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991.
Fear of negative evaluation, such as negative social performance feedback, is the core symptom of social anxiety. The present study investigated the neural correlates of anticipation and perception of social performance feedback in social anxiety. High (HSA) and low (LSA) socially anxious individuals were asked to give a speech on a personally relevant topic and received standardized but appropriate expert performance feedback in a succeeding experimental session in which neural activity was measured during anticipation and presentation of negative and positive performance feedback concerning the speech performance, or a neutral feedback‐unrelated control condition. HSA compared to LSA subjects reported greater anxiety during anticipation of negative feedback. Functional magnetic resonance imaging results showed deactivation of medial prefrontal brain areas during anticipation of negative feedback relative to the control and the positive condition, and medial prefrontal and insular hyperactivation during presentation of negative as well as positive feedback in HSA compared to LSA subjects. The results indicate distinct processes underlying feedback processing during anticipation and presentation of feedback in HSA as compared to LSA individuals. In line with the role of the medial prefrontal cortex in self‐referential information processing and the insula in interoception, social anxiety seems to be associated with lower self‐monitoring during feedback anticipation, and an increased self‐focus and interoception during feedback presentation, regardless of feedback valence. Hum Brain Mapp 35:6023–6031, 2014. © 2014 Wiley Periodicals, Inc.  相似文献   
992.
Apathy is a relatively common psychiatric syndrome in HIV infection, but little is known about its neural correlates. In the present study, we examined the associations between apathy and diffusion tensor imaging (DTI) indices in key frontal white matter regions in the thalamocorticostriatal circuit, which has been implicated in the expression of apathy. Nineteen participants with HIV infection and 19 demographically comparable seronegative comparison subjects completed the Apathy subscale of the Frontal Systems Behavioral Scale as a part of a comprehensive neuropsychiatric research evaluation. When compared to the seronegative participants, the HIV+ group had significantly more frontal white matter abnormalities. Within HIV+ persons, and as predicted, higher ratings of apathy were associated with greater white matter alterations in the anterior corona radiata, genu, and orbital medial prefrontal cortex. The associations between white matter alterations and apathy were independent of depression and were stronger among participants with lower current cluster of differentiation 4 (CD4) counts. All told, these findings indicate that apathy is independently associated with white matter abnormalities in anterior, medial brain regions in persons infected with HIV, particularly in the setting of lower current immune functioning, which may have implications for antiretroviral therapy.  相似文献   
993.
The visual word form area (VWFA) is a region in the posterior left occipitotemporal cortex adjacent to the fusiform gyrus hypothesized to mediate word recognition. Evidence supporting the role of this area in reading comes from neuroimaging studies of normal subjects, case-controlled lesion studies, and studies of patients with surgical resection of the VWFA for tumors or epilepsy. Based on these prior reports, a small discrete lesion to the VWFA would be expected to cause alexia in a literate person without prior brain process, but such a case has not previously been reported to our knowledge. Here, we report the case of a previously-healthy 63-year-old man with the acute onset of alexia without other significant impairments. Magnetic resonance imaging (MRI) of the brain revealed a small ischemic stroke localized to the inferior left occipitotemporal cortex, corresponding to the approximate location of the putative VWFA. Characteristic of pure alexia, testing in the weeks following the stroke revealed a letter-by-letter reading strategy and a word length effect on single word reading. Formal visual field testing was normal. There was no color anomia, or object or face recognition deficits, although a mild agraphia may have been present. This case of acute-onset alexia in a previously normal individual due to a small stroke restricted to the VWFA and sparing occipital cortex and white matter pathways supports the conclusion that the VWFA is crucial for reading.  相似文献   
994.
《Clinical neurophysiology》2014,125(12):2384-2389
ObjectiveTo assess the interest of specifically targeting Brodmann Areas (BA) 9 or 46 for rTMS treatment of depression.MethodsPatients with Treatment-Resistant Depression were randomly assigned to two treatment groups to receive either rTMS on BA 9 or on BA 46. Each patient underwent 10 sessions of 1 Hz-rTMS for 2 weeks. The Hamilton and Montgomery–Asberg Depression Rating Scales (HDRS, MADRS) were used under blind conditions to assess the therapeutic response (50% improvement). A Wilcoxon signed-rank test was used to compare the depression rating scales scores obtained before and after the 10 rTMS sessions for each of the two groups. The therapeutic results in the two groups were compared using the Mann–Whitney–Wilcoxon test. We also reported the effect sizes using Hedges’s g.ResultsFifteen patients were included. Stimulation of both BA 9 (n = 7) and BA 46 (n = 8) led to similar therapeutic responses in the two groups (with moderate effect size), such as the mean decrease in HDRS (BA 9: p = 0.015; BA 46: p = 0.010) and MADRS (BA 9: p = 0.042; BA 46: p = 0.038) scores.ConclusionOur results do not come out in favor of one or the other BA.SignificanceStimulation of BA 9 and BA 46 appears to be equally effective in the treatment of depression.  相似文献   
995.
996.
997.
目的 探讨肾上腺皮质腺瘤的诊断及治疗.方法 结合2013年8月收治的1例巨大无功能性肾上腺皮质腺瘤的临床资料进行回顾性分析,从发病机制、临床表现、诊断和治疗方面加以总结.结果术后病理:肿瘤大小约22 cm×15 cm×12 cm,重约3 500 g,类圆形,包膜完整,切开后见肿瘤内有出血.结合免疫组织化学考虑为肾上腺皮质腺瘤伴出血、囊性变;免疫组织化学:S100(±),Ki67约2%(+),A103(+ + +),Syn(+ +),嗜铬素A(CgA)为(+).结论本病缺乏特异性临床表现,术前诊断困难,手术难度大,但手术治疗是唯一有效的治疗方法.  相似文献   
998.
目的:研究大鼠内侧前额叶皮质(mPFC)边缘前区(PrL)GluN2亚基在海洛因诱导条件位置性偏爱(CPP)及戒断状态的表达。方法:24只SD大鼠随机分为对照组(control)和海洛因诱导组。海洛因诱导组大鼠按实验进程分为两种状态,即海洛因诱导CPP状态(heroin)和海洛因戒断状态(withdrawal)。用小剂量递增法皮下注射海洛因,行大鼠海洛因诱导CPP建模,并自然戒断,免疫荧光染色检测各组大鼠PrL区GluN2亚基NR2A、NR2B、NR2C、NR2D的表达。结果:大鼠经过连续7 d小剂量递增法注射海洛因,形成了稳定的CPP;免疫荧光染色结果显示,大鼠CPP状态PrL区NR2B表达较对照组显著增强(P<0.01),其他亚基无明显变化。海洛因自然戒断7 d后,戒断状态大鼠PrL区NR2A、NR2C表达较对照组和CPP状态皆显著增强(P<0.01)。戒断状态NR2B表达水平显著高于对照组(P<0.01),但与CPP状态无显著差异。结论:大鼠海洛因依赖CPP的形成与PrL区NR2B亚基的活性密切相关,NR2A和NR2C可能参与药物戒断症状的调控。推测PrL区GluN2不同亚基在海洛因成瘾不同阶段作用不同,并可能成为临床海洛因成瘾干预和治疗的重要靶点。  相似文献   
999.
All children experience pain, and although many recover quickly, some go on to develop chronic pain. Adolescent chronic pain is a growing epidemic. It is unknown why some adolescents recover without incident and others experience persistent pain. Although unexplored, early life adversity may contribute to the development and maintenance of chronic pain. This study investigated the effects and underlying neurobiological mechanisms of an early life stressor on nociceptive (pain) sensitivity and emotional function in male and female Sprague-Dawley rats. Using maternal separation (MS) as an established model of early life stress, we addressed two aims: investigation of the effects of MS on behavior (anxiety and pain sensitivity), and investigation of the effects of MS on mRNA and pathophysiological changes associated with an acutely painful stimulus. Our results indicate that MS increased anxiety-like behavior and altered nociceptive responsivity in adolescent rats, with decreased mechanical withdrawal thresholds indicative of heightened and prolonged pain-related behavior. The MS groups also demonstrated increased expression of genes involved in regulating the stress and fight-or-flight response, mood, and neuroplasticity; as well as increased levels of inflammatory markers. We conclude that nociception, both at the behavioral and molecular level, is altered in response to the MS stressor.  相似文献   
1000.
Monocarboxylates cannot cross the blood-brain barrier freely to participate in brain energy metabolism. Specific monocarboxylate transporters (MCTs) are needed to cross cellular membranes. Monocarboxylate transporter 2 (MCT2) is a major monocarboxylate transporter encoded by the SLC16A7 gene. Recent studies reported that neurodegenerative diseases of the CNS, such as Alzheimer's disease (AD) and Parkinson's disease (PD), were related to energy metabolic impairment. MCT2 also plays an important role in energy metabolism in the CNS. To provide experimental evidence for future research on the role of MCT2 in the pathological process of CNS degenerative diseases, the distribution and density of MCT2 in different subregions of wild-type mouse brain was examined using immunohistochemistry, western blot and immunogold post-embedding electron microscopic techniques. The amount of MCT2 was higher in cerebellum than in cortex and hippocampus on western blots, and there was no statistical difference between cortex and hippocampus. Immunohistochemistry assay revealed the highest density of MCT2 in the CA3 of the hippocampus. The granular cell layer of the cerebellum contained more MCT2 than the molecular layer. The MCT2 density on the end feet of astrocytes of molecular layer was lower than in hippocampus, but the postsynaptic densities (PSDs) of asymmetric synapses in the molecular layer exhibited a high density using immunogold post-embedding electron microscopic techniques.  相似文献   
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