医源性胆管狭窄X线表现

本文报道了１３例医源性胆管狭窄，分析其影像表现。特点为：环形狭窄；线样狭窄，包括规则的和不规则的线样狭窄；闭塞性狭窄；胆管闭塞和胆管中断分离。ＥＲＣＴ和ＰＣＴ对狭窄的形态，位置及长度显示优于ＣＴ和ＵＳ。     

功能性消化不良与幽门螺杆菌关系探讨

功能性消化不良是一种人群中发病率很高的消化系统症状群，其发病机理未完全阐明，本文通过对２７４２例各类型功能性消化不良患者的胃粘膜的幽门螺杆菌感染情况作分析，发现动力障碍型ＨＰ阳性率６５．３％，溃疡型ＨＰ阳性率７４％，胃食管反流型ＨＰ阳性率２４％，特发型ＨＰ阳性率２１．４％，前两型与后两型的阳性率差异有显著性（Ｐ〈０．０５），而前两型之间阳性率差异无显著性（Ｐ〉０．０５），说明ＨＰ与动力障碍型和溃疡     

羧乙基锗倍半氧化物对大鼠脑缺血再灌注损伤的保护作用

采用结扎双侧颈总动脉后再通的方法复制大鼠脑缺血再灌注损伤模型，通过测定再灌注后大鼠海马组织中脂质过氧化产物丙二醛（ＭＤＡ），超氧化物歧化酶（ＳＯＤ）与谷胱甘肽过氧化物酶（ＧＳＨ—Ｐｘ）及ＡＴＰａｓｅ的活性，观察了有机锗─羧乙基锗倍半氧化物（ＣＧＳ）对大鼠脑缺血再灌注后大鼠海马组织中ＭＤＡ水平，明显保护ＳＯＤ、ＧＳＨ─Ｐｘ、Ｎａ＋Ｋ＋─ＡＴＰａｓｅ及Ｃａ２＋─ＡＴ─Ｐａｓｅ活性。表明ＣＧＳ对大鼠脑缺血再灌注损伤具有保护作用。     

Regional patterns of bone loss and altered bone remodeling in response to calcium deprivation in laboratory rabbits

Summary This study explores the effects of a calcium-deficient diet on patterns of bone remodeling, and examines regional differences in the amount of bone lost. Skeletally mature female rabbits (n=6) were fed a calcium-deficient diet (0.10% Ca²⁺ and 0.50% P) for 14 weeks. A separate group of rabbits (n=4) were fed a maintenance diet (1.2% Ca²⁺ and 0.45% P). Bone mineral content, serum calcium, and serum phosphorus were measured each week during the experimental period. Following sacrifice, the L₃ vetebra, femoral head, proximal tibial metaphysis, and tibial midshaft were analyzed histomorphometrically. Rabbits had 20% less vertebral bone after only 14 weeks of a calcium-deficient diet. As in human postmenopausal osteoporosis, bone loss in calcium-deficient rabbits occurs in the trabecular bone of the lumbar spine before that in the trabecular bone of the lower extremity. Calcium-deficient diets alone do not lead to increased osteoid volume or thickness. Because bone loss is relatively rapid and because the pattern of loss is similar in some respects to that found in humans, adult rabbits may provide an attractive model of calcium deficiency osteoporosis in a skeletally mature mammal in which remodeling is predominant over modeling.     

Regulatory properties of brain glutamate decarboxylase (GAD): the apoenzyme of GAD is present principally as the smaller of two molecular forms of GAD in brain

The apoenzyme of glutamate decarboxylase [enzyme without bound cofactor, pyridoxal 5'-phosphate (pyridoxal-P)] serves as a reservoir of inactive glutamate decarboxylase (GAD) that can be activated when additional GABA synthesis is required. We have investigated which of two molecular forms of GAD is present as apoenzyme in synaptosomes and in cortex, caudate nucleus, hippocampus, and cerebellum of rat brain. Endogenous glutamate apodecarboxylase (apoGAD) was labeled by incubating extracts of synaptosomes or punches of each region with 32P-pyridoxal-P, followed by reduction with NaBH4, to link covalently the 32P-pyridoxal-P to GAD. Proteins were separated by SDS-PAGE. Punches from all four brain regions and forebrain synaptosomes contained two forms of GAD with apparent Mrs of 63 and 65 kDa as identified by immunoblotting with four antiGAD sera. Punches and synaptosomes contained a major 32P-pyridoxal-P-labeled band with an apparent Mr of 63 kDa that was stained on immunoblots by the antiGAD serum 1440 and the monoclonal antibody GAD-6, and a minor labeled band at 65 kDa that was stained by the 1440, 6799, and K2 antisera. Synaptosomes contained remarkably few other strongly labeled proteins, but punches contained several other labeled bands. Three additional lines of evidence indicate that the labeled 63-kDa protein is apoGAD: (1) it was purified by immunoaffinity chromatography with the GAD-1 monoclonal antibody; (2) it yielded one major labeled peptide when digested with chymotrypsin, and that peptide appeared identical in peptide-mapping experiments to the labeled active-site peptide isolated from chromatographically prepared rat brain GAD; and (3) its labeling was selectively blocked by 4-deoxypyridoxine 5'-phosphate, a competitive inhibitor of the binding of pyridoxal-P to GAD.(ABSTRACT TRUNCATED AT 250 WORDS)     

Efficacy of radiology of the esophagus for evaluation of dysphagia

The efficacy of radiology in evaluating dysphagia was studied in 86 patients by comparison to endoscopic findings. In the 66 patients with endoscopic abnormalities radiology was correct in 54, for a sensitivity of 82%. Sensitivity of radiology improved to 95% if mild esophagitis was excluded. In the 20 patients with normal endoscopy, radiology was normal in 18 (90%). Thus radiology proved to be a reliable means of evaluating the esophagus in patients with dysphagia.     

ELISA法检测可溶性人类白细胞抗原—I及广东人参考值的测定

OBJECTIVE: To explore a method for quantitative detection of soluble human leukocyte antigen class I(HLA-I) antigens, with the assistance of which we attempt to define the reference value of the antigen in the population of Guangdong Province. METHODS: Sandwich enzyme-linked immunosorbent assay (ELISA) was employed with W6/32 monoclonal antibody serving as the solid phase antibody and beta2 microglobulin antibody as the first antibody. HRP-labeled second antibody and the substrate were added for enzyme-catalyzed coloring. On the basis of the standard curve obtained by sHLA-I standard reagent in serial dilution, the concentration of sHLA-I antigens in the samples of 60 normal subjects from the population of Guangdong province was detected. RESULTS: The sensitivity of this assay was 2.84 ng/ml with variation coefficients of 5.80% within the same batch and 9.00% between batches. The recovery rate ranged from 98.57% to 100.15%. The level of sHLA-I antigens in normal individuals was 699.54+/-360.10 ng/ml. CONCLUSION: Sandwich ELISA is sensitive, specific and stable in the detection of sHLA-I.     

中南邵阳、华东南京、西南成都组织胞浆菌感染流行病学调查

目的 :组织胞浆菌是一种真菌 ,由家禽及鸟类传播 ,可引起人的深部真菌病。我们进行的流调工作 ,对掌握疾病流行情况、制定防治措施及对结核病的防治工作具有重要意义。方法 :调查对象是健康人、住院的肺结核病人、住院的非结核性肺疾患病人。使用的方法是在前臂内侧皮内注射酵母相组织胞浆菌素 (Histolyn -CYL)。同时在另一前臂做PPD皮试 (1∶1万 )。结果 :中南邵阳地区健康人组织胞浆菌素皮试阳性率2 2 .4 0 %。肺结核病人阳性率 31.6 0 %。非结核病肺部疾病阳性率 15 .85 %。华东南京地区健康人阳性率15 .10 %。肺结核病等阳性率 17.74 %。西南成都地区健康人阳性率 2 1.77%。肺结核病人阳性率 5 4 .4 4 %。结论 :组织胞浆菌感染率很高 ,与人文地理条件密切相关 ,差异很大。因此制订防治措施也应有所不同 ,应结合当地具体情况。     

On the Role of Proteasomes in Cell Biology and Proteasome Inhibition as a Novel Frontier in the Development of Immunosuppressants

The proteasome, a large protease complex in cells, is the major machinery for protein degradation. It was previously considered a humble garbage collector, performing housekeeping duties to remove misfolded or spent proteins. Until recently, the interests of immunologists in proteasomes were focused largely on its role in antigen processing. Its real importance in cell biology has only been revealed contemporarily due to the availability of relatively specific inhibitors. It has now become increasingly clear that many aspects of immune responses highly depend on proper proteasome activity. Recently, a proteasome inhibitor has been successfully used to prevent acute as well as ongoing heart allograft rejection in mice. Such inhibitors are also efficacious in treating several autoimmune diseases, such as arthritis, psoriasis, and probably type I diabetes, in animal models. Phase II and III clinical trials of proteasome inhibitors in treating various tumors have shown promising results, and the side-effects of these drugs are tolerable. Therefore, proteasome inhibition represents a new and promising frontier in immunosuppressant development.