Interleukin-6 in bronchoalveolar lavage fluid from patients with COPD

目的　本研究通过检测支气管肺灌洗液 (BALF)中及肺泡巨噬细胞 (AM)产生的IL 6 ,揭示IL 6与慢性支气管炎(COPD)肺气肿发生的关系 ,为IL 6提供新的研究领域。方法　检测 6名正常无吸烟人及 2 1名COPD患者BALF中及AM释放的IL 6 ,根据正常人组BALF中IL 6的 95 %正常值可信区限 ,将COPD患者分为二组 ,在正常值可信区限内为第一组 ,在正常值可信区限外为第二组。结果　表明 2组中AM产生的IL 6第二组明显高于第一组 ,且 2组患者肺功能 (Dlco ,FEV1,FEV1/FVC和RV/TLC)有明显差异结论　AM产生的IL 6可能与COPD患者肺功能变化有关 ,在COPD患者肺气肿发生发展过程中发挥重要作用     

脑外伤后脑干组织中血管内皮细胞及血浆蛋白分布改变的免疫？…

目的:探讨脑外伤后脑干组织中血脑屏障和神经细胞的病理学改变.方法:采用免疫组化染色显示人体脑干组织中的血管内皮细胞(CD31)和某些血浆蛋白(白蛋白及 IgM).结果:1.在正常脑干组织中, CD31阳性物呈连续的线条状,围成规则的血管腔,其周围无明显间隙;血浆蛋白位于血管内,未见到血浆/蛋白阳性神经细胞或神经纤维.2.脑外伤后,脑干中的 CD31阳性物呈不规则弯曲的小片段状,围成不规则的血管腔,其周围间隙明显增宽;同时可见到白蛋白及IgM阳性神经细胞和神经纤维.结论:脑外伤后,脑干组织中的血脑屏障受到了破坏,而且神经细胞也有不同程度的损伤.     

可吸收内固定治疗松质骨骨折22例

目的 总结可吸收内固定材料自身增强聚丙交脂（ＳＲ－ＰＬＬＡ）的临床应用体会。方法 采用波兰进口ＳＲ－ＰＬＬＡ螺钉、棒、线治疗四肢松质骨骨折２２例,随访摄片观察骨折愈合情况,检查关节活动功能。结果 术后有两侧出现并发症,一例局部少量积液,经２次穿刺抽液加压包扎痊愈;一例患者过早去除石膏功能锻炼,螺钉松动滑出,经手术复位石膏外固定治愈,无感染或过敏等情况发生。结论 掌握可吸收材料的生物力学特点,并选择适当的病例,可以最大限度地发挥可吸收内固定材料的优势。     

Traumatic cervical distraction complicated by delayed reduction due to traumatic vertebral artery pseudo-aneurysm

A 23-year-old male involved in a high-speed collision acquired, among other injuries, a wide fracture distraction at C2/C3. Reduction was delayed by an enlarging vertebral artery pseudo-aneurysm at the site of injury which was successfully treated by proximal endovascular occlusion with a detachable polymer-filled balloon. A traumatic arachnoid cyst or pseudomeningocele was also demonstrated at the injury site but intervention was not required. The treatment and outcome of these three uncommon injuries in the literature is reviewed and discussed. Given the severity of the injury, the absence of severe long-term neurological disability is notable.     

No association between an intronic presenilin-1 gene polymorphism and schizophrenia in a Chinese population

We investigated the association between schizophrenic psychosis and an intronic polymorphism of the presenilin-1 (PS1) gene in a Chinese population. Schizophrenic and control groups had similar PS1 genotype distributions and allele frequencies, indicating that this polymorphism may not be involved in the development of schizophrenia.     

Effects of TGFbeta on bone ingrowth in the presence of polyethylene particles

We implanted bone harvest chambers (BHCs) bilaterally in ten mature male New Zealand white rabbits. Polyethylene particles (0.3+/-0.1 microm in diameter, 6.4 x 10(12) particles/ml) were implanted for two, four or six weeks bilaterally in the BHCs, with subsequent removal of the ingrown tissue after each treatment. In addition to the particles, one side also received 1.5 microg of recombinant transforming growth factor beta1 (TGFbeta1). At two weeks, the bone area as a percentage of total area was less in chambers containing TGFbeta compared with those with particles alone (7.8+/-1.3% v 16.9+/-2.7% respectively; 95% confidence interval (CI) for difference -14.0 to -4.30; p = 0.002). At four weeks, the percentage area of bone was greater in chambers containing TGFbeta compared with those with particles alone (31.2+/-3.4% v 22.5+/-2.0% respectively; 95% CI for difference 1.0 to 16.4; p = 0.03). There were no statistical differences at six weeks, despite a higher mean value with TGFbeta treatment (38.2+/-3.9% v 28.8 +/-3.5%; 95% CI for difference -4.6 to 23.3; p = 0.16). The number of vitronectin-receptor-positive cells (osteoclast-like cells) was greater in the treatment group with TGFbeta compared with that with particles alone; most of these positive cells were located in the interstitium, rather than adjacent to bone. TGFbeta1 is a pleotropic growth factor which can modulate cellular events in the musculoskeletal system in a time- and concentration-dependent manner. Our data suggest that there is an early window at between two and six weeks, in which TGFbeta may favourably affect bone ingrowth in the BHC model. Exogenous growth factors such as TGFbeta may be a useful adjunct in obtaining osseointegration and bone ingrowth, especially in revisions when there is compromised bone stock and residual particulate debris.     

常见大气细菌对动物肺损伤的实验研究

为研究大气微生物对人体健康的影响,于１９９７年对上海市大气细菌污染进行了调查。在此基础上,采用大鼠经气管灌注细菌悬液２４小时后,分析肺灌洗液组成的方法,就大气细菌对动物呼吸系统损伤方面进行了研究。同时比较了不同地区大气细菌对大鼠肺细胞的损伤效应。结果发现大气细菌污染严重地区的细菌染毒组ＡＬＢ、ＬＤＨ、ＡＣＰ、ＡＫＰ、中性粒细胞等指标比清洁区升高更为显著,提示大气中常见细菌可对肺组织造成损伤。     

Early and delayed cardioprotection by heat stress is mediated by calcitonin gene-related peptide

Brief ischaemia or heat stress protects the myocardium against ischaemia-reperfusion injury. Heat stimulus evokes release of sensory nerve transmitters, including calcitonin gene-related peptide (CGRP). Since CGRP has been shown to play an important role in the mediation of ischaemic preconditioning, the present study examined whether early or delayed preconditioning induced by retrograde hyperthermic perfusion in vitro or by whole-body hyperthemia in vivo also involves endogenous CGRP. Isolated rat hearts were perfused in the Langendorff mode and subjected to 30 min global ischaemia and 30 min reperfusion. Heart rate, coronary flow, left ventricular pressure and its first derivatives (±dp/dt) were recorded and the CGRP-like immunoreactivity (CGRP-LI) content and the release of creatine kinase (CK) during reperfusion were measured. Retrograde hyperthermic perfusion (42 °C) for 5 min improved the recovery of cardiac function, decreased the release of CK and elevated the content of CGRP-LI in the coronary effluent. CGRP_8–37 (10^–7 mol/l), a selective CGRP receptor antagonist, abolished the cardioprotection by heat stress. Pretreatment with capsaicin (50 mg/kg s.c.), which specifically depletes sensory nerve transmitter content, abolished both the cardioprotection and the increased release of CGRP-LI. Whole-body hyperthermia (42 °C for 15 min) caused an increase in the plasma concentration of CGRP-LI. Early or delayed protection was shown in the hearts obtained from the animals subjected to whole-body hyperthermia 10 min or 48 h before the experiments. The early or delayed protection by heat stress was also abolished by pretreatment with capsaicin. The present study suggests that, in the rat, the early and delayed cardioprotection induced by heat stress involves endogenous CGRP. Received: 31 December 1998 / Accepted: 6 April 1999