Violence Exposure and the Development of School-Related Functioning: Mental Health, Neurocognition, and Learning

The relation between history of violence exposure and the development of academic and mental health problems is explored. Violence exposed children have an increased risk of developing school-related problems including: mental health problems, learning disabilities, language impairments, and other neurocognitive problems. These problems interact to create a complex web of deficits and disabilities where intervention access points are difficult to assess. Often mental health problems and academic problems develop in parallel. Timing of violence exposure and the developmental stage of the child during exposure complicate our understanding of the underlying mechanism. A model is presented that explores pathways linking violence exposure to aspects of school-related functioning, both academically and behaviorally. Early life stress, in the form of violence exposure, is related to neurocognitive deficits, including executive functioning and problems in self-regulation. Deficits in self-regulation at the level of behavior, and cognitive control and executive functioning, at the level of brain processing, are related to both academic and mental health problems, suggesting a possible psychological mechanism. Biological mechanisms are also included in the model to illustrate the contribution of the stress response, neuroendocrine system response, and neuroanatomical structural and functional impairments associated with violence exposure.     

Self‐Reported Family Socioeconomic Status,the 5‐HTTLPR Genotype,and Delinquent Behavior in a Community‐Based Adolescent Population

Twin and adoption studies have demonstrated a significant contribution of both genetic and environmental factors to antisocial and delinquent behavior. Associations have been reported between the serotonin transporter (5‐HTT) and aggression, and between socioeconomic status (SES), aggression, and serotonergic functions of the brain. We aimed to investigate associations between the 5‐HTTLPR genotype and family SES in relation to delinquent behavior among adolescents. A total of 1,467 17‐ to 18‐year‐old students in the county of Västmanland, Sweden, anonymously completed a questionnaire and gave a saliva sample. Family SES had a U‐shaped relation to delinquency, where adolescents with low and high family SES were the most delinquent. There were curvilinear interactions between the 5‐HTTLPR genotype and family SES in relation to delinquency. Among individuals having high family SES, boys with the LL (homozygous for the long allele) or LS (heterozygous) genotypes and girls with the SS (homozygous for the short allele) or LS (heterozygous) genotypes showed the highest delinquency scores. Among individuals having low family SES, boys with the LL (homozygous for the long allele) genotype and girls with the LS (heterozygous) genotype showed the highest delinquency scores. The present study suggests evidence for an interaction between family SES and the 5‐HTTLPR genotype in relation to juvenile delinquency. Aggr. Behav. 39:52‐63, 2013. © 2012 Wiley Periodicals, Inc.     

不同5-HT3受体拮抗剂预防腹腔镜术后恶心呕吐的临床观察

观察使用不同5-HT3受体拮抗剂预防全麻下腹腔镜手术术后恶心呕吐的临床效果。选择160例气管内插管全身麻醉下腹腔镜手术,随机分四组,每组40例,手术结束前30min分别静脉注射昂丹司琼4mg（A组）;托烷司琼2mg（B组）;格拉司琼3mg（C组）;D组为对照组。记录术后2h、6h、12h、24h患者恶心、呕吐出现的例数。结果四组患者术后恶心呕吐的发生率是一个逐渐下降的趋势,A、B、C三组与D组相比较有显著性差异（P〈0．05）;术后2h、6h、12hB组与A组、C组相比较有显著性差异（P〈0．05）;而术后24hA、B、C三组差异无统计学意义,A、B、C三组抑制恶心呕吐的有效率分别为67．5％、87．5％和70．0％,与对照组比较差异有统计学意义（P〈0．05）,随访患者24h内无与药物相关的不良反应。结论：三种药物都能有效地预防术后恶心呕吐,但12h内托烷司琼的有效性更为明显。     

晚期非小细胞肺癌TKIs治疗：关注与思考

以表皮生长因子受体（EGFR）为靶点的酪氨酸激酶抑制剂（TKIs）对晚期非小细胞肺癌EGFR突变患者的治疗效果令人瞩目。本文分析总结近年国内外相关研究,指出低剂量TKIs的应用虽有待进一步证实,但优于标准剂量组,并从安全性、改善肿瘤血管结构和功能、与细胞毒化疗的关系三方面探讨大剂量TKIs的应用效果。进一步分析指出大剂量联合小剂量TKIs能够最大程度地防止或延迟耐药的发生,进而控制疾病的进展。从而,为晚期非小细胞肺癌EGFR突变患者的TKIs治疗选择提供参考。     

前列腺素E2及其在肾脏调控中的作用

前列腺素E2(PGE2)是最主要的前列腺素化合物,参与几乎所有的细胞代谢活动并介导多种不同的生理病理功能。PGE2的生物学效应是通过与不同的EP受体结合从而激活不同的信号转导通路来实现的。因为各类EP受体在肾脏的高分布,所以近来PGE2在肾脏中的作用日趋引起人们的重视。     

维生素D_3及其受体的临床意义

1,25-(OH)2D3是维生素D在体内发挥生理作用的活性形式。活性维生素D3通过与细胞内特异性维生素D受体结合,除了具有调节钙磷代谢的功能外,还发现其可预防和治疗骨质疏松、心血管疾病、自身免疫性疾病和一些肿瘤等。然而,维生素D缺乏在人群中非常普遍。     

Depression

Abstract— The theory of clinical depression presented here integrates etiological factors, changes in specific structural and cellular substrates, ensuing symptomatology, and treatment and prevention. According to this theory, important etiological factors, such as stress, can suppress the production of new neurons in the adult human brain, thereby precipitating or maintaining a depressive episode. Most current treatments for depression are known to elevate brain serotonin neurotransmission, and such increases in serotonin have been shown to significantly augment the ongoing rate of neurogenesis, providing the neural substrate for new cognitions to be formed, and thereby facilitating recovery from the depressive episode. This theory also points to treatments that augment neurogenesis as new therapeutic opportunities.     

Behavioral profile of L–741,741, a selective D4 dopamine receptor antagonist,in social encounters between male mice

Although the role of dopamine D1–D2–D3 receptors in the modulation of aggression has been extensively documented, there is not information with respect to the implication of D4 receptor. The aim of this study was to examine the acute effects of L–741,741 (0.75, 1.5 and 3 mg/kg, i.p), a selective D4 receptor antagonist, on social encounters between male mice using an ethopharmacological approach. Ten min of diadic interactions were staged between a singly housed and an anosmic mouse in a neutral area. These encounters were videotaped and the accumulated time allocated by subjects to ten broad behavioral categories was estimated. Besides other behaviors, the aggressive and motor behaviors were evaluated 30 min after injection using an ethologically based analysis. L–741,741 did not affect significantly offensive behaviors (threat and attack), as compared with the control group. Likewise, motor and anxiety‐related behaviors (such as social investigation, avoidance/flee or defense submission) were not altered after drug administration. These results suggest that dopamine D4 receptor is not involved in the modulation of aggressive behavior. Aggr. Behav. 29:552–557, 2003. © 2003 Wiley‐Liss, Inc.     

Depotentiation of vdccLTP Requires NMDAR Activation

Long-term potentiation is an enduring increase in synaptic efficacy following repeated stimulation of afferent fibers that is thought to underlie memory. In area CA1 of the hippocampus at least two forms of synaptic potentiation coexist at the same synapses; nmdaLTP and vdccLTP. NmdaLTP is induced by Ca2+ entry through NMDARs and is dependent on serine/threonine kinase activation, while vdccLTP is induced through Ca2+ entry through VDCCs and is dependent on tyrosine kinase activation. Depotentiation is a mechanism known to reverse nmdaLTP through phosphatase activation. The depotentiation of vdccLTP has not been previously investigated. We used hippocampal slices (area CA1) from male Long-Evans rats to induce vdccLTP with a 200-Hz tetanus in the presence of 50 microM APV. The 200-Hz tetanus resulted in a slowly developing vdccLTP that remained stable for at least 30 min. Thirty minutes after vdccLTP was induced, a low-frequency tetanus (3, 10, 20, 30, or 40 Hz) was applied in the presence of APV in an attempt to depotentiate vdccLTP. The 3- and 10-Hz low-frequency tetani resulted in no depotentiation. The 20- and 30-Hz tetani partially depotentiated vdccLTP (by approximately 13%), whereas the 40-Hz tetanus resulted in further potentiation. When APV was washed out prior to the 3-Hz low-frequency tetanus, the vdccLTP was completely depotentiated--presumably by NMDAR mechanisms. Our results indicate that vdccLTP is resistant to depotentiation under low-frequency stimulation conditions that readily depotentiate nmdaLTP. As tetanus frequencies are increased a small depotentiation is observed, suggesting that vdccLTP can be depotentiated to a small extent. When NMDARs are unblocked, vdccLTP can be completely depotentiated by a 3-Hz low-frequency tetanus, suggesting that vdccLTP can be depotentiated via activation of NMDAR mechanisms.