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51.
目的 探讨多功能红外治疗宫颈糜烂的疗效。方法 将 171例宫颈糜烂患者随机分为两组 ,治疗组用多功能红外治疗仪探头点状光凝子宫颈 ,每点 2~ 3秒 ,对照组用CO2 激光治疗。结果 治疗组治愈 84例 ,占 97.67% ,对照组治愈 73例 ,占 85.88% ,两组疗效比较P <0 .0 5。结论 采用多功能红外治疗仪治疗宫颈糜烂疗效明显优于对照组。 相似文献
52.
西京医院冠心病介入治疗537例 总被引:1,自引:1,他引:0
目的 总结西京医院冠心病介入治疗的成功率及并发症发生率 .方法 回顾性分析 1998- 12前所有冠心病介入治疗病历完整患者的临床资料 .结果 在 5 37例患者中 ,6 9.3%为不稳定性心绞痛 ,2 0 .3%射血分数≤ 40 .0 % ,6 4.6 %为多支病变 .治疗血管 6 71支、病变 76 9处 ,B,C型病变77.9% .介入治疗病例成功率为 89.2 % .病变成功率 89.1% ,严重并发症发生率为 3.4% (死亡 1.9% ,Q波心梗 2 .0 % ,急症冠脉搭桥术 0 .2 % ) .普遍应用支架前后对比 ,病例成功率提高 (91.0 % vs80 .0 % ,P<0 .0 1) ,严重并发症发生率下降 (2 .6 % vs 6 .4% ,P<0 .0 5 ) .结论 我院病例病情严重 ,介入治疗成功率和并发症发生率与国外文献报道相似 .支架提高了介入治疗的安全性 相似文献
53.
Journal of Digital Imaging - Although medical imaging is frequently used to diagnose diseases, in complex diagnostic situations, specialists typically need to look at different modalities of image... 相似文献
54.
Ma S Li X Fang Q Ross MG Chao CR 《Brain research. Developmental brain research》1999,118(1-2):119-127
Transition from fetal to newborn life is accompanied by a marked rise in circulating norepinephrine (NE) concentrations though arterial blood pressure does not substantively change. Nitric oxide (NO) plays an important role in the central regulation of sympathetic tone in the nucleus tractus solitarius (NTS) and neuronal NO synthase (nNOS) expression is functionally regulated in the brain. The purpose of these studies was to determine the influence of transition at birth on nNOS expression in the brainstem nuclei, particularly in the NTS, associated with changes in arterial pressure and plasma NE concentration. Experiments were performed using time-dated gestational ewes with twin fetuses. Arterial blood pressure was recorded and arterial blood NE concentrations were measured in the term fetus (gestational 147-148 days) and newborn lambs (4 h of postnatal age). The fetal and newborn animals were then perfused with 4% paraformaldehyde. Sections of the medulla were examined by using both immunolabeling with a polyclonal antibody directed against nNOS and nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) histochemistry, a marker for expression of nNOS. Micrographs were quantified using a microscope with reticule grid to measure the number of positive cells containing color staining in the brainstem nuclei. Plasma NE concentration in the newborn was more than two-fold greater compared to fetal values but mean arterial blood pressure was similar between fetus and newborn. The nNOS positive cells and NADPHd positive cells were significantly increased in the medial NTS (mNTS) of the newborn compared to fetus. nNOS immunoreactivity and NADPHd reactivity tended to increase in the rostral ventral medulla (RVM) in newborn, but were not altered in other brainstem nuclei during the transition from fetal to newborn life. The results suggest that nNOS expression in the mNTS is predominately enhanced at 4 h of neonatal age vs. the term fetus. We conclude that elevated circulating NE is associated with up-regulation of nNOS in the mNTS which may serve a protective role in central regulation of neonatal arterial blood pressure. 相似文献
55.
56.
报道58例非心脏手术的围手术期心脏起搏临床应用,重点讨论围手术期心脏起搏的方法与适应症。认为经静脉右室起搏疗效恒定可靠,适应症范围广。对伴有缓慢型或快速型心律失常的心脏病或潜在心脏病患者,围手术期心脏起搏适应症可适当放宽,以确保麻醉手术顺利进行 相似文献
57.
Neuroprotective mechanism of glial cell line-derived neurotrophic factor on dopamine neurons: role of antioxidation. 总被引:5,自引:0,他引:5
Recombinant human GDNF was infused into the rat striatum either acutely or subchronically. Its effects and its interactions with MPP+ on antioxidant enzyme activities were examined. Results indicated that acute GDNF infusion significantly increased glutathione peroxidase, superoxide dismutase and catalase activities. Subchronic GDNF treatment decreased the DA level and enhanced DA turnover. Pre-treatment with GDNF markedly protected DA neurons against MPP+-induced toxicity. These results suggest that GDNF protects DA neurons through its activation of the antioxidant enzyme systems. 相似文献
58.
Chao CC 《Environmental toxicology and pharmacology》1996,1(3):199-205
We have previously reported a cisplatin-resistant HeLa variant cell line (HeLa/CPR) which exhibited an enhancement in repairing cisplatin-DNA adducts (Chao, 1994, Mol. Pharmacol. 45, 1137-1144). In this study, using this cell line, we investigated the modification, by arsenite, of cisplatin-induced cytotoxicity and DNA repair in the resistant cell line. By a sublethal dose of arsenite, cytotoxicity of the resistant cells was enhanced by 2.5-fold, compared to 1.62-fold in the parental cells. Using enzyme-linked immunosorbent assay (ELISA) and a monoclonal antibody specific for cisplatin-DNA adducts, we found that the resistant cells showed a 5.15-fold decrease in the adduct formation compared to the parental cells. However, in the presence of arsenite, the resistant cells showed only a 1.47-fold decrease in the adduct formation, indicating a more than 3-fold modification. Using host cell reactivation of transfected plasmid DNA carrying cisplatin damage (an indirect detection of DNA repair), arsenite also revealed a ~2-fold modification of adduct formation in the resistant cells. In addition, the time-dependent potentiation of cytotoxicity by arsenite in both cell lines was parallel to the increase of adduct formation. These results indicate that arsenite is an effective modifier of cisplatin-induced resistance and enhanced DNA repair in HeLa/CPR cells. The results are consistent with the notion that the cisplatin-resistant phenotype in HeLa cells is mainly mediated by enhancement of DNA repair. 相似文献
59.
60.
Objective To investigate the activation of apoptotic genes of the brain with hypoxia- ischemia (HI) in newborn SD rats, and MRI changes and memory and learning ability in adulthood. Methods HI was induced by right carotid artery ligation followed by 2.5 h of hypoxia (6% O2) on 3-day-old SD rats (n=36). Control pups were sham-operated (n = 27). Right brain hemisphere was collected at 12 h and 7 d after HI and subjected to an apoptosis Oligo GEArrayR. MRI and Morris water maze test were performed on both groups at 42 and 44 days old, respectively. Results Comparing to 12 h after HI, up-regulated apoptotic genes included TNF, Caspase and pro-apoptotit genes of Bcl2 families, whereas the anti-apoptotic genes of Bcl2 family were down-regulated at 7 d after HI. The MRI assessment of the rats in HI group demonstrated that the area of the right cerebra l cortex was significantly smaller than the left side and control [periventricular layer: (23.5±3.6) mm2 vs (33.0±4.3) mm2, (34.5±3.9) mm2; hippocampus layer: (18.9±4.4) mm2 vs (29.1±5.0) mm2,(30.8±4.5) mm2, both P<0.01]. During the navigation trial, the HI rats demonstrated longer escape latency (4th day: (52.7±35.9) vs (17.8±8. 9) s, P<0.01). HI rats passed the platform less times than the control ones (T= 292.5, P<0.05) in space probe trial. Conclusions The activation of apoptotic genes induced by HI brain injury remains until 7 days later, involving intrinsic and extrinsic apoptotic pathway. The apoptosis of neural cells may lead to poor development of the cortex and impair the memory and learning ability in the adult rats after neonatal hypoxia- ischemia injury. 相似文献