Non-human primate models in drug addiction deserve more attention

正Dear Editor,The process of relapse involves firm or aberrant memories of environmental cues associated with drug craving or addiction.To date,it is not known where these memories are stored in the brain,what kinds of regulatory biological factors or molecules are involved,nor why it is so difficult to stop addiction psychologically.Currently,rodent animal models,such as the self-administration and conditioning place preference/aversion paradigm are still widely used in the studies of drug withdrawal syndromes or drug-associate memories.However,the differences between humans and rodents—particularly in terms of genetics,and pathology and pharmacology—     

Increased expression of mdig predicts poorer survival of the breast cancer patients

Breast cancer is the most common cancer and the second leading cause of cancer death among women of all races and Hispanic origin populations in the United States. In the present study, we reported that the survival time of the breast cancer patients is influenced by the expression level of mdig, a previously identified lung cancer-associated oncogene encoding a JmjC-domain protein. By checking the expression levels of mRNA and protein of mdig through both RT-PCR and immunohistochemistry in samples from 204 patients, we noticed that about 30% of breast cancer samples showed increased expression of mdig. Correlation of the mdig expression levels with the survival time of the breast cancer patients indicated a clear inverse relationship between mdig expression and patient survival, including poorer overall survival, distant metastasis free survival, relapse free survival, and post-progression survival. Taken together, these data suggest that an increased expression of mdig is an important prognostic factor for poorer survival time of the breast cancer patients.     

Causal interactions between the cerebral cortex and the autonomic nervous system

Mental states such as stress and anxiety can cause heart disease.On the other hand,meditation can improve cardiac performance.In this study,the heart rate variability,directed transfer function and corrected conditional entropy were used to investigate the effects of mental tasks on cardiac performance,and the functional coupling between the cerebral cortex and the heart.When subjects tried to decrease their heart rate by volition,the sympathetic nervous system was inhibited and the heart rate decreased.When subjects tried to increase their heart rate by volition,the parasympathetic nervous system was inhibited and the sympathetic nervous system was stimulated,and the heart rate increased.When autonomic nervous system activity was regulated by mental tasks,the information flow from the post-central areas to the pre-central areas of the cerebral cortex increased,and there was greater coupling between the brain and the heart.Use of directed transfer function and corrected conditional entropy techniques enabled analysis of electroencephalographic recordings,and of the information flow causing functional coupling between the brain and the heart.     

Evidences for mutations in the histone modifying gene SETD2 as critical drivers in leukemia development

<正>Cancer is thought to be largely caused by genetic mutations that alter nucleotide sequences of DNA,yet epigenetic factors are increasingly recognized to also play causative roles in cancer development.The idea of"epimutations"involves aberrations in chemical modification of the chromatin or DNA that do not change nucleotide sequence.While it is widely accepted that aberrations of DNA methylation contribute to carcinogenesis,the functional importance of his-     

Asthma incidence,remission, relapse and persistence: a population-based study in southern Taiwan

Background

In western countries, late-onset asthmatics are more severe than early-onset asthmatics in clinic-based studies. However, whether asthma occurrence rates were higher in late ages than in younger ages was inconclusive. This information is essentially lacking in Asian population.

Methods

The participants were schoolchildren’s parents recruited from 94 elementary and middle schools in 2004. A cross-sectional self-administered questionnaire was sent through the children to their parents to survey their respiratory health. We investigated typical asthma symptoms occurring at different ages and subsequent remission or relapse after the first asthma event. Person-years of the participants from birth to the time of survey were used as the denominator.

Results

Among the 25,377 participants consisting of 949,807 total person-years, 860 reported ever having asthma. Highest incidences occurred at ages 0–12 and 36–40 years. The incidence of asthma was higher in males before puberty, and higher in females after puberty, with overall incidences 1.00 and 0.77 per 1000 person-years for females and males, respectively. Participants with late-onset asthma (onset age >12 years) comprised a large portion of adult current asthmatics. More than 52% of persistence or relapse was observed in early-onset asthma (onset age ≤12 years). The younger birth cohort had a more prominent later peak of asthma incidence than the older one.

Conclusions

In Asian population, asthma occurrence showed a U-shape age distribution with a prominent second peak in the thirties. A high proportion of early-onset asthma relapsed and most of late-onset asthma persisted or relapsed in adulthood.     

Mechanisms of cohesin-mediated gene regulation and lessons learned from cohesinopathies

Cohesins are conserved and essential Structural Maintenance of Chromosomes (SMC) protein-containing complexes that physically interact with chromatin and modulate higher-order chromatin organization. Cohesins mediate sister chromatid cohesion and cellular long-distance chromatin interactions affecting genome maintenance and gene expression. Discoveries of mutations in cohesin's subunits and its regulator proteins in human developmental disorders, so-called “cohesinopathies,” reveal crucial roles for cohesins in development and cellular growth and differentiation. In this review, we discuss the latest findings concerning cohesin's functions in higher-order chromatin architecture organization and gene regulation and new insight gained from studies of cohesinopathies. This article is part of a Special Issue entitled: Chromatin and epigenetic regulation of animal development.     

城市绿地对居民身心福祉的影响

城市绿地是人工与自然耦合的城市景观之一,是改善居民居住环境重要组成部分,更是提高居民身心健康的有效途径。以杭州主城区为研究对象,通过GIS技术对城市绿地遥感图像进行解译得到杭州主城区绿地空间布局图,同时,以人口密度为阻力要素,基于交通路网的500m网络距离可达范围内绿地数量和面积作为分类标准。通过对45个高、中、低不同档次的居民区进行问卷调查得到665份居民感知数据并进行统计整理。利用结构方程模型进行以绿地数量及游玩时间为标准的组间分析,区别不同组别的差异及其原因,分析城市绿地数量、面积,居民认知、动机,绿地吸引力等与居民身心健康福祉及满意度之间的关系。结果显示:城市绿地数量、居民游玩绿地次数时间等与居民福祉有显著的正向关系;居民对绿地作用的认知、去往绿地的动机进一步影响居民身心健康福祉;城市绿地的自身引力会激发居民去往绿地的积极性,从而增加去往绿地频次。另外,不同社会属性的个体对绿地需求不同,所产生的福祉效应及满意度也会有所差异。从增加居民区周围的街头绿地及邻里公园数量、提升绿地吸引力、提升居民对城市绿地作用的认知3个方面对城市绿地今后的发展规划提出建议。     

短期身心训练可以引起大脑灰质变化吗

持续数月的运动学习或者工作记忆训练可以引发成年人大脑灰质的变化,其结构变化的区域与任务有关.是否短期身心训练可以引起类似的大脑大脑灰质变化尚不清楚.在前期工作基础上,本文研究了连续两周的整体身心调节法训练以及放松训练对大脑可塑性的影响.结果表明:采用基于像素的形态学方法,没有发现两周整体身心调节法训练以及放松训练可以引起大脑结构变化.下一步的研究将以大样本并增加训练时间采探索训练引发的神经可塑性规律.     

Fragile X mental retardation protein is required for chemically-induced long-term potentiation of the hippocampus in adult mice

Fragile X syndrome (FXS), a common form of inherited mental retardation, is caused by the lack of fragile X mental retardation protein (FMRP). The animal model of FXS, Fmr1 knockout mice, have deficits in the Morris water maze and trace fear memory tests, showing impairment in hippocampus-dependent learning and memory. However, results for synaptic long-term potentiation (LTP), a key cellular model for learning and memory, remain inconclusive in the hippocampus of Fmr1 knockout mice. Here, we demonstrate that FMRP is required for glycine induced LTP (Gly-LTP) in the CA1 of hippocampus. This form of LTP requires activation of post-synaptic NMDA receptors and metabotropic glutamateric receptors, as well as the subsequent activation of extracellular signal-regulated kinase (ERK) 1/2. However, paired-pulse facilitation was not affected by glycine treatment. Genetic deletion of FMRP interrupted the phosphorylation of ERK1/2, suggesting the possible role of FMRP in the regulation of the activity of ERK1/2. Our study provide strong evidences that FMRP participates in Gly-LTP in the hippocampus by regulating the phosphorylation of ERK1/2, and that improper regulation of these signaling pathways may contribute to the learning and memory deficits observed in FXS.