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1.
Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. A prospective investigation 总被引:36,自引:0,他引:36
S D Boden D O Davis T S Dina N J Patronas S W Wiesel 《The Journal of bone and joint surgery. American volume》1990,72(3):403-408
We performed magnetic resonance imaging on sixty-seven individuals who had never had low-back pain, sciatica, or neurogenic claudication. The scans were interpreted independently by three neuro-radiologists who had no knowledge about the presence or absence of clinical symptoms in the subjects. About one-third of the subjects were found to have a substantial abnormality. Of those who were less than sixty years old, 20 per cent had a herniated nucleus pulposus and one had spinal stenosis. In the group that was sixty years old or older, the findings were abnormal on about 57 per cent of the scans: 36 per cent of the subjects had a herniated nucleus pulposus and 21 per cent had spinal stenosis. There was degeneration or bulging of a disc at at least one lumbar level in 35 per cent of the subjects between twenty and thirty-nine years old and in all but one of the sixty to eighty-year-old subjects. In view of these findings in asymptomatic subjects, we concluded that abnormalities on magnetic resonance images must be strictly correlated with age and any clinical signs and symptoms before operative treatment is contemplated. 相似文献
2.
Leslee J. Shaw Romalisa Miranda-Peats Piotr Slomka John Friedman Sean W. Hayes Daniel S. Berman Gary V. Heller Marcin Dada William E. Boden Paul Casperson Robert A. O’Rourke Ronald Schwartz William S. Weintraub David J. Maron Spencer King Koon Teo Pamela Hartigan 《Journal of nuclear cardiology》2006,13(5):685-698
Background Stress gated myocardial perfusion single photon emission computed tomography (gSPECT) is increasingly used before and after
intercurrent therapeutic intervention and is the basis for ongoing evaluation in the Department of Veterans Affairs clinical
outcomes utilizing revascularization and aggressive drug evaluation (COURAGE) trial.
Methods and Results The COURAGE trial is a North American multicenter randomized clinical trial that enrolled 2287 patients to aggressive medical
therapy vs percutaneous coronary intervention plus aggressive medical therapy. Three COURAGE nuclear substudies have been
designed. The goals of substudy 0 are to examine the diagnostic accuracy of the extent and severity of inducible ischemia
at baseline in COURAGE patients compared with patient symptoms and quantitative coronary angiography and to explore the relationship
between inducible ischemia and the benefit from revascularization when added to medical therapy. Substudy 1 will correlate
the extent and severity of provocative ischemia with the frequency, quality, and instability of recurrent symptoms in postcatheterization
patients. Substudy 2 (n _ 300) will examine the usefulness of sequential gSPECT monitoring 6 to 18 months after therapeutic
intervention. Together, these nuclear substudies will evaluate the role of gSPECT to determine the effectiveness of aggressive
risk-factor modifications, lifestyle interventions, and anti-ischemic medical therapies with or without revascularization
in reducing patients’ ischemic burdens.
Conclusions The unfolding of evidence on the application of gSPECT in trials such as COURAGE defines a new era for nuclear cardiology.
We hope the evidence that emerges from the COURAGE trial will further establish the role of nuclear imaging in the evidence-based
management of patients with stable coronary disease.
The COURAGE trial was supported by the Cooperative Studies Program of the Department of Veterans Affairs Office of Research
and Development in collaboration with the Canadian Institutes of Health Research. Unrestricted research grants were obtained
from Merck & Co; Pfizer Pharmaceuticals; Bristol-Myers Squibb Medical Imaging; Astellas Pharma; Kos Pharmaceuticals; Data
Scope; Astra Zeneca Pharmaceuticals; Astra-Zeneca-Canada; Schering-Plough Coorporation, Ltd; Sanofi-Aventis, Inc; First Horizon;
and GE Healthcare. All industrial funding for this trial was directed through the Department of Veterans Affairs. Additional
funding for this substudy was provided by grants to the Department of Veterans Affairs and Canadian Institutes of Health Research
from Astellas Pharma and Bristol-Myers-Squibb Medical Imaging. 相似文献
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Studies of proteins that inhibit tissue factor activity have generally been conducted using either an extracted tissue homogenate ("thromboplastin") or tissue factor protein reconstituted into phospholipid vesicles rather than with tissue factor expressed in cell membranes (its physiological environment). In the present study, a human fibroblast cell strain was used to evaluate the effects of lipoprotein associated coagulation inhibitor (LACI), placental anticoagulant protein (PAP), and apolipoprotein A-II (apo A-II) on human tissue factor in cell membranes. LACI was tested from 7.8 to 500 pmol/L on fibroblasts cultured at cell densities ranging from 3,500 to 9,925 cells/well, and caused a progressive inhibition of tissue factor activity. PAP was tested from 3.9 nmol/L to 1 mumol/L at cell densities ranging from 4,500 to 15,400 cells/well and caused up to 83% inhibition of tissue factor activity. Inhibition by these proteins appeared to be influenced by cell density as well as whether the cells were intact or disrupted. Apo A-II, up to 1 mumol/L, did not inhibit the tissue factor activity of intact or disrupted fibroblasts at any cell density examined even though it did inhibit the activity of tissue factor in phospholipid vesicles. Of these inhibitors of tissue factor-dependent activation of factor X, LACI was the most effective in suppressing the generation of factor Xa activity. The effects obtained with apo A-II are clearly dependent on the nature of the tissue factor preparation with which it is tested. The disparity between the inhibitory effect of apo A-II on the activity of tissue factor reconstituted into lipid vesicles and the absence of effect on the activity of tissue factor remaining in cell membranes serves to reemphasize the necessity of reexamining results obtained with model systems using as nearly physiological reagents as possible. 相似文献
7.
Myosin VIIA gene: heterogeneity of the mutations responsible for Usher syndrome type IB 总被引:8,自引:1,他引:8
Levy G; Levi-Acobas F; Blanchard S; Gerber S; Larget-Piet D; Chenal V; Liu XZ; Newton V; Steel KP; Brown SD; Munnich A; Kaplan J; Petit C; Weil D 《Human molecular genetics》1997,6(1):111-116
Usher syndrome is recognized as the most frequent cause of hereditary
deaf-blindness. Usher syndrome type I (USH1), the most severe form of the
disease, is characterized by profound congenital sensorineural deafness,
constant vestibular dysfunction, and retinitis pigmentosa of prepubertal
onset. This form is genetically heterogeneous and five loci (USH1A-E) have
been mapped thusfar. However, only the gene responsible for USH1 B (which
accounts for approximately 75% of USH1 cases) has been characterized. It
encodes a long-tailed unconventional myosin, myosin VIIA, with a predicted
2215 amino acid sequence. Primers covering the complete myosin VIIA coding
sequence as well as the 3' non coding sequence were designed, allowing
direct sequence analysis of each of the 48 coding exons and flanking splice
sites in seven patients affected by USH1. Four novel mutations were thereby
identified. The possibility should now be considered of a sequence-based
prenatal diagnosis in some of the families affected by this very severe
form of Usher syndrome.
相似文献
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Enhanced factor H binding to sialylated Gonococci is restricted to the sialylated lacto-N-neotetraose lipooligosaccharide species: implications for serum resistance and evidence for a bifunctional lipooligosaccharide sialyltransferase in Gonococci
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Gulati S Cox A Lewis LA Michael FS Li J Boden R Ram S Rice PA 《Infection and immunity》2005,73(11):7390-7397
We isolated serologically identical (by serovar determination and porin variable region [VR] typing) strains of Neisseria gonorrhoeae from an infected male and two of his monogamous female sex partners. One strain (termed 398078) expressed the L1 (Galalpha1 --> 4 [corrected] Galbeta1 --> 4Glcbeta1 --> 4HepI) lipooligosaccharide (LOS) structure exclusively; the other (termed 398079) expressed the lacto-N-neotetraose (LNT; Galbeta1 --> 4GlcNAcbeta1 --> 3Galbeta1 --> 4Glcbeta1 --> 4HepI) LOS structure. The strain from the male index case expressed both glycoforms and exhibited both immunotypes. Nuclear magnetic resonance analysis revealed that sialic acid linked to the terminal Gal of L1 LOS via an alpha2 --> 6 linkage and, as expected, to the terminal Gal of LNT LOS via an alpha2--> 3 linkage. Insertional inactivation of the sialyltransferase gene (known to sialylate LNT LOS) abrogated both L1 LOS sialylation and LNT LOS sialylation, suggesting a bifunctional nature of this enzyme in gonococci. Akin to our previous observations, sialylation of the LNT LOS of strain 398079 enhanced the binding of the complement regulatory molecule, factor H. Rather surprisingly, factor H did not bind to sialylated strain 398078. LOS sialylation conferred the LNT LOS-bearing strain complete (100%) resistance to killing by even 50% nonimmune normal human serum (NHS), whereas sialylation of L1 LOS conferred resistance only to 10% NHS. The ability of gonococcal sialylated LNT to bind factor H confers high-level serum resistance, which is not seen with sialylated L1 LOS. Thus, serum resistance mediated by sialylation of gonococcal L1 and LNT LOS occurs by different mechanisms, and specificity of factor H binding to sialylated gonococci is restricted to the LNT LOS species. 相似文献
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