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Biomedical subjects

S Tomisawa

Publications and source records attributed to S Tomisawa.

13 recordsLinked to original sources
PubMed1999

Apolipoprotein E epsilon 4 allele and nephrotic glomerular diseases in children.

Hyperlipidemia is a well-recognized complication of the nephrotic syndrome and is a factor contributing to the progression of the initial glomerular injury and the development of glomerulosclerosis. Apolipoprotein E (apoE) is a plasma protein and apoE epsilon 4 allele is associated with higher plasma cholesterol levels. With this in mind, we studied apoE phenotypes and alleles in children with nephrotic glomerular diseases (NGD, n=29), including idiopathic nephrotic syndrome (n=16), membranoproliferative glomerulonephritis (n=7), and focal segmental glomerulosclerosis (FSGS, n=6). Children with NGD had a higher epsilon 4 allele frequency (20.7%) than controls (10.8%), and those with FSGS had both higher apoE4/3 (66.7%) and epsilon 4 allele (33.3%) frequencies than controls (20.4% and 10.8%, respectively). In IgA nephropathy (n=30, disease controls), no significant association with specific apoE was found. Further studies are needed to clarify the significance of the observed high frequencies of apoE epsilon 4 allele in children with NGD and apoE4/3 phenotype distribution in FSGS.

Adolescent↗
PubMed1996

Study on proteinase-inhibiting capacity of plasma alpha 2-macroglobulin in idiopathic nephrotic syndrome.

We studied the relationship between plasma alpha 2-macroglobulin (alpha 2M) and depressed cell-mediated immunity in idiopathic nephrotic syndrome (INS). Plasma alpha 2M concentrations (mumol/l) were increased during relapses of INS; however, the proteinase inhibitory activity, measured using bacterial thermolysin, was significantly decreased when calculated per 1 mol of alpha 2M, implying a reduced proteinase-inhibiting capacity of alpha 2M. The decreased proteinase-inhibiting capacity of alpha 2M was associated with the inhibitory activity of plasma on normal lymphocyte blastogenesis. Purified alpha 2M, when complexed with chymotrypsin, intensively inhibited normal lymphocyte blastogenesis induced by concanavalin A, as compared with the free form of alpha 2M. From these results it is suggested that, although the amount of alpha 2M protein has increased in the plasma of INS patients during relapse, its binding capacity to proteinases has relatively decreased. The results of this study may provide speculation for both the well-known high plasma alpha 2M concentrations and the immunodepression, both of which have been observed in INS patients in the past few decades.

Adolescent↗
PubMed1996

Serum carnitine concentrations in different glomerular diseases with normal renal function.

Serum carnitine concentrations are known to decrease in patients on regular hemodialysis and to increase in chronic renal failure. However, there is little information available concerning serum levels of carnitine in different glomerular diseases in patients whose renal functions have not yet deteriorated. In this study, we measured serum carnitine concentrations in 40 pediatric patients with idiopathic nephrotic syndrome, IgA nephropathy, non-IgA glomerulonephritis, focal segmental glomerular sclerosis, and normal controls. The results showed that there were no significant differences in the serum-free and total carnitine concentrations (S-FCC and S-TCC, respectively) between patients with different glomerular diseases and the controls. Of interest was the statistically weak correlations of both S-TCC and S-FCC with BUN in these patients, despite their normal renal functions. The ratio of S-FCC to S-TCC was significantly higher as compared with that of the controls. These findings suggest that serum carnitine concentrations are not affected by the types of glomerular lesions and that serum levels of carnitine depend mostly on the glomerular excretory capacity of urea nitrogens, even when the renal functions have not yet deteriorated. The increase in the ratio of S-FCC to S-TCC may be an early reflection of changes in the serum carnitine profiles of these patients.

Adolescent↗
PubMed1992

Glomerular deposition of alpha 2-macroglobulin in a child with steroid refractory nephrotic syndrome.

A four-year-old male with steroid refractory nephrotic syndrome was found to have diffuse deposition of alpha 2-macroglobulin (alpha 2M) in the glomeruli which showed diffuse mesangial proliferation and partial hyalinization by light microscopy. Camostat mesylate, a commercially available synthetic proteinase inhibitor, led to biochemical and clinical improvement. Twenty-two patients with 7 biopsy-proven renal diseases did not have any deposition of alpha 2M in their kidney tissue. Though the pathogenetic mechanism is unknown, this is probably the first report of the deposition of alpha 2M in renal tissue.

Child, Preschool↗
PubMed1989

P blood group and proneness to urinary tract infection in Japanese children.

The globoseries of glycolipids are antigens in the P blood group system as well as epithelial cell receptors for uropathogenic Escherichia coli. The P1 blood group is overrepresented in Swedish girls with recurrent pyelonephritis. In this study, Japanese children with urinary tract infection (UTI) were analyzed for P blood group phenotype. Out of 26 children with recurrent UTI, 50% were of the P1 blood group compared to the 31% of P1 individuals in the Japanese population at large (p less than 0.05). Of children defined as having febrile UTI 62% were P1. The P1 blood group was thus significantly enriched (3.5 times) in the children with febrile UTI. These results support the hypothesis that individuals of blood group P1 run an increased risk for recurrent pyelonephritis.

Adolescent↗
PubMed1980

Enhancement of PGI2 formation by a new vasodilator, 2-nicotinamidoethyl nitrate in the coupled system of platelets and aortic microsomes.

Exogenous arachidonate addition to the coupled system of platelets and aortic microsomes resulted in production of TXA2 and PGI2 (detected as the stable degradation products, TXB2 and 6-keto PGF1 alpha, respectively). Imidazole, papaverine and dipyridamole increased PGI2 and decreased TXA2 in the coupled system. All of these agents inhibited TXA2 formation by platelets from arachidonate. Nitroglycerin did not show any effect on PGI2 and TXA2 formation in the coupled system and on TXA2 formation by platelets. In contrast with these compounds, in spite of showing no inhibitory effect on TXA2 formation by platelets alone, 2-nicotinamidoethyl nitrate (SG-75) increased PGI2 and decreased TXA2 in the coupled system. It is suggested that SG-75 accelerated the conversion of PGH2 to PGI2 so that smaller amounts of TXA2 was produced in the coupled system.

Animals↗
PubMed1976

Allometric method for the long term observation of adjuvant arthritis in rats.

An allometric method for estimating the volume change in inflamed paw of rats is described. The technique is effective and advantageous for long term observation of adjuvant arthritis which lacks a suitable reference criterion due to the simultaneous swelling of the control paw. In the present method, the inflammatory intensity (IF) of paw edema is estimated by means of the formula; IF(%)=(2Vr/cXd(I+Wt/aXb)-I) X 100 where Vt is the paw volume, Wt is the body weight weight and X is the tail length of the inflamed rat. The constants a, b, c, and d are obtained from tthe normal rats using the relative growth law, W=aXb and V=cXd (where W is the body weight, V is the paw volume and X is the tail length).

Adjuvants, Immunologic↗
PubMedDate not supplied

Delayed cardioprotection is associated with the sub-cellular relocalisation of ventricular protein kinase C epsilon, but not p42/44MAPK.

Both noradrenaline administration to rats and rapid cardiac pacing in dogs induces delayed protection of the heart against ischaemia-induced ventricular arrhythmias. In an attempt to establish molecular mechanisms underlying the delayed cardioprotection, we have examined the potential role of two kinases, PKC epsilon and p42/44MAPK. These protein kinases are expressed in the ventricles of the heart and are characterised by their ability to regulate ion-flux and gene transcription. In the rat p42MAPK is predominantly localised in the high-speed supernatant fraction of the ventricle homogenate, whereas p44MAPK is enriched in the nuclear low speed pellet. A small proportion of the p42MAPK is activated even in hearts from control animals. However, neither kinase is relocalised or activated by noradrenaline administration and this provides preliminary evidence the p42/44MAPK may not play a significant role in delayed protection in this species. In contrast, noradrenaline does induce the translocation of PKC epsilon to cell membranes, a response that is sustained for up to 4 h. However, PKC epsilon is down-regulated from the cytoplasm after 24 h post noradrenaline treatment. PKC epsilon is also translocated to the membrane in dogs that have been classically pre-conditioned and cardiac paced. In the latter case, translocation of PKC epsilon from the cytoplasm to the cell membrane is evident 24 h after pacing. These results indicate that the release of endogenous mediators may either inhibit down-regulation or elicit an increase in PKC epsilon mRNA expression. Therefore, in dog heart the subcellular relocalisation of PKC epsilon persists into the 'second window' and may play a central role in the molecular mechanism governing delayed cardioprotection. It is important in the future to identify either the gene products that are induced or the target protein(s) that are phosphorylated by PKC epsilon.

Animals↗