1981年至1997年甲真菌病分析

对１７年间甲真菌病动态分析发现：甲真菌病就诊患者逐渐增多;红色毛癣菌为主要致病菌,皮肤癣菌因酵母菌分离增多呈相对下降趋势;甲中分离出糠秕马拉色菌。     

1968年至1979年美国血友病病人死因分析

作者分析了美国国家卫生统计中心提供的1968-1979年949个死亡血友病人记录,发现其死亡年龄中位数呈线性增长,10中从35岁增至55岁。死因分析:(1)死亡与血友病有关476例,占50%,若加出血或疑为出血的死亡病例,则为70%;(2)心血管系统139例,以脑出血最常见;(3)意外死亡127例,包括自杀,他杀、药物中毒、事故等;(4)胃肠道疾病67例,包括溃疡性结肠炎、胃炎、憩室炎所致出血及酒精性和病毒性肝炎后肝硬化:(5)恶性肿瘤55例,多发生于老年患者,以肺癌最多;(6)感染24例,最多是肝炎,其次有败血症、肠炎、食物中毒、艾滋病;(7)肺部疾病22例,多数为肺炎,病菌未确定;(8)泌尿生殖道7例,可能     

《中国神经再生研究（英文版）》（NRR）杂志审稿专家名单（2009年4月至2010年4月）

经过2009年3月至2009年6月审稿工作的考核及编委会讨论，聘任下述专家为本刊审稿专家，聘任时间为2009年6月至2010年6月，任期1年。感谢这些审稿专家为保证本刊客观、公正、及时、规范的审稿工作所做出的贡献。     

《中国神经再生研究（英文版）》（NRR）杂志审稿专家名单（2009年6月至2010年6月）

经过2009年3月至2009年6月审稿工作的考核及编委会讨论,聘任下述专家为本刊审稿专家,聘任时间为2009年6月至2010年6月,任期1年。感谢这些审稿专家为保证本刊客观、公正、及时、规范的审稿工作所做出的贡献。     

《中国神经再生研究（英文版）》（NRR）杂志审稿专家名单（2009年7月至2010年7月）

至2009年7月经过审稿工作的考核及编委会讨论,聘任下述专家为本刊审稿专家,聘任时间为2009年7月至2010年7月,任期1年。感谢这些审稿专家为保证本刊客观、公正、及时、规范的审稿工作所做出的贡献。     

1972年西藏阿里的故事（连载一）

<正>去阿里兮路漫漫其修远离开北京城,一路西行,此去路途坎坷,千里迢迢,像是换了人间。最初一段时间,思家心切,人之常情。父母双亲己是古稀老人,圈在一间小小的陋室里,抚养着我四岁的女儿。夫人在上海,天各一方,爱莫能助。这次专程赶来。妈妈对我说:"你要去西藏,我把家管好,把你的女几带好。"我懂得妈妈在想着什么。我懂得她承诺的分量。临行,两老一小站在小屋门前,面无表情,要说的话都说了。我和夫人用一木棍,肩扛着两只行李     

呼吸衰竭（一）

呼吸衰竭（一）母双何权瀛呼吸衰竭（简称呼衰）是由多种原因引起的肺通气和／或换气功能严重障碍，以致不能进行有效气体交换，导致缺氧伴或不伴二氧化碳潴留，而产生的一系列病理生理改变的综合征。通常以在海平面大气压、静息状态下、呼吸室内空气、无异常的心内或体循...     

Inhibition of improgan antinociception by the cannabinoid (CB)(1) antagonist N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide (SR141716A): lack of obligatory role for endocannabinoids acting at CB(1) receptors

Improgan, a nonopioid antinociceptive agent, activates descending, pain-relieving mechanisms in the brain stem, but the receptor for this compound has not been identified. Because cannabinoids also activate nonopioid analgesia by a brain stem action, experiments were performed to assess the significance of cannabinoid mechanisms in improgan antinociception. The cannabinoid CB(1) antagonist N-(piperidin-1-yl)-5-(4-chloro phenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide (SR141716A) induced dose-dependent inhibition of improgan antinociception on the tail-flick test after i.c.v. administration in rats. The same treatments yielded comparable inhibition of cannabinoid [R-(+)-(2,3-dihydro-5-methyl-3-[(4-mor pholinyl)methyl]pyrol[1,2,3-de]-1,4-benzoxazin-6-yl)(1-naphthalenyl)methanone monomethanesulfonate, WIN 55,212-2] analgesia. Inhibition of improgan and WIN 55,212-2 antinociception by SR141716A was also observed in Swiss-Webster mice. Radioligand binding studies showed no appreciable affinity of improgan on rat brain, mouse brain, and human recombinant CB(1) receptors, ruling out a direct action at these sites. To test the hypothesis that CB(1) receptors indirectly participate in improgan signaling, the effects of improgan were assessed in mice with a null mutation of the CB(1) gene with and without SR141716A pretreatment. Surprisingly, improgan induced complete antinociception in both CB(1) (-/-) and wild-type control [CB(1) (+/+)] mice. Furthermore, SR141716A inhibited improgan antinociception in CB(1) (+/+) mice, but not in CB(1) (-/-) mice. Taken together, the results show that SR141716A reduces improgan antinociception, but neither cannabinoids nor CB(1) receptors seem to play an obligatory role in improgan signaling. Present and previous studies suggest that Delta(9)-tetrahydrocannabinol may act at both CB(1) and other receptors to relieve pain, but no evidence was found indicating that improgan uses either of these mechanisms. SR141716A will facilitate the study of improgan-like analgesics.     

Diagnostic protocol of toxoplasmosis in materno-fetal infections (1981-1984 statistics)

The authors describe the most important methods in use for the laboratory diagnosis of toxoplasmosis, with special reference to the presence of IgM and to their significance in the diagnosis of acute infection. Statistics of tests carried out on pregnant women at the "Giovanni Lelli" Centre (Rome, Italy) during the years 1981-1984 are quoted. The recommended diagnostic protocol to be followed to prevent congenital infections is given.     

Nephrotoxicity of 1-(2-chloroethyl)-3-(trans-4-methylcyclohexyl)-1-nitrosourea (MeCCNU) in the Fischer 344 rat

A single s.c. injection of 1-(2-chloroethyl)-3-(trans-4-methylcyclohexyl)-1-nitrosourea (MeCCNU; 20-140 mg/kg) resulted in rapid decreases in renal function as well as leading to a chronic progressive nephropathy in male Fischer 344 rats. Disturbances in renal function were proportional to the dose of MeCCNU administered and included impaired tubular transport of p-aminohippuric acid, a decrease in urine concentrating ability, an increase in urine pH, polyuria, proteinuria and enzymuria. The tubular accumulation of p-aminohippuric acid by kidney slices was decreased as early as 1 hr after MeCCNU administration (100 mg/kg), was maximal within 12 hr and remained depressed for at least 28 days after a single injection of either 40 or 80 mg/kg. Changes in other measures of renal function (increased lactate dehydrogenase excretion, alkalinuria and decreased urine concentrating ability) were delayed from 1 to 6 days after MeCCNU administration and in some cases progressed in severity throughout the 28-day duration of the experiment. The delay between the first evidence of renal damage (decreased p-aminohippuric acid uptake) and the subsequent appearance of enzymuria, proteinuria, polyuria and alkalinuria appears to correspond to a similar delay between the initial insult and the eventual development of cellular necrosis and other histopathological changes. These results demonstrate that MeCCNU is a nephrotoxicant in rats and indicate that even a single acute dose may lead to chronic and irreversible effects on the kidney. The in vivo toxicity model defined herein appears to be an appropriate one for further study of the mechanism of nephrotoxicity of MeCCNU.     

Effects of buthionine sulfoximine on the nephrotoxicity of 1-(2-chloroethyl)-3-(trans-4-methylcyclohexyl)-1-nitrosourea (MeCCNU)

Administration of 1-(2-chloroethyl)-3-(trans-4-methylcyclohexyl)-1 1-nitrosourea (MeCCNU; 50-500 mg/kg) to male F344 rats caused a time- and dose-related decrease of glutathione (GSH) preferentially in the liver, but not in the kidney. A 500-mg/kg dose of MeCCNU decreased liver, lung and kidney GSH by 69, 15 and 3%, respectively, 2 hr after dosing. However, MeCCNU had no effect on the ratio of GSH/oxidized GSH or on GSH reductase activity in any tissue tested. A single i.p. dose of DL-buthionine-SR-sulfoximine, an inhibitor of GSH biosynthesis, caused tissue GSH levels to decrease at a rate which reflected the biological half-life of GSH in the respective organs. The T 1/2 for GSH in kidney, liver and lung was found to be 1.5, 5 and 9 hr, respectively. MeCCNU administered s.c. to DL-buthionine-SR-sulfoximine-pretreated rats resulted in a depletion of hepatic and renal GSH concentrations which was additive to the effects of either of these treatments alone. DL-Buthionine-SR-sulfoximine also markedly increased the nephrotoxicity of MeCCNU and resulted in a hepatotoxicity not ordinarily seen when MeCCNU was administered alone. These results suggest that a reactive electrophilic intermediate may be involved in the mechanism of MeCCNU nephrotoxicity. Moreover, that renal GSH may play a protective role against MeCCNU-induced nephrotoxicity.     

Role of CYP2A5 in the bioactivation of the lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in mice

The tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a potent lung carcinogen. Previously, we have demonstrated that NNK-induced lung tumorigenesis in mice depends on target-tissue bioactivation by pulmonary cytochrome P450 (P450) enzymes. The present study was designed to test the hypothesis that mouse CYP2A5 plays an essential role in NNK bioactivation in mouse lung. The role of CYP2A5 in NNK bioactivation was studied both in vitro and in vivo, by comparing the kinetic parameters of microsomal NNK metabolism and tissue levels of O(6)-methylguanine (O(6)-mG) (the DNA adduct highly correlated with lung tumorigenesis) between wild-type (WT) and Cyp2a5-null mice. In both liver and lung microsomes, the loss of CYP2A5 resulted in significant increases in the apparent K(m) values for the formation of 4-oxo-4-(3-pyridyl)butanone, which represents the reactive intermediate that produces O(6)-mG in vivo. The loss of CYP2A5 did not change circulating levels of NNK or 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol in mice treated intraperitoneally with NNK at either 20 or 100 mg/kg. However, the levels of lung O(6)-mG were significantly lower in Cyp2a5-null than in WT mice; the extent of the reduction was greater at the 20 mg/kg dose (～40%) than at the 100 mg/kg dose (～20%). These results indicate that CYP2A5 is the low-K(m) enzyme for NNK bioactivation in mouse lung. It is noteworthy that the remaining NNK bioactivation activities in the Cyp2a5-null mice could be inhibited by 8-methoxypsoralen, a P450 inhibitor used previously to demonstrate the role of CYP2A5 in NNK-induced lung tumorigenesis. Thus, P450 enzymes other than CYP2A5 probably also contribute to NNK-induced lung tumorigenesis in mice.