Biomedical subjects

M Hafez

Publications and source records attributed to M Hafez.

77 records · Page 5Linked to original sources

PubMedDate not supplied

Histochemical studies of renal biopsies of nephrotic children.

Histopathological and histochemical studies were done on renal biopsies taken from twenty nephrotic children and thirty Albino rats of which fifteen were rendered nephrotic by the intravenous injection of nephrotoxic serum and the other fifteen served as controls. There were reduced activities of succinic dehydrogenase, alkaline phosphatase, acid phosphatase and non-specific esterases enzymes. These changes may be secondary to the insult which caused the nephrotic syndrome, or the result of the heavy proteinuria. In conclusion, a derangement in carbohydrate metabolism may underlie the disturbed metabolism of the basement membrane, the distortion of the foot-processes, and the tubular dysfunction.

Acid Phosphatase↗

PubMedDate not supplied

Clinico-immunogenetic study on Egyptian multicase tuberculous families.

Thirteen multicase Egyptian families (having more than one sib affected) with pulmonary tuberculosis have been studied. They include 26 parents (4 were tuberculous) and 53 sibs (30 tuberculous and 23 healthy). For all of them the following have been carried out: (a) Clinical, radiological, and bacteriological examination for diagnosis and evaluation of the disease severity; HLA-antigen determination using 9(A), 16(B) and 6(DR) antigens. The analysis of data revealed: (1) high incidence of tuberculosis among sibs in families having A2 B5 in their haplotypes compared to those having A2 X or B5 X--affected sibs with A2 B5 showed more severe manifestations than those having only one of the two antigens; (2) aggregation of HLA concordance among the sib pairs, both fully identical and haploidentical, while none of the sib pairs is non-identical; (3) Lod score studies showed linkage between the genetic control of susceptibility to pulmonary tuberculosis and HLA; (4) identity by descent study confirms the dominant pattern of transmission. The recommendation is that in a clinical setting of genetic counselling healthy individuals having either A2 or B5 antigens in their haplotypes should be vaccinated with BCG. Furthermore tuberculous patients having these HLA antigens should be managed aggressively, especially those having A2 B5 haplotypes in whom the disease is likely to run a severe course.

Adolescent↗

PubMedDate not supplied

Evidence of HLA-linked susceptibility gene(s) in primary congenital glaucoma.

The study included 82 individuals. Twenty-two were sporadic unrelated patients with Primary Congenital Glaucoma (PCG), and 60 were the members of 10 multiplex families. They were enrolled into two groups; GI:10 multiplex families; GII:32 unrelated patients with PCG (22 sporadic plus 10 probands of the multiplex families). The following were carried out for all the individuals: (1) detailed history; (2) ophthalmologic examination for diagnosis of PCG; (3) clinical examination to exclude any other disease; (4) HLA antigen typing using 30 antigens, 9 for A locus, 15 for B locus, and 6 for DR locus. Genetic and statistical analysis revealed the following: (1) significant association between HLA-B8 and PCG; (2) family studies revealed a susceptibility gene, probably recessive, predisposing to PCG; (3) this gene is linked to HLA, with strong linkage disequilibrium with B8.

Disease Susceptibility↗

PubMedDate not supplied

Evidence of HLA-linked susceptibility gene(s) in respiratory distress syndrome.

In a prospective study 101 newborns were enrolled into four groups: Group I included 38 unrelated newborns suffering from RDS and four sets of twin sibs (seven of whom had RDS; Group II included prematures free from RDS and any other disease; Group III included 21 newborns) delivered by C.S. and free from RDS and any other disease; Group IV included 20 infants of diabetic mothers free from RDS. HLA antigens were typed for all the newborns. The analysis of results could be summarized as follows. (1) Strong association between A3 antigen (RR = 19.4, WY2 = 59.8, S = 0.599) and B14 antigen (RR = 14.1, WY2 = 50.7, S = 0.489) and RDS. (2) HLA haplotypes were identical in twins sibs suffering from RDS and nonidentical in twins when one sib had RDS and the other is free. (3) The frequencies of A3 and B14 among the other three groups were insignificantly different from the general population and highly significantly low compared to RDS group. In conclusion, the development of RDS depends probably on the presence of susceptibility gene(s) in linkage disequilibrium with A3 and B14 antigens. Environmental factors, magnified by prematurity, in such susceptible newborns affect the production of surfactant leading to the development of RDS.

Disease Susceptibility↗

PubMedDate not supplied

Clinical, biochemical and histochemical studies on infants with Acrodermatitis enteropathica chronica.

7 infants diseased with Acrodermatitis enteropathica and 10 normal controls were included in this study. The values of anthranilic acid glucuronide, 6- aminohippuric, anthranilic acid, N-acetyl Kneurine, Kneurine and 30 H Kneurenine, were estimated in mg/24 hours urine, both basal and after tryptophane load. In addition, histopathological and histochemical studies for lactase, succinic dehydrogenase, alkaline phosphatase, acid phosphatase, and alpha-non-specific esterases activities were done for the intestinal mucosal biopsies. All the previous investigations were then repeated after two months treatment with 500 mg/day diiodohydroxyquinoline. The tryptophan metabolites were significantly low in the diseased infants, both basal and after tryptophan load. Moreover, the intestinal enzymes activities were altered. After 2 months treatment with diiodohydroxyquinoline the diseased infants became clinically improved, tryphtophan metabolites became normal, but the activities of the intestinal enzymes were not altered. The biochemical and histochemical findings were discussed, giving the possibility of competitive inhibition of the diiodohydroxyquinolines and the by-product 8 OH Quinololic acid resulting in more degradation of Kneurine and 3 OH Kneurenine to nicotinamide adenine dinucleotide.

Acrodermatitis↗