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32.
Ida Alzira Gomes Duarte Karen Levy Korkes Vanessa Alice M. Amorim Clarice Kobata Roberta Buense Rosana Lazzarini 《Anais brasileiros de dermatologia》2013,88(2):306-308
Whether parapsoriasis represents an early stage of T-cell cutaneous lymphoma is still
the subject of controversy. We evaluated the efficacy of phototherapy in the
treatment of parapsoriasis and its relation with TCCL. Patients diagnosed with
parapsoriasis and treated with phototherapy PUVA or UVB-NB were selected. Between 1
to 8 years following treatment the evolution of their disease was evaluated. In 62
patients the cure rate was 79.3% and 17.2% showed improvement of the lesions. Only
two patients developed full blown T-cell cutaneous lymphoma. Phototherapy is an
excellent treatment for parapsoriasis, with high cure rates, regardless of the type
of phototherapy employed. Of the 62 patients under study, parapsoriasis showed no
general tendency to progress to T-cell cutaneous lymphoma. 相似文献
33.
Koichiro Kinugawa Ryozo Nagai Hiroshi Inoue Hirotsugu Atarashi Yoshihiko Seino Takeshi Yamashita Wataru Shimizu Takeshi Aiba Masafumi Kitakaze Atsuhiro Sakamoto Takanori Ikeda Yasushi Imai Takashi Daimon Katsuhiro Fujino Tetsuji Nagano Tatsuaki Okamura Masatsugu Hori 《Advances in therapy》2014,31(5):577-578
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To obtain insight into the role of the mitochondrial ATP-sensitive K(+) (mitoK(ATP)) channel in ischemic preconditioning (PC), we aimed to clarify the mitoK(ATP) channel-dependent phase of PC in two PC protocols with different intervals between PC ischemia and an index ischemia. The possible contribution of mitoK(ATP) channel opening to protein kinase C activation in PC was also examined by Western blotting. Myocardial infarction was induced by 30-min coronary occlusion/2-h reperfusion in rat hearts in situ, and infarct size was expressed as a percentage of the area at risk (% IS/AR). PC was performed with 2 episodes of 5-min ischemia, and each heart was subjected to 30-min ischemia either 5 min or 20 min after PC. At 5 min after PC, both PKC-delta and -epsilon were translocated and the myocardium was protected against infarction (% IS/AR = 28.3 +/- 2.7 % vs. 72.7 +/- 2.2 in controls p < 0.05). Pretreatment with a selective mitoK(ATP) channel blocker, 5-hydroxydecanoate (5-HD, 10 mg/kg), abolished the cardioprotection but not PKC translocation by PC. At 20 min after PC, PKC translocation remained at the same level as that 5 min after PC, but the anti-infarct tolerance was attenuated (%IS/AR = 43.5 +/- 4.7 %). Injection of 5-HD after PC did not affect anti-infarct tolerance at 5 min after PC but abolished the protection at 20 min after PC without any effects on PKC. These results suggest that the mitoK(ATP) channel plays a role in triggering of PC in a PKC-independent manner and that the role of the mitoK(ATP) channel as a mediator of protection is detectable after, but not before, the PC effect starts to decay without a change in the level of PKC translocation in the rat heart. 相似文献
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Kita H Miura T Miki T Genda S Tanno M Fukuma T Shimamoto K 《Cardiovascular drugs and therapy / sponsored by the International Society of Cardiovascular Pharmacotherapy》2000,14(5):497-502
Earlier studies have shown that activation of bradykinin B2 receptor triggers protein kinase C (PKC)-mediated cardioprotective mechanism in ischemic preconditioning (PC). In the present study, we examined whether the effector in this B2-receptor triggered pathway of PC is the ATP sensitive potassium (KATP) channel in the mitochondria (mito-KATP channel) or KATP channel in the sarcolemma (sarc-KATP channel). Isolated rabbit hearts were perfused with modified Krebs-Henseleit buffer in a Langendorff mode, and regional myocardial ischemia was induced by occluding a left coronary artery for 30 min and then reperfusing for 2 hours. Infarct size was determined by triphenyltetrazolium chloride staining and expressed as a percentage of area at risk (% IS/AR). Infusion of bradykinin (500 nmol/L) for 15 min prior to ischemia significantly reduced % IS/AR from 37.4 ± 2.9 (SE) of the untreated controls to 12.0 ± 3.3%. This protective effect of bradykinin was completely abolished by coinfusion of 5-hydroxydecanoate (5-HD, 50 mol/L), a selective mito-KATP channel blocker (% IS/AR = 44.2 ± 6.4). In contrast, a high dose of HMR1098 (20 mol/L), which is a newly developed sarc-KATP channel selective blocker with IC50 of 0.6 mol/L, failed to modify the infarct size limitation by preischemic infusion of bradykinin (% IS/AR = 11.7 ± 3.4). Neither 5-HD nor HMR1098 alone modified infarct size (% IS/AR = 37.8 ± 3.8 and 35.1 ± 6.2, respectively). These results suggest that opening of the mito-KATP channel but not the sarc-KATP channel is involved in infarct size limitation by a mechanism triggered by bradykinin B2 receptor activation. 相似文献