基质金属蛋白酶1在不同程度退变腰椎间盘髓核与纤维环中的表达及意义

背景：基质金属蛋白酶在椎间盘退变中通过影响基质合成及降解导致基质成分紊乱及功能的改变。 目的：观察基质金属蛋白酶1在人类退变腰椎间盘组织中的表达变化。 方法：获取经手术治疗腰椎间盘突出症患者椎间盘标本30份,突出型、脱出型、游离型各10份,分离髓核与纤维环,设为实验组;腰椎损伤致椎体骨折切除椎间盘10份设为对照组。应用免疫组织化学法检测基质金属蛋白酶1在椎间盘中髓核与纤维环细胞中的表达。 结果与结论：①苏木精-伊红染色显示,对照组椎间盘标本纤维环仍保持着致密的板层结构,实验组椎间盘组织多呈纤维化样改变。②两组髓核细胞中基质金属蛋白酶1表达均高于纤维环细胞中的表达。③实验组突出型椎间盘标本中基质金属蛋白酶1表达明显高于对照组(P < 0.01),脱出型和游离型椎间盘标本中基质金属蛋白酶1表达明显高于突出型 (P < 0.01)。 关键词：椎间盘退变;基质金属蛋白酶1;椎间盘突出症;髓核;纤维环 doi:10.3969/j.issn.1673-8225.2012.13.015     

程序性死亡分子5在退变腰椎间盘中的表达

背景:细胞凋亡在腰椎间盘退变中起重要作用。程序性死亡分子5是一个促细胞凋亡的蛋白,在骨关节炎的软骨细胞中表达增高,但是至今未见在退变椎间盘中表达的报道。目的:观察程序性死亡分子5在正常、突出和脱出腰椎间盘髓核细胞中的表达规律,分析其在腰椎间盘退变中的作用。方法:用SP免疫组织化学方法、免疫荧光方法检测程序性死亡分子5在2例正常、23例突出和17例脱出腰椎间盘髓核细胞中的表达,用脱氧核苷酸转移酶末端标记法和透射电镜检测髓核细胞凋亡情况;用天狼星红染色观察髓核组织细胞外基质Ⅰ,Ⅱ型胶原纤维的变化。结果与结论:脱出组髓核细胞表达程序性死亡分子5的阳性率高于突出组(P0.05),脱出组髓核细胞脱氧核苷酸转移酶末端标记阳性率高于突出组(P0.05)。荧光显微镜和激光共聚焦显微镜观察结果显示程序性死亡分子5表达定位于退变椎间盘的髓核细胞的细胞核;用透射电镜检测到凋亡的髓核细胞;天狼星红染色结果显示,随着年龄增长,髓核中Ⅱ型胶原纤维减少,Ⅰ型胶原纤维增多。结果提示退变椎间盘髓核细胞表达程序性死亡分子5上调,细胞凋亡增加,程序性死亡分子5介导的细胞凋亡在椎间盘退变中起到重要作用。     

人颈椎间盘退变与细胞凋亡及基质金属蛋白酶11的表达

背景：前期研究发现基质金属蛋白酶11基因在人退变颈、腰椎间盘组织中明显上调。 目的：观察人退变颈椎间盘髓核组织中基质金属蛋白酶11的表达与细胞凋亡的关系。 方法：纳入30个经MRI确认的退变颈椎间盘髓核组织和20个因颈椎创伤治疗获得的正常颈椎间盘髓核组织。 结果与结论：苏木精-伊红染色显示退变的颈椎间盘髓核组织中髓核细胞较正常髓核组织明显减少(P < 0.01),而凋亡细胞较正常髓核组织明显增多(P < 0.01)。免疫组化染色显示退变的颈椎间盘髓核组织中基质金属蛋白酶11的表达明显高于正常髓核组织(P < 0.01),且基质金属蛋白酶11表达与TUNEL染色检测到的细胞凋亡正相关(r=0.44,P < 0.05)。说明高表达的基质金属蛋白酶11不仅可直接破坏细胞外基质尚可诱导髓核细胞凋亡,在椎间盘退变的过程中发挥重要作用。     

腰椎髓核组织中缺氧诱导因子1α的表达:与凋亡率正相关

背景:缺氧诱导因子1α在缺氧的环境下对细胞凋亡起着双重调控作用。缺氧的严重程度决定细胞是出现凋亡还是适应缺氧生存。当细胞暴露于慢性或极度缺氧时由缺氧诱导因子1α引起的保护机制不足而发生凋亡。目的:观察缺氧诱导因子1α和凋亡在人不同突出类型腰椎髓核组织中的表达,判断两者有无相关性。方法:腰椎髓核组织标本取自腰椎间盘突出症行腰椎后路椎板开窗髓核摘除患者60例,41例取自L4-5髓核组织,19例取自L5-S1髓核组织。将髓核组织分为突出组、游离组各30例,同时选取腰椎骨折脱位患者腰椎髓核组织标本10例作为对照组。采用免疫组织化学技术,观察各组突出腰椎髓核组织缺氧诱导因子1α的表达;采用Tunel技术,观察不同突出类型腰椎髓核细胞凋亡程度;分析各组髓核组织缺氧诱导因子1α的表达与髓核细胞凋亡率有无相关性。结果与结论:游离组、突出组和对照组都可观察到缺氧诱导因子1α的表达,游离组缺氧诱导因子1α在髓核的表达显著高于突出组和对照组(P0.01)。3组都可观察到髓核细胞的凋亡,游离组髓核细胞凋亡的表达显著高于突出型和对照组(P0.01)。髓核细胞缺氧诱导因子1α表达和凋亡呈正相关(P0.01)。结果提示,腰椎间盘突出症髓核组织中缺氧诱导因子1α的表达与突出类型有关,在脱垂游离型中表达最高。腰椎髓核组织中缺氧诱导因子1α的表达与凋亡率呈正相关。     

腰椎间盘突出髓核的自身免疫性CSCD

背景:引起椎间盘源性腰腿痛的发病机制很多,在椎间盘退变的发生和发展过程中血管内皮生长因子与T,B淋巴细胞的表达与突出类型、病程等是否具有相关性还未完全清楚。目的:观察不同类型腰椎间盘突出症患者腰椎间盘组织中T,B淋巴细胞及血管内皮生长因子的表达变化,分析其与患者症状、体征的相关性。方法:选取腰椎间盘突出症患者的腰椎间盘标本作为实验组,包括游离脱出型、突出型及膨出型;以腰椎骨折患者的正常椎间盘作为对照。采用苏木精-伊红染色法观察椎间盘标本中血管形成及周边淋巴细胞聚集情况,免疫组化法检测CD4,CD8,IgG,IgM及血管内皮生长因子的分布。结果与结论:①在突出髓核组织中有大量新生血管形成并可见血管内皮细胞,在其周围可见明显的淋巴细胞聚集。②实验组均有活化的CD4,CD8阳性T细胞、IgG,IgM阳性B细胞和血管内皮生长因子表达,其中脱出游离组和突出组的阳性细胞率高于膨出组(P<0.05),而对照组均无阳性表达。提示髓核组织暴露于自身免疫系统中可以激活T、B细胞,引起自身免疫反应,血管内皮生长因子参与了退变椎间盘新生血管的形成,并可能与T,B细胞引起的自身免疫反应对椎间盘突出腰腿痛机制有协同作用。     

TRAIL受体在肿瘤细胞系上的表达及意义

目的 检测TNF相关凋亡诱导配体（TRAIL）的受体，在来源于血液系统、肝脏、肺脏和大肠的8个肿瘤细胞系中的表达，并探讨其意义。方法 采用半定量RT－PCR，对TRAIL受体的表达进行半定量检测。结果 TRAIL凋亡通路中，能够诱导凋亡反应的死亡受体DR4和DR5，在所检测的肿瘤细胞系中都有表达，其中DR5在所有肿瘤细胞系中的表达水平均显著高于DR4（P＜0．05）。而能够竞争性与TRAIL诱导的凋亡反应的诱骗受体DcR1和DcR2，在所有的肿瘤细胞中都呈低水平表达或不表达。结论 DR5可能在TRAIL诱导凋亡的通路中发挥最重要的作用。TRAIL死亡受体和诱骗受体在肿瘤细胞系中的表达具有差异性，这种差异性可在一定程度上解释不同细胞对TRAIL诱导凋亡的敏感度。     

退行性变腰椎间盘中基质细胞衍生因子1的表达及意义

背景：目前腰椎间盘退行性变确切的发病机制并不十分清楚。炎症参与腰椎间盘退行性变的发病机制,基质细胞衍生因子1属于趋化因子家族成员,与炎症有关。 目的：检测腰椎间盘退行性变患者椎间盘中基质细胞衍生因子1的表达水平,分析其与病情严重程度的关系。 方法：选取84例腰椎间盘退行性变患者和28例椎体爆裂性骨折患者,收集2组患者术后的椎间盘组织,用酶联免疫吸附的方法测定椎间盘中基质细胞衍生因子1的表达水平。根据Schneiderman标准进行分级,分析椎间盘中的基质细胞衍生因子1水平与疾病分级的关系。 结果与结论：与椎体爆裂性骨折患者相比,腰椎间盘退行性变患者的腰椎间盘组织中基质细胞衍生因子1水平明显升高,差异有显著性意义(P < 0.01)。Schneiderman 4级的患者椎间盘组织中基质细胞衍生因子1水平明显高于Schneiderman 2级和3级的患者,而Schneiderman 3级的患者椎间盘组织中基质细胞衍生因子1水平明显高于2级患者。另外,Spearman相关分析也显示,基质细胞衍生因子1的蛋白水平与Schneiderman分级呈正相关(r=0.412, P < 0.01)。提示腰椎间盘退行性变患者椎间盘中基质细胞衍生因子1的表达增高,与疾病严重程度呈正相关,可能参与了腰椎间盘退行性变的发病机制。     

MCP-1在腰椎间盘突出症髓核中的表达及临床意义

目的 研究单核细胞趋化蛋白-1(MCP-1)在突出的腰椎间盘髓核组织中的表达及其临床意义.方法 应用半定量RT-PCR和免疫组织化学法检测48例突出的腰椎间盘(实验组)和10例正常腰椎间盘(对照组)髓核组织中MCP-1 mRNA和蛋白的表达.结果 MCP-1在实验组中的表达明显高于对照组(P<0.01);在实验组中,后外层纤维环破裂型MCP-1的表达明显高于后外层纤维环完整型(P<0.01).结论 在腰椎间盘突出症的病理生理过程中,MCP-1可能是一个重要的炎性调节因子,在突出的椎间盘组织周围炎性反应中发挥重要的始动作用.     

甲状腺癌中肿瘤坏死因子相关凋亡诱导配体及其受体的表达

目的　研究肿瘤坏死因子相关凋亡诱导配体 (TRAIL)和肿瘤坏死因子相关凋亡诱导配体受体(TRAILR)在甲状腺癌中的表达及意义。　方法　采用免疫组织化学方法 ,检测 5例正常甲状腺、13例乳头状甲状腺癌、3例滤泡状甲状腺癌和 12例甲状腺癌旁组织中TRAIL和TRAILR的表达和分布。　结果　乳头状、滤泡状甲状腺癌组织和正常甲状腺组织中的甲状腺滤泡细胞均表达TRAIL和全部的TRAILR ,其中诱捕受体TRAILR4在正常甲状腺组织和甲状腺癌旁组织表达较弱。　结论　甲状腺癌组织中的甲状腺滤泡细胞表达TRAIL和全部的TRAILR ,提示癌变的甲状腺滤泡细胞通过自身表达TRAIL ,以自分泌或旁分泌的形式和其死亡受体TRAILR1、TRAILR2结合 ,诱导癌变的甲状腺滤泡细胞发生凋亡 ,诱捕受体TRAILR3、TRAILR4的存在也不能影响其对TRAIL诱导的细胞凋亡的敏感性     

退行性变椎间盘组织中TGF-β1和Bax的表达及意义

目的探讨退行性变椎间盘组织中TGF-β1和Bax的表达及其意义。方法收集正常与退变椎间盘组织,并根据病理改变将退变椎间盘组织分成4级,采用HE、免疫组化、TUNEL染色和RT-PCR法进行研究。结果免疫组化和RT-PCR均显示在正常组织中有TGF-β1表达,Bax只有微量表达;在病变组织中随病理分级加大TGF-β1随之增加,与正常组相比,差异有显著性;Bax也逐步增加,与正常组相比,差异有显著性,Bax表达升高与凋亡指数(AI)呈正相关性。结论退变椎间盘的病理分级与TGF-β1的表达增高相关,由此调控了Bax的表达,导致了细胞凋亡,促进了椎间盘的退变。     

Role of growth differentiation factor-5 and bone morphogenetic protein type II receptor in the development of lumbar intervertebral disc degeneration

The present study was designed to evaluate the role of growth differentiation factor-5 (GDF-5) and bone morphogenetic protein type II receptor (BMPR-II) in the development of lumbar intervertebral disc degeneration (IDD). A total of 24 patients with lumbar IDD (experiment group) and 6 patients with lumbar vertebral fracture (control group) were enrolled in the study. Tissue samples of IVD from the experiment group and control group were obtained during lumbar fusion operation, respectively. Fixation and decalcification of IVD tissue were performed, and then HE staining was carried out to observe the morphological changes of the lumbar IVD tissues. The expression of GDF-5 and BMPRII in human lumbar IVD was detected by immunohistochemical staining. HE staining results showed that non- and minimal degeneration was found in 11 cases (score range, 0-3), moderate degeneration in 12 cases (score range, 4-8), and severe degeneration in 7 cases (score range, 9-12). According to the immunohistochemical results, the positive expression rates of GDF-5 and BMPRII in NP were higher than those in AF of the non- and minimal degeneration group, moderate degeneration group and severe degeneration group (all P < 0.05). However, no significant difference in GDF-5 or BMPRII positive expression was observed among the normal, non- and minimal, moderate and severe degeneration groups in neither NP area nor AF area (all P > 0.05). In conclusion, our results showed that GDF-5 and BMPRII expressed both in normal and degenerated IVD tissues, and GDF-5 might have an inhibition effect on degenerated lumbar IVD, suggesting that gene therapy may be a useful approach in producing physiological effects during early- and late-phase of lumbar IDD.     

DcR1 expression in endometrial carcinomas

The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family, which mediates apoptosis by the extrinsic pathway. Up-regulation of decoy receptors, DcR1 and DcR2, may result in diminished binding of TRAIL to their functional receptors. DcR1 expression was assessed in normal endometrial tissue (NE) and endometrial carcinoma (EC) samples by immunohistochemistry (IHC) and quantitative real-time polymerase chain reaction (PCR). IHC was performed in two tissue microarrays; one composed of 80 samples of NE and a second one constructed from paraffin-embedded blocks of 62 EC. For quantitative real-time RT-PCR analysis, RNA was obtained from 19 NE and 28 EC samples using Trizol®. mRNA expression of DcR1 was assessed with Taqman®-based assays in an Abi-Prism 700 SDS. Results were correlated with stage, histological type, and grade. By IHC, cytoplasmic expression of DcR1 was frequently seen in NE (79.6%) and varied according to the menstrual cycle. Positive DcR1 immunostaining was also detected in EC (98.1% of the cases) without any specific statistical association with histological type, grade, and stage. By quantitative real-time PCR, all NE had similar levels of DcR1expression (0.8–1.7 RQ), which were considered the basal levels of DcR1 expression in NE. Increased DcR1 expression (≥5-fold higher than the basal levels) was detected in 13 of 28 EC (46.4%). High DcR1 expression levels were found in ECs of different stages: IA, four of 12 (33%); IB, two of four (50%); IC, four of six (66%); and IIA and IIB three of six (50%). Results suggest that DcR1 expression occurs in a subset of EC and may contribute to resistance to TRAIL-induced apoptosis.     

DcR3 对肝纤维化动物模型的影响

目的:研究DcR3 基因对肝纤维化大鼠的预防性治疗的作用。方法:SPF 级健康雄性Wistar 大鼠30 只,体重范围180 ~220 g,随机分为3 组,每组10 只,分别为正常对照组、DcR3 基因预防性治疗组(1% DMN+DcR3 组)、造模组(1%DMN 组)。采用1%DMN 诱导大鼠肝纤维化模型,腹腔注射DcR3 质粒进行预防性干预。分别采用HE 染色和Masson 染色观察肝组织病理情况;qRT-PCR 和Western blot 法检测DcR3、Fas、FasL、-SMA 和TGF-1 的mRNA 和蛋白表达水平。结果:与模型组相比,DcR3 预防治疗组大鼠肝组织炎性细胞浸润及胶原类物质沉积有所改善;DcR3 基因可显著降低肝纤维化大鼠Fas、FasL、 SMA 和TGF-1 mRNA 和蛋白表达水平,DcR3 基因预防性治疗组与对照组和造模组有显著性差异(P<0.05);同时DcR3 基因预防性治疗组DcR3 mRNA 和蛋白表达水平显著升高(P<0.05)。结论:DcR3 基因可有效防治大鼠肝纤维化,其作用机制可能是DcR3 通过降低肝脏炎症反应,减少胶原类物质沉积,抑制 SMA 和TGF-1 表达,从而抑制HSC 活化;下调Fas和FasL 表达,抑制Fas/ FasL 途径诱导的肝细胞凋亡。     

Apoptosis resistance in ulcerative colitis: high expression of decoy receptors by lamina propria T cells

Intestinal mucosa is constantly exposed to normal environmental antigens. A significant number of intestinal mucosal T cells are being deleted through apoptosis. In contrast, T cells from inflamed mucosa of ulcerative colitis patients did not undergo apoptosis. In this study, we determined whether the apoptosis of normal mucosal T cells was induced by antigen receptor stimulation and further determined pathways that mediated the apoptosis. Freshly isolated lamina propria T cells were stimulated with CD3 mAb and apoptosis was determined by Annexin V staining. Normal mucosal T cells underwent apoptosis upon CD3 mAb stimulation whereas the T cells from inflamed mucosa did not. The apoptosis in normal T cells was blocked by TRAIL-R1:Fc and an inhibiting CD95 antibody. Interestingly, decoy receptor (DcR)1, DcR2, and DcR3 that compete with death receptor (DR)4/5 and CD95 were highly expressed by the T cells from inflamed mucosa, but much lower by T cells from normal mucosa. Our data suggest that normal mucosal T cells are constantly deleted in response to environmental antigens mediated through DR4/5 and CD95 pathways and mucosal T cells from ulcerative colitis resist to undergoing apoptosis due to highly expression of DcR1, DcR2, and DcR3.     

Expression of TRAIL (TNF-related apoptosis-inducing ligand) and its receptors in normal colonic mucosa,adenomas, and carcinomas

Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis in tumour cell lines. Four membrane-bound receptors for TRAIL have been identified, two apoptosis-mediating receptors, DR4 and DR5, and two apoptosis-inhibiting receptors, DcR1 and DcR2. The aim of this study was to examine the role of TRAIL and its receptors in colorectal cancer development. The immunohistochemical expression and localization of TRAIL and its receptors were investigated in normal mucosa (n=10), adenomas (n=19), and carcinomas (n=21). Correlations between the expression of TRAIL and its receptors and the degree of apoptosis (assessed by M30 expression) and histopathological characteristics were explored. TRAIL and its receptors were expressed in normal mucosal epithelium. Expression of the receptors was seen in adenomas and carcinomas. TRAIL expression was lost in a subset of colorectal tumours, more frequently in carcinomas than in adenomas (p<0.05). DR4 and DR5 staining was stronger in neoplastic cells than in normal cells and was accompanied by a higher degree of apoptosis. No differences were found between tumour and normal cells regarding DcR1 and DcR2 expression. No correlations were found between TRAIL or TRAIL receptor expression and histopathological characteristics. In conclusion, marked changes were seen in the course of the adenoma-carcinoma sequence with respect to the expression of TRAIL and TRAIL receptors DR4 and DR5. The stronger expression of DR4 and DR5 in neoplastic cells than in normal cells, together with a higher degree of apoptosis, suggests a possible functional role for these receptors in apoptosis induction in neoplastic colorectal cells.     

头针及整脊治疗腰椎间盘突出症髓核大小的改变

背景：临床上通过一定的方法可减少突出椎间盘内容、降低椎间盘内压的效果,使已突出的间盘组织还纳或复位。 目的：观察腰椎间盘突出物髓核治疗前后大小的变化情况。 方法：随机将60例腰椎间盘突出症患者按就诊先后顺序随机数字抽签法均分为头针组、整脊组、头针合整脊组,进行不同手法的治疗。另取同期健康体检人群20例设为正常对照组。观察各组患者椎间盘突出髓核经治疗后能否回纳。 结果与结论：与正常对照组比较,其他3组治疗前突出髓核的大小差异有非常显著性意义(P < 0.01);3组治疗前后突出髓核的大小比较,差异无显著性意义(P > 0.05);3组疗效比较,差异亦无显著性意义(P > 0.05)。结果证明3种手法治疗腰椎间盘突出症对椎间盘突出髓核的回纳无明显作用。     

肝细胞癌中DcR3表达与癌细胞凋亡的关系研究

目的探讨诱捕受体3（decoy receptor 3,DcR3）蛋白在原发性肝细胞癌（HCC）中的表达及其与癌细胞凋亡和HCC预后的关系。方法应用免疫组织化学（EnVision法）及和脱氧核糖核酸末端转移酶介导的缺口末端标记（TUNEL）技术检测43例HCC,16例非癌肝组织（单纯性肝硬化及肝血管瘤周围正常肝组织）中DcR3蛋白的表达及凋亡情况,并分析其与临床病理参数的关系。结果DcR3明确定位于肝细胞胞质内;HCC组织中的DcR3蛋白的阳性率为74．42％（32／43）,明显高于非癌肝组织43．75％（7／16,P〈0．05）;HCC中有转移癌组DcR3阳性率为100％（22／22）,明显高于无转移组52．94％（9／17,P〈0．01）;DcR3蛋白的表达与AFP水平（r=0．444,P〈0．01）、门静脉癌栓（r=0．414,P〈0．01）有关,与年龄、性别、有无肝硬化、包膜浸润、肿瘤结节数及分化程度无关（P〉0．05）。HCC中细胞凋亡指数[AI（0．78±0．64）％]明显低于非癌肝组织[（3．32±1,81）％,P〈0．01];HCC临床TNM分期Ⅰ、Ⅱ期AI（1．03±0．69）％高于Ⅲ、Ⅳ期[（0．52±0．48）％,P〈0．01];HCC无转移组AI（1．10±0．72）％高于转移组[（0．44±0．27）％,P〈0．01];AI与AFP水平（r=-0．468,P〈0．01）、门静脉癌栓（r=-0．434,P〈0．01）、包膜浸润（r=-0,331,P〈0．05）有关,与年龄、性别、有无肝硬化、肿瘤结节数及分化程度无关（P〉0．05）。在HCC和非癌肝组织中,DcR3阳性者的AI均分别低于阴性者的AI（均P〈0．01）。结论DcR3表达可影响凋亡并在HCC的发生发展中起重要作用;检测DcR3蛋白与AI有助于判断HCC患者预后。     

神经肽Y/降钙素基因相关肽在腰椎间盘中的分布与共表达

背景：研究发现,神经肽Y与降钙素基因相关肽在交感神经节中有共存现象。 目的：观察神经肽Y/降钙素基因相关肽在正常腰椎间盘的共分布及在突出腰椎间盘髓核组织中的共表达。 方法：从10例尸体中收集完整的腰椎间盘,在另10例尸体中收集腰椎间盘髓核组织作为对照组。收集30例有症状的腰椎间盘突出症患者,其中L4/5或L5/S1需行腰椎间盘髓核摘除,取出髓核组织作为实验组。 结果与结论：①正常椎间盘组织中神经肽Y/降钙素基因相关肽荧光双标染色阳性的神经纤维较多的分布于椎间盘纤维环外1/3,但在椎间盘内2/3及髓核中未见或少量分布。②髓核的共表达,神经肽Y/降钙素基因相关肽荧光双标染色神经纤维的阳性率实验组均高于对照组(P < 0.05)。提示在正常腰椎间盘组织中神经肽Y/降钙素基因相关肽分布于纤维环外1/3部分,在纤维环内2/3部分及髓核组织未分布,但在突出椎间盘髓核组织中有大量的神经肽Y/降钙素基因相关肽共表达。     

合并移行椎腰椎间盘突出症患者腰骶神经根支配区的变化

背景:腰骶移行椎是一种常见的先天脊柱畸形,国内外学者均有报道移行椎患者的腰骶神经根支配I区可能会发生改变,但并未系统阐述其支配区的变化以及该种改变对腰椎间盘突出症患者手术的指导意义。目的:探讨当存在腰骶移行椎时,腰骶神经根的运动和感觉支配区发生改变的可能性。方法:研究方案的实施符合滨州医学院附属医院对研究的相关伦理要求,参与试验的患病个体及其家属对试验过程完全知情同意。回顾分析321例单一节段腰椎间盘突出症行手术治疗患者的病历资料。其中38例(11.8%)存在腰骶移行椎,包括骶椎腰化26例、腰椎骶化12例。26例骶椎腰化患者中,23例为L5/S1(L6)椎间盘突出,压迫S1(L6)神经根。12例腰椎骶化患者中,8例为L3/4椎间盘突出,压迫L4神经根。在283例正常结构的患者中,138例患者L5/S1椎间盘突出压迫S1神经根,95例患者L4/L5椎间盘突出压迫L5神经根,47例患者L3/L4椎间盘突出压迫L4神经根。比较术前骶椎腰化患者S1神经根受压的症状、腰椎骶化患者L4神经根受压的症状与正常腰骶椎患者L4、L5或S1神经根受压的症状。结果与结论:(1)S1神经根受压所致运动功能减退的分布在骶椎腰化患者组和正常组之间差异有显著性意义(P<0.05);(2)L4神经根受压所致运动功能减退的分布在腰椎骶化患者组和正常组之间差异有显著性意义(P<0.05);(3)骶椎腰化患者S1神经根受压所致的运动功能减退与正常状态下L5神经根受压所致的运动功能减退相似;而腰椎骶化患者L4神经根受压所致的运动功能减退与正常状态下L5神经根受压所致的运动功能减退相似;皮肤感觉异常的分析也显示了相似的结果;(4)结果说明,腰骶神经根的功能在移行椎患者中发生改变,使得骶椎腰化患者的S1神经根起到L5神经根的通常功能(神经根功能上移),腰椎骶化患者的L4神经根起到L5神经根的通常功能(神经根功能下移)。     

DcR3-TL1A signalling inhibits cytokine-induced proliferation of rheumatoid synovial fibroblasts

Decoy receptor?3 (DcR3), a member of the tumour necrosis factor receptor (TNFR) superfamily, lacks the transmembrane domain of conventional TNFRs in order to be a secreted protein. DcR3 competitively binds and inhibits members of the TNF family, including Fas?ligand (FasL), LIGHT and TL1A. We previously reported that TNFα-induced DcR3 overexpression in rheumatoid synovial fibroblasts (RA-FLS) protects the cells from Fas-induced apoptosis and that DcR3 induces VLA-4 expression in THP-1 macrophages to inhibit cycloheximide-induced apoptosis. Meanwhile, recent studies have suggested that DcR3 acting as a ligand directly induces the differentiation of macrophages to osteoclasts. Therefore, in the present study, we analyzed the direct effects of DcR3 as a ligand in RA-FLS. The experiments showed that DcR3 binds to TL1A expressed in RA-FLS resulting in the negative regulation of cell proliferation induced by inflammatory cytokines. DcR3-TL1A signalling may be involved in the pathogenesis of rheumatoid arthritis (RA).