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61.
Shigetoshi Chiba Hidehiko Watanabe 《Clinical and experimental pharmacology & physiology》1983,10(1):1-5
1. Effects of 2-phenylaminoadenosine on SA nodal pacemaker activity and atrial contractility were studied, using eleven isolated, blood-perfused dog atrial preparations. The compounds were administered via the cannulated sinus node artery of the isolated atrium. 2. 2-Phenylaminoadenosine induced negative chronotropic and inotropic effects and was 100 times less potent than adenosine in this action. 3. The interaction between adenosine and 2-phenylaminoadenosine was studied. 2-Phenylaminoadenosine potentiated the effect of adenosine on atrial muscle, but not that of acetylcholine. 相似文献
62.
63.
The Secondary Structure of Human Hageman Factor (Factor XII) and its Alteration by Activating Agents 总被引:9,自引:5,他引:4 下载免费PDF全文
Carl R. McMillin Hidehiko Saito Oscar D. Ratnoff Alan G. Walton 《The Journal of clinical investigation》1974,54(6):1312-1322
Hageman factor (factor XII) is activated by exposure to surfaces such as glass or by solutions of certain compounds, notably ellagic acid. Changes in the structure of Hageman factor accompanying activation have been examined in this study by circular dichroism spectroscopy. The spectrum of unactivated Hageman factor in aqueous solutions suggests that its conformation is mainly aperiodic. Various perturbants altered the conformation of Hageman factor in differing ways, demonstrating the sensitivity of Hageman factor to its environment.After activation of Hageman factor with solutions of ellagic acid, a negative trough appeared in the region of the circular dichroism spectrum commonly assigned to tyrosine residues, along with other minor changes in the peptide spectral region. Some of these changes are similar to changes that occurred upon partial neutralization of the basic residues at alkali pH. Activation of Hageman factor by adsorption to quartz surfaces (in an aqueous environment) also produced changes similar to those in the ellagic acid-activated Hageman factor, including the negative ellipticity in the tyrosine region.These observations suggest that the activation process may be related to a change in status of some of the basic amino acid residues, coupled with a specific change in the environment of some tyrosine residues. The importance of these changes during the activation process remains to be determined. The sensitivity of Hageman factor to its environment is consistent with the view that the initiation of clotting by exposure of plasma to appropriate agents is brought about by alterations in the conformation of Hageman factor that occur in the apparent absence of Fletcher factor or other recognized clotting factors. 相似文献
64.
Mechanism of Adherence of Streptococcus mutans to Smooth Surfaces II. Nature of the Binding Site and the Adsorption of Dextran-Levan Synthetase Enzymes on the Cell-Wall Surface of the Streptococcus 总被引:45,自引:40,他引:5 下载免费PDF全文
The mechanism of adsorption of the Streptococcus mutans enzymes responsible for the synthesis of insoluble dextran-levan to the S. mutans cell-wall binding sites has been studied. Certain characteristics of these binding sites are presented. The adsorption of these enzymes to the cell surface occurred rapidly without the addition of a source of energy and over a pH range of 3 to 11. The adsorption was inhibited by soluble dextran, probably due to the strong affinity of the polymer to the enzyme. All other polymers and sugars studied showed little or no inhibition. The adsorption was also inhibited by antibody globulin to the a-d immunologically specific group antigen surface polysaccharide of S. mutans and by anti-dextran globulin. The inhibition by anti-a-d globulin is considered to be due to a restriction of access of enzyme to the binding site of the enzyme which may be located in close proximity to the group antigen. On the other hand, anti-dextran globulin appeared to directly inhibit the adsorption by covering the binding site. Dextranase destroyed the binding site and released glucose from the S. mutans cells. These data indicate that S. mutans grown in media containing glucose possesses a small amount of dextran on the cell surface, and that this dextran is, or is a part of, the binding site for enzymes which synthesize the insoluble dextran-levan polymer. Trypsin inhibited the synthesis of insoluble polysaccharide and the adherence of cells. It is not clear in this case that destruction of the binding sites occurred. These data present a partial explanation of the processes which may be concerned in the formation of dental plaque on the smooth surfaces of teeth. 相似文献
65.
Overexpression of Aurora-A potentiates HRAS-mediated oncogenic transformation and is implicated in oral carcinogenesis 总被引:4,自引:0,他引:4
Tatsuka M Sato S Kitajima S Suto S Kawai H Miyauchi M Ogawa I Maeda M Ota T Takata T 《Oncogene》2005,24(6):1122-1127
Aurora kinases are known to play a key role in maintaining mitotic fidelity, and overexpression of aurora kinases has been noted in various tumors. Overexpression of aurora kinase activity is thought to promote cancer development through a loss of centrosome or chromosome number integrity. Here we observed augmentation of G12V-mutated HRAS-induced neoplastic transformation in BALB/c 3T3 A31-1-1 cells transfected with Aurora-A. Aurora-A-short hairpin RNA (shRNA) experiments showed that the expression level of Aurora-A determines susceptibility to transformation. Aurora-A gene amplification was noted in human patients with tongue or gingival squamous carcinoma (4/11). Amplification was observed even in pathologically normal epithelial tissue taken at sites distant from the tumors in two patients with tongue cancer. However, overexpression of Aurora-A mRNA was observed only within the tumors of all patients examined (11/11). Our data indicate that Aurora-A gene amplification and overexpression play a role in human carcinogenesis, largely due to the effect of Aurora-A on oncogenic cell growth, rather than a loss of maintenance of centrosomal or chromosomal integrity. 相似文献
66.
Aurora-B, previously known as AIM-1, is a conserved eukaryotic mitotic protein kinase. In mammals, this kinase plays an essential role in chromosomal segregation processes, including chromosome condensation, alignment, control of spindle checkpoints, chromosome segregation, and cytokinesis. Aurora-B is overexpressed in various cancer cells, suggesting that the kinase activity perturbs chromosomal segregation processes. Its forced overexpression induces chromosomal number instability and progressive tumorigenicity in rodent cells in vitro and in vivo. Nevertheless, based on focus formation in BALB/c 3T3 A31-1-1 cells, Aurora-B is not oncogenic. Here, we show that Aurora-B kinase activity augments Ras-mediated cell transformation. RNA interference with short hairpin RNA inhibits transformation by Ras and its upstream oncogene Src, but not by the downstream oncogene Raf. In addition, the inner centromere protein, which is a passenger protein associated with Aurora-B, has a similar ability to potentiate the activity of oncogenic Ras. These data indicate that elevated Aurora-B activity promotes transformation by oncogenic Ras by enhancing oncogenic signaling and by converting chromosome number-stable cells to aneuploid cells. 相似文献
67.
We experienced acute myocardial infarction due to coronary artery spasm after caesarean section. A 41-year-old multigravida woman with no previous cardiac history or coronary risk factor developed acute myocardial infarction after caesarean section, and was successfully resuscitated with emergency percutaneous transluminal coronary angioplasty. Acute myocardial infarction during pregnancy and postpartum period is a rare event, but could be associated with high mortality if it occurs. It is necessary to consider the possibility of acute myocardial infarction and provide early diagnosis and treatment by multidisciplinary team when a pregnant woman complains of retrosternal chest pain. 相似文献
68.
Ishimitsu T Ohta S Saito M Teranishi M Inada H Yoshii M Minami J Ono H Hikawa A Shibata N Sugaya T Kamijo A Kimura K Ohrui M Matsuoka H 《Clinical and experimental nephrology》2005,9(1):34-39
Background Messenger RNA of liver fatty acid-binding protein (L-FABP) is expressed in proximal tubules of the kidney, and a certain amount is excreted into urine. We analyzed factors relating to the urinary L-FABP excretion in health-check participants.Methods We measured L-FABP in the first morning urine by ELISA in 715 men and 193 women 30–79 years of age who entered a 2-day hospitalized health checkup program. In addition to the routine physical examination and laboratory tests, plasma high-sensitivity C-reactive protein (HSCRP) was assayed.Results In 150 healthy subjects, urinary L-FABP averaged 3.6 ± 0.2µg/g creatinine, whereas the values were significantly increased in patients with hypertension (5.2 ± 0.4, P = 0.010), diabetes mellitus (5.5 ± 0.5, P < 0.001), and chronic hepatitis (5.8 ± 1.0, P = 0.022). Urinary L-FABP excretion was significantly greater in women than in men when the value was related to creatinine. In regression analysis in men, urinary L-FABP was positively correlated with fasting plasma glucose (r = 0.103, P = 0.033) and plasma HSCRP (r = 0.135, P = 0.006).Conclusions It is suggested that renal production and urinary excretion of L-FABP are increased in situations in which arteriosclerosis is promoted, such as hypertension, diabetes mellitus, and cardiovascular inflammation. 相似文献
69.
Postoperative cerebral hyperperfusion associated with impaired cognitive function in patients undergoing carotid endarterectomy 总被引:7,自引:0,他引:7
Ogasawara K Yamadate K Kobayashi M Endo H Fukuda T Yoshida K Terasaki K Inoue T Ogawa A 《Journal of neurosurgery》2005,102(1):38-44
OBJECT: Cognitive impairment occurs in 20 to 30% of patients following carotid endarterectomy (CEA). The purpose of the present study was to determine whether postoperative cerebral hyperperfusion is associated with impairment of cognitive function in patients undergoing that procedure. METHODS: Cerebral blood flow (CBF) was measured using single-photon emission computerized tomography scanning before and immediately after CEA and on the 3rd postoperative day in 92 patients with ipsilateral internal carotid artery stenosis of 70% or greater. Hyperperfusion post-CEA was defined as a 100% increase or greater in CBF compared with preoperative values. Neuropsychological testing was also performed preoperatively and at the 1-, 3-, and 6-month follow-up examinations. At the 1-month postoperative neuropsychological assessment, 11 patients (12%) displayed evidence of cognitive impairment. In addition, the incidence of postoperative cognitive impairment in patients with post-CEA hype perfusion (seven [58%] of 12 patients) was significantly higher than that in patients without post-CEA hyperperfusion (four [5%] of 80 patients; p < 0.0001). A logistic regression analysis demonstrated that post-CEA hyperperfusion was the only significant independent predictor of postoperative cognitive impairment. Of the seven patients in whom post-CEA hyperperfusion and cognitive impairment were identified 1 month postoperatively, four (including three patients with hyperperfusion syndrome) remained cognitively impaired at the 3- and 6-month follow-up examinations. CONCLUSIONS: Postoperative cerebral hyperperfusion is associated with impairment of cognitive function in patients undergoing CEA. Furthermore, the development of hyperperfusion syndrome is associated with the persistence of postoperative cognitive impairment. 相似文献
70.