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151.
肉毒碱治疗TPN大鼠肝脂肪变性的研究 总被引:4,自引:1,他引:3
目的 探讨在全胃肠外营养(TPN)中补充肉毒碱减轻肝脂肪变性的作用。方法 18只正常Wistar大鼠和19只肝硬化Wistar大鼠分别随机分为6组,A1组、A2组,自由进食和进水(各6只);B1组、B2组,TPN(分别6只、7只);C1组、 ,TPN加肉毒碱(各6只)。各组实验结束后测肝功能,肝脂肪及行肝脏的组织学检查。结果 TPN组肝内脂肪显著2,TPN+肉毒碱组肝内脂肪明显减少。结论 在TPN 相似文献
152.
An echovirus 30 outbreak with a high meningitis attack rate among children and household members at four day-care centers 总被引:2,自引:0,他引:2
U.C. Vieth M. Kunzelmann S. Diedrich H. Timm A. Ammon O. Lyytikäinen L.R. Petersen 《European journal of epidemiology》1999,15(7):655-658
Echovirus 30 (E 30) outbreaks in defined cohorts have rarely been reported. In June 1996, an outbreak of E 30 occurred in four day-care centers (DCCs) in neighboring villages in Germany. A retrospective cohort study of DCC children, employees and household members was done to determine the extent of the outbreak and risk factors for illness. Forty-two percent (39/92) of DCC children, 13% (30/228) of their household members, 5% (1/19) of employees and 2% (1/49) of household members of employees were ill. Onsets occurred over 31 days. Thirteen percent (12/92) of DCC children had meningitis. In only one of 16 households with multiple family members ill, illness in a family member preceeded that of the DCC child. Household members of ill DCC children were 15 times more likely to report illness than those of non-ill DCC children. We conclude that this outbreak was associated with a very high incidence of meningitis, the outbreak began in the DCCs and then spread to household members, and that household members of ill children compared to those of non-ill children were much more likely to report illness. 相似文献
153.
李军艳 《山东中医药大学学报》1999,23(2):134-136
就《伤寒论》水气的涵义、致病特点、形成与发病、证治等方面进行了分析和探讨。认为:水气是一个病理概念,具有病理产物和致病因素的双重性,其本质是体内停蓄之水,其致病过程具有动而不居的特点;痰饮、水肿、湿痹皆是水气为患。水气的形成机制是阳虚,阳不制阴。治疗以“温药和之”为常法,振奋阳气以祛除水气;非尽以温药和之为变法,攻逐、清热、滋阴皆在其中。 相似文献
154.
155.
大鼠实验性视网膜光损伤中的视细胞凋亡 总被引:7,自引:1,他引:6
目的
进一步探讨视网膜光损伤的发病机制。
方法
20只Wistar大鼠分为实验组、对照组,分别在光照后12,24,36小时摘除眼球,视网膜组织行HE染色和核苷酸末端转移酶介导的DUTP缺口翻译法(TdT-mediated dUTP nick end labelling method,TUNEL)标记凋亡细胞。
结果
光照后12小时,视杆细胞外节出现少量空泡变性;24小时后,外核层出现明显的细胞核破碎、浓染和DNA裂解;36小时后,视杆细胞内、外节溶解,外核层大量细胞核丢失。
结论
视细胞凋亡是大鼠实验性视网膜光损伤的重要机制之一。
(中华眼底病杂志, 1999, 15: 167-169) 相似文献
156.
Acute toxic inhalation by irritant, and particularly oxidant, gases has until recently been considered to be no more complicated conceptually than a chemical burn of the epithelial surface. More recently, however, toxic inhalation has been appreciated to be a complex process involving biochemical, morphological and functional changes which are quantitatively similar, although inducible by different agents. Recent advances in pulmonary pathophysiology, inhalation toxicology, and particularly endothelial biology have clarified the events occurring at the moment of, and immediately following, exposure to oxidant gases. Studies of the pathophysiologic mechanisms associated with toxic inhalation by oxidant gases have been relatively static, however. Implications of recent findings in related fields illuminate the pathophysiology of toxic inhalation. Several principal speakers in this workshop are collaborating in an effort to develop a research facility for the study of toxic inhalation injury. This would be an international registry to serve as a teaching and research facility for documentation of cases of occupational and environmental toxic inhalation, considered as lung injury resulting from the inhalation of a toxic substance in a workplace setting or an uncontrolled release affecting residents of a community. The registry, as proposed, would encourage submissions by clinicians and institutions of a data set on each patient and on each incident; the registry would further encourage long-term follow-up of subjects and documentation of residual effects.Work presented at the 23rd Congress on Occupational and Environmental Health in the Chemical Industry (Medichem 1995) The Chemical Industry as a Global Citizen - Balancing Risks and Benefits, 19–22 September 1995, Massachusetts Institute of Technology, Cambridge, Massachusetts 相似文献
157.
恶性肿瘤体内外生长和发展过程与细胞外基质相关性的研究 总被引:12,自引:0,他引:12
目的探讨细胞外基质在肿瘤侵袭转移中的作用。方法利用小鼠肺腺癌细胞母系LA795移植于T739小鼠皮下和肾包膜下,以及人鼻咽癌细胞系CNE-2Z移植于裸小鼠皮下等体内移植模型,通过间接免疫酶标和间接免疫荧光技术,测定纤维粘连蛋白(FN)、层粘连蛋白(LN)与Ⅳ型胶原(ⅣC)在肿瘤移植后不同时间的表达,并利用多种体外实验方法(琼脂糖滴瘤细胞移动实验、软琼脂上瘤细胞集落生长速度测定、斑点杂交等),分析瘤细胞运动能力、瘤细胞集落生长速度等与LN、FN和ⅣC之间的关系。结果随着肿瘤的生长,FN、LN与ⅣC的表达均增强,且呈不同的分布;外源性FN、LN及ⅣC能提高瘤细胞的体外运动能力和促进瘤细胞集落的体外生长。结论细胞外基质的分布及其合成和降解的变化,与恶性肿瘤的侵袭和转移有关,对预测肿瘤生物学行为有参考价值。观察细胞外基质与瘤细胞侵袭的关系,肾包膜下移植模型较为理想 相似文献
158.
Neutropenia, fever, and infection 总被引:5,自引:0,他引:5
A E Brown 《The American journal of medicine》1984,76(3):421-428
With the advances in the management of various neoplastic diseases and subsequent improvement in "disease-free" states, complications of therapy--particularly, infectious complications--have evolved as stumbling blocks to survival. Among neutropenic (absolute neutrophil count below 1,000/mm3) patients with cancer, infection is the major autopsy-determined cause of death. With expected "cure rates" of childhood leukemia approaching 60 to 70 percent, it seems unreasonable to lose such patients to an infectious cause of death, yet this, indeed, happens. The purpose of this review is to (1) define the magnitude of the problem; (2) describe the various agents responsible for infections in neutropenic patients; (3) attempt to more sharply define degrees of neutropenia and mechanical defenses; and (4) consider various approaches to studying and treating these infections. 相似文献
159.
By intra-adnexal injection of glucose in the rabbit embryo, we were able to stimulate all the anomalies associated with "Amniotic Disease". Since we were even able to obtain amniotic bands, this study provides an excellent experimental model of this disease. Resulting lesions occur early in development, corresponding to the first trimester of human gestation. All of the anomalies can ultimately be explained by the destruction of the most superficial cells: epiblastic cells of the embryo and the amnion, subjacent mesenchyme, and endothelial cells. The subsequent lack of interaction between these cells and the importance of the anatomical localizations of resulting hematomas can lead to the pathogenetic approach to this disease. In light of the present study, the disease appears to be caused by an external factor within the amniotic fluid. The exact nature of the destructive agent(s) remains a mystery in man. 相似文献
160.