Biomedical subjects

Hiroji Shimomura

Publications and source records attributed to Hiroji Shimomura.

3 recordsLinked to original sources

PubMed2006

[Age specific reference ranges and clinical trial for complexed prostate specific antigen (cPSA)].

We compared the complexed PSA (cPSA) reference range of values by age against that for total PSA. The subjects were 1,210 men who underwent a complete medical checkup at our center between September and November 2003. We found an upward trend of the measured values associated with age and defined a set of expected result range by age groups. The cPSA 95th percentile upper limit value increased across all age groups: for men under 40 years, 1.38ng/ml: for men 40 to 49 years, 1.60ng/ml; for men 50 to 59 years, 2.25 ng/ml; for men 60 to 69 years, 2.50 ng/ml; and for men 70 years older, 4.31 ng/ml (The number of subjects in each group was 153, 323, 429, 220 and 77). The total PSA also increased with age: 1.85 ng/ml, 2.11 ng/ml, 2.80 ng/ml, 4.20 ng/ml, and 5.69 ng/ml, respectively. We also compared other prostatic tumor markers in urology patients.

Adult↗

PubMed2003

Blood extracellular superoxide dismutase levels in hemodialysis patients pre- and post-hemodialysis and its association with lipoprotein lipase mass and free fatty acid.

BACKGROUND: Hemodialysis (HD) is a method of chronic therapy for patients with renal failure. Diabetic nephropathy is the most common underlying disease among HD patients in Japan. A characteristic problem associated with this condition is endothelial cell damage. We have been using extracellular superoxide dismutase (EC-SOD) attached to the heparan sulfate on the endothelial cell surface as a marker of vascular damage. METHODS: This study examined the pre- and post-HD levels of lipoprotein lipase (LPL). The increase in free fatty acid (FFA) is affected by a type of cytokine-like substances, which induces insulin resistance and causes abnormal lipid metabolism. RESULTS: Pre-HD blood samples showed highly significant correlations between EC-SOD and LPL mass (r = 0.792) and between EC-SOD and FFA (r = 0.675) (p < 0.0001). EC-SOD, LPL mass, and FFA were remarkably high among the patients who had been placed on HD treatment for over 20 years. CONCLUSION: Because EC-SOD and LPL mass represent heparin-binding proteins, these results were considered to reflect severe vascular damage.

Adult↗

PubMed2003

Glycated high-density lipoprotein regulates reactive oxygen species and reactive nitrogen species in endothelial cells.

Nonenzymatic glycosylation of plasma proteins may contribute to the excess risk of developing atherosclerosis in patients with diabetes mellitus. Although it is believed that high-density lipoprotein (HDL) is glycosylated at an increased level in diabetic individuals, little is known about a possible linkage between glycated HDL and endothelial dysfunction in diabetes. To clarify whether glucose-modified HDL affects the function of endothelial cells, we first examined herein the level of H(2)O(2) generation from cultured human aortic endothelial cells (HAECs) exposed to a glycated oxidized HDL (gly-ox-HDL) prepared in vitro. Incubation for 48 hours with 100 microg/mL of gly-ox-HDL induced significant release of H(2)O(2) from cells and gly-ox-HDL-induced H(2)O(2) formation was inhibited in the presence of diphenyleneiodonium, an inhibitor of NADPH oxidase. In addition, stimulation of HAECs with gly-ox-HDL for 48 hours elicited a marked downregulation of catalase and Cu(2+), Zn(2+)-superoxide dismutase (CuZn-SOD), suggesting H(2)O(2) formation by gly-ox-HDL to be due to a disturbance involving oxidant and antioxidant enzymes in the cells. Treatment of HAECs with gly-ox-HDL attenuated the expression of endothelial nitric oxide synthase (eNOS), but not inducible nitric oxide synthase (iNOS), and this was followed by decreased production of nitric oxide (NO) by the cells. Furthermore, in vitro experiments with glycated HDL (gly-HDL) in the presence of 2 mmol/L EDTA and Cu(2+)-oxidized HDL suggested the effect of gly-HDL on endothelial function to be possibly potentiated by additional oxidative modification. Taking all of the above findings together, gly-ox-HDL may lead to the deterioration of vascular function through altered production of reactive oxygen species and reactive nitrogen species in endothelial cells.

Blotting, Western↗