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21.
Abstract: In experimental diabetic neuropathy, defective arachidonic acid metabolism characterized by a decrease in the proportion of glycerophospholipid arachidonoyl-containing molecular species (ACMS) occurs and has been implicated in the pathogenesis of the disorder. In this study, we evaluated the suitability of a tumor-derived human Schwann cell line (NF1T) as a model to investigate the mechanism underlying the loss of ACMS. NF1T cells grown in 30 versus 5.5 m M glucose undergo a marked reduction in ACMS in phosphatidylcholine, phosphatidylethanolamine, and phosphatidylinositol, in a manner resembling that of diabetic nerve. The depletion of ACMS can be reversed on transferring the cells from 30 m M glucose to medium containing physiological levels of glucose. Cells maintained in 5.5 m M glucose plus 25 m M mannitol or sorbitol did not exhibit decreased ACMS levels, indicating that osmotic effects were not responsible for ACMS depletion. However, growth in 25 m M fructose elicited a reduction of ACMS similar to that produced by 30 m M glucose. Excessive glucose flux through the polyol pathway has been implicated in the neural and vascular abnormalities associated with diabetes. Therefore, we examined the effects of polyol pathway inhibitors, including two aldose reductase inhibitors, zopolrestat and sorbinil, and a sorbitol dehydrogenase inhibitor (SDI), CP166,572, on ACMS levels in NF1T cells cultured in elevated glucose concentrations. At 200 µ M , zopolrestat fully and sorbinil partially corrected ACMS depletion. The SDI at concentrations up to 100 µ M failed to affect diminished ACMS levels. Neither zopolrestat nor the SDI restored ACMS levels reduced in the presence of elevated fructose concentrations. These findings suggest that enhanced flux through the polyol pathway and, in particular, elevated aldose reductase activity may play a significant role in the reduction of ACMS levels in the cells brought about by elevated glucose levels. 相似文献
22.
23.
Robinette ED Gulley KT Cassity KJ King EE Nielsen AJ Rozelle CL Warren TJ Morrow JM Kuruvilla HG 《The Journal of eukaryotic microbiology》2008,55(2):86-90
Chemorepellents are compounds that cause ciliated protozoans to reorient their swimming direction. A number of chemorepellents have been studied in the ciliated protozoans, Paramecium and Tetrahymena. Chemorepellents, such as polycations, cause the organism to exhibit "avoidance behavior," a swimming behavior characterized by jerky movements and other deviations from normal forward swimming, which result from ciliary reversal. One well-characterized chemorepellent pathway in Tetrahymena is that of the proposed polycation receptor that is activated by lysozyme and pituitary adenylate cyclase activating polypeptide (PACAP). In this study, we compare the response of Paramecium to the chemorepellents lysozyme, vasoactive intestinal peptide (VIP), and PACAP to the previously studied polycation response in Tetrahymena. Our results indicate that lysozyme, VIP, and PACAP are all chemorepellents in Paramecium, just as they are in Tetrahymena. However, the signaling pathways involved appear to be different. While previous pharmacological characterization indicates that G-proteins are involved in polycation signaling in Tetrahymena, we present evidence that similar reception in Paramecium involves activation of a tyrosine kinase pathway in order for lysozyme avoidance to occur. Polycation responses of both organisms are inhibited by neomycin sulfate. While PACAP is the most effective of the three chemorepellents in Tetrahymena, lysozyme is the most effective chemorepellent in Paramecium. 相似文献
24.
Kuruvilla SJ Fox SD Cullen DM Akhter MP 《Journal of musculoskeletal & neuronal interactions》2008,8(1):71-78
Over 25 million Americans suffer from osteoporosis. Bone size and strength depends both upon the level of adaptation due to physical activity (applied load), and genetics. We hypothesized that bone adaptation to loads differs among mice breeds and bone sites. Forty-five adult female mice from three inbred strains (C57BL/6 [B6], C3H/HeJ [C3], and DBA/2J [D2]) were loaded at the right tibia and ulna in vivo with non-invasive loading devices. Each loading session consisted of 99 cycles at a force range that induced approximately 2000 microstrain (microepsilon) at the mid-shaft of the tibia (2.5 to 3.5 N force) and ulna (1.5 to 2 N force). The right and left ulnae and tibiae were collected and processed using protocols for histological undecalcified cortical bone slides. Standard histomorphometry techniques were used to quantify new bone formation. The histomorphometric variables include percentage mineralizing surface (%MS), mineral apposition rate (MAR), and bone formation rate (BFR). Net loading response [right-left limb] was compared between different breeds at tibial and ulnar sites using two-way ANOVA with repeated measures (p<0.05). Significant site differences in bone adaptation response were present within each breed (p<0.005). In all the three breeds, the tibiae showed greater percentage MS, MAR and BFR than the ulna at similar in vivo load or mechanical stimulus (strain). These data suggest that the bone formation due to loading is greater in the tibiae than the ulnae. Although, no significant breed-related differences were found in response to loading, the data show greater trends in tibial bone response in B6 mice as compared to D2 and C3 mice. Our data indicate that there are site-specific skeletal differences in bone adaptation response to similar mechanical stimulus. 相似文献
25.
Background
The endocardial endothelium that lines the inner cavity of the heart is distinct from the microvascular endothelial cells and modulates cardiac muscle performance in a manner similar to the vascular endothelial modulation of vascular structure and vasomotor tone. Although the modulatory effects of endocardial endothelium (EE) on cardiomyocytes are firmly established, the regulatory effects of endocardial endothelium on the cardiac interstitium and its cellular components remain ill defined.Methods and Results
We investigated whether the stimulatory effect of EE on cardiac fibroblasts would be altered when EECs are activated by the cytokine tumor necrosis factor-α (TNF-α) or the endotoxin bacterial lipopolysaccharide (LPS). Both TNF-α and LPS were found to independently attenuate the stimulatory effect of EE on cardiac fibroblasts. These agents lowered the synthesis or release of ET-1 and increased the secretion of TGF-β and NO.Conclusion
The findings of this study using endocardial endothelial cells (EECs) and neonatal cardiac fibroblasts demonstrate that pro-inflammatory cytokines cause altered secretion of paracrine factors by EECs and inhibit proliferation and lower collagen synthesis in fibroblasts. These changes may influence fibroblast response and extra cellular matrix remodeling in pathological conditions of the heart. 相似文献26.
27.
S. R. Mace J. G. Dean J. R. Murphy J. L. Rhodes H. G. Kuruvilla 《Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology》2000,186(1):39-43
Pituitary adenylate cyclase activating peptide (PACAP-38) is a peptide hormone which functions in many mammalian systems,
including the nervous and digestive systems. Using in vivo behavioral studies, we have found that this hormone functions as
a chemorepellent in Tetrahymena thermophila with an EC50 of 10 nM. Cells previously adapted to PACAP-38 were found to be adapted to lysozyme, and vice versa. Furthermore, the in
vivo behavioral activity of PACAP-38 was blocked by addition of the anti-lysozyme receptor antibody, 5545. Chemorepellent
activity of PACAP-38 was also inhibited by the addition of neomycin sulfate (inhibition constant K
i=0.080 μmol · l−1), a competitive inhibitor of lysozyme binding to its receptor. PACAP-38 is a more potent and specific agonist for the lysozyme
receptor than either intact lysozyme or CB2, a 24-amino acid fragment of lysozyme.
Accepted: 11 October 1999 相似文献
28.
Sindhu Raveendran Binod Parameswaran Mathew Anil Kuruvilla Abraham Amith Pandey Ashok Gnansounou Edgard Castro Galliano Eulogio 《Bioprocess and biosystems engineering》2018,41(4):565-571
Bioprocess and Biosystems Engineering - Surfactants play major role in the delignification of lignocellulosic biomass. Surfactant-assisted hydrothermal pretreatment was evaluated for chili... 相似文献
29.
Rajshri Singh Priya Dagar Shyama Pal Bhakti Basu Bhavani S. Shankar 《Biochimica et Biophysica Acta (BBA)/General Subjects》2018,1862(3):669-683
Background
Tumor microenvironment is composed of a largely altered extracellular matrix with different cell types. The complex interplay between macrophages and tumor cells through several soluble factors and signaling is an important factor in breast cancer progression.Methods
We have extended our earlier studies on monocyte and macrophage conditioned medium (M?CM) and have carried out proteomic analysis to identify its constituents as well as validation. The 8-gene signature identified through macrophage-breast cancer cell interactions was queried in cBioportal for bioinformatic analyses.Results
Proteomic analysis (MALDI-TOF and LC-MS/MS) revealed integrin and matrix metalloproteinases in M?CM which activated TGF-β1, IL-6, TGF- βRII and EGFR as well as its downstream STAT and SMAD signaling in breast cancer cells. Neutralization of pro-inflammatory cytokines (TNF-α. Il-1β, IL-6) abrogated the M?CM induced migration but invasion to lesser extent. The 8- gene signature identified by macrophage-tumor interactions (TNF-α, IL-1β, IL-6, MMP1, MMP9, TGF-β1, TGF-βRII, EGFR) significantly co-occurred with TP53 mutation, WTAPP1 deletion and SLC12A5 amplification along with differential expression of PSAT1 and ESR1 at the mRNA level and TPD52and PRKCD at the protein level in TCGA (cBioportal). Together these genes form a novel 15 gene signature which is altered in 63.6% of TCGA (1105 samples) data and was associated with high risk and poor survival (p < 0.05) in many breast cancer datasets (SurvExpress).Conclusions
These results highlight the importance of macrophage signaling in breast cancer and the prognostic role of the15-gene signature.General significance
Our study may facilitate novel prognostic markers based on tumor-macrophage interaction. 相似文献30.
David M. Bishai Robert Cohen Y. Natalia Alfonso Taghreed Adam Shyama Kuruvilla Julian Schweitzer 《PloS one》2016,11(1)