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41.
42.
Ultraviolet-light induced p53 mutational spectrum in yeast is indistinguishable from p53 mutations in human skin cancer 总被引:1,自引:2,他引:1
Inga A; Scott G; Monti P; Aprile A; Abbondandolo A; Burns PA; Fronza G 《Carcinogenesis》1998,19(5):741-746
Ultraviolet (UV) light has been associated with the development of human
non-melanoma skin cancers (NMSC). Such cancers often exhibit mutations in
the p53 tumour suppressor gene. In order to determine the UV-induced p53
mutation spectrum, a yeast expression vector that harbours a human
wild-type p53 cDNA was UV-irradiated in vitro and transfected into a yeast
strain that contained the ADE2 gene regulated by a p53-responsive promoter.
Forty-five mutant clones contained 51 mutations. Seven mutations were
tandem base pair substitutions, four of which being CC-->TT, hallmark
mutations of UV mutagenesis. Eighty percent (41/51) of the mutations were
single or non-tandem base pair substitutions, the majority of which (27/41)
were C-->T transitions. Ninety-five percent of such mutations occurred
at dipyrimidine sites. Through a rigorous statistical test, the UV-induced
p53 mutation spectrum appears to differ significantly (P < 0.008) from
the one induced by the antineoplastic drug
chloroethyl-cyclohexyl-nitrosourea, and to be indistinguishable from the
one observed in NMSC (P = 0.4). These results demonstrate that the assay
allows the determination of carcinogen-specific p53 mutation fingerprints
and represents a new tool for molecular epidemiology.
相似文献
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44.
Monatsschrift Kinderheilkunde - 相似文献
45.
46.
Mireille G.F. Gerrits Peter G. Schnabel Teun M. Post Pierre A.M. Peeters 《Contraception》2013,87(2):193-200
BackgroundThe pharmacokinetics of the monophasic oral contraceptive nomegestrol acetate (NOMAC) plus 17β-estradiol (E2) were investigated after a single dose and multiple dosing.Study designNOMAC/E2 (2.5 mg/1.5 mg) was administered daily to healthy women (18–50 years, n= 23) for 24 days; blood samples for pharmacokinetic analysis were obtained on Day 24 and again, after a 10-day pill-free interval, on Day 35 after a single dose.ResultsNOMAC reached steady state after 5 days with mean ± standard deviation (SD) trough NOMAC concentration (Cav) of 4.4±1.4 ng/mL. On Day 24, mean±SD peak NOMAC concentration (Cmax, 12.3±3.5 ng/mL) was reached in mean 1.5 h (tmax); the mean±SD elimination half-life (t½) was 45.9±15.3 h. After a single dose, NOMAC mean±SD Cmax was 7.2±2.0 ng/mL and mean±SD t½ was 41.9±16.2 h. On Day 24, E2 mean±SD Cav was 50.3±25.7 pg/mL; mean±SD Cmax was 86.0±51.3 pg/mL. After a single dose, mean±SD E2 Cmax was 253±179 pg/mL.ConclusionsThese data demonstrate that NOMAC/E2 has a pharmacokinetic profile consistent with once-daily dosing. 相似文献
47.
Comparison of Bilateral vs. Staged Unilateral Deep Brain Stimulation (DBS) in Parkinson's Disease in Patients Under 70 Years of Age
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48.
Dr. A.V. Kristen S.O. Sch?nland A. Remppis U. Hegenbart P.A. Schnabel H.A. Katus T.J. Dengler 《Der Pathologe》2009,30(3):212-218
Cardiac amyloidoses are a heterogeneous group of cardiomyopathies that are resistant to treatment and are associated with a poor outcome. Standard heart failure treatment is usually not well tolerated and the underlying disease remains unaffected. The clinical picture is uncharacteristic. Cardiac amyloidosis is often associated with dysfunction of additional organs. Early cardiac amyloid involvement usually reveals left ventricular hypertrophy, impairment of longitudinal shortening and diastolic ventricular function. Without adequate therapy (bi-)ventricular hypertrophy will progress to severe systolic ventricular function decrease. The combination of low voltage pattern, left ventricular hypertrophy and granular sparkling is characteristic for advanced cardiac amyloid involvement. Cardiac magnetic resonance imaging and scintigraphy yield further information on the pattern and severity of cardiac involvement. In unclear cases (left ventricular) endomyocardial biopsy is necessary. Detection of early cardiac involvement and proper identification of patients at high risk for sudden cardiac death due to rapid progressive amyloidosis is still incompletely defined. Referral to specialized centers is strongly recommended. 相似文献
49.
Expression of fibrinogen receptors during activation and subsequent desensitization of human platelets by epinephrine 总被引:2,自引:0,他引:2
Epinephrine causes platelet aggregation and secretion by interacting with alpha 2-adrenergic receptors on the platelet surface. Platelet aggregation requires the binding of fibrinogen to a specific receptor on the membrane glycoprotein IIb-IIIa complex. Although the IIb-IIIa complex is identifiable on the surface of resting platelets, the fibrinogen receptor is expressed only after platelet activation. The current studies were designed to examine the effect of occupancy of platelet alpha 2-adrenergic receptors by epinephrine on the expression of fibrinogen receptors and on the aggregation of platelets. The ability of epinephrine to induce the expression of fibrinogen receptors was studied under two different conditions: acute stimulation (less than 1 min) and prolonged stimulation (50 to 90 min), the latter of which is associated with a reduction or "desensitization" of the platelet aggregation response. Expression of the fibrinogen receptor was monitored with 125I-fibrinogen as well as with 125I-PAC-1 (PAC-1), a monoclonal antibody that binds to the glycoprotein IIb-IIIa complex only after platelets are activated. Epinephrine caused an immediate increase in PAC-1 and fibrinogen binding that was dependent on occupancy of the alpha 2-receptor by epinephrine and on the presence of extracellular free Ca (KCa = 30 mumol/L). By itself, 1 mmol/L Mg was unable to support induction of the fibrinogen receptor by epinephrine. However, it did decrease the Ca requirement by about two orders of magnitude. Prolonged stimulation of unstirred platelets by epinephrine led to a 70% decrease in the aggregation response when the platelets were subsequently stirred. Despite their decreased aggregation response, desensitized platelets bound PAC-1 and fibrinogen normally, indicating that the loss of aggregation was not due simply to a decrease in fibrinogen receptor expression. Although desensitization was not affected by pretreatment of the platelets with aspirin, it was partially prevented when extracellular Ca was chelated by EDTA during the long incubation with epinephrine. These studies demonstrate that once platelet alpha 2-adrenergic receptors are occupied by epinephrine, extracellular Ca is involved in initiating the aggregation response by supporting the induction of the fibrinogen receptor and the binding of fibrinogen. Furthermore. Ca-dependent reactions subsequent to fibrinogen binding may be necessary for maximal platelet aggregation and are impaired when platelets become desensitized to epinephrine. 相似文献
50.
Glycoprotein Ib and glycoprotein IX are fully complexed in the intact platelet membrane 总被引:3,自引:6,他引:3
Two new murine monoclonal antibodies, AK 1 and SZ 1, reactive with the human platelet glycoprotein (GP) Ib-IX complex have been produced by the hybridoma technique. Both AK 1 and SZ 1 immunoprecipitated the GP Ib-IX complex from Triton X-100-solubilized, periodate-labeled platelets. With trypsinized, labeled platelets, AK 1, SZ 1, and FMC 25 (epitope on GP IX) immunoprecipitated a membrane-bound proteolytic fragment of the GP Ib-IX complex consisting of GP IX and an congruent to 25,000 mol wt remnant of the alpha-chain of GP lb disulfide-linked to the beta-subunit. Unexpectedly, although AK 1 and SZ 1 immunoprecipitated purified GP Ib-IX complex, neither antibody immunoprecipitated the individual components of this complex, GP Ib or GP IX. When GP Ib and GP IX were recombined, however, AK 1 and SZ 1 again immunoprecipitated the reformed complex, strongly suggesting that both antibodies were recognizing an epitope present only on the intact complex. Cross-blocking studies indicated that AK 1 and SZ 1 recognized a very similar or identical epitope that was proximal to the epitope for FMC 25. Both AK 1 and SZ 1 bound to a similar number of binding sites (congruent to 25,000) on intact platelets as monoclonal antibodies directed against either GP lb or GP IX. The combined data suggests that GP lb and GP IX are fully complexed in the intact platelet membrane. 相似文献