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61.
Impact of p16 expression,nodal status,and smoking on oncologic outcomes of patients with head and neck unknown primary squamous cell carcinoma 下载免费PDF全文
62.
High-level gentamicin resistance mediated by a Tn4001-like transposon in seven nonclonal hospital isolates of Streptococcus pasteurianus 下载免费PDF全文
Chow VC Hawkey PM Chan EW Chin ML Au TK Fung DK Chan RC 《Antimicrobial agents and chemotherapy》2007,51(7):2508-2513
We report on the first occurrence of high-level gentamicin resistance (MICs > or = 512 microg/ml) in seven clinical isolates of Streptococcus pasteurianus from Hong Kong. These seven isolates were confirmed to be the species S. pasteurianus on the basis of nucleotide sequencing of the superoxide dismutase (sodA) gene. Epidemiological data as well as the results of pulse-field gel electrophoresis analysis suggested that the seven S. pasteurianus isolates did not belong to the same clone. Molecular characterization showed that they carried a chromosomal, transposon-borne resistance gene [aac(6')Ie-aph(2')Ia] which was known to encode a bifunctional aminoglycoside-modifying enzyme. The genetic arrangement of this transposon was similar to that of Tn4001, a transposon previously recovered from Staphylococcus aureus and other gram-positive isolates. Genetic linkage with other resistance elements, such as the ermB gene for erythromycin resistance, was not evident. On the basis of these findings, we suggest that routine screening for high-level gentamicin resistance should be recommended for all clinically significant blood culture isolates. This is to avoid the inadvertent use of short-course combination therapy with penicillin and gentamicin, which may lead to the failure of treatment for endocarditis, the selection of drug-resistant Streptococcus pasteurianus and other gram-positive organisms, as well as the unnecessary usage of gentamicin, a drug with potential toxicity. 相似文献
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An inhibitory monoclonal antibody to factor X that blocks prothrombin activation but not prothrombinase enzyme assembly 总被引:1,自引:0,他引:1
A monoclonal antibody (designated alpha BFX-2b) prepared against bovine factor X inhibited factor X activity in human, bovine, porcine, rabbit, and canine plasma. In assays using purified prothrombinase components, factor Xa, factor Va, phospholipid vesicles, and calcium ion with the fluorescent active site thrombin inhibitor dansylarginyl-N-(3-ethyl-1,5- pentanediyl)amide, the antibody inhibited the conversion of prothrombin to thrombin. Antibody alpha BFX-2b also blocked prothrombinase cleavage of the macromolecular substrates prethrombin 1 and prethrombin 2 but did not inhibit factor Xa hydrolysis of the synthetic substrate benzoyl- Ile-Glu-Gly-Arg-p-nitroanilide. The antibody also prevented the inactivation of factor Xa by antithrombin III but did not prevent the inactivation by soybean trypsin inhibitor. Antibody alpha BFX-2b bound factor Xa with a stoichiometry of 1:1 and an apparent dissociation constant of 9.0 x 10(-11) mol/L as estimated from its inhibition of prothrombinase activity. Antibody alpha BFX-2b did not prevent binding of factor Xa to factor Va-phospholipid as measured by using fluorescence polarization or high-pressure liquid gel chromatography with the fluorescent Factor Xa analogue dansyl-glutamyl-glycyl-arginyl- Xa. Immunoblotting of factor X following electrophoresis on sodium dodecyl sulphate-polyacrylamide gels and transfer to nitrocellulose indicated that the antigenic determinant recognized by antibody alpha BFX-2b was found on the heavy chain of factors X and Xa. From these observations it can be concluded that antibody alpha BFX-2b recognizes a highly conserved epitope on the factor X heavy chain that is remote from the topographic sites required for prothrombinase complex assembly and substrate hydrolysis but may be located at or near a portion of the macromolecular substrate binding site. 相似文献
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The reproductive capabilities of 6- and 24-month-old C57BL/6NNia male mice were compared after being paired for one month with a 4-month-old proven-fertile female. All of the younger males mated, with 96% yielding a litter; only 42% of aged males mated, with 65% siring young. There were no statistical differences in the litter sizes, nor any congenital defects noted in offspring from either age group. There was no evidence of aneuploidy in 10-day-old embryos sired from males of either age group. Aged males that failed to mate had lower body weight, a lower hematocrit, hypertrophied adrenal glands and seminal vesicles, decreased fructose levels in seminal vesicle fluid, atrophied testes with fewer sperm that were less motile, lower testosterone levels, and a greater percentage of degenerating epithelium lining seminiferous tubules. The latter group of aged mice, while appearing and acting as vigorous as aged mice that had mated, may have been experiencing disease processes associated with aging which subsequently impaired reproduction. 相似文献
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Kaharu Sumino Katiuscia O’Brian Brian Bartle David H. Au Mario Castro Todd A. Lee 《The Journal of asthma》2014,51(3):306-314
Objective: Many asthma patients suffer from chronic conditions other than asthma. We investigated the specific contribution of common comorbidities on mortality and morbidity in adult asthma. Methods: In an observational study of adults with incident asthma identified between 1999 and 2003 using National Veterans Affairs and Centers for Medicare and Medicaid Services encounter databases (n?=?25?975, follow-up 3.0?±?1.7 years), association between 13 most prevalent comorbidities (hypertension, ischemic heart disease (IHD), osteoarthritis, rheumatoid arthritis, diabetes, mental disorders, substance/drug abuse, enlarged prostate, depression, cancer, alcoholism, HIV and heart failure) and four conditions previously associated with asthma (sleep apnea, gastroesophageal reflux disease (GERD), rhinitis and sinusitis) and mortality, hospitalizations and asthma exacerbations were assessed using multivariate regression analyses adjusted for other clinically important covariates. Results: HIV followed by alcoholism and mental disorders among 18–45-years old, and heart failure, diabetes, IHD and cancer among those ≥65 years old were associated with an increased risk of all-cause mortality. Many conditions were associated with increased risk for all-cause hospitalizations, but the increased risk was consistent across all ages for mental disorders. For asthma exacerbations, mental disorder followed by substance abuse and IHD were associated with increased risk among those 18–45 years old, and chronic sinusitis, mental disorder and IHD among those ≥65-years old. GERD was associated with decreased risk for asthma exacerbation in all ages. Conclusions: Many comorbidities are associated with poor outcome in adult asthmatics and their effect differs by age. Mental disorders are associated with increased risk of mortality and morbidity across ages. 相似文献
68.
Kuan Rong Chan Eugenia Z. Ong Hwee Cheng Tan Summer Li-Xin Zhang Qian Zhang Kin Fai Tang Nivashini Kaliaperumal Angeline Pei Chiew Lim Martin L. Hibberd Soh Ha Chan John E. Connolly Manoj N. Krishnan Shee Mei Lok Brendon J. Hanson Chao-Nan Lin Eng Eong Ooi 《Proceedings of the National Academy of Sciences of the United States of America》2014,111(7):2722-2727
Viruses must evade the host innate defenses for replication and dengue is no exception. During secondary infection with a heterologous dengue virus (DENV) serotype, DENV is opsonized with sub- or nonneutralizing antibodies that enhance infection of monocytes, macrophages, and dendritic cells via the Fc-gamma receptor (FcγR), a process termed antibody-dependent enhancement of DENV infection. However, this enhancement of DENV infection is curious as cross-linking of activating FcγRs signals an early antiviral response by inducing the type-I IFN-stimulated genes (ISGs). Entry through activating FcγR would thus place DENV in an intracellular environment unfavorable for enhanced replication. Here we demonstrate that, to escape this antiviral response, antibody-opsonized DENV coligates leukocyte Ig-like receptor-B1 (LILRB1) to inhibit FcγR signaling for ISG expression. This immunoreceptor tyrosine-based inhibition motif-bearing receptor recruits Src homology phosphatase-1 to dephosphorylate spleen tyrosine kinase (Syk). As Syk is a key intermediate of FcγR signaling, LILRB1 coligation resulted in reduced ISG expression for enhanced DENV replication. Our findings suggest a unique mechanism for DENV to evade an early antiviral response for enhanced infection.Despite long-lived serotype-specific immunity upon initial infection, predicted global prevalence of dengue now surpasses World Health Organization estimates by more than threefold with 390 million cases annually (1). Furthermore, the risk of severe disease is augmented by cross-reactive or subneutralizing levels of antibody (2, 3), which opsonize dengue virus (DENV) to ligate Fc-gamma receptor (FcγR) for entry into monocytes, macrophages, and dendritic cells, a phenomenon known as antibody-dependent enhancement (ADE) of DENV infection (4, 5). The resultant greater viral burden leads to increased systemic inflammation that precipitates plasma leakage, a hallmark of dengue hemorrhagic fever (6). However, ligation of the activating FcγRs by immune complexes has been shown to induce type-I IFN stimulated genes (ISGs), independent of autocrine or paracrine IFN activity, unless the inhibitory FcγRIIB is coligated (7). We and others reported recently that coligation of FcγRIIB by DENV immune complexes requires high antibody concentration, and such coligation inhibited the entry of DENV immune complexes into monocytes (8, 9). At low antibody concentrations where ADE occurs, the inhibitory FcγRIIB is not coligated (9). Ligation of the activating FcγRs by DENV opsonized with subneutralizing levels of antibody would thus induce the expression of ISGs and hinder DENV replication (10). Here, we demonstrate that DENV employs a unique evasive mechanism by coligating LILRB1 to down-regulate the early antiviral responses triggered by activating FcγRs for ADE. 相似文献
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70.
Jesse Mez MD MS Daniel H. Daneshvar MD PhD Bobak Abdolmohammadi BA Alicia S. Chua MS Michael L. Alosco PhD Patrick T. Kiernan BA Laney Evers BA Laura Marshall BA Brett M. Martin MS Joseph N. Palmisano MS Christopher J. Nowinski PhD Ian Mahar PhD Jonathan D. Cherry PhD Victor E. Alvarez MD Brigid Dwyer MD Bertrand R. Huber MD PhD Thor D. Stein MD PhD Lee E. Goldstein MD PhD Douglas I. Katz MD Robert C. Cantu MD Rhoda Au PhD Neil W. Kowall MD Robert A. Stern PhD Michael D. McClean MS ScD Jennifer Weuve MPH ScD Yorghos Tripodis PhD Ann C. McKee MD 《Annals of neurology》2020,87(1):116-131