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排序方式: 共有3908条查询结果,搜索用时 15 毫秒
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Kiyoshi Nakatsuka Yoshiki Nishizawa Satoshi Hagiwara Hidenori Koyama Takami Miki Hironobu Ochi Hirotoshi Morii 《Calcified tissue international》1990,47(6):378-382
Summary Total body bone mineral (TBBM) content in rats was measured by dual photon absorptiometry (DPA). TBBM showed significant increases
over 4 weeks in control groups with significant bone loss over the same time in prednisolone-injected rats on low calcium
feed. Daily injections of calcitonin significantly reduced loss of bone mass. Both prednisolone- and prednisolone-calcitonin-injected
groups showed significantly elevated serum alkaline phosphatase with the prednisolone-calcitonin group also exhibiting elevated
serum calcium and phosphate levels, confirming the impact of the experimental protocol. TBBM measured by DPA in all groups
correlated well (r=0.928,P<0.001 n=20) with the total ash weight suggesting that the method reflects total skeletal mineral content in the small animal.
TBBM measurement by DPA proves well-suited to monitoring bone mineral in a small animal experimental setting. 相似文献
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Changes in phosphorus metabolites and intracellular pH in acute liver failure induced by D-galactosamine (GAL) were evaluated non-destructively and continuously using 31P-NMR spectroscopy. Furthermore, changes in these parameters under ischemia were also examined. GAL(1.0g/kg) was injected intravenously to male Wistar rats. NMR measurements in perfused livers were performed with a GX-270FT NMR spectrometer (JEOL). Typical changes in 31P-NMR spectra were observed after GAL administration. ATP levels decreased to 57.4 +/- 12.4% at 12 hours and to 65.4 +/- 7.7% at 24 hours after the administration compared with that in control rats. Pi levels increased remarkably to 632.1 +/- 76.4% at 3 hours and recovered to 127.5 +/- 22% at 24 hours. NAD+/NADH and UDP-sugar levels gradually increased to 253.5 +/- 33.4 and 456.3 +/- 60.9%, respectively, at 24 hours. In GAL treated livers, ATP levels fell rapidly and Pi levels rose correspondingly during ischemia, and they rapidly recovered by reperfusion. The intracellular pH decreased to 7.16 +/- 0.032 from 7.38 +/- 0.065 at 3 hours after GAL administration. However, significant changes in pH were not observed until 24 hours. In GAL treated livers, slight changes in pH were observed under ischemia. These results indicate that 31P-NMR is a useful method to evaluate the damage of acute liver failure, and to diagnose liver diseases involving the intrahepatic energy metabolism. 相似文献
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Usefulness of magnetic motor evoked potentials in the surgical treatment of hemiplegic patients with intractable epilepsy. 总被引:2,自引:0,他引:2
Tohru Kamida Hiroshi Baba Kenji Ono Masato Yonekura Minoru Fujiki Hidenori Kobayashi 《Seizure》2003,12(6):373-378
Five hemiplegic patients with intractable epilepsy were studied with transcranial magnetic stimulation (TMS) before and after various surgical treatments. These patients had unilateral widespread cerebral lesions acquired at various times, including congenital, infantile and childhood injury. Motor evoked potentials (MEPs) of the abductor pollicis brevis (APB) muscles were simultaneously recorded on both sides following TMS of the motor cortex in the respective hemisphere using a figure-8 or circular coil. In all patients with congenital disease, the abolition of motor function in the affected hemisphere was estimated by magnetic MEPs, and the hemiplegia did not deteriorate after functional hemispherectomy (HS) was performed in two of them. In two patients with acquired disease, HS was not performed because it was shown by magnetic maps that the motor function in the affected hemisphere remained. Furthermore, it was shown by electric MEPs using subdural electrodes that a patient who had had encephalitis in early childhood had a reorganised motor area in the parietal cortex of the affected hemisphere. The present findings indicate that magnetic MEPs are a very useful non-invasive method of assessing whether the motor area in the affected hemisphere can be resected in hemiplegic patients with intractable epilepsy. 相似文献
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Yusuf K. Durlu Sei-ichi Ishiguro Akiko Yoshida Takezo Mito Makio Tsuchiya Makoto Tamai 《Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie》1990,228(1):44-48
We used morphological, biochemical and immunohistochemical methods to assess the response of Müller cells after experimental
lensectomy-vitrectomy in rabbits. We observed widened intercellular spaces between the Müller cells and nerve fibers of ganglion
cells, and increased electron opacity in the Müller cells of eyes injected with silicone oil. No apparent morphological changes
were detected in the Müller cells of air-injected eyes. The specific and total activities of Müller cell-marker enzymes (glucose
6-phosphatase and glutamine synthetase) showed an initial increase, followed by a decrease. Glial fibrillary acidic protein
immunoreactivity was not found in the Müller cells of the normal rabbit retina but was exhibited after surgery. Our results
showed that markers of Müller cells associated with glycogenolysis and/or gluconeogenesis, glutamate-glutamine cycle and cytoskeletal
protein metabolism were affected by the experimental lensectomy-vitrectomy. 相似文献
8.
Yoshinori Yamashita Toshihiro Hirai Hidenori Mukaida Takashi Iwata Tetsuya Toge Hong Jae Hoon 《Surgery today》1990,20(6):671-676
This report presents the effect of repeated heating every 24 hrs using bleomycin (BLM) which, although seemingly contrary
to the usual agreement that hyperthermia should be carried out with a long interval due to thermotolerance, holds many possibilities.
FM3A cells on the foot pad of C3H mouse were immersed in a heated water bath at 43 and 44°C for 30 min. The effect of repeated
heating was appreciated by an improved growth curve and 50 day survival compared to mice which received heating twice with
a 96-hr interval. Repeated heating every 24 hrs 5 times with BLM suppressed tumor growth significantly as compared to heating
twice with a 96-hr interval without BLM. The longest survival time was obtained by the repeated heating with BLM among all
protocols. There is therefore a good possibility that more effective results could be obtained clinically by repeated heating
over a short period. 相似文献
9.
Hidenori Endo Chikako Nito Hiroshi Kamada Tatsuro Nishi Pak H Chan 《Journal of cerebral blood flow and metabolism》2006,26(12):1479-1489
Recent studies have revealed that the phosphatidylinositol 3-kinase (PI3-K) pathway is involved in apoptotic cell death after experimental cerebral ischemia. The serine-threonine kinase, Akt, functions in the PI3-K pathway and prevents apoptosis by phosphorylation at Ser473 after a variety of cell death stimuli. After phosphorylation, activated Akt inactivates other apoptogenic factors, including glycogen synthase kinase-3beta (GSK3beta), thereby inhibiting cell death. However, the role of Akt/GSK3beta signaling in the delayed death of hippocampal neurons in the CA1 subregion after transient global cerebral ischemia (tGCI) has not been clarified. Transient global cerebral ischemia for 5 mins was induced by bilateral common carotid artery occlusion combined with hypotension. Western blot analysis showed a significant increase in phospho-Akt (Ser473) and phospho-GSK3beta (Ser9) in the hippocampal CA1 subregion after tGCI. Immunohistochemistry showed that expression of phospho-Akt (Ser473) and phospho-GSK3beta (Ser9) was markedly increased in the vulnerable CA1 subregion, but not in the ischemic-tolerant CA3 subregion. Double staining with phospho-GSK3beta (Ser9) and terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end labeling showed different cellular distributions in the CA1 subregion 3 days after tGCI. Phosphorylation of Akt and GSK3beta was prevented by LY294002, a PI3-K inhibitor, which facilitated subsequent DNA fragmentation 3 days after tGCI. Moreover, transgenic rats that overexpress copper/zinc-superoxide dismutase, which is known to be neuroprotective against delayed hippocampal CA1 injury after tGCI, had enhanced and persistent phosphorylation of both Akt and GSK3beta after tGCI. These findings suggest that activation of the Akt/GSK3beta signaling pathway may mediate survival of vulnerable hippocampal CA1 neurons after tGCI. 相似文献
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