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991.
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993.
目的探讨肝病患者转化生长因子-β1(TGF-β1)水平、肝纤维化标志物(HA、LN、CIV、PⅢP)、HBV—DNA及丙氨酸氨基转移酶(ALT)与肝脏炎症分级和纤维化分期的关系。方法测定80例肝病患者血清TGF—β1、HA、LN、CIV、PⅢP、HBV—DNA、ALT,同时对30例慢性乙型肝炎患者行肝穿刺活检并进行病理分级分期,分析TGF-β1、HA、LN、CIV、PⅢP、HBVDNA、ALT与肝脏病理分级分期的关系。结果乙型肝炎患者血清TGF—β1水平随肝纤维化程度加重而升高,各期之间有显著性差异,但其在肝脏炎症各级之间差异无统计学意义(P〉0.05);肝纤维化各期和炎症各级之间HBV—DNA、ALT均无明显差异(P〉0.05);TGF-β1变化趋势与HA、LN、CIV、PⅢP均呈正相关(P〈0.05)。结论血清TGF—β1水平与乙型肝炎患者纤维化程度密切相关,且不受肝组织炎症程度的影响,血清TGF-β1水平测定有助于肝纤维化的早期诊断。 相似文献
994.
Stefan A. Doderer Gabor Gäbel Vivianne B.C. Kokje Bernd H. Northoff Lesca M. Holdt Jaap F. Hamming Jan H.N. Lindeman 《Journal of vascular surgery》2018,67(6):1891-1900.e4
Objective
The processes driving human abdominal aortic aneurysm (AAA) progression are not fully understood. Although antiinflammatory and proteolytic strategies effectively quench aneurysm progression in preclinical models, so far all clinical interventions failed. These observations hint at an incomplete understanding of the processes involved in AAA progression and rupture. Interestingly, strong clinical and molecular associations exist between popliteal artery aneurysms (PAAs) and AAAs; however, PAAs have an extremely low propensity to rupture. We thus reasoned that differences between these aneurysms may provide clues toward (auxiliary) processes involved in AAA-related wall debilitation. A better understanding of the pathophysiologic processes driving AAA growth can contribute to pharmaceutical treatments in the future.Methods
Aneurysmal wall samples were collected during open elective and emergency repair. Control perirenal aorta was obtained during kidney transplantation, and reference popliteal tissue obtained from the anatomy department. This study incorporates various techniques including (immuno)histochemistry, Western Blot, quantitative polymerase chain reaction, microarray, and cell culture.Results
Histologic evaluation of AAAs, PAAs, and control aorta shows extensive medial (PAA) and transmural fibrosis (AAA), and reveals abundant adventitial adipocytes aggregates as an exclusive phenomenon of AAAs (P < .001). Quantitative polymerase chain reaction, immunohistochemistry, Western blotting, and microarray analysis showed enrichment of adipogenic mediators (C/EBP family P = .027; KLF5 P < .000; and peroxisome proliferator activated receptor-γ, P = .032) in AAA tissue. In vitro differentiation tests indicated a sharply increased adipogenic potential of AAA adventitial mesenchymal cells (P < .0001). Observed enrichment of adipocyte-related genes and pathways in ruptured AAA (P < .0003) supports an association between the extent of fatty degeneration and rupture.Conclusions
This translational study identifies extensive adventitial fatty degeneration as an ignored and distinctive feature of AAA disease. Enrichment of adipocyte genesis and adipocyte-related genes in ruptured AAA point to an association between the extent of fatty degeneration and rupture. This observation may (partly) explain the failure of medical therapy and could provide a lead for pharmaceutical alleviation of AAA progression. 相似文献995.
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997.
目的对遗传性凝血因子V(FV)缺陷症进行诊断。方法通过检测先证者及家系成员的活化部分凝血活酶时间(APTT)、凝血酶原时间(PT)、FV促凝活性(FV:C)和FV抗原(FV:Ag)等进行临床表型诊断,应用聚合酶链反应(PCR)方法对先证者F5基因的25个外显子及其侧翼序列进行扩增,PCR产物进行直接测序以发现其基因突变,进行家系调查以期发现遗传规律。结果先证者APTT和PT显著延长,FV:C为3.5%,FV:Ag为1.47%。F5基因测序发现,先证者F5基因外显子区共有7处与GenBank AY364535序列不同的位点,其中外显子10区的C38591T杂合突变导致产生1个终止密码(R506Term),外显子13区的C47504T纯合变异导致编码氨基酸L1369F替换,该变异被证实为基因多态性。家系分析表明,前者遗传于先证者母亲,后者遗传于其父母双亲。结论通过表型检测、家系调查和基因诊断,明确该先症者为遗传性凝血因子V缺陷症,C38591T杂合突变产生终止密码是导致先证者FV缺陷的原因之一。 相似文献
998.
本研究旨在观察静脉血栓栓塞患者凝血因子V(Factor V,F V)活性改变,检测活化蛋白C抗性(activated protein C resistance,APCR)和凝血因子V基因F V Leiden、F V Cambridge、F V Hong Kong、F V Asp79His和F V I359T多态性.对95例静脉血栓栓塞患者(其中下肢深静脉血栓79例,肺栓塞4例,下肢深静脉血栓合并肺栓塞12例)和95例正常对照者.应用限制性内切酶片段长度多态性测定FV Leiden、F V Cambridge和F V Hong Kong多态性,用MassARRAYTM技术检测F V Asp79His、F V I359T多态性.以一期法和校正的APTT试验分别对其中的65例静脉血栓栓塞患者和60例正常对照者行凝血因子V活性水平和活化蛋白C抵抗检测.结果表明静脉血栓栓塞患者血浆凝血因子V活性水平(108.03%±28.29%)高于对照组(95.17%±29.75%),差异有显著性统计学意义(P=0.008);静脉血栓栓塞组活化蛋白C抵抗阳性13例(20.0%),对照组3例(5.0%),二组比较,有统计学意义(P=0.012).二组均未发现FV Leiden、F V Cambridge、F V Hong Kong、FV Asp79His和FV I359T多态性.结论凝血因子V活性升高和活化蛋白C抵抗是静脉血栓栓塞的危险因素,但APCR与F V Leiden、F V Cambridge、F V HongKong、F V Asp79His和F V I359T多态性无关. 相似文献
999.
Q. M. ANSTEE R. D. GOLDIN M. WRIGHT† A. MARTINELLI R. COX‡ M. R. THURSZ 《Journal of thrombosis and haemostasis》2008,6(8):1336-1343
Summary. Background: There is strong evidence demonstrating that coagulation system activation contributes to wound healing and promotes organ fibrosis. Several epidemiological studies have now shown that prothrombotic status, including carriage of the factor (F)V Leiden mutation, is associated with rapid progression of hepatic fibrosis. Objectives: To assess the effect of a procoagulant state on progression of hepatic fibrosis in a controlled environment and to test whether anticoagulation could attenuate fibrogenesis. Methods: We investigated the effects of coagulation status on liver fibrosis development in a mouse model of chronic toxic liver injury. Prothrombotic FV Leiden mutant mice, C57BL/6 control animals and anticoagulated mice were studied after chronic exposure to carbon tetrachloride. Results: Carriage of the FV Leiden mutation caused a significant increase in hepatic fibrosis. Anticoagulation with warfarin significantly reduced fibrosis progression in wild-type mice but was less effective against the profibrotic FV Leiden mutation. Changes in the fibrosis scores were mirrored by changes in liver hydroxyproline content and hepatic stellate cell activation detected by α-smooth muscle actin expression. Conclusions: These results demonstrate that coagulation status has a strong influence on hepatic fibrogenesis. It is likely that thrombin signaling through the proteinase-activated receptor 1 (PAR1 ) receptor expressed on hepatic stellate cells is responsible for this relationship. These results represent the first reported use of anticoagulation to slow hepatic fibrogenesis and suggest a potential novel anti-fibrotic therapeutic approach for the future. 相似文献
1000.
Visual scenes are frequently composed of objects that move in different directions. To segment such scenes into distinct objects or image planes, local motion cues have to be evaluated and integrated according to criteria of global coherence. When several populations of coherently moving random dots penetrate each other, the visual system tends to assign them to different planes-perceived as transparent motion. This process of integration was studied by changing the angle of motion trajectories with which groups of dots penetrate each other or by varying the spatial constellation of dots moving in opponent directions. Psychophysical testing revealed that stimuli providing almost identical local motion cues could be perceived in three very different ways: (1) as a matrix of stationary flickering dots, (2) as a single surface of coherently moving dots, and (3) as two transparent dot matrices moving in different directions. Behaviorally controlled functional magnetic resonance imaging (fMRI) was used to identify brain regions that contribute to the integration of local motion cues into coherently moving surfaces. Activation of the human motion complex (hMT+/V5) and of areas in the fusiform gyrus (FG) as well as in the intraparietal sulcus (IPS-occ) was correlated with the perception of coherent motion and especially hMT+/V5 took a central role in differentiating transparent motion from single-surface coherent motion. 相似文献