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81.
A patient with Waardenburg syndrome type II associated with Hirschsprung megacolon and Marcus Gunn ptosis is presented. It is suggested that these different anomalies are manifestations of the same neurocrestopathy. 相似文献
82.
Jocelyne Fleury-Feith Laurence Kheuang Lin Zeng Jean Bignon Christian Boutin Isabelle Monnet Marie-Claude Jaurand 《The Journal of pathology》1995,177(2):209-215
The aim of this study was to determine, by transmission electron microscopy, the differentiation features of 21 human malignant mesothelioma cell lines (HMCLs) established from 13 specimens of 12 confirmed human malignant mesotheliomas, and of tumours induced in nude mice injected with 16 HMCLs. Fifty per cent of HMCLs showed typical mesothelial differentiation (long and slender microvilli, desmosomes, perinuclear intermediate filaments); 29 per cent did not show differentiation; and the remainder were poorly differentiated. Three human tumour specimens gave several different HMCLs; the cell lines obtained from a given tumour exhibited variable mesothelial differentiation. Eleven HMCLs were compared with the native tumour. Four were similar to the tumour and seven were less well differentiated, in most cases in relation to their microvilli. With six HMCLs, tumours induced in nude mice were less well differentiated than the corresponding cell lines, whereas with four HMCLs, tumours were equally or better differentiated. However, in most nude mice tumours, typical mesothelial microvilli were present. These results show that cell lines established from malignant mesothelioma may exhibit dedifferentiated features. However, while the variability in ultrastructural differentiation may result from the culture microenvironment, it could also be related to the state of differentiation, of the native tumour sample and to tumour cell heterogeneity. 相似文献
83.
构建7q32区域鼻咽癌和正常鼻咽上皮细胞部分基因的表达图谱 总被引:7,自引:2,他引:7
目的构建7q32区域鼻咽癌细胞和组织及原代培养人正常鼻咽上皮细胞的部分基因表达图谱。方法通过差异RT-PCR和Northern杂交的方法检测定位于7q32区域的20个EST在鼻咽癌细胞和鼻咽癌组织及原代培养人正常鼻咽上皮细胞mRNA的表达水平。结果8个EST在鼻咽癌细胞HNE1和原代培养人正常鼻咽上皮细胞中表达量较一致,7个EST在两种细胞中均无表达,3个EST(W72688、H19830、AA130630)在鼻咽癌细胞株中表达上调,而2个EST(AA070437、H90882)在原代培养人鼻咽上皮细胞中表达上调。在13例鼻咽癌活检组织中30.7%(4/13)的AA070437表达下调,77%(10/13)的W72688和77%(10/13)的H19830表达上升。结论构建了7q32区域鼻咽癌细胞和组织及原代培养人正常鼻咽上皮细胞部分基因表达图谱,并初步认为A070437的表达下调和W72688、H19830的过表达与鼻咽癌的发生有关。 相似文献
84.
不同年龄人脑视皮质毛细血管密度的计量分析 总被引:1,自引:1,他引:1
本文应用碱性磷酸酶染色,按立体学方法观测了不同年龄(14岁以下儿童4例,成年人2例,60岁以上老人2例)共8例人脑视皮质有纹区各层毛细血管的密度(各层均取40个数据).结果:成年组视皮质第三层血管网3c亚层(位于皮质第Ⅳc层)毛细血管密度平均为1580.79±47.73mm/mm~3;儿童组为1087.19±44.90mm/mm~3;老年组为619.95±21.39mm/mm~3.经方差分析检验,P<0.01,说明在第三层血管网3c亚层三个年龄组之间具有非常显著性差异.讨论了各年龄组之间视皮质有纹区毛细血管密度差异与机能的关系. 相似文献
85.
86.
Rosiglitazone, an agonist of peroxisome proliferator-activated receptor γ, reduces pulmonary inflammatory response in a rat model of endotoxemia 总被引:3,自引:0,他引:3
Objective: The effect of rosiglitazone, a potent peroxisome proliferator-activated receptor γ (PPAR-γ) agonist, on pulmonary inflammation
in endotoxemia was investigated.
Materials and methods: Male Wistar rats were given either lipopolysaccharide (LPS, 6 mg/kg i.v.) or saline, pretreated with rosiglitazone (0.3 mg/kg
i.v.) or its vehicle (dimethyl sulphoxide) 30 min before LPS. The selective PPAR-γ antagonist GW9662 (0.3 mg/kg i.v.) was
given 20 min before rosiglitazone. Wet/dry weight (W/D) ratio, myeloperoxidase (MPO) activity, malondialdehyde (MDA) as well
as TNF-α and CINC-1 concentrations were measured in lung tissues 4 h after LPS injection. Expression of ICAM-1, NF-κB p65
and PPAR-γ were also determined by immunohistochemistry or Western blot analysis.
Results: Rosiglitazone pretreatment significantly attenuated the increases in W/D ratio, MPO activity and MDA levels, and reduced
pulmonary overproduction of TNF-α and CINC-1 as well as expression of ICAM-1 following endotoxemia. Rosiglitazone also inhibited
the nuclear localization of NF-κB and up-regulated the expression of PPAR-γ protein. The specific PPAR-γ antagonist GW9662
abolished the effect of rosiglitazone.
Conclusion: These findings suggest that PPAR-γ agonists might be used as therapeutic agents in the therapy of inflammatory lung injury
related to endotoxemia.
Received 8 January 2005; returned for revision 6 July 2005; returned for final revision 20 July 2005; accepted by M. Katori
31 July 2005 相似文献
87.
Chen YN Chen SY Zeng LJ Ran JM Xie B Wu MY Wu YZ 《British journal of biomedical science》2003,60(1):9-13
Sulphonylurea (SU) stimulates insulin secretion by pancreatic beta-cells and is generally used as a first-line treatment for type 2 diabetes. However, after long-term SU treatment (six months or over), some patients begin to show an increase in blood glucose once again (secondary SU failure). Two theories have been put forward to explain this failure--dysfunction of the proinsulin conversion machinery or insulin resistance. However, the primary pathogenesis behind secondary SU failure still needs to be investigated. Using a reliable technique that specifically identifies intact proinsulin (IPI), total proinsulin (TPI) and specific insulin (SI), this study aims to discover if a defect in the proinsulin converting mechanism plays a role in SU failure. Three groups were recruited for this study: healthy controls (n=8), SU responders (n=38) and secondary SU failures (n= 46). Serum concentrations of insulin-related molecules released in response to a standard glucose challenge test were compared between the groups. It was found that total SI was lower in the patient groups (P<0.05 compared to the control group), while TPI and IPI showed no distinct difference between the three groups (P>0.05). TPI:SI ratio and IPI:SI ratio showed marked increases in the patient groups (P<0.05 compared to control group), with no obvious quantitative difference between SU responders and secondary SU failures (P>0.05). Similar results for the Homa Insulin Resistant Index were found between the two patient groups. Interestingly, blood glucose at 180 mins after glucose challenge was significantly higher in the secondary SU failure group (P<0.05), with no correlation to SI, while the SU responder group showed good correlation between the parameters (P<0.05). We conclude that type 2 diabetes is associated with obvious dysfunction in the proinsulin-converting process and shows severe SI deficiency in responding to glucose challenge. Dysfunction of the proinsulin conversion mechanism was not an extra cause responsible for SU failure. 相似文献
88.
检测Epstein-Barr病毒特异性细胞毒性T淋巴细胞方法的建立及其初步研究 总被引:4,自引:0,他引:4
目的建立一种非放射性、简便易行的可检测特异性细胞毒性T淋巴细胞的方法,并且初步应用于Epstein-Bar病毒的细胞免疫应答。方法用重组的EBV-LMP1痘苗病毒、TK+痘苗病毒和杆状病毒系统表达的EBV-LMP1蛋白分别免疫Balb/C小鼠,用P815细胞和乳酸脱氢酶法检测EB病毒特异性细胞毒性T细胞的杀伤效应。结果重组EBV-LMPI痘苗病毒免疫组原发CTL水平和体外诱生的二次CTL水平均高于TK+痘苗病毒免疫组和正常组;杆状病毒系统表达的EBV-LMP1蛋白免疫组的CTL水平也明显高于正常鼠。结论本法可以较好的反映EB病毒特异性细胞毒性T细胞的水平,而且再一次说明LMP1基因能够诱发特异性的细胞免疫。 相似文献
89.
Lattice constants (LCs) of all possible 96 apatite compounds, A(5)(BO(4))(3)C, constituted by A[double bond]Ba(2+), Ca(2+), Cd(2+), Pb(2+), Sr(2+), Mn(2+); B[double bond]As(5+), Cr(5+), P(5+), V(5+); and C[double bond]F(1-), Cl(1-), Br(1-), OH(1-), are predicted from their elemental ionic radii, using pattern recognition (PR) and artificial neural networks (ANN) techniques. In particular, by a PR study it is demonstrated that ionic radii predominantly govern the LCs of apatites. Furthermore, by using ANN techniques, prediction models of LCs a and c are developed, which reproduce well the measured LCs (R(2)=0.98). All the literature reported on 30 pure and 22 mixed apatite compounds are collected and used in the present work. LCs of all possible 66 new apatites (assuming they exist) are estimated by the developed ANN models. These proposed new apatites may be of interest to biomedical research especially in the design of new apatite biomaterials for bone remodeling. Similarly these techniques may also be applied in the study of interface growth behaviors involving other biomaterials. 相似文献
90.
Progressive deterioration of beta-cell function is proposed as a disease-related factor of sulphonylurea (SU) failure in type 2 diabetes. If it gradually worsens over time then disease duration may mirror the progressive beta-cell deterioration. The aim of the present study is to assess whether or not disease duration is influential in remodelling the secretion pattern of insulin-like molecules and in glucose control of SU-treated type 2 diabetes. A research model is used to investigate proinsulin secreting capacity over time, using two groups of patients: i) disease duration <5 years (n=62), comprising SU responders (SUr; n=48) and SU failures (SUf; n=14); and ii) disease duration > or = 5 years (n= 37), comprising an SUr group (n=17) and an SUf group (n=20). Blood samples are taken at 0 h, 0.5 h 1 h, 2 h and 3 h during a standard oral glucose tolerance test and measured for glucose, total proinsulin (TPI), intact proinsulin (IPI) and specific insulin (SI) concentrations. Pairwise comparison of estimated marginal means of blood glucose, SI, IPI and TPI levels at each time point are carried out between groups and subgroups. (SUr vs. SUf). Homa insulin resistance index (IR index) is applied to analyse IR between the groups. It was found that patients with shorter disease duration had higher proinsulin (TPI and IPI) levels at all time points (P<0.05), together with a lower glucose level at 2 h and 3 h (P<0.05). Homa insulin index analysis showed no difference between the two groups (P=0.26). Results also showed that the SUr group had a significantly lower glucose level at Oh and 3h (P<0.05), although no significant difference in insulin and proinsulin levels was found between the SUr and SUf groups. In conclusion, proinsulin may play an important role in glucose control in SU-treated type 2 diabetes, but the effect is reduced in SUf patients. 相似文献