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Biomedical subjects

M N Musa

Publications and source records attributed to M N Musa.

At least 19 recordsLinked to original sources
PubMed1998

Haemophilus influenzae meningitis in Malaysia.

OBJECTIVE: To determine the pattern of postneonatal childhood meningitis in Malaysia. METHODS: Retrospective cross-sectional study involving five pediatric departments in Malaysia. RESULTS: There were 435 cases of clinical meningitis admitted to the five centers. More than 90% of the patients were <5 years old, and one-half were <6 months of age. The estimated overall incidence of childhood meningitis in the first 5 years of life was 76.7 per 100000 per year. However, of the 435 cases only 71 (16.3%) fulfilled laboratory diagnostic criteria and in only 58 of these was an organism isolated. Nearly one-half (48%) of all bacteriologically proved cases were caused by Haemophilus influenzae type b (Hib). The mortality rate was 12.5% and 21 patients (30%) suffered neurologic sequelae. CONCLUSIONS: More than one-half of all cases of culture-positive childhood bacterial meningitis were caused by Hib, although successful isolation of a pathogen occurred in only a small proportion of cases. For this reason the true incidence of Hib meningitis in Malaysia remains unknown. These findings are consistent with previous studies in Malaysia.

Child↗
PubMed1995

Patulin-induced inhibition of protein synthesis in hepatoma tissue culture.

Patulin is a mycotoxin produced by several species of fungi and is commonly found in fruits. It is regulated in several countries at a tolerance level of 50 micrograms/Kg. We investigated its ability to inhibit cell growth in hepatoma tissue culture and its ability to inhibit protein synthesis. It was found to be cytostatic at concentration of 1 microgram/mL (6.4 microM). It inhibits protein synthesis by two mechanisms: inhibition of amino acid uptake into the cell and their incorporation into proteins. The former mechanism appears to be more significant than the latter. This is consistent with previous work showing the ability of patulin to perturb plasma membrane function.

Animals↗
PubMed1994

On mixtures of three normal populations caused by monogenic inheritance: application to desipramine metabolism.

For a mixture of three normal distributions, which represent genotypes AA, Aa and aa, a method of estimation of the seven unknown parameters is proposed which works well whenever the phenotype (aa) is sufficiently well separated from the phenotype (AA, Aa). It is based on p-values of Kolmogorov's test of goodness of fit to normality. Initial parameter values for this iterative algorithm can be found by visual check and/or by using the EM algorithm. In an example of a data set of size 59 from a study of the metabolic rate of desipramine, the usefulness of this method is demonstrated. Extensions to more complex situations are feasible and are indicated at the end.

Adolescent↗
PubMed1994

Pharmacogenetics of desipramine metabolism.

There is wide interindividual variation in steady-state plasma concentration of desipramine and other tricyclic antidepressants primarily due to differences in rates of hydroxylation. Several studies have shown that the rate of hydroxylation of desipramine is correlated with the rate of hydroxylation of the genetic probe drug, debrisoquine, which is controlled by monogenic inheritance. However, no population studies of the polymorphic metabolism of antidepressants have been reported. In this study, 59 patients with endogenous depression received a fixed dose of desipramine and the steady-state plasma concentration of desipramine and 2-hydroxydesipramine were determined by high-pressure chromatography. A new statistical approach based on optimizing the fit to a specific stochastic model was utilized to separate the mixture of the three genotypes: homozygous extensive (AA), heterozygous extensive (Aa) and poor (aa) metabolizers. The proportions of the genotypes are 0.43, 0.45 and 0.12, respectively. The gene frequency of the low-activity allele is 0.34 and that of the high-activity allele is 0.66. The means (SD) of the desipramine/2-hydroxydesipramine metabolic ratios of the three genotypes are 1.71 (0.44), 3.32 (1.68) and 23.32 (10.03). These data suggest that the heterozygous genotype has half the metabolic activity of the homozygous extensive metabolizer and that the poor metabolizer genotype has negligible metabolic activity.

Adolescent↗
PubMed1989

Nonlinear kinetics of trimipramine in depressed patients.

An increase of the dose of trimipramine (TM) results in a markedly disproportionate increase of the steady-state plasma concentration of the major active metabolite desmethyltrimipramine (DMT). Ten patients receiving 75 mg/day of TM had a mean steady-state plasma concentration of 53.8 ng/ml TM and 26.3 ng/ml DMT. Ten others receiving 150 ng/ml TM had a mean concentration of 122.5 ng/ml TM and 133.8 ng/ml DMT. This is most likely due to the saturation within therapeutic dosage range of the subspecies of cytochrome P-450 responsible for hydroxylation of DMT. Available data on metabolism of tricyclic antidepressants shows that the hydroxylation of desmethylimipramine (desipramine) but not that of desmethylamitriptyline (nortriptyline) reaches saturation within therapeutic dosage range. Clinicians should take into consideration the possibility of dose-dependent kinetics when adjusting the dose of tricyclic antidepressants. This finding highlights the value of monitoring of blood levels of antidepressants.

Adult↗
PubMed1988

Sleep apnea following withdrawal of amitriptyline.

A 41-year-old man developed sleep apnea following abrupt cessation of amitriptyline. Cessation of antidepressants may result in excessive release of acetylcholine, which increases REM sleep. This in turn increases disordered breathing time and decreases nocturnal oxygenation. Sleep apnea did not recur when amitriptyline was reinstated and later gradually discontinued.

Adult↗
PubMed1978

Phenobarbital--thioridazine interaction in man.

Plasma thioridazine levels were estimated in seven retarded patients during the course of gradual phenobarbital withdrawal. In each patient, plasma levels of thioridazine plus metabolites increased with decreasing phenobarbital dose. Possible mechanisms of the interaction are discussed.

Adult↗