Search PubMed⌕ Search

Biomedical subjects

Tadashi Suehiro

Publications and source records attributed to Tadashi Suehiro.

25 records · Page 2Linked to original sources
PubMed2002

Double deletions and missense mutations in the first nucleotide-binding fold of the ATP-binding cassette transporter A1 ( ABCA1) gene in Japanese patients with Tangier disease.

Tangier disease (TD) is a rare autosomal recessive disease characterized by plasma high-density lipoprotein deficiency caused by an ATP-binding cassette transporter A1 ( ABCA1) gene mutation. We describe three different mutations in Japanese patients with TD. The first patient was homozygous for double deletions of 1221 bp between intron 12 and 14 and 19.9 kb between intron 16 and 31. The breakpoint sequence analyses suggest that it is a simultaneous event caused by double-loop formation through multiple Alu. The second patient was homozygous for a novel mutation of A3198C in exon 19, resulting in Asn935His. The third patient was homozygous for A3199G of exon 19 that leads to Asn935Ser, which is the same mutation found in German and Spanish families. Both Asn mutations involved Walker A motif of the first nucleotide-binding fold.

ATP Binding Cassette Transporter 1↗
PubMed2002

Diabetes mellitus associated with Klinefelter's syndrome: a case report and review in Japan.

We report a case of Klinefelter's syndrome in a 48-year-old man who had diabetes mellitus associated with severe insulin resistance. We diagnosed him with Klinefelter's syndrome from his atrophic testicles, primary hypogonadism in hormonal examination, and a chromosomal aberration of 47,XXY. He showed severe decreased insulin sensitivity in a hyper-insulinemic euglycemic clamp test. He had injected over 100 units of insulin per day, however, testosterone replacement and administration of pioglitazone improved his glycemic control, which resulted in a decrease of insulin dose to less than 50 units per day. Here, we discuss the characteristics of diabetes mellitus associated with Klinefelter's syndrome in Japanese patients including this case.

Blood Glucose↗
PubMed2002

Acute-phase, but not constitutive serum amyloid A (SAA) is chemotactic for cultured human aortic smooth muscle cells.

The human serum amyloid A (SAA) protein family is subclassified as acute phase SAA (A-SAA), which comprises the SAA1 and SAA2 allelic variants, and constitutive SAA (C-SAA), which is the SAA4 isoform. Extrahepatic production of A-SAA occurs in many organs and tissues of the body, including smooth muscle cells (SMC) of the aorta. A-SAA has been shown to act locally as a chemoattractant for neutrophils, monocytes and lymphocytes via the N-formyl peptide receptor-like (fPRL1). In order to gain further understanding of the physiological significance of local production of A-SAA by SMC, the effect of exogenous A-SAA on the in vitro migration of human aortic SMC was investigated. Increased SMC migration in the presence of A-SAA was detectable after six hours and continued to increase up to 24 hours after incubation. The increased migration was dose-dependent over the concentration range 10 to 100 micrograms/ml. The mode of A-SAA stimulated SMC migration was by chemotaxis not chemokinesis. Exogenous constitutive SAA (C-SAA) did not affect SMC migration. Stimulation of SMC migration by A-SAA was inhibited by both polyclonal and monoclonal antibodies to human SAA1 and also by the inhibitors of fPRL1 signaling, wortmannin, bisindolylmaleimide and pertussis toxin. The results herein indicate that A-SAA, but not C-SAA, may serve as an autocrine factor to influence SMC migration in situations of aortic tissue injury and inflammation.

Amino Acid Sequence↗
PubMed2002

Proinflammatory cytokines but not acute phase serum amyloid A or C-reactive protein, downregulate paraoxonase 1 (PON1) expression by HepG2 cells.

The expression of paraoxonase1 (PON1) during inflammation has been investigated in vitro. The alteration of steady state PON1 mRNA in HepG2 cells by interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha), was investigated relative to acute-phase serum amyloid A (A-SAA) mRNA. PON1 mRNA expression by HepG2 cells was decreased within three hours of stimulation by IL-1beta or TNF-alpha. Relative to PON1 mRNA expression, the pattern of steady state A-SAA mRNA expression was altered reciprocally and inversely by IL-1beta. These findings suggested that the decrease in serum PON activity after abdominal surgery in our previous clinical study may be ascribed to a decrease in steady state PON1 mRNA expression by liver with proinflammatory cytokines.

Apolipoproteins↗
PubMed2002

Serum paraoxonase (PON1) concentration in patients undergoing hemodialysis.

Cardiac death from atherosclerosis is common in patients undergoing hemodialysis. Although the enzymic activity of human serum paraoxonase (PON1) has been reported to be decreased in such patients, serum PON1 concentrations have not been measured. We investigated serum PON1 concentrations in 81 patients undergoing hemodialysis and 103 age-matched healthy subjects using an enzyme immunoassay. The PON1 concentration was significantly lower in the patient group than the control group (mean +/- SD: 6.78 +/- 3.56 vs 18.01 +/- 4.55 U/ml, respectively. p < 0.0001). There were no significant relationships between serum PON1 concentrations and the PON1 genetic polymorphisms, 55Leu/Met (L/M) and 192Gln/Arg (Q/R). The concentration adjusted for HDL-cholesterol or apolipoprotein A-I was also lower in the patient group. However, the specific activities (enzyme activity divided by the PON1 concentration) of paraoxonase and arylesterase were increased in the patient group compared with the control group. In the male patients, but not the female patients, PON1 concentrations were significantly lower in subjects with than without coronary heart disease (CHD) (mean +/- SD: 4.48 +/- 2.77 vs 7.34 +/- 3.22 U/ml, respectively. p < 0.01). In conclusion, the serum PON1 concentration in hemodialyzed patients was significantly decreased, resulting in an attenuation of PON1 enzymic activity. This decrease may be in part involved in the development of cardiovascular disease.

Aged↗