28 results match your criteria: "University of Missouri-Kansas City 64108-2792[Affiliation]"

Objective: The objective of this study was to evaluate the effect of adding a spiroorthocarbonate (SOC) or a polyol on the cytotoxicity of epoxy-based dental resins.

Methods: Resins contained one of the epoxies: diglycidyl ether Bisphenol A (GY-6004); 3,4-epoxycyclohexanemethyl-3,4-epoxycyclohexane carboxylate (UVR-6105); vinyl cyclohexane dioxide (ERL-4206) or the three-epoxy mixture (Epoxy-M). The SOC was t/t-2,3,8,9-di(tetramethylene)-1,5,7,11-tetraoxaspiro[5.

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Glycyl-L-glutamine (Gly-Gln; beta-endorphin 30-31) is an endogenous dipeptide that is synthesized through the post-translational processing of beta-endorphin. Previously, we showed that Gly-Gln inhibits the hypotension and respiratory depression produced by central beta-endorphin administration. In this study, we tested whether cyclo(Gly-Gln), a non-polar, cyclic Gly-Gln derivative, was similarly effective following intracerebro-ventricular (i.

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Estrogen-regulated uterine vascularization modulates the guinea pig intrauterine environment.

Biol Neonate

February 1998

Division of Cell Biology and Biophysics, School of Biological Sciences, University of Missouri-Kansas City 64108-2792, USA.

The effects of experimentally-induced, uterine vascular restriction on uterine blood flow (UBF) and uterine blood volume (UBV) capacity, as well as the dependent intrauterine oxygen tension (IUpO2) measurements used as an indication of luminal nutrient availability, were examined using ovariectomized, estrogen (E)-treated guinea pigs. Following 3 days of E treatment, both UBF and UBV measurements were found to be elevated and associated with a causally-related increase in intraluminal uterine oxygen availability levels. Following the acute clamping of the uterine arteries, both UBF and UBV levels decreased dramatically and induced a rapid fall in associated intrauterine luminal oxygen tension measurements.

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To assess the effects of long-term pressure overload on sympathetic presynaptic components in the left ventricle, young adult male rats were subjected to surgical constriction of the suprarenal abdominal aorta. At 4 and 8 wk postsurgery, but not at 1 wk, left ventricular sympathetic activity, measured by the net fractional norepinephrine (NE) decrease after alpha-methyl-p-tyrosine methyl ester administration, was elevated in the aortic-banded rats. However, left ventricular NE was reduced only at 8 wk.

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Age-related functional alterations in a variety of neurotransmitter systems result in modulation of interneuronal communications which has some relevance in neurological deficits observed in the aging process. The synergistic interactions between protein kinase and inositol 1,4,5-trisphosphate (insP3)/Ca2+ pathways underlie a variety of cellular responses to external stimuli. To determine whether age-dependent changes occur in the regulation of protein kinase C and inositol 1,4,5-trisphosphate/Ca2+ pathways, insP3 contents as a marker for the release of intracellular calcium, saturation binding analysis of Ins P3 receptor using [3H]inositol 1,4,5-trisphosphate, slot/northern blot analysis of Ins P3 receptor-encoding mRNA transcripts, and the activities of Ca2+/phospholipid-dependent protein kinase C isozymes were investigated in the rat spinal cord.

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Studies show that peroxisome proliferators inhibit mitochondrial beta-oxidation of fatty acids. However, mechanism(s) of this inhibitory effect has not been identified. This study was undertaken to delineate such mechanism(s).

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The phosphodiesterase inhibitor, enoximone, was previously shown to cause paradoxical effects on cardiac lipid metabolism. The present study was undertaken to elucidate the effects of enoximone on the hepatic mitochondrial pathway of fatty acid oxidation. Results presented here show that in isolated rat liver mitochondria, palmitate oxidation was inhibited progressively by increasing concentrations of enoximone.

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Although septic shock may be the most common cause of distributive shock, to our knowledge, no studies have defined the likelihood and type of infection among patients with distributive shock. We performed a retrospective study of 100 consecutive patients who were admitted to a city-county hospital with hemodynamic evidence of distributive shock. Forty-nine of 100 patients with distributive shock had microbiological documentation of infection.

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Hepatotoxicity induced by various therapeutic agents, industrial chemicals and environmental pollutants is a well-recognized phenomenon. These chemicals are known to cause liver damage that is localized to either periportal or centrilobular regions of the liver lobule (1-3). Depending on dose, duration, and route of exposure, the resultant liver injury may regress or progress and becomes irreversible (1).

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Substance P- and opioid peptide-immunoreactive nerve terminals functionally interact in the spinal cord as two opposing systems in the regulation of the nociceptive pathway. In order to determine how SP-ergic system adapts to chronic opioid receptor blockade, the effects of naltrexone on SP level, SP receptor and the second messenger system coupled to the SP receptor were examined in the rat spinal cord. Male Sprague-Dawley rats were treated with naltrexone or vehicle for seven days by constant minipump infusion.

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Microbial growth and antimicrobial bacterial killing are both diminished in abscesses. It was postulated that zinc depletion in abscesses, perhaps secondary to a neutrophil protein resembling calprotectin, may be partly responsible for these effects. In a rabbit tissue-cage abscess model, pooled abscess supernatant concentration of zinc was < 1.

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Chronic blockade of opioid receptors by naltrexone increases opioid peptides in the striatum, and up-regulates brain opioid receptors resulting in functional supersensitivity. Striatal SP content was increased 3.5-fold after 8 days of naltrexone treatment relative to control animals.

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Human placenta was used to investigate the effects of chronic methadone use during pregnancy on villus tissue opioid receptors. Patients included in this investigation received 35-60 mg methadone per day. Methadone-exposed placenta villus tissue had no detectable opioid receptor binding sites measured by tritiated opioid agonists.

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The purpose of this study was to clarify the role of the mitochondria as a site for the reported hepatotoxic effects of the anti-AIDS drug dideoxyinosine (ddI). Data show that ddI interfered with the mitochondrial redox state in perfused livers leading to more oxidized mitochondria. This effect was reflected by a significant decrease in the mitochondrial NADH/NAD+ ratios from basal values of 0.

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Very little information is available on the permeability of the blood-brain barrier (BBB) to small polar drugs in chronic hypertension. The blood and cerebrospinal fluid (CSF) pharmacokinetics of libenzapril (LZP), a potent angiotensin converting enzyme inhibitor, were investigated in hypertensive (SH) and normotensive (SD) rats. Following intravenous bolus administration of this hydrophilic drug, the terminal rate constant for elimination (beta), steady-state volume of distribution (Vdss), and systemic clearance (CL) were similar in these two animal groups.

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Opioid ligands were investigated for their effect on hCG release from trophoblast tissue obtained from term human placenta. Data obtained indicate that opiate agonists stimulate in vitro basal hCG release from trophoblast tissue. The potency of these opioid agonists correspond to their kappa receptor selectivity, i.

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A method for simultaneous serial sampling of blood, bile, and urine from rats is described. Techniques for cannulation of jugular and femoral veins, bile duct, and bladder are described that make serial sampling of these three fluids possible. A saline infusion regimen was developed that prevents dehydration and maintains constant hematocrit values throughout the experiment.

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Characterization of a cocaine binding protein in human placenta.

Life Sci

April 1990

Division of Molecular Biology and Biochemistry, School of Basic Life Sciences, University of Missouri-Kansas City 64108-2792.

[3H]-Cocaine binding sites are identified in human placental villus tissue plasma membranes. These binding sites are associated with a protein and show saturable and specific binding of [3H]-cocaine with a high affinity site of 170 fmole/mg protein (Kd 16.7 nM).

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Elevated serum cholesterol is a risk factor in the development of coronary artery disease. Magnesium has been reported to decrease total serum cholesterol, low density lipoprotein, and very low density lipoprotein, and increase high density lipoprotein. A randomized, double-blind, placebo-controlled, crossover study was completed to determine if supplemented magnesium, in the form of magnesium oxide, would produce changes in the lipid profile.

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In perfused livers from fed rats, rates of glucose production (glycogenolysis) were 133 +/- 12 mumol/g/hr. Infusion of 2 microM verapamil into these livers decreased the rates of glucose production significantly to 97 +/- 15 mumol/g/hr within 10 min. Conversely, rates of production of lactate plus pyruvate (glycolysis) of 64 +/- 6 mumol/g/hr were not significantly altered by verapamil (60 +/- 3 mumol/g/hr).

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A glycoprotein with a molecular weight of 63,000 has been purified, in an active form, from human placental villus tissue membranes. The binding properties of this glycoprotein to opioid alkaloids and peptides indicates that it is the kappa opiate receptor of human placenta. The receptor binds the tritiated ligands etorphine, bremazocine, ethylketocyclazocine and naloxone specifically and reversibly with Kd values of 3.

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Mitochondrial enzymes and respiration were studied in the hearts of mice exposed to ethanol in utero from gestational Day 8 to parturition. This treatment had previously been shown by electron microscopy to result in myofibril loss and mitochondrial abnormalities. Ethanol was administered to pregnant mice by a liquid diet paradigm and pair-fed dams were used as controls.

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The mutagenicities of [1R] and [1S] aflatoxicol were measured using the Salmonella microsome test. In strain TA100 the [1R] form (unnatural aflatoxicol, aflatoxicol B) had a mutagenic potency approximately four times that of the [1S] epimer (natural aflatoxicol, aflatoxicol A, Ro) in the presence of S-9 liver microsomal fraction. The order in mutagenic potency compared to some other toxicologically important aflatoxins was as follows: B1 greater than [1R] approximately equal to G1 much greater than [1S] much much greater than B2.

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