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1.
sa Andersson Susanne M. Grunewald Albert Duschl Alain Fischer James P. Disanto 《European journal of immunology》1997,27(7):1762-1768
The common γ chain (γc) forms a critical component of the receptors for interleukins (IL)-2, IL-4, IL-7, IL-9, and IL-15. We analyzed γc-deficient mice to define a role for γc signaling in the development and function of the macrophage lineage. No major differences in absolute cell numbers, cell surface phenotype, or in vitro function of γ?c compared to γ+c macrophages were observed. We therefore conclude that signaling through the γc chain is not essential for the differentiation of mouse macrophages. Although B and T cells require γc for IL-4 responses, IL-4 up-regulated major histocompatibility class II molecules and inhibited nitric oxide production from γ?c macrophages following stimulation with lipopolysaccharide and interferon-γ. γ?c macrophages could also respond to IL-13, consistent with the model of a type II IL-4 receptor α/IL-13R which can function in the absence of γc. Both IL-4 and IL-13 responses could be completely inhibited with the mouse IL-4 antagonist QY, suggesting that all of the observed IL-13 responses pass through the type II receptor, making it the primary signaling receptor complex for IL-13 in mouse macrophages. 相似文献
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Cho WS Duffin R Poland CA Duschl A Oostingh GJ Macnee W Bradley M Megson IL Donaldson K 《Nanotoxicology》2012,6(1):22-35
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Sara Michelini Muamera Sarajlic Albert Duschl Jutta Horejs-Hoeck 《Human immunology》2018,79(8):610-615
Dendritic cells play an important role in the initiation of immune reactions. Due to their high capacity to prime T-cell responses, the activation of dendritic cells must be tightly controlled. Because Interleukin-1β (IL-1β) is a key player in autoinflammatory diseases, we compared the ability of IL-1β to activate human dendritic cells and induce immune-regulatory molecules versus the effects induced by pathogen-derived stimuli.Upon activation with either IL-1β or microbial stimuli, monocyte-derived dendritic cells showed enhanced expression of costimulatory molecules, increased secretion of chemokines and cytokines, and the ability to activate T cells. In contrast, immune-feedback molecules, including PD-L1, IL-1RA, IL-10 and SOCS1, were exclusively upregulated in response to microbial stimuli, whereas IL-1β treatment had no inducing effect on them. Thus, the limited capacity of IL-1β to induce potential feedback inhibitors may support its key etiologic role in chronic inflammation and autoinflammatory responses. 相似文献
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Mller-Hess Ziemke Gutzeit R. Riebeling Stern F. Klieneberger Bratz Gierlich Mendel Kurt Flatau G. Wiethold Kockel Heinz Binswanger H. Klestadt Oblath Koch Lurz L. Buhtz Brieger Schellenberg Duschl L. Strassmann Gg. Reich Liguori-Hohenauer Baruch v. Neureiter Schwarz O. A. Zavka Ruge Ullmann K. 《International journal of legal medicine》1932,18(6):271-283
International Journal of Legal Medicine - 相似文献
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Josef Duschl 《Langenbeck's archives of surgery / Deutsche Gesellschaft fur Chirurgie》1929,215(3-5):343-344
Ohne Zusammenfassung 相似文献
10.
Röder-Stolinski C Fischäder G Oostingh GJ Eder K Duschl A Lehmann I 《Inhalation toxicology》2008,20(9):813-820
Chlorobenzene is a volatile organic compound that is used as a solvent in many industrial settings and has been shown to be related with irritations of the respiratory tract. Exposure to chlorobenzene induces the release of monocyte chemoattractant protein 1 (MCP-1) by lung epithelial cells, a chemokine involved in inflammatory reactions. To characterize the underlying mechanisms we investigated the influence of chlorobenzene on the activation of two intracellular signalling pathways: the nuclear factor-kappa B (NF-kappa B) and the p38 mitogen-activated protein kinase (MAPK) pathways. Human lung epithelial cells (A549) were stimulated with tumor necrosis factor (TNF)-alpha in the presence or absence of specific inhibitors of NF-kappaB or the p38 MAP kinase and exposed to chlorobenzene using an air-liquid cell culture system. Exposure of lung epithelial cells to chlorobenzene resulted in an activation of NF-kappa B and p38 MAP kinase and a release of the chemokine MCP-1. In the presence of IKK-NBD, a specific NF-kappa B inhibitor, or the inhibitors of the p38 MAP kinase SB 203580 and SB 202190, the chlorobenzene-related MCP-1 release was suppressed, suggesting an involvement of both pathways in the chlorobenzene induced expression of MCP-1. Our data show that the release of MCP-1 following chlorobenzene exposure is dependent on the NF-kappa B and MAPK pathways. 相似文献