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Biomedical subjects

L Moore

Publications and source records attributed to L Moore.

At least 217 records · Page 12Linked to original sources
PubMed1985

Meeting the terminal functions of a baccalaureate curriculum: the students' perception.

Nursing faculty have established terminal functions which graduates are expected to be able to accomplish after successfully completing the nursing program. Students have asked themselves and faculty if they are ready to perform as professional nurses after graduation. This study utilized the terminal functions established by one medium-size state university to obtain data regarding the students' perceptions of their competencies based on the terminal functions. The assessment was conducted at the time of graduation and again one year post-graduation. The data may provide other faculty with a method to further evaluate nursing curricula and illustrate the changes in graduates' perceptions of their abilities over time.

Clinical Competence↗
PubMed1984

Effect of t-butyl hydroperoxide on liver microsomal membranes and microsomal calcium sequestration.

In vitro exposure of hepatocytes or liver microsomes to t-butyl hydroperoxide resulted in a marked decrease of liver microsomal calcium pump activity. Decreased calcium pump activity was dependent upon both concentration and time. Liver microsomes could be protected from this effect by glutathione or dithiothreitol. In addition to decreased calcium pump activity, exposure of liver microsomes to t-butyl hydroperoxide produced a concentration-dependent aggregation of microsomal membrane protein as determined by polyacrylamide gel electrophoresis. Inhibition of microsomal calcium pump activity was observed when intact hepatocytes were incubated, in vitro, with t-butyl hydroperoxide. However, aggregation of microsomal membrane protein was not observed when hepatocytes were incubated with t-butyl hydroperoxide. The effects produced by exposure of liver microsomes to this compound do not appear to be a complete model of actions of the compound on intact cells.

Animals↗
PubMed1984

Evaluation of provocative tests in suspected medullary carcinoma of the thyroid:heterogeneity of calcitonin responses to calcium and pentagastrin.

Abnormal calcitonin secretion provides a reliable marker for the presence of medullary carcinoma of the thyroid (MCT) and its precursor form, C-cell hyperplasia (CCH). Since this tumor may be transmitted by a dominant autosomal gene, the coincidence of a sensitive marker and an easily identified "at risk" population affords an unusual opportunity for cancer prophylaxis. To evaluate the specificity and sensitivity of provocative tests used for detection of C-cell disease, we have compared the calcitonin (hCT) responses to calcium (3 mg/kg body weight over 10 minutes intravenously), pentagastrin (0.5 microgram/kg body weight), and injection of calcium (1.0 mg/kg body weight) plus pentagastrin (0.25 microgram/kg body weight) over 60 seconds in 13 patients with subsequently proven MCT or CCH and in 31 normal volunteers. The ranges of hCT observed in normals after injection of pentagastrin and combined calcium and pentagastrin were lower than those seen in all nine patients with MCT. One subject, the only MCT patient with normal basal hCT values, had a normal response to calcium whereas all others achieved supranormal levels. Basal hCT levels were normal in the four patients with CCH but the hCT response to calcium was to a value in excess of 300 pg/mL, a level exceeded by only 3 of 31 normal subjects; the hCT response to pentagastrin in CCH and in normal subjects was indistinguishable. Combined calcium and pentagastrin administration was associated with abnormal hCT responses in two of the CCH patients and in the MCT patient with a normal response to calcium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Excretion of ouabain by Malpighian tubules of Oncopeltus fasciatus.

An in vitro preparation of Malpighian tubules was used to investigate the excretion of the polar cardiac glycoside, ouabain, in Oncopeltus fasciatus. Tubules were found to consist of at least two morphologically and physiologically distinct segments, both of which metabolized ouabain. The distal segment (segment II) secreted primary urine and ouabain. Secretion of ouabain by segment II was not observed to occur against a concentration gradient and increased with increasing fluid secretion. The proximal segment (segment I) reabsorbed fluid and ouabain but not metabolites. Ouabain was reabsorbed against a strong concentration gradient (23-fold), was independent of fluid reabsorption, and increased with increasing fluid secretion by segment II. In rapidly secreting Malpighian tubules (a situation of high cardiac glycoside secretion by segment II), the presence of segment I reduced the excretion of ouabain by 84-93%, mainly by reducing ouabain concentration. It appears excretory loss of cardiac glycosides can be reduced in O fasciatus and thus may be a factor in the sequestration of cardiac glycosides in this insect.

Absorption↗
PubMed1983

Enhanced hepatotoxicity and inhibition of liver endoplasmic reticulum calcium pump by CCl4 in rats fed a thiamine deficient diet.

Male Sprague-Dawley rats were fed a thiamine deficient diet for three weeks, then treated with a range of CCl4 doses (0.01-1-ml/kg). Rats fed the deficient diet grew more slowly (body weight 65 percent of control) and had elevated liver glutathione (GSH) (220 percent of control). CCl4 hepatotoxicity, assessed by serum glutamicpyruvic transaminase (SGPT) activity and histological examination 24 hours after the hepatotoxin, was augmented in the group fed the thiamine deficient diet. Likewise, CCl4 inhibition of liver endoplasmic reticulum (ER) function (glucose-6-phosphatase (G6Pase) and calcium pump activities one hour after CCl4) was enhanced in rats fed the deficient diet. These results suggest that thiamine deficiency enhances CCl4 damage to membranes of the ER and enhances CCl4 hepatotoxicity.

Alanine Transaminase↗
PubMed1983

Enhanced inhibition of hepatic microsomal calcium pump activity by CCl4 treatment of isopropanol-pretreated rats.

Pretreatment of rats with isopropanol enhanced both hepatotoxicity and calcium pump inhibition after CCl4 exposure in vivo or in vitro. Animals were given isopropanol (1.25 ml/kg) 18 hr before CCl4 (0.01 to 1.0 ml/kg). CCl4 hepatotoxicity, judged as increased appearance of glutamic-pyruvate transaminase in serum, was enhanced by isopropanol pretreatment. Pretreatment of rats with isopropanol made CCl4 as much as 20- to 30-fold more potent as an inhibitor of the calcium pump. Inhibition of another endoplasmic reticulum enzyme, glucose 6-phosphatase, was also enhanced by isopropanol pretreatment. In contrast to the effect of CCl4 in control animals, in isopropanol-pretreated rats given CCl4, depletion of liver glutathione was observed. Altered CCl4 metabolism in isopropanol-pretreated animals may result in production of increased amounts of phosgene (or other metabolites) responsible for inhibition of the liver microsome calcium pump and glutathione depletion.

1-Propanol↗
PubMed1983

Isopropanol enhancement of cytochrome P-450-dependent monooxygenase activities and its effects on carbon tetrachloride intoxication.

Acute or chronic treatment of rats with isopropanol caused a significant increase in hepatic cytochrome P-450 content and a two- to threefold increase in aniline hydroxylase and 7-ethoxycoumarin O-deethylase activities, but no significant change in ethylmorphine N-demethylase or benzo(a)pyrene hydroxylase activity. In rats treated with isopropanol and challenged with CCl4, liver toxicity of CCl4 was characteristically potentiated, as assessed by elevation of serum glutamic-pyruvic transaminase (SGPT) levels. Isopropanol pretreatment also potentiated CCl4-induced damage to the hepatic monooxygenase system. In addition to a decrease in cytochrome P-450, rats treated with isopropanol and challenged with CCl4 showed a nonspecific decrease not only in aniline hydroxylase and 7-ethoxycoumarin O-deethylase activities, but also in ethylmorphine N-demethylase, benzo(a)pyrene hydroxylase, and NADPH-cytochrome c reductase activities. These results were confirmed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis of solubilized microsomes. The electrophoretic results showed that isopropanol pretreatment markedly potentiated the CCl4-caused destruction of cytochrome P-450 hemeproteins. The data strongly suggest that isopropanol increases one or more forms of cytochrome P-450 which selectively enhance the metabolism of CCl4 to an active metabolite. This active metabolite then causes a nonselective damage to the microsomal mixed-function oxidase system.

1-Propanol↗
PubMed1983

Duodenal microflora in infants with acute and persistent diarrhoea.

The duodenal bacterial population was determined qualitatively and quantitatively in 3 groups of infants with diarrhoeal disease of varying duration. Infants with acute self limiting diarrhoea (group 1) had an abnormal overgrowth of organisms in the upper small bowel which was similar to that found in infants whose diarrhoea persisted after 4 days in hospital (group 2). The total duodenal organism count in infants with diarrhoea persisting after 7 days in hospital (group 3) was almost 100 times greater than either of the other groups. The findings may have important implications in preventing persistent diarrhoea from becoming protracted.

Acute Disease↗
PubMed1982

Evidence for an osmotic effect of glucose in the in vivo rat proximal tubule.

A series of micropuncture experiments were performed to assess whether phlorizin inhibition of proximal tubular glucose reabsorption inhibits proximal tubular fluid reabsorption due to a change in the transepithelial osmotic gradient for glucose. End proximal tubular filtrate reabsorption was measured, control vs experimental, in the same rat. The effects of infusing phlorizin in one group were compared to those of graded small infusions of mannitol in a second group of rats. In the phlorizin series tubular fluid and peripheral plasma were analyzed for glucose. Net renal sodium and renal oxygen consumption were measured in these same rats. In the mannitol series tubular fluid and peripheral plasma mannitol concentrations were determined. The results show that phlorizin inhibits proximal tubular fluid and glucose reabsorption without changing renal oxygen consumption. Mannitol inhibits proximal fluid reabsorption per unit transepithelial concentration difference to the same extent as does glucose during phlorizin infusion. We interpret these data as most consistent with the conclusion that the reduction in proximal tubular fluid reabsorption during phlorizin infusion is primarily due to the resultant change in the effective transepithelial osmotic gradient for glucose. Normally this gradient favors net fluid reabsorption. During phlorizin it favors retention of fluid in the proximal tubular lumen.

Animals↗
PubMed1982

1,1-Dichloroethylene inhibition of liver endoplasmic reticulum calcium pump function.

This study shows that 1,1-DCE promptly inhibits a calcium homeostatic function of liver ER. The correlation with GSH depletion and the effect of MFOS induction on calcium pump inhibition suggest that this is a direct effect of a 1,1-DCE metabolite on the calcium pump. As a result of calcium pump inhibition, calcium released from the ER may serve to trigger changes that result in a massive influx of extracellular calcium and, ultimately, cytotoxicity.

Animals↗
PubMed1982

Carbon disulfide hepatoxicity and inhibition of liver microsome calcium pump.

This work has shown that CS2 promptly inhibits the liver ER calcium pump only in those animals that subsequently develop hepatic necrosis. In this respect, inhibition of the ER calcium pump by CS2 resembles the actions of chlorinated hydrocarbon hepatotoxins. This lends further support to the suggestion that disruption of calcium homeostasis is an important early step in the action of at least some hepatotoxins [1-5]. CS2 appears to be the first example of a hepatotoxin other than chlorinated hydrocarbons that inhibit the liver ER calcium pump early in the course of intoxication. Finally, studies by others [17,18] suggest a mechanism by which CS2 can interact with and inhibit the liver ER calcium pump.

Animals↗
PubMed1982

Effect of essential amino acids (EAA) on chronic hemodialysis (CHD) patients (PTS).

1. Oral administration of EAA and calories was demonstrated to improve nutritional status of chronic stable hemodialysis patients. 2. This improvement was manifested by an increase of hematocrit, total protein, serum albumin, transferrin, and TLC in those patients with low values, as well as an increase in cortical and trabecular bone thickness. 3. Improvement occurred in patients receiving a diet with one gm protein/kg/day. 4. Administration of calories without EAA did not show any beneficial effect.

Amino Acids, Essential↗
PubMed1980

Xylose absorption in infants with severe prolonged diarrhoea.

Energy supply may be a limiting factor in tissue repair when infants with severe prolonged diarrhoea are fed orally. Xylose tolerance tests were done on 8 female infants who had had severe dehydrating diarrhoea requiring treatment in hospital for 7 days. Seven infants had flat xylose tolerance curves, 5 of these being at very low levels. Very early intervention with hyperalimentation, elemental diets or antibacterial agents and basic anion exchange resins may reduce morbidity.

Absorption↗
PubMed1980

Nucleotide-induced alteration of rat liver microsome calcium pump activity.

Rat liver microsomes sequester calcium by an energy dependent process that may be a nonmuscle cell analog of the sarcoplasmic reticulum Ca2+ pump of skeletal muscle (Moore, L., Chen, T.S., Knapp, H.R., Jr. and Landon, E.J. (1975) J. Biol. Chem. 250, 4562-4568). Homogenization of rat liver in the presence of ATP (5 mM) results in a 2-fold increase of the specific activity of the microsome Ca2+ pump. The effect of ATP is concentration dependent and is detected at ATP levels as low as 0.1 mM. ATP will produce this effect if added before homogenization, after homogenization or after any of the centrifugation steps of microsome isolation. Homogenization of rat liver in the presence of ADP and AMP also increases specific activity of the microsome Ca2+ pump, but to a lesser extent than ATP. Other nucleoside triphosphates have been tested and are in general less effective than ATP in increasing microsome Ca2+ pump activity. The phosphate group of nucleotides appears to be improtant to his effect in that adenosine does not affect Ca2+ pump activity, while sodium pyrophosphate will increase pump activity but to a smaller extent than ATP. The presence of nucleotides or pyrophosphate during microsome isolation results in the release of a small amount of protein material from microsomes. These proteins can be detected in 105 000 Xg supernatant by SDS-polyacrylamide gel electrophoresis. Three bands of molecular weight 46 000, 42 000 and 36 000 comprise the majority of protein material released from microsomes. The ability of nucleotides to release one of the these proteins, the 42 000 molecular weight band, from microsomes correlates with the ability of the nucleotide to increase microsome Ca2+ pump activity. Preliminary evidence indicates that the protein released from ATP-treated microsomes is able to suppress the stimulated calcium uptake measured in ATP-treated microsomes. It is possible that this protein functions to regulate Ca2+ pump activity in the endoplasmic reticulum of liver.

Adenosine Diphosphate↗