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Biomedical subjects

A Mazur

Publications and source records attributed to A Mazur.

At least 91 records · Page 5Linked to original sources
PubMed1997

Parenteral magnesium loading test in the assessment of magnesium status in healthy adult French subjects.

Parenteral magnesium loading test has been proposed as an adequate mean to evaluate magnesium status. However, applied tests vary among different laboratories and standardized procedure is not available. In the present study, we assessed magnesium status in 32 healthy adult French subjects by magnesium loading test using MgCl2 and determination of magnesium concentrations in plasma and erythrocytes. We observed a positive correlation between plasma and erythrocyte magnesium concentrations, but there was no correlation between magnesium retention and basal urinary excretion of magnesium, and plasma or erythrocyte magnesium concentrations.

Adult↗
PubMed1996

Increased hepatic synthesis and accumulation of plasma apolipoprotein B100 in copper-deficient rats does not result from modification in apolipoprotein B mRNA editing.

Experimentally induced copper deficiency in the rat results in increased plasma apolipoprotein B100 (apo B100) concentration in association with increased hepatic apo B100 synthesis. This enhancement of apo B100 synthesis and plasma accumulation accounts for the rise of plasma low density lipoprotein in these animals. In the present study, we have investigated if the selective increase in hepatic apo B100 synthesis is accounted for by changes in apo B mRNA editing. Reverse transcription coupled with polymerase chain reaction amplification and primer extension analysis of apo B cDNA revealed no differences in apo B mRNA editing in either the liver or small intestine between control and copper-deficient rats. We speculate that the increase in apo B100 synthesis in the liver of copper-deficient rats reflects posttranslational alterations in gene expression accompanying changes in very low density lipoprotein assembly and secretion.

Animals↗
PubMed1996

Functional alterations in sarcoplasmic reticulum membranes of magnesium-deficient rat skeletal muscle as consequences of free radical-mediated process.

Free radical-induced physiopathologies are generally thought to be mediated by membrane injuries. Using a pro-oxidant model induced by dietary magnesium deficiency, we have recently shown that skeletal muscle lesions occurred with a rise in the calcium level and enhanced free radical production. In this study, we investigated the physicochemical and biochemical properties of sarcoplasmic reticulum membranes isolated from hind limb muscles of weanling male rats pair fed magnesium-deficient or control diets for 12 d. The calcium-induced calcium efflux from preloaded vesicles was increased in membranes isolated from Mg-deficient rat muscle. In agreement with this latter observation, we demonstrated increased ryanodine binding affinity of the calcium channel. The Ca2(+)-ATPase activity of the pump was shown to be reduced. The viscosity state of the membranes, assessed by 1,6-diphenyl-1,3,5-hexatriene fluorescence anisotropy, was significantly increased in Mg-deficient membranes. Moreover, these membranes demonstrated an increased content of protein carbonyls as compared with controls. These functional as well as structural changes are closed to those described in sarcoplasmic reticulum membranes oxidatively modified in vitro. Together, these data fitted well with the concept that free radical-induced membrane damages resulting in calcium overload may be at the origin of skeletal muscle lesion during Mg-deficiency.

Animals↗
PubMed1996

Acceleration of retarded growth in children with Gaucher disease after treatment with alglucerase.

OBJECTIVES: The incidence and severity of growth retardation in children with type 1 Gaucher disease and the response to enzyme replacement therapy with alglucerase were studied. STUDY DESIGN: A retrospective analysis of growth in 99 children and adolescents with type 1 Gaucher disease before treatment, and in 54 of those subjects during treatment, was done. Growth was compared with gender, age, and dosage of replacement enzyme. RESULTS: Linear growth was normal in the first 1 to 2 years of life and then decelerated. Height was at or below the 5th percentile in 50% of all subjects immediately before treatment. The mean z score was -1.49 (95% confidence interval, -1.83 to -1.16), corresponding to the 6.8th percentile for height. Seventy-two percent were below the 50th percentile and 50% were at or below the 5th percentile for mid-parental height (p <0.001). One and one-half years after treatment was started, the estimated mean z score for all subjects was -1.01, which corresponds to the 16th percentile for height. Normal growth was achieved within 4 to 30 months in eight of nine subjects who were at or below the 5th percentile. It occurred only in those receiving higher doses (60 to 120 U/kg per 4-week period) of alglucerase. There was a significant association between z scores for height before treatment and liver enlargement (r= 0.57; p < 0.01). CONCLUSIONS: Half of the subjects who manifest type 1 Gaucher disease in childhood have growth retardation. Treatment with adequate amounts of modified enzyme replacement was effective in normalizing linear growth.

Adolescent↗
PubMed1996

Diets deficient in selenium and vitamin E affect plasma lipoprotein and apolipoprotein concentrations in the rat.

The present study examined the effects of Se, vitamin E and combined Se and vitamin E deficiencies in rats on plasma lipid, lipoprotein and apolipoprotein (apo) concentrations. Deficiencies were induced by feeding rats the respective diets for 6 weeks. The study shows that Se deficiency results in increased concentrations of plasma cholesterol and apo E. Both could be explained by an increase in the HDL1 fraction. Vitamin E deficiency alone had no significant effect on plasma lipid, lipoprotein and apo concentrations. Se deficiency in combination with vitamin E deficiency leads to an increase in plasma LDL and apo B concentrations. These results point to the need for further investigations on the mechanism by which Se deficiency affects lipoprotein metabolism.

Animals↗
PubMed1996

Lipid fluidity of triacylglycerol-rich lipoproteins isolated from copper-deficient rats.

Triacylglycerol-rich lipoproteins (TGRLP) were isolated from Cu-deficient and control rats. TGRLP from Cu-deficient rats appeared more fluid than those from controls as sensed by the fluorescence anisotropy of 1,6-diphenyl-1,3,5-hexatriene (DPH). This high fluidity was related to a low cholesterol:phospholipid ratio and high triacylglycerol content in these lipoproteins. TGRLP from Cu-deficient rats were more susceptible to in vitro peroxidation than lipoproteins from control rats as shown by the rate of diene conjugation. The damage induced by the peroxidation resulted in a more ordered state of the lipid fraction especially in lipoproteins from Cu-deficient rats. Thus, after in vitro peroxidation, TGRLP from Cu-deficient rats were more rigid than those from controls. These results suggest that Cu deficiency induces modifications in physicochemical properties of TGRLP which could affect their metabolism.

Animals↗
PubMed1996

Apolipoprotein B mRNA editing is preserved in the intestine and liver of zinc-deficient rats.

Apolipoprotein B (apo B) mRNA editing is a site-specific, post transcriptional cytidine deamination reaction that generates apo B48 in the mammalian small intestine and in the liver of certain animals. This reaction is mediated by an enzyme complex that includes the catalytic subunit apobec-1, a zinc-dependent cytidine deaminase. To determine the importance of zinc status to apo B mRNA editing in vivo, we examined the effects of experimentally induced zinc deficiency in rats upon hepatic and serum lipid levels and several indices of apo B gene expression. Rats were either given unlimited access to or were pair-fed a semipurified zinc-supplemented (30 mg Zn/kg) diet or were fed a zinc-deficient diet (approximately 1 mg Zn/kg) for 17 d. Significant differences were detected in the ratio of serum apo B100/B48 in the unlimited access, zinc-supplemented group compared with either zinc-deficient rats or pair-fed controls. There were no alterations in hepatic triglyceride and cholesterol concentrations, hepatic apo B mRNA abundance or apo B mRNA editing in either the small intestine or liver. Taken together, these data suggest that the altered ratios of serum apo B isomorphs seen in zinc deficiency are not mediated through changes in hepatic or intestinal apo B mRNA editing.

Animals↗
PubMed1995

Biosocial models of deviant behavior among male army veterans.

Measures of hormones (testosterone, cortisol and thyroxin) and of deviant or antisocial behavior are examined in a sample of 4179 Vietnam veterans. Hormone levels were found to vary with veterans' age, social status and race, and all three hormones were significantly related to deviant behavior. Biosocial models, combining hormonal variables with social background variables, tended to explain more variance in deviance than did traditional models based on social background alone. Several propositions regarding hormones and behavior were assessed. While the role of hormones in causing deviance remains unclear, it is argued that hormones should be included in models of deviant behavior.

Antisocial Personality Disorder↗
PubMed1995

QT prolongation and polymorphous ventricular tachycardia associated with trasodone-amiodarone combination.

Trasodone, a second generation antidepressant, has been shown to equal standard tricyclics in clinical efficacy while causing significantly fewer cardiac side effects. Although clinical trials have demonstrated a relatively safe arrhythmogenic profile, trasodone has been implicated in the pathogenesis of ventricular arrhythmias. This report describes a patient in whom the administration of trasodone in addition to previously well-tolerated long-term amiodarone therapy was associated with a marked prolongation of the QT interval and polymorphous ventricular tachycardia. Caution in the concurrent use of trasodone and other medications known to cause QT prolongation and polymorphous ventricular tachycardia is recommended.

Aged↗
PubMed1995

Magnesium deficiency modulates hepatic lipogenesis and apolipoprotein gene expression in the rat.

The present study was performed to determine the effects of magnesium (Mg) deficiency upon plasma lipoproteins and hepatic apolipoprotein gene expression in the rat. The most obvious effect of Mg-deficiency on plasma lipids is a marked increase in post-prandial triacylglycerol concentration. This increased triglyceridemia persists in fasted rats. Density gradient ultracentrifugation analysis revealed marked alterations in the distribution of plasma lipoproteins in Mg-deficient rats. An increase in triacylglycerol-rich lipoproteins (TGRLP) was associated with a significant increase in plasma apolipoprotein B (apo B) concentration and was accompanied by selective accumulation of apo B-48. A decrease in high-density lipoproteins (HDL) was accompanied by a corresponding decrease in plasma apo E concentration and a concordant decrease in hepatic apo E mRNA abundance and biosynthesis. Hepatic apo B-100 synthesis was reduced by over 75% in Mg-deficient animals despite an increase in hepatic apo B mRNA abundance. However, this change in hepatic apo B gene expression was not associated with alterations in posttranscriptional apo B mRNA editing. These changes in apolipoprotein gene expression were associated with increased hepatic lipogenesis, despite the observation that net triacylglycerol secretion rates were not different between Mg-deficient and control animals. Taken together, the data demonstrate a complex pattern of alterations in hepatic lipid metabolism and apolipoprotein gene expression in the Mg-deficient rat and suggest a defect in the catabolism rather than secretion of TGLRP as the major factor underlying the altered plasma lipoprotein profile.

Animals↗
PubMed1995

Hepatic apolipoprotein and LDL receptor gene expression in the genetically hypercholesterolemic (RICO) rat.

The present study was designed to examine apolipoprotein and LDL receptor gene expression in genetically hypercholesterolemic RICO rats. In the plasma of RICO rats as compared to SW (control) rats, the hypercholesterolemia (+41%) was associated with a significant increase in plasma apo B (+23%) and apo E (+68%) concentrations. Study of apolipoprotein synthesis in the liver has shown that this increase in plasma apo B and apo E concentrations was not associated with modification in their synthesis and mRNA levels. Study of apo E mRNA level in various tissues has shown only the modification in adrenals in RICO as compared to SW rats (2.7-fold increase). Study of LDL binding, LDL receptor mass and LDL receptor mRNA level in the liver of RICO and SW rats has shown no significant differences between these two strains. EDTA-resistant binding of rat LDL was lower in RICO than in SW rats suggesting that binding sites others than the LDL receptor are present in lesser amount in this hypercholesterolemic strain.

Adrenal Glands↗