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Biomedical subjects

J Kadowaki

Publications and source records attributed to J Kadowaki.

At least 19 recordsLinked to original sources
PubMed1998

Connatal Pelizaeus-Merzbacher disease: a missense mutation in exon 4 of the proteolipid protein (PLP) gene.

We investigated the proteolipid protein (PLP) gene in two brothers in a Japanese family with a connatal form of Pelizaeus-Merzbacher disease (PMD). Direct sequencing of the PLP gene revealed an A-to-T transition in exon 4, which led to an Asp-to-Val substitution at residue 202. Their mother was confirmed to be heterozygous for the mutation. The mutation was not found in 78 X-chromosomes of normal Japanese individuals. A correlation between the clinical severity of the disease in the brothers and the Asp202-to-Val mutation in the PLP gene was suggested.

Child↗
PubMed1994

[Glucocorticoid therapy for children with idiopathic nephrotic syndrome].

The glucocorticoid treatment of patients with idiopathic nephrotic syndrome in children was reported especially focused upon the dose of initial treatment and different effect of various glucocorticoids if they were used equivalently. It appeared that lower dose prednisolone; 40 mg/m2 bsa (body surface area) was also effective same as 60 mg/m2 bsa of protocol of ISKDC (International Study of Kidney Disease in Children) for the initial treatment if time for free proteinuria was taken as index. Therefore, it was considered favorable that we could use lower dose to avoid various adverse effects of glucocorticoids. Clinically it was felt that some different effects were present despite of their equivalent use. The equivalency of various glucocorticoids was based upon anti-inflammatory effect experimentally. The etiology of idiopathic nephrotic syndrome has not been well known, however some sort of immune disorder has been thought most important. Therefore, it might be acceptable if effect of glucocorticoid treatment of nephrotic syndrome is evaluated on the basis of immunosuppression. It is hoped that these empirically proven evidence should be analysed fundamentally in the near future.

Adolescent↗
PubMed1992

In vitro glucoregulation of prolactin secretion.

In this study we have examined the direct glucoregulation of prolactin secretion from normal anterior pituitary cells in vitro and have found that changes in medium glucose concentration regulate the amount of prolactin released. Nature and/or degree of this response to glucose was influenced by some effect, long-lived in vitro, which was correlatable to serum insulin levels. When the cells were derived from animals with mean low-normal serum insulin levels, there was a stimulation of prolactin secretion by hypoglycemia, the response was rapid, transient, dose-dependent, and could be duplicated by 2-deoxyglucose. When the cells were derived from animals with a higher mean serum insulin level, the prolactin secretion from the cells was slowly, adversely affected by hypoglycemia. Conversely, elevated glucose caused a depression in prolactin secretion in the first group and a stimulation of prolactin secretion in the second. We conclude (1) that modulation of glucose levels in vitro regulates prolactin release from pituitary mammotrophs and (2) that this glucose regulation of prolactin release is in turn coregulated with or regulated by insulin.

Animals↗
PubMed1984

Mammotroph autoregulation: uptake of secreted prolactin and inhibition of secretion.

A dissociated preparation of normal adult rat pituitary cells has been used to study PRL autoregulation at the level of the mammotroph . Female rat pituitary cells previously cultured for 48 h on polylysine-coated petri dishes were washed to remove serum and accumulated PRL and then incubated in fresh medium in the absence or presence of increasing concentrations of rat PRL. Accurate balance sheets, allowing for degradation and nonspecific adsorption of PRL, showed exogenous PRL to regulate the amount of PRL released by the cells. That this regulation was partly produced by uptake of secreted PRL from the medium was demonstrated by supplementing the medium with [125I]iodo-rat PRL. Inhibition of secretion also played a role and was implied by experiments showing that ease of reversal of the inhibition was inversely proportional to the density of cell culture, which was itself proportional to the amount of PRL in the medium and the duration of autoregulation. These results indicate that normal adult rat pituitary cells in primary culture are capable of regulating the amount of PRL in their external milieu and that uptake of already secreted PRL is an important component of the regulatory mechanism.

Animals↗
PubMed1977

Dermatoglyphs of Klinefelter's syndrome.

The dermatoglyphs of 28 Japanese with Klinefelter's syndrome [24 XXY; 2 XXYY; 1 XXXY; 1 XXXXY] were compared with 544 male and 129 female controls. These patients showed high frequencies of fingertip arches pattern, right third interdigital loops, right hypothenar patterns (Lr) and line C terminating 0 in the right hand. The mean summed a-b ridge count of Klinefelter's syndrome patients was significantly lower than that of the male controls. We suggest that an increase in the number of X or Y chromosomes decreased the a-b ridge count in a similar way to the decrease in total finger ridge count.

Adolescent↗
PubMed1975

Hepatitis-associated (Australia) antigen and Down's syndrome.

Hepatitis-Associated (Australia) Antigen (HAA) was detected in 13 (5.8%) of 223 patients with Down's syndrome and in 14 (3.7%) of 378 patients with other forms of mental retardation. The frequency of HAA was 2.4 per cent in 127 noninstitutionalized patients with Down's syndrome, and 10.4 per cent in 96 institutionalized patients. The frequency of HAA with Down's syndrome was lower on the average in Japan than in the United States or Germany. HAA was detected in one (1.3%) of 78 mothers of infants with Down's syndrome. Our study suggests that maternal exposure to HAA, as reflected by the presence of either HAA or anti-HAA, was not associated with the subsequent birth of an infant with Down's syndrome.

Adolescent↗