神经调节蛋白（neuromodulin）

神经调节蛋白是一种神经组织特异性的钙调素结合蛋白,与钙调素结合有反Ｃａ＾２＋依赖性。它与突触的可靠性、神经生长和再生有关。本简述其分离纯化、结构与功能以及ｃＤＮＡ克隆与表达等方面的研究现状。     

神经调节中的新概念：神经递质与调质

一、神经调节物——递质和调质 (一)神经化学传递——历史的回顾自20年代初,在Otto Loewi应用蛙心灌流,为神经的化学传递奠定基础以后的半个世纪里,大量的研究工作揭示了乙酰胆碱(ACh)和去甲肾上腺素(NE)在外周神经传递中的作用。首先是运动神经对横纹肌的支配,由于是神经末梢同肌纤维之间的点对点联系,其作用既迅速又精确,是由在神经肌接头处释放的ACh,在以毫秒计的时间内跨越突触间隙,作用于突触后受体,引起离子通道的启闭而实现的。其次是交感神经末梢释放NE,副交感释放ACh对平滑肌和腺体分泌的支配。由于缺乏点对点的直接联系,其作用较慢而持久。如此,ACh和NE在很长一段时间里基本概括了一切已     

"神经调节"备考复习随想

以“神经调节”单元的备考复习为例,探讨高三生物学的系统复习阶段,教师应如何确定单元复习目标,重组单元课题内容和设计单元复习方案,从而将培养学生科学素养的理念落到实处。     

脂肪组织的神经调控概况

脂肪组织是重要的代谢器官,也是内分泌器官,其生理功能的稳定执行依赖于神经系统的调控.中枢神经系统起源的交感神经同时支配棕色脂肪组织和米色脂肪细胞,调控分解代谢,进行能量消耗.虽然棕色脂肪组织中副交感神经的存在和生理功能还未明确,但是啮齿类动物白色脂肪组织中的副交感神经调控合成代谢,维持能量储存.同时,脂肪组织中还可能存...     

肠道菌群在肥胖发病中的作用

近十年来,肠道菌群在人类许多疾病发病机制中的潜在作用引起了人们的广泛关注。已被证实肠道菌群与肥胖和肥胖相关的代谢性疾病的发生发展密切相关。与肥胖相关的肠道微生物可调控宿主的能量代谢、胰岛素抵抗和脂肪组织堆积,这些在肥胖发生中都起着至关重要的作用。本综述重点介绍了代谢紊乱中肠道菌群组成的变化以及肠道菌群在肥胖发病机制中的作用,包括能量代谢、中枢食欲、免疫系统和宿主昼夜节律。在不久的将来,该领域的研究将为治疗肥胖及其并发症开辟新的途径。     

茶及其多酚类化合物调节肥胖及并存症的研究进展

肥胖是备受全球关注的健康问题,主要表现在机体营养代谢失衡和脂肪积累。多项研究表明茶及其多酚类化合物具有降脂减肥、改善代谢、保护肝脏、降血压、降血糖等多种生理功能。本综述总结十年来有关茶及其多酚类化合物调节肥胖及并存症的研究,归纳出调节机理,主要包括调节食欲、减少能量摄入、促进脂质代谢和产热、抑制脂质生成和积累、调节肠道微生物、介导炎症及免疫反应。本综述在分析前人研究成果的基础上,为茶叶功能成分研究提供了新的研究思路和方向,有利于茶产品开发及应用推广。     

“神经调节与体液调节的关系”的教学设计

“神经调节与体液调节的关系”一节内容,人教版和苏教版教材都有安排,但侧重点有所不同。这需要教师从课程标准的角度去分析教材的内涵,从新的层面去发掘知识的内在联系。     

“神经调节”的简笔画复习设计

通过"简笔画"分析法,充分借助形象思维,最大限度地挖掘学生的思维潜力,从而使学生的理解能力、获取信息能力、综合应用能力、探究能力等各方面能力得以提高。通过借图读表,学生掌握神经调节的最基本结构——反射弧的结构特点、功能;通过过程图,学生掌握并理解兴奋在神经纤维上的传导;通过对突触的简笔画分析,学生掌握兴奋在神经元之间的传递特点;再借助相应高考题针对性的评析及训练,学生不仅掌握了知识,获得了能力,而且在潜移默化中养成了借助适当的方法解决生物学问题的良好习惯。     

神经反馈调节失衡与帕金森病(Parkinson's desease)

机体的各种组织、器官和系统能维持正常的生理功能,离不开各种形式的反馈调节,这些调节包括神经调节,体液调节和局部的自身调节。机体生理活动的调节在分子、细胞和系统的各种水平都存在,而且每种反馈调节都必须得到精确控制,否则将会引起各种疾病。帕金森病的产生就是大脑有关脑区兴奋和抑制的反馈调节失衡造成的,它为我们理解生命活动过程中的反馈调节机制提供了一个极为典型的有重要价值的模型。[第一段]     

Molecular genetics of human obesity: A comprehensive review

Obesity and its related health complications is a major problem worldwide. Hypothalamus and their signalling molecules play a critical role in the intervening and coordination with energy balance and homeostasis. Genetic factors play a crucial role in determining an individual's predisposition to the weight gain and being obese. In the past few years, several genetic variants were identified as monogenic forms of human obesity having success over common polygenic forms. In the context of molecular genetics, genome-wide association studies (GWAS) approach and their findings signified a number of genetic variants predisposing to obesity. However, the last couple of years, it has also been noticed that alterations in the environmental and epigenetic factors are one of the key causes of obesity. Hence, this review might be helpful in the current scenario of molecular genetics of human obesity, obesity-related health complications (ORHC), and energy homeostasis. Future work based on the clinical discoveries may play a role in the molecular dissection of genetic approaches to find more obesity-susceptible gene loci.     

Ghrelin: a new peptide regulating growth hormone release and food intake

Ghrelin, identified as an endogenous ligand for the growth hormone secretagogue receptor, is a 28 amino acid peptide hormone possessing an unusual octanoyl group on the serine in position 3, crucial for its biological activity. Ghrelin is predominantly produced by the stomach but also by many other tissues such as pituitary, hypothalamus, duodenum, jejunum, ileum, colon, lung, heart, pancreas, kidney, and testis. In addition to stimulation of GH release, ghrelin stimulates appetite and food intake, enhancing fat mass deposition and weight gain. Besides these main actions, ghrelin regulates gastric motility and acid secretion, exerts cardiovascular and anti-inflammatory effects, modulates cell proliferation and influences endocrine and exocrine pancreatic secretion, as well as glucose and lipid metabolism. Therefore, ghrelin agonists and antagonists might be valuable for some clinical aspects.     

Beyond the metabolic role of ghrelin: a new player in the regulation of reproductive function

Ghrelin is a gastric peptide, discovered by Kojima et al. (1999) [55] as a result of the search for an endogenous ligand interacting with the “orphan receptor” GHS-R1a (growth hormone secretagogue receptor type 1a). Ghrelin is composed of 28 aminoacids and is produced mostly by specific cells of the stomach, by the hypothalamus and hypophysis, even if its presence, as well as that of its receptors, has been demonstrated in many other tissues, not least in gonads. Ghrelin potently stimulates GH release and participates in the regulation of energy homeostasis, increasing food intake, decreasing energy output and exerting a lipogenetic effect. Furthermore, ghrelin influences the secretion and motility of the gastrointestinal tract, especially of the stomach, and, above all, profoundly affects pancreatic functions. Despite of these previously envisaged activities, it has recently been hypothesized that ghrelin regulates several aspects of reproductive physiology and pathology. In conclusion, ghrelin not only cooperates with other neuroendocrine factors, such as leptin, in the modulation of energy homeostasis, but also has a crucial role in the regulation of the hypothalamic–pituitary gonadal axis. In the current review we summarize the main targets of this gastric peptide, especially focusing on the reproductive system.     

Global analysis of cellular protein translation by pulsed SILAC

Current methods for system‐wide gene expression analysis detect changes in mRNA abundance, but neglect regulation at the level of translation. Pulse labeling with stable isotopes has been used to measure protein turnover rates, but this does not directly provide information about translation rates. Here, we developed pulsed stable isotope labeling by amino acids in cell culture (pSILAC) with two heavy isotope labels to directly quantify protein translation on a proteome‐wide scale. We applied the method to cellular iron homeostasis as a model system and demonstrate that it can confidently identify proteins that are translationally regulated by iron availability.     

Adrenal medullary function and expression of catecholamine-synthesizing enzymes in mice with hypothalamic obesity

The mechanisms underlying the onset of obesity are complex and not completely understood. An imbalance of autonomic nervous system has been proposed to be a major cause of great fat deposits accumulation in hypothalamic obesity models. In this work we therefore investigated the adrenal chromaffin cells in monosodium glutamate (MSG)-treated obese female mice. Newborn mice were injected daily with MSG (4 mg/g body weight) or saline (controls) during the first five days of life and studied at 90 days of age. The adrenal catecholamine content was 56.0% lower in the obese group when compared to lean controls (P < 0.0001). Using isolated adrenal medulla we observed no difference in basal catecholamine secretion percentile between obese and lean animals. However, the percentile of catecholamine secretion stimulated by high K+ concentration was lower in the obese group. There was a decrease in the tyrosine hydroxylase enzyme expression (57.3%, P < 0.004) in adrenal glands of obese mice. Interestingly, the expression of dopamine beta-hydroxylase was also reduced (47.0%, P < 0.005). Phenylethanolamine N-methyltransferase expression was not affected. Our results show that in the MSG model, obesity status is associated with a defective adrenal chromaffin cell function. We conclude that in MSG obesity the low total catecholamine content is directly related to a decrease of key catecholamine-synthesizing enzymes, which by its turn may lead to a defective catecholamine secretion.     

Feedback models allowing estimation of thresholds for self-promoting body weight gain

Objective: Most people maintain almost constant body weight over long time with varying physical activity and food intake. This indicates the existence of a regulation that works well for most individuals. Yet some people develop obesity, indicating that this regulation sometimes fails. The difference between the two situations is typically an energy imbalance of about 1% over a long period of time.Theory: Weight gain increases basal metabolic rate. Weight gain is often associated with a decrease in physical activity, although not to such an extent that it prevents an increase in total energy expenditure and energy intake. Dependent on the precise balance between these effects of weight gain, they may make the body weight unstable and tend to further promote weight gain. With the aim of identifying the thresholds beyond which such self-promoting weight gain may take place, we develop a simple mathematical model of the body as an energy-consuming machine in which the changes in physical activity and food intake are described as feedback effects in addition to the effect of the weight gain on basal metabolic rate. The feedback parameters of the model may differ between individuals and only in some cases do they take values that make weight gain self-promoting.Results: We determine the quantitative conditions under which body weight gain becomes self-promoting. We find that these conditions can easily be met, and that they are so small that they are not observable with currently available techniques. This phenomenon encourages emphasis on even minor changes in food intake and physical activity to abate or stop weight gain.     

Obesity linking to hepatocellular carcinoma: A global view

Hepatocellular carcinoma (HCC) is the commonest primary liver cancer and the second leading cause of cancer death worldwide. Obesity is rapidly becoming pandemic and associated with increased carcinogenesis. In this review, we describe the obesity-related factors that influence the development of HCC. We provide evidence of strong links between neural regulation, endocrine and HCC in obesity. We discuss recent advances in our understanding of how adipose tissue alters hepatic metabolism and immune response in HCC development through inter-organ communication. Taken together, our review aims to provides a concise and up-to date summary about the connection between obesity and HCC, with emphasis on the opportunities for effective strategies in preventing the development of HCC in obese individuals.