PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Chlorates”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,027 records · Page 57Linked to original sources
PubMed1992

Molybdoenzyme biosynthesis in Escherichia coli: in vitro activation of purified nitrate reductase from a chlB mutant.

All molybdoenzyme activities are absent in chlB mutants because of their inability to synthesize molybdopterin guanine dinucleotide, which together with molybdate constitutes the molybdenum cofactor in Escherichia coli. The chlB mutants are able to synthesize molybdopterin. We have previously shown that the inactive nitrate reductase present in a chlB mutant can be activated in a process requiring protein FA and a heat-stable low-molecular-weight substance. We show here that purified nitrate reductase from the soluble fraction of a chlB mutant can be partially activated in a process that requires protein FA, GTP, and an additional protein termed factor X. It appears that the molybdopterin present in the nitrate reductase of a chlB mutant is converted to molybdopterin guanine dinucleotide during activation. The activation is absolutely dependent upon both protein FA and factor X. Factor X activity is present in chlA, chlB, chlE, and chlG mutants.

Bacterial Proteins↗
PubMed2006

Preparation and characterization of (PVP + NaClO4) electrolytes for battery applications.

A sodium ion-conducting polymer electrolyte based on polyvinyl pyrrolidone (PVP) complexed with NaClO(4) was prepared using the solution-cast technique. The cathode film of V(2)O(5) xerogel modified with polyvinyl pyrrolidone was prepared using the sol-gel method. Investigations were conducted using X-ray diffractometry (XRD), Fourier transformation infrared (FT-IR) spectroscopy. The ionic conductivity and transference number measurements were performed to characterize the polymer electrolyte for battery applications. The transference number data indicated that the conducting species in these electrolytes are the anions. Using the electrolyte, electrochemical cells with a configuration Na/(PVP + NaClO(4))/V(2)O(5) modified by (PVP) were fabricated and their discharge profiles studied.

Chlorates↗
PubMed2002

Mechanism of thrombin-induced vasodilation in human coronary arterioles.

Thrombin (Thromb), activated as part of the clotting cascade, dilates conduit arteries through an endothelial pertussis toxin (PTX)-sensitive G-protein receptor and releases nitric oxide (NO). Thromb also acts on downstream microvessels. Therefore, we examined whether Thromb dilates human coronary arterioles (HCA). HCA from right atrial appendages were constricted by 30-50% with endothelin-1. Dilation to Thromb (10(-4)-1 U/ml) was assessed before and after inhibitors with videomicroscopy. There was no tachyphylaxis to Thromb dilation (maximum dilation = 87.0%, ED(50) = 1.49 x 10(-2)). Dilation to Thromb was abolished with either hirudin or denudation but was not affected by PTX. Neither N(omega)-nitro-l-arginine methyl ester (n = 7), indomethacin (n = 9), (1)H-[1,2,4] oxadiazolo-[4,3-a]quinoxalin-1-one (n = 6), tetraethylammonium chloride (n = 5), nor iberiotoxin (n = 4) reduced dilation to Thromb. However, KCl (maximum dilation = 89 +/- 5 vs. 20 +/- 10%; P < 0.05; n = 7), tetrabutylammonium chloride (maximum dilation = 79 +/- 7 vs. 21 +/- 4%; P < 0.05; n = 5), and charybdotoxin (maximum dilation = 89 +/- 4 vs. 10 +/- 2%; P < 0.05; n = 4) attenuated dilation to Thromb. In contrast to animal models, Thromb-induced dilation in human arterioles is independent of G(i)-protein activation and NO release. However, Thromb dilation is endothelium dependent, is maintained on consecutive applications, and involves activation of K(+) channels. We speculate that an endothelium-derived hyperpolarizing factor contributes to Thromb-induced dilation in HCA.

Adult↗
PubMed2004

A novel efflux-recapture process underlies the mechanism of high-density lipoprotein cholesteryl ester-selective uptake mediated by the low-density lipoprotein receptor-related protein.

OBJECTIVE: To determine the mechanism of low-density lipoprotein (LDL) receptor-related protein (LRP)-mediated selective uptake of high-density lipoprotein (HDL)-derived cholesteryl esters (CE). METHODS AND RESULTS: Apolipoprotein E (apoE) and heparin sulfate proteoglycans are required for LRP-mediated selective uptake in adipocytes. Furthermore, 2-deoxyglucose and NaN(3) abolish this process, indicating that cellular energy is required. LRP-mediated selective uptake is also abolished by monensin or when clathrin-mediated internalization is inhibited (using hypotonic, K(+)-free medium or hyperosmolar sucrose), clearly implicating receptor endocytosis. The receptor-associated protein (RAP), an inhibitor of ligand binding to LRP, reduced the transport of CE into an intracellular compartment but not into the plasma membrane. Remarkably, the CE that is ultimately transported by LRP first enters the plasma membrane then undergoes apoE-mediated CE efflux before being recaptured and internalized by LRP. CONCLUSIONS: According to this "efflux-recapture" model, LRP contributes to selective uptake because it recovers CE that would normally be lost by efflux mediated by apoE. In adipocytes, the LDL receptor-related protein contributes to selective uptake when it recaptures and internalizes HDL-derived cholesteryl esters that are otherwise lost by apoE-mediated efflux. This novel "efflux-recapture" process explains some conflicting observations of selective uptake and underscores the bi-directional nature of efflux.

Adipocytes↗
PubMed1997

Tissue factor pathway inhibitor in endothelial cells colocalizes with glycolipid microdomains/caveolae. Regulatory mechanism(s) of the anticoagulant properties of the endothelium.

Tissue factor pathway inhibitor (TFPI), the main downregulator of the procoagulant activity of tissue factor.factor VIIa complex, locates in human endothelial cells (EC) in culture as well-defined clusters uniformly distributed both on the cell surface and intracellularly. We here demonstrate by immunofluorescence that TFPI colocalizes in EC with caveolin, urokinase-type plasminogen activator receptor, and glycosphingolipids. The localization of TFPI in caveolae in resting endothelium is proved by double immunogold electron microscopy for TFPI and caveolin. After ultracentrifugation of rat lung or EC homogenates through density gradients of Nycodenz, TFPI was highly enriched at densities of 1.05 to 1.08 g/mL, together with caveolin and alkaline phosphatase. By ELISA, more than half of the cellular TFPI was detected in Triton X-100-insoluble extracts of EC. TFPI incorporates [1-3H]ethanolamine and is cleaved from the cell surface by phosphatidylinositol-phospholipase C, indicating a specific glycosylphosphatidylinositol-anchorage mechanism for TFPI in the plasma membrane. Clustering of TFPI and its localization in caveolae are dependent on the presence of cholesterol in the membrane. Agonist-induced stimulation of EC caused marked changes of distribution for both TFPI and caveolin at subcellular level, with subsequent increase of the cell surface-associated inhibitory activity toward tissue factor.factor VIIa. Our findings suggest that, beside their function in transcytosis, potocytosis, cell surface proteolysis, and regulation of signal transduction, caveolae also play a direct role in the regulation of EC anticoagulant properties.

Animals↗
PubMed2002

Interaction of human chondrocytes and NIH/3T3 fibroblasts on chloric acid-treated biodegradable polymer surfaces.

It has been recognized that adhesion and proliferation of cells on biodegradable polymers such as poly(lactic acid) (PLA), poly(glycolic acid) (PGA), and poly(lactide-co-glycolide) (PLGA) depend on the surface properties. The chloric acid (CA) treatment of these films was developed to increase surface wettability and to improve adhesion and proliferation of human chondrocytes and NIH/3T3 fibroblasts. The CA-treated films were characterized by the measurement of water contact angle, electron spectroscopy for chemical analysis (ESCA), and scanning electron microscopy (SEM). The changes of the film surface water contact angle gradually decreased with increase of CA treatment time, owing to the oxygen-based functional groups incorporated on the surface by CA treatment and were in the order PGA > PLGA > PLA due to the number of methyl group on the backbone chain. In ESCA analysis, as CA treatment time increased, the carbon (binding energy, approximately 285 eV) ratio decreased in film surfaces, whereas the oxygen (approximately 532 eV) ratio increased. The human chondrocytes from articular cartilage and mouse NIH/3T3 fibroblasts adhered for 1 day and grown for 2 days on the CA-treated films were counted and observed by SEM. As the surface wettability increased, the number of cells adhered and grown on the surface increased. In conclusion, this study demonstrated that the surface wettability of the biodegradable polymer plays an important role for cell adhesion and proliferation behavior for the application of the tissue engineering.

3T3 Cells↗
PubMed1996

Involvement of wound-associated factors in rat brain astrocyte migratory response to axonal injury: in vitro simulation.

The poor ability of mammalian central nervous system (CNS) axons to regenerate has been attributed, in part, to astrocyte behavior after axonal injury. This behavior is manifested by the limited ability of astrocytes to migrate and thus repopulate the injury site. Here, the migratory behavior of astrocytes in response to injury of CNS axons in vivo was simulated in vitro using a scratch-wounded astrocytic monolayer and soluble substances derived from injured rat optic nerves. The soluble substances, applied to the scratch-wounded astrocytes, blocked their migration whereas some known wound-associated factors such as transforming growth factor-beta 1 (TGF-beta 1), basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), transforming growth factor-alpha (TGF-alpha), and heparin-binding epidermal growth factor in combination with insulin-like growth factor-1 (HB-EGF + IGF-1) stimulated intensive migration with consequent closure of the wound. Migration was not dominated by proliferating cells. Both bFGF and HB-EGF + IGF-1, but not TGF-beta 1, could overcome the blocking effect of the optic nerve-derived substances on astrocyte migration. The induced migration appeared to involve proteoglycans. It is suggestive that appropriate choice of growth factors at the appropriate postinjury period may compensate for the endogenous deficiency in glial supportive factors and/or presence of glial inhibitory factors in the CNS.

Animals↗
PubMed2006

Involvement of the adenylyl cyclase/protein kinase A signaling pathway in the stimulatory effect of PACAP on frog adrenocortical cells.

We have previously shown that PACAP stimulates in vitro the secretion of corticosteroids by frog adrenal explants and that PACAP increases cAMP formation and cytosolic calcium concentration ('Ca2+'i) in adrenocortical cells. The aim of the present study was to investigate the involvement of cAMP and 'Ca2+'i in the stimulatory effect of PACAP on steroid production. Incubation of adrenal explants with PACAP resulted in a significant increase in total inositol phosphate formation. Administration of the protein kinase A inhibitor, H89, markedly reduced the stimulatory effect of PACAP on corticosterone and aldosterone secretion by perifused adrenal slices. In contrast, chelation of intracellular or extracellular calcium, or incubation with calcium channel blockers, had no effect on PACAP-evoked steroid secretion. Incubation of the cells with BAPTA or thapsigargin totally suppressed the stimulatory effect of PACAP on 'Ca2+'i. In contrast, suppression of extracellular calcium with EGTA or blockage of voltage-dependent Ca2+ channels did not impair PACAP-induced Ca2+ response. These data indicate that, in frog adrenocortical cells, the stimulatory effect of PACAP on steroid secretion is mediated through activation of the cAMP/PKA pathway. Concurrently, PACAP causes calcium mobilization from IP(3)-dependent intracellular stores through activation of a phospholipase C, while the calcium response is not involved in the stimulatory effect of PACAP on corticosteroid secretion.

Adenylyl Cyclases↗
PubMed2003

Anion selectivity by the sodium iodide symporter.

The iodide transporter of the thyroid (NIS) has been cloned by the group of Carrasco. The NIS-mediated transport was studied by electrophysiological methods in NIS-expressing Xenopus oocytes. Using this method, the anion selectivity of NIS was different from that previously reported for thyroid cells, whereas perchlorate and perrhenate were found not transported. In this study we compared the properties of human NIS, stably transfected in COS-7 cells to those of the transport in a thyroid cell line, the FRTL5 cells, by measuring the transport directly. We measured the uptake of (125)I(-), (186)ReO(4)(-), and (99m)TcO(4)(-) and studied the effect on it of known competing anions, i.e. ClO(4)(-), SCN(-), ClO(3)(-), ReO(4)(-), and Br(-). We conclude that the properties of the NIS transporter account by themselves for the properties of the thyroid iodide transporter as described previously in thyroid slices. The order of affinity was: ClO(4)(-) > ReO(4)(-) > I(-) >/= SCN(-) > ClO(3)(-) > Br(-). NIS is also inhibited by dysidenin (as in dog thyroid).

Animals↗
PubMed1987

Age-related failure of endocytosis may be the pathogenetic mechanism responsible for "cold" follicle formation in the aging mouse thyroid.

With advancing age, 60-80% of the follicles of the mouse thyroid gland turn "cold", i.e. they lose their normal capacity to iodinate thyroglobulin (Tgb). Cold follicles are morphologically characterized by their large size, by deeply periodic acid-Schiff-stained colloid and by flat epithelial cells. We investigated the hypothesis that a progressive, age-related failure of endocytosis, leading to a gradually increasing mismatch between production of new Tgb and resorption of stored Tgb, could lead to overfilling of colloid stores with consecutive impediment of diffusion. To this purpose, labeling of the thyroids was started when mice were 3 months old, and 125I was continuously administered thereafter for 2-6 months. After this time, all follicles were homogeneously labeled in autoradiographs. Tracer application was then discontinued. Autoradiographs obtained at intervals during the washout of the tracer yielded a mirror image of that observed after acute labeling. The large follicles which were cold after acute labeling in old animals now still retained labeled iodoproteins even after 7 weeks of washout, i.e. at a time when morphologically normal follicles had long lost their labeled Tgb stores. Thus, the cold follicles of the old thyroid must have been functioning normally during equilibration of young thyroids, but have then gradually lost their capacity to iodinate and to remove stored Tgb from the colloid. The observation supports the thesis that aging primarily affects the cytoskeleton and, thus, the cell's endocytotic machinery. This effect of aging on the thyroid can be prevented by life-long stimulation of the gland by TSH.

Aging↗
PubMed1996

Proteoglycans are required for maintenance of Wnt-11 expression in the ureter tips.

Development of the metanephric kidney requires the concerted interaction of two tissues, the epithelium of the ureteric duct and the metanephric mesenchyme. Signals from the ureter induce the metanephric mesenchyme to condense and proliferate around the ureter tip, reciprocal signals from the mesenchyme induce the ureter tip to grow and to branch. Wnt genes encode secreted glycoproteins, which are candidate mediators of these signaling events. We have identified three Wnt genes with specific, non-overlapping expression patterns in the metanephric kidney, Wnt-4, Wnt-7b and Wnt-11. Wnt-4 is expressed in the condensing mesenchyme and the comma- and S-shaped bodies. Wnt-7b is expressed in the collecting duct epithelium from 13.5 days post coitum onward. Wnt-1l is first expressed in the nephric duct adjacent to the metanephric blastema prior to the outgrowth of the ureteric bud. Wnt-l1 expression in Danforth's short-tail mice suggests that signaling from the mesenchyme may regulate Wnt-ll activation. During metanephric development, Wnt-11 expression is confined to the tips of the branching ureter. Maintenance of this expression is independent of Wnt-4 signaling and mature mesenchymal elements in the kidney. Moreover, Wnt-ll expression is maintained in recombinants between ureter and lung mesenchyme suggesting that branching morphogenesis and maintenance of Wnt-ll expression are independent of metanephric mesenchyme-specific factors. Interference with proteoglycan synthesis leads to loss of Wnt-ll expression in the ureter tip. We suggest that Wnt-11 acts as an autocrine factor within the ureter epithelium and that its expression is regulated at least in part by proteoglycans.

Animals↗