动物瘢痕模型的相关研究进展

皮肤损伤后的异常愈合会导致病理性瘢痕的产生。病理性瘢痕的出现不仅影响美观,严重时还会造成心理和生理功能障碍。病理性瘢痕的机制研究对于瘢痕治疗有极为重要的意义。其中,动物瘢痕模型是目前研究病理性瘢痕的重要模型手段之一。理想的动物瘢痕模型应该在组织学、细胞学等层面尽可能接近于人类的病理性瘢痕。该文分别从传统技术动物瘢痕中的啮齿类动物模型、兔耳模型和猪模型,以及新技术动物瘢痕模型这两个方面,结合近年来在瘢痕领域应用较多的研究,进行了相应系统的阐述。     

得宝松单独注射与得宝松加利多卡因治疗瘢痕疙瘩效果比较

目的:观察得宝松加与不加利多卡因皮损内注射对瘢痕疙瘩的疗效.方法:患者随机分为两组,A组16例,单纯得宝松皮损内注射,B组16例,得宝松加利多卡因注射,每4周注射1次,连续观察3个月.结果:经过3次注射,A组痊愈12例(75%),B组痊愈5例(31%),A组痊愈率明显高于B组,(u=2.83,P＜0.01).两组注射后疼痛情况无明显差异.结论:单纯得宝松皮损内注射对瘢痕疙瘩的疗效优于得宝松加利多卡因.     

瘢痕疙瘩成纤维细胞p53基因突变的研究

目的　探讨瘢痕疙瘩成纤维细胞中 p5 3基因第 4～ 8外显子的突变规律及其意义。　方法　取瘢痕患者手术切除的瘢痕疙瘩和增生性瘢痕标本各 12例 ,并设患者自身正常皮肤标本及血标本为对照。体外分离、培养上述组织标本的成纤维细胞。采用聚合酶链式反应 单链构象多态性(PCR SSCP)分析方法和基因测序法 ,检测各种组织成纤维细胞中p5 3基因的突变情况。　 结果　 12例瘢痕疙瘩标本中有 9例p5 3基因外显子 4、5、6、7出现点突变和移码突变 ,增生性瘢痕标本、正常皮肤标本及血标本中均未检出突变。　结论　p5 3基因突变是瘢痕疙瘩形成和发展的重要因素之一。     

巢蛋白(nestin)在瘢痕疙瘩和增生性瘢痕中的表达

目的探讨巢蛋白（nestin）在瘢痕疙瘩和增生性瘢痕中的表达。方法采用免疫组织化学技术方法检测8例正常皮肤、7例扁平瘢痕、8例瘢痕疙瘩、8例增生性瘢痕中nestin^＋细胞，计数分析nestin^＋细胞在瘢痕疙瘩和增生性瘢痕中的表达。结果①nestin在8例正常皮肤组织中表皮基底细胞和棘细胞、汗腺、毛囊、皮脂腺、血管内皮细胞和7例成纤维细胞的胞浆中表达。nestin在扁平瘢痕、瘢痕疙瘩、增生性瘢痕组织中表皮基底细胞和棘细胞、血管内皮细胞和成纤维细胞的胞浆及残留的汗腺、毛囊、皮脂腺中表达。②瘢痕疙瘩和增生性瘢痕组织中nestin^＋表皮细胞、nestin^＋成纤维细胞和nestin^＋血管内皮细胞的数量明显高于正常皮肤和扁平瘢痕（P〈0．05），而正常皮肤与扁平瘢痕组织中nestin^＋细胞的表达差异无显著性（P〉0．05）。结论巢蛋白在瘢痕疙瘩和增生性瘢痕表皮、成纤维细胞和血管内皮细胞中表达增高提示瘢痕疙瘩和增生性瘢痕的过度增生可能与巢蛋白相关。     

染色体1pter-p36.21杂合性缺失与瘢痕疙瘩的关系

目的寻找瘢痕疙瘩1pter-36.21中可能存在的肿瘤抑制基因的杂合性丢失(LOH)区域,为发现和定位瘢痕抑制基因提供线索和依据。方法采用聚合酶链反应(PCR)-变性聚丙烯酰胺凝胶电泳技术,对25例瘢痕疙瘩组织和外周静脉血标本进行微卫星分析。结果瘢痕疙瘩组织在所选的位点上的LOH发生率为60%(15/25),明显高于正常对照组织的4%(1/25,P<0.05),在所选的位点上均未发现微卫星不稳定性(MSI)。D1S243位点、D1S468位点、D1S507位点、D1S199位点的LOH发生率分别为28%(7/25)、40%(10/25)、52%(13/25)、12%(3/25),其中D1S243、D1S468、D1S507的LOH发生率比较具有统计学意义(P<0.05)。结论发生在D1S243-D1S468-D1S507位点的LOH存在与瘢痕疙瘩有关的潜在瘢痕抑制基因(SSG),而1pter-36.21上LOH微卫星不稳定性与瘢痕疙瘩发生的关系不大。     

细胞周期蛋白E在瘢痕疙瘩不同区域中的表达及意义

目的探讨细胞周期蛋白E在瘢痕疙瘩形成过程中的作用及意义。方法应用免疫组织化学链霉亲和素-过氧化物酶（SP）法检测瘢痕疙瘩不同区域和正常皮肤组织成纤维细胞（fibro-blast,FB）中细胞周期蛋白E的表达。结果在瘢痕疙瘩周边部FB中存在细胞周期蛋白E的高表达;而在瘢痕疙瘩中央部阳性表达的FB数量少,8例标本FB中细胞周期蛋白E表达阴性。正常皮肤FB中细胞周期蛋白E表达阴性。经统计学处理,周边部与正常皮肤组及中央部比较,差异有统计学意义（P〈0.01及P〈0.05）;中央部与正常皮肤（NS）组比较差异无统计学意义（P〉0.05）。结论细胞周期蛋白E在瘢痕疙瘩周边部FB中的高表达,不仅可能促进了瘢痕疙瘩的形成,并可能是瘢痕疙瘩侵犯周围正常组织,呈浸润性生长的原因之一。     

手术联合术后放疗治疗瘢痕疙瘩的临床研究

目的：研究手术联合术后放疗治疗瘢痕疙瘩的临床效果。方法：瘢痕疙瘩85例,随机分为2组,实验组50例,采用瘢痕疙瘩切除缝合或植皮,术后即时放疗;对照组35例,仅行瘢痕疙瘩切除植皮。结果：术后随访6个月－3年,实验组40例（80％）治愈,无复发;5例（10％）轻度瘢痕增生,局部注射康宁克通－A后未复发;5例（10％）复发;对照组6例（17．14％）治愈,29例（82．86％）复发,实验组治愈率明显高于对照组。结论：手术联合术后放疗是治愈瘢痕疙瘩的有效方法。     

Long non-coding RNA LINC01116 accelerates the progression of keloid formation by regulating miR-203/SMAD5 axis

BackgroundEmerging evidence reveals the importance of long non-coding RNAs (lncRNAs) in the development and progression of keloid formation. However, the roles and molecular mechanism of lncRNA LINC01116 in the progression of keloid formation remain largely unknown.MethodsThe expression levels of LINC01116, microRNA-203 (miR-203) and SMAD family member 5 (SMAD5) were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Cell proliferation, migration and invasion were detected by Cell counting Kit-8 (CCK-8) assay and transwell assay. Flow cytometry and western blot assay were used to examine cell apoptosis and extracellular matrix (ECM) production. The interaction between miR-203 and LINC01116 or SMAD5 was predicted by bioinformatics analysis and verified by dual-luciferase reporter and RNA Immunoprecipitation (RIP) and RNA pull-down assays.ResultsLINC01116 and SMAD5 were upregulated while miR-203 was downregulated in keloid tissues and keloid fibroblasts. LINC01116 knockdown suppressed the proliferation, migration, invasion, and ECM production but induced apoptosis in keloid fibroblasts through enhancing miR-203 and inhibiting SMAD5. Moreover, SMAD5 was identified as a direct target of miR-203 and miR-203 could directly bind to LINC01116. Besides, LINC01116 regulated SMAD5 expression by targeting miR-203.ConclusionDownregulation of LINC01116 inhibited the progression of keloid formation by regulating miR-203/SMAD5 axis, which might provide a novel target for keloid therapy.     

A better incision for pectus excavatum repair: avoiding the keloid triangle

The most common approach to the pepair of pectus excavatum and pectus carinatum deformities is via a central transverse submammary incision. The subsequent suprasternal scar is conspicuous and prone to hypertrophic and keloid scarring. To avoid the keloid triangle and to produce a less noticeable scar, we have utilized bilateral inframammary incisions for repairs of five female and two male patients with pectus defects. This approach provides excellent access for cartilage resection, sternotomy, and sternal tupport without increasing opearative time or compromising operative exposure. On follow-up for up to 25 months, all patients have had excellent cosmetic and functional results. Chest wall configuration and stability, wound healing, and scar formation have all been without complication. No keloid or hypertrophic scars have developed. To date, there has been no recurrence of pectus defects. We believe bilateral inframammary incisions are a superior approach for pectus repairs by enchancing cosmesis with less noticeable scars and fewer hypertropic and keloid scars, all without compromising operative exposure or increasing operative time.     

非瘢痕体质性耳垂瘢痕瘤的病因及手术治疗

目的研究耳垂瘢痕瘤的病因与手术治疗。方法对21例耳垂瘢痕瘤实施瘢痕切除、耳垂成形术,其中10例为双耳,11例为单耳;12例为黑人,9例为华人。结果经过6个月以上随访,21例病人未见有耳垂瘢痕瘤复发者。结论耳垂瘢痕瘤患者可以进行瘢痕切除、耳垂成形术,并取得良好的效果。