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81.
82.
83.
Interleukin 1 production by human lung tissue. II. Inhibition by anti-inflammatory steroids 总被引:5,自引:0,他引:5
B S Bochner B K Rutledge R P Schleimer 《Journal of immunology (Baltimore, Md. : 1950)》1987,139(7):2303-2307
Glucocorticoids block the localized accumulation of leukocytes as sites of inflammation by preventing their adherence to vascular endothelium. This implies that glucocorticoids are acting either on the leukocytes, endothelium, or cells which produce adherence-promoting factors (such as interleukin 1 (IL-1)). Previous studies have shown that dexamethasone (DEX) treatment of either polymorphonuclear leukocytes (PMN) or human umbilical vein vascular endothelial cells (VEC) or both in vitro does not prevent adherence induced by thrombin or formylmethionyl-leucyl-phenylalanine (f-met peptide). We now show that pretreatment of PMN and/or VEC for 24 hr with 0.1 microM DEX had no effect on adherence of PMN to VEC activated with IL-1 (2 U/ml), lipopolysaccharide (1 microgram/ml), or 12-O-tetradecanoylphorbol-13-acetate (30 ng/ml) suggesting that glucocorticoids may inhibit adherence in vivo by blocking formation of IL-1 and other adherence-inducing stimuli. We have recently established that cultured human lung fragments produce IL-1 in vitro. To investigate whether glucocorticoids could inhibit the production of adherence-inducing factors, we examined the effect of glucocorticoids on IL-1 production from human lung tissue. Treatment of human lung fragments in vitro for 18 hr with glucocorticoids such as DEX and hydrocortisone resulted in dose dependent inhibition of IL-1 production; these and other glucocorticoids, at concentrations ranging between 0.1 and 1 microM, produced greater than 50% inhibition of IL-1 release. Nonglucocorticoid steroids including testosterone and beta-estradiol (1 microM) had no effect. Inhibition of IL-1 production occurred after a lag period 5 of 16 hr, and the relative glucocorticoid potencies agreed with their known anti-inflammatory potencies in vivo (beta-methasone approximately triamcinolone acetonide greater than DEX greater than fludrocortisone greater than prednisolone greater than hydrocortisone). Inhibition of IL-1 production in vivo may, in part, explain the remarkable ability of glucocorticoids to prevent the adherence of leukocytes to endothelium and their accumulation at an inflammatory site. 相似文献
84.
B S Bochner S D Landy M Plaut C A Dinarello R P Schleimer 《Journal of immunology (Baltimore, Md. : 1950)》1987,139(7):2297-2302
Crucial to the development of inflammatory infiltrates is the localized production of mediators which promote adherence of leukocytes to the vascular endothelium. Previous in vitro studies, using monolayers of cultured human vascular endothelial cells (VEC), have identified various agents which promote the acquisition of adhesiveness in VEC for polymorphonuclear leukocytes. In the present studies, we report that human lung fragments cultured for 4 to 24 hr release a factor which acts on VEC to promote adherence of polymorphonuclear leukocytes. Adhesiveness in VEC stimulated by lung fragment culture supernatants was time- and dose-dependent. This adherence-promoting factor appears to be a mixture of the alpha and beta forms of interleukin 1 (IL-1) and has the following properties: 1) it is heat-labile; 2) it is not inactivated by polymyxin B; 3) it has mobility on Sephadex G-75 column chromatography corresponding to apparent m.w. of approximately 15,000, 30,000, and 70,000 (a pattern observed previously for IL-1); 4) it has activity in the thymocyte costimulation IL-1 assay, but no interleukin 2 activity, and 5) it is neutralized by anti-human IL-1 antisera but not by anti-human tumor necrosis factor antiserum. Production and release of IL-1 in vivo may play a role in the development of inflammatory infiltrates in human lung and other tissues by acting on endothelium to promote the localized adherence of leukocytes. 相似文献
85.
Adaptive evolution of G-protein coupled receptor genes 总被引:2,自引:0,他引:2
The phylogeny and patterns of nucleotide substitutions in the visual
pigment genes, adrenergic receptor genes, muscarinic receptor genes, and in
the human mas oncogene were studied by comparing their DNA sequences. The
evolutionary tree obtained shows that the visual pigment genes and mas
oncogene form one cluster and that the receptor genes form another. In the
evolution of rhodopsin genes, synonymous substitutions outnumber
nonsynonymous substitutions. This is consistent with the neutral theory of
molecular evolution. However, the early evolutionary stages of alpha- and
beta-adrenergic and muscarinic receptors are notable for significantly more
nonsynonymous substitutions than synonymous substitutions, suggesting the
acquisition of novel functional adaptations. Variable rates of
nonsynonymous changes in different domains of these proteins reveal DNA
segments that might have been important in their functional adaptations.
相似文献
86.
Diadenosine 5',5"'-P1,P4-tetraphosphate and related adenylylated nucleotides in Salmonella typhimurium 总被引:16,自引:0,他引:16
Salmonella typhimurium LT2 rapidly accumulates high levels of a family of five adenylylated nucleotides following exposure to a bacteriostatic quinone, 6-amino-7-chloro-5,8-dioxoquinoline. These compounds have been analyzed using our recently described two-dimensional thin layer chromatographic method. The five dinucleotides, which cannot be detected in exponentially growing cells, have been identified as diadenosine 5',5"'-P1,P4-tetraphosphate (AppppA), ApppGpp (guanosine 3'-diphosphate-5'-adenosine-5'-(P1,P3-triphosphate)), AppppG (adenosine 5'-guanosine-5'-(P1,P4-tetraphosphate)), ApppG (adenosine 5'-guanosine-5'-(P1,P3-triphosphate)), and ApppA (diadenosine 5',5"'-P1,P3-triphosphate). AppppA has been previously detected in vitro as an enzymatic product of aminoacyl-tRNA synthetases and in vivo at submicromolar levels in eucaryotic cells. The induced intracellular concentration of AppppA and the other adenylylated nucleotides in S. typhimurium is approximately 100-fold higher than that found in eucaryotic cells. We propose that these dinucleotides are alarmones, regulatory molecules signaling a particular metabolic stress. 相似文献
87.
A. terreus isolates isolated from some bakery products, corn and rice were found to be able to produce territrems. 90% of theA. terreus isolated from bakery products were able to produce territrem A, with a mean of 0.09 ppm, while 80% ofA. terreus isolates produce territrem B with a mean of 0.24 ppm. On the other hand 31.8% of the isolates ofA. terreus from corn were able to produce territrem A with a mean of 0.44 ppm. ConcerningA. terreus isolates from rice, 66.7% were found to produce territrem A, with a mean of 5.28 ppm, and 77.8% of the isolates produced
territrem B with a mean of 1.79 ppm. 相似文献
88.
S Jadhav B S Bochner K Konstantopoulos 《Journal of immunology (Baltimore, Md. : 1950)》2001,167(10):5986-5993
The ability of tumor cells to metastasize hematogenously is regulated by their interactions with polymorphonuclear leukocytes (PMNs). However, the mechanisms mediating PMN binding to tumor cells under physiological shear forces remain largely unknown. This study was designed to characterize the molecular interactions between PMNs and tumor cells as a function of the dynamic shear environment, using two human colon adenocarcinoma cell lines (LS174T and HCT-8) as models. PMN and colon carcinoma cell suspensions, labeled with distinct fluorophores, were sheared in a cone-and-plate rheometer in the presence of the PMN activator fMLP. The size distribution and cellular composition of formed aggregates were determined by flow cytometry. PMN binding to LS174T cells was maximal at 100 s(-1) and decreased with increasing shear. At low shear (100 s(-1)) PMN CD11b alone mediates PMN-LS174T heteroaggregation. However, L-selectin, CD11a, and CD11b are all required for PMN binding to sialyl Lewis(x)-bearing LS174T cells at high shear (800 s(-1)). In contrast, sialyl Lewis(x)-low HCT-8 cells fail to aggregate with PMNs at high shear conditions, despite extensive adhesive interactions at low shear. Taken together, our data suggest that PMN L-selectin initiates LS174T cell tethering at high shear by binding to sialylated moieties on the carcinoma cell surface, whereas the subsequent involvement of CD11a and CD11b converts these transient tethers into stable adhesion. This study demonstrates that the shear environment of the vasculature modulates the dynamics and molecular constituents mediating PMN-tumor cell adhesion. 相似文献
89.
Exogenous eosinophil activation converts PSGL-1-dependent binding to CD18-dependent stable adhesion to platelets in shear flow 总被引:1,自引:0,他引:1
McCarty OJ Tien N Bochner BS Konstantopoulos K 《American journal of physiology. Cell physiology》2003,284(5):C1223-C1234
Thisstudy examined the binding kinetics and molecular requirements ofeosinophil adhesion to surface-anchored platelets in shear flow.P-selectin glycoprotein ligand-1 (PSGL-1) binding to plateletP-selectin initiates tethering and rolling of eosinophils to plateletsunder flow. These primary interacting cells assist in the capture offree-flowing eosinophils through homotypic tethering (secondaryinteractions) mediated via L-selectin-PSGL-1 interactions. Differencesbetween eosinophils and neutrophils in PSGL-1 and L-selectin expressionlevels predict the pattern and relative extent of their adhesiveinteractions with immobilized platelets under shear, as well as therelative magnitude of their average rolling velocities. The majority oftethered eosinophils become rapidly stationary on the platelet layer, aprocess that is predominantly mediated via eosinophil PSGL-1 binding toplatelet P-selectin and has an absolute requirement for intactcytoskeleton. Only a small fraction of these stationary eosinophilsdevelop shear-resistant attachments mediated by CD18 integrins.However, stimulation of eosinophils with eotaxin-2 convertsPSGL-1-P-selectin-dependent stationary adhesion to CD18-mediatedshear-resistant stable attachment. These studies provide insights fordesigning strategies based on blocking of eosinophil-plateletinteractions to combat thrombotic disorders in hypereosinophilic patients. 相似文献
90.
Nutku E Hudson SA Bochner BS 《Biochemical and biophysical research communications》2005,336(3):918-924
Sialic acid binding immunoglobulin like lectin (Siglec)-8 crosslinking with specific antibodies causes human eosinophil apoptosis. Mechanisms by which Siglec-8 crosslinking induces apoptosis are not known. Peripheral blood eosinophils were examined for caspase, mitochondria and reactive oxygen species (ROS) involvement after incubating the cells with anti-Siglec-8 crosslinking Abs or control Abs, in the presence or absence of selective inhibitors. Siglec-8 crosslinking induced rapid cleavage of caspase-3, caspase-8, and caspase-9 in eosinophils. Selective caspase-8 and/or caspase-9 inhibitors inhibited this apoptosis. Siglec-8 crosslinking on eosinophils increased dissipation of mitochondrial membrane potential upstream of caspase activation. Rotenone and antimycin, inhibitors of mitochondrial respiratory chain components, completely inhibited apoptosis. Additional experiments with an inhibitor of ROS, diphenyleneiodonium, demonstrated that ROS was also essential for Siglec-8-mediated apoptosis and preceded Siglec-8-mediated mitochondrial dissipation. These experiments show that Siglec-8-induced apoptosis occurs through the sequential production of ROS, followed by induction of mitochondrial injury and caspase cleavage. 相似文献