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91.
92.
急性出血坏死性胰腺炎手术治疗的临床观察 总被引:1,自引:0,他引:1
朱义强 《中国危重病急救医学》1996,8(2):82-84
总结了经手术证实为急性出血坏死性胰腺炎的53例患者的手术疗效。发现该病应早期手术。若发病4天后手术,体温在38℃以上、脉搏超过120次/分、收缩压在12kPa(1kPa=7.5mmHg)以下、有弥漫性腹膜炎、白细胞高于16×109/L和术后有重要器官功能衰竭者,术后病死率明显增高。手术方法以胰腺坏死组织清除加三造瘘、腹腔三套管持续冲洗为优。抑制胰腺分泌的药物主要选用5氟脲嘧啶。引起胰腺感染的常见病原菌依次是大肠杆菌、肺炎克雷白杆菌、肠球菌、金黄色葡萄球菌、绿脓杆菌、奇异假单胞菌、链球菌、产气肠杆菌和脆弱类杆菌9种细菌。选用抗生素应遵守3个原则:①抗生素必须能通过血胰屏障。②能在胰腺组织中形成有效的治疗浓度。③能有效地抑制引起胰腺感染的病原菌。这样,才能取得良好的治疗效果。 相似文献
93.
对液化气燃烧后室内空气污染进行了流行病学调查,结果显示,液化气燃烧可造成SO_2、NO_2、空气总悬浮颗粒物和总烃类的室内空气污染。小鼠接触三个月出现T淋巴细胞计数降低、睡眠时间延长、骨髓嗜多染红细胞微核率增加、肺组织匀浆Ames试验阳性率增高、雄性小鼠精子畸形率增加,并有明显的剂量-反应关系。对接触5年以上的人群调查发现,呼吸道、鼻和眼的自觉症状明显增加,咽炎、鼻炎、结膜炎患病率增高。人群尿液浓缩物Ames试验和外周血红细胞微核率检出阳性结果,可能与液化气燃烧废气中含有致突变污染物有关。 相似文献
94.
Six human cytochrome P450s expressed in HepG2 cells using vaccinia virus cDNA-directed expression, were used to study the biotransformation of caffeine and its metabolites. CYP1A2 alone was responsible for caffeine 3-demethylation and paraxanthine 7-demethylation; in addition, 1A2 catalysed virtually all reactions related to caffeine and its metabolites. The metabolic profile of caffeine biotransformation by CYP1A2 averaged 81.5% for paraxanthine, 10.8% for theobromine and 5.4% for theophylline formation. It remained quite uniform when caffeine concentrations were varied. The most striking finding was that CYP2E1 (the ethanol-inducible form) had major influences upon caffeine metabolism: in particular, it catalysed the formation of theophylline and theobromine from caffeine. Thus, the in vivo metabolite profiling of caffeine may reveal CYP2E1 activities in addition to the previously documented activities of CYP1A2, polymorphic N-acetyltransferase and xanthine oxidase. 相似文献
95.
Yasuyuki Yamashita Katsuhiko Mitsuzaki Yi Tang Tomohiro Namimoto Mutsumasa Takahashi 《Journal of magnetic resonance imaging : JMRI》1997,7(4):623-628
MR angiography (MRA) was performed in 50 consecutive subjects (mean age, 59 years), who had been referred for abdominal MRA, on a 1.5-T superconductive unit that used a body phased-array coil. Three breath-hold three-dimensional sequences were evaluated both in phantom and clinical studies: (a) standard fast three-dimensional gradient-echo sequence (TR = 15, TE = 6; imaging time, 32 seconds), (b) ultrafast three-dimensional gradient-echo sequence (TR = 8.2, TE = 3; imaging time, 18 seconds), and (c) ultrafast magnetization-prepared (MP) rapid acquisition gradient echo (RAGE) (TR = 5.8, TE = 2.9, inversion time [TI] = 20; imaging time, 15 seconds). The initial 30 patients were randomized into three groups by three separate sequences. For the remaining 20 patients, ultrafast-gradient-echo and ultrafast MP-RAGE sequences were performed. Conventional angiography was performed on 36 patients. Signal measurements of the phantom and clinical images of the aorta, visceral branches of the aorta, iliac arteries, inferior vena cavae, and portal veins were performed. The overall image quality and background fatty tissue contrast of the vessels were rated subjectively. Comparison of images between MRA and conventional angiography also was performed. The contrast between the vessels and background fatty tissue was significantly higher in the ultrafast MP-RAGE sequence in both quantitative and qualitative analysis, and image-quality ultrafast MP-RAGE was superior to the other two sequences (P < .01). The aorta and iliac arteries could be visualized in all pulse sequences, and abnormalities of these vessels were diagnosed correctly. The renal artery was visualized more clearly with the two ultrafast sequences. 相似文献
96.
观察了食饵性高血脂对新西兰兔血小板功能、纤溶系统和血液流变学的影响以及去纤酶的调节作用,并动态观察了指标的变化.结果发现,高血脂能引起兔的血小板数增加,粘附力增强,血液粘滞性增加,红细胞流动变慢,呈现高凝和低纤溶状态,且主动脉形成明显粥样斑块.去纤酶在降低血脂的同时,可明显降低血小板的粘附力,降低血液粘滞性,呈现低凝和高纤溶状态,其主动脉粥样斑块亦明显减轻和缩小.提示去纤酶既能降低血脂又能降低血粘稠度,促进纤溶,起到抗凝及防止血栓形成,抑制动脉硬化的形成和发展. 相似文献
97.
Anti-rat thymocyte antibody-induced injury of glomerular mesangial cells is characterized initially by lysis (1 h) and is followed by proliferation (beginning at 3 to 4 days), with resolution that can include a focal increase in mesangial matrix (by 28 days). Chronic administration (every 12 h) of heparin (anticoagulant or nonanticoagulant) resulted in a decrease in antibody-induced mesangial cell proliferation, which, in turn, was associated with a decrease in the size and number of areas of focal mesangial matrix increase. The effect could not be attributed to the effect of heparin on complement, to alterations in the small numbers of la-positive cells that characterize the lesion, or to binding of antibody to glomeruli. The beneficial effects of heparin in reducing mesangial cell proliferation, with a subsequent reduction in matrix increase, suggest that mesangial cell responses are a major element in the development of at least some forms of glomerulosclerosis. The possible mechanisms by which these effects of heparin may be achieved are discussed. 相似文献
98.
Lynn R. Sorbara Zhichun Tang Alessandro Cama Jinru Xia Esther Schenker Ronald A. Kohanski Leonid Poretsky Elizabeth Koller Simeon I. Taylor Andrea Dunaif 《Metabolism: clinical and experimental》1994,43(12)
Women with polycystic ovary syndrome (PCOS) are markedly insulin-resistant, but the molecular mechanisms of these changes and their relationship to the hyperandrogenic state remain to be clarified. Mutations have recently been identified in the insulin receptor gene of patients with extreme forms of insulin resistance associated with hyperandrogenism (eg, type A insulin resistance), and these mutations account for the insulin resistance in such patients. We performed this study to determine whether mutations in the coding portion of the insulin receptor gene were responsible for insulin resistance in PCOS. Insulin binding studies using cultured skin fibroblasts of three obese (body mass index > 27 kg/m2) women with PCOS (ie, mild hyperandrogenemia and chronic anovulation of unknown etiology) and documented insulin resistance showed no apprarent abnormalities in either the number or affinity of insulin binding sites. Direct sequencing of all 22 exons of the insulin receptor gene from two of the women with PCOS did not reveal any mutations. Furthermore, both alleles of the gene were expressed at equal levels. In a third insulin-resistant PCOS woman, there was no evidence for a mutation in the coding portion of the insulin receptor gene as determined by denaturing gradient gel electrophoresis (DGGE). We conclude that the insulin resistance in these PCOS women was caused by a defect extrinsic to the insulin receptor. 相似文献
99.
Chih-Hsin Tang Rong-Sen Yang Houng-Chi Liou Wen-Mei Fu 《Journal of bone and mineral research》2003,18(3):502-511
The skeletal extracellular matrix produced by osteoblasts contains the glycoprotein fibronectin (Fn), which regulates the adhesion, differentiation, and function of osteoblasts. Fn fibrillogenesis is involved in the process of bone mineralization. Bone morphogenetic proteins (BMPs) can be isolated from organic bone matrix and are able to initiate de novo cartilage and bone formation. In this study, the effect of BMP-4 on Fn fibrillogenesis in cultured rat osteoblasts was examined. BMP-4 enhanced Fn synthesis and extracellular Fn assembly in primary cultured osteoblasts. In addition, the extracellular assembly of Fn from exogenously applied soluble human Fn was also increased by BMP-4. It has been reported that alpha5beta1 integrin is related to Fn fibrillogenesis. The synthesis of both alpha5 and beta1 integrins was upregulated by BMP-4. Immunocytochemistry showed that the clustering of alpha5 and beta1 integrins was also increased by BMP-4. BMP-4 increased fibril formation of Fn and the adhesion of osteoblasts onto Fn matrix, which was inhibited by disintegrin triflavin and Gly-Arg-Gly-Asp-Ser (GRGDS) peptide. Phosphorylation of extracellular signal-regulated kinase (ERK) and focal adhesion kinase (FAK) was increased by BMP-4. Enhancement of extracellular Fn fibrillogenesis and the mRNA expression of beta1 integrin by BMP-4 were inhibited by ERK kinase (MEK) inhibitor PD98059. These results suggest that the enhancement of extracellular Fn fibrillogenesis by BMP-4 in cultured osteoblasts is related to the increase of the synthesis of Fn and clustering of alpha5 and beta1 integrins. ERK is involved in the signaling pathway of BMP-4 in regulating Fn fibrillogenesis in osteoblasts. 相似文献
100.