EGFR、p53在db/db自发性糖尿病小鼠颌下腺的表达

目的 观察表皮生长因子受体（EGFR）、p53在糖尿病小鼠颌下腺中的表达。方法 选取3、4、6、8、10月龄db／db糖尿病小鼠及相应月龄的db／＋m正常小鼠颌下腺。应用HE染色及免疫组织化学方法染色后进行图像分析，统计EGFR、p53在颌下腺组织内表达的细胞阳性率。结果 随着糖尿病的发展，颌下腺组织出现腺叶萎缩及实质细胞排列不整齐，堆集呈簇。纤维及血管增多；EGFR、p53在对 照组及糖尿病组颌下腺中均有表达。其细胞阳性率随月龄增大均呈增高趋势。且糖尿病组显著高于对照组。结论 ①db／db糖尿病可导致颌下腺组织萎缩及实质细胞形态学改变。②EGFR、p53表达增多。说明糖尿病时EGFR作为多效应受体，可能被激活从而诱导了颌下腺的细胞凋亡；p53表达的上升。提示随着糖尿病发展，颌下腺实质细胞有凋亡趋势。     

纤溶酶相关蛋白在冠心病患者中的表达

目的:了解冠心病患者是否存在组织型纤溶酶原激活物(t-PA)及纤溶酶原激活抑制物Ⅰ(PAI-Ⅰ)功能紊乱,以及这两个指标与血脂、胰岛素抵抗的相关关系。方法:选择2004年1月至2006年1月于我院住院就诊的冠心病患者作为观察对象。按临床类型分为SAP组、UAP组、AMI组、OMI组,并设健康对照组。检测t-PA、PAI-Ⅰ、胰岛素敏感性指数(IAI)、胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL)等指标。结果:(1)健康对照组t-PA高于各型冠心病组(P<0.05),AMI组t-PA低于其余各型冠心病组(P<0.05);健康对照组PAI-Ⅰ低于各型冠心病组(P<0.05),AMI组PAI-Ⅰ高于其余各型冠心病(P<0.05)。(2)t-PA与IAI呈正相关,与TC、TG、LDL呈负相关;PAI-Ⅰ则与IAI呈负相关,与TC、TG、LDL呈正相关。(3)各病例组t-PA于治疗后有所升高,PAI-Ⅰ于治疗后有所下降(P<0.05)。结论:冠心病患者存在明显的纤溶功能紊乱,且以急性期为重,并且纤溶功能紊乱与胰岛素抵抗、血脂异常等因素有关。     

Polycystic Kidney Disease Re-evaluated: A Population-based Study

A genetic register of all known cases of autosomal dominantpolycystic kidney disease occurring in South and Mid-Wales hasbeen established. In a population of 2.1 million, 209 familieswith affected members were identified, 303 of whom are currentlyalive, 70 on renal replacement therapy. An additional 551 caseswould be predicted amongst family members at 50 per cent and25 per cent risk, giving an apparent prevalence of 1:2459 inthe general population. Five possible new mutations were seenwhere adults with phenotypic autosomal dominant polycystic kidneydisease had both parents alive, age > 55 years with no cystsvisible on ultrasound. The take-on rate for renal replacementtherapy increased during 1970–79 but has apparently reacheda plateau of 4.8 cases per million population per year overthe last 8 years, despite a rapidly increasing acceptance ofuraemic patients as a whole (72/10⁶/year in 1988–89).Considerably more patients with autosomal dominant polycystickidney disease aged over 50 years were started on treatmentin 1980–89 than in 1970–79, but the survival overallimproved with time. All cases of autosomal dominant polycystickidney disease reaching end-stage renal disease are now beingtreated, but the apparent clinical prevalence of this conditionin our region is less than half the supposed gene frequency,suggesting that undiagnosed cases have a benign prognosis.     

Inhalational anesthetics inhibit spreading depression: relevance to migraine

Cortical spreading depression (SD) has not been shown in the human neocortex by direct cortical recordings. However, animal studies suggest that cortical injury, such as that occurring during neurosurgical procedures, should result in the initiation of SD. It is possible that inhibition of SD by volatile anesthetic agents may partially explain the failure to observe SD in the human neocortex during surgery. This study examines the effect of the anesthetic agents α-chloralose, halothane, nitrous oxide and isoflurane on the initiation of cortical SD in the cat neocortex. SD was seen in 100% of cats anesthetized with α-chloralose ( n = 15), in 3 of 7 (42%) animals anesthetized with isoflurane ( p < 0.05, χ² with Yates correction) and none of the animals ( n = 4, 6 hemispheric preparations) anesthetized with halothane ( p < 0.005, χ² with Yates correction, halothane vs α-chloralose group). In all cases this inhibitory effect was reversible. In four animals the administration of nitrous oxide (66%) reduced the inspired concentration of isoflurane required to inhibit SD by 0.75%. This study suggests that halothane, and to a lesser extent isoflurane and nitrous oxide, protect against the initiation of cortical SD. This observation may partially explain why SD has not been demonstrated in human neocortex during surgery. Further studies are needed to determine if SD may occur under pathological conditions, such as during migraine with aura, where the cortex may be predisposed to SD.     

Propylene glycol-induced side effects during intravenous nitroglycerin therapy

Propylene glycol, an alcohol frequently used as a solvent in medical preparations, is considered non-toxic. We found that this solvent, used in a commercially available IV nitroglycerin solution, may cause hyperosmolality, hemolysis and lactic acidosis. The influence of kidney function as the main determinant in causing accumulation of this solvent and consequently hyperosmolality is emphasized. A review of the literature dealing with propylene glycol is given. The possible mechanisms of neurological disturbances occurring during IV nitroglycerin therapy are discussed.