VEGF对缺血/再灌注损伤胰腺细胞凋亡的影响

目的 研究血管内皮生长因子(VEGF)对缺血/再灌注损伤胰腺组织细胞凋亡的影响.方法 将雄性sD大鼠30只随机分为3组(n=10),A组为假手术组,B组为缺血/再灌注损伤组,C组为缺血/再灌注损伤+VEGF反义寡核苷酸组.通过血管夹阻断大鼠腹腔干及肠系膜上动脉30 min,然后去除血管夹再灌注6 h,建立大鼠胰腺缺血/再灌注损伤模型.对各组胰腺组织进行VEGF免疫组化染色及TUNEL法细胞凋亡检测.结果 缺血/再灌注损伤后胰腺组织出现细胞凋亡,同时VEGF蛋白表达上调.缺血/再灌注损伤+VEGF反义寡核苷酸组的胰腺组织VEGF蛋白表达较缺血/再灌注损伤组显著减少(P<0.05),前者细胞凋亡指数较后者明显升高(P<0.05).结论 VEGF能抑制缺血/再灌注损伤胰腺细胞凋亡,可能对胰腺缺血再灌注损伤具有保护作用.     

系膜细胞来源的白细胞介素-13对系膜细胞细胞因子基因表达的研究(英文)

目的　白细胞介素 1 3(IL 1 3)是新近发现的一种抗炎性细胞因子 ,其在肾小球肾炎中的作用尚不清楚 ,该研究探讨脂多糖 (LPS)对体外培养的人肾小球系膜细胞 (HMC)表达IL 1 3作用以及IL 1 3对HMC促炎性细胞因子、趋化因子和促纤维化因子基因表达的影响。方法　体外培养HMC ,加入不同浓度的LPS和 (或 )IL 1 3后 ,用逆转录 -聚合酶链反应和ELISA检测HMCIL 1 3mRNA表达和细胞培养上清液中IL 1 3蛋白含量 ;应用核酸酶保护法检测HMC肿瘤坏死因子 α(TNF α)、白介素 - 1α(IL 1α)、白介素 - 1 β(IL 1 β)、单核细胞趋化蛋白 1(MCP 1 )、白介素 8(IL 8)、转化生长因子 - β1 (TGF β1 )mRNA的表达。 结果　未予LPS刺激的HMC不表达IL 1 3mRNA和蛋白 ;LPS呈剂量依赖性和时间依赖性诱导HMC表达IL 1 3mRNA和分泌IL 1 3蛋白。HMC受LPS刺激后 1 2h即可表达IL 1 3mRNA ,4 8h达高峰 ,72h仍维持在较高的水平。HMC受LPS刺激后 2 4h ,其培养上清液中检测到IL 1 3蛋白 ,4 8h和 72h进一步增加。外源性IL 1 3呈剂量依赖性地抑制LPS诱导的系膜细胞TNF α ,IL 1α ,IL 1 β ,MCP 1 ,IL 8,TGF β1mRNA的表达。应用抗IL 1 3抗体中和内源性IL 1 3后 ,上述炎症因子表达增强。结论　IL 1 3是HMC自分泌因子。IL 1 3可抑制LPS诱导     

Late-onset epilepsy and occult cerebrovascular disease

The interface between cerebrovascular disease (CVD) and epilepsy is complex and multifaceted. Late-onset epilepsy (LOE) is increasingly common and is often attributed to CVD, and is indeed associated with an increased risk of stroke. This relationship is easily recognizable where there is a history of stroke, particularly involving the cerebral cortex. However, the relationship with otherwise occult, subcortical CVD is currently less well established yet causality is often invoked. In this review, we consider the diagnosis of LOE in clinical practice—including its behaviour as a potential mimic of acute ischemic stroke and transient ischemic attack; evidence for an association between occult CVD and LOE; and potential mechanisms of epileptogenesis in occult CVD, including potential interrelationships between disordered cerebral metabolism and perfusion, disrupted neurovascular unit integrity, blood–brain barrier dysfunction, and inflammation. We also discuss recently recognized issues concerning antiepileptic drug treatment and vascular risk and consider a variety of less common CVD entities associated with seizures.     

Immunohistochemical localization of basic fibroblast growth factor in choroid plexus of the rat

Abstract

In the present study, we report that an intense bFGF-immunoreactivity has been detected in the choroid plexus of the brain ventricles of adult rats. These results suggest that epithelial choroid plexus cells may be the source of the cerebrospinal fluid bFGF. [Neurol Res 1994; 16: 310-312]     

Analysis of the KRT9 Gene in a Mexican Family with Epidermolytic Palmoplantar Keratoderma

Epidermolytic palmoplantar keratoderma (EPPK), an autosomal‐dominant genodermatosis, is the most frequently occurring hereditary palmoplantar keratoderma. EPPK is characterized by hyperkeratosis of the palms and soles. Approximately 90% of patients present with mutations in the KRT9 gene, which encodes for keratin 9. Many of these mutations are located within the highly conserved coil 1A region of the alpha‐helical rod domain of keratin 9, an important domain for keratin heterodimerization. The objective was to assess the clinical and molecular characteristics of a Mexican family with EPPK. The clinical characteristics of members of this family were analyzed. The KRT9 gene of affected members was polymerase chain reaction amplified from genomic DNA and sequenced. All affected members of the family had hyperkeratosis of the palms and soles with knuckle pads. The R163W mutation in the KRT9 gene was present in all affected individuals who were tested. Although R163W is the most frequent KRT9 mutation in patients with EPPK, only two families have been reported with knuckle pads associated with this mutation. Our findings indicate that knuckle pads can be associated with EPPK and the R163W mutation in a family with a genetic background different from that described here.