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51.
Yanni Li Lianne M. Nieuwenhuis Michiel D. Voskuil Ranko Gacesa Shixian Hu Bernadien H. Jansen Werna T. U. Venema Bouke G. Hepkema Hans Blokzijl Henkjan J. Verkade Ton Lisman Rinse K. Weersma Robert J. Porte Eleonora A. M. Festen Vincent E. de Meijer 《American journal of transplantation》2021,21(9):3133-3147
Thrombosis after liver transplantation substantially impairs graft- and patient survival. Inevitably, heritable disorders of coagulation originating in the donor liver are transmitted by transplantation. We hypothesized that genetic variants in donor thrombophilia genes are associated with increased risk of posttransplant thrombosis. We genotyped 775 donors for adult recipients and 310 donors for pediatric recipients transplanted between 1993 and 2018. We determined the association between known donor thrombophilia gene variants and recipient posttransplant thrombosis. In addition, we performed a genome-wide association study (GWAS) and meta-analyzed 1085 liver transplantations. In our donor cohort, known thrombosis risk loci were not associated with posttransplant thrombosis, suggesting that it is unnecessary to exclude liver donors based on thrombosis-susceptible polymorphisms. By performing a meta-GWAS from children and adults, we identified 280 variants in 55 loci at suggestive genetic significance threshold. Downstream prioritization strategies identified biologically plausible candidate genes, among which were AK4 (rs11208611-T, p = 4.22 × 10−05) which encodes a protein that regulates cellular ATP levels and concurrent activation of AMPK and mTOR, and RGS5 (rs10917696-C, p = 2.62 × 10−05) which is involved in vascular development. We provide evidence that common genetic variants in the donor, but not previously known thrombophilia-related variants, are associated with increased risk of thrombosis after liver transplantation. 相似文献
52.
Risk of thromboembolism in relation to an in-vitro fertilization programme: three case reports 总被引:2,自引:3,他引:2
Aurousseau M.H.; Samama M.M.; Belhassen A.; Herve F.; Hugues J.N. 《Human reproduction (Oxford, England)》1995,10(1):94-97
Severe thrombotic events following ovarian stimulation for in-vitrofertilization (IVF) procedures in three women are reported.None of these patients presented any concomitant clinical signof ovarian hyperstimulation syndrome. Coagulation inhibitorswere in the normal range but cardiovascular risk factors werepresent. It is postulated that early thrombosis could be favouredby high endogenous plasma oestrogen concentrations subsequentto ovarian stimulation when associated with another risk factor.Our data are discussed in relation to previous publications.It is suggested that risk factors must be considered individuallybefore each IVF attempt. In patients at high risk, clinicalmanagement of the post-transfer period is recommended. 相似文献
53.
Cheras PA Freemont AJ Sikorski JM 《Osteoarthritis and cartilage / OARS, Osteoarthritis Research Society》1993,1(4):219-232
It has been proposed that nontraumatic ischemic necrosis of bone (INB) is a result of lipid associated intraosseous thrombosis. A histological study of 15 patients with INB confirmed the presence of intravascular lipid and thrombosis in the vessels of the femoral head. A similar analysis of 11 patients with primary osteoarthritis (OA) showed similar changes at lower levels. These changes were not observed in seven control femoral heads. The possibility that both INB and OA result from intraosseous thrombosis is discussed. 相似文献
54.
目的 研究妇科腹腔镜术后深静脉血栓的发生率。方法 在澳大利亚悉尼Liverpool医院 1997年 5月~ 1997年 9月 72例妇科腹腔镜手术采用Doppler超声检查静脉血流的通畅性和血管腔内的回声团用以诊断深静脉血栓。 61例患者充气时间 <60分钟为小手术组 ,11例 >60分钟为大手术组。每例患者在术后 2 4小时内及术后 7天行两次超声Doppler检查 ,所有 72人均行术后 2 4小时内的超声Doppler检查 ,小手术组 61例中 4 0例、大手术组 11例中 9例行二次超声检查。 2 3例未行二次超声检查者均行电话随访。结果 在我们的研究中两组患者均未发现DVT。本文同时报道北京复兴医院一例腹腔镜下右卵巢巧克力囊肿剥除术、左卵巢及部分输卵管切除术患者术后并发DVT ,其诊断及治疗经过。结论 这项研究证实妇科腹腔镜手术DVT虽发生率极低 ,一旦发生需及时诊治 ,以免发生肺栓塞等致命并发症。 相似文献
55.
56.
57.
多烯脂肪酸对脑血栓伴高脂血症病人降脂作用的疗效观察 总被引:2,自引:0,他引:2
目的:研究多烯脂肪酸胶囊对脑血栓伴高脂血症病人的降脂作用。选血脂康作对照。方法:60例脑血栓伴高脂血症病人随机分为二组:治疗组(n=31)及对照组(n=29)。服药前及服药后4周,8周查血脂。结果:⑴服药4周后TC和LDL-C分别降低21.02%和28.93%(多烯脂肪酸组)。⑵多烯脂肪酸组降低了34.06%的血清TG水平,效果显,结论:多烯脂肪酸胶囊降TG和LDL-C水平与血脂康作用相近,其降 相似文献
58.
Reiichiro Kondo Yasuko Iwakiri Masayoshi Kage Hirohisa Yano 《Pathology international》2023,73(9):381-393
Liver is the largest solid organ in the abdominal cavity, with sinusoid occupying about half of its volume. Under liver disease, hemodynamics in the liver tissue dynamically change, resulting in injury to liver sinusoidal endothelial cells (LSECs). We discuss the injury of LSECs in liver diseases in this article. Generally, in noninflamed tissues, vascular endothelial cells maintain quiescence of circulating leukocytes, and unnecessary blood clotting is inhibited by multiple antithrombotic factors produced by the endothelial cells. In the setting of inflammation, injured endothelial cells lose these functions, defined as inflammatory endotheliopathy. In chronic hepatitis C, inflammatory endotheliopathy in LSECs contributes to platelet accumulation in the liver tissue, and the improvement of thrombocytopenia by splenectomy is attenuated in cases with severe hepatic inflammation. In COVID-19, LSEC endotheliopathy induced by interleukin (IL)-6 trans-signaling promotes neutrophil accumulation and platelet microthrombosis in the liver sinusoids, resulting in liver injury. IL-6 trans-signaling promotes the expression of intercellular adhesion molecule-1, chemokine (C-X-C motif) ligand (CXCL1), and CXCL2, which are the neutrophil chemotactic mediators, and P-selectin, E-selectin, and von Willebrand factor, which are involved in platelet adhesion to endothelial cells, in LSECs. Restoring LSECs function is important for ameliorating liver injury. Prevention of endotheliopathy is a potential therapeutic strategy in liver disease. 相似文献
59.
Shunsuke Kageyama Hiroshi Yamamoto Mitsuyo Nagano Harumi Arisaka Takashi Kayahara Ryota Yoshimoto 《British journal of pharmacology》1997,122(1):165-171
- A murine anti-human vWF monoclonal antibody, AJvW-2, was developed that inhibited the interaction between platelet glycoprotein Ib (GPIb) and von Willebrand factor (vWF) during the ristocetin- (IC50=0.7±0.1 μg ml−1) and botrocetin- (IC50=1.8±0.3 μg ml−1) induced aggregation of human platelets.
- AJvW-2 inhibited the high shear stress (10.8 N m−2) induced aggregation of human platelets dose-dependently with an IC50=2.4±0.3 μg ml−1, but had no effect on low shear stress induced platelet aggregation (1.2 N m−2) up to 100 μg ml−1.
- AJvW-2 also inhibited the high shear stress (5.0 N m−2) induced adhesion of human platelets to collagen I with the same efficacy (IC50=2.4±0.3 μg ml−1), but had no effect at low shear conditions (1.5 N m−2).
- AJvW-2 inhibited the botrocetin-induced aggregation of platelets from guinea-pig, rat, rabbit, dog and pig at the same concentration range as human platelets; it likewise also inhibited the high shear stress induced aggregation and adhesion to collagen I of guinea-pig platelets.
- AJvW-2 prevented arterial thrombus formation in guinea-pigs at a dose of 100 μg kg−1 without prolonging the template bleeding time, whereas the GPIIb/IIIa antagonist lamifiban mediated inhibition of thrombosis at 1000 μg kg−1 was accompanied by a significant prolongation of the bleeding time.
- These results suggest that AJvW-2 is a potent inhibitor of the GPIb-vWF interaction and a potential novel antithrombotic agent with lower bleeding risk than GPIIb/IIIa antagonists.
60.
We report eight cases of vein of Galen aneurysmal malformation (VGAM) assoicated with a Chiari type I malformation. In four cases magnetic resonance imaging (MRI) or computed tomography performed in the neonatal period did not demonstrate the posterior fossa anomaly, which appeared on later scans. In the other cases the MRI was performed in infancy and the anomaly was already present. We compared the venous phases of the posterior fossa angiograms and the MRI in these patients. In all eight cases, the angiograms showed a reflux in the cerebellar veins, via the petrous vein, associated with a uni-or bilateral stenosis or thrombosis of the distal posterior dural sinuses. Furthermore, in two cases the posterior fossa returned to normal on MRI following endovascular treatment, while in three cases the herniation of the cerebellar tonsils decreased after the embolization. Tonsillar prolapse becomes irreversible when the venous outlet is incapable of taking the flow even when the VGAM has been treated adequately. In eight additional cases of VGAM for which MRI and angiogram studies were available and in which stenosis or thrombosis of posterior dural sinuses was present without tonsillar prolapse, no reflux into the cerebellar veins was shown. We suggest that the posterior fossa hydrovenous congestion is a result of inadequate venous drainage and that the tonsillar descent is reversible if adequate venous drainage is reconstituted following therapeutic embolization of the fistula. Tonsillar prolapse is not a consequence of mass or raised intraventricular pressure. Our observation suggests that in some other conditions, the Chiari I malformations may be secondary to early hydrovenous dysfunction of the posterior fossa. 相似文献