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151.
We describe a simple procedure for isolation of Vicia villosa lectin with binding specificity for N-acetyl-D-galactosamine >D-galactose. Also, a rosette assay using V. villosa lectin coupled-SRBC is described which enables us to both visualize lectin binding cells and to fractionate lymphocytes from in vitro primary mixed lymphocyte cultures on the basis of ability to bind V. villosa lectin. 相似文献
152.
The belief is widely held, on the basis of indirect evidence, that a substantial, even brief elevation of red cell Ca content must result in a marked shortening of circulatory survival. To test this notion directly, we exposed rabbit red cells in vitro to the ionophore A23187 and Ca so as to produce sustained uniform cell Ca levels of 40 to 360 mumol/L cells for one to 60 minutes, and compared the survival of the Ca-loaded cells in vivo with that of ionophore-treated controls, simultaneously, in the same rabbits. Despite marked reductions in cell adenosine triphosphate and dehydration of the Ca-exposed cells prior to reinfusion, the majority of cells, all of which had experienced these high cytoplasmic Ca levels, showed normal or near-normal survival in the circulation. 相似文献
153.
154.
Interaction between complement receptor gC1qR and hepatitis C virus core protein inhibits T-lymphocyte proliferation 总被引:16,自引:0,他引:16
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Kittlesen DJ Chianese-Bullock KA Yao ZQ Braciale TJ Hahn YS 《The Journal of clinical investigation》2000,106(10):1239-1249
Hepatitis C virus (HCV) is an important human pathogen that is remarkably efficient at establishing persistent infection. The HCV core protein is the first protein expressed during the early phase of HCV infection. Our previous work demonstrated that the HCV core protein suppresses host immune responses, including anti-viral cytotoxic T-lymphocyte responses in a murine model. To investigate the mechanism of HCV core-mediated immunosuppression, we searched for host proteins capable of associating with the core protein using a yeast two-hybrid system. Using the core protein as bait, we screened a human T cell-enriched expression library and identified a gene encoding the gC1q receptor (gC1qR). C1q is a ligand of gC1qR and is involved in the early host defense against infection. Like C1q, HCV core can inhibit T-cell proliferative responses in vitro. This core-induced anti-T-cell proliferation is reversed by addition of anti-gC1qR Ab in a T-cell proliferation assay. Furthermore, biochemical analysis of the interaction between core and gC1qR indicates that HCV core binds the region spanning amino acids 188 to 259 of gC1qR, a site distinct from the binding region of C1q. The inhibition of T-cell responsiveness by HCV core may have important implications for HCV persistence in humans. 相似文献
155.
mdx muscle pathology is independent of nNOS perturbation 总被引:2,自引:0,他引:2
Crosbie RH; Straub V; Yun HY; Lee JC; Rafael JA; Chamberlain JS; Dawson VL; Dawson TM; Campbell KP 《Human molecular genetics》1998,7(5):823-829
In skeletal muscle, neuronal nitric oxide synthase (nNOS) is anchored to
the sarcolemma via the dystrophin-glycoprotein complex. When dystrophin is
absent, as in Duchenne muscular dystrophy patients and in mdx mice, nNOS is
mislocalized to the interior of the muscle fiber where it continues to
produce nitric oxide. This has led to the hypothesis that free radical
toxicity from mislocalized nNOS may contribute to mdx muscle pathology. To
test this hypothesis directly, we generated mice devoid of both nNOS and
dystrophin. Overall, the nNOS- dystrophin null mice maintained the
dystrophic characteristics of mdx mice. We evaluated the mice for several
features of the dystrophic phenotype, including membrane damage and muscle
morphology. Removal of nNOS did not alter the extent of sarcolemma damage,
which is a hallmark of the dystrophic phenotype. Furthermore, muscle from
nNOS-dystrophin null mice maintain the histological features of mdx
pathology. Our results demonstrate that relocalization of nNOS to the
cytosol does not contribute significantly to mdx pathogenesis.
相似文献
156.
Class I major histocompatibility complex (MHC) restricted T lymphocytes preferentially recognize fragments of polypeptides processed through a nonendosomal presentation pathway. At present the intracellular compartment(s) in which polypeptide fragmentation occurs and factors which influence the formation of an antigenic epitope are not well understood. To assess the role of residues flanking an antigenic site in the generation of the antigenic moiety recognized by class I MHC restricted T lymphocytes we have moved the coding sequence for an immunodominant H-2Kd restricted site on the influenza A/JAPAN/57 hemagglutinin (residues 202-221) by site-directed mutagenesis to six different positions along the coding sequence of the hemagglutinin gene. We have found that all six classes of mutants are recognized by MHC class I restricted T cells as efficiently as the wild type hemagglutinin gene product. Thus neither N-terminal to C-terminal position within the translation product nor sequences flanking the antigenic site influence processing. 相似文献
157.
Mark T. Esser Doris M. Haverstick Claudette L. Fuller Charles A. Gullo Vivian Lam Braciale 《The Journal of experimental medicine》1998,187(7):1057-1067
Cytolytic T cells use two mechanisms to kill virally infected cells, tumor cells, or other potentially autoreactive T cells in short-term in vitro assays. The perforin/granule exocytosis mechanism uses preformed cytolytic granules that are delivered to the target cell to induce apoptosis and eventual lysis. FasL/Fas (CD95 ligand/CD95)–mediated cytolysis requires de novo protein synthesis of FasL by the CTL and the presence of the death receptor Fas on the target cell to induce apoptosis. Using a CD8+ CTL clone that kills via both the perforin/granule exocytosis and FasL/Fas mechanisms, and a clone that kills via the FasL/Fas mechanism only, we have examined the requirement of intra- and extracellular Ca2+ in TCR-triggered cytolytic effector function. These two clones, a panel of Ca2+ antagonists, and agonists were used to determine that a large biphasic increase in intracellular calcium concentration, characterized by release of Ca2+ from intracellular stores followed by a sustained influx of extracellular Ca2+, is required for perforin/granule exocytosis. Only the sustained influx of extracellular Ca2+ is required for FasL induction and killing. Thapsigargin, at low concentrations, induces this small but sustained increase in [Ca2+]i and selectively induces FasL/Fas-mediated cytolysis but not granule exocytosis. These results further define the role of Ca2+ in perforin and FasL/Fas killing and demonstrate that differential Ca2+ signaling can modulate T cell effector functions. 相似文献
158.
Heterogeneity and specificity of cloned lines of influenza-virus specific cytotoxic T lymphocytes 总被引:9,自引:16,他引:9
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Continuous lines of murine cytotoxic T lymphocytes (CTL) directed to type A influenza viruses have been generated in vitro by stimulation of individual CTL precursors in the presence of T cell-growth factor TCGF and syngeneic virus-infected stimulator cells. The cloned CTL lines are H-2 restricted in their target cell recognition and exhibit distinct patterns of influenza virus recognition. All CTL lines appear to be restricted in target cell recognition to either the H-2K or the H-2D end of the appropriate H-2 haplotype. Likewise, CTL lines of F1 origin are restricted in recognition exclusively to one of the parental haplotypes. All CTL lines examined express the Thy-1.2 and the Lyt-2- surface antigen markers. 4 of 11 cytotoxic lines examined also expressed detectable levels of the Lyt-1- surface antigen. These findings confirm at the clonal level previous observations on the H- 2K/D restriction of virus-specific CTL and also demonstrate heterogeneity among H-2 restricted CTL both from the standpoint of viral antigen recognition and cell surface phenotype. 相似文献