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991.
T. Wang Y.T. Zhou X.N. Chen A.X. Zhu 《Brazilian journal of medical and biological research》2014,47(9):738-745
Hypoxia-inducible factor-1α (HIF-1α) is one of the most potent angiogenic growth
factors. It improves angiogenesis and tissue perfusion in ischemic skeletal muscle.
In the present study, we tested the hypothesis that ischemic postconditioning is
effective for salvaging ischemic skeletal muscle resulting from limb
ischemia-reperfusion injury, and that the mechanism involves expression of HIF-1α.
Wistar rats were randomly divided into three groups (n=36 each): sham-operated (group
S), hindlimb ischemia-reperfusion (group IR), and ischemic postconditioning (group
IPO). Each group was divided into subgroups (n=6) according to reperfusion time:
immediate (0 h, T0), 1 h (T1), 3 h (T3), 6 h
(T6), 12 h (T12), and 24 h (T24). In the IPO
group, three cycles of 30-s reperfusion and 30-s femoral aortic reocclusion were
carried out before reperfusion. At all reperfusion times
(T0-T24), serum creatine kinase (CK) and lactate
dehydrogenase (LDH) activities, as well as interleukin (IL)-6, IL-10, and tumor
necrosis factor-α (TNF-α) concentrations, were measured in rats after they were
killed. Histological and immunohistochemical methods were used to assess the skeletal
muscle damage and HIF-1α expression in skeletal muscle ischemia. In groups IR and
IPO, serum LDH and CK activities and TNF-α, IL-6, and IL-10 concentrations were all
significantly increased compared to group S, and HIF-1α expression was up-regulated
(P<0.05 or P<0.01). In group IPO, serum LDH and CK activities and TNF-α and
IL-6 concentrations were significantly decreased, IL-10 concentration was increased,
HlF-1α expression was down-regulated (P<0.05 or P<0.01), and the pathological
changes were reduced compared to group IR. The present study suggests that ischemic
postconditioning can reduce skeletal muscle damage caused by limb
ischemia-reperfusion and that its mechanisms may be related to the involvement of
HlF-1α in the limb ischemia-reperfusion injury-triggered inflammatory response. 相似文献
992.
Signals mediated by members of the tumor necrosis factor receptor superfamily modulate a network of diverse processes including initiation of inflammatory responses and altering cell fate between pathways favoring survival and death. Although such pathways have been well-described for the TNF-α receptor, less is known about signaling induced by the TNF superfamily member LIGHT and how it is differentially altered by expression of its two receptors LTβR and HVEM in the same cell. We used cell lines with different relative expression of HVEM and LTβR to show that LIGHT-induced signals mediated by these receptors were associated with altered TRAF2 stability and RelA nuclear translocation. Production of the inflammatory chemokine CXCL10 was primarily mediated by LTβR. Higher expression of HVEM was associated with cell survival, while unopposed LTβR signaling favored pathways leading to apoptosis. Importantly, restoring HVEM expression in cells with low endogenous expression recapitulated the phenotype of cells with higher endogenous expression. Together, our data provide evidence that relative expression of HVEM and LTβR modulates canonical NF-κB and pro-apoptotic signals stimulated by LIGHT. 相似文献
993.
Ibrahim Hatipoglu Duygu Ercan Ceyda Acilan Aynur Basalp Deniz Durali Ahmet Tarik Baykal 《Immunobiology》2014
Hepatitis B virus (HBV) continues to be a serious worldwide health problem despite the use of protective HBV vaccines and therapeutic regimens against chronic HBV infection. Chronic HBV patients cannot induce sufficient immune responses against the virus. HBV and its antigens are believed to suppress immune responses during chronic infection. Hence, studying the role of HBV in immune suppression is very important for the development of alternative therapeutic strategies for HBV infections. 相似文献
994.
995.
B型主动脉夹层腔内治疗已有10余年历史,目前国内越来越多医院在起步尝试开展此项技术,对此我们总结开展B型主动脉夹层腔内治疗的经验与教训,认为技术开展初期应注意如下几点:充分重视术前血管评估与测量,准确选择近端锚定区,勿轻易覆盖左锁骨下动脉,合理选择移植物长度,合理选择远端移植物口径以预防破裂,重视围手术期血压管理,加强远期随访。总之,把握技术要点,有助于缩短学习曲线,避免治疗误区,提高手术安全性。 相似文献
996.
《Journal of clinical virology》2014,59(2):100-103
BackgroundEquine influenza virus (EIV) is considered enzootic in Europe (except Iceland), Asia, North Africa, and North and South America. When EIV outbreaks occur they may severely impact the equine and tourist industries. Australia faced its first EIV outbreak beginning in August of 2007. The outbreak was concentrated in New South Wales and Queensland, with more than 1400 confirmed EIV infections in horses during the first month. Rapid response from the equine industry and the federal government was successful and Australia was declared free from EIV by the end of 2007.ObjectivesThis cross-sectional study was designed to examine associations between exposure to EIV-infected horses and evidence of EIV infection in humans.Study designEmploying informed consent, between October 2007 and April 2008, 100 subjects (89 with horse exposures and 11 non-exposed) were enrolled during equine events and at the University of the Sunshine Coast. All subjects provided a blood sample and were asked to complete an online questionnaire including health history, animal exposure and demographic information. Sera samples were tested for the presence of antibodies against two H3N8 EIV strains using microneutralization, hemagglutination inhibition, and enzyme-linked lectin assays.ResultsEvidence for H3N8 infection was sparse, with only 9 study participants having any indication of H3N8 infection and the seroreactivity seen was low and easily explained by cross-reactions against human influenza strains or vaccines.ConclusionsThese data provide little evidence to support the premise that EIV infections occurred among humans exposed to EIV-infected horses during the 2007 Australian epizootic. 相似文献
997.
Jing Zhu Xiang Cheng Rongkai Xie Zhengqiong Chen Youfei Li Guilan Lin Jianmei Liu Ying Yang 《International journal of clinical and experimental pathology》2014,7(9):6085-6090
Background: Hypoxia-inducible factor-1 alpha (HIF-1α) P582S polymorphism has been reported to increase transactivation capacity of HIF-1α, which is prone to tumorigenesis. Several published case-control studies on the association between P582S polymorphism and cervical cancer have shown mixed results. In this study, we chose to perform a meta-analysis to assess the association. Methodology/Principal findings: We conducted a meta-analysis consisting of four studies with a total of 846 cases and 991 controls. All data were collected and overall comparison was performed among all subjects. Using the fi xed effects model, the homozygous and the recessive models showed a significant increase in the risk of cervical cancer (the pooled OR=6.32, 95% CI=2.28-17.55, Phet=0.348; the pooled OR=5.86, 95% CI=2.13-16.11, Phet=0.394 respectively). Publication bias was not significantly indicated in this analysis. Conclusions: This meta-analysis demonstrates that HIF-1α P582S polymorphism may be associated with the risk of cervical cancer. 相似文献
998.
999.
Andrew K. Kwegyir-Afful Senthilmurugan Ramalingam Puranik Purushottamachar Vidya P. Ramamurthy Vincent C.O. Njar 《Oncotarget》2015,6(29):27440-27460
Galeterone (Gal) is a first-in-class multi-target oral small molecule that will soon enter pivotal phase III clinical trials in castration resistant prostate cancer (CRPC) patients. Gal disrupts androgen receptor (AR) signaling via inhibition of CYP17, AR antagonism and AR degradation. Resistance to current therapy is attributed to up-regulation of full-length AR (fAR), splice variants AR (AR-Vs) and AR mutations. The effects of gal and VNPT55 were analyzed on f-AR and AR-Vs (AR-V7/ARv567es) in LNCaP, CWR22Rv1 and DU145 (transfected with AR-Vs) human PC cells in vitro and CRPC tumor xenografts. Galeterone/VNPT55 decreased fAR/AR-V7 mRNA levels and implicates Mdm2/CHIP enhanced ubiquitination of posttranslational modified receptors, targeting them for proteasomal degradation. Gal and VNPT55 also induced significant apoptosis in PC cells via increased Bax/Bcl2 ratio, cytochrome-c release with concomitant cleavage of caspase 3 and PARP. More importantly, gal and VNPT55 exhibited strong in vivo anti-CRPC activities, with no apparent host toxicities. This study demonstrate that gal and VNPT55 utilize cell-based mechanisms to deplete both fAR and AR-Vs. Importantly, the preclinical activity profiles, including profound apoptotic induction and inhibition of CRPC xenografts suggest that these agents offer considerable promise as new therapeutics for patients with CRPC and those resistant to current therapy. 相似文献
1000.