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Biomedical subjects

M Hoshi

Publications and source records attributed to M Hoshi.

358 records · Page 20Linked to original sources
PubMedDate not supplied

Angiotensin II (AII) induced hypertension chemotherapy (IHC) for unresectable gastric cancer: with reference to resection after down staging.

Angiotensin II induced hypertension chemotherapy (IHC) is a drug delivery system for augmentation of anti-cancer effects on the experimental basis of the functional difference of microcirculation between tumor and normal tissue. Blood flow in tumor tissue increased selectively when the blood pressure was elevated by the infusion of angiotensin II. Two randomized controlled trials (RCT) for advanced gastric cancer using AFM regimen; a combination of adriamycin (ADM), 5-fluorouracil (5-FU), and mitomycin (MMC), showed increased response rate by IHC (response rate: IHC/non-IHC; 42.9% vs 10.5% in RCT-1, and 31.3% vs 6.7% in RCT-2, respectively). Toxicities were not different statistically between groups. In phase II for stage IVB gastric cancer patients (the criteria according to the General Rules of the Gastric Cancer Study of Japanese Research Society for Gastric Cancer), 5 complete response (CR) and 10 partial response (PR) (58%) were observed out of 26 unresectable cases without prior chemotherapy. Moreover, 5 of 15 responders could received curative gastrectomy and obtained conclusive down staging (19%). Here we discuss the role of enhancement of drug delivery for cancer chemotherapy on the basis of a series of clinical and experimental evidences.

Adult↗
PubMedDate not supplied

Effects of low-dose simvastatin therapy on serum lipid levels in patients with moderate hypercholesterolemia: a 12-month study. The Simvastatin Study Group.

The aim of this study was to investigate the safety and long-term effects on serum lipid levels of low-dose simvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, in Japanese patients with moderate primary hypercholesterolemia. We assigned 201 patients (68 men and 133 women; mean +/- SD age, 61.3 +/- 10.2 years) with serum total cholesterol levels > or = 220 mg/dL to receive simvastatin 5 mg each evening; the treatment period was 1 year. Serum total cholesterol, triglycerides, and low-density lipoprotein (LDL) cholesterol levels decreased significantly in response to simvastatin therapy, and the changes were maintained throughout the treatment period. Mean total cholesterol decreased from 269.9 +/- 35.4 mg/dL to 215.2 +/- 34.5 mg/dL (20.3%), triglycerides decreased from 183.0 +/- 110.2 mg/dL to 155.5 +/- 88.5 mg/dL (15.0%), and LDL cholesterol decreased from 180.0 +/- 33.1 mg/dL to 130.1 +/- 35.1 mg/dL (27.7%). Total cholesterol, triglycerides, and LDL cholesterol tended to decline when the pretreatment values were higher; the critical values and the bidirectional changes of the serum lipid levels were 188.1, 109.5, and 91.6 mg/dL, respectively. Although the serum level of high-density lipoprotein cholesterol did not change significantly, it tended to increase more when the pretreatment values were lower; the "critical value" was 70 mg/dL. Nine patients experienced mild adverse events, but none discontinued simvastatin during the 12-month treatment period. We found that low-dose simvastatin therapy is effective in achieving long-term decreases in serum lipid levels and is well tolerated by patients with moderate hypercholesterolemia. Simvastatin therapy may result in normalization of serum lipid levels.

Adult↗
PubMedDate not supplied

Possible role of tau protein kinases in pathogenesis of Alzheimer's disease.

Tau protein kinases (TPK) I and II were isolated as candidate enzymes responsible for the hyperphosphorylation observed in PHF-tau. Four phosphorylation sites of tau were identified for each kinase, accounting for most, but not all, of the major phosphorylation sites of PHF-tau. Immunostaining with anti-TPKI antibody indicated that this kinase is up-regulated in AD brain. Such up-regulation of TPKI and phosphorylatioin of tau were reproduced by treating cultured hippocampal cells with amyloid beta (Abeta) protein. In addition, we found that TPKI can phosphorylate and inactivate pyruvate dehydrogenase (PDH), which is expected to result in depletion of acetyl-CoA, a key substrate of acetyl choline synthesis. Indeed, when septum cells were treated with Abeta, the level of acetyl choline decreased dramatically.

Alzheimer Disease↗