网络成瘾的生物学机制研究与展望

网络成瘾是指由于过度使用网络而导致社会及心理损害的现象,危害极大,故受到广泛关注。网络成瘾主要受生物学机制的调控。在脑神经机制方面,通过对成瘾者的自发脑电、事件相关电位以及成瘾者静息态BOLD-f MRI的分析,发现成瘾者脑功能区出现异常。同时,网络成瘾也受到自主神经功能的影响。另外,脑内奖赏系统和成瘾记忆模型也可能成为引发网络成瘾的脑神经机制。体内化学物质的失衡也能引发网络成瘾。鉴于此,一些治疗方法如药物干预、行为干预、认知干预以及综合干预疗法使得根治网络成瘾成为可能。本文拟从网络成瘾的概念、表现特点、不良影响及其发生的生物学机制等方面的研究进展进行阐述,以期为相关研究提供一些有价值的参考依据。     

儿童强迫症、抑郁症患者血小板5-羟色胺浓度的比较研究

目的:通过检测儿童强迫症、抑郁症患者血小板5-羟色胺(5-HT)的浓度,探讨血小板5-HT在儿童强迫症、抑郁症发病中的作用.方法:采用高效液相色谱法检测22例强迫症患儿(包括强迫思维15例,强迫动作7例)和20例抑郁症惠儿血小板5-HT的浓度,并与20名正常儿童进行比较.结果:强迫症患儿(173.43±90.67)ng/109和抑郁症患儿(251.62±152.72)ng/109血小板5-HT的浓度低于正常儿童(351.91±170.97)ng/109(P<0.05),强迫症患儿的血小板5-HT的浓度和抑郁症惠儿的差异没有显著性(P>0.05).强迫症患儿中,强迫思维惠儿的血小板5-HT的浓度(147.09±44.92)ng/109低于强迫动作患儿(229.88±1:136.44)ng/109(P<0.05).结论:儿童强迫症、抑郁症患者血小板5-HT浓度明显下降,并且强迫思维患儿的血小板5-HT浓度与强迫动作患儿的差异有显著性.     

磁场的细胞生物学效应不统一之现状分析

随着无线电通讯设备和家用电器的日益普及,磁场对生物体健康的影响越来越受到人们的关注。目前,已有一些磁场对细胞影响的初步探索,但是由于现有研究中各种细胞的差异、磁场参数的不同,影响了人们对磁场的细胞生物学效应的正确认识。该文将系统比较目前此领域的研究成果,分别从磁场类型和强度、细胞种类及密度等方面来阐明磁场对细胞增殖的影响,并且通过分析磁场对细胞信号通路的影响来探究磁场生物学效应的潜在机制。该文旨在对现有的结论进行总结分析并且找到存在差异和矛盾的原因,从而为该领域的深层次探讨提供线索,为进一步在基础和临床研究中探究磁场生物学效应提供可借鉴的依据。     

纳米铁氧化物磁热疗相关机制研究进展

热疗作为继手术、放疗和化疗后的肿瘤治疗的重要方法之一,自其诞生之初便受到研究人员和产业部门的关注.磁热疗目前已经应用到前列腺癌、脑部肿瘤等临床实验或治疗中,并取得较好的疗效.本文主要介绍基于磁性纳米颗粒的磁热疗产热物理机制与影响因素,以及磁热的亚细胞水平生物学效应.     

肠道菌群与结核病之间相关性的研究进展

随着新一代测序技术的发展,肠道菌群成为生物学研究领域的一大热点,特别是肠道菌群与人体各种疾病之间的关系受到广泛关注。目前已有研究发现结核分枝杆菌感染会引起肠道菌群改变,而肠道菌群失调也会增加机体对结核分枝杆菌的易感性,两者通过机体免疫反应、菌群代谢产物等因素相互影响。本文就肠道菌群与结核病的关系、肠道菌群与结核病相互影响的可能机制、抗结核治疗对肠道菌群的影响等方面的相关研究进行综述。     

血型与气质类型和疾病相关性的生物学机制

血型与气质类型关系的研究属于人格的生物学研究范畴,其最早的研究在日本,1927年日本学者古川竹二(Furukawa)提出气质血型学说,在学术界和社会上都产生很大影响。早期对气质血型论的研究主要是通过统计学方法进行研究,缺少对其相关生物学机制的探讨,从而引起较大的争论。上世纪五十年代血型与疾病相关性的研究也引起许多学者的关注。气质类型与遗传因素、机体生活环境和文化因素等都具有相关性,本文介绍了血型与气质类型和疾病现阶段的主要研究结果,重点是从生物学角度阐述血型与气质类型和疾病等方面具有相关性的原因。     

保护演化生物学——保护生物学的新分支

离开演化谈保护,往往难窥其道.保护生物学建立之初旨在阐释受人类活动或其他因素干扰下的物种、种群、群落和生态系统的保护问题,在其发展过程中其逐渐从生态、行为等宏观层面深入到生理、遗传、基因组、适应性演化等分子机制层面.特别是近年来,越来越多的研究聚焦到物种演化历史及其成因、适应性演化机制与演化潜力等方面,这些研究超越了传统保护生物学分支学科如保护生态学和行为学等的研究内容.将演化生物学原理引入保护生物学研究则能更好地揭示问题的本质,因而越来越受到保护生物学家的重视.因此,我们提出"保护演化生物学"这一新分支学科,以强化演化生物学原理和方法在解决物种保护问题中的应用.保护演化生物学是将演化生物学原理和方法整合进保护生物学研究中,旨在从演化的视角探讨物种的过去、现在与未来,揭示物种如何适应和响应环境变化以维持长期生存的机制,阐明物种濒危过程与演化潜力,以期为制定前瞻性的物种保护策略提供科学依据.本文从保护演化生物学的产生、发展、研究内容、研究方法及研究意义等方面进行了简要介绍,以推动保护演化生物学分支学科的发展.     

磁场与辐照联合的生物学效应

利用辐照的放射治疗(放疗)是临床治疗肿瘤的主要方法之一。近年来,随着磁共振成像引导放疗以及多方法联合治疗的逐渐推广,磁场与辐照联合对人体的影响逐渐引起了人们的关注。大量研究表明,磁场会对辐照效应产生一定的影响,但目前并没有统一的结论。本文系统比较并分析了多种参数的磁场与辐照联合所产生的生物学效应,发现其结果不一致性与研究对象、磁场参数(包括磁场强度、方向、处理时间等)和辐照剂量等都有关。虽然目前对相关机制的探索并不多,但已有证据表明,磁场可能通过影响细胞周期和凋亡相关信号转导通路、DNA损伤修复以及线粒体功能等影响辐照效应。这不仅有助于我们深入了解磁场与辐照联合的生物学效应,并且可能为未来磁场与放疗联用在肿瘤治疗中的参数优化设计提供依据。     

UV对昆虫的生物学效应及昆虫适应机制

紫外光（Ultraviolet light,UV）源于太阳辐射,是一种重要的环境因子,昆虫作为地球生态系统中的重要参与者其生命活动也会受到UV辐射的影响。UV辐射对昆虫造成的生物学效应除与波长、辐射强度等光学特性有关,还与其他非生物因素和生物因素有关。昆虫长期与UV共存,也进化出了行为适应、生理适应等各种抵御UV辐射的能力。本文从多方面综述了UV对昆虫的生物学效应,以及昆虫对UV胁迫的适应机制,有利于认识和理解昆虫应对物理胁迫的生理对策,为丰富和完善害虫物理防治策略提供科学依据,对促进害虫物理防治产业的发展具有重要意义。     

细胞因子抗瘢痕的研究进展

瘢痕是创伤修复的必然结果影响,瘢痕的产生,发展的因素很多,虽然国内外学者在病理性瘢痕领域研究取得了一些进展,但其确切的发病机制仍未完全清楚,目前对治疗瘢痕的研究主要集中在生化,细胞水平,对分子机制和基因水平的研究还在不断的深入,人们对细胞因子在瘢痕形成方面起了关键的调节作用这一观点已逐步形成共识,并将细胞因子引入瘢痕的治疗中.常见的细胞因子在抗瘢痕中的应用也将成为可能.本文主要介绍了常见细胞因子的在创面修复中的生物学特征及抗瘢痕的研究情况.     

An Inherited Small Microdeletion at 15q13.3 in a Patient with Early- Onset Obsessive-Compulsive Disorder

Copy number variations (CNVs) have been previously associated with several different neurodevelopmental psychiatric disorders, such as autism, schizophrenia, and attention deficit hyperactivity disorder (ADHD). The present study consisted of a pilot genome-wide screen for CNVs in a cohort of 16 patients with early-onset obsessive-compulsive disorder (OCD) and 12 mentally healthy individuals, using array-based comparative genomic hybridization (aCGH) on 44K arrays. A small rare paternal inherited microdeletion (∼64 kb) was identified in chromosome 15q13.3 of one male patient with very early onset OCD. The father did not have OCD. The deletion encompassed part of the FMN1 gene, which is involved with the glutamatergic system. This finding supports the hypothesis of a complex network of several genes expressed in the brain contributing for the genetic risk of OCD, and also supports the glutamatergic involvement in OCD, which has been previously reported in the literature.     

COMT and MAO-A Polymorphisms and Obsessive-Compulsive Disorder: A Family-Based Association Study

Objective

Obsessive-compulsive disorder (OCD) is a common and debilitating psychiatric illness. Although a genetic component contributes to its etiology, no single gene or mechanism has been identified to the OCD susceptibility. The catechol-O-methyltransferase (COMT) and monoamine oxidase A (MAO-A) genes have been investigated in previous OCD studies, but the results are still unclear. More recently, Taylor (2013) in a comprehensive meta-analysis of genetic association studies has identified COMT and MAO-A polymorphisms involved with OCD. In an effort to clarify the role of these two genes in OCD vulnerability, a family-based association investigation was performed as an alternative strategy to the classical case-control design.

Methods

Transmission disequilibrium analyses were performed after genotyping 13 single-nucleotide polymorphisms (eight in COMT and five in MAO-A) in 783 OCD trios (probands and their parents). Four different OCD phenotypes (from narrow to broad OCD definitions) and a SNP x SNP epistasis were also analyzed.

Results

OCD, broad and narrow phenotypes,were not associated with any of the investigated COMT and MAO-A polymorphisms. In addition, the analyses of gene-gene interaction did not show significant epistatic influences on phenotype between COMT and MAO-A.

Conclusions

The findings do not support an association between DSM-IV OCD and the variants of COMT or MAO-A. However, results from this study cannot exclude the contribution of these genes in the manifestation of OCD. The evaluation of broader spectrum phenotypes could help to understand the role of these and other genes in the pathophysiology of OCD and its spectrum disorders.     

整合转录组数据鉴定大型真菌原基形成的潜在通路

[背景]大型真菌子实体发育特别是从菌丝体到原基转变的分子机制,目前仍不清楚.现有的研究大多集中在有限的真菌种类或环境因素上,但对在发育中起关键作用的基因提供的信息有限.[目的]研究大型真菌原基形成的分子机制.[方法]对11个物种及4个环境因子相关的转录组数据进行分析.[结果]与对照组相比,上调基因数量从白灵菇(Pleu...     

Neurobiology of obsessive-compulsive disorder: insights into neural circuitry dysfunction through mouse genetics

The precise causal factors for obsessive-compulsive disorder (OCD) are not known, although, decades of research have honed in on the cortico-striatal-thalamo-cortical (CSTC) circuitry in the brain as a critical pathway involved in obsessions and the intimately linked compulsive-repetitive behaviors. Recent progress in human and mouse genetics have led to the identification of novel candidate susceptibility genes, which in turn have facilitated a more focused approach to unraveling the nature of circuitry dysfunction in OCD. The ability to perform invasive techniques in genetic animal models of OCD will be crucial for rapid advances in this field, and as such we review the most recent developments and highlight the importance of searching out common circuitry defects underlying compulsive-repetitive behaviors.     

Genomewide linkage analysis in Costa Rican families implicates chromosome 15q14 as a candidate region for OCD

Obsessive compulsive disorder (OCD) has a complex etiology that encompasses both genetic and environmental factors. However, to date, despite the identification of several promising candidate genes and linkage regions, the genetic causes of OCD are largely unknown. The objective of this study was to conduct linkage studies of childhood-onset OCD, which is thought to have the strongest genetic etiology, in several OCD-affected families from the genetically isolated population of the Central Valley of Costa Rica (CVCR). The authors used parametric and non-parametric approaches to conduct genome-wide linkage analyses using 5,786 single nucleotide repeat polymorphisms (SNPs) in three CVCR families with multiple childhood-onset OCD-affected individuals. We identified areas of suggestive linkage (LOD score ≥ 2) on chromosomes 1p21, 15q14, 16q24, and 17p12. The strongest evidence for linkage was on chromosome 15q14 (LOD = 3.13), identified using parametric linkage analysis with a recessive model, and overlapping a region identified in a prior linkage study using a Caucasian population. Each CVCR family had a haplotype that co-segregated with OCD across a ~7 Mbp interval within this region, which contains 18 identified brain expressed genes, several of which are potentially relevant to OCD. Exonic sequencing of the strongest candidate gene in this region, the ryanodine receptor 3 (RYR3), identified several genetic variants of potential interest, although none co-segregated with OCD in all three families. These findings provide evidence that chromosome 15q14 is linked to OCD in families from the CVCR, and supports previous findings to suggest that this region may contain one or more OCD susceptibility loci.     

A novel algorithm based on bi-random walks to identify disease-related lncRNAs

Background

It’s a very urgent task to identify cancer genes that enables us to understand the mechanisms of biochemical processes at a biomolecular level and facilitates the development of bioinformatics. Although a large number of methods have been proposed to identify cancer genes at recent times, the biological data utilized by most of these methods is still quite less, which reflects an insufficient consideration of the relationship between genes and diseases from a variety of factors.

Results

In this paper, we propose a two-rounds random walk algorithm to identify cancer genes based on multiple biological data (TRWR-MB), including protein-protein interaction (PPI) network, pathway network, microRNA similarity network, lncRNA similarity network, cancer similarity network and protein complexes. In the first-round random walk, all cancer nodes, cancer-related genes, cancer-related microRNAs and cancer-related lncRNAs, being associated with all the cancer, are used as seed nodes, and then a random walker walks on a quadruple layer heterogeneous network constructed by multiple biological data. The first-round random walk aims to select the top score k of potential cancer genes. Then in the second-round random walk, genes, microRNAs and lncRNAs, being associated with a certain special cancer in corresponding cancer class, are regarded as seed nodes, and then the walker walks on a new quadruple layer heterogeneous network constructed by lncRNAs, microRNAs, cancer and selected potential cancer genes. After the above walks finish, we combine the results of two-rounds RWR as ranking score for experimental analysis. As a result, a higher value of area under the receiver operating characteristic curve (AUC) is obtained. Besides, cases studies for identifying new cancer genes are performed in corresponding section.

Conclusion

In summary, TRWR-MB integrates multiple biological data to identify cancer genes by analyzing the relationship between genes and cancer from a variety of biological molecular perspective.

     

Role of GAD2 and HTR1B genes in early‐onset obsessive‐compulsive disorder: results from transmission disequilibrium study

One of the leading biological models of obsessive‐compulsive disorder (OCD) is the frontal‐striatal‐thalamic model. This study undertakes an extensive exploration of the variability in genes related to the regulation of the frontal‐striatal‐thalamic system in a sample of early‐onset OCD trios. To this end, we genotyped 266 single nucleotide polymorphisms (SNPs) in 35 genes in 84 OCD probands and their parents. Finally, 75 complete trios were included in the analysis. Twenty SNPs were overtransmitted from parents to early‐onset OCD probands and presented nominal pointwise P < 0.05 values. Three of these polymorphisms achieved P < 2 × 10^?4, the significant P‐value after Bonferroni corrections: rs8190748 and rs992990 localized in GAD2 and rs2000292 in HTR1B. When we stratified our sample according to gender, different trends were observed between males and females. In males, SNP rs2000292 (HTR1B) showed the lowest P‐value (P = 0.0006), whereas the SNPs in GAD2 were only marginally significant (P = 0.01). In contrast, in females HTR1B polymorphisms were not significant, whereas rs8190748 (GAD2) showed the lowest P‐value (P = 0.0006). These results are in agreement with several lines of evidence that indicate a role for the serotonin and γ‐Aminobutyric acid (GABA) pathways in the risk of early‐onset OCD and with the gender differences in OCD pathophysiology reported elsewhere. However, our results need to be replicated in studies with larger cohorts in order to confirm these associations.     

The effects of boron on some biochemical parameters: A review

BackgroundBoron; It is used mainly in glass and ceramics, in the defense industry, in jet and rocket fuel, as a disinfectant, and even in the agricultural sector to increase or prevent vegetation development. Its use in the health field has become more widespread when studies in recent years are reviewed. Although it has been reported that boron has essential biological effects on minerals, some enzymes, and hormones, the mechanism of these biological effects has yet to be fully elucidated. This review aims to bring a new perspective to researchers by combining the results of experimental studies in the literature on the effects of boron on some biochemical parameters.MethodsWorks of literature on boron were brought together using more than one database (WOS, PubMed, Scopus, Google Scholar). The animal, boron type and dose used in the experimental study, and biochemical parameters (glucose, urea, BUN (blood urea nitrogen), uric acid, creatinine, creatine kinase, blood lipid profile, minerals, liver function tests) were systematically compiled.ResultsIt was observed that the studies mainly focused on glucose and lipid profiles and had a lowering effect on these parameters. From a mineral point of view, the studies are mostly related to the bone matrix.ConclusionAlthough the mechanism of action of boron on biochemical parameters has not yet been clarified, it would be beneficial to examine its relationship with hormones in more depth. A good understanding and analysis of the effect of boron, which is widely used, on biochemical parameters will be beneficial in taking necessary precautions for human and environmental health.     

A family study of Gilles de la Tourette syndrome.

Previous studies have demonstrated that Gilles de la Tourette syndrome (TS) is a familial disorder and that chronic tics (CT) and obsessive compulsive disorder (OCD) appear to be etiologically related to the syndrome. In the present study we report the results from a study of 338 biological relatives of 86 TS probands, 21 biologically unrelated relatives of adopted TS probands, and 22 relatives of normal subjects. The 43 first-degree relatives of the adopted TS and normal probands constituted a control sample. The rates of TS, CT, and OCD in the total sample of biological relatives of TS probands were significantly greater than in the relatives of controls. In addition, the morbid risks of TS, OCD, and CT were not significantly different in families of probands with OCD when compared to relatives of probands without OCD. These findings provide further evidence that OCD is etiologically related to TS.