Where and what is the paralaminar nucleus? A review on a unique and frequently overlooked area of the primate amygdala

The primate amygdala is composed of multiple subnuclei that play distinct roles in amygdala function. While some nuclei have been areas of focused investigation, others remain virtually unknown. One of the more obscure regions of the amygdala is the paralaminar nucleus (PL). The PL in humans and non-human primates is relatively expanded compared to lower species. Long considered to be part of the basal nucleus, the PL has several interesting features that make it unique. These features include a dense concentration of small cells, high concentrations of receptors for corticotropin releasing hormone and benzodiazepines, and dense innervation of serotonergic fibers. More recently, high concentrations of immature-appearing cells have been noted in the primate PL, suggesting special mechanisms of neural plasticity. Following a brief overview of amygdala structure and function, this review will provide an introduction to the history, embryology, anatomical connectivity, immunohistochemical and cytoarchitectural properties of the PL. Our conclusion is that the PL is a unique subregion of the amygdala that may yield important clues about the normal growth and function of the amygdala, particularly in higher species.     

Association between statin use and all-cause mortality in cancer survivors,based on the Korean health insurance service between 2002 and 2015

Background and aimsCancer is the number one cause of death in Korea. This study aimed to investigate if statin use in cancer survivors was inversely associated with all-cause mortality.Methods and resultsData from the 2002 to 2015 National Health Insurance Service-National Health Screening Cohort (NHIS-HEALS) were used. The Kaplan–Meier estimator was used to estimate the survival function according to statin usage. Cox proportional hazards regression models were adopted after stepwise adjustment for potential confounders to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause mortality. The median follow-up duration was 10.0 years. Statin users had a higher percentage of diabetes and hypertension in both sexes. Survival rates of statin users were higher than non-users (p-values <0.001 in men and 0.021 in women). Compared to non-users, the HRs (95% CIs) of statin users for all-cause mortality were 0.327 (0.194–0.553) in men and 0.287 (0.148–0.560) in women after adjustment for potential confounding factors.ConclusionsStatin users in cancer survivors had higher survival rate than non-users in both sexes.     

附子多糖预防高胆固醇血症的作用及其对肝脏CYP7α-1表达的影响

目的: 探讨附子多糖(FPS)预防高胆固醇血症的作用及其对肝脏胆固醇7α-羟化酶(CYP7α-1)表达的影响。方法: SPF级雄性Wistar大鼠50只,体重100 g,随机分为正常组(control)、高胆固醇组(HC)和HC+附子多糖(HC+FPS)低、中、高3个剂量组,每组10只,分别给予正常、高胆固醇及高胆固醇加附子多糖(224、448和896mg·kg^-1·d^-1 )饮食,持续2周,检测各组的血脂水平;观察control组、HC组和HC+FPS(224 mg·kg^-1·d^-1)组大鼠的体重、进食量和粪便量的变化,实验结束后取3组大鼠的肝脏行HE染色;并检测3组大鼠肝脏羟甲基戊二酰辅酶A(HMG-CoA)还原酶mRNA水平、CYP7α-1 mRNA和蛋白水平以及粪便总胆汁酸含量等方面的改变。结果: 附子多糖能显著抑制高胆固醇血症大鼠血清中总胆固醇(TC)和低密度脂蛋白胆固醇(LDL-C)的水平(P<0.05);HC+FPS组大鼠肝细胞脂肪变性较HC组轻微;real-time PCR和Western blotting结果显示附子多糖能显著上调高胆固醇大鼠肝脏CYP7α-1 mRNA水平和蛋白表达并明显降低HMG-CoA还原酶的mRNA水平(P<0.01);HC组大鼠粪便中胆汁酸的含量增多而HC+FPS组进一步增加(P<0.05)。结论: 附子多糖具有明显的降血胆固醇作用,其机制与上调CYP7α-1 mRNA及蛋白水平和下调大鼠肝脏HMG-CoA还原酶mRNA水平有关。     

基础血脂水平对HMG—CoA还原酶抑制剂降脂作用的影响

目的　观察治疗前基础血脂水平对HMG CoA还原酶抑制剂降低血清总胆固醇 (TC)、低密度脂蛋白胆固醇(LDL C)以及血清甘油三酯 (TG)作用的影响。方法　分析1994～ 1999年期间进行的 3项多中心临床药物试验 :辛伐他汀试验 (16 6例 ,平均年龄 5 8 9岁± 9 2岁 ) ,洛伐他汀试验(146例 ,平均年龄 5 7 9岁± 8 7岁 ) ,阿伐他汀试验 (10 5例 ,平均年龄 5 7 8岁± 9 3岁 )。治疗前血清TC≥ 5 98mmol·L-1,血清TG≤ 4 5 2mmol·L-1。按治疗前基础血脂水平分组。分别口服辛伐他汀 10mg·d-1,疗程 8周 ;或洛伐他汀2 0mg·d-1,疗程 8周 ;或阿伐他汀 10mg·d-1,疗程 6周。结果　治疗前基础血清TC、LDL C以及TG水平越高 ,HMG CoA还原酶抑制剂降低相应血脂的作用越明显。辛伐他汀、洛伐他汀或阿伐他汀降低血清TC、LDL C以及TG的幅度分别与治疗前相应的基础血脂水平呈正相关。结论　HMG CoA还原酶抑制剂降低血脂的作用与治疗前相应的基础血脂水平有关     

微生物来源的胆固醇酰基转移酶抑制剂研究.菌株分类、发酵、分离和生物学特性

用大鼠肝微粒体酶系统筛选脂酰辅酶 A:胆固醇酰基转移酶 (ACAT)抑制剂 ,获得了一株阳性菌株 ,经初步分类鉴定为 Aspergillussp.H717。曲霉 H717的发酵液经溶媒提取 ,硅胶柱层析 ,葡聚糖 L H- 2 0凝胶柱层析和反相中压液相柱层析得到两个活性化合物 NA- 2 0 9A、B。用大鼠肝微粒体酶系统测定其 IC5 0 分别为 6 0 .6和 86 .7μmol/ L。     

石榴叶鞣质对高血脂高血糖模型动物脂代谢的影响

目的 :观察石榴叶鞣质对高脂模型鼠脂代谢的影响 ,以及体外对HMG CoA还原酶的抑制作用。方法 :造大鼠高脂模型 ,以四氧嘧啶诱导高血糖伴高血脂小鼠模型 ,检测TC、TG等生化指标 ;制备大鼠肝微粒体HMG CoA还原酶液 ,测 1min内A34 0nm的变化。结果 :石榴叶鞣质大中剂量 (15 0、75mg kg)对高脂大鼠的TC和TG具有显著的降低作用 ,大小剂量 (30 0、75mg kg)对高血糖伴高血脂小鼠的TC降低作用明显 ,体外抑制HMG CoA还原酶的最低有效浓度为 1× 10 - 6 g mL ,抑制率 15 16 %。结论 :石榴叶鞣质对高脂模型鼠脂代谢紊乱具有较好的调节作用 ,体外可较强的抑制HMG CoA还原酶活性。     

Lipidstatus und basale Steroidhormonspiegel nach 16 Wochen Lovastatintherapie bei primärer Hypercholesterinämie

Summary We examined the effect of a 16 week therapy with the HMG CoA reductase inhibitor lovastatin in 29 patients (mean age 43 years) with primary hypercholesterolemia. All patients had cholesterol levels above 250 mg/dl (mean 348 ±96 mg/dl) inspite of a lipid lowering diet and a therapy with conventional lipid lowering drugs during a three month screening period. After 4 weeks on placebo 20 mg lovastatin was given orally for 4 weeks. If total cholesterol exceeded 200 mg/dl the dose of lovastatin was increased monthly by 20 mg up to the maximal dose of 80mg/day. After 16 weeks lipid values changed compared with the placebo period: total-cholesterol –25%, triglycerides –8.6%, LDL-cholesterol –31%, APO B –25%, HDL-cholesterol +5.8%, APO AI +0.8%, total-cholesterol/HDL-cholesterol –25%. There was a significant improvement of lipid parameters after lovastatin therapy compared with conventional lipid lowering drugs at the end of the screening period. Lovastatin was well tolerated. A small and reversible rise of transaminases and/or creatinine kinase was observed in 6 patients. Basal levels of ACTH in the morning increased significantly during lovastatin therapy within the normal range. This observation was more frequent in females (10/12) than in males (10/ 17).

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Abkürzungen HMG Co A 3-Hydroxy-3-Methyl-Glutaryl-Coenzym A - TChol Gesamtcholesterin - LDL low density lipoprotein - HDL high density lipoprotein - TG Triglyceride - APO AI/B Apolipoprotein AI/B - ACTH Adrenocorticotropes Hormon Diese Publikation enthält Ergebnisse des Dissertationsarbeit von Frau Angela Bink.     

Brain prostaglandin formation is increased by α-synuclein gene-ablation during global ischemia

We have previously demonstrated that α-synuclein (Snca) gene ablation reduces brain arachidonic acid (20:4n − 6) turnover rate in phospholipids through modulation of endoplasmic reticulum-localized acyl-CoA synthetase activity. Although 20:4n − 6 is a precursor for prostaglandin (PG), Snca effect on PG levels is unknown. In the present study, we examined the effect of Snca ablation on brain PG level at basal conditions and following 30 s of global ischemia. Brain PG were extracted with methanol, purified on C₁₈ cartridges, and analyzed by LC–MS/MS. We demonstrate, for the first time, that Snca gene ablation did not affect brain PG mass under normal physiological conditions. However, total PG mass and masses of individual PG were elevated ∼2-fold upon global ischemia in the absence of Snca. These data are consistent with our previously observed reduction in 20:4n − 6 recycling through endoplasmic reticulum-localized acyl-CoA synthetase in the absence of Snca, which may result in the increased 20:4n − 6 availability for PG production in the absence of Snca during global ischemia and suggest a role for Snca in brain inflammatory response.