外直肌超常量后徙固定在知觉性外斜视手术中的应用

目的 观察外直肌超常量后徙固定在知觉性外斜视手术中的远期疗效,分析其应用价值.方法 回顾性分析我科2012年5月至2013年9月行外直肌超常量后徙固定的知觉性外斜视病例12例.外斜视度数均＞50△,患眼固视功能差.在斜视眼行外直肌超常量后徙固定(缝合于原肌止点后12.0 mm)联合内直肌缩短术(4.0～7.0 mm),观察术后眼位、眼球运动、眼面外观及视功能远期疗效.结果 随访13 ～ 27个月后,12例患者术后眼位正位,眼球外转稍有受限;眼面外观良好;均获得较稳定的患眼固视能力,但未建立明确的双眼视功能.结论 外直肌超常量后徙固定稳定了后徙外直肌的位置,减少了手术肌肉条数,具有安全可行、远期疗效稳定等优点.     

骨髓间充质干细胞对球囊损伤的大鼠颈总动脉内皮修复的影响

目的 研究骨髓间充质干细胞对球囊损伤的大鼠颈总动脉内皮修复的影响.方法 球囊损伤24只SD大鼠颈总动脉,建立动脉内皮损伤模型,随机分为:(1)治疗组12只SD大鼠,球囊损伤颈总动脉即刻注射1 mL骨髓间充质干细胞溶液;(2)对照组12只SD大鼠,球囊损伤颈总动脉即刻注射1 mL磷酸盐缓冲液.14 d及28 d后,取颈总动脉标本作组织病理切片,行苏木精伊红及血管内皮生长因子受体2、α-平滑肌肌动蛋白免疫组化染色.结果 用苏木精伊红染色观察新生内膜的厚度,14 d及28 d治疗组血管内膜增生均较对照组轻(14 d时0.57±0.06 cm比1.09±0.06 cm,P<0.05;28 d时0.43±0.09 cm比4.72±0.15 cm,P<0.05);用血管内皮生长因子受体-2免疫组化染色观察内皮化程度,治疗组血管内皮细胞覆盖程度高于对照组(14 d时70.8%±1.3%比20.4%±1.1%,P<0.05;28 d时90.2%±1.3%比10.7%±0.4%,P<0.05),治疗组可见血管内皮生长因子受体-2/5-溴脱氧尿核苷双阳性细胞约占血管内皮生长因子受体-2单阳性细胞的50%.α-平滑肌肌动蛋白免疫组化染色观察平滑肌细胞浸润积分,14 d时治疗组平滑肌细胞浸润1.5分,对照组2分;28 d时两组分别为1分和3分.结论 骨髓间充质干细胞可减轻新生内膜增生,加快损伤血管的内皮化进程,减少平滑肌细胞浸润,从而促进球囊损伤的大鼠颈总动脉内皮完整性修复.     

平滑肌细胞源性生长因子的部分纯化

本文用超滤和肝素亲和层析法对培养的兔主动脉平滑肌细胞的无血清条件培养基进行纯化。用３Ｈ－ＴｄＲ掺入细胞ＤＮＡ法检测层析所得各组分对ＮＩＨ３Ｔ３纤维母细胞的致有丝分裂活性。用ＮａＤｏｄＳＯ４－聚丙烯酰胺凝胶电泳及等电聚焦电泳检测其分子量及等电点。结果表明，该条件培养基经肝素亲和层析，被１．０～１．６ｍｏｌ·Ｌ＇ＮａＣｌ洗脱下来的蛋白质成分对３Ｔ３细胞有致有丝分裂活性，其分子量范围为２３．０～２６．９ｋＤａ，等电点约为４．６。这些生物化学特性不同于ＰＤＧＦ、ＩＧＦ及ＦＧＦ，提示这种致有丝分裂蛋白质可能是一种独立的生长因子。     

上皮钙黏蛋白、雌激素受体α在子宫内膜癌变过程中的表达

目的探讨上皮钙黏蛋白(E-cadherin)、雌激素受体α(ERα)在子宫内膜癌变过程中的表达及临床意义。方法应用免疫组化En Vision二步法检测28例不典型增生子宫内膜(AH)和55例子宫内膜样腺癌(EA)组织中E-cadherin、ERα蛋白表达,另设18例增殖期子宫内膜组织作对照组。结果 1对照组、AH组、EA组组织中Ecadherin蛋白异常表达率分别为5.6%(1/18)、35.7%和60%,ERα阳性率分别为72.2%、53.6%和45.5%,ERα表达强度逐渐减弱,组间比较差异显著(均P0.05)。2EA组中,E-cadherin蛋白表达与肿瘤侵犯肌层相关(P0.05),与患者月经状态、组织学分级、临床分期无关(P0.05);ERα蛋白表达与肿瘤组织学分级相关(P0.01),与患者月经状态、肌层浸润及临床分期无关(P0.05)。E-cadherin与ERα的表达呈正相关(P0.05)。结论 Ecadherin和ERα改变可能参与了子宫内膜癌变过程,在EA的发生、发展过程中二者可能具有某种协同作用。     

Tanshinone IIA attenuates interleukin-17A-induced systemic sclerosis patient-derived dermal vascular smooth muscle cell activation via inhibition of the extracellular signal-regulated kinase signaling pathway

OBJECTIVE:Salvia miltiorrhiza has long been used to treat systemic sclerosis. Tanshinone IIA, one of the phytochemicals derived from the roots of Salvia miltiorrhiza, exhibits multiple biological activities. The present study aimed to investigate whether tanshinone IIA has an effect on the interleukin-17A-induced functional activation of systemic sclerosis patient-derived dermal vascular smooth muscle cells.METHODS:Systemic sclerosis patient-derived dermal vascular smooth muscle cells were incubated with various dosages of tanshinone IIA in the presence of interleukin-17A or the serum of systemic sclerosis patients. Cell proliferation was assessed using Cell Counting Kit-8. The expression of collagen 1 and 3 in cells was evaluated by immunofluorescence. Cell migration was measured using a transwell assay. The expression of phospho-extracellular signal-regulated kinase was detected by Western blotting.RESULTS:Our data demonstrate that tanshinone IIA exerts an inhibitory effect on interleukin-17A-induced systemic sclerosis patient-derived dermal vascular smooth muscle cell proliferation, collagen synthesis and migration.CONCLUSION:These findings suggest that tanshinone IIA might serve as a promising therapeutic agent for the treatment of systemic sclerosis.     

Vascular smooth muscle cell in atherosclerosis

Vascular smooth muscle cells (VSMCs) exhibit phenotypic and functional plasticity in order to respond to vascular injury. In case of the vessel damage, VSMCs are able to switch from the quiescent ‘contractile’ phenotype to the ‘proinflammatory’ phenotype. This change is accompanied by decrease in expression of smooth muscle (SM)‐specific markers responsible for SM contraction and production of proinflammatory mediators that modulate induction of proliferation and chemotaxis. Indeed, activated VSMCs could efficiently proliferate and migrate contributing to the vascular wall repair. However, in chronic inflammation that occurs in atherosclerosis, arterial VSMCs become aberrantly regulated and this leads to increased VSMC dedifferentiation and extracellular matrix formation in plaque areas. Proatherosclerotic switch in VSMC phenotype is a complex and multistep mechanism that may be induced by a variety of proinflammatory stimuli and hemodynamic alterations. Disturbances in hemodynamic forces could initiate the proinflammatory switch in VSMC phenotype even in pre‐clinical stages of atherosclerosis. Proinflammatory signals play a crucial role in further dedifferentiation of VSMCs in affected vessels and propagation of pathological vascular remodelling.