脑卒中后抑郁患者血清皮质醇水平变化分析

目的：分析脑卒中后抑郁患者血清皮质醇（cortisol,Cor）水平变化,探讨脑卒中后抑郁（poststroke depression,PSD）患者的内分泌功能变化.方法：采用放射免疫法检测59例PSD患者、36例非PSD患者及43例正常人的血清Cor水平;并观察29例PSD患者抗抑郁治疗后血清Cor水平变化.结果：治疗前,PSD组血清Cor水平显著高于非PSD组（P＜0.01）和正常对照组（P＜0.01）;治疗后,PSD抗抑郁治疗组与PSD未抗抑郁治疗组相比,HAMD评分（P＜0.01）和Cor水平（P＜0.01）均显著降低.在PSD组治疗前、PSD抗抑郁治疗组治疗后及PSD未抗抑郁治疗组中,HAMD评分与血清Cor水平呈显著性正相关.结论：PSD患者血清Cor水平明显升高并且与抑郁程度相关,提示脑卒中后抑郁可能引起了患者内分泌功能的变化.     

逍遥散联合百忧解治疗脑卒中后抑郁疗效观察

目的观察逍遥散联合百忧解辅以心理疗法治疗脑卒中后抑郁（PSD）及神经功能缺损的疗效.方法将85例PSD患者随机分为治疗组43例和对照组42例,在药物治疗基础上,对照组予百忧解配合心理治疗,治疗组在对照组的基础上加用逍遥散.治疗前后采用汉密尔顿抑郁量表（HAMD）、改良Barthel指数（MBI） 、斯堪的纳维亚卒中量表（SSS） 对患者进行评定,比较两组的疗效.结果治疗后,治疗组的有效率明显高于对照组（ P〈0.01）,HAMD评分和SSS 评分明显低于对照组（ P〈0.01） ,MBI评分明显高于对照组（ P〈0.01） .结论逍遥散联合百忧解并配以心理疗法治疗PSD不仅能明显改善患者的抑郁症状,而且能促进神经功能的恢复.     

增强型体外反搏联合舍曲林对卒中后抑郁患者抑郁状态和血清TNF-α、BDNF、VEGF水平的影响

目的:观察增强型体外反搏(EECP)联合舍曲林对缺血性脑卒中后抑郁(IPSD)患者抑郁状态、血清肿瘤坏死因子(TNF-α)、血清脑源性神经营养因子(BDNF)和血管内皮生长因子(VEGF)水平的影响。方法:80例IPSD患者随机分为对照组和观察组,每组40例。对照组患者在常规治疗(包括基础疾病的药物治疗和综合康复训练)的基础上给予口服盐酸舍曲林治疗,观察组患者在对照组治疗的基础上进行EECP治疗。2组患者在治疗前后均进行汉密顿抑郁量表(HAMD)、美国国立卫生研究院卒中量表(NIHSS)和改良Barthel指数(MBI)评定,以及血清TNF-α、VEGF和BDNF和VEGF含量检测。结果:治疗7周后,2组患者HAMD评分、NIHSS评分均较治疗前显著下降(P<0.01),而MBI评分较治疗前显著上升(P<0.01);观察组患者的HAMD评分、NIHSS评分均显著低于对照组(P<0.01),而MBI评分显著高于对照组(P<0.01)。2组患者血清TNF-a含量较治疗前显著下降(P<0.01),而BDNF和VEGF含量较治疗前显著上升(P<0.01);观...     

呼吸训练对卒中后抑郁患者自主神经功能及情绪状态的影响

目的 观察呼吸训练对卒中后抑郁（PSD）患者自主神经功能及情绪状态的影响。 方法 采用随机数字表法将52例PSD患者分为观察组及对照组,每组26例。对照组患者给予常规康复干预（包括药物治疗、物理因子治疗、偏瘫肢体综合训练等）,观察组患者在此基础上辅以呼吸训练(包括渐进性吸气肌抗阻训练及呼吸控制训练),每天训练2次。于治疗前、治疗4周后分别采用动态心电图、汉密尔顿抑郁量表（HAMD）及改良Barthel指数（MBI）量表评估患者自主神经功能、情绪状态及日常生活活动（ADL）能力改善情况。 结果 治疗后观察组患者心率变异性（HRV)指标24 h正常R-R间期标准差（SDNN）、24 h相邻R-R间期差值均方根（RMSSD）、24 h相邻R-R间期差值＞50 ms百分数（PNN50）及高频功率（HF）［分别为（128.36±8.34）ms,（15.63±3.63）ms,（8.62±2.33）%及（677.58±196.74）ms2/Hz］均较治疗前及对照组明显提高(P＜0.05)。另外治疗后观察组患者HAMD评分［（12.63±10.44）分］及MBI评分［（60.44±12.72）分］亦显著优于治疗前及对照组水平（P＜0.05）。 结论 在传统康复干预基础上辅以呼吸训练能进一步缓解PSD患者抑郁情绪,改善患者自主神经功能及ADL能力,该联合治疗模式值得在PSD患者中推广、应用。     

正念减压联合文拉法辛治疗焦虑抑郁状态患者的疗效观察

目的：探讨正念减压（MBSR）联合文拉法辛治疗焦虑抑郁状态的临床疗效。方法：焦虑抑郁状态患者 64例,随机分为观察组和对照组,各32例。2组均给与文拉法辛治疗,在药物治疗基础上,对照组接受常规心 理健康教育,观察组接受MBSR治疗。于治疗前、后分别采用汉密尔顿焦虑量表（HAMA）、汉密尔顿抑郁量表 （HAMD）和五因素正念量表（FFMQ）,评价患者的焦虑、抑郁症状和正念水平。结果：治疗前,2组的HAMA、 HAMD和FFMQ评分差异无统计学意义（P＞0.05）。干预后,2组的HAMA、HAMD评分均低于同组治疗前 （P＜0.05或P＜0.01）,且观察组低于对照组（P＜0.05）;观察组的FFMQ评分显著高于同组治疗前（P＜0.01）, 且观察组显著高于对照组（P＜0.01）。结论：MBSR联合文拉法辛治疗能更有效地缓解焦虑抑郁症状并提升 患者的正念水平。     

重复经颅磁刺激对脑卒中后抑郁患者抑郁情绪、睡眠障碍及日常生活活动能力的影响

目的探讨重复经颅磁刺激（rTMS）对脑卒中后抑郁（PSD）患者抑郁情绪、睡眠障碍及日常生活活动（ADL）能力的影响。 方法选取PSD患者90例,按随机数字表法将其分为对照组、治疗组和联合治疗组,每组30例。3组患者均给予基础治疗及综合康复训练,对照组在此基础上给予艾司西酞普兰治疗,治疗组给予rTMS治疗,联合治疗组在对照组基础上辅以rTMS治疗,疗程8周。治疗前及治疗8周后（治疗后）,采用汉密尔顿抑郁量表（HAMD）、匹斯堡睡眠质量指数量表（PSQI）、中国脑卒中量表（CSS）及改良Barthel指数（MBI）对患者的抑郁情绪、睡眠质量、神经功能缺损情况及ADL能力进行评定。 结果治疗前,3组患者HAMD、CSS、PSQI、MBI评分之间比较。差异无统计学意义（P&rt;0.05）。治疗8周后（治疗后）,3组患者HAMD评分、PSQI评分、CSS评分均较治疗前明显下降（P<0.05）,MBI评分较治疗前明显增高（P<0.05）。与对照组治疗后比较,治疗组及联合治疗组治疗后HAMD、CSS、PSQI、MBI评分均无显著变化,差异无统计学意义（P&rt;0.05）。与联合治疗组治疗后比较,治疗组治疗后HAMD［（9.76±4.59）分］、CSS［（7.65±2.35）分］、PSQI［（16.13±4.12）分］、MBI评分［（52.61±9.26）分］无显著变化,差异无统计学意义（P&rt;0.05）。 结论rTMS可显著改善PSD患者的抑郁症状、睡眠障碍及神经功能缺损状况,有效提高其ADL能力。     

早期心理护理干预对脑卒中后抑郁病人的疗效分析

[目的]探讨早期心理护理干预对脑卒中后抑郁(PSD)的疗效分析。[方法]将住院的112例PSD病人随机分为观察组和对照组各56例,对照组进行常规治疗和常规护理,观察组在此基础上实施早期心理护理干预。两组病人干预前后进行汉密尔顿抑郁量表(HAMD)评分、日常生活自理能力(MBI)评分、肢体运动功能(FMA)评分和临床疗效比较。[结果]两组病人进行早期心理护理干预前HAMD、MBI、FMA评分差异无统计学意义(P0.05)。干预4周后,HAMD评分观察组低于对照组,差异有统计学意义(P0.05);MBI评分观察组高于对照组,差异有统计学意义(P0.05);FMA评分观察组高于对照组,差异有统计学意义(P0.05)。观察组总有效率为91.1%,对照组为69.6%,差异有统计学意义(χ2=5.76,P0.05)。[结论]早期心理护理干预措施可以改善PSD病人的抑郁情绪,促进病人肢体运动功能和生活自理能力的恢复。     

中西医结合治疗脑卒中后抑郁130例疗效分析

目的:探讨中西医结合治疗对脑卒中后抑郁(PSD)的疗效。方法:PSD患者130例随机分为对照组和观察组,各65例。2组均按常规治疗,在此基础上,对照组给予草酸艾司西酞普兰片口服及综合康复治疗,观察组给予豁痰清窍解郁汤、草酸艾司西酞普兰片口服及综合康复治疗,均治疗8周。于治疗前后采用汉密尔顿抑郁量表(HAMD)、神经功能缺损程度评分、简易精神状态评定量表(MMSE)及改良Barthel(MBI)指数对患者的抑郁程度、运动功能、认知功能及ADL能力进行评定。结果:治疗前,2组患者HAMD、神经功能缺损程度、MMSE及MBI评分差异无统计学意义(P0.05)。治疗后,2组HAMD、神经功能缺损程度、MMSE及MBI评分均较组内治疗前有所改善(P0.05);观察组改善程度高于对照组(P0.05)。对照组和观察组抑郁治疗总有效率分别为78.5%和90.8%,神经功能缺损程度改善的总有效率为70.8%和86.1%,观察组的总有效率高于对照组(P0.05)。结论:中西医结合治疗有助于改善PSD患者的抑郁状态、运动功能、认知功能及生活质量。     

黛力新治疗脑卒中后抑郁状态的疗效观察

目的观察黛力新治疗脑卒中后抑郁状态（PSD）的临床疗效。方法采用平行对照研究方法,将98例脑卒中后抑郁患者按随机数字表法分为治疗组和对照组,每组49例。对照组只进行常规治疗;治疗组在常规治疗的基础上加用黛力新片治疗4周。对2组患者治疗前,治疗后2、4周的汉密顿抑郁量表（HAMD）及神经功能缺损评分进行比较。结果 2组患者治疗2、4周后HAMD及神经功能缺损评分均较治疗前明显下降（P〈0.05或P〈0.01）;治疗组治疗2、4周后HAMD及神经功能缺损评分明显低于对照组（P〈0.01）。结论黛力新治疗PSD疗效好,不良反应轻。     

醒脑开窍针法联合中医情志疗法在脑卒中后抑郁患者中的应用

目的 探讨醒脑开窍针法联合中医情志疗法在脑卒中后抑郁(PSD)患者中的应用效果。方法 选取2022年南昌大学第二附属医院康复科收治的70例PSD患者为研究对象,按照随机数字表法将其分为对照组和观察组,各35例。对照组在常规治疗的基础上予以醒脑开窍针法治疗,观察组在对照组治疗方案的基础上予以中医情志疗法干预。分别采用汉密尔顿抑郁量表(HAMD)、中国神经功能缺损量表(MSSS)以及日常生活活动能力量表(MBI)评估并比较2组治疗前后的抑郁症状、神经功能以及日常生活活动能力。结果 治疗4周后,2组HAMD评分和MSSS评分均较治疗前下降,且观察组HAMD评分和MSSS评分均低于对照组(P<0.05);2组MBI评分均较治疗前提高,且观察组MBI评分高于对照组(P<0.05)。结论 醒脑开窍针法结合中医情志疗法可以有效地改善PSD患者的抑郁症状和神经功能,提升其日常生活活动能力,且治疗效果较单纯使用醒脑开窍针法更好。     

Mechanisms of factor VIIa‐catalyzed activation of factor VIII

Summary. Background: Factor (F)VIIa, complexed with tissue factor (TF), is a primary trigger of blood coagulation, and has extremely restricted substrate specificity. The complex catalyzes limited proteolysis of FVIII, but these mechanisms are poorly understood. Objectives: In the present study, we investigated the precise mechanisms of FVIIa/TF‐catalyzed FVIII activation. Results: FVIII activity increased ～4‐fold within 30 s in the presence of FVIIa/TF, and then decreased to initial levels within 20 min. FVIIa (0.1 nm ), at concentrations present physiologically in plasma, activated FVIII in the presence of TF, and this activation was more rapid than that induced by thrombin. The heavy chain (HCh) of FVIII was proteolyzed at Arg⁷⁴⁰ and Arg³⁷² more rapidly by FVIIa/TF than by thrombin, consistent with the enhanced activation of FVIII. Cleavage at Arg³³⁶ was evident at ～1 min, whilst little cleavage of the light chain (LCh) was observed. Cleavage of the HCh by FVIIa/TF was governed by the presence of the LCh. FVIII bound to Glu‐Gly‐Arg‐active‐site‐modified FVIIa (K_d, ～0.8 nm ) with a higher affinity for the HCh than for the LCh (K_d, 5.9 and 18.9 nm ). Binding to the A2 domain was particularly evident. Von Willebrand factor (VWF) modestly inhibited FVIIa/TF‐catalyzed FVIII activation, in keeping with the concept that VWF could moderate FVIIa/TF‐mediated reactions. Conclusions: The results demonstrated that this activation mechanism was distinct from those mediated by thrombin, and indicated that FVIIa/TF functions through a ‘priming’ mechanism for the activation of FVIII in the initiation phase of coagulation.     

Heme binds to factor VIII and inhibits its interaction with activated factor IX

Summary. Background: Heme is a redox active macrocyclic compound that is released upon tissue damage or hemorrhages. The extracellular release of large amounts of heme saturates scavenging heme‐binding proteins. Free heme has been proposed to affect coagulation and has been co‐purified with the factor VIII (FVIII)‐von Willebrand factor (VWF) complex. The sites from which heme is released upon injury overlap with the sites to which FVIII is targeted for performing its hemostatic functions. Objectives: To investigate the interaction of heme with FVIII and the consequence for the procoagulant activity of FVIII in vitro. Methods and results: Heme bound to several sites on FVIII with high apparent affinity. Heme‐binding inhibited FVIII procoagulant activity in a dose‐dependent manner. FVIII inactivation in the presence of saturating amounts of heme implicated a reduced interaction of FVIII with activated FIX, as shown by ELISA, surface plasmon resonance and fluorescence quenching. Heme‐mediated inactivation of FVIII was prevented by VWF, but not by human serum albumin, a heme‐binding protein known for its protective activity in hemolytic conditions. Conclusions: Our data identify FVIII as a novel heme‐binding protein. Occupation of high affinity heme‐binding sites on FVIII at low concentrations of free heme did not inactivate FVIII. Conversely, large molar excesses of heme over FVIII, which correspond to conditions of extensive heme release, inhibited FVIII activity in vitro. It remains to be demonstrated whether, under such conditions, heme‐mediated modulation of the activity of FVIII plays some role in the regulation of coagulation.     

Structural and functional features of factor XI

Summary.  Factor XI (FXI) has structural and mechanistic features that distinguish it from other coagulation proteases. A relatively recent addition to vertebrate plasma coagulation, FXI is a homodimer, with each subunit containing four apple domains and a protease domain. The apple domains form a disk structure with binding sites for platelets, high molecular weight kininogen, and the substrate factor IX (FIX). FXI is converted to the active protease FXIa by cleavage of the Arg³⁶⁹−Ile³⁷⁰ bond on each subunit. This converts the catalytic domains to the active forms, and unmasks exosites on the apple domains required for FIX binding. FXI activation by factor XIIa or thrombin proceeds through an intermediate with only one activated submit (1/2-FXIa). 1/2-FXIa activates FIX in a similar manner to FXIa. While the importance of the homodimeric structure of FXI is not certain, it may represent a strategy for binding to FIX and a platelet surface simultaneously.     

肥厚腰椎黄韧带中成纤维细胞生长因子、转化生长因子及结缔组织生长因子的表达

背景：腰椎黄韧带肥厚是临床上引起腰椎管狭窄的主要因素之一,但其分子机制仍不是非常清楚。目的：分析纤维化相关细胞因子碱性成纤维细胞生长因子、转化生长因子β1和结缔组织生长因子在腰椎黄韧带肥厚过程中的作用。方法：取临床手术所取黄韧带,对照组6例（椎管内占位且无腰椎不稳患者黄韧带）、突出组（单纯腰椎间盘突出症患者黄韧带）6例、腰椎管狭窄症组6例。采用实时定量RT-PCR的方法检测各组黄韧带中碱性成纤维细胞生长因子、转化生长因子β1、结缔组织生长因子及Ⅰ、Ⅲ、Ⅴ型胶原蛋白的mRNA含量,分析3个细胞因子在黄韧带肥厚过程中的作用。结果与结论：腰椎管狭窄症组碱性成纤维细胞生长因子mRNA表达均明显高于突出组和对照组（均P 〈0.05）;腰椎管狭窄症组转化生长因子β1mRNA在3组中的表达明显高于对照组和突出组（均P 〈0.01）;结缔组织生长因子 mRNA 3组间差异无显著性意义（P 〉0.05）。腰椎管狭窄症组Ⅰ型胶原蛋白mRNA表达明显高于突出组和对照组（均P 〈0.05）;Ⅲ型胶原蛋白、Ⅴ型胶原蛋白mRNA表达3组之间差异无显著性意义（P 〉0.05）。结果说明碱性成纤维细胞生长因子、转化生长因子β1在腰椎黄韧带肥厚形成过程中有重要作用,引起黄韧带肥厚的主要胶原产物为Ⅰ型胶原蛋白。     

The relationship between ABO histo-blood group, factor VIII and von Willebrand factor

ABO histo-blood group is a major determinant of plasma levels of factor VIII (FVIII) and von Willebrand factor (vWF). Blood group O individuals have significantly (approximately 25%) lower plasma levels of both glycoproteins. This association is of clinical significance. Low plasma levels of either FVIII or vWF have long been established as causes of excess bleeding. Conversely, there is accumulating evidence that elevated FVIII-vWF levels may represent an important risk factor for ischaemic heart disease and venous thromboembolic disease. In spite of the well-documented association between ABO blood group and FVIII-vWF levels, the underlying mechanism remains unknown. However, it has been established that the ABO effect is primarily mediated through a direct functional effect of the ABO locus on plasma vWF levels. Theoretically, ABO blood group may alter the rate of vWF synthesis or secretion within endothelial cells. Alternatively, ABO group may affect vWF plasma clearance rates. ABH antigenic determinants have been identified on the N-linked oligosaccharide chains of circulating vWF and FVIII, according to the blood group of the individual. It remains unclear whether these carbohydrate structures are responsible for mediating the effect of ABO blood group on plasma vWF levels.     

急性心肌梗死患者组织因子及组织因子途径激活抑制物水平的变化

目的探讨急性心肌梗死(AMI)患者组织因子(TF)及组织因子途径激活抑制物(TF-PI)的变化及临床意义。方法用ELISA法分别检测50例AMI患者及20例健康对照的外周血TF及TFPI的抗原水平。比较15例支架手术患者冠状窦内及外周血的TFPI水平。比较并发糖尿病和/或高脂血症AMI患者与无并发症者的TFAg及TFPIAg水平。结果AMI患者的TFAg及TFPIAg较正常人均明显升高(P<0.01);支架患者冠状窦内的TFPI水平明显低于其外周血(P<0.01);有并发症患者的TF及TFPI水平均明显高于无并发症患者(分别为P<0.01和P<0.05)。结论AMI患者外周血凝血活性增高,并发糖尿病和/或高脂血症AMI患者的凝血活性较无并发症患者高,血栓形成使冠状动脉腔内的TFPI消耗而降低。     

转化生长因子-β、碱性成纤维生长因子和血小板衍生生长因子在骨折愈合中的表达

目的:观察转化生长因子-β(TGF-β)、碱性成纤维细胞生长因子(bFGF)和血小板衍生生长因子(PDGF)在骨折愈合中的表达和分布情况,进而探讨其作用机制。方法:选用SD大鼠制作胫骨骨折愈合模型,伤后不同时期处死取材,分别进行组织学和TGF-β、bFGF和PDGF免疫组化染色观察。结果:(1)伤后3d开始形成原始骨痂。1周时肉芽组织中的间质细胞开始分化为软骨细胞,软骨形成后再进行软骨内化骨。4周时形成连接骨折端的桥接骨痂。(2)伤后早期血肿中炎性细胞表达bFGF、PDGF。伤后1周骨膜增殖细胞、肉芽组织中的成纤维细胞、内皮细胞、骨端骨细胞以及原始骨痂成骨细胞表达TGF-β、bFGF和PDGF。伤后2周软骨细胞表达TGF-β、bFGF和PDGF。结论:TGF-β、bFGF和PDGF有着各自的表达和分布特点,并共同调解骨原细胞的增殖和成骨细胞、软骨细胞的分化,最终完成骨折愈合。