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排序方式: 共有10000条查询结果,搜索用时 15 毫秒
991.
Martje G. Pauly MD Marta Ruiz López MD Ana Westenberger PhD Gerard Saranza MD Norbert Brüggemann MD Anne Weissbach MD Raymond L. Rosales MD PhD Cid C. Diesta MD Roland D.G. Jamora MD Charles J. Reyes MSc Harutyun Madoev MSc Sonja Petkovic PhD Laurie J. Ozelius PhD Christine Klein MD Aloysius Domingo MD PhD 《Movement disorders》2020,35(11):1933-1938
992.
993.
Maria Grazia Forese Marta Pellegatta Paolo Canevazzi Giorgia S. Gullotta Paola Podini Cristina Rivellini Stefano C. Previtali Marco Bacigaluppi Angelo Quattrini Carla Taveggia 《Glia》2020,68(1):95-110
We have previously reported that prostaglandin D2 Synthase (L-PGDS) participates in peripheral nervous system (PNS) myelination during development. We now describe the role of L-PGDS in the resolution of PNS injury, similarly to other members of the prostaglandin synthase family, which are important for Wallerian degeneration (WD) and axonal regeneration. Our analyses show that L-PGDS expression is modulated after injury in both sciatic nerves and dorsal root ganglia neurons, indicating that it might play a role in the WD process. Accordingly, our data reveals that L-PGDS regulates macrophages phagocytic activity through a non-cell autonomous mechanism, allowing myelin debris clearance and favoring axonal regeneration and remyelination. In addition, L-PGDS also appear to control macrophages accumulation in injured nerves, possibly by regulating the blood–nerve barrier permeability and SOX2 expression levels in Schwann cells. Collectively, our results suggest that L-PGDS has multiple functions during nerve regeneration and remyelination. Based on the results of this study, we posit that L-PGDS acts as an anti-inflammatory agent in the late phases of WD, and cooperates in the resolution of the inflammatory response. Thus, pharmacological activation of the L-PGDS pathway might prove beneficial in resolving peripheral nerve injury. 相似文献
994.
Vito Antonio Baldassarro Alessandra Marchesini Luciana Giardino Laura Calzà 《Glia》2020,68(5):898-917
Impaired myelination is a key feature in neonatal hypoxia/ischemia (HI), the most common perinatal/neonatal cause of death and permanent disabilities, which is triggered by the establishment of an inflammatory and hypoxic environment during the most critical period of myelin development. This process is dependent on oligodendrocyte precursor cells (OPCs) and their capability to differentiate into mature oligodendrocytes. In this study, we investigated the vulnerability of fetal and adult OPCs derived from neural stem cells (NSCs) to inflammatory and HI insults. The resulting OPCs/astrocytes cultures were exposed to cytokines to mimic inflammation, or to oxygen–glucose deprivation (OGD) to mimic an HI condition. The differentiation of both fetal and adult OPCs is completely abolished following exposure to inflammatory cytokines, while only fetal-derived OPCs degenerate when exposed to OGD. We then investigated possible mechanisms involved in OGD-mediated toxicity: (a) T3-mediated maturation induction; (b) glutamate excitotoxicity; (c) glucose metabolism. We found that while no substantial differences were observed in T3 intracellular content regulation and glutamate-mediated toxicity, glucose deprivation lead to selective OPC cell death and impaired differentiation in fetal cultures only. These results indicate that the biological response of OPCs to inflammation and demyelination is different in fetal and adult cells, and that the glucose metabolism perturbation in fetal central nervous system (CNS) may significantly contribute to neonatal pathologies. An understanding of the underlying molecular mechanism will contribute greatly to differentiating myelination enhancing and neuroprotective therapies for neonatal and adult CNS white matter lesions. 相似文献
995.
Lubeiro Alba Fatjó-Vilas Mar Guardiola Maria Almodóvar Carmen Gomez-Pilar Javier Cea-Cañas Benjamin Poza Jesús Palomino Aitor Gómez-García Marta Zugasti Jone Molina Vicente 《European archives of psychiatry and clinical neuroscience》2020,270(4):433-442
European Archives of Psychiatry and Clinical Neuroscience - A deficit in task-related functional connectivity modulation from electroencephalogram (EEG) has been described in schizophrenia. The use... 相似文献
996.
Ana Clara Cristvo Filipa L. Campos Goun Je Marta Esteves Subhrangshu Guhathakurta Lichuan Yang M. Flint Beal Beatriz M. Fonseca Antonio J. Salgado Joo Queiroz Nuno Sousa Liliana Bernardino Gilberto Alves Kyung‐Sik Yoon Yoon‐Seong Kim 《The European journal of neuroscience》2020,52(4):3242-3255
Animal models of human diseases are crucial experimental tools to investigate the mechanisms involved in disease pathogenesis and to develop new therapies. In spite of the numerous animal models currently available that reproduce several neuropathological features of Parkinson disease (PD), it is challenging to have one that consistently recapitulates human PD conditions in both motor behaviors and biochemical pathological outcomes. Given that, we have implemented a new paradigm to expose rats to a chronic low dose of paraquat (PQ), using osmotic minipumps and characterized the developed pathologic features over time. The PQ exposure paradigm used lead to a rodent model of PD depicting progressive nigrostriatal dopaminergic neurodegeneration, characterized by a 41% significant loss of dopaminergic neuron in the substantia nigra pars compacta (SNpc), a significant decrease of 18% and 40% of dopamine levels in striatum at week 5 and 8, respectively, and a significant 1.5‐fold decrease in motor performance. We observed a significant increase of microglia activation state, sustained levels of α‐synucleinopathy and increased oxidative stress markers in the SNpc. In summary, this is an explorative study that allowed to characterize an improved PQ‐based rat model that recapitulates cardinal features of PD and may represent an attractive tool to investigate several mechanisms underlying the various aspects of PD pathogenesis as well as for the validation of the efficacy of new therapeutic approaches that targets different mechanisms involved in PD neurodegeneration. 相似文献
997.
Marta Campagnolo Federica Taioli Mario Cacciavillani Marta Ruiz Marco Luigetti Alessandro Salvalaggio Francesca Castellani Silvia Testi Moreno Ferrarini Tiziana Cavallaro Roberto Gasparotti Gian Maria Fabrizi Chiara Briani 《Journal of the peripheral nervous system : JPNS》2020,25(1):19-26
Hereditary neuropathies may be misdiagnosed with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). A correct diagnosis is crucial for avoiding unnecessary therapies and access genetic counseling. We report on nine patients (seven men, mean age 49.2 ± 16.1) diagnosed with and treated as CIDP, in whom mutations or variants of unknown significance (VUS) in genes associated with hereditary neuropathies were reported. All underwent neurological and neurophysiological examination, eight also cerebrospinal fluid (CSF) analysis. In 4/9, nerve ultrasound and/or MR‐neurography were performed. All the patients complained of progressive upper or lower limbs sensory‐motor symptoms, with heterogeneous disease duration (1‐34 years, mean 8.6 ± 10.8). Neurophysiology showed demyelinating signs in seven patients, mixed findings with predominant axonal damage in two patients. Neuroimaging disclosed diffuse abnormalities at proximal and distal segments. Molecular screening showed PMP22 duplication in two patients, mutations in the MPZ, EGR2, and GJB1 genes were reported in each of the remaining patients. The two patients with mixed neurophysiological findings had p.Val30Met mutation in the transthyretin gene. Two patients had VUS in the MARS and HSPB1 genes. Four patients had partial response to immunomodulant therapies, and CSF and neurophysiological features suggesting an inflammatory condition concomitant with the hereditary neuropathy. Hereditary neuropathy may be misdiagnosed with CIDP. The most common pitfalls are CSF (high protein levels and oligoclonal bands), incorrect interpretation of neurophysiology, and transient benefit from therapies. Neuroimaging may be helpful in cases with atypical presentations or when severe axonal damage complicate the neurophysiological interpretation. 相似文献
998.
Toniolo Sofia Cercignani Mara Mora-Peris Borja Underwood Jonathan Alagaratnam Jasmini Bozzali Marco Boffito Marta Nelson Mark Winston Alan Vera Jaime H. 《Journal of neurovirology》2020,26(5):754-763
Journal of NeuroVirology - We assessed changes in functional connectivity by fMRI (functional magnetic resonance imaging) and cognitive measures in otherwise neurologically asymptomatic people with... 相似文献
999.
Jiménez Isabel Carabia Júlia Bobillo Sabela Palacio Carles Abrisqueta Pau Pagès Carlota Nieto Juan C. Castellví Josep Martínez-Ricarte Francisco Escoda Lourdes Perla Cristóbal Céspedes Torrez Dennis H. Boix Joan Purroy Noelia Puigdefàbregas Lluís Seoane Joan Bosch Francesc Crespo Marta 《Journal of neuro-oncology》2020,149(1):13-25
Journal of Neuro-Oncology - Patients diagnosed with primary central nervous system lymphoma (PCNSL) often face dismal outcomes due to the limited availability of therapeutic options. PCNSL cells... 相似文献
1000.
Filippo Pietrantonio Fotios Loupakis Giovanni Randon Alessandra Raimondi Massimiliano Salati Dario Trapani Filippo Pagani Ilaria Depetris Giulia Maddalena Federica Morano Salvatore Corallo Michele Prisciandaro Francesca Corti Vincenzo Guarini Alessandro Bocconi Antonio Marra Carmen Belli Andrea Spallanzani Matteo Fassan Sara Lonardi Giuseppe Curigliano Giovanni Fucà Maria Di Bartolomeo Filippo de Braud 《The oncologist》2020,25(9):803-809