Biomedical subjects

M M Jadaon

Publications and source records attributed to M M Jadaon.

3 recordsLinked to original sources

PubMed2005

HR2 haplotype in Arab population and patients with venous thrombosis in Kuwait.

BACKGROUND: Venous thromboembolism (VTE) occurs due to a number of hereditary and acquired disorders of hemostasis. A recently identified polymorphism in factor V gene (A4070G; named HR2) has been reported to be a possible risk factor for the development of VTE, with a high prevalence of 9.5%-15.2% in patients of different ethnic groups in different parts of the world. However, the prevalence of HR2 has not yet been tested in VTE patients of Arab ethnicity. OBJECTIVES: To study the prevalence and possible risk of HR2 haplotype in Arabs. PATIENTS/METHODS: Exactly 188 VTE patients and 100 healthy subjects, all being of Arab ethnicity, were examined for HR2 using Polymerase chain reaction, restriction fragment length polymorphism and agarose gel electrophoresis. RESULTS: Data showed that 31 patients and seven healthy subjects had HR2 haplotype, with a prevalence of 16.5% and 7%, respectively. Furthermore, 43 patients (22.9%) had more than one risk factor for VTE. CONCLUSIONS: The prevalence of HR2 in Arabs is quite high, with a 2.62-fold greater risk of developing VTE. Moreover, coexistence of two or more genetic/acquired defects of VTE is quite common in Arab patients.

Arabs↗

PubMed2005

Megaloblastosis: from morphos to molecules.

OBJECTIVE: Megaloblastosis (i.e., megaloblastic transformation of erythroid precursor cells in the bone marrow) is the cytomorphological hallmark of megaloblastic anemia resulting from vitamin B12 and folate deficiency. It is characterized by a finely stippled lacy pattern of nuclear chromatin, which is believed to be an expression of deranged cellular DNA synthesis. However, the molecular basis of these cytomorphological aberrations still remains obscure. The current presentation describes the results of our studies on some molecular events associated with the development of megaloblastosis. METHODS: Transmission electron microscopy was used to study megaloblasts as well as DNA fibers extracted from megaloblastic and normoblastic bone marrows with and without treatment with proteinase K during the extraction procedure; cellular DNA synthesis in bone marrow cultures was studied by incorporation of 3H-thymidine and deoxyuridine suppression test, while histone biosynthesis in bone marrow cells was studied by in vitro incorporation of 3H-tryptophan, 3H-lysine and 3H-arginine into histones. RESULTS: Derangement of DNA synthesis occurred due to an impaired de novo pathway of thymidylate synthesis in both vitamin-B12- and folate-deficient human megaloblastic bone marrows as well as in the bone marrows of rhesus monkeys and rats with experimentally induced folate deficiency. Interestingly, folate-deficient monkeys developed frank megaloblastic bone marrows, but folate-deficient rats did not. On the other hand, megaloblastic changes in the bone marrow of human patients with myelodysplastic syndrome and erythroleukemia were not associated with this DNA synthetic abnormality. Biosynthesis of predominantly arginine-rich histones in megaloblastic bone marrows was markedly reduced as compared to normoblastic bone marrows, which was consistently associated with elongation and despiralization of chromosomes and finely stippled nuclear chromatin in megaloblasts. CONCLUSION: The impaired biosynthesis of predominantly arginine-rich nuclear histones appeared to be a common molecular event (a denominator) underlying the development of megaloblastosis with or without abnormal DNA synthesis.

Adolescent↗

PubMed1997

Zinc and liver cirrhosis: biochemical and histopathologic assessment.

Experimental liver cirrhosis was produced by administration of thioacetamide. Cirrhotic animals were divided into two groups: one group was given zinc sulphate and the second kept as cirrhotic control. Zinc-treated animals showed a restoration of normal hepatic and plasma zinc and copper levels. Similarly, plasma levels of aspartate aminotransferase, alanine aminotransferase, gamma-glutamyl aminotransferase, and total bilirubin decreased significantly. Light microscopic studies showed that most of the hepatocytes appeared normal in zinc-treated as compared with untreated cirrhotic animals. The amount of fibrin, reticulin, and collagen, which was high in the cirrhotic livers, decreased following zinc treatment. Staining with periodic acid Schiff's reagent showed the ability of hepatocytes to store glycogen after zinc treatment. These results revealed that zinc may have some beneficial effect in the treatment of liver cirrhosis.

Alanine Transaminase↗