剖宫产术后腹部切口愈合不良30例分析

目的 探讨剖宫产术后腹部切口愈合不良的处理.方法 回顾性分析剖宫产手术切口愈合不良30例,分析其危险因素.结果 妊娠合并症、产程延长、破膜时间长、手术及住院时间长、孕妇肥胖、营养不良、手术人员缝合技术等因素增加了剖宫产术后腹部切口愈合不良的几率.患者经术后积极治疗均获痊愈.结论 针对影响剖宫产切口愈合不良的高危因素制定有效的预防措施,并积极治疗.     

运用弹力绷带联合湿性愈合疗法缩短乳腺癌根治术后切口愈合不良病程

<正>切口愈合不良指切口愈合生物学阶段出现明显停滞或延迟而导致切口不愈合甚至切口范围扩大,伴有明显感染性或非感染性渗出,伴或不伴坏死组织,是外科手术并发症之一[1]。乳腺癌根治术后并发皮瓣下感染致皮瓣与胸壁之间形成潜行,多由于皮下积液合并感染和腋下引流管口感染引起,是乳腺癌根治术后最常见的并发症之一[2],也是影响术后切口愈合和后续治疗的主要原因。这不仅为患者带来极大痛苦和经济负担,而且影响乳腺癌的多元化治疗效果。我们对我院2011年1月至     

95例腹部手术后切口愈合不良的临床分析

腹部手术常因各种原因引起切口愈合不良.我院2006年至2008年进行腹部手术745例,其中发生切口感染、切口裂开、切口疝共达95例.为探讨腹部手术后切口愈合不良的相关因素,控制发生率,我们回顾性对这745例切口愈合不良的病例进行临床分析.现报告如下.     

庆大霉素联合地塞米松局部封闭预防与治疗剖宫产术腹部切口愈合不良的临床观察

目的：探讨剖宫产术后腹部切口愈合不良的治疗措施。方法回顾性分析我院2010年2月~2014年2月的56例剖宫产术后腹部切口愈合不良病例。结果妊娠合并症、产程延长、破膜时间长、急诊手术、手术及住院时间长、孕妇肥胖、贫血、营养不良、手术人员缝合技术等因素增加了剖宫产术后腹部切口愈合不良的几率。结论加强剖宫产术后腹部切口护理,合理预防性应用抗生素,及早发现切口感染征象,使用庆大霉素联合地塞米松局部封闭,可有效预防腹部切口愈合不良。     

胶原-壳聚糖/bFGF培养人成纤维细胞生物特性研究

目的：研究一种适于人成纤雏细胞生长的组织工程支架材料，确定碱性成纤维细胞生长因子(bFGF)的用量。材料与方法：采用胶原与壳聚糖整合bFGF做为人成纤维细胞生长的支架材料，用体外细胞培养法确定胶原与壳聚糖在材料中的配比，用体外细胞相容性直观法观察材料与人成纤维细胞的相容性。结果：选择出了胶原与壳聚糖在材料中较佳的配比，确定了bFGF在材料中的用量范围．人成纤维细胞在胶碌一壳聚糖／bFGF膜持续生长繁殖，具有生物降解性。材料与细胞呈低毒性反应。结论：胶原—壳聚糖／bFGF可做为组织工程的支架材料。     

bFGF对成年大鼠损伤的大脑皮质神经元的作用

实验用ＳＤ大鼠４０只，其中３０只分为实验组和对照组各１５只，切片用甲基绿－派洛宁染色；另１０只也分为实验组和对照组，各５只，切片用神经丝免疫组化染色．手术毁损大鼠大脑顶叶皮质，立即放入分别浸有碱性成纤维细胞生长因子（实验组）或ＰＢＳ（ｐＨ７．２，０．２ｍｏＬ／Ｍ）（对照组）的海绵胶粒（１ｍｍ３），于术后１４ｄ，２４ｄ，３４ｄ在损伤的皮质腔内重复注射相应的实验用液２５μｌ．术后４０ｄ取材，在大脑皮质损伤腔颞侧边缘Ⅱ～Ⅲ层距边缘５００μｍ范围内，对每只大鼠计数了１ｍｍ２面积中的存活神经元数目，并观察神经元的形态学变化．结果发现，实验组大脑皮质存活神经元数目较多，对照组存活神经元较少．经体视学定量方法分析，结果其均数±标准差为：实验组９１９．４５±１６５．４０，对照组６２８．３９±５７．５０／ｍｍ２，经两样本均数ｔ检验，Ｐ＜０．０５．提示碱性成纤维细胞生长因子对大鼠大脑皮质损伤神经元有一定的维持存活作用．     

自制便携式简易封闭负压引流装置在术后切口愈合不良中的应用

目的探讨一种自制便携式简易封闭负压引流装置在手术后切口愈合不良中的应用效果。 方法回顾性分析2015年1月至2018年10月在江苏省靖江市人民医院烧伤整形科进行术后切口愈合不良治疗的50例患者资料。其中，25例采用自制便携式简易封闭负压引流装置进行持续低负压吸引设为治疗组，25例采用碘伏纱条填塞引流换药，设为对照组。观察2组创面形态学变化；比较2组患者的切口愈合时间、换药次数、疼痛程度、换药材料费用指标。对数据行t检验。 结果治疗组患者创面清洁，肉芽组织新鲜红润；对照组患者创面肉芽组织生长不佳，渗液较多。治疗组患者的切口愈合时间、换药次数、疼痛程度、换药材料费用分别为(14.7±4.3) d、(5.1±1.4)次、(5.9±1.4)分、(639.5±127.4)元，对照组患者对应的指标分别为(38.6±5.9) d、(49.2±9.7)次、(8.2±1.8)分、(1 357.5±135.9)元，2组对应指标比较，差异均有统计学意义(t＝－16.3、－32.8、－4.9、－38.5，P值均小于0.05)。 结论自制便携式简易封闭负压引流装置在术后切口愈合不良患者中，能显著缩短切口愈合时间，减少换药次数，减轻疼痛程度，换药材料费用明显减少，大大提高了手术切口治愈率，优于传统方法换药，具有一定的推广价值。     

bFGF在骨组织工程学中的研究进展

碱性成纤维细胞生长因子(bFGF)是近年来研究较为广泛的生长因子之一，对骨组织有着广泛的生物学效应。本就bFGF的研究进展及其目前在骨组织工程学研究方面的应用做一综述。     

原位注射bFGF及其抗体对鼠胚神经细胞发育的影响

应用胚胎原位注射方法,通过形态学观察、Ｆｅｕｌｇｅｎ染色、蛋白含量测定及图像分析等技术,观察了ｂＦＧＦ及其抗体在体内对神经细胞发育的影响。结果显示,胚胎原位注射ａｎｔｉ－ｂＦＧＦ在本实验给予的剂量下,对胎鼠的体重、身长以及ＤＮＡ和蛋白合成无显著性影响;在高温致畸动物模型上给胚胎原位注射ｂＦＧＦ,对高温的胚胎毒和致畸作用具有保护作用,可促进胚胎的正常发育;高温可抑制细胞ＤＮＡ的合成,高温后并注射ｂＦＧＦ可促进蛋白合成,增加总蛋白含量。     

碱性成纤维细胞生长因子促进大鼠硬腭穿孔的愈合

目的:研究碱性成纤维细胞生长因子 (bFGF)对硬腭穿孔愈合的影响。方法:在大鼠硬腭部制作早期硬腭穿孔动物模型,外用bFGF治疗硬腭穿孔。采用肉眼观察、病理学检查的方法进行评价。结果:肉眼观察发现bFGF组伤口愈合率明显高于对照组(P＜0.01); 病理学检查表明bFGF能刺激肉芽组织的增长,成纤维细胞分裂增殖; bFGF组成纤维细胞的核仁形成区嗜银蛋白颗粒数目为3.73±0.52,对照组为2.11±0.31(P＜0.05)。结论: bFGF有助于肉芽组织的生长,具有显著促进硬腭穿孔创伤愈合的作用,有助于硬腭穿孔的修复。     

The mechanisms underlying fibroblast apoptosis regulated by growth factors during wound healing

While investigating the mechanisms underlying cell death during wound healing processes, we uncovered the pro‐apoptotic effects of basic fibroblast growth factor (bFGF) on granulation tissue fibroblasts following pretreatment with transforming growth factor (TGF)‐β1 in vitro. bFGF induced caspse‐3 activation and apoptosis in TGF‐β1‐pretreated granulation tissue‐derived fibroblasts (GF‐1) following bFGF treatment for 48 and 96 h. In contrast, fibroblasts that had been treated in the same manner and that originated from the uninjured dermis did not display apoptosis, indicating that the mechanisms underlying apoptosis events in fibroblasts that originate from normal dermal and wound tissues differ. In this process, we also found that bFGF inhibited Akt phosphorylation at serine 473 and induced a rapid loss of phosphorylation of focal adhesion kinase (FAK) at tyrosine 397 in pretreated GF‐1 cells, an event that coincided with the dissociation of phosphorylated FAK from the focal adhesions. Therefore, inhibition of survival signals relayed via the disrupted focal adhesion structures and inactivated Akt following bFGF treatment may lead to apoptosis in GF‐1 cells pretreated with TGF‐β1. Pretreatment of GF‐1 with TGF‐β1 followed by the addition of bFGF resulted in significantly greater inhibition of phosphorylation of Akt and FAK compared to treatment with TGF‐β1 or bFGF alone. The combinatorial treatment also led to proteolysis of FAK and inhibition of FAK and Akt protein expression in GF‐1 cells. These findings demonstrated a significant role for the two cytokines in apoptosis of granulation tissue fibroblasts during wound healing. In vivo studies also confirmed a marked decline in phosphorylation and protein expression of Akt and FAK in bFGF‐injected skin wounds. These results led to the hypothesis that temporal activation of TGF‐β1 and bFGF at the injury site promotes apoptosis in granulation tissue fibroblasts, an event that is critical for the termination of proliferative granulation tissue formation. Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.     

Dramatic promotion of wound healing using a recombinant human-like collagen and bFGF cross-linked hydrogel by transglutaminase

Abstract

The basic fibroblast growth factor (bFGF) plays an important role in the wound repair process. However, lacking of better biomaterials to carry bFGF still is a challenge in skin repair and regeneration. In this study, the human-like collagen (HLC) cross-linked with transglutaminase (TG) to fabricate a HLC/TG hydrogel to load bFGF. The physical properties of hydrogel, such as interior structure, mechanical property, were characterized in vitro using scanning electron microscopy (SEM), rheometer. Then, the effects of the HLC/TG hydrogel on the bFGF and cell attachmentwere evaluated, and the results showed that the HLC/TG hydrogel has good biocompatibility towards bFGF and cells. Finally, skin wound healing test was performed for the evaluation of HLC/TG hydrogels with bFGF in a mouse model. All results of macroscopic and microscopic analysis indicated that not only our HLC/TG hydrogel provide a delivery of growth factors, but also the HLC/TG hydrogel with bFGF achieving better skin regeneration in the structure and function.     

活血驳骨丸对内源性bFGF分泌影响的探讨

目的：分子学角度研究活血驳骨丸促进碱性成纤维细胞生长因子（bFGF）内源性分泌,以了解中医药在骨折后促进机体骨折愈合的作用机理。方法：应用双抗体夹心法ELISA检测驳骨丸治疗组和对照组在骨折后不同时期的内源性bFGF含量。结果：在伤后的8、14d时驳骨丸治疗组的bFGF含量明显高于对照组（P〈0．05）。结论：活血驳骨丸可以促进内源性bFGF分泌,刺激骨折端毛细血管的生长,为骨折端提供必要的血运。     

In Vivo Binding of Topically Applied Human bFGF on Rabbit Corneal Epithelial Wound

Abstract

We present the results of the first evaluation of human placenta extracted basic fibroblast growth factor (bFGF) in a rabbit corneal epithelium wound-healing model. Healing dose-response experiments after selective epithelial wounding with iodine vapors demonstrated that bFGF accelerated the repair process in a saturable manner. Corneal binding of topically applied ¹²⁵I-labeled bFGF was investigated using radioassay and autoradiographic techniques. Basic FGF was shown to bind specifically to denuded epithelial basement membrane in a very stable fashion and not to the intact epithelium. No transfer of the topical bFGF to the aqueous humor or any intraocular structure could be observed. The stability of this interaction was further demonstrated by reextracting and characterizing the labeled factor from treated corneas. The specificity of the fixation was documented by in vivo topical competition with unlabeled bFGF or heparin. We propose that bFGF-basement membrane interactions play a role in corneal wound healing.     

医用胶原蛋白海绵及负压封闭引流联合自体刃厚皮复合移植在足部毁损伤难愈性创面中的应用

目的观察医用胶原蛋白海绵及负压封闭引流(VSD)联合自体刃厚皮复合移植修复足部毁损伤难愈性创面的效果。方法选取2017年1月至2019年10月海南省人民医院烧伤与皮肤修复外科收治的足部毁损伤难愈性创面患者18例,其中合并足背肌腱外露12例,跖骨骨外露6例。创面清创后,予医用胶原蛋白海绵覆盖肌腱外露、骨外露创面,并安装VSD装置,待创面覆盖肉芽组织后,再给予自体刃厚皮移植修复创面。记录治疗时间、外露肌腱或骨质坏死率、皮片成活率,术后随访6个月,以Maryland足部功能评分标准评估外观及功能。结果18例患者足部均得以保存,外露的肌腱和骨质均保持活性,皮片成活率85%~95%,平均(90±5)%。残余创面给予间断换药治疗后全部愈合,治疗时长14.0~45.0 d,平均(29.5±15.5)d。出院后6个月复诊以Maryland足部功能评分标准评估足部功能,优3例,良4例,中6例,差5例。结论医用胶原蛋白海绵及VSD在促进肌腱、骨质外露创面肉芽组织生长的同时可保留外露的肌腱及骨组织活性,联合自体刃厚皮移植,能较好地修复足部毁损伤难愈性创面。     

大鼠皮肤创伤修复过程中转化生长因子β1和β3的表达

背景：转化生长因子β在组织创伤修复中发挥核心和关键作用。 目的：观察转化生长因子β1和转化生长因子β3在大鼠皮肤瘢痕性创伤愈合过程中表达量及表达部位的变化。 方法：制备大鼠皮肤全层切伤模型,长度1.5-2.0 cm,深及筋膜层。于伤后0 h,12 h,1 d,2 d,3 d,4 d,5 d,6 d,7 d处死大鼠,取损伤部位皮肤,采用免疫组织化学染色检测各时间点转化生长因子β1和转化生长因子β3的表达,并进行定量分析。 结果与结论：免疫组织化学染色显示,在创伤愈合的早期阶段(伤后1-5 d),转化生长因子β1和转化生长因子β3免疫阳性颗粒主要出现在上皮细胞、上皮基底层细胞胞浆、巨噬细胞等免疫细胞胞浆及肉芽组织中;随着创伤修复时间的持续,免疫阳性颗粒主要出现在真皮层的成纤维细胞及细胞外基质中。其中转化生长因子β1的表达在创伤后1-5 d最强,而转化生长因子β3在创伤后六七天时开始明显表达。可见在大鼠皮肤瘢痕性创伤愈合过程中,转化生长因子β1的表达先于转化生长因子β3,提示转化生长因子β1与胶原形成及创伤修复关系密切,而转化生长因子β3在愈合后期表达量有升高趋势,其可能与创伤后期的组织改建密切相关。     

低频电磁场在基因修饰表皮干细胞移植修复创面中的作用

背景：烧伤、慢性创面等大面积皮肤缺损的创面修复是临床上亟待解决的难题。表皮干细胞和角质化细胞生长因子可为创面的治疗提供新的策略。低频电磁场作为一种非侵入性物理刺激在创面修复中已被认为较佳的方法。 目的：探讨低频电磁场在角质化细胞生长因子基因修饰的表皮干细胞移植促进小鼠皮肤全层缺损创面修复中的作用。 方法：体外分离培养SD乳鼠表皮干细胞,用5-溴脱氧尿核苷进行标记,成功转染角质化细胞生长因子基因腺病毒表达载体后,移植于昆明小鼠全层缺损创面。建立全层缺损创面小鼠模型,分别进行表皮干细胞移植,角质化细胞生长因子修饰的表皮干细胞移植,角质化细胞生长因子修饰的表皮干细胞移植外加低频电磁场干预。 结果与结论：移植后第9,16天,低频电磁场干预的角质化细胞生长因子基因修饰的表皮干细胞移植组创面收缩率优于其他各组(P < 0.05)。移植后第9天,免疫荧光染色法检测显示,各组组创面中均有5-溴脱氧尿核苷阳性细胞分布。移植后第16天,Western blot检测显示,低频电磁场干预的角质化细胞生长因子基因修饰的表皮干细胞移植组和角质化细胞生长因子基因修饰的表皮干细胞移植组创面组织中角质化细胞生长因子蛋白表达高于表皮干细胞移植组(P < 0.05);移植后第16,30天,苏木精-伊红染色结果显示,低频电磁场干预的角质化细胞生长因子基因修饰的表皮干细胞移植组的创面组织上皮化现象较明显。结果证实,低频电磁场有促进角质化细胞生长因子基因修饰的表皮干细胞移植修复小鼠皮肤全层缺损创面的作用。     

Multiple roles of chemokine CXCL12 in the central nervous system: a migration from immunology to neurobiology

Chemotactic cytokines (chemokines) have been traditionally defined as small (10-14kDa) secreted leukocyte chemoattractants. However, chemokines and their cognate receptors are constitutively expressed in the central nervous system (CNS) where immune activities are under stringent control. Why and how the CNS uses the chemokine system to carry out its complex physiological functions has intrigued neurobiologists. Here, we focus on chemokine CXCL12 and its receptor CXCR4 that have been widely characterized in peripheral tissues and delineate their main functions in the CNS. Extensive evidence supports CXCL12 as a key regulator for early development of the CNS. CXCR4 signaling is required for the migration of neuronal precursors, axon guidance/pathfinding and maintenance of neural progenitor cells (NPCs). In the mature CNS, CXCL12 modulates neurotransmission, neurotoxicity and neuroglial interactions. Thus, chemokines represent an inherent system that helps establish and maintain CNS homeostasis. In addition, growing evidence implicates altered expression of CXCL12 and CXCR4 in the pathogenesis of CNS disorders such as HIV-associated encephalopathy, brain tumor, stroke and multiple sclerosis (MS), making them the plausible targets for future pharmacological intervention.