Search PubMed⌕ Search

Biomedical subjects

A Rasheed

Publications and source records attributed to A Rasheed.

At least 37 records · Page 2Linked to original sources
PubMed1992

The relationship between reduction in periodontal inflammation and diabetes control: a report of 9 cases.

The established correlation between diabetes and periodontal diseases and the increasing prevalence of Type II diabetes in the general population indicate that dental practitioners will probably treat an increasing number of diabetic patients. Despite the fact that there is little scientific evidence to support the concept, it has been generally accepted that treatment for periodontal disease in diabetic patients may reduce insulin requirements and improve metabolic balance. However, to date no one has evaluated the effects of periodontal therapy on the metabolic state of the poorly-controlled diabetic patient. The purpose of this pilot study was to evaluate the effect of controlling gingival inflammation on blood glucose levels as determined by glycosylation of hemoglobin and albumin.

Blood Glucose↗
PubMed1992

Biopharmaceutical studies of spirobishexahydropyrimidine.

Oral administration of spirobishexahydropyrimidine showed an increase in the activity of serum transaminases, lactate dehydrogenase and alkaline phosphatase. Biological half life and other pharmacokinetic parameters showed rapid absorption and slow elimination of the drug.

Alanine Transaminase↗
PubMed1992

Identification and quantitative determination of morphine in the urine of heroin dependents.

Morphine in the urine of heroin addicts was identified by TLC using methanol, water, benzene and glacial acetic acid (80:15:15:5) and ethyl acetate, methanol and ammonium hydroxide (25:10:5) as solvent systems and potassium iodoplatinate and iodine as the developing reagents. Potassium iodate in alkaline medium gives a yellowish golden colour having maximum absorbance at 450 nm. By this reaction the minimum limit of identification and quantitative determination of morphine is 2 microg/ml. It provides a basis for the spectrophotometric determination of morphine in the urine of heroin addicts.

Journal Article↗
PubMed1991

Expression of O6-methylguanine-DNA methyltransferase in malignant human glioma cell lines.

When animals are treated with carcinogenic agents that alkylate O6-guanine residues, the incidence of tumors in specific tissues often relates inversely to the level of the DNA repair enzyme O6-methylguanine-DNA methyltransferase (MGMT) present in the tissue. Similarly, the hypersensitivity to anticancer chloroethylnitrosoureas of some human tumor cell lines is believed to result from their deficiency in MGMT. We have undertaken a comprehensive investigation of MGMT expression in a panel of nine characterized human glioma cell lines. Methyltransferase activity determined by incubating protein extracts of these glioma lines with [3H]methylated DNA ranged from undetectable in six lines (the Mer- phenotype) to greater than 0.8 pmol/mg in two lines (U-373 MG and D-392 MG). MGMT protein was undetectable in Western blots of the Mer- cell extracts probed with specific anti-MGMT monoclonal antibodies. Consistent with these results, steady-state levels of MGMT mRNA, determined by Northern blot analysis, were detectable only in the three Mer+ glioma lines (U-373 MG, D-392 MG, D-263 MG). Southern analysis of EcoRI-digested DNA probed with MGMT cDNA revealed no amplification, rearrangement or deletions of the MGMT gene in any of the glioma cell lines. This is the first report that examines MGMT expression at the biochemical, molecular and genetic levels in a particular tumor type. These studies suggest that transcriptional regulation is the basis of the Mer- phenotype in these malignant human glioma cell lines, since no gross structural or quantitative abnormalities of the MGMT gene were seen in the phenotypically Mer- lines.

Blotting, Northern↗
PubMed1990

A technique for one stage repair of complete palatal cleft.

A technique for repairing in one stage, wide complete palatal cleft of congenital origin with obvious shortening of the soft palate, is described. Mucoperiosteal flaps were obtained from vomer bone and palate while muco-muscular flap from posterior pharyngeal wall by means of a simple technique. A layer closure was used to fill in the palatal defect. This technique was used successfully in 24 out of 25 cases, with a mean follow-up of 2 years. When fully healed, the palate attained a normal shape and function.

Child↗
PubMed1990

Biopharmaceutical studies of 3-substituted isatin derivatives.

The metabolic fate of isatin hydrazone (Ia), isatin-3-thiosemicarbazone (Ib), isatin-3-semicarbazone (Ic), isatin-3-phenylhydrazone (Id), isatin oxime (Ie) and 3-hydroxy-3-acetonyl oxindole (II) was studied in rabbits. The compounds were administered orally in the dose of 300 mg/kg body wt. Isatin anthranilic acid, tryptophan and nicotinic acid were identified as the major metabolites excreted in urine. The 3-hydroxy-3-acetonyl oxindole (II) gave on additional metabolite, oxindole. The major metabolites were separated and identified unambiguously on thin layer silica gel plate. Metabolic pathways have been proposed to explain the biotransformation of the compounds investigated.

Animals↗
PubMed1977

Incubations of testis myo-inositol-1-phosphate synthase with D-(5-18O)glucose 6-phosphate and with H218O show no evidence of Schiff base formation.

myo-Inositol-1-P synthase (EC 5.5.1.4) purified from rat testis and from bovine testis was allowed to react with D-[5-18O]glucose-6-P. myo-Inositol, obtained in these reactions, retained all of the 18O originally in the glucose-6-P. When these enzyme preparations were incubated with unlabeled glucose-6-P in a medium enriched in H2 18O no uptake of the oxygen isotope occurred that could be ascribed to the myo-inositol-1-P synthase reaction. By these criteria this enzyme, which is considered to use an aldolase mechanism in the cyclization step, cannot form a Schiff base during the reaction. In addition, these enzymes are not inhibited by 10 mM EDTA. One interpretation of this evidence is that the myo-inositol-1-P synthases we have studied are neither Class I nor Class II aldolases, and simply use base catalysis in the cyclization step.

Animals↗
PubMed1973

Partial reactions of D-glucose 6-phosphate-1L-myoinositiol 1-phosphate cyclase.

After removal of tightly bound NAD(+) by using charcoal, a preparation of d-glucose 6-phosphate-1 l-myoinositol 1-phosphate cyclase catalysed the reduction of 5-keto-d-glucitol 6-phosphate and 5-keto-d-glucose 6-phosphate by [4-(3)H]NADH to give [5-(3)H]-glucitol 6-phosphate and [5-(3)H]glucose 6-phosphate respectively. The position of the tritium atom in the latter was shown by degradation. Both enzyme-catalysed reductions were strongly inhibited by 2-deoxy-d-glucose 6-phosphate, a powerful competitive inhibitor of inositol cyclase. The charcoal-treated enzyme preparation also converted 5-keto-d-glucose 6-phosphate into [(3)H]myoinositol 1-phosphate in the presence of [4-(3)H]NADH, but less effectively. These partial reactions of inositol cyclase are interpreted as providing strong evidence for the formation of 5-keto-d-glucose 6-phosphate as an enzyme-bound intermediate in the conversion of d-glucose 6-phosphate into 1 l-myoinositol 1-phosphate. The enzyme was partially inactivated by NaBH(4) in the presence of NAD(+). Glucose 6-phosphate did not increase the inactivation, and there was no inactivation in the absence of NAD(+). There was no evidence for Schiff base formation during the cyclization. d-Glucitol 6-phosphate (l-sorbitol 1-phosphate) was a good inhibitor of the overall reaction. It did not inactivate the enzyme. The apparent molecular weight of inositol cyclase as determined by Sephadex chromatography was 2.15x10(5).

Animals↗