首页 | 本学科首页   官方微博 | 高级检索  
文章检索
  按 检索   检索词:      
出版年份:   被引次数:   他引次数: 提示:输入*表示无穷大
  收费全文   103篇
  免费   1篇
  国内免费   2篇
  2022年   1篇
  2021年   2篇
  2020年   1篇
  2019年   1篇
  2018年   1篇
  2017年   1篇
  2016年   5篇
  2015年   3篇
  2014年   3篇
  2013年   8篇
  2012年   2篇
  2011年   3篇
  2010年   6篇
  2009年   5篇
  2008年   6篇
  2007年   2篇
  2006年   5篇
  2005年   6篇
  2004年   7篇
  2003年   4篇
  2002年   2篇
  2001年   4篇
  1999年   1篇
  1997年   2篇
  1996年   1篇
  1995年   3篇
  1993年   1篇
  1992年   8篇
  1991年   1篇
  1990年   1篇
  1989年   1篇
  1988年   1篇
  1987年   2篇
  1984年   3篇
  1982年   1篇
  1980年   1篇
  1972年   1篇
排序方式: 共有106条查询结果,搜索用时 15 毫秒
51.
Research suggests that schizotypal personality disorder (SPD) is a part of the spectrum of schizophrenia-related illnesses. This article hypothesizes that a deficit in the representation and maintenance of context is a core cognitive disturbance in schizophrenia and that SPD individuals should demonstrate context-processing deficits. To test this hypothesis, the authors administered 3 versions of their AX-CPT task, designed to assess context processing, to 35 healthy controls and 26 individuals with DSM-IV SPD. They also administered working memory and selective attention tasks. SPD individuals displayed context representation deficits similar to those found in schizophrenia but did not show the same additional deficits in context maintenance. Context processing was strongly associated with working memory and selective attention performance in the SPD individuals.  相似文献   
52.
Huntington disease (HD) is a progressive neurodegenerative disorder. Presymptomatic genetic testing allows at-risk individuals to clarify their risk status. Understanding the characteristics and motivations of individuals seeking HD presymptomatic genetic testing better equips genetic counselors and other healthcare professionals to provide comprehensive and personalized care. The aims of this study were to (1) determine whether the average age when individuals seek presymptomatic HD genetic testing has decreased over time, (2) assess motivations for seeking testing, (3) explore whether there is a relationship between age and motivations, and (4) explore genetic counselors’ perceptions of the shift in age. Data from the US HD testing centers (N?=?4) were analyzed. A small but statistically significant decrease in age of individuals seeking presymptomatic testing was observed (p?=?0.045). HD community members (N?=?77) were surveyed regarding presymptomatic testing motivations. Younger individuals were more likely than older individuals to cite “To learn whether or not you would develop HD” and “To make choices about further education or a career” compared to older individuals (p?<?0.05). Conversely, older individuals more frequently cited “To give children a better idea of their risk” (p?<?0.002). Sixteen percent of genetic counselors surveyed (6/37) perceived a change in age of testing. All of these respondents had provided HD testing for ten or more years and anecdotally believed the age at testing has decreased over time. Study results help providers personalize counseling based on patient’s age and serve as a starting point for more research into the relationship between age at testing and motivations for testing.  相似文献   
53.
54.
The NMDA receptor (NMDAR) subunit GluN1 is an obligatory component of NMDARs without a known functional homolog and is expressed in almost every neuronal cell type. The NMDAR system is a coincidence detector with critical roles in spatial learning and synaptic plasticity. Its coincidence detection property is crucial for the induction of hippocampal long-term potentiation (LTP). We have generated a mutant mouse model expressing a hypomorph of the Grin1N598R allele, which leads to a minority (about 10%) of coincidence detection-impaired NMDARs. Surprisingly, these animals revealed specific functional changes in the dentate gyrus (DG) of the hippocampal formation. Early LTP was expressed normally in area CA1 in vivo, but was completely suppressed at perforant path-granule cell synapses in the DG. In addition, there was a pronounced reduction in the amplitude of the evoked population spike in the DG. These specific changes were accompanied by behavioral impairments in spatial recognition, spatial learning, reversal learning, and retention. Our data show that minor changes in GluN1-dependent NMDAR physiology can cause dramatic consequences in synaptic signaling in a subregion-specific fashion despite the nonredundant nature of the GluN1 gene and its global expression.According to Hebb''s postulate, neurons require a molecular mechanism to detect synchronous activity in order to change the strength of synaptic connectivity (Hebb 1949). NMDA receptors (NMDARs) are molecular coincidence detectors, and selective NMDAR antagonists block the induction of long-term potentiation (LTP) in both the dentate gyrus (DG) and CA1 regions of the hippocampus (Bliss and Collingridge 1993; Martin et al. 2000). NMDARs have been long known for their role in spatial learning, but more recently have been implicated in other forms of cognitive function and dysfunction (Gruart et al. 2006; Whitlock et al. 2006; Castner and Williams 2007; Kristiansen et al. 2007; Wilson and Linster 2008).Neuronal NMDARs are hetero-tetrameric ligand-gated ion channels typically comprised of two types of subunits. Two copies of the mandatory GluN1 subunit (or NR1 subunit [Collingridge et al. 2009] encoded by Grin1) are associated with two copies from the GluN2 family, GluN2A–D (or NR2A–D). The GluN1 subunit is expressed ubiquitously both spatially and temporally throughout the developing and adult brain. Global knockout mice models of the GluN1 subunit are postnatally lethal within hours after birth (Forrest et al. 1994; Li et al. 1994), and cell-specific GluN1 mice knockouts (Tsien et al. 1996; Nakazawa et al. 2002; McHugh et al. 2007; Niewoehner et al. 2007) have provided insights on how specific synapses and regional neuronal networks are dependent on NMDAR function.The early postnatal lethality of the global GluN1 knockout is in contrast to the null mutants of the four AMPA receptor genes and other major synaptic proteins, such as αCaMKII (Silva et al. 1992a,b; Jia et al. 1996; Zamanillo et al. 1999; Meng et al. 2003). This can be at least partially explained by the absence of any close GluN1 homologs, which could functionally compensate for the absence of the GluN1 subunit. Recombinant expression studies defined the GluN1 subunit as a mandatory component of NMDARs. This constellation provides a specific opportunity to test whether different local neuronal subnetworks are affected differentially by mutant Grin1 alleles associated with subtle alterations of the functional properties of NMDARs.GluN1 subunits with the N598R point mutation (GluN1R) yield functional NMDARs that are Mg2+ insensitive and Ca2+ impermeable (Burnashev et al. 1992; Mori et al. 1992). The Grin1N598R allele that codes for GluN1R subunits is a gain-of-function mutation that is dominant lethal, even in heterozygous and hemizygous lines (Single et al. 2000; Rudhard et al. 2003). NMDARs with GluN1R subunits do not act as coincidence detectors and, interestingly, mice expressing exclusively the GluN1R allele lack whisker-related pattern formation in the neonate brainstem (Rudhard et al. 2003).To investigate the functional importance of GluN1 subunits with the N598R point mutation, we took advantage of the generation of a variant mutant line of mice (GluN1Rneo/+) expressing a minority (around 10%) of these mutant NMDARs. Even though the majority of the NMDARs are normal, all neurons expressing NMDARs will contain a subset of receptors carrying this mutation.Therefore, this mouse model is an ideal candidate to study the impact of subtle alterations of NMDAR function on different neuronal networks, such as those comprising the hippocampal formation.Studies examining region-specific targeted disruption of GluN1 expression in subregions of the hippocampus have revealed subtle yet important contributions of this NMDAR subunit in synaptic plasticity and spatial learning and memory. CA1-restricted knockout of GluN1 expression in the hippocampus caused impaired spatial learning and memory as well as reduced CA1-LTP (Tsien et al. 1996). In the case of the disruption of GluN1 expression in the DG region of the hippocampus, more subtle behavioral impairments were apparent, including the inability to discriminate between two similar contexts (pattern separation) and deficits in spatial working memory despite normal LTP in the CA1 region (McHugh et al. 2007; Niewoehner et al. 2007).Our GluN1Rneo/+ mice differ from the region-specific GluN1 mutant mice in that they express the mutant hypomorph at the same level in different subregions of the hippocampus. Interestingly, we found that this allele leads to substantial differences in short- and long-term plasticity between area CA1 and the DG of the hippocampus. The specific impairment in the DG was accompanied by impaired spatial recognition, spatial learning, reversal learning, and retention. Our data establish the possibility of a circuit-specific phenotype caused by a mutant variant of a globally expressed major nonredundant synaptic protein.  相似文献   
55.
56.
Abstract

Over the course of 5 consecutive days, each author agreed to be ostracized for a day at work by the other four coauthors. All coauthors’ offices were in close proximity and were located solely on a single floor and wing of their academic building. Each morning, the name of that day's ostracized individual was drawn, and a scarlet letter “O” was placed above that individual's office door. Ostracizers were instructed to ignore the “Os” by not looking at them, speaking to them, or responding to anything they said. Open-ended individual event-contingent diaries were kept to record participants’ thoughts, feelings, and behaviors each time they were reminded of the ostracism. Despite foreknowledge and consent, attributional confusion surfaced and strong aversive reactions were reported. Findings are framed in terms of Williams's (1997) model of ostracism  相似文献   
57.
This article investigates child delinquency (offenders younger than 13 years of age). The population of child delinquents under various dispositions in the state of Louisiana, at one point in time, is described. Eighty youth are examined using the following characteristics: Race, Gender, Age, Offense Type (violent, nonviolent) Crime Category (felony, status offense, misdemeanor, and felony or misdemeanor) and Disposition (supervision, secure custody, and non-secure custody). Child delinquency is an important topic because the younger the age of first offense the greater the probability of a delinquent and criminal career. Findings reveal very few youth in secure custody and black males account for over half of the population of child delinquents. Over 75% of the population was 12 years of age.  相似文献   
58.
We propose a mixed belief model of self-deception. According to the theory, people distribute belief over two possible causal paths to an action, one where the action is freely chosen and one where it is due to factors outside of conscious control. Self-deceivers take advantage of uncertainty about the influence of each path on their behavior, and shift weight between them in a self-serving way. This allows them to change their behavior to provide positive evidence and deny doing so, enabling diagnostic inference to a desired trait. In Experiment 1, women changed their pain tolerance to provide positive evidence about the future quality of their skin, but judgments of effort claimed the opposite. This “effort denial” suggests that participants’ mental representation of their behavior was dissociated from their actual behavior, facilitating self-deception. Experiment 2 replicated the pattern in a hidden picture task where search performance was purportedly linked to self-control.  相似文献   
59.
The main goal of the present research was to demonstrate the interaction between category and causal induction in causal model learning. We used a two-phase learning procedure in which learners were presented with learning input referring to two interconnected causal relations forming a causal chain (Experiment 1) or a common-cause model (Experiments 2a, b). One of the three events (i.e., the intermediate event of the chain, or the common cause) was presented as a set of uncategorized exemplars. Although participants were not provided with any feedback about category labels, they tended to induce categories in the first phase that maximized the predictability of their causes or effects. In the second causal learning phase, participants had the choice between transferring the newly learned categories from the first phase at the cost of suboptimal predictions, or they could induce a new set of optimally predictive categories for the second causal relation, but at the cost of proliferating different category schemes for the same set of events. It turned out that in all three experiments learners tended to transfer the categories entailed by the first causal relation to the second causal relation.  相似文献   
60.
Family therapists emphasize introducing members of the caring professions to systemic ideas. Doctors in training usually gain some experience of systemic therapy. In this study two participatory styles of learning were used with medical students. Six groups of forty students were randomly allocated to learn about family therapy either by watching a video of a family or through role-play. The two mediums used are feasible, scored similarly on students' level of satisfaction, and result in gains in the students' knowledge of systemic principles.  相似文献   
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号