Human respiratory nasal mucosa in progressive systemic sclerosis (scleroderma). An electron microscopic study.

The fine structure of the respiratory nasal mucosa in cases of systemic scleroderma was studied in 5 patients. The cilia were absent in all the sections examined, and the epithelium showed characteristic morphological details. Absence of the mucous elements in the sero-mucinous glands was noticed with evidence of increased activity of the serous units. The capillaries and small arterioles showed severe changes. Electron-dense deposits were seen within the various constituents of the nasal mucosa. It was assumed that the characteristics of the disease are dependent on individual reactivity of a genetically determined immune system stimulated by an undetermined factor.

Histochemical and histopathologic studies of alveolar mucosa under complete dentures.

An investigation was made of the enzymatic, histochemical, and histopathologic characteristics of clinically healthy edentulous mucosae of non-denture wearers. The effects of dentures on the oral mucosa were examined and related to the length of time that dentures were worn. Succinodehydrogenase, acid phosphatase, and alkaline phosphatase enzymes were used along with periodic acid Schiff's stain. Hematoxylin and eosin stain was used for the histopathologic study. The results indicated that a denture stimulates the underlying mucosa for the first 3 years. A healthy mucosa results, showing slight hyperkeratinization and increased enzymatic activity. After 3 years there are atrophic changes which can lead to inflammatory changes. There is also a reduction in enzyme activity associated with wearing dentures for more than 3 years. Remaking the dentures after 3 years increases the enzymatic activity of the alveolar mucosa.

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.

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.