人角质形成细胞Notch信号通路与转化生长因子β调控受体蛋白的作用

背景：在皮肤中受体蛋白酪氨酸磷酸酶kappa的调控至关重要,而转化生长因子β似乎是其调控的上游因子,既然Notch信号和转化生长因子β信号通道如此相关,那么Notch是不是也参加了转化生长因子β信号对受体蛋白酪氨酸磷酸酶kappa的调控呢？ 目的：探讨Notch信号通道在人角质形成细胞中对转化生长因子β调控受体蛋白酪氨酸磷酸酶kappa的作用的影响。 方法：在分别用Jagged-1激活和用Γ-分泌酶抑制剂抑制Notch信号通道后,加入转化生长因子β,同时设立对照组,用Real-time PCR测试人角质形成细胞中受体蛋白酪氨酸磷酸酶kappa mRNA表达量。 结果与结论：覆盖率为40%的角质形成细胞在加入了转化生长因子β后,受体蛋白酪氨酸磷酸酶kappa mRNA量在各时间点均高于对照组。在用Jagged-1激活Notch通道的角质形成细胞中,单独加入Jagged-1、转化生长因子β及两者都加入时均高于对照组(P < 0.05,P < 0.01)。在用γ-分泌酶抑制剂抑制Notch通道的角质形成细胞中,只加入转化生长因子β显著高于对照组(P < 0.01),只加入γ-分泌酶抑制剂和两者均加入时与对照组比较,差异无显著性意义(P > 0.05)。说明加入转化生长因子β导致角质形成细胞中受体蛋白酪氨酸磷酸酶kappa表达增加,而分别对Notch信号进行激活和抑制后发现,受体蛋白酪氨酸磷酸酶kappa信号分别显著增加和显著被抑制。所以在转化生长因子β升高受体蛋白酪氨酸磷酸酶kappa表达过程中Notch信号通道是非常重要且不可或缺的。     

乳腺肿块多级分形特征提取方法研究

乳腺肿块是女性的常发病,严重影响着女性健康。准确检测及定位乳腺图像中的肿块将大大提高乳腺疾病诊断的准确率。研究表明,肿块的组织结构、表面粗糙度等构成了肿块图像的纹理特征,是判别肿块的重要依据。本文提出了一种乳腺肿块多级分形特征提取方法,通过对可疑病变区域建立分形特征向量,实现了乳腺图像中腺体和肿块部分的特征提取及分析。结合支持向量机(SVM)分类方法,得出最终的诊断结果。对110幅乳腺图像进行分形特征向量提取和分类,肿块准确率达到90%。实验结果表明,本文提出的多级分形特征提取及判别方法能够有效提高乳腺肿块诊断的准确率,对乳腺肿块的早期诊断具有良好的效果。     

Atonal homolog 1 expression in lung cancer correlates with inhibitors of the Wnt pathway as well as the differentiation and primary tumor stage

Atonal homolog 1 (Atoh1) is crucial to the differentiation of many cell types and participates in tumorigenesis and progression. This study investigated the role of Atoh1 in lung cancer development and its correlation with key members of the Wnt pathway. We used immunohistochemistry to examine the expressions of Atoh1, β‐catenin, Axin, chibby, and Disabled‐2 (Dab2) in 118 samples of lung cancer. We also detected the cytoplasmic and nuclear expression of Atoh1 in lung cancer tissues using western blot. Atoh1 nuclear expression was negatively correlated with differentiation level (p = 0.004) and primary tumor stage (p = 0.044) of lung cancer. Nuclear Atoh1 expression was positively correlated with nuclear expression of chibby (p < 0.001) and Dab2 (p < 0.001). Cytoplasmic Atoh1 expression was positively correlated with the cytoplasmic expression of Axin (p = 0.028), chibby (p < 0.001), and Dab2 (p < 0.001). We conclude that the nuclear expression of Atoh1 was inversely correlated with the differentiation and primary tumor stage of lung cancers. The expression and localization of Atoh1 correlated with Axin, chibby, or Dab2. Atoh1 may be a potential therapeutic target for the inhibition of growth and progression of lung cancers.     

渐进式肌肉放松法对医学生考试焦虑的干预

目的探讨渐进式肌肉放松法(PMR)对医学生考试焦虑的干预成效,以期为学生心理健康教育工作提供有利的方法。方法利用焦虑自评量表筛查出我院2010级大学新生存在考试焦虑并自愿参加该研究的20名同学,对其实施渐进式肌肉放松法,在每天放松前后进行血压、心率、呼吸的测量,在干预进行2周后和4周后分别再次给予焦虑自评量表调查。结果①和干预前相比,干预2周和4周后,学生的焦虑情况有非常显著的差异(F=14.653,P<0.01),学生的焦虑得分明显降低;②干预前后的收缩压有显著的差异(F=4.145,3.905,P<0.05)收缩压值逐渐下降;③干预前后的舒张压有非常显著的差异(F=11.385,7.911,P<0.05)舒张压值逐渐下降;④干预前后的呼吸频率有显著的差异(F=17.837,4.395,P<0.05),呼吸频率逐渐下降,心理紧张主观感受改善明显。⑤干预前后的脉搏无显著性差异(F=2.033,3.158,P>0.05)。结论渐进式肌肉放松法能降低医学生考试焦虑程度,降低医学生的血压和呼吸频率。     

兰州地区孕中期产前筛查血清指标MoM值分析

目的分析兰州地区孕中期唐氏综合征（Down syndrome,Ds）筛查人群中位数分布并探讨其临床应用价值。方法采用时间分辨荧光分析法检测7172例妊娠14—20“周妊娠女性血清甲胎蛋白（alpha fetoprotein,AFP）和游离绒毛促性腺激素（free—beta human chorionic gonadotropin,Freeβ—HCG）的浓度。利用DS筛查风险评估软件（LifeCycle3．0,LC3．0）的MediansTool统计不同孕用AFP和Freeβ-HCG的人群中位数、体质量,对LC3．0的中位数方程、体质量校正方程系数进行修正。结果各孕周血清AFP中位数平均水平均比软件内嵌值低,而Freeβ-HCG中位数水平在孕17周前中位数高于软件内嵌值而孕17周后中位数则低于软件内嵌值。各体重血清AFP与软件内嵌值几乎吻合,而Freeβ-HCG中位数平均水平比软件内嵌值低。结论不同地区血清中位数的筛查切割值制定标准可能存在差异,有必要进一步建立本地区孕中期产前筛查人群中位数系统。     

复合肌肉动作电位与周围神经损伤程度的相关性研究

目的:分析45例腓总神经不全损伤患者复合肌肉动作电位（CMAP）的波幅、时程,探讨其与周围神经损伤程度的关系。方法 :选择2012年1月至2012年12月就诊于我院的45例不同程度腓总神经不全损伤患者,根据患者胫前肌肌力级别将45例患者分为三组（n=15）:胫前肌肌力4-5级（P₁组）、胫前肌肌力2-3级（P₂组）、胫前肌肌力1级（P₃组）。应用肌电诱发电位仪记录45例患者的CMAP波形,测量CMAP波幅与时程。采用SPSS13.0统计软件对数据进行秩和检验,分析各组间CMAP波幅与时程的差别。结果 :（1）P₁组、P₂组和P₃组腓总神经-胫前肌CMAP平均波幅分别为7.1±0.2mv、3.3±0.3mv和0.5±0.1mv;P₂组、P₃组与P₁组相比,波幅均有显著性差异（P<0.05）;P₃组与P₂组相比,波幅亦有显著性差异（P<0.05）。（2）P₁组、P₂组和P₃组腓总神经-胫前肌CMAP平均时程分别为11.4±0.4ms、16.9±0.6ms和23.3±1.2ms;P₂组、P₃组与P₁组相比,时程均有显著性差异（P<0.05）;P₃组与P₂组相比,时程亦有显著性差异（P<0.05）。结论 :（1）CMAP波幅、时程有助于评价周围神经受损的严重程度。（2）CMAP波幅降低提示有功能的周围神经轴突数量减少,时程延长反映了周围神经的脱髓鞘损害。     

Sdc1 Overexpression Inhibits the p38 MAPK Pathway and Lessens Fibrotic Ventricular Remodeling in MI Rats

Expression of the proteoglycan syndecan-1 (Sdc1) is increased in rats with myocardial infarction (MI). This study investigated the effects of Sdc1 overexpression on ventricular remodeling and cardiac function in MI and explored the possible mechanism through in vivo transfection of rats with recombinant adenovirus-carrying rat Sdc1 cDNA. Sprague–Dawley rats (n?=?48) underwent intramyocardial injection in the marginal zone of the infarcted area immediately after ligation of the left anterior descending artery. The rats were divided into four groups according to the solution injected: MI Ad-GFP-Sdc1 transfection group, MI Ad-GFP control group, MI saline group, and sham operation group. Cardiac function and collagen expression of each group were examined, and the roles of inflammation, apoptosis, and p38 MAKP signal transduction pathway were investigated. Compared with the rats in the sham operation group, ventricular weight and collagen content increased in MI rats, and cardiac function declined. Substantial inflammatory cell infiltration was seen in the marginal zone of the infarction area, and a great number of myocardial cells were apoptotic. The p38 MAPK signaling pathway was clearly activated. Rats in the MI Ad-GFP-Sdc1 transfection group showed decreased ventricular weight, reduced collagen synthesis, and significant improvement of ventricular remodeling and cardiac function. Post-MI inflammatory cell infiltration and apoptosis was reduced, and the p38 MAPK signaling pathway was inhibited. Overexpression of Sdc1 can improve post-MI ventricular remodeling, and it is possible that the improvement is achieved through reducing apoptosis and suppressing inflammatory response and through the p38 MAPK signal transduction pathway.     

经鼻及皮下给予睾丸酮/丙酸睾丸酮对大鼠相关脑区c-Fos表达效能的影响

目的:探讨经鼻和皮下给予睾丸酮(T)或丙酸睾丸酮(TP)对大鼠中枢神经系统相关脑区激活的效能.方法:利用放射免疫分析法检测大鼠经鼻滴注给予TP后脑脊液和血清睾丸酮浓度的变化;以免疫组织化学观察大鼠各脑区cFos的表达.结果:放射免疫结果显示去势组大鼠脑脊液和血清中睾丸酮含量比正常组降低;去势大鼠皮下注射TP后只增加了血清巾睾丸酮的含量,去势大鼠和正常大鼠经鼻给予TP后脑脊液和血清中睾丸酮的含量均明显增加;去势大鼠经鼻给予TP脑脊液巾睾丸酮的含量高于去势皮下注射TP组,而血清巾睾丸酮的含量低于去势皮下注射TP组.免疫组织化学结果显示正常大鼠鼻腔给予TP或睾丸酮增加大鼠多数脑区的c-Fos免疫反应阳性神经元数目和c-Fos免疫反应强度,而皮下注射TP只增加了少数脑区c-Fos免疫反应阳性神经元数目以及c-Fos免疫反应强度.结论:经鼻给予睾丸酮或TP后能够激活多数脑区c-Fos蛋白的表达,经鼻给予睾丸酮或TP的给药方式有可能成为治疗大雄激素低下导致的巾枢神经系统疾病的一种有效手段.     

Hyperhomocysteinemia Associates with Small Vessel Disease More Closely Than Large Vessel Disease

Background: Hyperhomocysteinemia was believed to be an independent risk factor for stroke and associate with small vessel disease (SVD) related stroke and large vessel disease (LVD) related stroke differently. However it''s still unclear which type of stroke associated with homocysteine (HCY) more strongly because the conclusions of previous studies were contradictory. In this study we focused on the subclinical angiopathies of stroke, i.e., SVD and LVD instead of stroke subtypes and sought to compare the associations between HCY level and different angiopathies. Methods: 324 non-stroke patients were enrolled. Sex, age, HCY level and other vascular risk factors were collected. MRI and angiographies were used to determine the type of angiopathies and their severity, i.e., the scores of leukoaraiosis (LA), plaques and numbers of silent brain infarctions (SBI). LVD was defined as the presence of atherosclerotic plaques of cerebral arteries. SVD was defined as the presence of either LA or SBI. 230 patients were deemed to have LVD; 180 patients were deemed to have SVD. Spearman''s correlation test and logistic regression were used to analyze the association between HCY level and different angiopathies. Results: The correlation between HCY level and scores of plaques was weaker than that of the scores of LA and numbers of SBI. Hyperhomocysteinemia was an independent risk factor for SVD (OR = 1.315, P <0.001), whereas the association between HCY level and LVD was not that significant (OR = 1.058, P = 0.075). Conclusion: HCY level associated with SVD more strongly than LVD.     

Different roles of PD-L1 and FasL in immunomodulation mediated by human placenta-derived mesenchymal stem cells

Mesenchymal stem cells (MSCs) derived from either bone marrow (BMSCs) or placenta (PMSCs) have the capacity to suppress immune responses to mitogenic and allogeneic stimulations. Both cell contact and soluble factor dependent mechanisms have been proposed to explain this immunosuppression. This study explored the roles of some of cell surface molecules expressed on human PMSCs (hPMSCs) in hPMSC mediated immunomodulation. hPMSCs strongly suppressed mitogen and allogeneic peripheral mononuclear cells (PBMCs) induced T cell activation and proliferation. hPMSCs constituently expressed programmed death-ligand 1 (PD-L1) and Fas ligand (FasL) molecules. Neutralising antibodies to-PD-L1 and FasL significantly reduced the suppressive effect of hPMSCs on T cell proliferation. However, only anti-PD-L1 antibody partially restored early T cell activation suppressed by hPMSCs. Anti-FasL antibody but not anti-PD-L1 antibody reduced apoptosis of activated T cell indicating that FasL molecule plays a role in inducing apoptosis of activated T cells, although overall hPMSCs diminished T cell apoptosis. Different effects of PD-L1 and FasL molecules on T cell activation and activated T cell apoptosis suggest that these two molecules influence T cell response at different stages. hPMSCs significantly prevented activated T cells from going into S phase. Both antibodies to PD-L1 and FasL had significant effect on reversing the effect of hPMSCs on cell cycles. hPMSCs reduced INF-γ but increased IL-10 production by mitogen activated T cells. Both antibodies partially abolished the effect of hPMSCs on INF-γ and IL-10 production. These data demonstrated that PD-L1 and FasL molecules play significant roles in immunomodulation mediated by hPMSCs. This study provides a rational basis for modulation of negative costimulators on hPMSCs to increase their immunosuppressive properties in their therapeutic applications.