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111.
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The present study was designed to investigate the incorporation of zinc (Zn) into cultured UMR-106 osteoblasts in response
to mineralization caused by the addition of β-glycerophosphate. As a result of the induced mineralization, the contents of
calcium (Ca), phosphorus (P), and Zn in the monolayer increased, whereas the magnesium (Mg) content did not change. The activity
of alkaline phosphatase (ALP) also increased during the process.
The zinc distribution in the cell monolayer was studied using Zinquin, a fluorescent zinc ion chelator. The double fluorescent
labeling with Zinquin and calcein revealed that zinc was localized both as intracellular vesicles and extracellular clusters,
whereas calcium was colocalized with extracellular zinc. These results suggest that zinc is involved in the mineralization
process of UMR-106 cells. 相似文献
114.
Motomi Ito Tetsukazu Yahara Robert M King Kuniaki Watanabe Sanae Oshita Jun Yokoyama Daniel J Crawford 《Journal of plant research》2000,113(1):91-96
Neomirandea (x=17 and 25), Ageratina (x=17) and Sclerolepis (x=15) with the higher chromosome base numbers, and the other includes Mikania (x=17) and the remaining genera with lower chromosome base numbers (x=10–11). However, the monophyly of the former clade is supported with a low bootstrap value. In the latter clade, Mikania (x=17) diverged first, then Stevia (x=11), and finally eight genera with x=10 diverged in succession. This result supports the hypothesis that the genera in the tribe Eupatorieae with x =10 evolved from an ancestor with a higher base number, and the tribe is of polyploid origin.
Received 13 September 1999/ Accepted in revised form 20 January 2000 相似文献
115.
Emilie Tourneur Sanae Ben Mkaddem Cécilia Chassin Marcelle Bens Jean-Michel Goujon Nicolas Charles Christophe Pellefigues Meryem Aloulou Alexandre Hertig Renato C. Monteiro Stephen E. Girardin Dana J. Philpott Eric Rondeau Carole Elbim Catherine Werts Alain Vandewalle 《PLoS pathogens》2013,9(1)
Acute pyelonephritis (APN), which is mainly caused by uropathogenic Escherichia coli (UPEC), is the most common bacterial complication in renal transplant recipients receiving immunosuppressive treatment. However, it remains unclear how immunosuppressive drugs, such as the calcineurin inhibitor cyclosporine A (CsA), decrease renal resistance to UPEC. Here, we investigated the effects of CsA in host defense against UPEC in an experimental model of APN. We show that CsA-treated mice exhibit impaired production of the chemoattractant chemokines CXCL2 and CXCL1, decreased intrarenal recruitment of neutrophils, and greater susceptibility to UPEC than vehicle-treated mice. Strikingly, renal expression of Toll-like receptor 4 (Tlr4) and nucleotide-binding oligomerization domain 1 (Nod1), neutrophil migration capacity, and phagocytic killing of E. coli were significantly reduced in CsA-treated mice. CsA inhibited lipopolysaccharide (LPS)-induced, Tlr4-mediated production of CXCL2 by epithelial collecting duct cells. In addition, CsA markedly inhibited Nod1 expression in neutrophils, macrophages, and renal dendritic cells. CsA, acting through inhibition of the nuclear factor of activated T-cells (NFATs), also markedly downregulated Nod1 in neutrophils and macrophages. Silencing the NFATc1 isoform mRNA, similar to CsA, downregulated Nod1 expression in macrophages, and administration of the 11R-VIVIT peptide inhibitor of NFATs to mice also reduced neutrophil bacterial phagocytosis and renal resistance to UPEC. Conversely, synthetic Nod1 stimulating agonists given to CsA-treated mice significantly increased renal resistance to UPEC. Renal transplant recipients receiving CsA exhibited similar decrease in NOD1 expression and neutrophil phagocytosis of E. coli. The findings suggest that such mechanism of NFATc1-dependent inhibition of Nod1-mediated innate immune response together with the decrease in Tlr4-mediated production of chemoattractant chemokines caused by CsA may contribute to sensitizing kidney grafts to APN. 相似文献
116.
To clarify the mechanism of the cardiotoxic action of adriamycin (ADM), the participation of free radicals from ADM in cardiotoxicity was investigated through the protective action of glutathione (GSH) or by using electron spin resonance (ESR). Oxidation of ADM by horseradish peroxidase and H2O2 (HRP-H2O2) was blocked by GSH concentration dependently. Inactivation of creatine kinase (CK) induced during interaction of ADM with HRP-H2O2 was also protected by GSH. Other anthracycline antitumor drugs that have a p-hydroquinone structure in the B ring also inactivated CK, and GSH inhibited the inactivation of CK. These results suggest that ADM was activated through oxidation of the p-hydroquinone in the B ring by HRP-H2O2. Although ESR signals of the oxidative ADM B ring semiquinone were not detected, glutathionyl radicals were formed during the interaction of ADM with HRP-H2O2 in the presence of GSH. ADM may be oxidized to the ADM B ring semiquinone and then reacts with the SH group. However, ESR signals of ADM C ring semiquinone, which was reductively formed by xanthine oxidase (XO) and hypoxanthine (HX) under anaerobic conditions, were not diminished by GSH, but they completely disappeared with ferric ion. These results indicate that oxidative ADM B ring semiquinones oxidized the SH group in CK, but reductive ADM C ring semiquinone radicals may participate in the oxidation of lipids or DNA and not of the SH group. 相似文献
117.
Sujii Patricia Sanae Tambarussi Evandro Vagner Grando Carolina de Aguiar Silvestre Ellida Viana João Paulo Gomes Brancalion Pedro H. S. Zucchi Maria Imaculada 《Conservation Genetics》2021,22(3):383-396
Conservation Genetics - Gene flow may occur both through pollen movement and seed dispersal, although their relative contribution to overall species gene flow is not understood for most tropical... 相似文献
118.
119.
Sakakibara F Takagi K Kataoka R Kiyota H Sato Y Okada S 《Biochemical and biophysical research communications》2011,(1):76-81
We isolated a novel aerobic dieldrin-degrading bacterium from an enrichment culture in a soil–charcoal perfusion system. Enrichment culture using a soil–charcoal perfusion system was an effective way to obtain microorganisms that degrade recalcitrant compounds. The soil–charcoal perfusion was performed using aldrin trans-diol, which was a metabolite of dieldrin. Aldrin trans-diol had higher bioavailability (2.5 mg/l) than dieldrin (0.1–0.25 mg/l), therefore it is possible for microorganisms to utilize it as a substrate in soil. After 100 days of circulation and three exchanges of the medium, the enriched charcoal was harvested and a bacterium isolated. The isolate was designated as strain KSF27 and was found to be closely related to Pseudonocardia spp. as determined by 16S rRNA sequencing analysis. Strain KSF27 degraded aldrin trans-diol by 0.05 μmol/l from an initial concentration of 25.5 μmol/l. The metabolite of aldrin trans-diol was detected by HPLC/MS and determined to be aldrindicarboxylic acid based on retention time and the MS fragment. Moreover, strain KSF27 degraded dieldrin from 14.06 μmol/l to 2.01 μmol/l over a 10-day incubation at 30 °C. This strain degraded dieldrin and other persistent organochlorine pesticides, such as α-endosulfan, β-endosulfan, endosulfan sulfate, heptachlor, heptachlor epoxide and chlordecone. 相似文献
120.
The thermodynamics of cofactor binding to the isolated reductase domain (Red) of nNOS and its mutants have been studied by isothermal titration calorimetry. The NADP(+) and 2',5'-ADP binding stoichiometry to Red were both 1:1, consistent with a one-site kinetic model instead of a two-site model. The binding constant (K(D) = 71 nM) and the large heat capacity change (ΔC(p) = -440 cal mol(-1) K(-1)) for 2',5'-ADP were remarkably different from those for NADP(+) (1.7 μM and -140 cal mol(-1) K(-1), respectively). These results indicate that the nicotinamide moiety as well as the adenosine moiety has an important role in binding to nNOS. They also suggest that the thermodynamics of the conformational change in Red caused by cofactor binding are significantly different from the conformational changes that occur in cytochrome c reductase, in which the nicotinamide moiety of the cofactor is not essential for binding. Analysis of the deletion mutant of the autoinhibitory helix (RedΔ40) revealed that the deletion resulted in a decrease in the binding affinity of 2',5'-ADP with more unfavorable enthalpy gain. In the case of RedCaM, which contains a calmodulin (CaM) binding site, the presence of Ca(2+)/CaM caused a 6.7-fold increase in the binding affinity for 2',5'-ADP that was mostly due to the favorable entropy change. These results are consistent with a model in which Ca(2+)/CaM induces a conformational change in NOS to a flexible "open" form from a "closed" form that locked by cofactor binding, and this change facilitates the electron transfer required for catalysis. 相似文献