Decreased GDNF mRNA expression in dorsal spinal cord of unilateral arthritic rat

It is now well established that nerve growth factor (NGF) plays a key role in inflammation-induced hyperalgesia. It was also reported that brain derived neurotrophic factor (BDNF), another member of neurotrophins, contributed to the pain pathway as a neurotransmitter in the CNS. The present work demonstrated a down-regulation of glial cell line-derived neurotrophic factor (GDNF) mRNA expression in dorsal spinal cord in complete Freund's adjuvant-induced unilateral arthritic rats serving as a chronic pain model. The fast occurring and long lasting down-regulations suggest that GDNF might contribute to pain pathway in a way different from neurotrophins and might play a role in the maintenance of chronic pain status.     

Interactions between spatial attention and global/local feature selection: an ERP study

The present study examined the interaction between spatial attention and global/local feature processing of visual hierarchical stimuli. Event-related brain potentials (ERPs) were recorded from subjects who detected global or local targets at attended locations while ignoring those at unattended locations. Spatial attention produced enhanced occipital P1 and N1 waves in both global and local conditions. Selection of local features enhanced posterior P1, N1 and N2 waves relative to selection of global features. However, the modulations of the P1 and N2 by global/local feature selection were stronger when spatial attention was directed to the left than the right visual fields. The results suggest neurophysiological bases for interactions between spatial attention and hierarchical analysis at multiple stages of visual processing.     

Myositis ossificans of the chest wall simulating malignant neoplasm

Myositis ossificans originating from the chest wall is extremely rare. We report a case of myositis ossificans occurring in a young woman with progressive painful swelling in the chest wall. Preoperative examination suggested a malignant neoplasm originating from soft tissue. Although rare, myositis ossificans is one of the potential causes of painful swelling in the chest wall, and can be mistaken for a malignant neoplasm.     

大鼠心肌缺血缺氧损伤核转录因子-κB与细胞间粘附分子-1的表达

目的　研究异丙肾上腺素致大鼠心肌损伤对心肌核转录因子 κB(NF κB)以及细胞间粘附分子 1(ICAM 1)表达的影响。方法　大鼠皮下注射异丙肾上腺素造成心肌坏死模型,测定血清乳酸脱氢酶(LDH)、肌酸磷酸激酶(CK)活力和丙二醛(MDA)含量,观察心肌坏死程度,免疫组化检测心肌NF κBp65蛋白的表达,Western蛋白质印迹杂交检测IκBα的蛋白质表达,半定量RT PCR检测ICAM 1mRNA含量。观察腹腔注射地塞米松后上述指标的变化。结果　大鼠给予异丙肾上腺素后,血清LDH、CK和MDA含量升高,心肌坏死,NF κBp65蛋白大量表达,IκBα蛋白质表达减弱,ICAM 1mRNA表达上升。地塞米松使升高的LDH、CK和MDA明显下降,减轻心肌坏死程度,显著抑制NF κBp65蛋白和ICAM 1mRNA表达,IκBα蛋白质表达增强。结论　儿茶酚胺大量释放引起的心肌缺血缺氧损伤中,NF κB和ICAM 1mRNA表达增加,表明抑制NF κB激活,减少ICAM 1mRNA的表达及炎性细胞因子产生是减少心肌缺血缺氧损伤的关键点之一。     

细菌对MLS类和糖肽类抗生素产生耐药性的作用机制

MLS类和糖肽类抗生素在人类与细菌感染性疾病的对抗中发挥着重要作用.与其他抗生素一样,随着这些抗生素的临床使用,细菌耐药性的出现和不断发展给人们带来新的挑战.本综述对这两类抗生素的细菌耐药性产生机制进行了剖析,并就已开发的若干个新型MLS类和糖肽类抗生素作了介绍.     

氯诺昔康与美施康定对照治疗肢体缺血性疼痛68例

目的:观察氯诺昔康治疗肢体缺血性疼痛的疗效和安全性.方法:在无用药禁忌的前提下,将68例肢体缺血性疼痛的患者随机分为氯诺昔康(可塞风)组和美施康定组,观察时间为12h,每半小时记录1次.结果:可塞风的缓解率为93.8%,与美施康定对照组(89.7%)无显著性差异;不良反应发生率17.6%(6 /34),与美施康定组比(41.2%)其差别有统计学意义(P＜0.05).结论:可塞风在治疗肢体缺血性疾病中安全且具良好疗效.     

海洛因依赖性人格概念的建构及其与心理健康的关系

目的:了解海洛因依赖性人格的概念结构,建立海洛因依赖性人格量表。方法:对10 5名海洛因戒除者的海洛因依赖性人格问卷的测试数据进行验证性因素分析。结果:(1)海洛因依赖性人格由海洛因渴求感和戒除效能感两个维度构成,二维模型对样本数据的拟合度较好;(2 )海洛因渴求感α=0 .86 6 ,戒断效能感α=0 . 92 3,所有项目与所属因素因子分的相关系数在0. 6 81- 0 . 876之间,P <0 .0 0 1,两个分量表的相关系数r =- 0 4 4 2 ,P <0 . 0 0 1;(3)海洛因渴求感和戒除效能感与自尊、孤独、抑郁的相关系数的绝对值在0 . 2 2 1- 0. 5 11之间,达到显著性水平;回归分析的结果显示,戒断效能感可解释自尊、孤独和抑郁14 . 4 %、10 . 8%和2 6 . 2 %的变异。结论:海洛因依赖性人格的概念的构想合理,其量表具有良好的项目区分度、内部一致性信度和效度。     

Induction of cell-cycle arrest by all-trans retinoic acid in mouse embryonic palatal mesenchymal (MEPM) cells.

all-trans retinoic acid (atRA), the oxidative metabolite of vitamin A, is essential for normal embryonic development. Also, high levels of atRA are teratogenic in many species and can effectively induce cleft palate in the mouse. Most cleft palate resulted from the failed fusion of secondary palate shelves, and maintenance of the normal cell proliferation is important in this process of shelf growth. To clarify the mechanism by which atRA causes cleft palate, we investigated the effect of atRA on proliferation activity and cell cycle distribution in mouse embryonic palatal mesenchymal (MEPM) cells. atRA inhibited the growth of MEPM cells by inducing apoptosis in a dose-dependent manner. atRA also caused a G1 block in the cell cycle with an increase in the proportion of cells in G0/G1 and a decrease in the proportion of cells in S phase, as determined by flow cytometry. We next investigated the effects of atRA on molecules that regulate the G1 to S phase transition. These studies demonstrated that atRA inhibited expression of cyclins D and E at the protein level. Furthermore, atRA treatment reduced phosphorylated Rb and decreased cdk2 and cdk4 kinase activity. These data suggest that atRA had antiproliferative activity by modulating G1/S cell cycle regulators and by inhibition of Rb phosphorylation in MEPM cells, which might account for the pathogenesis of cleft palate induced by retinoic acid.