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Biomedical subjects

M Hamza

Publications and source records attributed to M Hamza.

At least 91 records · Page 5Linked to original sources
PubMed1987

[A new form of metaphyseal chondrodysplasia].

The authors report a new form of metaphyseal chondrodysplasia revealed in a 5 1/2 year-old boy with seizures. This disorder associated coxa vara, large terminal phalanges, bilateral cataracts and severe mental deficiency. Both parents were healthy, suggesting autosomal recessive transmission. There is no associated calcium phosphate metabolism disorder. An enzymatic abnormality might be the cause of the bone, ocular and neuronal lesions.

Bone and Bones↗
PubMed1987

Large artery involvement in Behçet's disease.

Ten (2.2%) of 450 patients with Behçet's disease seen over a 10 year period had arterial manifestations. This was demonstrated by occlusion of radial and superficial femoral arteries in 3, aneurysm of subclavian, innominate, common and external iliac arteries and abdominal aorta in 4, both occlusion and aneurysm of pulmonary, external iliac and renal arteries in 3. All patients were male except one. Their ages ranged from 24-36 years with a mean age of 30 +/- 5 years.

Adult↗
PubMed1986

[Renal and digestive amyloidosis and Behçet's disease. Apropos of a case].

The authors report the case of a 33-year old male Tunisian who, 7 years after the onset of complete Behçet's disease (diagnosed on international criteria) developed a nephrotic syndrome diagnosed as renal amyloidosis on histological evidence. Attenuation of Congo red staining by potassium permanganate pointed to AA type amyloidosis. Despite treatment with colchicine and cyclophosphamide the patient's condition deteriorated. Amyloid deposits were found in a small bowel biopsy performed for persistent diarrhoea. The patient died 3 years after amyloidosis was diagnosed. The authors have reviewed the literature concerning this exceptional association: in all cases where it was typed the amyloidosis was AA. Attention is drawn to the failure of colchicine in this patient.

Adult↗
PubMed1985

Action of hemicholinium-3 on phospholipid metabolism in Krebs II ascites cells.

Incorporation of [Me-14C]choline or/and [2-14C]ethanolamine into phospholipids of Krebs II ascites cells in toto have been tested in the presence of hemicholinium-3. With [Me-14C]choline, labelling of cell pellet, intracellular choline, phosphocholine and total lipid extract is inhibited by hemicholinium-3 in a dose-dependent way between 6.25 X 10(-6) M and 10(-3) M. These effects are caused by a diminution of the choline or/and ethanolamine transport across the cell membrane and by a choline-kinase inhibition. In Krebs cells, choline is taken up by a low affinity Na+ sensitive uptake system (KT = 46 X 10(-6) M) which is competitively inhibited by hemicholinium-3 (KTi = 161 X 10(-6) M). Krebs cells exert a counter-transport (i.e. an exchange of choline across the membrane) against a concentration gradient of 10 mM choline whereas 10 mM hemicholinium-3 has no effect. Choline-kinase is also inhibited (I50 = 57 X 10(-6) M) in Krebs cells in toto and time-course data suggest that choline transport and phosphorylation might be tightly coupled. Specific radioactivities of phosphocholine and choline-glycerophospholipids decrease owing to the effect of the drug on the uptake and phosphorylation system. With 4 X 10(-5) M hemicholinium-3 and [Me-14C]choline as a marker, labelled choline-glycerophospholipids are decreased by 22%. With [2-14C]ethanolamine, labelled ethanolamine-phospholipids are decreased by 26% and choline-glycerophospholipids remain unlabelled. With the two markers, the additional effect produces a 35% decrease. It is concluded that hemicholinium-3 might be able to induce a depression of the intracellular choline and phosphocholine pool which could provoke a serious quantitative deficiency of major phospholipids in Krebs cells.

Animals↗
PubMed1985

Carrier-mediated choline uptake by Krebs II ascites cells.

Krebs II ascites cells have a low affinity uptake system for choline (Km = 36 microM, Vm = 76 nmol/min per 2 X 10(8). Choline entered the cells and was rapidly phosphorylated (95% of total intracellular soluble label). Trans acceleration of labeled choline from cells preloaded with radiolabeled choline and postincubated in the presence of unlabeled choline indicates that choline transport in Krebs II ascites cell is carrier mediated. Ethanolamine competed for the choline carrier. The uptake was reduced by hemicholinium-3, iodoacetamide and ouabain. The mechanism of choline transport in Krebs II ascites cells is in agreement with a linear transport model.

2,4-Dinitrophenol↗