Frequency of seroreactors to Legionella among the patients with pulmonary infections

A prospective study was conducted with patients with pulmonary infections who were consecutively admitted to the three community hospitals in Benghu from July 1986 to May 1987, and to the children's hospital in Nanjing from September 1986 to January 1987. Antibodies to Lpi-8, Lm, Ld, and Lg were measured by the micro-agglutination test. During the study period, 150 adult patients (100 pairs sera) and 212 control healthy people and 110 pairs sera of childhood patients and 173 children without respiratory tract infections were investigated. The diagnosis of legionellosis was based on seroconversion (fourfold rise in titer to greater than 1:32 or static titer of greater than 1:32) and clinical and radiographic features of legionnaires' disease. About 11% legionella infection in hospitalized adult patients with pulmonary infections, and about 5.45% in children with atypical pneumonias.     

胸部类癌

本文报道了３１例胸部类癌，其中胸腺类癌１４例，支气管类癌１７例，伴有异位ＡＣＴＨ综合征者１７例。１２例患者发生转移（３９％），２４例行原发肿瘤全部或部分切除，术后放疗或化疗或两者均有者１７例，４例仅行探查并取活检，２８例经手术及病理证实。     

四氧嘧啶诱发糖尿病大鼠血管紧张素的变化

实验观察了四氧嘧啶诱发糖尿病大鼠连续饲养１１０ｄ后体内肾素一血管紧张素系统的变化。结果表明，血浆和心脏的血管紧张素Ⅱ含量无明显变化，而肾脏的ＡｎｇⅡ含量却明显低于正常对照组。另外，心脏的心钠素（ＡＮＰ）含量在糖尿病大鼠与正常对照组之间无差别，血中的糖化血红蛋白含量基本无变化。上述结果表明，糖尿病大鼠早期心脏可能无明显损伤，而肾脏的肾素一血管紧张素系统活性降低。     

Biological significance of enhanced mitochondrial ketogenesis during the early stages after 70% hepatectomy in rats

Ketogenic capacity of mitochondria from the remnant liver of 70% hepatectomized rats was studied in relation to mitochondrial phosphorylative activity. Ketogenic capacity increased to a maximum of 6.04 +/- 0.39 from 3.84 +/- 0.13 of control, with an enhancement of mitochondrial phosphorylative activity 6 hr after hepatectomy, and then decreased to normal levels within 24 hr. Adenylate energy charge, (ATP + 1/2ADP)/(ATP + ADP + AMP), of the remnant liver decreased to 0.825 +/- 0.006 as compared to 0.849 +/- 0.002 of control 6 hr after operation. At 12 hr, total ketone body concentrations of the arterial blood increased concomitant with a fall in ketone body ratio (acetoacetate/3-hydroxybutyrate) which reflects the decreased liver mitochondrial redox (NAD+/NADH) state. These findings suggest that an enhancement of mitochondrial fatty acid oxidation and ketogenesis occurs concomitant with an enhancement of mitochondrial phosphorylative activity in the remnant liver in response to a decreased energy charge after 70% hepatectomy.     

Effects of different types of diet and sodium saccharin on proliferation at the limiting ridge of the rat forestomach

Sodium saccharin, at high doses in the diet, has been reported to cause hyperplasia of the forestomach (squamous portion of stomach), at the limiting ridge in F344 rats, in addition to its potential to induce proliferative effects on the urinary bladder epithelium. We have characterized this hyperplasia of the squamous epithelium of the forestomach at the limiting ridge in F344 and Sprague-Dawley rats given various doses of sodium saccharin for 4 to 95 wk. With increasing doses of sodium saccharin, the limiting ridge of the forestomach showed dose-related morphological changes: basal-cell hyperplasia, early papillary hyperplasia with basal-cell hyperplasia and papillary hyperplasia. Calcium saccharin in Prolab diet caused hyperplasia of the forestomach at the limiting ridge, similar to that caused by sodium saccharin. The severity of hyperplasia was influenced by the type of diet and by the strain of rats. AIN-76A diet without added sodium saccharin caused basal-cell hyperplasia in F344 rats, whereas Prolab, Purina and NIH-07 diets without added sodium saccharin had little or no effect on the forestomach. The effect of AIN-76A diet alone persisted through 95 wk of feeding without any evidence of tumour formation. In Sprague-Dawley rats, which appeared more sensitive to effects on the forestomach than F344 rats, Prolab 3200 and Purina diets without sodium saccharin caused basal-cell hyperplasia in more than half of the treated rats. The forestomach hyperplasia associated with AIN-76A or saccharin administration appears to be mild, limited in extent to the limiting ridge, and not associated with carcinogenesis.     

Brain natriuretic peptide enhances the endothelium-independent cAMP and vasorelaxant responses of calcitonin gene-related peptide in rat aorta

Calcitonin gene-related peptide (CGRP) causes vasorelaxation in rat aorta involving endothelium/nitric oxide (NO)-dependent elevations of both cAMP and cGMP levels. When endothelium is removed, preincubation with exogenous NO uncovers and potentiates direct (endothelium-independent) cAMP elevations and vasorelaxations caused by CGRP. This enhancing effect of NO potentially involves elevation of cGMP and inhibition of Type III (cGMPinhibitable) phosphodiesterase, causing accumulation of cAMP. However, NO may have other actions. The aim of the present study was to determine if brain natriuretic peptide (BNP), which elevates cGMP levels independent of NO, could enhance cAMP accumulations and vasorelaxations induced by CGRP in rat aortic rings denuded of endothelium. When added separately, neither CGRP (100 nM) nor BNP (10 nM) altered cAMP levels. When added in combination, CGRP (100 nM) and BNP (10 nM) significantly elevated cAMP levels (from control of 0.95 ± 0.08 to 1.53 ± 0.09 pmol/mg protein) at 2 min. BNP (10 nM) elevated cGMP levels 10-fold at 2 min and this response was not altered by co-administration of CGRP (100 nM).Pretreatment with BNP at concentrations as low as 1 nM in endothelium-denuded aortic rings greatly enhanced the direct vasorelaxant effects of CGRP (100 nM) (from control of 0% to 57.6 ± 6.8% relaxation of phenylephrineprecontractions). Our findings indicate that BNP enhances direct (endothelium-independent) cAMP elevations and vasorelaxations caused by CGRP in rat aorta, thus supporting the concept that cGMP inhibits cAMP metabolism and enhances CGRP-induced responses in aortic smooth muscle cells.     

胫骨延长术后的功能康复程序初探

胫骨延长术是矫治小儿麻痹后遗症下肢短缩最常见的术式，但如何恢复或改善术后的功能，目前尚无一套系统的程序。本文作者根据自行设计的胫骨延长休后功能康复的临床观察，作较系统地介绍，并就该程序的合理性，进行了讨论与论证。     

心间隔缺损并哑性动脉导管未闭4例

我院治疗６６例心间隔缺损的病例中，有４例合并哑性动脉导管未闭（简称ＰＤＡ），发生率６％。全组病例术前均无ＰＤＡ临床体征，１例术前再次复查心脏彩超时发现，其余３例均漏诊。１例先处理ＰＤＡ，３例在纠正心内畸形同时处理ＰＤＡ。心间隔缺损合并哑性ＰＤＡ容易漏诊，但有其临床特点，手术可先处理ＰＤＡ，或在体外循环下处理ＰＤＡ。