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31.
Bucello Sebastiano Annovazzi Pietro Ragonese Paolo Altieri Marta Barcella Valeria Bergamaschi Roberto Bianchi Alessia Borriello Giovanna Buscarinu Maria Chiara Callari Graziella Capobianco Marco Capone Fioravante Cavalla Paola Cavarretta Rosella Cortese Antonio De Luca Giovanna Di Filippo Massimiliano Dattola Vincenzo Fantozzi Roberta Ferraro Elisabetta Filippi Maria Maddalena Gasperini Claudio Grimaldi Luigi Maria Edoardo Landi Doriana Re Marianna Lo Mallucci Giulia Manganotti Paolo Marfia Girolama Alessandra Mirabella Massimiliano Perini Paola Pisa Marco Realmuto Sabrina Russo Margherita Tomassini Valentina Torri-Clerici Valentina Liliana Adriana Zaffaroni Mauro Zuliani Cristina Zywicki Sofia Filippi Massimo Prosperini Luca 《Journal of neurology》2021,268(8):2922-2932
Journal of Neurology - To identify baseline factors associated with disease activity in patients with relapsing–remitting multiple sclerosis (RRMS) under teriflunomide treatment. This was an... 相似文献
32.
Toffano Roberta Burgio Francesca Palmer Katie Benavides-Varela Silvia Meneghello Francesca Orrù Graziella Sartori Giuseppe Arcara Giorgio Semenza Carlo 《Neurological sciences》2021,42(10):4183-4191
Neurological Sciences - Financial capacity is the ability to manage money and finances according to a person’s values and self-interests. In Italy, the first instrument specifically designed... 相似文献
33.
de Sousa Graziella Ribeiro Lira Régia Caroline Peixoto de Almeida Magalhães Taciani da Silva Keteryne Rodrigues Nagano Luis Fernando Peinado Saggioro Fabiano Pinto Baroni Mirella Marie Suely Kazue Nagahashi Oba-Shinjo Sueli Mieko Brandelise Silvia de Paula Queiroz Rosane Gomes Brassesco María Sol Scrideli Carlos Alberto Tone Luiz Gonzaga Valera Elvis Terci 《Journal of molecular medicine (Berlin, Germany)》2021,99(8):1101-1113
Journal of Molecular Medicine - Although ependymoma (EPN) molecular subgroups have been well established by integrated high-throughput platforms, low- and middle-income countries still need... 相似文献
34.
Martin H. Berryer Fadi F. Hamdan Laura L. Klitten Rikke S. Møller Lionel Carmant Jeremy Schwartzentruber Lysanne Patry Sylvia Dobrzeniecka Daniel Rochefort Mathilde Neugnot‐Cerioli Jean‐Claude Lacaille Zhiyv Niu Christine M. Eng Yaping Yang Sylvain Palardy Céline Belhumeur Guy A. Rouleau Niels Tommerup LaDonna Immken Miriam H. Beauchamp Gayle Simpson Patel Jacek Majewski Mark A. Tarnopolsky Klaus Scheffzek Helle Hjalgrim Jacques L. Michaud Graziella Di Cristo 《Human mutation》2013,34(2):385-394
De novo mutations in SYNGAP1, which codes for a RAS/RAP GTP‐activating protein, cause nonsyndromic intellectual disability (NSID). All disease‐causing point mutations identified until now in SYNGAP1 are truncating, raising the possibility of an association between this type of mutations and NSID. Here, we report the identification of the first pathogenic missense mutations (c.1084T>C [p.W362R], c.1685C>T [p.P562L]) and three novel truncating mutations (c.283dupC [p.H95PfsX5], c.2212_2213del [p.S738X], and (c.2184del [p.N729TfsX31]) in SYNGAP1 in patients with NSID. A subset of these patients also showed ataxia, autism, and a specific form of generalized epilepsy that can be refractory to treatment. All of these mutations occurred de novo, except c.283dupC, which was inherited from a father who is a mosaic. Biolistic transfection of wild‐type SYNGAP1 in pyramidal cells from cortical organotypic cultures significantly reduced activity‐dependent phosphorylated extracellular signal‐regulated kinase (pERK) levels. In contrast, constructs expressing p.W362R, p.P562L, or the previously described p.R579X had no significant effect on pERK levels. These experiments suggest that the de novo missense mutations, p.R579X, and possibly all the other truncating mutations in SYNGAP1 result in a loss of its function. Moreover, our study confirms the involvement of SYNGAP1 in autism while providing novel insight into the epileptic manifestations associated with its disruption. 相似文献
35.
Yael Lahav David Levy Avi Ohry Gabi Zeilig Meir Lahav Hava Golander Anat-Chacham Guber Orit Uziel Ruth Defrin 《The journal of pain》2021,22(2):209-218
Chronic pain induces a multitude of harmful effects; recently it has been suggested that chronic pain is also associated with premature aging, manifested in shortened telomere length (TL). However, evidence for this hypothesis is scarce and inconsistent. The aim was twofold: 1) Investigate whether chronic pain is associated with premature aging, and 2) Determine whether physical exercise (PE) moderates this association if it exists. Participants were 116 male subjects, with (n = 67) and without chronic pain (n = 49). Blood samples for TL analysis were collected and participants were interviewed and completed questionnaires. As a part of the cohort, we included people with physical disability; this variable was controlled in the analysis. The TL of individuals with chronic pain was significantly shorter than that of pain-free individuals. Regression analysis revealed a significant moderating effect of PE on chronic pain and TL, above and beyond the effects of disability, age, and weight. Whereas chronic pain was associated with shorter telomeres in participants who did not exercise, this association was nonsignificant among participants who did exercise. The results suggest that chronic pain is associated with premature ageing; however, PE may mitigate this association and may protect individuals against the harmful effects of chronic pain.PerspectiveThe study suggests that it is important to monitor signs of premature ageing among chronic pain patients as they are at risk. However, chronic pain patients may benefit from regular PE in this respect as it may moderate premature ageing. 相似文献
36.
37.
Durand S Richard G Bontems F Uzan M 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(18):7073-7078
The bacteriophage T4-encoded RegB endoribonuclease is produced during the early stage of phage development and targets mostly (but not exclusively) the Shine-Dalgarno sequences of early genes. In this work, we show that the degradation of RegB-cleaved mRNAs depends on a functional T4 polynucleotide kinase/phosphatase (PNK). The 5'-OH produced by RegB cleavage is phosphorylated by the kinase activity of PNK. This modification allows host RNases G and E, with activity that is strongly stimulated by 5'-monophosphate termini, to attack mRNAs from the 5'-end, causing their destabilization. The PNK-dependent pathway of degradation becomes effective 5 min postinfection, consistent with our finding that several minutes are required for PNK to accumulate after infection. Our work emphasizes the importance of the nature of the 5' terminus for mRNA stability and depicts a pathway of mRNA degradation with 5'- to 3'-polarity in cells devoid of 5'-3' exonucleases. It also ascribes a role for T4 PNK during normal phage development. 相似文献
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40.
Fede G Spadaro L Tomaselli T Privitera G Germani G Tsochatzis E Thomas M Bouloux PM Burroughs AK Purrello F 《Hepatology (Baltimore, Md.)》2012,55(4):1282-1291
In patients with cirrhosis, adrenal insufficiency (AI) is reported during sepsis and septic shock and is associated with increased mortality. Consequently, the term "hepato-adrenal syndrome" was proposed. Some studies have shown that AI is frequent in stable cirrhosis as well as in cirrhosis associated with decompensation other than sepsis, such as bleeding and ascites. Moreover, other studies showed a high prevalence in liver transplant recipients immediately after, or some time after, liver transplantation. The effect of corticosteroid therapy in critically ill patients with liver disease has been evaluated in some studies, but the results remain controversial. The 250-μg adreno-cortico-tropic-hormone stimulation test to diagnose AI in critically ill adult patients is recommended by an international task force. However, in liver disease, there is no consensus on the appropriate tests and normal values to assess adrenal function; thus, standardization of normal ranges and methodology is needed. Serum total cortisol assays overestimate AI in patients with cirrhosis, so that direct free cortisol measurement or its surrogates may be useful measurements to define AI, but further studies are needed to clarify this. In addition, the mechanisms by which liver disease leads to adrenal dysfunction are not sufficiently documented. This review evaluates published data regarding adrenal function in patients with liver disease, with a particular focus on the potential limitations of these studies as well as suggestions for future studies. 相似文献