Distinct effects of acute and chronic sleep loss on DNA damage in rats

The aim of this investigation was to evaluate genetic damage induced in male rats by experimental sleep loss for short-term (24 and 96 h) and long-term (21 days) intervals, as well as their respective recovery periods in peripheral blood, brain, liver and heart tissue by the single cell gel (comet) assay. Rats were paradoxically deprived of sleep (PSD) by the platform technique for 24 or 96 h, or chronically sleep-restricted (SR) for 21 days. We also sought to verify the time course of their recovery after 24 h of rebound sleep. The results showed DNA damage in blood cells of rats submitted to PSD for 96 h. Brain tissue showed extensive genotoxic damage in PSD rats (both 24 and 96 h), though the effect was more pronounced in the 96 h group. Rats allowed to recover from the PSD-96 h and SR-21 days treatments showed DNA damage as compared to negative controls. Liver and heart did not display any genotoxicity activity. Corticosterone concentrations were increased after PSD (24 and 96 h) relative to control rats, whereas these levels were unaffected in the SR group. Collectively, these findings reveal that sleep loss was able to induce genetic damage in blood and brain cells, especially following acute exposure. Since DNA damage is an important step in events leading to genomic instability, this study represents a relevant contribution to the understanding of the potential health risks associated with sleep deprivation.     

老年脑梗死后抑郁与老年功能性抑郁临床特征对比分析

目的对老年脑梗死后抑郁与老年功能性抑郁临床特征进行对比分析。方法选择老年脑梗死后抑郁患者30例（观察组）和单纯功能性抑郁患者30例（对照组）作为研究对象,使用汉密尔顿抑郁量表（HAMD）和简易精神状况检查量表（MMSE）对二组患者抑郁特征及抑郁认知情况进行评定和对比。结果观察组HAMD激越性抑郁因子（￡=18．00,P〈0．01）、焦虑反应因子（t=16．15,P〈0．01）突出,与对照组比较差异有统计学意义,对照组以躯体症状因子（t=21．48,P〈0．01）、迟滞性抑郁因子（t=44．41,P〈0．01）突出,与观察组比较差异有统计学意义;观察组MMSE不同时间（1,2,3d）评定值均明显优于对照组,二组比较差异有统计学意义（t=13．70,22．50,22．11;P〈0．01）。结论老年脑梗死后抑郁与老年功能性抑郁在临床特征上差异显著,存在本质区别。     

Quantitative analysis of pre‐ and postsynaptic sex differences in the nucleus accumbens

The nucleus accumbens (NAc) plays a central role in motivation and reward. While there is ample evidence for sex differences in addiction‐related behaviors, little is known about the neuroanatomical substrates that underlie these sexual dimorphisms. We investigated sex differences in synaptic connectivity of the NAc by evaluating pre‐ and postsynaptic measures in gonadally intact male and proestrous female rats. We used DiI labeling and confocal microscopy to measure dendritic spine density, spine head size, dendritic length, and branching of medium spiny neurons (MSNs) in the NAc, and quantitative immunofluorescence to measure glutamatergic innervation using pre‐ (vesicular glutamate transporter 1 and 2) and postsynaptic (postsynaptic density 95) markers, as well as dopaminergic innervation of the NAc. We also utilized electron microscopy to complement the above measures. Clear but subtle sex differences were identified, namely, in distal dendritic spine density and the proportion of large spines on MSNs, both of which are greater in females. Sex differences in spine density and spine head size are evident in both the core and shell subregions, but are stronger in the core. This study is the first demonstration of neuroanatomical sex differences in the NAc and provides evidence that structural differences in synaptic connectivity and glutamatergic input may contribute to behavioral sex differences in reward and addiction. J. Comp. Neurol. 518:1330–1348, 2010. © 2009 Wiley‐Liss, Inc.     

脑卒中后抑郁的疗效与诸因素的关系

目的了解影响中风后抑郁疗效的因素,尽可能及早消除可干预因素.方法观察74例中风后抑郁的疗效与年龄、性别、病因、病程、病情、病前性格、文化程度、心理社会因素、病灶部位的关系.结果中风后抑郁的疗效与患者以上诸因素及病灶部位有关,与病因及性别无关.结论积极有效的治疗可减轻患者的病情,尽早作心理治疗并动员患者亲人及社会对患者适当关怀和照顾,可提高中风后抑郁的疗效.     

Radiation Exposure of Patients and Interventional Radiologists during Prostatic Artery Embolization: A Prospective Single-Operator Study

Purpose

To prospectively analyze the radiation exposure of patients and interventional radiologists during prostatic artery embolization (PAE).

艾司西酞普兰与帕罗西汀治疗精神分裂症后抑郁障碍对照研究

目的探讨艾司西酞普兰与帕罗西汀治疗精神分裂症后抑郁障碍的临床疗效和安全性。方法将72例精神分裂症后抑郁障碍患者随机分为两组,研究组37例,对照组35例,两组均维持原用抗精神病药物治疗,在此基础上研究组口服艾司西酞普兰治疗,对照组口服帕罗西汀治疗,观察8周。于治疗前及治疗1周、2周、4周、8周末采用汉密顿抑郁量表评定抑郁状况,副反应量表评定不良反应。结果治疗后两组汉密顿抑郁量表评分均较治疗前有显著下降（P〈0．01）,但研究组治疗第1周末较对照组下降更显著（P〈0．01）,其他时段评分两组比较差异均无显著性（P〉0．05）;治疗8周末,研究组有效率为81．1％,对照组为72．3％,两组比较差异无显著性（x2=0．48,P〉o．05）;两组不良反应均较轻微,总体不良反应发生率比较差异无显著性（x2=1．34,P〉0．05）,但研究组性功能障碍发生率显著低于对照组（x2=4．58,P〈0．05）。结论艾司西酞普兰与帕罗西汀均能显著改善精神分裂症后抑郁障碍患者的抑郁症状,总体疗效相当,但艾司西酞普兰起效更快,对性功能影响较小,安全性更高,依从性更好。     

卒中后抑郁心理护理的临床观察

卒中后抑郁是卒中患者最常见的心理障碍,发挥中医心理治疗与护理的优势,加强对PSD患者的情志调护,使其早日进入躯体、心理康复的良性循环,显得尤为重要,对PSD患者进行中医情志护理,具有重要的临床治疗价值。     

Influence of the NR3A subunit on NMDA receptor functions

Various combinations of subunits assemble to form the NMDA-type glutamate receptor (NMDAR), generating diversity in its functions. Here we review roles of the unique NMDAR subunit, NR3A, which acts in a dominant-negative manner to suppress receptor activity. NR3A-containing NMDARs display striking regional and temporal expression specificity, and, unlike most other NMDAR subtypes, they have a low conductance, are only modestly permeable to Ca²⁺, and pass current at hyperpolarized potentials in the presence of magnesium. While glutamate activates triheteromeric NMDARs composed of NR1/NR2/NR3A subunits, glycine is sufficient to activate diheteromeric NR1/NR3A-containing receptors. NR3A dysfunction may contribute to neurological disorders involving NMDARs, and the subunit offers an attractive therapeutic target given its distinct pharmacological and structural properties.     

PKMζ is necessary and sufficient for synaptic clustering of PSD‐95

The persistent activity of protein kinase Mzeta (PKMζ), a brain‐specific, constitutively active protein kinase C isoform, maintains synaptic long‐term potentiation (LTP). Structural remodeling of the postsynaptic density is believed to contribute to the expression of LTP. We therefore examined the role of PKMζ in reconfiguring PSD‐95, the major postsynaptic scaffolding protein at excitatory synapses. In primary cultures of hippocampal neurons, PKMζ activity was critical for increasing the size of PSD‐95 clusters during chemical LTP (cLTP). Increasing PKMζ activity by overexpressing the kinase in hippocampal neurons was sufficient to increase PSD‐95 cluster size, spine size, and postsynaptic AMPAR subunit GluA2. Overexpression of an inactive mutant of PKMζ did not increase PSD‐95 clustering, and applications of the ζ‐pseudosubstrate inhibitor ZIP reversed the PKMζ‐mediated increases in PSD‐95 clustering, indicating that the activity of PKMζ is necessary to induce and maintain the increased size of PSD‐95 clusters. Thus the persistent activity of PKMζ is both necessary and sufficient for maintaining increases of PSD‐95 clusters, providing a unified mechanism for long‐term functional and structural modifications of synapses. © 2011 Wiley Periodicals, Inc.