不同民族冷适应水平的研究

冬季在乌鲁木齐市对维族(25名)、藏族(12名)和汉族(43名)战士及21名维族大学生的冷适应水平进行测试。以血浆CPK和FFA、尿中儿茶酚胺和VMA,以及左中指泡冰水20min的皮温作为指标。结果表明藏、维族战士的适应水平优于汉族战士及维族大学生。但进新疆2年以上的汉族战士与藏、维族问无明显差别,加强体力锻炼之后,可使某些生化指标得到改善。作者认为尿中儿茶酚胺和VMA由于测试方法简便,结果稳定,可考虑作为人群冷适应的评价指标。     

Neonatal and fetal exposure to trans-fatty acids retards early growth and adiposity while adversely affecting glucose in mice

Industrially produced trans-fatty acids (TFAs) consumed in Western diets are incorporated into maternal and fetal tissues and are passed linearly to offspring via breast milk. We hypothesized that TFA exposure in utero and during lactation in infants would promote obesity and poor glycemic control as compared with unmodified fatty acids. We further hypothesized that in utero exposure alone may program for these outcomes in adulthood. To test this hypothesis, we fed female C57/BL6 mice identical Western diets that differed only in cis- or trans-isomers of C18:1 and then aimed to determine whether maternal transfer of TFAs through pregnancy and lactation alters growth, body composition, and glucose metabolism. Mice were unexposed, exposed during pregnancy, during lactation, or throughout pregnancy and lactation to TFA. Body weight and composition (by computed tomography) and glucose metabolism were assessed at weaning and adulthood. Trans-fatty acid exposure through breast milk caused significant early growth retardation (P < .001) and higher fasting glucose (P = .01), but insulin sensitivity was not different. Elevated plasma insulin-like growth factor-1 in mice consuming TFA-enriched milk (P = .02) may contribute to later catch-up growth and leanness and preserved peripheral insulin sensitivity observed in these mice. Mice exposed to TFA in utero underwent rapid early neonatal growth with TFA-free breast milk and had significantly impaired insulin sensitivity (P < .05) and greater abdominal fat (P = .01). We conclude that very early catch-up growth resulted in impaired peripheral insulin sensitivity in this model of diet-related fetal and neonatal programming. Trans-fatty acid surprisingly retarded growth and adiposity while still adversely affecting glucose metabolism.     

非动脉炎性AION中缺血部位及水肿程度对中心视力的影响

目的 :探讨非动脉炎性前部缺血性视神经病变 (nonarteriticanteriorischemicopticneuropathy ,NAION)中视盘水肿程度、缺血部位对中心视力的影响 ,以利于疗效评定及预后判断。方法 :2 40例NAION患者 (160例接受住院治疗 )的临床资料 ,结合视野和荧光眼底血管造影 (fundusfluoresceinangiography ,FFA)检查进行治疗前中心视力与水肿程度、缺血部位两方面统计分析 ,并分析治疗效果。结果 :2 40例NAION患者发病时中心视力的损害程度 ,依视盘缺血部位、水肿程度之不同而均有显著的差异 (P <0 0 0 5 )。 160例住院患者 ,视盘水肿消退时间最长为 3 5天 ,最短 11天 ,平均时间 2 1 5天 ,FFA复查四项指标改善率 88 1% ,中心视力两行行上者 10 4例 ,占 65 %。结论 :视盘的缺血部位及水肿程度是影响NAION中心视力的重要因素之一 ,积极针对性的治疗对防止NAION致盲有重要意义。     

前部缺血性视神经病变诊断要点探讨

目的：报告19例22眼前部缺血性视神经病变的多种临床表现，探讨本病诊断要点。方法：应用眼底血管荧光造影和静态定量视野检查的方法，探讨多种改变形式。结果：视盘荧光充盈延缓和视盘荧光充盈缺损为造影主要表现；半盲，象限盲或扇形视野缺损为视野主要改变。结论：本病我发于50岁以上老年患者，其诊断主要依据较有特点的发病史，眼底血管荧光造影和视野改变特点来判断。及时诊断与治疗有利于本病的恢复。     

非酒精性脂肪性肝病发生中Perilipin和ADRP表达变化实验研究

目的：探讨高脂饮食诱导大鼠非酒精性脂肪性肝病（NAFLD）形成过程中，肝组织Perilipin（脂滴包被蛋白）和ADRP（脂肪分化相关蛋白）的表达变化及意义。方法：建立大鼠高脂饮食NAFLD模型并设正常对照组，观察时间点为建模后4w、8w和12w，观察大鼠肝组织病理变化，检测血浆游离脂肪酸及甘油三酯水平，免疫组织化学染色法检测肝组织中Perilipin和ADRP蛋白水平。结果：成功制作大鼠NAFLD实验模型，与正常组相比，NAFLD组大鼠血浆FFA水平和TG水平从第4w起显著升高（P〈0．01），NAFLD组大鼠肝组织Perilipin蛋白表达水平显著低于正常组（P〈0．01），ADRP蛋白表达水平显著高于同期正常组（P〈0．01）。Perilipin及ADRP表达与FFA及TG具有显著相关性。结论：高脂饮食可制作NAFLD大鼠模型，Perilipin和ADRP与NAFLD的形成有关。     

The Mechanism of Action of Clofibrate and Tetranicotinoylfructose (Bradilan) on the Kinetics of Plasma Free Fatty Acid and Triglyceride Transport in Type IV und Type V Hypertriglyceridaemia

Abstract. The kinetics of plasma free fatty acid and triglyceride transport were assessed in 20 patients with idiopathic hypertriglyceridaemia. These patients were subdivided according to lipoprotein pattern into Type IV and Type V patients. The effects of clofibrate therapy on plasma free fatty acid and triglyceride kinetics were assessed in these patients. Clofibrate produced a marked reduction in serum triglyceride associated with a significant reduction in triglyceride turnover as well as enhancement of triglyceride clearance. The reduction in triglyceride concentration produced by clofibrate was found to correlate with the reduction in free fatty acid turnover indicating that this drug decreased the availability of free fatty acid turnover indicating that this drug decreased the availability of free fatty acids for hepatic esterification. Clearance of endogenous plasma triglyceride was markedly enhanced in those patients in whom it was markedly impaired before treatment. – Having discontinued clofibrate for six weeks the same patients received bradilan (tetranicotinoylfructose) and kinetic measurements were repeated. It was evident that bradilan had a greater hypotriglyceridaemic effect than clofibrate in both groups of patients. The effect of bradilan was the result of inhibition of free fatty acid turnover and consequently a marked reduction in triglyceride turnover. Bradilan, unlike clofibrate, did not affect the mechanisms responsible for the clearance of plasma triglycerides.     

Sterol regulatory element-binding protein-1c knockdown protected INS-1E cells from lipotoxicity

Objective: The reduction in insulin secretory capacity and β-cell mass has been attributed, at least partially, to lipotoxicity, which may contribute to the development of type 2 diabetes. Chronic free fatty acids (FFA) exposure impairs pancreatic β-cell function and induces β-cell apoptosis. This study is to elucidate the underlying molecular mechanisms.
Research design and methods: We exposed INS-1E pancreatic β-cell line to palmitate or oleate, and measured the glucose stimulated insulin secretion (GSIS). The effect of FFA on sterol regulatory element-binding protein (SREBP)-1c lipogenic pathway, and expression of genes involved in β-cell functions, including AMPK (AMP-activated protein kinase), UCP-2 (uncoupling protein-2), IRS-2 (insulin receptor substrate-2), PDX-1 (pancreatic duodenal homeobox-1), GLUT-2 (glucose transporter-2) and B cell lymphoma/leukaemia-2 (Bcl-2) were investigated. Apoptosis of these exposed cells was determined by MitoCapture, Annexin V-Cy3 or terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay. Cell lipid accumulation was measured by oil red O staining or TG extraction. Also SREBP-1c expression knockdown were used.
Results: FFA treatment resulted in SREBP-1c overexpression, impaired GSIS, lipid accumulation, apoptosis of INS-1E cells. In addition, the expression of lipogenic genes and UCP-2 were upregulated, but AMPK, IRS-2, PDX-1, GLUT-2 and Bcl-2 were downregulated in the exposed cells. However, these lipotoxic effects of FFA were largely prevented by induction of a SREBP-1c small interfering RNA.
Conclusions: These data suggest a strong correlation between FFA treatment and SREBP-1c activation in INS-1E cells. SREBP-1c might be a major factor responsible for β-cell lipotoxicity, and SREBP-1c knockdown could protect INS-1E cells from lipotoxicity, which is implicating a therapeutic potential for treating diabetes related to lipotoxicity.     

Identification of a possible role for atrial natriuretic peptide in MDMA-induced hyperthermia

MDMA (3,4-methylenedioxymethamphetamine) induces thermogenesis in a mitochondrial uncoupling protein 3-dependent manner. There is evidence that this hyperthermia is mediated in part by the lipolytic release of free fatty acids, that subsequently activate uncoupling protein 3 in skeletal muscle mitochondria. We hypothesize that atrial natriuretic peptide (ANP), a strong lipolytic mediator, may contribute to the induction and maintenance of MDMA-induced thermogenesis. The specific aims of this study were to (1) determine if ANP is released following MDMA administration, and (2) use the ANP receptor antagonist, Anantin, to ascertain the role of ANP in MDMA-induced hyperthermia. ANP levels were measured in plasma at baseline, 10, 20, 30 and 60 min following MDMA (40 mg/kg, sc) administration in 16 male Sprague-Dawley rats. A robust increase in ANP was seen within 10 min of MDMA administration. ANP levels returned to baseline at 20 min and then gradually rose over the 60 min monitoring period. The administration of Anantin (40 mg, ip), 15 min before and after MDMA, significantly attenuated the MDMA-induced hyperthermia. We conclude that ANP signaling contributes to the hyperthermia induced by MDMA.     

氩激光治疗中心性浆液性脉络膜视网膜病变疗效观察

目的：观察氩离子激光治疗中心性浆液性脉络膜视网膜病变的疗效。方法：对89例（93只眼）的中浆病人行氩激光治疗,根据眼底荧光造影检查,喷出型者36只眼,圆点扩大型者57只眼。结果：93只眼均达到临床治愈,其中激光一次治愈91只眼,二次治愈2只眼,无并发症发生。结论：氩激光是治疗中心性浆液性脉络膜视网膜病变安全有效的方法。