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51.
Dynamic body weight and body composition changes in response to subordination stress 总被引:3,自引:1,他引:2
Tamashiro KL Hegeman MA Nguyen MM Melhorn SJ Ma LY Woods SC Sakai RR 《Physiology & behavior》2007,91(4):440-448
Social stress is prevalent in many facets of modern society. Epidemiological data suggest that stress is linked to the development of overweight, obesity and metabolic disease. Although there are strong associations between the incidence of obesity with stress and elevated levels of hormones such as cortisol, there are limited animal models to allow investigation of the etiology of increased adiposity resulting from exposure to stress. Perhaps more importantly, an animal model that mirrors the consequences of stress in humans will provide a vehicle to develop rational clinical therapy to treat or prevent adverse outcomes from exposure to chronic social stress. In the visible burrow system (VBS) model of chronic social stress mixed gender colonies are housed for 2 week periods during which male rats of the colony quickly develop a dominance hierarchy. We found that social stress has significant effects on body weight and body composition such that subordinate rats progressively develop characteristics of obesity that occurs, in part, through neuroendocrine alterations and changes in food intake amount. Although subordinate rats are hyperphagic following social stress they do not increase their intake of sucrose solution as control and dominants do suggesting that they are anhedonic. Consumption of a high fat diet does not appear to affect development of a social hierarchy and appears to enhance the effect that chronic stress has on body composition. The visible burrow system (VBS) model of social stress may be a potential laboratory model for studying stress-associated metabolic disease, including the metabolic syndrome. 相似文献
52.
Ana Maria Brailean Ernst H.W. KosterKristof Hoorelbeke Rudi De Raedt 《Journal of behavior therapy and experimental psychiatry》2014
Background and objectives
Research indicates that individuals at-risk for depression are characterized by high sensitivity to loss and reduced sensitivity to reward. Moreover, it has been shown that attentional bias plays an important role in depression vulnerability. The current study aimed to examine the interplay between these risk factors for depression by examining the development of attentional bias toward reward and loss signals in dysphoric participants (individuals with elevated levels of depressive symptoms).Methods
Shapes were conditioned to reward and loss and subsequently presented in a dot probe task in a sample of dysphoric and nondysphoric participants.Results
Nondysphoric individuals oriented towards reward-related signals whereas dysphoric individuals failed to develop a reward-related attentional bias. This attentional effect was observed in the absence of group differences in motivational factors. No group differences were found for attentional bias for loss-related signals, despite the fact that dysphoric individuals performed worse in response to losing.Limitations
The current sample is not clinical thus generalization to clinical depression is not warranted.Conclusions
We argue that impaired early attentional processing of rewards are an important cognitive risk factor for anhedonic symptoms in persons with dysphoria. 相似文献53.
54.
Miura S Kida H Nakajima J Noda K Nagasato K Ayabe M Aizawa H Hauser M Taniwaki T 《Clinical neurology and neurosurgery》2012,114(4):352-355
Background
Anhedonia, a lowered ability to experience physical or social pleasure, has recently been recognized as a non-motor symptom of Parkinson's disease.Objective
To identify the frequency of anhedonia and the factors influencing hedonic tone in Japanese patients with Parkinson's disease.Patients and methods
We recruited 86 consecutive outpatients with a clinical diagnosis of PD attending two Japanese hospitals (one university hospital and one community hospital) in February 2010. We used the self-rating Snaith–Hamilton Pleasure Scale (SHAPS) translated into Japanese language from the original English version to assess and quantify hedonic tone as a subjectively experienced phenomenon. We studied the association of anhedonia with the variables age, age at onset, gender, disease duration, disease severity and antiparkinsonian drugs.Results
Thirty-nine patients (45%) were male and 47 (55%) were female. Mean age was 72.01 ± 9.07 (49–89) years, with mean age at onset of 64.93 ± 11.42 (31–88) years. Mean disease duration was 7.20 ± 5.54 (1–23) years. The mean Hoehn and Yahr scale was 2.76 ± 0.78. The mean SHAPS score of the total sample was 1.19 ± 1.86. The SHAPS score of 14 patients (16.3%) was 3 or more, indicating anhedonia. The mean SHAPS score was lower in patients taking pramipexole (0.58 ± 0.97) than in patients not taking pramipexole (1.57 ± 2.16). Multiple linear regression analysis identified pramipexole as a significant negative influencing factor on the SHAPS score, while disease severity and entacapone treatment were identified as positive influencing factors. The age, onset age, gender, disease duration, and use of pergolide, amantadine, zonisamide, selegiline, anticholinergic agents and droxidopa did not significantly affect the SHAPS score.Conclusion
Anhedonia is not rare non-motor symptom in Japanese patients with Parkinson's disease. This study suggests an anti-anhedonic property of pramipexole. 相似文献55.
Berry A Bellisario V Capoccia S Tirassa P Calza A Alleva E Cirulli F 《Psychoneuroendocrinology》2012,37(6):762-772
Stress is a main risk factor that can trigger psychiatric disorders, including anxiety and major depression. Neurotrophins, such as Brain-Derived Neurotrophic Factor (BDNF), have been identified as neuroendocrine effectors involved in the response to stress and in the neurobehavioural changes associated with depression. Aim of this paper was to study the relationship between neuroendocrine activation (circulating corticosterone and brain BDNF levels) and a wide array of depression- and anxiety-like behaviours (anhedonia, behavioural despair, generalised and social anxiety) resulting from exposure to chronic stress. To this end, 3-month-old C57BL/6J male mice were exposed to either chronic disruption of the social structure (SS), to a stable social structure (SG) or to social deprivation (SD), a condition lacking social stimuli. Results show that, despite not developing anhedonia (decreased preference for a sucrose solution), SD mice were characterised by increased emotionality and hypothalamic-pituitary-adrenal axis reactivity in addition to reduced BDNF levels. By contrast, SG and SS mice showed increased anhedonia accompanied by no alterations in the behavioural and neuroendocrine profile. The results here reported indicate that mice exposed to different social housing conditions use different behavioural strategies to cope with external challenges. In addition they suggest that social deprivation might represent a stressful condition triggering the emergence of both anxiety- and depression-like behaviours and clearly indicate BDNF as a main neurobiological variable mediating these responses. 相似文献
56.
KT Warnock AR Yang HS Yi HL June T Kelly AS Basile P Skolnick HL June 《Pharmacology, biochemistry, and behavior》2012,103(1):111-118
The co-occurrence of alcoholism and depression is highly prevalent and difficult to treat. In an animal model of binge drinking that exhibits abstinence-induced behaviors reminiscent of negative affective states, the triple monoamine uptake inhibitor, amitifadine, produced a selective, dose dependent attenuation of binge drinking. Amitifadine also reversed abstinence-induced increases in the intracranial self-stimulation threshold, a model of anhedonia, and immobility in the forced swim test, reflecting behavioral despair. In view of the safety profile of amitifadine in humans, including low risk for weight gain, lack of sexual side effects, and low potential for abuse, we hypothesize that amitifadine will be effective in treating co-occurring alcoholism and depression. 相似文献
57.
Jessica L. Bolton Jenny Molet Limor Regev Yuncai Chen Neggy Rismanchi Elizabeth Haddad Derek Z. Yang Andre Obenaus Tallie Z. Baram 《Neuropsychopharmacology》2018,83(2):137-147
Background
Anhedonia, the diminished ability to experience pleasure, is an important dimensional entity linked to depression, schizophrenia, and other emotional disorders, but its origins and mechanisms are poorly understood. We have previously identified anhedonia, manifest as decreased sucrose preference and social play, in adolescent male rats that experienced chronic early-life adversity/stress (CES). Here we probed the molecular, cellular, and circuit processes underlying CES-induced anhedonia and tested them mechanistically.Methods
We examined functional brain circuits and neuronal populations activated by social play in adolescent CES and control rats. Structural connectivity between stress- and reward-related networks was probed using high-resolution diffusion tensor imaging, and cellular/regional activation was probed using c-Fos. We employed viral-genetic approaches to reduce corticotropin-releasing hormone (Crh) expression in the central nucleus of the amygdala in anhedonic rats, and tested for anhedonia reversal in the same animals.Results
Sucrose preference was reduced in adolescent CES rats. Social play, generally considered an independent measure of pleasure, activated brain regions involved in reward circuitry in both control and CES groups. In CES rats, social play activated Crh-expressing neurons in the central nucleus of the amygdala, typically involved in anxiety/fear, indicating aberrant functional connectivity of pleasure/reward and fear circuits. Diffusion tensor imaging tractography revealed increased structural connectivity of the amygdala to the medial prefrontal cortex in CES rats. Crh-short hairpin RNA, but not control short hairpin RNA, given into the central nucleus of the amygdala reversed CES-induced anhedonia without influencing other emotional measures.Conclusions
These findings robustly demonstrate aberrant interactions of stress and reward networks after early-life adversity and suggest mechanistic roles for Crh-expressing amygdala neurons in emotional deficits portending major neuropsychiatric disorders. 相似文献58.
The medial prefrontal cortex (mPFC), hippocampus, and amygdala are implicated in the regulation of affect and physiological processes, including hypothalamic-pituitary-adrenal (HPA) axis function. Anhedonia is likely associated with dysregulation of these processes. Dense-array resting electroencephalographic and cortisol were obtained from healthy and anhedonic groups. Low-resolution electromagnetic tomography was used to compute intracerebral current density. For the control group, voxelwise analyses found a relationship between current density in beta and gamma bands and steeper cortisol slope (indicative of more adaptive HPA axis functioning) in regions of the hippocampus, parahippocampal gyrus, and mPFC. For the anhedonic group, the mPFC finding was absent. Anhedonia may be characterized by disruptions of mPFC-mediated neuroendocrine regulation, which could constitute a vulnerability to the development of stress-related disorders. 相似文献
59.
目的探索首发精神分裂症患者快感缺乏的成分特征及其与临床症状、认知功能和社会功能的相关性。方法纳入符合《国际疾病分类(第10版)》(ICD-10)诊断标准的31例首发精神分裂症患者和33例健康对照组。使用愉快情绪体验量表(TEPS)、阳性和阴性症状量表(PANSS)、重复性成套神经心理状态测验(RBANS)以及个人和社会功能量表(PSP)对患者的快感缺乏情况、精神症状、认知功能和社会功能进行评定。采用Pearson相关分析测查快感缺乏与临床症状、认知功能和社会功能的相关性。结果首发精神分裂症患者TEPS消费性快感评分低于健康对照组,差异有统计学意义[(27.71±5.48)分vs.(31.58±5.92)分,t=2.705,P=0.009]。相关分析显示,首发精神分裂症患者消费性快感缺乏与PANSS、RBANS和PSP评分的相关均无统计学意义(P均0.05)。结论首发精神分裂症患者存在消费性快感缺乏,其消费性快感缺乏可能独立于临床症状、认知功能损害和社会功能损害之外。 相似文献
60.