肌成纤维细胞在胆道愈合过程中的表达及意义

目的探讨肌成纤维细胞在医源性胆管狭窄形成过程中的作用及意义。方法通过制作犬肝外胆管损伤修复模型，分别于术后1周、3周、3个月、6个月取材行透射电镜观察和α-平滑肌肌动蛋白(α-SMA)免疫组织化学染色观察。结果肌成纤维细胞功能活跃，持续存在于整个胆道愈合过程，细胞外基质过度沉积。α-SMA表达于肌成纤维细胞胞浆，术后1周至6个月表达均较强,与正常对照比较差异有显著性（P<0.01）,术后各期表达差异无显著性（P>0.05）。结论肌成纤维细胞是导致胆道瘢痕性挛缩和管腔狭窄的主要原因。     

良性胆管狭窄形成机制的研究

目的：探讨良性胆管狭窄的形成机制。方法：用28只犬建立犬胆总管损伤修复的动物模型，分别于术后3d、1周、3周、3月、6月取材行光镜、电镜观察及免疫组化观察巨噬细胞、转化生长因子（TGF-β1）、平滑肌肌动蛋白（α-SMA）在胆管愈合过程不同时期组织中的表达强度、阳性细胞数和组织分布。结果：光镜及电镜显示：在整个胆管修复过程中炎性渗出期较长，胆道粘膜上皮愈合较慢，瘢痕组织细胞持续增生活跃，细胞外基质过度沉积，胶原纤维排列致密杂乱。肌成纤维细胞（MFB）功能活跃，持续存在于整个愈合过程中。免疫组化：巨噬细胞、TGF-β1）、α-SMA 在胆管愈合过程中表达较强，且持续较长时间。Mφ阳性主要表达于胆道粘膜下固有层；TGF-β1主要表达于肉芽组织、成纤维细胞、Mφ及血管内皮细胞浆和细胞膜；α-SMA 表达于MFB胞浆、平滑肌组织。Mφ、TGF-β1及α-SMA的表达呈正相关。结论：①胆管愈合方式属于过度愈合。②肌成纤维细胞功能活跃，地、持续存在，是导致胆管瘢痕性挛缩的重要原因。③Mφ、TGF-β1及α-SMA高表达是造成胆管愈合过程中成纤维细胞增殖旺盛、细胞外基质过度沉积、胆管瘢痕性挛缩的重要因素。     

良性胆管狭窄形成机制的研究

目的 探讨良性胆管狭窄的形成机制。方法 用28只犬建立犬胆总管损伤修复的动物模型,分别于术后3d、1周、3周、3月、6月取材行光镜、电镜观察及免疫纵化观察巨噬细胞、转化生长因子（TGF-β1）、平滑肌肌动蛋白（α-SMA）在胆管愈合过程不同时期组织中的表达强度、阳性细胞数和组织分布。结果 光镜及电镜显示:在整个胆管修复过程中炎性渗出期较长,胆道粘膜上皮愈合较慢,瘢痕组织细胞持续增生活跃,细胞外基质过度沉积,胶原纤维排列致密杂乱。肌成纤维细胞（MFB）功能活跃,持续存在于整个愈合过程中。免疫组化:巨噬细胞、TGF-β1、α-SMA在胆管愈合过程中表达较强,且持续较长时间。MΦ阳性主要表达于胆道粘膜下固有层;TGF-β1主要表达于肉芽组织、成纤维细胞、MΦ由及血管内皮细胞胞浆和细胞膜;α-SMA表达于MFB胞浆、平滑肌组织。MΦ、TGF-β1及α-SMA的表达呈正相关。结论 ①胆管愈合方式属于过度愈合。②肌成纤维细胞功能活跃,持续存在,是导致胆管瘢痕性挛缩的重要原因。③MΦ、TGF-β1及α-SMA高表达是造成胆管愈合过程中成纤维细胞增殖旺盛、细胞外基质过度沉积、胆管瘢痕性挛缩的重要因素。     

巨噬细胞及转化生长因子—β1在肝外胆管务修复过程中的 …

目的 观察巨噬细胞（ＭΦ）及转化生长因子－β１（ＴＧＦ－β１）在胆道愈合过程中的表达和分布,探讨其在良性胆管狭窄形成过程中的作用及意义。方法 通过制作犬胆管损伤修复模型,术后分为１周组、３周组、３个月组、６个月组。采用免疫组织化学过氧化酶标记的链霉卵白素（ＳＰ）法对ＭΦ、ＴＧＦ－β１在各组中的表达和分布进行研究。结果 ＭΦ１周时表达＋＋＋,与其他各期比较差异有显著性（Ｐ〈０．０５）,３周～６个月表     

良性胆管狭窄形成机制的实验研究

目的：探讨良性胆管狭窄形成机制。方法：通过制作犬胆管损伤修复模型,术后采用免疫组化SP法法对巨噬细胞（MΦ）、TGF－β1及α－SMA在胆管愈合过程不同时期组织中的表达和分布进行研究。结果：MΦ、TGF－β1及α－SMA愈合过程中表达较强,且持续较长时间。MΦ阳性表达于粘膜固有层;TGF－β1主要表达于肉芽组织、成纤维细胞、MΦ及血管内皮细胞。α－SMA表达于肌纤维细胞胞浆。结论：MΦ、TGF－β1及α－SMA高表达是造成胆道愈合过程成纤维细胞增殖旺盛、细胞外基质过度沉积、胆道瘢痕性挛缩的重要因素。     

术后狭窄胆管转化生长因子-β1的表达及意义

目的　观察转化生长因子 β1(TGF β1)在术后狭窄胆道中的表达和分布 ,探讨其在良性胆管狭窄形成过程中的作用及意义。方法　采用免疫组织化学streptavidin biotincomplex(SABC)法检测了 12例术后 3～ 6个月狭窄胆道组织中TGF β1的的表达和分布情况 ,并与 5例正常胆道组织进行对照研究。结果　狭窄胆道组织中TGF β1主要表达于肉芽组织、成纤维细胞、巨噬细胞及血管内皮细胞。正常胆管壁纤维组织表达较弱 ,阳性细胞均数为 12 .45± 6.2 4;TGF β1在术后狭窄胆道组织中的表达较强 ,本组 12例标本中 10例表达 ,2例表达 ,阳性细胞均数为5 9 .5 2± 8.3 3 ,与正常胆管比较差异有非常显著性 (P <0 .0 1)。结论　TGF β1高表达是造成胆道狭窄过程中成纤维细胞增殖旺盛、细胞外基质过度沉积、瘢痕增生的重要因素。     

PDGF—A及bFGF表达与移植血管平滑肌细胞增殖的关系

目的 探讨血小板源性生长因子－Ａ（ＰＤＧＦ－Ａ）和碱性成纤维细胞生长因子（ｂＦＧＦ）与移植血管平滑肌细胞增殖的关系。方法 建立３２例大鼠自体列脉移植模型,分别于术后６小时、４８小时、１周、２周、４周切取移植静脉,应用免疫组织化学动态观察不同时期移植血管ＰＤＧＦ－Ａ及ｂＦＧＦ表达情况。结果 ＰＤＧＦ－Ａ的在时间上与血管平滑肌细胞（ＳＭＣ）增殖活性的变化是相对平行的：均于术后逐渐增加,于１周达高峰,与     

转化生长因子β1在胆管愈合过程中的表达及意义

目的 观察转化生长因子β１（ＴＧＦ－β１）在胆管愈合过程中的表达和分布，探讨其在良性胆管狭窄形成过程中的作用及意义。方法 通过昨犬胆管损伤修复模型，术后采用免疫组化ＳＰ法对ＴＧＦ－β１在胆管愈合过程不同时期组织中的表达和分布进行研究。结果ＴＧＦ－β１主要表达于肉芽组织、成纤维细胞、巨噬细胞及血管内皮细胞。ＴＧＦ－β１术后各期表达均较强，且持续较长时间。结论 ＴＧＦ－β１高表达是造成胆管愈合过程成     

中华整形烧伤外科杂志1999年第15卷文题索引

以汉语拼音字母顺序排列Ａ艾滋病　艾滋病病毒感染者烧伤治疗应注意的几个问题（赵东彦等）（５）：３６２Ｂ白细胞　胶体金标记法测定烧伤性休克时外周血单核白细胞表面ＬＦＡ１的表达（王妍春等）（５）：３９９白细胞介素　白细胞介素１对病理性瘢痕成纤维细胞胶原合成的影响（杨东元等）（６）：４３４瘢痕　ＴＧＦβ１,对瘢痕形成的影响（贾赤宇等）（１）：７２烧伤后颈部瘢痕挛缩松解术致副神经损伤二例（沈余明等）（２）：１１４瘢痕成纤维细胞的钙网蛋白表达研究（赵烨德等）（３）：１６７ＰＣＭＶ４－ｈＴＧＦβ１在大鼠深…     

点状切口治疗斜颈

肌性斜颈系胸锁乳突肌发育不良挛缩所致，常用的方法是将该肌的起、止点作一３～５ｃｍ长的切口，予以离断松解［１～２］，术后常会留下明显切口瘢痕，影响美观。为了寻求一种简单实用、并发症少的术式，于１９９６年１月至１９９７年１２月，用点状切口术式治疗斜颈６例...     

炎性狭窄胆管壁中成纤维细胞表型改变及增殖的意义

目的 探讨炎性狭窄胆管壁中成纤维细胞表型改变及增殖在炎性胆管狭窄发生中的作用。方法 对人正常胆管壁及炎性狭窄胆管壁组织学结构及其纤维细胞的密度和超微结构进行观察。结果 厉纤维细胞是胆管壁中合成胶原的主要细胞;炎性狭窄胆管壁的纤维化增厚明显,其成纤维细胞表型改变,由相对静止转化为功能活跃状态,并进一步向肌成纤维细胞转化,且大量增殖。结论 静止型成纤维细胞转化为功能活跃的成纤维细胞及肌成纤维细胞并大量     

Control of wound contraction. Basic and clinical features

Although a substantial amount of molecular and cellular data have been generated in an effort to understand the process of wound contraction and scar contracture formation, questions remain. What seems apparent is that the myofibroblast is not the only cell that generates contractile forces within wounds, but it does appear to be intrinsically linked to the development of hypertrophic scars. The supposition that the formation of scar contractures is solely the result of a continuation of wound contraction is an oversimplification. Figure 4 provides a model of the possible evolution of contractile forces during the wound healing process and their role in the development of scar contractures. Migration of fibroblasts into and through the extracellular matrix during the initial phase of wound healing, prior to the expression of alpha-SMA, appears to be a fundamental component of wound contraction. During this migration, the pulling of collagen fibrils into a streamlined pattern in their wake, and the associated production of collagenase, may facilitate a more normal arrangement of collagen. Once the wound has been repopulated and the chemotactic gradient that was established by inflammatory cells is decreased, fibroblast migration will cease. It is at this point that myofibroblasts appear and play a key role in the production of hypertrophic scars, given that their prolonged presence and over-representation are hallmarks of this pathology. One of the pivotal differences between wounds that proceed to normal scar compared with those that develop hypertrophic scars and scar contractures may be a lack (or late induction) of myofibroblast apoptotic cell death. The combined contribution of fibroblasts and myofibroblasts to abnormal extracellular matrix protein production results in an excessive and rigid scar. The isometric application of contractile forces by myofibroblasts probably contributes to the formation of the whorls, nodules, and scar contractures characteristic of hypertrophic scars. Because the prolonged presence of myofibroblasts, producing an imbalance in extracellular matrix proteins and proteases, probably exacerbates hypertrophic scars and wound contraction, accelerating the rate of apoptotic cell death to reduce the cell number to that seen in normal scar may be a useful strategy for providing effective and efficient treatment of scar contracture.     

TGF-β1及CTGF在胆管缺血性损伤修复过程中的表达及意义

目的 观察TGF-β1 及CTGF 在胆管损伤修复过程中的表达,探讨良性胆管狭窄形成机制.方法 建立大鼠胆管缺血损伤模型,观察术后胆总管及肝脏组织病理改变;免疫组化检测两组胆管组织TGF-β1 及CTGF的表达,计算阳性细胞数.结果 实验组夹闭处胆管管腔狭窄伴纤维组织增生,钳夹部位以上胆管扩张;肝脏炎性细胞浸润.对照组...     

An approach to the hepatic hilus with marked fibrosis: A surgical technique for reconstruction of the bile duct with a benign stricture

It is very difficult to approach the hepatic hilus safely in patients with common and/or hepatic bile duct strictures in which normal tissue has been replaced by scarred tissue with firm fibrous adhesions. In this report, we describe how eight patients with benign strictures of the bile duct underwent an operation which involved dividing the superior mesenteric and portal veins from the lower margin of the pancreas in a dorsal direction using a finger in a tunneling technique. The common bile duct, which was buried in scar tissue, was then explored, while the common and/or proper hepatic arteries in the hepatoduodenal ligament were confirmed, after transsection at the superior margin of the pancreas. Biliary reconstruction was successfully performed after resection of the constricted bile duct in all the patients, none of whom have experienced recurrence from 6 months to 5 years after the operation.     

应用局部皮瓣治疗会阴区瘢痕挛缩

目的：探讨各种原因引起的会阴区瘢痕挛缩的修复方法。方法：1991年1月－2000年1月共治疗会阴区瘢痕挛缩20例分别采用局部皮瓣转移术＋游离皮片移植，皮瓣移植术修复。如会阴周围有可供利用的正常皮肤，最好首先采用扩张术，将正常皮肤扩张后形成局部皮瓣加游离皮片移植修复。功能重要区域如耻骨联合，阴囊部可采用轴型皮瓣修复。结果：20例会阴区瘢痕，其中一次手术修复18例，近期效果满意。10例患者获得随访仍有部分功能障碍，需再次手术修复。结论：会阴区瘢痕挛缩的治疗，功能重要区域采用轴型皮瓣修复，其他区域以局部皮瓣加游离皮片移植修复为佳。     

Contraction and the control of contraction

Wound contraction is a basic mechanism for wound closure that can be lifesaving. Yet, wound contraction can also produce considerable deformity and misery in conditions as diverse as burn scar contracture, cirrhosis, Dupuytren's contracture, and contracture around silicone tissue implants. Current evidence suggests that wound contraction is a cellular function of contractile fibroblasts (myofibroblasts). These cells share the electron microscopic appearance of both fibroblasts and smooth muscle cells. Pharmacologically and immunologically, myofibroblasts have many characteristics of smooth muscle cells. Active wound contraction caused by myofibroblasts can lead to fixed, rigid scar contracture. Contracture associated with poor joint positioning can also occur passively due to collagen reorganization alone, without myofibroblast involvement. Control of contraction (and contracture) can be achieved theoretically by 3 modes of therapy. Physical means, including range of motion exercises, splinting, and full thickness skin grafting after surgical release, are used currently. Biochemical control of myofibroblast contraction by agents that affect tissue-cultured fibroblasts has the potential of reducing wound contraction. Inhibition of collagen synthesis, inhibition of cross-linking, or increased collagenolysis may eventually be clinically useful, and would be of value in controlling both contracture due to active wound contraction, and contracture due to passive positioning.     

A型肉毒毒素治疗挛缩性瘢痕的初步研究

目的：探讨A型肉毒毒素（BTXA）治疗挛缩性瘢痕的效果及其作用机制.方法：10例烧伤后挛缩性瘢痕患者,每人选取两处挛缩性瘢痕,随机分为BTXA组（瘢痕内注射BTXA,间隔3个月1次,共2次）和空白对照组（瘢痕内注射等积生理盐水）,于注射前及首次注射后1、3、6个月测量瘢痕长轴长度,观察其长度变化用以反映瘢痕挛缩程度;切取5例药物治疗6个月后行瘢痕切除手术患者的瘢痕组织,HE染色观察病理学改变,免疫组化染色观察α-平滑肌肌动蛋白及肌球蛋白-Ⅱ的表达.结果：BTXA组较空白对照组瘢痕挛缩程度明显减轻（P〈0.01）,尤以6个月时差异明显[（1.103±0.158）cm比（0.187±0.221）cm].常规HE染色观察到BTXA组瘢痕组织内胶原纤维排列稀疏且规则,瘢痕内成纤维细胞数量较空白对照组减少.免疫组化结果显示BTXA组瘢痕内α-平滑肌肌动蛋白及肌球蛋白-Ⅱ表达较空白对照组明显减少（P〈0.01）.结论：BTXA可用于治疗挛缩性瘢痕,作用机制可能与BTXA能够抑制瘢痕内成纤维细胞中α平滑肌肌动蛋白及肌球蛋白-Ⅱ的表达有关.     

两阶段医源性胆道损伤处理及其疗效的对比研究

目的 探讨医源性胆道损伤处理原则的演变及其效果的对比.方法 回顾性分析和总结1996～2001年和2004～2009年间我院收治的50例医源性胆道损伤的临床资料和随访结果.结果 前阶段处理28例,其中术中即时修复11例,术后17例,术中修复以胆管端端吻合为主,后期修复以胆管-空肠Roux-Y吻和为主,后阶段处理22例...     

Influence of the anti‐inflammatory cytokine interleukin‐4 on human joint capsule myofibroblasts

Post‐traumatic joint contracture was reported to be associated with elevated numbers of contractile myofibroblasts (MFs) in the healing capsule. During the physiological healing process, the number of MFs declines; however, in fibroconnective disorders, MFs persist. The manifold interaction of the cytokines regulating the appearance and persistence of MFs in the pathogenesis of joint contracture remains to be elucidated. The objective of our current study was to analyze the impact of the anti‐inflammatory cytokine interleukin (IL)‐4 on functional behavior of MFs. Cells were isolated from human joint capsule specimens and challenged with three different concentrations of IL‐4 with or without its neutralizing antibody. MF viability, contractile properties, and the gene expression of both alpha‐smooth muscle actin (α‐SMA) and collagen type I were examined. Immunofluorescence staining revealed the presence of IL‐4 receptor (R)‐alpha (α) on the membrane of cultured MFs. The cytokine IL‐4 promoted MF viability and enhanced MF modulated contraction of collagen gels. Moreover, IL‐4 intervened in gene expression by up‐regulation of α‐SMA and collagen type I mRNA. These effects could be specifically lowered by the neutralizing IL‐4 antibody. On the basis of our findings we conclude that the anti‐inflammatory cytokine IL‐4 specifically regulates viability and the contractile properties of MFs via up‐regulating the gene expression of α‐SMA and collagen type I. IL‐4 may be a helpful target in developing anti‐fibrotic therapeutics for post‐traumatic joint contracture in human. © 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:1290–1298, 2017.