纤维粘连蛋白和层粘连蛋白与子宫内膜异位症发病关系的研究

目的探讨纤维粘连蛋白（Fibronectin,FN）和层粘连蛋白（Laminin,LN）与子宫内膜异位症的关系。方法采用免疫组化方法分析了子宫内膜异位症患者异位内膜35例、在位内膜20例及对照组子宫内膜24例的FN和LN的表达变化。结果1.与对照组相比子宫内膜异位症异位内膜组FN、LN的表达均明显下降,差异有显著性（均为P〈0.05）;2.在位内膜组FN、LN的表达同样也呈明显下降,有显著性差异（FN,P〈0.01;LN,P〈0.05）。提示细胞外基质中FN、LN的表达减少与子宫内膜异位症的发生、发展有关。     

层粘连蛋白和纤维粘连蛋白在着床期小鼠子宫内膜中的表达

目的：为探讨层粘连蛋白和纤维粘连蛋白在胚泡着床过程中的生物学作用。方法：本实验使用昆明雌性小鼠30只,分为未孕和早期妊娠共6组。通过免疫组织化学方法,检测了层粘连蛋白和纤维粘连蛋白在着床期小鼠子宫内膜中的分布状况。结果：胚泡着床开始时（即受精后4－5天）,层粘连蛋白和纤维粘连蛋白均出现一个表达高峰,尔后纤维粘连蛋白迅速减少。受精后6－8天,细胞外基质中的层粘连蛋白逐渐增加。结论：层粘连蛋白和纤维粘连蛋白在胚泡着床微环境和植入调节中发挥重要作用。     

Survivin和CD44v6在子宫内膜异位症中的表达及意义

目的研究Survivin、CD44v6在卵巢子宫内膜异位症中的表达，以探讨二者与卵巢子宫内膜异位症发病的关系。方法用免疫组化S-P方法检测卵巢子宫内膜异位症31例异位内膜、5例在位内膜、15例正常内膜中Survivin和CD44v6的表达。结果Survivin蛋白在异位内膜中表达明显高于在位内膜、正常内膜（P〈0．05）；CD44v6蛋白在异位内膜组与增生期内膜比较有统计学意义（P〈0．05），与其他两组比较无统计学意义（P〉0．05）；二者的表达不随AFS分期的变化而变化；并且二者在卵巢子宫内膜异位症中的表达呈相关性（r=0．24），但无统计学意义（P〉0．05）。结论Survivin和CD44v6在卵巢子宫内膜异位症中的异常表达对卵巢子宫内膜异位症的发生及发展起着重要的作用.     

子宫内膜异位症相关卵巢癌的发病机制研究

子宫内膜异位症相关卵巢癌(EAOC)与其他类型卵巢癌相比,有发病年龄早,一般50岁左右,病变期别较早,且预后很好等特点,目前关于EAOC发病机制的研究尚未定论.但有专家提出,子宫内膜异位症(EMs)增加了卵巢子宫内膜样癌和透明细胞癌的发生风险.EAOC的发生可能与ARID1A、HNF、miRNAs等基因突变,雌激素和氧化应激等因素密切相关.     

CD38和CD138在子宫内膜异位症患者中的表达及意义

目的 检测子宫内膜异位症（EMs）患者子宫内膜组织中CD38、CD138的表达情况,探讨二者在EMs发病中的作用。方法 选取2020年7月至2021年7月于广西壮族自治区妇幼保健院妇科收治的育龄女性200例,其中通过检查确诊子宫内膜异位症患者100例作为观察组,排除子宫内膜异位症并需要行宫腔镜检查的育龄女性100例作为对照组。免疫组化实验检测两组患者子宫内膜组织中CD38和CD138的表达水平;酶联免疫吸附测定血清中辅助T细胞因子干扰素（INF）-γ、肿瘤坏死因子（TNF）-α、白介素（IL）-6和血管内皮细胞生长因子（VEGF）表达水平,同时检测外周血中炎症因子WBC、CRP、CA125数值。采用多因素Logistic回归方程分析EMs的相关影响因素,采用受试者操作特征（ROC）曲线分析CD38、CD138与INF-γ、IL-6、TNF-α、VEGF、WBC、CRP、CA125对EMs的预测价值。结果 观察组子宫内膜组织中CD38、CD138阳性比例,血清中TNF-α、IL-6、VEGF和外周血中WBC、CRP、CA125高于对照组（P<0.05）;血清中INF-γ低于对照组（...     

子宫内膜异位症与免疫的关系

子宫内膜异位症与免疫的关系山东省计划生育科研所（２５０００２）张丽凤山东医科大学附院妇产科李秀花李叔平审校子宫内膜异位症（ｅｎｄｏｍｅｔｒｉｏｓｉｓ）是较常见的妇科疾病，主要引起不孕、流产及痛经。１９７８年，美国生育协会根据腹腔镜检或剖腹探查术中所见...     

GnRHⅡ蛋白在子宫内膜异位症患者中的表达及意义

目的：检测GnRHⅡ蛋白在子宫内膜异位症患者异位子宫内膜、在位子宫内膜和正常子宫内膜中的表达情况,同时分析其表达是否与子宫内膜月经周期有关。方法：采用免疫组织化学SP法检测GnRHⅡ蛋白在异位内膜、在位内膜及正常子宫内膜组织中的表达情况,并分析和比较其表达是否有差异。结果：GnRHⅡ蛋白在子宫内膜异位症患者异位、在位子宫内膜及正常子宫内膜中均有表达,阳性表达定位于子宫内膜腺体及间质细胞的细胞质;GnRHⅡ蛋白在异位内膜、在位内膜及对照组正常内膜的表达依次增强,两两比较差异有统计学意义（P＜0.05）;GnRHⅡ蛋白在正常子宫内膜分泌期表达强于增生期（P＜0.05）,且以分泌早中期最强,显著强于增生期和分泌晚期（P＜0.01）,而异位组或在位组的分泌期与增生期比较,差异无统计学意义（P＞0.05）。结论：GnRHⅡ蛋白在子宫内膜异位症的发病中以及在人类月经生理方面可能起重要作用。     

层粘连蛋白在早孕小鼠子宫内膜中的表达

层粘连蛋白 (ＬａｍｉｎｉｎＬＮ)是细胞外基质中重要的大分子非胶原糖蛋白 ,由座落于基膜上的上皮细胞、内皮细胞及被基膜包绕的肌细胞、垂体细胞合成并分泌贮存于基质中。研究表明 ,ＬＮ与细胞膜表面受体结合后可产生多种生物学作用 ,如介导上皮细胞生长、增殖、分化 ,促进细胞粘附、辅展、移动 ,并在肿瘤细胞转移过程中起重要作用。有人曾用间接免疫荧光方法对小鼠早期胚胎进行研究 ,发现ＬＮ在桑椹胚和内细胞团及其滋养层均有较强的阳性反应 ,在外胚层与内胚层之间的细胞外基质中可见ＬＮ呈条带状荧光。但有关胚泡植入前后子宫内膜中Ｌ…     

Survivin与子宫内膜异位症的研究现状

Survivin是近年来新发现的一种凋亡抑制蛋白,与细胞分裂、增殖有关,具有高度的组织分布特异性和强大的抗凋亡功能。本文就其生物学特点及在子宫内膜异位症中的研究现状作一概述。     

细胞凋亡与子宫内膜异位症的关系

越来越多的证据表明,子宫内膜异位症患者与正常人子宫内膜存在许多不同之处,表现为内异症患者的子宫内膜细胞粘附、侵袭和血管形成能力明显增强,使之具有异位种植和生长的能力,在内异症的发生和发展中起重要作用。最近研究表明,子宫内膜细胞自发性凋亡减弱和对凋亡信号不敏感,可能是内膜细胞具有异位种植和生长能力的重要因素。本文将细胞凋亡在正常子宫内膜周期变化中的作用,以及对子宫内膜异位症发生发展的影响作一综述。     

骨质疏松性骨折骨痂软骨细胞CD44和纤连蛋白的表达

目的:探讨骨质疏松性骨折愈合过程中胞内信号因子CD44及其配体纤连蛋白(FN)在骨痂软骨细胞的表达情况。方法:建立SD大鼠骨质疏松性股骨骨折愈合模型作为实验组以及二期股骨骨折愈合模型作为对照组,分别于骨折后10、20、30d和40d取材,对骨痂进行H-E染色及CD44、FN免疫组织化学显色。结果:在骨痂组织中CD44和FN的表达及分布在时空上有一致性。在实验组中,随着骨折愈合进程的发展,软骨细胞CD44与FN的表达逐渐减少,而对照组中,CD44与FN共同表达于骨折愈合各阶段的各区软骨细胞中。结论:大鼠骨质疏松性骨折愈合过程中骨痂软骨细胞CD44、FN的表达明显弱于正常二期骨折愈合过程中的表达,提示CD44和FN在软骨细胞中表达的明显减少可能是造成骨质疏松性骨折骨痂软骨组织向骨组织演变缓慢的原因之一。     

非小细胞肺癌患者CD44及其变异体V6的测定

目的：探讨测定粘附分子CD44及其变异体V₆在非小细胞肺癌（non-smallcelllungcarcinoma, NSCLC）中的意义。方法：采用酶联免疫吸附试验检测血清中可溶性CD44S（sCD44S）和可溶性CD44V₆（sCD44V₆）含量;流式细胞术测定细胞表面CD44S、CD44V₆的表达。结果：NSCLC患者血清CD44S、CD44V₆水平明显高于肺良性疾病（P<0.05, P<0.01）。原发肺鳞癌（SCC）和腺癌（ADC）细胞的CD44S表达率明显高于对照组（P<0.01）;3组的CD44V₆表达率均低,差异无显著。NSCLC原发癌细胞表面CD44S、CD44V₆表达与其血清的可溶性含量之间均无相关性。结论：提示血清CD44S、CD44V₆水平可作为鉴别NSCLC和肺良性疾病的辅助指标。     

CD44 expression in benign and malignant nevomelanocytic lesions

CD44 is an integral membrane glycoprotein that is a principal receptor for hyaluronan and plays a role in cell-extracellular matrix interactions. Recent studies of melanomas in mouse models have suggested that increased CD44 expression by these tumors may relate to metastatic potential. Immunohistochemical expression of CD44 (standard [s] and variant [v6]) in benign and malignant nevomelanocytic lesions was assessed in formalin-fixed, paraffin-embedded tissue and was correlated with histological parameters and prognostic factors. Cases included benign nevi (three junctional, four compound, five intradermal, five blue, six Spitz, one deep penetrating), architecturally disordered (dysplastic) nevi (three, and primary (22) and metastatic melanomas (eight). All of the benign lesions showed diffuse and essentially uniform membrane staining of CD44s in nevomelanocytic cells, regardless of lesion size, depth, or extent of dermal involvement. In contrast, semiquantitative analysis (0 to 3+) of the primary melanomas showed heterogeneous and decreased staining of CD44s, which inversely correlated with lesion size (−0.569) and depth of invasion (−0.622 and −0.617 for Breslow's depth and Clark's level, respectively). These results were significant at P < .05. CD44s expression in metastases paralleled that of their respective primaries. None of the benign nevomelanocytic lesions showed CD44v6 staining. In contrast, all of the malignant nevomelanocytic lesions showed cytoplasmic staining of the tumor cells. Pretreatment with chondroitinase did not alter CD44s staining. CD44s expression by immunohistochemical determination is uniform in benign nevomelanocytic lesions. Malignant melanomas show decreased, heterogeneous staining that inversely correlates with increasing size, depth, and level of invasion. CD44 expression may be a prognostic indicator in malignant melanomas. Tumor staining with anti-chondroitin sulfate monoclonal antibodies suggests that CD44s may be expressed as a chondroitin sulfate proteoglycan in primary melanomas.     

Physical association between CD155 and CD44 in human monocytes

Regulation of CD44-mediated binding to hyaluronan is critical in normal and diseased immune cell function. In earlier work by others (Shepley and Racaniello, J. Virol., 68, 1301–1309), anti-CD44 mAb blocked poliovirus binding to CD155 (the poliovirus receptor) in HeLa cells, suggesting that CD155 and CD44 may be physically associated. Here, we present evidence that CD155 and CD44 are physically associated in human monocytes. In co-modulation experiments in U937 monocytic cells, CD155 and CD44 reciprocally co-modulated. In primary human monocytes, CD155 syn-capped with CD44. In immunofluorescence flow cytometric experiments, anti CD44 mAb inhibited up to 94% of binding by anti-CD155 mAb which blocks poliovirus binding to CD155. This inhibition was specific for CD155. Culturing monocytes increased the extent of inhibition. In addition, mAb against PRR2, a novel molecule that is related to CD155, was inhibited by anti-CD44 in a dose-dependent manner, but not by anti-CD14. These data support the interpretation that CD155 (and related proteins) are physically associated with CD44 on monocyte cell surfaces. Although the current study does not address functional significance, we speculate that this interaction may have a role in regulating monocyte CD44 ligand binding which may be critical in pathological processes such as tumor metastasis and arthritis.     

尼古丁对中性粒细胞活化及细胞间粘附分子基因表达的影响

目的:观察尼古丁对中性粒细胞(PMNs)的活化,PMNs与内皮细胞的粘附及内皮细胞表达ICAM-1mRNA,有助于阐明尼古丁在慢性阻塞性肺疾患(COPD)炎症发病中的作用。方法:测定β-葡萄糖醛酸苷酶及溶菌酶活性,以反映PMNs的活化;培养人脐静脉内皮细胞,观察PMNs与内皮细胞的粘附;制备探针,提取总RNA,Northern杂交测细胞间粘附分子-1(ICAM-1)mRNA。结果:尼古丁可活化PMNs,增加PMNs－内皮细胞粘附;增强ICAM-1mRNA表达,764-3可明显抑制尼古丁的上述作用。结论:尼古丁通过活化PMNs,促进PMNs－内皮细胞粘附,在COPD慢性炎症发病中起重要作用。而这种粘附作用的增加与粘附分子表达增强有关;抑制尼古丁的上述作用可能是764-3抗炎作用的部分机理。     

Integrin–fibronectin interactions at the cell-material interface: initial integrin binding and signaling

Integrin receptors mediate cell adhesion to extracellular matrices and provide signals that direct proliferation and differentiation. Integrin binding involves receptor–ligand interactions at the cell-substrate interface and assembly and reorganization of structural and signaling elements at the cytoplasmic face. Using a cross-linking/extraction/reversal method to quantify bound integrins, we demonstrate that the density of α₅β₁ integrin-fibronectin bonds increases linearly with ligand density, as predicted by simple receptor–ligand equilibrium. This linear relationship is consistent with linear increases in cell adhesion strength with receptor and ligand surface densities. Furthermore, we show that phosphorylation of FAK, a tyrosine kinase involved in early integrin-mediated signaling, increases linearly with the number of integrin–Fn bonds. These linear relationships suggest the absence of cooperative effects in the initial stages of mechanical coupling and adhesion-mediated signaling.     

丹参注射液对动脉粥样硬化大鼠血脂及细胞间粘附分子-1表达的影响

目的:研究丹参注射液对大鼠动脉粥样硬化(AS)的治疗作用及其作用机制。方法:采用高脂饲料加大剂量VitD₃复制大鼠AS模型,用全自动生化分析仪检测血清甘油三酯、总胆固醇含量。用Westernblot和RT-PCR方法分别检测动脉壁细胞间粘附分子-1(ICAM-1)蛋白及mRNA含量。结果:丹参注射液组大鼠血清甘油三酯、总胆固醇明显低于AS大鼠,丹参注射液组大鼠血管壁ICAM-1蛋白及mRNA的表达显著低于AS大鼠。结论:丹参注射液可抑制动脉粥样硬化大鼠血脂及ICAM-1蛋白及mRNA的表达。     

血清sCD44s及sCD44v6变化与乳腺癌的初步研究

目的:测定血清中sCD44s和sCD44v6含量并探讨其在乳腺癌中的临床意义。方法:用酶联免疫吸附试验(ELISA)检测38例乳腺癌患者及15例乳腺良性疾病患者和40例正常人血清中可溶性CD44s(sCD44s)和可溶性CD44v6(sCD44v6)的水平。结果:乳腺癌患者血清sCD44s和sCD44v6水平明显高于正常人和乳腺良性疾病患者(P＜0.01)。Ⅲ、Ⅳ期患者血清sCD44s和sCD44v6明显高于Ⅰ、Ⅱ期(P＜0.05);乳腺癌手术后1周sCD44v6明显低于手术前(P＜0.05),手术后2周sCD44v6更加明显(P＜0.01);手术后2周sCD44s明显低于手术前(P＜0.05)。结论:血清sCD44s和sCD44v6水平可作为诊断、治疗乳腺癌的辅助指标;乳腺癌血清中sCD44s和sCD44v6升高及降低与肿瘤负荷有关。     

Effects of injecting fibronectin and antifibronectin antibodies on cushion mesenchyme formation in the chick

Summary During heart development in the chick some of the endocardial cells that cover the cushion areas leave the cushion endocardium, seed the underlying cardiac jelly, and are transformed into mesenchyme. Cushion mesenchymal (CM) cells migrate from the endocardium toward the myocardium using the cardiac jelly as substratum. Developing cushions have been microinjected with fibronectin (FN), antifibronectin antibodies (AbFN), and four synthetic peptide probes. Two of these peptides (P7 and P10) contained the sequence Arg-GlyAsp-Ser (RGDS), while the other two (P15 and PColl) did not. Cushion area, individual cell area, cell density, cell orientation and a factor of form were evaluated in both experimental and control cushions. CM cell migration was inhibited by FN and AbFN, only partially inhibited by P10 and unaffected by P7. Cushions injected with P15 and PColl were unaffected. These results can be explained by steric modifications of the extracellular matrix, that may render cardiac jelly nonpermissive for CM cell migration, or by interaction of the substances injected at the endocardial cell surface. Migrating CM cells do not present any preferential orientation in any particular direction. CM cell migration seems to depend upon intrinsic migratory behaviour and the presence of FN at the CM cell surface. The enforcement of the direction of CM cell migration does not appear to rely upon matrix signals but be the result of randomly migrating cells becoming distributed more evenly in the matrix.Formerly at the Department of Anatomy, University of Chicago, Chicago, Illinois, USA