前列腺素E2干预后交叉韧带成纤维细胞和滑膜细胞的迁移

背景:细胞迁移是组织损伤后修复过程中的重要环节之一,但是膝关节交叉韧带损伤后局部产生的细胞因子前列腺素E2对后交叉韧带成纤维细胞和滑膜细胞迁移的影响尚未见报道。目的:在后交叉韧带成纤维细胞与滑膜细胞单培养和共培养的条件下,研究前列腺素E2对此2种细胞迁移的影响。方法:体外培养人后交叉韧带成纤维细胞和滑膜细胞,分别进行2种细胞的单培养和Transwell共培养,并用质量浓度10μg/L的前列腺素E2干预。比较单培养和共培养下细胞生长状态;细胞划痕试验检测24h时细胞的迁移率。结果与结论:共培养使后交叉韧带成纤维细胞和滑膜细胞的迁移率较单培养增高128%和48%。前列腺素E2分别使单培养下后交叉韧带成纤维细胞和滑膜细胞的迁移率降低了28%和14%;使共培养下细胞的迁移率较相应的共培养组未处理细胞下降37%和24%。证实,在前列腺素E2的刺激下,后交叉韧带成纤维细胞和滑膜细胞迁移率均明显降低,尤其对共培养下后交叉韧带成纤维细胞迁移率的抑制更显著。     

世界胃肠病学组织全球指南——发展中国家幽门螺杆菌感染

世界上有一半人口感染幽门螺杆菌（H．pylori）,其感染率因地理位置、种族、年龄和社会经济状况不同而存在很大差异．在发展中国家较高．发达国家较低。但总体而言,近年世界许多地区的H．pylori感染率均呈下降趋势。     

Chronic social stress in a changing dietary environment

The human population has slowly transformed from the "hunter-gatherer" period to the current environment of high energy consumption, minimal physical activity and a lifestyle that includes stress and anxiety. Modeling the current environment in the laboratory can help to elucidate mechanisms responsible for the development of obesity, diabetes and, ultimately, the metabolic syndrome. Using the visible burrow system (VBS) model of social stress we have begun to examine the short- and long-term consequences of chronic social stress on energy homeostasis. We demonstrated that social stress has significant effects on body weight and body composition such that subordinate rats progressively develop characteristics of obesity and have additionally determined that this occurs, in part, through changes in food intake amount and behavior. Changes in body weight and body composition are similar or greater when animals are maintained on a high fat diet. These data suggest that consumption of a high-fat diet during social stress in the VBS, while it does not appear to affect development of a social hierarchy, enhances the effect that chronic stress has on body composition and may be more representative of what happens in humans in modern society where the typical diet has progressively moved toward higher calorie, high-fat foods.     

Cost-utility of living donor liver transplantation in a single Japanese center

BACKGROUND/AIMS: Living donor liver transplantation is becoming increasingly important in the Western world, but the economic issues remain controversial. We conducted a cost-utility analysis to evaluate whether living donor liver transplantation is cost-effective. METHODOLOGY: Cost and utility analyses were performed in a longitudinal survey of a single center in Sapporo, Japan. Medical costs were derived from 11 patients who underwent living donor liver transplantation. Health utility was measured in quality-adjusted life year. Data for health utility scores were derived from 19 patients who underwent living donor liver transplantation. RESULTS: Median medical cost was U.S. dollars 154,626 from the first day of preoperative evaluation to 24 months post-transplantation. Cumulative quality-adjusted life years were 1.60 at 24 months after transplantation. Medical cost per quality-adjusted life year decreased progressively, leading to medical cost of U.S. dollars 605,131 per quality-adjusted life year at 3 months to U.S. dollars 94,169 at 24 months after transplantation. The results were sensitive to medical cost. CONCLUSIONS: Follow-up survey identified progressive increases in the cost-effectiveness of living donor liver transplantation for patients with end-stage liver disease. Living donor liver transplantation appears to represent a cost-effective medical technology.     

共培养下后交叉韧带成纤维细胞中赖氨酰氧化酶的基因表达

背景：后交叉韧带对人膝关节结构的稳定以及功能的发挥起着重要作用。与内侧副韧带相比,损伤后的后交叉韧带难以很好的自我愈合,甚至会导致半月板撕裂和软骨损伤。为了提高后交叉韧带的愈合能力,这就需要寻找新的途径来再生和修复损伤的后交叉韧带。近年来的研究表明,赖氨酰氧化酶在组织损伤修复过程中起到非常重要的作用,但其在后交叉韧带修复过程中的分子机制研究尚未涉猎。 目的：观察与滑膜细胞共培养后交叉韧带成纤维细胞中赖氨酰氧化酶基因的表达。 方法：将第4代的后交叉韧带成纤维细胞和滑膜细胞分别种植于6孔板和Tanswell中。实验分为2组,即后交叉韧带成纤维细胞与滑膜细胞共培养组和后交叉韧带成纤维细胞单层培养组。培养6 h后,提取总RNA,通过半定量PCR和实时定量PCR检测单层培养组和共培养组中后交叉韧带成纤维细胞中赖氨酰氧化酶基因表达。 结果与结论：与单层培养组相比,赖氨酰氧化酶、赖氨酰氧化酶样蛋白1、赖氨酰氧化酶样蛋白2、赖氨酰氧化酶样蛋白3和赖氨酰氧化酶样蛋白4的基因表达在共培养的后交叉韧带细胞中都明显升高,分别增加了1.1,1.4,1.1,1.3,1.1倍(P < 0.05)。单层培养组家族成员在单层培养和共培养中表达情况的差异性,说明细胞之间的相互作用会影响后交叉韧带组织的损伤修复,对后交叉韧带损伤修复的机制研究有极其重要的参考价值。     

全球195个国家18亿青少年健康调查:慢病占青少年疾病负担一半以上,是青年人健康状况每况愈下的主因

正一项针对全球195个国家的18亿10-24岁的青少年健康状况的调查研究显示,这些年轻人正面临比25年前更大的健康挑战。文章称,目前的10～24岁的人口是有史以来最多的,截至2016年达到18亿,印度和中国拥有全球三分之一的青少年(6.22亿)。印度青少年人口增长了40%,然而,中国青少年人口从1990年的3.52亿减少到2016年的2.53亿。2016年青少年的DALYs为2.53亿,非传染性疾病(NCD)占青少年疾病负担的56%(1.42亿),NCD是所有国家青年人健康状况每况愈下的主要     

Pleasurable behaviors reduce stress via brain reward pathways

Individuals often eat calorically dense, highly palatable "comfort" foods during stress for stress relief. This article demonstrates that palatable food intake (limited intake of sucrose drink) reduces neuroendocrine, cardiovascular, and behavioral responses to stress in rats. Artificially sweetened (saccharin) drink reproduces the stress dampening, whereas oral intragastric gavage of sucrose is without effect. Together, these results suggest that the palatable/rewarding properties of sucrose are necessary and sufficient for stress dampening. In support of this finding, another type of natural reward (sexual activity) similarly reduces stress responses. Ibotenate lesions of the basolateral amygdala (BLA) prevent stress dampening by sucrose, suggesting that neural activity in the BLA is necessary for the effect. Moreover, sucrose intake increases mRNA and protein expression in the BLA for numerous genes linked with functional and/or structural plasticity. Lastly, stress dampening by sucrose is persistent, which is consistent with long-term changes in neural activity after synaptic remodeling. Thus, natural rewards, such as palatable foods, provide a general means of stress reduction, likely via structural and/or functional plasticity in the BLA. These findings provide a clearer understanding of the motivation for consuming palatable foods during times of stress and influence therapeutic strategies for the prevention and/or treatment of obesity and other stress-related disorders.     

Prolactin prevents acute stress-induced hypocalcemia and ulcerogenesis by acting in the brain of rat

Stress causes hypocalcemia and ulcerogenesis in rats. In rats under stressful conditions, a rapid and transient increase in circulating prolactin (PRL) is observed, and this enhanced PRL induces PRL receptors (PRLR) in the choroid plexus of rat brain. In this study we used restraint stress in water to elucidate the mechanism by which PRLR in the rat brain mediate the protective effect of PRL against stress-induced hypocalcemia and ulcerogenesis. We show that rat PRL acts through the long form of PRLR in the hypothalamus. This is followed by an increase in the long form of PRLR mRNA expression in the choroid plexus of the brain, which provides protection against restraint stress in water-induced hypocalcemia and gastric erosions. We also show that PRL induces the expression of PRLR protein and corticotropin-releasing factor mRNA in the paraventricular nucleus. These results suggest that the PRL levels increase in response to stress, and it moves from the circulation to the cerebrospinal fluid to act on the central nervous system and thereby plays an important role in helping to protect against acute stress-induced hypocalcemia and gastric erosions.