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Biomedical subjects

S Abid

Publications and source records attributed to S Abid.

9 recordsLinked to original sources
PubMed1991

Yet another cause of chronic viral hepatitis?

The clinical features, course and histology of liver in 20 patients; mostly middle aged to elderly females, closely resembling chronic Non A Non B hepatitis is presented. They presented quite late in their disease and therefore, complications such as variceal bleeds, ascites and encephalopathy were frequent. Our patients were negative for hepatitis B and C virus serology. Metabolic and immune causes of chronic liver disease were also ruled out. To the best of our knowledge, this is the first study of its kind elaborating the clinical features, course and histology of liver in chronic Non B Non C hepatitis and raises a number of questions as to the nature of the infecting virus and the epidemiology of disease.

Chronic Disease↗
PubMed1991

Supervised training of practical procedures in the internal medicine residency.

In order to get feedback whether the medical residents are getting adequate supervised training to perform practical procedures, a questionnaire was distributed among the residents asking their involvement in sixteen frequently performed procedures in the medical unit of the Aga Khan University Medical Centre. Though the residents were satisfied about their training in doing lumbar punctures, pleural and peritoneal aspirations, bone marrow aspiration and trephine and chest tubes placement, they showed their concern about training in putting central lines, venous cut downs, cardiac pacing and biopsies. A better schedule training programme, organized subspecialty rotation, continuous evaluation of resident's skill, credentialing procedures and willingness on the part of faculty to teach and residents to learn may improve the training.

Internal Medicine↗
PubMed1990

Protection against gentamicin-induced early renal alterations (phospholipidosis and increased DNA synthesis) by coadministration of poly-L-aspartic acid.

Coadministration of polyaspartic acid protects against functional and pathological signs of gentamicin-induced nephrotoxicity in rats without reduction of drug accumulation in renal cortex (Williams et al., J. Pharmacol. Exp. Ther. 237: 919-925, 1986; Gilbert et al., J. Infect. Dis. 159: 945-953, 1989). We have assessed the influence of polyaspartic acid on the early alterations induced in kidney cortex by gentamicin, namely the lysosomal phospholipidosis and the increase in cell turnover. We used an infused rat model in which animals received a total dose of 100 mg/kg of gentamicin over 12 hr. Renal cortex was examined 2 hr (day 0) and 48 hr (day 2) after treatment. All animals received an injection of [3H]thymidine (200 microCi i.p.) before sacrifice. Coadministration of polyaspartic acid (drug-polypeptide mass ratio 1:2.5) did not modify the drug serum levels, as recorded during or shortly after the infusion. Yet, it was associated with 1) an increased (approximately 35%) drug cortical content at day 0; 2) a significant protection against both biochemical (decrease of sphingomyelinase activity at day 0; increase of lipid phosphorus content at day 2) and morphological (enlargement of lysosomes and deposition of myeloid bodies at day 2) signs of lysosomal phospholipidosis in proximal tubular cells; and 3) an almost complete protection against increased cell turnover (mostly in proximal tubules) in cortex at day 2, as assessed by the measurement of [3H]thymidine incorporation into DNA and the enumeration of S-phase cells after histoautoradiography. In addition, morphological studies revealed a larger number of apical vacuoles in proximal tubular cells of animals receiving polyaspartic acid alone (but not in combination with gentamicin), and the deposition of osmiophilic, homogenous material in the lysosomes of animals receiving the combination of gentamicin and polyaspartic acid. Together with the results reported in two companion papers (Kishore et al., J. Pharmacol. Exp. Ther. 867-874, and 875-885, 1990), these results provide evidence that protection afforded by polyaspartic acid extends to the earliest cellular alterations described in kidney for gentamicin, namely the lysosomal phospholipidosis, suggesting that this protecting agent exerts blocking effect from this step in the cascade of events relating drug cortical accumulation to renal toxicity.

Animals↗