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Syed M. Gilani Muhammad Khan Andrea Barbieri Manju L. Prasad 《Diagnostic Histopathology》2021,27(6):263-271
Anaplastic thyroid carcinoma (ATC) is an aggressive thyroid malignancy with high mortality rate. This malignancy arises in thyroid follicular cells either denovo or with an associated differentiated thyroid carcinoma component. Clinically, it usually presents as a rapidly enlarging mass, pain and locally compressive symptoms. Histopathologic variability and heterogeneity often pose diagnostic challenges, especially in scant and paucicellular specimens. This article describes the clinical, histopathologic and molecular features of ATC and also addresses the associated diagnostic limitations and challenges. 相似文献
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Ahmed I. Gilani Muhammad O. Chohan Melis Inan Scott A. Schobel Nashid H. Chaudhury Samuel Paskewitz Nao Chuhma Sara Glickstein Robert J. Merker Qing Xu Scott A. Small Stewart A. Anderson Margaret Elizabeth Ross Holly Moore 《Proceedings of the National Academy of Sciences of the United States of America》2014,111(20):7450-7455
GABAergic interneuron hypofunction is hypothesized to underlie hippocampal dysfunction in schizophrenia. Here, we use the cyclin D2 knockout (Ccnd2−/−) mouse model to test potential links between hippocampal interneuron deficits and psychosis-relevant neurobehavioral phenotypes. Ccnd2−/− mice show cortical PV+ interneuron reductions, prominently in hippocampus, associated with deficits in synaptic inhibition, increased in vivo spike activity of projection neurons, and increased in vivo basal metabolic activity (assessed with fMRI) in hippocampus. Ccnd2−/− mice show several neurophysiological and behavioral phenotypes that would be predicted to be produced by hippocampal disinhibition, including increased ventral tegmental area dopamine neuron population activity, behavioral hyperresponsiveness to amphetamine, and impairments in hippocampus-dependent cognition. Remarkably, transplantation of cells from the embryonic medial ganglionic eminence (the major origin of cerebral cortical interneurons) into the adult Ccnd2−/− caudoventral hippocampus reverses these psychosis-relevant phenotypes. Surviving neurons from these transplants are 97% GABAergic and widely distributed within the hippocampus. Up to 6 mo after the transplants, in vivo hippocampal metabolic activity is lowered, context-dependent learning and memory is improved, and dopamine neuron activity and the behavioral response to amphetamine are normalized. These findings establish functional links between hippocampal GABA interneuron deficits and psychosis-relevant dopaminergic and cognitive phenotypes, and support a rationale for targeting limbic cortical interneuron function in the prevention and treatment of schizophrenia.Precursors of most γ-aminobutyric acid (GABA)-releasing interneurons of the cerebral cortex and the hippocampus originate in the embryonic medial ganglionic eminence (MGE) (1–3). A subpopulation of MGE-derived cells differentiates into fast-spiking, parvalbumin-expressing (PV+) interneurons that tightly regulate the activity and synchronization of cortical projection neurons (2, 4). Structural and functional deficits in PV+ interneurons are hypothesized as a pathophysiological mechanism in schizophrenia and psychotic disorders (4–6).Although psychotic disorders are clearly heterogeneous in etiology, disinhibition within temporolimbic cortical circuits is postulated as a core pathophysiology underlying positive symptoms (e.g., delusions and hallucinations) and a subset of cognitive disturbances that manifest with psychosis (4, 5, 7). Postmortem studies of brains from individuals with psychotic disorders show reduced molecular markers of the number and/or function of PV+ interneurons in the hippocampus (6, 8). Consistent with these observations, basal metabolic activity in the hippocampus, as measured with functional magnetic resonance imaging (fMRI), is increased in schizophrenia, a phenotype that predicts psychosis and positive symptom severity (5, 7). This abnormal resting activity is postulated to underlie abnormal recruitment of hippocampal circuits during cognitive performance (5, 9). Striatal dopamine (DA) release capacity is also increased and correlated with positive symptoms in schizophrenia and its risk states (10, 11). Importantly, hippocampal hyperactivity may contribute to DA dysregulation (12), because rodent studies show that caudoventral hippocampal (in the primate, anterior hippocampal) efferents regulate the activity of DA neurons and medial striatal DA release (13, 14).Thus, converging evidence implicates hippocampal disinhibition in the abnormal striatal DA transmission and cognitive impairment in schizophrenia. However, the role of hippocampal inhibitory interneurons in psychosis-relevant circuitry remains to be established. To this end, we used the cyclin D2 (Ccnd2) knockout mouse model (15), which displays a relatively selective deficit in cortical PV+ interneurons, and transplantation of interneuron precursors from the MGE to elucidate relationships between reduced hippocampal GABA interneuron function and multiple psychosis-relevant phenotypes, and to explore a novel treatment strategy for psychosis. 相似文献
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Evaluation of atypical human immunodeficiency virus immunoblot reactivity in blood donors 总被引:6,自引:0,他引:6
NL Dock ; HV Lamberson Jr ; TA O''Brien ; DE Tribe ; SS Alexander ; BJ Poiesz 《Transfusion》1988,28(5):412-418
Blood donors reactive by enzyme-linked immunosorbent assay for antibody to the human immunodeficiency virus (HIV) who showed atypical patterns of viral core protein reactivity on Western blot were monitored for several months. Characterization of their antibodies was performed by 1) use of recombinant HIV proteins; 2) determination of cross-reactivity to HTLV-I, HTLV-II, and HTLV-IV: 3) assessment of immune status; and 4) identification of potentially interfering autoantibodies. Nineteen of 20 donors maintained the same HIV antibody reactivity throughout the follow-up period; the other donor became fully antibody-positive. Eighteen of 20 donors' sera showed clear reactivity with HIV recombinant core proteins. Ten of 19 donor samples demonstrated cross-reactivity to HTLV-IV; 3 of these 10 also cross-reacted with HTLV-I. The immune status of all donors was normal, although the medical histories and HLA antibody screens suggested possible autoimmune reactivity in 9 of 18 donors. During follow-up interviews, three donors reported possible risk factors for HIV infection that had not been acknowledged at the time of blood donation. We conclude that exclusion of donors with these atypical serologic test results is warranted while further studies to determine significance are being conducted. 相似文献
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Transfusion practice in central Virginia 总被引:4,自引:0,他引:4
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目的:已有理论提出急性心肌梗死后骨髓和外周血中的CD34 干细胞具有自身动员的潜能,观察这一潜能的变化特征及其对心肌梗死组织再生能力的影响。方法:实验于2004-09/2005-02在阜外心血管病医院完成。①实验动物:雄性SD大鼠40只,随机数字表法分为心肌梗死组、假手术组,20只/组。②实验方法:心肌梗死组大鼠采用冠状动脉结扎法建立心肌梗死模型。心电图ST段抬高或有室性心律出现,前壁心肌呈苍白色为造模成功。假手术组仅作开胸手术,前降支不予结扎。③实验评估:于心肌梗死后3,7,14,28d,流式细胞仪检测骨髓和外周血中CD34 干细胞的含量。用免疫组化方法检测梗死心肌组织中的Ki67细胞和毛细血管数量。结果:①外周血及骨髓CD34 干细胞含量的变化:心肌梗死组外周血中的CD34 干细胞数量于造模后3d开始上升,7d后明显高于假手术组(P<0.01),至14,28d时逐渐回落至假手术组水平(P>0.05)。心肌梗死组骨髓中的CD34 干细胞数量于造模后各时间点始终无明显变化(P>0.05)。②组织学评定:心肌梗死组梗死区Ki67细胞和毛细血管数量于造模后3d开始增多,7d时明显多于非梗死区(P<0.05);至14,28d梗死区Ki67细胞数量明显少于造模后7d(P<0.05),毛细血管数量的减少不明显(P>0.05)。免疫组化染色显示少数Ki67细胞分化为血管内皮细胞,未见向心肌细胞分化。③相关性分析:梗死区Ki67细胞、毛细血管数量于造模后7d与外周血中CD34 干细胞数量呈显著正相关(r=0.913,P=0.021;r=0.887,P=0.035)。结论:机体CD34 干细胞的自体动员、增殖反应的潜能随急性心肌梗死时间的延长而逐渐减弱,自体动员的干细胞功能尚不足以达到修复梗死心肌组织的效果。 相似文献
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对QT离散度实质的探讨 总被引:2,自引:0,他引:2
为探讨QT离散度(QTd)的真实意义,观察139例急性心肌梗死(AMI,AMI组)及109例正常人(对照组)的最长QT间期(QTmax)、校正QTmax(QTcmax)及QTd的变化。结果:①AMI组的QTmax、QTcmax和QTd均显著高于对照组(分别为422.60±30.51msvs382.46±23.40ms、460.21±28.96msvs388.51±20.15ms、59.80±28.40msvs39.43±12.21ms,P均<0.001)。②AMI组中发生严重室性心律失常(VA)患者(114例)的QTmax、QTcmax、QTd与无VA的患者(25例)相比,均有显著差异(分别为448.58±33.40msvs416.10±35.30ms、481.43±35.17msvs439.60±27.10ms、66.90±20.72msvs48.32±23.61ms,P均<0.001)。认为AMI时QTd系T向量环在不同导联上的“投影”差异所引起的,其异常的本质是QT间期延长 相似文献