Biomedical subjects

Osamu Hanyu

Publications and source records attributed to Osamu Hanyu.

4 recordsLinked to original sources

PubMed2003

LCAT-dependent conversion of prebeta1-HDL into alpha-migrating HDL is severely delayed in hemodialysis patients.

Prebeta1-HDL is a minor HDL subfraction that acts as an efficient initial acceptor of cell-derived free cholesterol. During 37 degrees C incubation, plasma prebeta1-HDL decreases over time due to its conversion to alpha-migrating HDL by lecithin:cholesterol acyltransferase (LCAT). This conversion may be delayed in hemodialysis patients who have decreased LCAT activity. To clarify whether LCAT-dependent conversion of prebeta1-HDL to alpha-migrating HDL is delayed in hemodialysis patients, prebeta1-HDL concentrations were determined in 45 hemodialysis patients and 45 gender-matched control subjects before and after 37 degrees C incubation with and without the LCAT inhibitor. It was found that the baseline prebeta1-HDL concentration in hemodialysis patients was more than twice that in the controls (44.9 +/- 21.4 versus 19.8 +/- 6.7 mg/L apoAI; P < 0.001). After 2-h incubation, the LCAT-dependent decrease in prebeta1-HDL in hemodialysis patients was about one-third of that in the controls (30 +/- 27 versus 97 +/- 17% of baseline; P < 0.01). The LCAT-dependent rate of decrease in prebeta1-HDL levels (DR(prebeta1)) was the same for samples from hemodialysis patients exhibiting normal (> or =1.03 mmol/L) and low HDL-cholesterol levels (32 +/- 32 versus 28 +/- 23% of baseline; NS). DR(prebeta1) was positively correlated with LCAT activity (r = 0.617; P < 0.001). In conclusion, the LCAT-dependent conversion of prebeta1-HDL to alpha-migrating HDL is severely delayed in hemodialysis patients. The impaired catabolism of prebeta1-HDL may accelerate atherosclerosis in hemodialysis patients.

Adult↗

PubMed2002

Analytical performance of a sandwich enzyme immunoassay for pre beta 1-HDL in stabilized plasma.

We have established an immunoassay for pre beta 1-HDL (the initial acceptor of cellular cholesterol) using a monoclonal antibody, MAb55201. Because pre beta 1-HDL is unstable during storage, fresh plasma must be used for pre beta 1-HDL measurements. In this study, we describe a method of stabilizing pre beta 1-HDL, and evaluate the analytical performance of the immunoassay for pre beta 1-HDL. Fresh plasma was stored under various conditions with or without a pretreatment consisting of a 21-fold dilution into 50% (v/v) sucrose. Pre beta 1-HDL concentration was measured by immunoassay. In nonpretreated samples, pre beta 1-HDL decreased significantly from the baseline after 6 h at room temperature. Although pre beta 1-HDL was more stable at 0 degrees C than at room temperature, it increased from 30.2 +/- 8.5 (SE) to 56.5 +/- 5.5 mg/l apolipoprotein A-I (apoA-I) (P < 0.001) in hyperlipidemics, and from 18.4 +/- 1.2 to 37.9 +/- 3.3 mg/l apoA-I (P < 0.001) in normolipidemics after 5-day storage. After 30-day storage at -80 degrees C, pre beta 1-HDL increased from 29.0 +/- 4.0 to 38.0 +/- 5.7 mg/l apoA-I (P < 0.001) in hyperlipidemics, whereas it did not change in normolipidemics. In pretreated samples, pre beta 1-HDL concentration did not change significantly under any of the above conditions. Moreover, pre beta 1-HDL concentrations determined by immunoassay correlated with those determined by native two-dimensional gel electrophoresis (n = 24, r = 0.833, P < 0.05). An immunoassay using MAb55201 with pretreated plasma is useful for clinical measurement of pre beta 1-HDL.

Electrophoresis, Gel, Two-Dimensional↗

PubMed2002

LDL-cholesterol and HDL-cholesterol concentrations decrease during the day.

BACKGROUND: Homogenous assays for LDL-cholesterol (LDL-C) and HDL-cholesterol (HDL-C) are highly accurate, with little interference from triglyceride. Using these methods, we measured postprandial LDL-C and HDL-C. Earlier studies suggested a postprandial decrease in LDL-C. METHODS: To elucidate whether LDL-C and HDL-C decrease significantly during the day, we determined daily profiles of LDL-C and HDL-C using homogeneous assays in subjects with normal coronary arteries (N; n=10), and subjects with coronary artery disease (CAD; n=23). RESULTS: In both groups, LDL-C and HDL-C were significantly lower from after breakfast until midnight than they were before breakfast. The next morning, they returned to baseline levels. The mean reduction in LDL-C was 0.09-0.13 mmol/L in N and 0.05-0.20 mmol/L in CAD, while that in HDL-C was 0.02-0.06 mmol/L in N and 0.00-0.05 mmol/L in CAD. CONCLUSION: LDL-C and HDL-C decrease significantly over the course of the day.

Adult↗

PubMed2002

Adrenocorticotropin-producing pituitary carcinoma with metastasis to the liver in a patient with Cushing's disease.

A 61-year-old woman who had a nonfunctioning pituitary tumor removed was later found to have a pituitary carcinoma with metastasis to the liver that produced adrenocorticotropic hormone (ACTH), causing Cushing's disease. Despite the second removal of the pituitary tumor, Cushing's disease persisted. Endocrinologic examination demonstrated marked elevation of plasma ACTH, beta-endorphin, and serum cortisol concentrations, which were not suppressed by low- or high-dose dexamethasone administration. A computed tomographic scan of the abdomen revealed a solitary hypodense area in the liver consistent with a metastatic lesion. Immediately after resection of the liver tumor, plasma ACTH concentrations fell to normal range. Such a decline in ACTH secretion was not observed even after the pituitary tumor was removed. Histologic characteristics of both the pituitary and liver tumors were similar. The immunohistochemical study using anti-ACTH antibody showed similar ACTH-positive cells in the pituitary and liver tumors. Based on these findings, the patient was diagnosed as having liver metastasis of ACTH-secreting pituitary carcinoma. This is the first case report in which a metastatic liver tumor of a pituitary carcinoma caused ACTH.

Adrenocorticotropic Hormone↗