition of natural killer (NK) cell-mediated cytotoxicity. Rat interleukin-2-activated NK cells express the PKA alpha-isoforms RIalpha, RIIalpha, and Calpha and contain both PKA type I and type II. Prostaglandin E2, forskolin, and cAMP analogs all inhibit NK cell lysis of major histocompatibility complex class I mismatched allogeneic lymphocytes as well as of standard tumor target cells. Specific involvement of PKA in the cAMP-induced inhibition of NK cell cytotoxicity is demonstrated by the ability of a cAMP antagonist, (Rp)-8-Br-adenosine 3',5'-cyclic monophosphorothioate, to reverse the inhibitory effect of complementary cAMP agonist (Sp)-8-Br-adenosine 3',5'-cyclic monophosphorothioate. Furthermore, the use of cAMP analog pairs selective for either PKA isozyme (PKA type I or PKA type II), shows a preferential involvement of the PKA type I isozyme, indicating that PKA type I is necessary and sufficient to completely abolish killer activatory signaling leading to NK cell cytotoxicity. Finally, combined treatment with phorbol ester and ionomycin maintains NK cell cytotoxicity and eliminates the cAMP-mediated inhibition, demonstrating that protein kinase C and Ca2+-dependent events stimulate the cytolytic activity of NK cells at a site distal to the site of cAMP/PKA action.     

西北四省区西电东送两端市场研究报告(摘录)

分析西北送电端和东部受电端的电力市场,指出西北电力开发的优势和劣势;提出西北电源和电网开发规划,给出西北电力东送的效益评价。     

将生态旅游认证纳入我国认证认可体系范畴可行性研究

生态旅游是遵循可持续发展的原则,依托自然生态系统以及与之共生的人文生态系统,追求人与自然和谐的高级旅游形态,是现代社会发展的必然需求和产物.     

环境友好型水产养殖业发展战略

本项研究在总结我国水产养殖业发展主要经验基础上,论述了进一步发展水产养殖业的战略意义。在绿色、低碳和碳汇渔业发展新理念引导下,提出环境友好型水产养殖业发展战略,主要包括:推动水产养殖业现代化发展的"养护、拓展和高技术"三大发展战略;实现水产养殖业"高效、优质、生态、健康、安全"可持续发展的任务目标;近期需着力构建的现代水产养殖业创新发展体系的重点任务等。针对目前产业存在的问题和发展需求,提出重视水产养殖对发展空间的需求、建立养殖水域容纳量评估制度、发展生态系统水平的新型养殖生产模式、实施养殖装备提升工程、加强水产养殖管理与执法能力建设等对策建议。     

The gene encoding the catalytic subunit C alpha of cAMP-dependent protein kinase (locus PRKACA) localizes to human chromosome region 19p13.1

OBJECTIVE: The importance of portal hypertensive gastropathy, as a potentially bleeding lesion in cirrhotics with portal hypertension, has recently been appreciated. Histologically, dilation of the mucosal and submucosal vessels of the stomach is noted in this entity. The possibility of nitric oxide acting as a mediator for this mucosal vascular dilation has not been explored. METHODS: We determined, in a group of 10 male cirrhotic patients with esophageal varices and endoscopic changes consistent with severe portal hypertensive gastropathy (Group A), the gastric mucosal nitric oxide synthase activity. This was determined by measuring the rate of conversion of [3H]-arginine to [3H]-citrulline. Serum levels of nitrates and nitrites, the end products of nitric oxide, were also measured. The results were compared with those of a group of 10 male controls with no liver disease (Group B). RESULTS: Gastric mucosal constitutive and inducible nitric oxide synthase levels were significantly higher in group A (125.4 +/- 4.3 and 259.7 +/- 5.5 pmol/mg protein/minute, respectively) than in group B (88 +/- 8.6 and 130.8 +/- 6.6 pmol/mg protein/minute, respectively) ( p < 0.002 and < 0.0001, respectively). Serum nitrate/nitrite levels were 30.1 +/- 3.2 nmol/ml in group A and 15.5 +/- 0.09 nmol/ml in group B (p < 0.001). CONCLUSIONS: We conclude that the significantly increased gastric mucosal nitric oxide synthase activity, in patients with portal hypertensive gastropathy, suggests an important role for nitric oxide in the pathogenesis of this mucosal lesion.