Biomedical subjects

M A Kabir

Publications and source records attributed to M A Kabir.

6 recordsLinked to original sources

PubMed2006

Low T3 syndrome in psychiatric depression.

In euthyroid sick syndrome [non-thyroidal illness (NTI)], a number of investigators have described TSH and serum thyroid hormone abnormalities, low T3, low T3 and T4, increased T4, low TSH, etc. Those cases of NTI where there is only T3 decrease [and normal serum T4, free T4 (FT4), and TSH levels] are specifically referred to as low T3 syndrome. However, the information in regard to low T3 syndrome in psychiatric subjects who are clinically euthyroid and do not have any other systemic illness is scanty. In our facility, since thyroid function is routinely assessed in psychiatric patients at admission, this provided the opportunity to study low T3 syndrome in a large group of psychiatric patients. Out of 250 subjects with major psychiatric depression, 6.4% exhibited low T3 syndrome (mean serum T3 concentration 0.94 nmol/l vs normal mean serum concentration of 1.77 nmol/l). The low T3 levels could not be ascribed to malnutrition or any other illness and the metabolic parameters were all normal. Possible mechanisms contributing to low T3 are discussed. The depression might constitute an illness having the same relation to low T3 as found in the low T3 syndrome previously described in euthyroid sick subjects. The present findings, besides describing low T3 syndrome in psychiatric patients without systemic illnesses, suggest the possibility of subgrouping in clinical psychiatric depression which may have a broader clinical significance.

Major Depressive Disorder↗

PubMed2006

Tobacco consumption and its association with illicit drug use among men in Bangladesh.

AIMS: This study examined the association of tobacco consumption (smoking and chewing) with illicit drug use among Bangladesh males. DESIGN: Cross-sectional survey data from the Bangladesh Demographic and Health Survey 2004 were used. SETTING: Bangladesh. PARTICIPANTS: A total of 4297 males aged 15-54 years. MEASUREMENTS: Age, education, religion, marital status, place of residence; tobacco consumption such as cigarette and bidi smoking, chewing sada, pata, tobacco leaves, gul, betel quid with zarda; taking illicit drugs such as ganja, charas, heroin, pethedine, phensidyl; having sexually transmitted diseases (STDs). FINDINGS: Overall prevalence of tobacco consumption was 59%. Bidi smoking (29.6%), cigarette smoking (27.8%) and chewing betel quid with tobacco/zarda (17.5%) were predominant. Overall prevalence of illicit drug use was 4%. Ganja was the main drug (3%), followed by phensidyl (0.8%), heroin (0.3%) and charas (0.3%). Age, education, place of residence, marital status, having STDs, premarital and extra-marital sex were associated significantly with tobacco smoking. Almost all variables were also associated significantly with illicit drug use. Smoking cigarettes and bidi and eating tobacco leaves/shada pata/gul showed significantly positive associations with illicit drug use when adjusted for other variables. CONCLUSIONS: Tobacco consumption is common and associated positively with the illicit drug use among males in Bangladesh.

Adolescent↗

PubMed2000

Multiple copies of MRG19 suppress transcription of the GAL1 promoter in a GAL80-dependent manner in Saccharomyces cerevisiae.

A plasmid clone that suppresses galactose toxicity in a gal7 yeast strain has been isolated from a multicopy genomic DNA library. Molecular analysis revealed that the region responsible for the suppression of galactose toxicity corresponds to the ORF YPR030w, which was named MRG19. A CEN-based plasmid carrying the above ORF was unable to suppress the toxicity. Galactokinase activity was substantially reduced in cell extracts obtained from transformants bearing multiple copies of MRG19. Multiple copies of MRG19 were also able to suppress galactokinase expression driven by the CYC1 promoter but not the TEF1 promoter. Multiple copies of MRG19 could not suppress GAL1-driven galactokinase expression in a gal80 strain. However, MRG19-mediated suppression of CYC1-driven galactokinase expression was independent of GAL80 function. These results imply that multiple copies of MRG19 suppress galactokinase expression probably at the level of transcription. In agreement with this idea, multiple copies of MRG19 also suppress beta-galactosidase expression driven by the GAL1 promoter in a GAL80-dependent manner. Disruption of MRG19 leads to an increase in the cell density at stationary phase in synthetic complete medium. MRG19 encodes a previously uncharacterised 124-kDa protein that shows no sequence homology to any known proteins.

Chromosome Mapping↗

PubMed1999

Hepatobiliary dysfunction as the initial manifestation of disseminated cryptococcosis.

A case of hepatobiliary dysfunction as the initial manifestation of disseminated cryptococcosis is described. The patient was admitted with symptoms of hepatitis with cholestatic jaundice. Antibody tests for hepatitis B and C and human immunodeficiency virus were negative. The patient continued to deteriorate clinically. Eventually, the patient succumbed to hepatic failure. Autopsy disclosed systemic cryptococcosis that caused extensive necrosis of the liver. In review of the literature, only nine cases of cryptococcal infection presenting as hepatitis, cholangitis, and cholecystitis as initial manifestation were reported. Four of these patients had been subjected to exploratory laparotomy for clinical suspicion of acute abdomen. One patient developed cirrhosis as a result of cryptococcal hepatitis. Two patients succumbed to hepatic failure. Cryptococcosis is known to occur commonly in immunocompromised patients, yet only two reported cases presenting as hepatitis were associated with immunocompromised status.

Aged↗

PubMed1984

Ethanol feeding and thyroid hormone monodeiodination.

Adult male rats were placed on a 3 week regimen of ethanol (as 20% of total calories) in a nutritionally adequate diet, and controls were matched equicalorically without ethanol. Serum measurements of T4, T3, FT4, rT3, and TSH were performed in both the fed and the fasted state (18 hours). In the fed state, serum hormone measurements did not differ between control and ethanol-treated rats. Overnight fasting had a significant effect in decreasing serum T3 level in both experimental and control rats and in decreasing serum T4 level in ethanol-treated animals; FT4 and rT3 levels were not affected. Fasting also decreased in vitro hepatic T4 to T3 production to an equivalent degree in control and ethanol-treated rats, but did not alter hepatic T4 to rT3 production rates in control animals. In the fed state, hepatic rT3 neogenesis in animals given ethanol declined relative to the levels observed in control fed rats; fasting restored the depressed rT3 neogenesis to the levels noted in the fed state. Because decreased rT3 production in ethanol-treated rats in the fed state could not be explained on the basis of a change in 5'-deiodinase activity, it is suggested that ethanol administered with a nutritionally adequate diet may inhibit hepatic rT3 generation by inhibiting T4(5)-deiodinase.

Analysis of Variance↗

PubMed1984

Ethanol inhibition of pituitary-thyroid axis: an effect secondary to nutritional deficiency.

Ethanol as either 20% or 36% of total calories in a Lieber diet was administered to male rats. At these concentrations, ethanol consumption relative to body weight did not differ. Pair-fed controls were restricted to the amount of calories consumed by rats given ethanol. Under these conditions, a direct effect of ethanol on the hypothalamic-hypophyseal-thyroid axis could not be demonstrated. There were no differences between pair-fed control and ethanol treated rats in serum or pituitary TSH, TSH response to TRH, or T4 and T3 levels. On the other hand, in rats given ethanol as 36% of total calories ("36%" ethanol-treated), and in their pair-fed controls, a marked decrease in serum T4 levels occurred (25% and 30%), relative to the corresponding "20%" groups. The decreased T4 in the "36%" groups was associated with a pronounced fall in caloric intake, decreased serum TSH, and declines in adenohypophyseal and body weights -- all of which were of similar magnitude in experimental and control rats. Thus, inanition was probably the primary cause of reduced thyroid function in the "36%" groups. An interesting aspect of this change was the finding of no difference in serum T3 levels between pair-fed control and ethanol treated rats in the 36% and 20% groups despite the reduced T4 and caloric intake in 36% animals; the lack of decrease in T3 concentration in 36% animals may reflect augmented peripheral conversion of T4 to T3 or reduced T3 clearance.

Animals↗