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Biomedical subjects

M Fujioka

Publications and source records attributed to M Fujioka.

At least 307 records · Page 17Linked to original sources

The sphenoidal sinuses: radiographic patterns of normal development and abnormal findings in infants and children.

Developmental patterns of sphenoidal sinuses were determined from lateral radiographs of 1702 patients from newborn to 15 years of age. Pneumatization of the conchal sinuses was seen as early as 6 months of age; 90% showed sphenoidal sinus pneumatization by 4 years of age; 100% by 10 years of age. Extension of pneumatization into the basisphenoid may be evident after 4 years of age, and 95% showed basisphenoidal pneumatization after age 12. An apparent lack of pneumatization of the sphenoidal sinuses in patients over 10 should stimulate investigation for sphenoidal sinus disease. Although isolated sphenoidal sinus abnormalities were rare, sphenoidal sinus involvement was common (67--75%).

Adolescent↗

Primary IgA glomerulonephritis and Schönlein-Henoch purpura nephritis: Clinicopathological and immunohistological characteristics.

A comparative analysis on clinicopathological and immunohistological characteristics was performed of 205 cases with primary IgA nephritis and 35 with Schönlein-Henoch purpura nephritis (purpura nephritis). Diagnostic criteria for primary IgA nephritis were set out so that IgA was either the most prominent immunoglobulin or, at least, equal to IgG and/or IgM, if present, irrespective of mesangial or peripheral localization. In primary IgA nephritis, one half of the cases were discovered by asymptomatic proteinuria, and one-third presented recurrent upper respiratory tract infection and gross hematuria, one-fourth abdominal pain and a few cases joint pain, while purpura nephritis was associated with a significantly higher incidence of such systemic symptoms as abdominal and joint pains, in addition to purpura. Both diseases shared a tendency toward conspicuous hematuria in contrast to the modest proteinuria, with normal renal function in three-fourths to two-thirds. Moreover, four of 35 with purpura nephritis showed preceding proteinuria and had been regarded as primary IgA nephritis until purpura appeared. The glomerular pathology had a common feature in that there was frequent occurrence of mesangial proliferative and focal and segmental lesions. The immunohistology in the two diseases was indistinguishable with regard to the glomerular immunoglobulins and mediators, whether purpura was present or absent. Thus, we propose a unifying concept that, by analogy with SLE, primary IgA nephritis may be regarded as 'sine lupo,' lying on one side of the nosological spectrum with less systemic symptoms, whereas purpura nephritis may occupy the other side with more systemic aspects. Furthermore, we confirmed the epimembranous granular deposition of IgA in both diseases as the most characteristic morphological expression of circulating immune complexes.

Adolescent↗

Saccharopine dehydrogenase. Substrate inhibition studies.

In the direction of reductive condensation of alpha-ketoglutarate and lysine, saccharopine dehydrogenase (N6-(glutar-2-yl)-L-lysine:NAD oxidoreductase (lysine-forming) is inhibited by high concentrations of alpha-ketoglutarate and lysine, but not by NADH. NAD+ and saccharopine show no substrate inhibition in the reverse direction. Substrate inhibition by alpha-ketoglutarate and lysine is linear uncompetitive versus NADH. However, when the inhibition is examined with alpha-ketoglutarate or lysine as the variable substrate, the double reciprocal plots show a family of curved lines concave up. The curvature is more pronounced with increasing concentrations of the inhibitory substrate, suggesting an interaction of variable substrate with the enzyme form carrying the inhibitory substrate. These inhibition patterns, the lack of interaction of structural analogs of lysine such as ornithine and norleucine with the E-NAD+ complex (Fujioka M., and Nakatani, Y. (1972) Eur. J. Biochem. 25, 301-307), the identity of values of inhibition constants of alpha-ketoglutarate and lysine obtained with either one as the substrate inhibitor, and the substrate inhibition data in the presence of a reaction product, NAD+, are consistent with the mechanism that substrate inhibition results from the formation of a dead-end E-NAD+-alpha-ketoglutarate complex followed by the addition of lysine to this abortive complex.

Ketoglutaric Acids↗