Inositol phosphate levels in WRK-1 cells during hyperthermia.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to R Manning.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND: Unavoidable exposure to disease and to patients susceptible and vulnerable to disease warrants that students entering medical school be immunized against many of the illnesses for which vaccines are available. The validity of immunization records presented at the time of registration, however, is largely dependent on the provision of accurate and reliable documentation by the student. METHODS: We evaluated for authenticity the immunization and tuberculin testing records of 85 students entering medical school in 1990. Five levels of valid documentation were defined, and the information on each record was reviewed accordingly. RESULTS: Only 43% of the records were original documents or laboratory reports of antibody titers, and 7.5% were not date-specific. We found that 8% to 20% of the forms were missing physician and/or student signatures, and 12% to 19% of the forms did not have health care provider addresses. CONCLUSIONS: Even though medical student preventive health programs may have strict requirements, there may be substantial deficiencies in the quality of the documentation provided by the students. Such deficiencies undermine the purpose of these programs.
Several organizations have made recommendations about medical students' health. To determine the University of South Florida College of Medicine's concurrence with published guidelines, a prospective analytic study of the 1990 entering class was carried out, using the 1989 class as a control. Enforcement measures not present in 1989 were initiated in 1990. The requirements for the 1990 matriculants were a history and physical examination; tuberculin testing; immunizations to rubella, rubeola, tetanus-diphtheria, and hepatitis B; status of immunity to chickenpox; and proof of health insurance. The results showed that in 1990 expensive requirements had the lowest rates of compliance, and inexpensive ones, the highest rates of compliance. Comparing 1990 with 1989 showed that the enforcement measures significantly improved compliance for expensive requirements, and for requirements that obligated a student to incur a fee because they needed to be updated. The authors conclude that cost is a major deterrent to compliance and that, in order to improve compliance, medical schools must either implement effective enforcement measures or transfer the cost from the student to the institution.
Twenty-eight Angora goat doelings (average BW 22.1 kg) were used in a 150-d study to examine the effects of dietary CP level and degradability on mohair fiber production. A 2 x 2 factorial arrangement was instituted using conventional, solvent-extracted soybean meal (high degradability) or expelled, heat-treated soybean meal (low degradability) incorporated into low- (12%) or high- (19%) CP diets. Grease and clean mohair weights were greater (P less than .05) in goats fed the diets containing 19% CP. Mohair fiber diameter was not affected (P greater than .10) by dietary CP level. Clean mohair weight tended (P less than .08) to be higher in the goats fed diets containing expelled, heat-treated soybean meal. Body weight gains were not affected (P greater than .10) by CP level or degradability, whereas DMI increased (P less than .01) with increasing CP level. Ruminal fluid pH and total VFA concentrations were not affected (P greater than .10) by diet. Ruminal ammonia N concentration increased (P less than .05) as CP level in the diet increased, and postprandial changes in concentrations were less noticeable in the group fed expelled, heat-treated soybean meal. Plasma urea N (P less than .001) and total protein (P less than .01) concentration increased as dietary CP level increased. Plasma glucose was elevated (P less than .001) 2 h after feeding in the goats fed conventional, solvent-extracted soybean meal, whereas glucagon concentrations were greater at 0 and 4 h in the group fed expelled, heat-treated soybean meal.(ABSTRACT TRUNCATED AT 250 WORDS)
The haemiglobincyanide (HiCN) method for measuring haemoglobin is used extensively worldwide; its advantage is the ready availability of a stable and internationally accepted reference standard/calibrator. However, its use may create a problem, especially in automated analysers, as the waste disposal of large volumes of reagent containing cyanide may constitute a potential toxic hazard. As an alternative, conversion of haemoglobin to a sulphate derivative by nontoxic sodium lauryl sulphate has been proposed and is available as a commercial product from Toa Medical Electronics Co. Ltd., Japan. This evaluation has shown it to be as reliable and reproducible as HiCN for measuring haemoglobin at all concentrations, by both spectrophotometry and automated analyser. Maximum absorbance is at 534 nm. Total conversion occurs almost instantaneously, and includes methaemoglobin but not sulphaemoglobin. HbF is also measured. The only disadvantage is that solutions of haemoglobin-sulphate are stable for only a few hours at room temperature and up to three weeks at 4 degrees C. Thus, for standardization and calibration of instruments it is necessary to use a sample of blood or lysate the haemoglobin value of which has been assigned initially by the HiCN method.
1. Male chickens (Gallus domesticus) were treated with a single intramuscular injection of oestradiol-17 beta, then changes in the liver and plasma levels of triacylglycerol, phospholipid, nonesterified fatty acids and in the hepatic activities of acetyl-CoA carboxylase and fatty acid synthetase were measured at various times after injection. 2. The results suggest that the initial phase (less than 20 hr) of oestrogen-induced hyperlipidaemia occurs in the absence of changes in the hepatic activities of the major enzymes of fatty acid biosynthesis, but a subsequent increase in these enzyme activities may contribute to the later phase (greater than 20 hr) of oestrogen-induced lipogenesis in avian liver.
1. Early changes (0-44 hr) in liver and plasma lipid levels and in the rate of hepatic lipogenesis were measured in male chicks after a single intramuscular injection of oestradiol-17 beta. 2. Chick liver slices were employed to measure the rate of lipogenesis de novo using 3H2O and the rate of triacylglycerol synthesis from [9, 10-3H] palmitate at various times after injection. 3. The results suggest that oestrogen-induced lipogenesis occurs initially by a rapid and coordinated stimulation of the total hepatic capacity for lipogenesis de novo and for triacyglycerol synthesis from fatty acids. 4. The results are discussed in relation to oestrogen-induced changes in hepatic lipogenic enzymes.
Explore the source record for details and available documents.
Male chickens (Gallus domesticus) were treated with 17 beta-oestradiol then injected with a mixture of [6-3H]glucose and [U-14C]glucose. Subsequently, blood samples were taken to determine plasma lipid levels and several parameters of glucose metabolism, including entry rate, carbon recycling, mean transit time, the total body glucose mass, the mass of the sampling pool and the rate of outflow from this pool. Oestrogen-treated birds exhibited typical hyperlipidaemia, with significantly elevated plasma levels of triacylglyerol and nonesterified fatty acids. Oestrogen administration significantly decreased the glucose entry rate, the total body glucose mass and the rate of outflow from the sampling pool.
Explore the source record for details and available documents.
In the presence of Ca2+ (2.5 mM) and using [14C]arachidonoyl phosphatidylinositol (PI) membrane as substrate, phosphatidylinositol-specific phospholipase C (PI-PLC) (EC 3.1.4.10) in rat brain synaptosomes was activated by deoxycholate but not taurocholate. Calcium stimulated enzymic hydrolysis by both detergents, but the stimulatory effect of taurocholate was less than that of deoxycholate. Peak stimulation for deoxycholate was observed at 1 mg/ml, whereas that for taurocholate was 4 mg/ml. When 1 mM EDTA was added to the taurocholate (4 mg/ml) and Ca2+ (3.5 mM) system, synaptosomal PI-PLC activity was greatly stimulated, to almost the same level as the deoxycholate + Ca2+ system. This system required the presence of all three factors, and EGTA could not effectively replace EDTA in the stimulatory action. The detergent-induced hydrolysis of synaptosomal PI by the deoxycholate + Ca2+ and the taurocholate + Ca2+ + EDTA systems was strongly inhibited by divalent metal ions such as Zn2+, Cu2+, Pb2+, and Fe2+, whereas Mg2+ and Ca2+ were ineffective. Nevertheless, only the deoxycholate + Ca2+ system was responsive to enzyme inhibition by membrane-perturbing agents such as lysophospholipids and free fatty acids. The specific requirement for EDTA in the taurocholate system may be due to the release of a pool of inhibitory divalent metal ions from the membranes.
Synaptosomal phosphoglycerides were labeled after incubation with [1-14C]arachidonic acid, ATP, Mg2+, CoASH, and a small amount of 1-acylglycerophosphocholines. Under this incubation system, radioactivity was directed largely to diaclyglycerophosphocholines but diacylglycerophosphoinositols were also labeled to a lesser extent. Synaptosomes obtained after a 5-min ischemic treatment indicated a decrease (10-20%) in incorporation of radioactivity into the phospholipids. The ischemic synaptosomes also tended to retain a larger portion of the labeled arachidonate during the wash with bovine serum albumin. Upon incubation of the prelabeled synaptosomes in a sucrose-Tris (pH 7.4) medium at 37 degrees C, a time-dependent release of labeled arachidonate from the phospholipids was observed in both control and ischemic samples. Arachidonate release from the prelabeled synaptosomes was not affected by EDTA (1 mM) or taurocholate (0.4%) but was stimulated by Ca2+ (2.5 mM) or Ca2+ (3.5 mM) together with EDTA (1 mM). After incubation at 37 degrees C for 1 hr without added factors, the phospholipid degradation, as well as the appearance of free fatty acids, were higher in the ischemic samples (especially after 1 min of treatment) as compared to controls.
The hydrolysis of acyl-CoA by acyl-CoA hydrolase (EC 3.1.2.2.) in brain synaptosomes was inhibited by calcium. This inhibition was partly due to interaction of Ca2+ with the acyl-CoA, which was present in the soluble form, and partly due to complex formation among acyl-CoA, Ca2+ and membrane phospholipids. The inhibition of acyl-CoA hydrolase activity, as well as the complex formation, could be reversed if incubation was carried out in the presence of Ca2+ chelating agents. Synaptosomes isolated from brain samples after 1 min of postdecapitative treatment showed a decrease in oleoyl-CoA hydrolase activity. The physiological implication of acyl-CoA metabolism in relation to synaptic function is discussed.
Rats subjected to mild hypoxic and postdecapitative ischemic treatments indicated a decrease (8-16%) in the proportion of polyunsaturated acyl groups of diacyl glycerophosphocholines (diacyl-GPC), diacyl glycerophosphoethanolamines (diacyl-GPE), and alkenylacyl glycerophosphoethanolamines (alkenylacyl-GPE) in brain synaptosomes. In general, the acyl group changes due to mild hypoxic treatment were less obvious than those due to the ischemic treatment. The decrease in polyunsaturated acyl groups was marked by an increase in the saturated (16:0 and 18:0) and monoenoic (18:1) acyl groups. Among the polyunsaturated acyl groups, arachidonate (20:4) indicated the greatest decrease in response to ischemic and hypoxic treatments. The decrease in polyunsaturated fatty acids of diacyl glycerophosphocholines was largest in the first minute of ischemic treatment and the first 30 min of hypoxic treatment. After the initial decrease, there was a slight recovery. The biphasic type of change was thought to be due to active reacylation of the lyso phospholipids. This biphasic change, however, was not observed with ethanolamine phosphoglycerides which indicated a steady decrease in the polyunsaturated acyl group content with time of ischemic treatment. The increased hydrolysis of polyunsaturated acyl groups in brain membrane phosphoglycerides due to the ischemic and hypoxic treatments seemed to correlate well with the implication of phospholipase A(2) involvement in eliciting the increase in free fatty acids during brain stimulation.
1. Acetyl-Coa carboxylase from lactating-rabbit mammary gland was purified to homogeneity by the criterion of polyacrylamide-gel electrophoresis in the presence of sodium dodecyl sulphate. 2. Use of phosphate buffer throughout the purification gave low recovery of enzyme. Consequently, Tris buffers were used in the extraction and in selected stages of the purification procedure. 3. The purified enzyme had a specific activity of 5.15 +/- 0.3 mumol of bicarbonate incorporated/min per mg of protein (mean +/- S.E.M. of five preparations). This represents a purification of 257 +/- 16-fold and a yield of 4.3 +/- 0.13%. 4. The kinetic parameters of the purified enzyme were similar to those reported for the enzyme from other tissue sources. 5. The enzyme was assayed by a spectrophotometric assay and by a [14C]bicarbonate-fixation assay. Short incubation were used in the radio-chemical assay to avoid substantial loss of [14C]bicarbonate.
Antisera were raised to acetyl-CoA carboxylase and 6-phosphogluconate dehydrogenase from mammary glands of lactating rabbits, and cytochrome oxidase from rat liver. The enzymes were all highly purified but gave rise to multispecific antisera when tested against tissue extracts. Absorption procedures were devised to free the antisera of contaminating antibodies. Antisera to acetyl-CoA carboxylase and cytochrome oxidase were absorbed with fractions discarded during enzyme purification. The antiserum to 6-phospho-gluconate dehydrogenase was absorbed with a tissue extract from an early stage in mammary-gland differentiation. Monospecific antisera are essential for enzyme turnover studies and therefore antisera should be extensively tested and absorbed before use. A general procedure for the absorption of antisera to purified enzymes has been devised on the basis of accepted principles of antisera absorption.