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排序方式: 共有458条查询结果,搜索用时 125 毫秒
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Sonja M Wojcik Martesa Tantra Beata Stepniak Kwun-nok M Man Katja Müller-Ribbe Martin Begemann Anes Ju Sergi Papiol Anja Ronnenberg Artem Gurvich Yong Shin Iris Augustin Nils Brose Hannelore Ehrenreich 《Molecular medicine (Cambridge, Mass.)》2013,19(1):135-148
Anxiety disorders and substance abuse, including benzodiazepine use disorder, frequently occur together. Unfortunately, treatment of anxiety disorders still includes benzodiazepines, and patients with an existing comorbid benzodiazepine use disorder or a genetic susceptibility for benzodiazepine use disorder may be at risk of adverse treatment outcomes. The identification of genetic predictors for anxiety disorders, and especially for benzodiazepine use disorder, could aid the selection of the best treatment option and improve clinical outcomes. The brain-specific angiogenesis inhibitor I–associated protein 3 (Baiap3) is a member of the mammalian uncoordinated 13 (Munc13) protein family of synaptic regulators of neurotransmitter exocytosis, with a striking expression pattern in amygdalae, hypothalamus and periaqueductal gray. Deletion of Baiap3 in mice leads to enhanced seizure propensity and increased anxiety, with the latter being more pronounced in female than in male animals. We hypothesized that genetic variation in human BAIAP3 may also be associated with anxiety. By using a phenotype-based genetic association study, we identified two human BAIAP3 single-nucleotide polymorphism risk genotypes (AA for rs2235632, TT for rs1132358) that show a significant association with anxiety in women and, surprisingly, with benzodiazepine abuse in men. Returning to mice, we found that male, but not female, Baiap3 knockout (KO) mice develop tolerance to diazepam more quickly than control animals. Analysis of cultured Baiap3 KO hypothalamus slices revealed an increase in basal network activity and an altered response to diazepam withdrawal. Thus, Baiap3/BAIAP3 is gender specifically associated with anxiety and benzodiazepine use disorder, and the analysis of Baiap3/BAIAP3-related functions may help elucidate mechanisms underlying the development of both disorders. 相似文献
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Donato Inverso Jingjing Shi Ki Hong Lee Moritz Jakab Shani Ben-Moshe Shubhada R. Kulkarni Martin Schneider Guanxiong Wang Marziyeh Komeili Paula Argos Vélez Maria Riedel Carleen Spegg Thomas Ruppert Christine Schaeffer-Reiss Dominic Helm Indrabahadur Singh Michael Boutros Sudhakar Chintharlapalli Hellmut G. Augustin 《Developmental cell》2021,56(11):1677-1693.e10
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How do environmental factors influence life cycles and development? An experimental framework for early‐diverging metazoans 下载免费PDF全文
Thomas C. G. Bosch Maja Adamska René Augustin Tomislav Domazet‐Loso Sylvain Foret Sebastian Fraune Noriko Funayama Juris Grasis Mayuko Hamada Masayuki Hatta Bert Hobmayer Kotoe Kawai Alexander Klimovich Michael Manuel Chuya Shinzato Uli Technau Seungshic Yum David J. Miller 《BioEssays : news and reviews in molecular, cellular and developmental biology》2014,36(12):1185-1194
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Cristobal Rodero Marina Strocchi Maciej Marciniak Stefano Longobardi John Whitaker Mark D. ONeill Karli Gillette Christoph Augustin Gernot Plank Edward J. Vigmond Pablo Lamata Steven A. Niederer 《PLoS computational biology》2021,17(4)
Cardiac anatomy plays a crucial role in determining cardiac function. However, there is a poor understanding of how specific and localised anatomical changes affect different cardiac functional outputs. In this work, we test the hypothesis that in a statistical shape model (SSM), the modes that are most relevant for describing anatomy are also most important for determining the output of cardiac electromechanics simulations. We made patient-specific four-chamber heart meshes (n = 20) from cardiac CT images in asymptomatic subjects and created a SSM from 19 cases. Nine modes captured 90% of the anatomical variation in the SSM. Functional simulation outputs correlated best with modes 2, 3 and 9 on average (R = 0.49 ± 0.17, 0.37 ± 0.23 and 0.34 ± 0.17 respectively). We performed a global sensitivity analysis to identify the different modes responsible for different simulated electrical and mechanical measures of cardiac function. Modes 2 and 9 were the most important for determining simulated left ventricular mechanics and pressure-derived phenotypes. Mode 2 explained 28.56 ± 16.48% and 25.5 ± 20.85, and mode 9 explained 12.1 ± 8.74% and 13.54 ± 16.91% of the variances of mechanics and pressure-derived phenotypes, respectively. Electrophysiological biomarkers were explained by the interaction of 3 ± 1 modes. In the healthy adult human heart, shape modes that explain large portions of anatomical variance do not explain equivalent levels of electromechanical functional variation. As a result, in cardiac models, representing patient anatomy using a limited number of modes of anatomical variation can cause a loss in accuracy of simulated electromechanical function. 相似文献