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991.
猴指神经皮下植入后感觉神经电生理的研究 总被引:2,自引:0,他引:2
探讨感觉神经植入术后神经再生的机制。方法:用神经电生理单纤维放电引导技术,从放电纤维检出率、外周感受野分布和感觉纤维种类等方面,评价灵长类动物失神经手指无毛皮肤中再生神经纤维的功能。结果:触、压、痛、温冷觉纤维均可再生,而且具有正常传导功能。在各类再生的感觉纤维中触、压觉纤维占优势;各类纤维的比例和其感受野的分布类似于正常皮肤。结论:猴手指神经皮下植入后感觉神经再生良好。 相似文献
992.
血浆S100蛋白在体外循环术后脑损伤评价中的意义 总被引:6,自引:1,他引:5
目的:探讨血浆S100蛋白在体外循环术中和术后脑损伤评价中的意义。方法:体外循环下心内直视手术病人40例,在体外循环中和结束后不同时间点采血测定血浆S100浓度,并观测病人术后精神神经系统并发症。结果:体外循环可引起病人血浆S100蛋白明显升高,水平最高的3例术后均出现明显的精神神经系统症状,术后24~48h无精神神经并发症者血浆S100蛋白恢复到术前水平。结论:体外循环引起的血浆S100蛋白水平变化对体外循环术后脑损伤的评价具有重要意义。 相似文献
993.
The influence of cultured Schwann cells on regeneration through acellular basal lamina grafts 总被引:1,自引:0,他引:1
Acellular basal lamina grafts have been shown to be less immunogenic in comparison to cellular grafts, but possess a limited potential for supporting axonal regeneration through them. The present study describes the effect of cultured Schwann cells on enhancing regeneration through acellular grafts. 2 cm long acellular grafts, and in vitro Schwann cell populated acellular grafts were used to repair a surgically created gap in the host peroneal nerve. The transplants were analyzed at 1, 2, 4 and 8 weeks to determine their ability to support axonal regeneration. Host axonal regeneration through Schwann cell cocultured acellular grafts occurred rapidly and was significantly better as compared to non-cultured acellular grafts. The results demonstrate a beneficial effect of Schwann cell culture pretreatment on regeneration through acellular grafts and an improved recovery of the target muscle. The procedure of first preparing acellular grafts with subsequent coculture with Schwann cells offers a novel approach for the repair of injured nervous tissue. 相似文献
994.
995.
Toshiko Shibayama-Imazu Ikuko Okahashi Kumiko Omata Shigeo Nakajo Hidehiko Ochiai Yasumitsu Nakai Tokiko Hama Yasuharu Nakamura Kazuyasu Nakaya 《Brain research》1993,622(1-2)
In the present paper, the distribution of a neuron-specific phosphoneuroprotein 14 (PNP 14) in cell and tissue was investigated in detail by the immunoblot method using affinity-purified antibody against this protein. The immunoblot of the supernatant fractions of various tissue homogenates of rat clearly demonstrated that PNP 14 was enormously rich in the brain. The content in rat brain was as much as 0.1% of the homogenate. The immunocytochemical study showed that the protein was localized at nerve endings in the cerebellum. Existence of the protein was also comfirmed in cultured neuronal cells from postnatal rat midbrain, but not in glial cells. Examination of subcellular localization of PNP 14 indicates that the protein was present in synaptic plasma membranes and synaptic supernatant fractions, but not in synaptic vesicles. During the development of rat brain, PNP 14 came into existence after birth and it's amount linearly increased to a maximum at 21–28 days after birth. The content of the protein then remained at the same level for more than 10 months. We concluded that this protein is neuron specific and supposed that it may be involved in neuronal formation and function. 相似文献
996.
Yukio Abe Kazuteru Doi Yoshihiko Katoh Hisashi Yamamoto Hideo Kataoka Shinya Kawai 《Journal of the neurological sciences》1996,140(1-2):61-66
We studied peripheral nerve elongation of rabbit sciatic nerves. External fixators developed in our department were applied to 32 rabbit femurs in vivo. The rabbits underwent osteotomy of the femur and were divided into two groups subjected to different sciatic nerve elongation speeds: group I (0.45 mm/day) and group II (1.35 mm/day). The sciatic nerves were elongated 1.5, 3.0, 4.5, 6.0 and 7.0 cm by the external fixators, and the corresponding actual percentage of elongation of the nerves were 8, 16, 24, 30 and 40%. After elongation, nerve electrophysiology, nerve blood flow and pathology were studied. Forty percent elongation decreased nerve blood flow to 69 ± 5.1 % of contralateral controls in group I and to 20 ± 4.8% in group II. Although no decrease in motor conduction velocity (MCV) was observed at any elongation distance, compound muscle action potential (CMAP) amplitude gradually decreased with increasing elongation. In group I, after 40% elongation, specimens showed the following pathologic changes: thinning of myelin sheath, atrophy and detachment of the axon from the myelin sheath. Furthermore, in group II, 40% elongation induced disorganization of the myelin sheath and Wallerian degeneration. Consequently 40% elongation was regarded as critical at speeds of both 0.45 and 1.35 mm/day. 相似文献
997.
998.
脉冲电磁场、碱性成纤维细胞生长因子促进坐骨神经延长的实验研究 总被引:1,自引:0,他引:1
目的探讨减轻周围神经在缓慢牵拉过程中的损伤,增加神经延长率的方法。方法采用改良的组织扩张器,对大白兔坐骨神经行扩张延长的同时,辅以脉冲电磁场(PEMF)及碱性成纤维细胞生长因子(bFGF)处理。最后,测定神经延长率(NER)、运动传导速度(MCV)及组织病理观察。结果NER在PEMF组及bFGF组均显著高于对照组,而MCV的降低却显著较轻。组织病理显示,PEMF及bFGF组的神经变性轻,雪旺氏细胞增殖,新生毛细血管及髓鞘却较明显。结论PEMF及bFGF可减轻神经在扩张期间的损伤,增加延长率 相似文献
999.
Cultured Postnatal Rat Medial Septal Neurons Respond to Acute Ethanol Treatment and Nerve Growth Factor By Changing Intracellular Calcium Levels 总被引:2,自引:0,他引:2
B. Webb S.S. Suarez M.B. Heaton D.W. Walker 《Alcoholism, clinical and experimental research》1996,20(8):1385-1394
Ethanol neurotoxicity results in the loss of neurons during the development of the nervous system. Nerve growth factor (NGF) can ameliorate the neurotoxic effects of ethanol (EtOH) in rat medial septal (MS) neurons. These experiments study the effects of EtOH and NGF on neuronal calcium (Ca2+) homeostasis in cultured postnatal day of birth (PO) rat MS neurons. Previously, we observed that EtOH and NGF modulate intracellular Ca2+ levels ([Ca2+]i) in unstimulated and high potassium stimulated (30 mM KCI) cultured rat embryonic day 21 (E21) MS neurons (Webb et al., Brain Res 701:61-74, 1995). The purpose of the present study was to explore whether the effects of EtOH and NGF on Ca2+ homeostasis were altered by developmental stage. The hypotheses tested were the following: treatment with EtOH affects Ca2+ homeostasis in postnatal day of birth (PO) rat MS neurons by causing transient and persistent changes in [Ca2+]i; NGF modulates Ca2+ homeostasis in MS neurons by regulating [Ca2+]i; the action of NGF changes the response of MS neurons to EtOH, thus altering Ca2+ homeostasis; and that EtOH and or NGF effects on Ca2+ homeostasis are developmentally regulated. Our results indicated that behaviorally relevant levels of EtOH caused a rapid transient increase in basal [Ca2+]i, whereas there was no effect of NGF on basal [Ca2+]i. Ethanol and NGF interacted, resulting in the lowering of [Ca2+]i. During stimulation with high K+, EtOH inhibited the change in [Ca2+]i. NGF partially ameliorated this effect of higher levels of EtOH, allowing [Ca2+]i to increase. NGF and the lowest level of EtOH potentiated the high K+ stimulated increase in [Ca2+]i. Ethanol and NGF effects on [Ca2+]i were different in the PO neurons compared with our previously published observations in E21 neurons. Therefore, these data suggest that EtOH neurotoxicity and NGF protection involve mechanisms that regulate neuronal Ca2+ homeostasis, and the magnitude of these effects depend on developmental stage. 相似文献
1000.