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1.
Steven M. Melemis 《The Yale journal of biology and medicine》2015,88(3):325-332
There are four main ideas in relapse prevention. First, relapse is a gradual process with distinct stages. The goal of treatment is to help individuals recognize the early stages, in which the chances of success are greatest. Second, recovery is a process of personal growth with developmental milestones. Each stage of recovery has its own risks of relapse. Third, the main tools of relapse prevention are cognitive therapy and mind-body relaxation, which are used to develop healthy coping skills. Fourth, most relapses can be explained in terms of a few basic rules. Educating clients in these rules can help them focus on what is important: 1) change your life (recovery involves creating a new life where it is easier to not use); 2) be completely honest; 3) ask for help; 4) practice self-care; and 5) don’t bend the rules. 相似文献
2.
Riccardo E. Marioni Lars Penke Gail Davies Jennifer E. Huffman Caroline Hayward Ian J. Deary 《Proceedings. Biological sciences / The Royal Society》2014,281(1781)
Human cognitive ability shows consistent, positive associations with fitness components across the life-course. Underlying genetic variation should therefore be depleted by selection, which is not observed. Genetic variation in general cognitive ability (intelligence) could be maintained by a mutation–selection balance, with rare variants contributing to its genetic architecture. This study examines the association between the total number of rare stop-gain/loss, splice and missense exonic variants and cognitive ability in childhood and old age in the same individuals. Exome array data were obtained in the Lothian Birth Cohorts of 1921 and 1936 (combined N = 1596). General cognitive ability was assessed at age 11 years and in late life (79 and 70 years, respectively) and was modelled against the total number of stop-gain/loss, splice, and missense exonic variants, with minor allele frequency less than or equal to 0.01, using linear regression adjusted for age and sex. In both cohorts and in both the childhood and late-life models, there were no significant associations between rare variant burden in the exome and cognitive ability that survived correction for multiple testing. Contrary to our a priori hypothesis, we observed no evidence for an association between the total number of rare exonic variants and either childhood cognitive ability or late-life cognitive ability. 相似文献
3.
Meta‐analyses evaluating the association between the serotonin transporter polymorphism (5‐HTTLPR) with neuroticism and depression diagnosis as phenotypes have been inconclusive. We examined a gene–environment interaction on a cognitive vulnerability marker of depression, cognitive reactivity (CR) to sad mood. A total of 250 university students of European ancestry were genotyped for the 5‐HTTLPR, including SNP rs25531, a polymorphism of the long allele. Association analysis was performed for neuroticism, CR and depression diagnosis (using a self‐report measure). As an environmental pathogen, self‐reported history of childhood emotional abuse was measured because of its strong relationship with depression. Participants with the homozygous low expressing genotype had high CR if they had experienced childhood emotional maltreatment but low CR if they did not have such experience. This interaction was strongest on the Rumination subscale of the CR measure. The interaction was not significant with neuroticism or depression diagnosis as outcome measures. Our results show that 5‐HTTLPR is related to cognitive vulnerability to depression. Our findings provide evidence for a differential susceptibility genotype rather than a vulnerability genotype, possibly because of the relatively low levels of abuse in our sample. The selection of phenotype and environmental contributor is pivotal in investigating gene–environment interactions in psychiatric disorders. 相似文献
4.
Ximena J. Nelson Alex H. Taylor Erica A. Cartmill Heidi Lyn Lauren M. Robinson Vincent Janik Colin Allen 《Biological reviews of the Cambridge Philosophical Society》2023,98(5):1548-1563
The nature and evolution of positive emotion is a major question remaining unanswered in science and philosophy. The study of feelings and emotions in humans and animals is dominated by discussion of affective states that have negative valence. Given the clinical and social significance of negative affect, such as depression, it is unsurprising that these emotions have received more attention from scientists. Compared to negative emotions, such as fear that leads to fleeing or avoidance, positive emotions are less likely to result in specific, identifiable, behaviours being expressed by an animal. This makes it particularly challenging to quantify and study positive affect. However, bursts of intense positive emotion (joy) are more likely to be accompanied by externally visible markers, like vocalisations or movement patterns, which make it more amenable to scientific study and more resilient to concerns about anthropomorphism. We define joy as intense, brief, and event-driven (i.e. a response to something), which permits investigation into how animals react to a variety of situations that would provoke joy in humans. This means that behavioural correlates of joy are measurable, either through newly discovered ‘laughter’ vocalisations, increases in play behaviour, or reactions to cognitive bias tests that can be used across species. There are a range of potential situations that cause joy in humans that have not been studied in other animals, such as whether animals feel joy on sunny days, when they accomplish a difficult feat, or when they are reunited with a familiar companion after a prolonged absence. Observations of species-specific calls and play behaviour can be combined with biometric markers and reactions to ambiguous stimuli in order to enable comparisons of affect between phylogenetically distant taxonomic groups. Identifying positive affect is also important for animal welfare because knowledge of positive emotional states would allow us to monitor animal well-being better. Additionally, measuring if phylogenetically and ecologically distant animals play more, laugh more, or act more optimistically after certain kinds of experiences will also provide insight into the mechanisms underlying the evolution of joy and other positive emotions, and potentially even into the evolution of consciousness. 相似文献
5.
Pierre Valeix Paul Preziosi Claude Rossignol Marie-Alice Farnier Serge Hercberg 《Biological trace element research》1992,32(1-3):259-266
Urinary iodine excretion was assessed in 642 healthy children aged 10 mo (n=243), 2 yr (n=183), and 4 yr (n=216) living in the Paris area and originating from continental France (60.3%), North Africa (13.8%), the West Indies (9.1%),
West Africa (8.3%), Southeast Asia (4.8%), and southern Europe (3.8%). Mild impairment of neurological (reflexes, tone, audiometry)
and intellectual development (Brunet-Lézine scale) was assessed in relation to iodine status. Iodine excretions (median values)
were 18.4, 11.9, and 10.9 μg/100 mL at 10 mo, 2 yr, and 4 yr, respectively, and risk of mild iodine deficiency (5–10 μg/100
mL) was 18.1%, 34.8%, and 38.3% for the same age groups. No relationship was found between anthropometry, global development
quotient, and iodine status. High hearing thresholds were more commonly associated with lower iodine excretion, suggesting
mild hearing defects. In spite of iodine prophylaxis, the risk of mild to moderate iodine deficiency still exists in France
and in a number of European countries. Evaluation of neurological sequels of borderline iodine status is a major public health
problem in European communities. 相似文献
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8.
目的:探讨更有利于术后认知功能障碍早期诊断的评估方法。方法:选择青年患者(18-45岁)60例,ASAⅠ~Ⅱ级,在全凭静脉麻醉或椎管内麻醉下行手术;青年健康志愿者30例为对照组,术前一天(T1),术后3天(T2)行认知功能6项测定。所得结果分别采用1个标准差法(SD)和Z计分法对术后认知功能进行评定。P<0.05差异有统计学意义。结果:术后3天,依据SD法诊断认知功能受损25/90例(27.8%),术后认知功能障碍2/90例(2.2%),Z计分法认知受损18/90(20%)例,认知障碍3/90例(3.3%),两种诊断方法之间差异无统计学意义(P>0.05)。经K系数检验,SD法与Z计分法诊断吻合度无统计学意义(kappa=0.000,P>0.05)。结论:两种评估方法同时进行评估,可以弥补相互不足,较大程度地避免了术后认知功能受损假阴性的诊断,更有利于术后认知功能障碍的早期发现。 相似文献
9.
Basavanahalli Nanjundaiah Rohith Baragur Venkatanarayanasetty Shyamala 《Developmental neurobiology》2019,79(3):236-251
Neural identity and wiring specificity are fundamental to brain function. Factors affecting proliferation of the progenitor cells leading to an expansion or regression of specific neuronal clusters are expected to challenge the process of formation of precise synaptic connections with their partners and their further integration to result in proper functional neural circuitry. We have investigated the role of scalloped, a Hippo pathway gene in Drosophila brain development and have shown that its function is critical to regulate proliferation of Mushroom Body Neuroblasts and to limit the neuronal cluster size to normal in the fly brain. Here we investigate the consequent effect of the anatomical phenotype of mutant flies on the brain function, as exemplified by their cognitive performance. We demonstrate that the neural expansion in important neural clusters of the olfactory pathway, caused due to Scalloped inactivation, imparts severe disabilities in learning, short‐term memory and long‐term memory. Scalloped knockdown in αβ Kenyon Cell clusters drastically reduces long‐term memory performance. Scalloped deficiency induced neural expansion in antennal lobe and ellipsoid body neurons bring down short‐term memory performance significantly. We also demonstrate that the cognitive impairments observed here are not due to a problem in memory formation or execution in the adult, but are due to the developmental deformities caused in the respective class of neurons. Our results strongly indicate that the additional neurons generated by Scalloped inactivation are not synergistically integrated into, but rather perturb the formation of precise functional circuitry. 相似文献
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