手部动力支具在多区肌腱损伤修复术后的应用

【】目的：探讨手部动力支具在多区肌腱修复术后的临床应用效果。方法：选取2016年6月～2018年6月我院收治的81例肌腱损伤患者,采用随机数表法分为支具治疗组45例和对照组36例,分别予安装手部动力支具功能锻炼及常规治疗,患指肌腱修复后功能用TAM[总主动活动度测定法(total active movement,TAM)]评定。结果：随访3个月,支具组综合优良率为87.9％,对照组综合优良率为63.9％ ,两组间差异有显著性意义(P<0．05);支具治疗组二次松解手术率明显低于常规治疗组,组间数据对比差异显著(X₂=3.854,p=0.048),且未发生不良反应。结论：手部动力支具能较明显地减轻肌腱修复术后粘连的发生,降低二次手术的几率,由此可见手部动力支具在在肌腱修复术后的康复治疗是安全有效的。     

Influence of agitation methods of irrigants after methylene blue-mediated PDT on the bonding interface of a fiber post cementation system

BackgroundThis study evaluated the effects of final agitation methods of irrigants to remove methylene blue and sodium hypochlorite residues after PDT-assisted endodontic treatment on the bond strength of fiber posts cemented with etch-and-rinse adhesive and conventional resin cement.MethodsNinety bovine teeth were endodontically treated. In sequence, post space preparation followed by methylene blue-mediated PDT and sodium hypochlorite (NaOCl) irrigation were performed. Six final irrigations protocols for dye and NaOCl removal were performed prior to cementation with etch-and-rinse adhesive (Adper Scocthbond Multipurpose) and conventional dual resin cement (RelyX ARC): Conventional endodontic irrigation (CEI), passive ultrasonic irrigation (PUI), mechanical agitation with XP Endo Finisher (XPF), XP Clean (XPC) or Easy Clean (ECL) and distilled water (NCO - control). After fiber post cementation, push-out bond strength test was performed at different thirds of the post space. Failure mode was also analyzed. ANOVA and Tukey's post-hoc test was used for data analysis (α=5%).ResultsPUI, XPF e XPC protocols showed the highest bond strength values with no difference among them (p > 0.05), although they were similar to NCO, regardless of the post space third. CEI e ECL showed similar bond strength values, regardless of the third (p > 0.05). Adhesive failure was the most incident for CEI and ECL, while mixed and cohesive failures were predominant in PUI, XPF, XPC and NCO groups.ConclusionsMechanical agitation of distilled water with XPF, XPC and PUI after methylene blue-mediated PDT and irrigation with 2.5% sodium hypochlorite promoted bond strength of the resin cementation system in post space dentin comparable to control group.     

Reduction of oxidative stress by oral N-acetyl-L-cysteine treatment decreases plasma soluble vascular cell adhesion molecule-1 concentrations in non-obese, non-dyslipidaemic, normotensive, patients with non-insulin-dependent diabetes

Summary To assess in vivo effects of antioxidants on vascular cell adhesion molecule (VCAM)-1 expression, circulating soluble VCAM-1 and intraerythrocytic reduced glutathione (GSH) and GSH disulphide (GSSG) concentrations were evaluated in non-insulin-dependent diabetic patients without complications (9 men, 6 women, 48 ± 6 years old) before and after 1 month of either oral N-acetyl-L-cysteine (1.200 mg/day) or placebo treatments, given in randomized, cross-over, double-blind fashion. Ten healthy subjects (7 men, 3 women, 52 ± 4 years old) served as control subjects. Baseline plasma VCAM-1 concentrations were higher (p = 0.007) in non-insulin-dependent diabetic patients (707.9 ± 52.5 ng/ml) than in control subjects (627.3 ± 84.6 ng/ml). Intraerythrocytic GSSG content was higher (non-insulin dependent diabetic patients: 0.618 ± 0.185 μmol/g Hb; control subjects: 0.352 ± 0.04 μmol/g Hb, p = 0.0002), whereas intraerythrocytic GSH concentrations were lower (p = 0.001) in non-insulin dependent diabetic patients (6.0 ± 0.7 μmol/g Hb) than in control subjects (7.1 ± 0.5 μmol/g Hb). The mean GSH:GSSG ratio was also lower (p = 0.0001) in the first (10.9 ± 4.5) than in the second group (20.2 ± 1.4). Circulating VCAM-1 and intraerythrocytic GSH concentrations were negatively correlated in non-insulin diabetic patients (r = 0.605, p = 0.01). Treatment with N-acetyl-L-cysteine decreased plasma VCAM-1 (p = 0.01) and intraerythrocytic GSSG (p = 0.006) but increased GSH concentrations (p = 0.04) and the GSH:GSSG ratio (p = 0.004) in non-insulin dependent diabetic patients. Our data indicate that the vascular endothelium is activated in non-insulin dependent diabetes. Antioxidant treatment counterbalanced such endothelial activation. Thus, antioxidant agents might protect against oxidant-related upregulation of endothelial adhesion molecules and slow down the progression of vascular damage in non-insulin dependent diabetes. [Diabetologia (1998) 41: 1392–1396] Received: 15 May 1998 and in revised form: 8 July 1998     

重组腺相关病毒介导的细胞色素P450表氧化酶基因对TNF-α诱导人脐静脉内皮细胞炎症的影响

目的研究过度表达细胞色素P450表氧化酶基因引起内源性EETs产生增加是否能抑制由TNF—α诱导的内皮炎症。方法以携带三种不同表氧化酶基因的重组腺相关病毒rAAV- CYP2C11、rAAV—CYP2J2和rAAV—CYPF87V转染人脐静脉内皮细胞,然后再以TNF—α干预,来研究它们对内皮VCAM-1的表达及外周血单核细胞PBMC与内皮细胞粘附的影响。结果TNF-α诱导了 HUVEC中VCAM-1蛋白质的表达,rAAV—CYP2C11、rAAV—CYP2J2能明显抑制TNF-α的这一作用。 TNF-α诱导了PBMC与HUVEC的粘附(100±0．0％ vs 620．1±65．3％),rAAV-CYP2C11、rAAV- CYP2J2能明显抑制TNF-α的这一作用(分别为120．3±33．4％ vs 387．7±27．4％．131．0±28．7％ vs 535．0±69．7％)。结论CYP2C11和CYP2J2基因具有显著的保护内皮细胞、对抗炎症介质介导的内皮损伤的作用。     

糖尿病大鼠坐骨神经病变与细胞黏附分子-1和P-选择素变化的相关性及西洛他唑的治疗作用

目的　研究糖尿病 (DM )大鼠黏附分子CD5 4、CD6 2p变化及其与坐骨神经病变的关系 ,探讨西洛他唑对糖尿病神经病变 (DPN)和黏附分子的影响。　方法　将实验大鼠分为正常组 (8只 )、糖尿病组 (8只 )、胰岛素组 (7只 )和西洛他唑组 (7只 )。测定各组坐骨神经传导速度和血浆单个核细胞CD5 4、血小板CD6 2p含量 ,观察坐骨神经超微结构变化。　结果　西洛他唑治疗组与DM组相比 :(1)坐骨神经传导速度明显加快 ;DM组 =(2 0 .3± 2 .2 )m/s ,西洛他唑组 =(2 8.9± 7.9)m /s ,q =3 .50 ,P <0 .0 5。 (2 )血浆单个核细胞表面CD5 4水平明显降低 ;DM组 =(65± 15) % ,西洛他唑组 =(2 5± 9) % ,q =7.50 ,P <0 .0 5。 (3 )西洛他唑有降低血小板表面CD6 2p的趋势 ,与DM组相比无显著差异。 (4)坐骨神经超微结构的病理变化明显改善。　结论　DM大鼠CD5 4、CD6 2p表达增加与DPN有明显的相关性 ,西洛他唑可降低其表达并改善糖尿病神经病变     

氧化型低密度脂蛋白促进单核细胞－内皮细胞体外粘附反应

体外培养猪胸主动脉内皮细胞，观察氧化型低密度脂蛋白对内皮细胞－单核细胞体外粘附反应的影响，同时观察氧化型低密庆脂蛋白对内皮细胞表面粘附分子颗粒膜蛋白－１４０及内皮细胞分泌前列环素的影响。结果发现氧化型低密度脂蛋白（０、５０、１００和２００ｍｇ／Ｌ）增加内皮细胞－单核细胞粘附率并呈剂量依赖性，其中以１００ｍｇ／Ｌ作用最强；氧化型低密度脂蛋白（１００ｍｇ／Ｌ）与内皮细胞孵育０．５ｈ，粘附率上升但无显著性，１ｈ后显著升高，３ｈ达高峰，４８ｈ回复接近正常水平。同时发现１００ｍｇ／Ｌ氧化型低密度脂蛋白使内皮细胞表面颗粒膜蛋白－１４０含量从９２．８±４７．６上升到２９３．０±１４０．７μｇ／Ｌ（Ｐ＜０．０５），内皮细胞分泌前列环素量从８４．６±１８．７降低到６．０±３．１ｎｇ／Ｌ（Ｐ＜０．０１）．结果表明氧化型低密度脂蛋白可显著促进单核细胞－内皮细胞粘附，其作用机制可能同内皮细胞表面粘附分子颗粒膜蛋白－１４０增加有关。关键词     

不同来源的CD34^＋细胞归巢相关分子的表达

目的 研究不同来源CD34^＋细胞归巢相关分子（HRM）的表达情况。方法采用免疫磁珠法（MACS）分选不同来源的CD34^＋细胞，免疫荧光标记流式细胞仪测定HRM的表达。结果骨髓（BM）、动员后的外周血（mPB）及脐血（UCB）来源的CD34^＋细胞均高表达细胞黏附分子CD49d、CD49e、CD54、CD11a、CD62L、CD44、CD31。UCB来源的CD34^＋细胞表面表达的细胞黏附分子中，CD49e表达显著低于BM和mPB来源的CD34^＋细胞（P〈0．05），CD54表达显著低于mPB来源者（P〈0．05），CXCR4表达显著低于BM来源者（P〈0．05）。结论UCB来源的造血干／祖细胞归巢能力低可能是UCB移植造血重建延迟的原因之一。     

High glucose induces plasminogen activator inhibitor-1 expression through Rho/Rho-kinase-mediated NF-kappaB activation in bovine aortic endothelial cells

Recently, it has become evident that elevated levels of plasminogen activator inhibitor-1 (PAI-1) are associated with myocardial infarction and stroke, especially in patients with diabetes. The molecular mechanisms involved in hyperglycemia-induced PAI-1 expression in bovine aortic endothelial cells (BAEC) were investigated. PAI-1 expression in BAEC was significantly increased in accordance with the concentration of glucose in media from 5.7 mM to 23 mM. Stimulation with high glucose (23 mM) significantly increased small GTPase Rho A activation. Pretreatment with a Rho-kinase inhibitor, Y-27632 (1-10 microM), significantly blocked high glucose-induced PAI-1 expression. NF-kappaB activity determined using the luciferase reporter gene assay was significantly enhanced by high glucose, and pretreatment with Y-27632 inhibited high glucose-induced PAI-1 expression at the basal level. An inhibitor of NF-kappaB action, namely parthenolide (0.1 microM), BAY 11-7082 (5 microM) and SN50 (1 microM), significantly blocked high glucose-mediated PAI-1 expression to a level with low glucose (5.7 mM). These data suggested that high glucose-induced PAI-1 expression in endothelial cells is mediated by NF-kappaB activation through the Rho/Rho-kinase pathway. Inhibition of Rho/Rho-kinase signaling might be a novel target for diabetes and metabolic syndrome.     

Possible Involvement of Altered RGD Sequence in Reduced Adhesive and Spreading Activities of Advanced Glycation End Product-Modified Fibronectin to Vascular Smooth Muscle Cells

Although fibronectin (FN) modified by advanced glycation end products (AGEs) has been shown to contribute to the development of diabetic vascular complications through its reduced adhesive activity to vascular cells, little is known about changes in the cell binding domain of AGE-modified FN. Here we examined the mechanism of reduced adhesive and spreading activities of AGE-modified FN to vascular smooth muscle cells (SMCs), particularly the contribution of modification of Arg-Gly-Asp (RGD) sequence. Incubation with glucose caused not only the formation of N-carboxymethyllysine and pentosidine, but also polymerization of FN in a dose- and time-dependent manner. AGE-modified FN had significantly low adhesive and spreading activities to cultured SMCs. On the other hand, multimeric FN formed by disulfide bonds did not show any effect on either cell adhesion or spreading. The adhesive activity of type I collagen, one of the RGD sequence-containing proteins, to SMCs also decreased by AGE-modification. The inhibitory effect of AGE-modification on cell adhesion was significantly greater in type I collagen than in FN. Although the extent of AGE-modification of type I collagen was indistinguishable from that of FN, AGE-modification decreased the arginine content of type I collagen by 69.5% and of FN by 30.6%, compared with their non-glycated forms. The addition of RGD peptides caused a decrease in adhesion of SMCs to non-glycated FN, but not to AGE-modified FN. Modification of RGD sequence with glyoxal eliminated its inhibitory effect on cell adhesion. Our results suggest that a marked decrease in adhesive and spreading activities of AGE-modified FN to SMCs might largely be due to a modification of its RGD sequence by AGE, thus suggesting a potential link between AGE modification of FN and the pathogenesis of diabetic angiopathy.     

Keratinocyte Differentiation and Proliferation are Regulated by Adhesion to the Three-Dimensional Meshwork Structure of Type IV Collagen

We examined the behavior of human foreskin keratinocytes (HFKs) on reconstituted type IV collagen gel. HFKs survived for several days and the upper layer cells expressed a differentiation marker, involucrin. Apoptosis was induced after involucrin expression while cell proliferation was suppressed. On molecular type IV collagen, integrins shifted from α2β1 to α3β1 during HFK culture. On type IV collagen gel, HFKs initially expressed integrin α2β1, and later expressed integrin α3β1 in the presence of α2β1 did not disappear. Using synthetic peptides, we examined integrin α2-mediated adhesion to type IV collagen gel. Addition of synthetic peptide dose-dependently inhibited cell adhesion both on type IV collagen gel and on molecular type IV collagen. On type IV collagen gel, weaker phosphorylation of focal adhesion kinase, paxillin, and Akt was observed compared with the molecular forms. Based on these observations, we think type IV collagen gel is a novel culture substrate that mimics the physiological environment for HFKs.