对比分析多种介入途径治疗门静脉系统血栓的临床疗效

目的：对比分析多种介入途径治疗门静脉系统血栓的临床疗效。方法：收集从2001年1月至2009年3月经我科治疗的37例门静脉系统（包括门静脉、肠系膜上、下静脉及脾静脉）血栓形成患者,根据介入治疗途径的不同分为三组：A组（13例）行经TIPS途径门静脉行碎栓溶栓及置管溶栓术;B组（19例）行直接经皮穿肝门静脉碎栓和或置管溶栓术;C组（5例）行经肠系膜上动脉置管溶栓治疗。所有的患者术后定期随访1—12个月,复查CT或彩超了解门静脉系统的血流变化及临床症状恢复情况。结果：A组：经治疗出院时11例（85％）患者门静脉完全再通,;1例（8％）门静脉血流部分再通,1例（8％）术后第二天因出血死亡。术后随访1、3、6、12月门静脉通畅率分别为：85％,77％,77％,62％;所有患者的临床症状均明显缓解。B组：经治疗出院时7例（37％）门静脉完全再通,9例（47％）部分再通,3例（16％）因出血中止溶栓;随访1、3、6月、12月门静脉通畅率分别为：32％,26％,16％,16％。C组：经治疗出院时5例（100％）患者门静脉均未再通,通畅率为0％,术后随访1-3个月内4例患者I临床症状得到部分缓解。结论：经TIPS途径治疗后门静脉的再通率及临床症状改善均好于直接经皮穿肝及经肠系膜上动脉途径。经肠系膜上动脉置管溶栓法无法使已有侧支形成的门静脉主干复通,仅能一定程度缓解患者的临床症状。     

综合护理对脑卒中患者下肢深静脉血栓形成的预防效果

目的:分析综合护理干预在脑卒中偏瘫患者下肢深静脉血栓形成中的预防效果及临床效应。方法:将120例经颅部CT或MRI确诊的脑卒中患者分为观察组和对照组,每组各60例。对照组给予常规护理干预,观察组进行综合护理干预,比较不同干预措施患者下肢深静脉血栓形成情况。结果:观察组DVT发生率为3.33%,对照组为18.33%,观察组干预效果明显优于对照组,差异有统计学意义(P0.05)。结论:综合护理干预可有效降低脑卒中偏瘫患者DVT的形成,在脑卒中偏瘫患者DVT方面具有显著的预防作用与临床效应,值得借鉴。     

应用手持激光器建立光化学法脑梗死动物模型

目的应用手持激光器作为光源建立光化学法局灶性脑梗死动物模型。方法将36只SD大鼠随机分为4组,即A组：开骨窗至硬脑膜,不注射玫瑰红,手持激光器照射5rain;B组：开骨窗至硬脑膜,注射玫瑰红,手持激光器照射5min;C组：保留颅骨内板,注射玫瑰红,手持激光器照射5min;D组：开骨窗至硬脑膜,注射玫瑰红,冷光源照射40rain。于术后24、48h对各组大鼠进行神经功能的行为学评分,进行MR扫描,术后48h处死动物,TTC染色测量梗死体积,光镜下观察病理改变,比较各组的模型制作成功率。结果不同方法进行动物模型制作时,24h神经功能的行为学评分有显著性差异,48h后差异消失。头部MR扫描显示,A组未见脑梗死形成,B组、c组全部有脑梗死灶形成,D组仅部分大鼠形成梗死灶,但体积明显较B、C组小,另外C组有2例合并硬膜外血肿。TTC染色A组未见梗死灶形成,B组、C组可见恒定的梗死灶,D组仅部分形成梗死灶。B、C、D组模型制作成功率分别为100％、80％、50％,将B组、C组合并为手持激光器组,与冷光源组（D组）比较,两种方法间有显著性差异（P=0．026）。结论应用手持激光器作为照射光源与冷光源相比,有更高的模型制作成功率。     

对比分析多种介入途径治疗门静脉系统血栓的临床疗效

目的:对比分析多种介入途径治疗门静脉系统血栓的临床疗效。方法:收集从2001年1月至2009年3月经我科治疗的37例门静脉系统(包括门静脉、肠系膜上、下静脉及脾静脉)血栓形成患者,根据介入治疗途径的不同分为三组:A组(13例)行经TIPS途径门静脉行碎栓溶栓及置管溶栓术;B组(19例)行直接经皮穿肝门静脉碎栓和或置管溶栓术;C组(5例)行经肠系膜上动脉置管溶栓治疗。所有的患者术后定期随访1-12个月,复查CT或彩超了解门静脉系统的血流变化及临床症状恢复情况。结果:A组:经治疗出院时11例(85%)患者门静脉完全再通,;1例(8%)门静脉血流部分再通,1例(8%)术后第二天因出血死亡。术后随访1、3、6、12月门静脉通畅率分别为:85%,77%,77%,62%;所有患者的临床症状均明显缓解。B组:经治疗出院时7例(37%)门静脉完全再通,9例(47%)部分再通,3例(16%)因出血中止溶栓;随访1、3、6月、12月门静脉通畅率分别为:32%,26%,16%,16%。C组:经治疗出院时5例(100%)患者门静脉均未再通,通畅率为0%,术后随访1-3个月内4例患者临床症状得到部分缓解。结论:经TIPS途径治疗后门静脉的再通率及临床症状改善均好于直接经皮穿肝及经肠系膜上动脉途径。经肠系膜上动脉置管溶栓法无法使已有侧支形成的门静脉主干复通,仅能一定程度缓解患者的临床症状。     

Thrombosis during pregnancy: Risks,prevention, and treatment for mother and fetus—harvesting the power of omic technology,biomarkers and in vitro or in vivo models to facilitate the treatment of thrombosis

Maternal thromboembolism and a spectrum of placenta‐mediated complications including the pre‐eclampsia syndromes, fetal growth restriction, fetal loss, and abruption manifest a shared etiopathogenesis and predisposing risk factors. Furthermore, these maternal and fetal complications are often linked to subsequent maternal health consequences that comprise the metabolic syndrome, namely, thromboembolism, chronic hypertension, and type II diabetes. Traditionally, several lines of evidence have linked vasoconstriction, excessive thrombosis and inflammation, and impaired trophoblast invasion at the uteroplacental interface as hallmark features of the placental complications. “Omic” technologies and biomarker development have been largely based upon advances in vascular biology, improved understanding of the molecular basis and biochemical pathways responsible for the clinically relevant diseases, and increasingly robust large cohort and/or registry based studies. Advances in understanding of innate and adaptive immunity appear to play an important role in several pregnancy complications. Strategies aimed at improving prediction of these pregnancy complications are often incorporating hemodynamic blood flow data using non‐invasive imaging technologies of the utero‐placental and maternal circulations early in pregnancy. Some evidence suggests that a multiple marker approach will yield the best performing prediction tools, which may then in turn offer the possibility of early intervention to prevent or ameliorate these pregnancy complications. Prediction of maternal cardiovascular and non‐cardiovascular consequences following pregnancy represents an important area of future research, which may have significant public health consequences not only for cardiovascular disease, but also for a variety of other disorders, such as autoimmune and neurodegenerative diseases. Birth Defects Research (Part C) 105:209–225, 2015. © 2015 Wiley Periodicals, Inc.     

Erythrocyte hyperaggregation in obesity: determining factors and weight loss influence

Objective: To compare erythrocyte aggregation (EA) in patients with severe obesity without other cardiovascular risk factors with a control group, using the Myrenne and the Sefam aggregometers, and to evaluate the effect of weight loss on this parameter. Research Methods and Procedures: This was a longitudinal, clinical intervention study of a very low‐calorie diet for 4 weeks followed by a low‐calorie diet for 2 months. In 67 severely obese patients, an anthropometric and analytical evaluation [plasmatic lipids, fibrinogen (Fbg), and EA] was performed at baseline and 3 months after diet. The same determinations were performed in 67 normal‐weight volunteers. EA was measured with the Myrenne MA₁, which determines EA at stasis (EA₀) and at a low shear of 3 seconds^?1 (EA₁), and the Sefam aggregometer, which determines aggregation index at 10 seconds^?1 (IA₁₀), aggregation time (Ta), and disaggregation threshold (γD). Insulin resistance (IR) was calculated by homeostasis model assessment. Results: Obese patients showed higher Fbg levels, EA₀, EA₁, IA₁₀, and γD values, and lower Ta values. Differences between obese patients and control group for EA₀, EA₁, Ta, IA₁₀, and γD disappeared after adjusting for BMI or for homeostasis model assessment but were maintained after adjusting for Fbg or low‐density lipoprotein‐cholesterol. Obese patients with IR showed higher EA₀ and EA₁ values. After weight loss, EA₁ showed a significant improvement. Discussion: Obese patients show increased EA. Erythrocyte hyperaggregation does not seem to be related to a high Fbg level or to an abnormal lipid profile but to IR. Hyperagreggation improves after weight loss.     

Thrombosis in pregnancy and maternal outcomes

Pregnancy increases the risk of thrombosis four‐ to five‐fold. Seventy‐five to eighty percent of pregnancy‐related thrombotic events are venous and twenty to –twenty‐five percent are arterial. The main reason for the increased risk is hypercoagulability. Women are hypercoagulable because they have evolved so that they are protected against the bleeding challenges of pregnancy, miscarriage, or childbirth. Both genetic and acquired risk factors can further increase the risk of thrombosis. The maternal consequences of thrombosis of pregnancy include permanent vascular damage, disability, and death. While the maternal outcomes of thrombosis can be modified by anticoagulation therapy, management of thrombosis during pregnancy is the subject of another paper in this issue (see paper by B. Konkle). This review will focus on the epidemiology, pathophysiology, risk factors, and maternal consequences of thrombosis in pregnancy. Birth Defects Research (Part C) 105:159–166, 2015. © 2015 Wiley Periodicals, Inc.     

Effects of platelets on the protein expression in aortic segments: A proteomic approach

It is well known the effects of the vascular wall on platelet activity but little is known about the effects of platelets on the proteins expression in the vascular wall. We analyzed whether platelets may modify the protein expression in the vascular wall. We used an in vitro model coincubating human platelet rich plasma (PRP) with control and 10 ng/ml tumor necrosis factor‐α (TNF‐α)‐preincubated bovine aortic segments. 2DE, mass spectrometry and Western blot analysis were used to determine changes in the expression of proteins associated with the cytoskeleton and energetic metabolism in the aortic segments. In control healthy vascular wall, only the cytoskeleton‐related proteins expression was modified by PRP. However, when PRP was coincubated with TNF‐α pre‐stimulated aortic segments lesser number of cytoskeleton‐related proteins were modified. With respect to energetic metabolism, in control segments, PRP failed to modify any of the analyzed energetic‐related proteins. However, in TNF‐α‐preincubated segments the presence of PRP upexpressed glyceraldehyde‐3‐phosphate dehydrogenase. Moreover, by western blot experiments it was observed that in TNF‐α‐preincubated segments the expression of fructose 1,6‐bisphosphate aldolase was downregulated by platelets. However, no differences were found in the expression of triosephosphate isomerase and ATP synthase α‐chain. In addition, the activity of fructose 1,6‐bisphosphate aldolase and piruvate content was significantly reduced without modification on triosephosphate isomerase activity. In conclusion, the crosstalk between platelets and vascular wall is bidirectional and platelets regulated in the vascular wall the expression of proteins associated with the cytoskeleton and energetic metabolism, particularly in the healthy vascular wall. J. Cell. Biochem. 111: 889–898, 2010. © 2010 Wiley‐Liss, Inc.