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Biomedical subjects

Jun Sasaki

Publications and source records attributed to Jun Sasaki.

58 records · Page 4Linked to original sources
PubMed2002

Report of the Japan Atherosclerosis Society (JAS) Guideline for Diagnosis and Treatment of Hyperlipidemia in Japanese adults.

This paper described the Guideline for Diagnosis and Management of Hyperlipidemias for Prevention of Atherosclerosis proposed by The Japan Atherosclerosis Society (JAS) Guideline Investigating Committee (1,995-2,000) under the auspices of the JAS Board of Directors. 1) The guideline defines the diagnostic criteria for serum total cholesterol (Table 1), LDL-cholesterol (Table 1), triglycerides (Table 4) and HDL-cholesterol (Table 7). It also indicates the desirable range (Table 1), the initiation levels of management (Table 2) and the target levels of treatment (Table 2) for total and LDL-cholesterol. 2) Though both total and LDL-cholesterol are shown as atherogenic parameter in the guideline, the use of LDL-cholesterol, rather than total cholesterol, is encouraged in daily medical practice and lipid-related studies, because LDL-cholesterol is more closely related to atherosclerosis. 3) Elevated triglycerides and low HDL-cholesterol are included in the risk factors, since no sufficient data have been accumulated to formulate the guideline for these two lipid disorders. 4) Emphasis is laid on evaluation of risk factors of each subject before starting any kind of treatment (Table 2). 5) This guideline is applied solely for adults (age 20-64). Lipid abnormalities in children or the youth under age 19, and the elderly with an age over 65 have to be evaluated by their own standard. 6) This part of the guideline gives only the diagnostic aspects of hyperlipidemias. The part of management and treatment will follow in the second section of the guideline that will be published in future.

Adult↗
PubMed2002

Clinical effects of rosuvastatin, a new HMG-CoA reductase inhibitor, in Japanese patients with primary hypercholesterolemia: an early phase II study.

The effects and tolerability of the new HMG-CoA reductase inhibitor rosuvastatin were assessed in 68 hypercholesterolemic Japanese patients (22 men and 46 postmenopausal women; age range 28-72 years) in a multicenter, double-blind, dose-ranging, early phase II study. Patients were randomized into three groups and received once-daily doses of 1, 2, or 4 mg rosuvastatin. Sixty evaluable patients (19 men and 41 women) with mean total cholesterol (TC) 294 mg/dl (7.60 mmol/l) and mean triglyceride (TG) 150 mg/dl (1.69 mmol/l) provided data in the efficacy analysis based on percentage changes in lipids at 4 and 8 weeks. All doses of rosuvastatin improved lipid parameters after both 4 and 8 weeks of therapy. On average, TC decreases were 22-29%, low-density lipoprotein cholesterol (LDL-C) decreases 32-42%, TG decreases 2% to 22%, and HDL-C increases 3-7%. There were no remarkable differences between efficacy at 4 and at 8 weeks, and dose-dependent reductions were noted for LDL-C, with 30, 39, and 42% decreases in the 1-, 2-, and 4-mg/ day dose groups, respectively, at 8 weeks. The drug was well tolerated over the 8 weeks of therapy. These preliminary results indicate that rosuvastatin is a potent cholesterol-lowering agent, capable of achieving marked reductions in LDL-C even at low doses.

Adult↗
PubMed2002

Structure-function studies of apoA-I variants: site-directed mutagenesis and natural mutations.

Five mutants of apolipoprotein A-I (apoA-I), apoA-I(Delta63-73), apoA-I(Delta140-150), apoA-I(63-73@140-150), apoA-I(R149V), and apoA-I(P143A) were compared with human plasma apoA-I for their ability to promote cholesterol and phospholipid efflux from HepG2 cells. A significantly lower capacity to promote cholesterol and phospholipid efflux was observed with lipid-free apoA-I(Delta63-73), while mutations apoA-I(Delta140-150) and apoA-I(P143A) affected phospholipid efflux only. When added as apoA-I/palmitoyloleoyl phosphatidylcholine (POPC) complex, mutations apoA-I(63-73@140-150) and apoA-I(Delta140-150) affected cholesterol efflux. None of the mutations affected alpha-helicity of the lipid-free mutants or their self-association. Five natural mutations of apoA-I, apoA-I(A95D), apoA-I (Y100H), apoA-I(E110K), apoA-I(V156E), and apoA-I (H162Q) were studied for their ability to bind lipids and promote cholesterol efflux. None of the mutations affected lipid-binding properties, cholesterol efflux, or alpha-helicity of lipid-free mutants. Two mutations affected self-association of apoA-I: apoA-I(A95D) was more prone to self-association, while apoA-I(E100H) did not self-associate. The following conclusions could be made from the combined data: i) regions 210-243 and 63-100 are the lipid-binding sites of apoA-I and are also required for the efflux of lipids to lipid-free apoA-I, suggesting that initial lipidation of apoA-I is rate limiting in efflux; ii) in addition to the lipid-binding regions, the central region is important for cholesterol efflux to lipidated apoA-I, suggesting its possible involvement in interaction with cells.

Apolipoprotein A-I↗