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Kazuhiro Izawa Yasuyuki Hirano Sumio Yamada Koichiro Oka Kazuto Omiya Setsu Iijima 《Circulation journal》2004,68(4):315-320
BACKGROUND: The present study examined the impact of an 8-week cardiac rehabilitation (CR) program on physiological outcomes and health-related quality of life (HRQOL) of patients with acute myocardial infarction (AMI). METHODS AND RESULTS: A total of 124 consecutive AMI patients were divided into a supervised outpatient CR group (n=82) and a non-CR group as a control (n=42). Peak oxygen uptake, handgrip strength, and knee extension muscular strength were used as physiological outcome measures. HRQOL outcomes were assessed by the Medical Outcome Study Short Form 36 (SF-36). CR group patients performed both aerobic exercise and moderate resistance training from 1 month (T1) to 3 months (T2) after AMI onset. Age, sex, body mass index, medications, and ejection fraction were similar in both groups. Significantly greater increases in overall physiological outcomes from T1 to T2 were measured in the CR group compared with those of the non-CR group. There were also significantly greater improvements in 4 of the 8 SF-36 health status subscales (physical functioning, role-physical, general health, and vitality) in the CR group compared with the non-CR group. CONCLUSIONS: Eight weeks of exercise training have specific effects on improvement in HRQOL and physiological outcomes in Japanese patients. 相似文献
86.
Koichiro Higasa Jun-Ichi Manabe Toshitsuga Yubisui Hideki Sumimoto Parichat Pung-amritt Varavarn S. Tanphaichitr & Yasuyuki Fukumaki 《British journal of haematology》1998,103(4):922-930
Hereditary methaemoglobinaemia, caused by deficiency of NADH-cytochrome b5 reductase (b5R), has been classified into two types, an erythrocyte (type I) and a generalized (type II). We analysed the b5R gene of two Thai patients and found two novel mutations. The patient with type II was homozygous for a C-to-T substitution in codon 83 that changes Arg (CGA) to a stop codon (TGA), resulting in a truncated b5R without the catalytic portion. The patient with type I was homozygous for a C-to-T substitution in codon 178 causing replacement of Ala (GCG) with Val (GTG). To characterize effects of this missense mutation, we investigated enzymatic properties of mutant b5R (Ala 178 Val). Although the mutant enzyme showed normal catalytic activity, less stability and different spectra were observed. These results suggest that this substitution influenced enzyme stability due to the slight change of structure. In conclusion, the nonsense mutation led to type II because of malfunction of the truncated protein. On the other hand, the missense mutation caused type I, due to degradation of the unstable mutant enzyme with normal activities in patient's erythrocytes, because of the lack of compensation by new protein synthesis during the long life-span of erythrocytes. 相似文献
87.
Andrei Brydun Yuichiro Watari Yoshiyuki Yamamoto Koichiro Okuhara Hiroki Teragawa Fujiko Kono Kazuaki Chayama Tetsuya Oshima Ryoji Ozono 《Hypertension research》2007,30(4):341-348
Heme oxigenase-1 (HO-1) is known to be an inducible cytoprotective enzyme that copes with oxidative stress. However, changes in HO-1 expression and their association with human diseases have not been studied. To test the hypothesis that the capacity to upregulate HO-1 in response to oxidative stress is an intrinsic marker for susceptibility to coronary atherosclerosis, we assessed stimulation-induced change in HO-1 expression in blood cells in 110 patients who underwent coronary angiography, comparing the results with the extent of coronary atherosclerosis and (GT)(n) repeat polymorphism in the HO-1 gene promoter region, which is believed to affect the gene expression level. The extent of coronary atherosclerosis was assessed by coronary score. Mononuclear cells were incubated with 10 micromol/l hemin or vehicle for 4 h to maximally stimulate HO-1 expression, then the HO-1 expression level was determined by real-time polymerase chain reaction (PCR). The difference between the HO-1 mRNA levels of hemin- and vehicle-treated cells (DeltaHO-1 mRNA) was taken as an index of the capacity to upregulate HO-1 mRNA. The coefficient of variance of DeltaHO-1 mRNA was 7.2%. Consistent with previous studies, DeltaHO-1 mRNA was significantly lower in patients carrying a long (GT)(n) repeat. DeltaHO-1 mRNA negatively and significantly correlated with the coronary score (r(2)=0.50, p<0.01). In conclusion, the capacity to upregulate HO-1 expression may be determined, at least in part, by genetics, and reduced ability to induce HO-1 may be involved in the mechanism of coronary atherosclerosis. 相似文献
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Ishiguro T Takayanagi N Kurashima K Matsushita A Harasawa K Yoneda K Tsuchiya N Miyahara Y Yamaguchi S Yano R Tokunaga D Saito H Ubukata M Yanagisawa T Sugita Y Kawabata Y 《Internal medicine (Tokyo, Japan)》2008,47(11):1021-1025
This report describes a 65-year-old woman who developed granulomatous lesions consistent with sarcoidosis during etanercept therapy for rheumatoid arthritis. Hilar and mediastinal lymphadenopathy and multiple nodules in both lung fields developed 21 months after administration of etanercept. Noncaseating epithelioid cell granulomas consistent with sarcoidosis were detected in a lung biopsy specimen and in the parietal pleura obtained via thoracotomy. Diseases showing similar histologic changes were excluded, and a diagnosis of sarcoidosis was made. Etanercept was discontinued, which resulted in symptomatic relief, improvement of oxygenation and radiologic findings. There is substantial evidence of tumor necrosis factor-alpha involvement in the induction and maintenance of granuloma formation; however, we should keep in mind that granulomatous disease, such as sarcoidosis, can develop during treatment with a tumor necrosis factor-alpha blocking agent, such as etanercept. 相似文献
90.
Akira Endo Yoshio Kano Koichiro Mihara Kunzo Orita Masayoshi Namba 《Journal of cancer research and clinical oncology》1993,119(9):522-526
Genetic analysis was carried out in human fibroblasts (KMST-6) immortalized by treatment with60Co gamma rays in order to determine if any genetic change was involved in the immortal transformation of human cells. Analysis by restriction fragment length polymorphism revealed an alteration in chromosome 13q12–14, in which the retinoblastoma (RB) gene locus (13q14) is located. Then the RB gene itself was examined. Structural abnormalities in the RB gene were detected by Southern blot analysis. Furthermore, abnormal RB protein (pRB) was expressed in immortalized KMST-6 cells, as shown by in vitro phosphorylation, whereas normal KMS-6 cells expressed the intact pRB. These findings indicated that inactivation of the RB gene is one of the key events of the immortalization of human cells.Abbreviations RB
retinoblastoma
- pRB
retinoblastoma gene product (protein)
- T
simian virus 40 large T antigen
- E1A
adenovirus E1A protein 相似文献