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81.
Effect of human recombinant cytokines on the induction of macrophage procoagulant activity 总被引:9,自引:1,他引:8
A panel of human recombinant cytokines was tested for induction of procoagulant activity (PCA) in human monocyte-derived macrophages. Nonadherent culture conditions were used, and PCA was determined with whole cells rather than cell lysates. It was assured by Limulus amebocyte lysate assay that tested cytokines displayed low levels of endotoxin activity within the range of biologic activity. Additional evidence to rule out an endotoxin effect was provided by heat- inactivation experiments. Interferon-gamma (IFN-gamma), interleukin-1 beta (IL-1 beta), and tumor necrosis factor-alpha (TNF-alpha) were strong macrophage PCA inducers. The low level of PCA induced by IL-2, granulocyte-macrophage colony-stimulating factor (GM-CSF), M-CSF, IL-4, IL-6, IL-10, and IFN-alpha could not be distinguished from that induced by traces of endotoxin contaminating the preparations. Transforming growth factor-beta decreased constitutively expressed PCA within 24 hours of exposure. PCA induced by IFN-gamma, IL-1 beta, and TNF-alpha depended largely on tissue factor expression, as evidenced by experiments with factor X-deficient plasma and antitissue factor antibodies. In macrophages subcultured in adherence, IL-1 beta was a strong PCA inducer, whereas IFN-gamma and TNF-alpha promoted little PCA increase. This observation and different kinetics of PCA induction suggested that mechanisms of PCA induction are distinct for the three cytokines. Thus, we showed that well-characterized cytokines critically involved in the promotion of cell-mediated antimicrobial defense/delayed-type hypersensitivity and considered for clinical application promote local fibrin deposition by a direct effect on macrophages. 相似文献
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Absence of TNFRp55 influences virus-induced autoimmunity despite efficient lymphocytic infiltration 总被引:2,自引:1,他引:2
McKall-Faienza KJ; Kawai K; Kundig TM; Odermatt B; Bachmann MF; Zakarian A; Mak TW; Ohashi PS 《International immunology》1998,10(4):405-412
Tumor necrosis factor (TNF)-alpha is a multipotent cytokine associated with
many cellular functions, including inflammation and anti-viral defense.
Many studies have implicated TNF-alpha in the pathogenesis of autoimmune
diseases. TNF-alpha responses are mediated through binding to specific cell
surface receptors, TNFRp55 and TNFRp75. The objective of the present study
was to investigate the contribution of the TNFRp55 in the inflammatory
response associated with autoimmune diabetes development in a viral
transgenic model. In this model, the animals express lymphocytic
choriomeningitis virus (LCMV)-glycoprotein (gp) in the beta cells of the
pancreas under the control of the rat insulin promoter (RIP-gp). Diabetes
is induced following LCMV infection due to beta cell destruction by
LCMV-specific CD8+ cytotoxic T lymphocytes. TNFRp55-deficient RIP-gp
animals were examined to assess the importance of the TNFRp55. The kinetics
and onset of lymphocytic infiltration into the pancreatic islets and
hyperglycemia was not altered in the absence of TNFRp55 after LCMV
infection. Animals were evaluated following recombinant LCMV-gp vaccinia
virus infection to test whether properties of the infectious agent
influence autoimmunity. Interestingly, the kinetics were accelerated and
the frequency of diabetes was increased in TNFRp55-deficient mice compared
with control animals. This accelerated onset of diabetes is likely a result
of increased viral replication in the TNFRp55-deficient host. Thus, these
data demonstrate that TNFRp55 is not essential for producing the local
inflammatory effects which contribute to organ-specific autoimmunity in
this transgenic model. However, the absence of TNFRp55 altered the kinetics
and incidence of the disease in a pathogen-dependent fashion.
相似文献
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Normal thymic selection, superantigen-induced deletion and Fas-mediated apoptosis of T cells in IL-2 receptor beta chain-deficient mice 总被引:1,自引:0,他引:1
Mice lacking the IL-2 receptor beta chain (IL-2R beta) exhibit an
autoimmune reaction characterized by generalized T cell activation,
production of autoantibodies, myeloproliferation and severe anemia. T cells
of IL-2R beta-/- mice were examined to elucidate the mechanism responsible
for their abnormal activation and to determine how such abnormal activation
might affect other cell lineages. Elevated levels of IgG, IgE and
autoantibodies in IL-2R beta-/- mice were found to be associated with
activated CD4+ T cells which secreted elevated levels of IL-4. Thymocytes
in IL-2R beta-/- mice showed normal negative and positive selection
patterns when analyzed in transgenic mice bearing a TCR specific for HY
antigen, suggesting that neither IL-2 nor IL-15 is essential for thymic
selection. Peripheral T cells in IL-2R beta- deficient mice underwent
normal programmed cell death in response to staphylococcal enterotoxin B
superantigen, in contrast to cells from mice deficient for either IL-2 or
IL-2R alpha. Activated T cells in IL- 2R beta-deficient mice expressed
normal levels of Fas antigen and underwent normal apoptosis in response to
induction with anti-Fas mAb. Thus, the accumulation of activated T cells in
IL-2R beta-/- mice does not appear to be derived from abnormalities in
either thymic selection or Fas-mediated apoptosis.
相似文献
90.
Zito JM Safer DJ de Jong-van den Berg LT Janhsen K Fegert JM Gardner JF Glaeske G Valluri SC 《Child and adolescent psychiatry and mental health》2008,2(1):26