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Biomedical subjects

T Hamazaki

Publications and source records attributed to T Hamazaki.

104 records · Page 6Linked to original sources

Effects of ceruloplasmin and the haptoglobin-hemoglobin complex on the oxygen-dependent reduction in growth of human diploid fibroblasts in serum-free, albumin containing medium.

We examined that growth-promoting activity of two different human albumin (HSA) preparations for human diploid fibroblasts in serum-free RITC 80-7 medium. The activity of one preparation (sample A) was affected markedly by environmental oxygen, whereas the other (sample B) was little affected. Sample B contained ceruloplasmin (Cp) and haptoglobin (Hp) as impurities. To detect the generation of superoxide anion in the media the amount of reduction of cytochrome c that is inhibited by superoxide dismutase (SOD) was determined. In an aerobic environment it was relatively large in comparison with reduction inhibited in a hypoxic environment. Reduction in the sample A with HSA-supplemented medium was relatively large in comparison with that in sample B with HSA-supplemented medium. The reduction of cytochrome c also was inhibited by Cp (25 mg/l) and catalase (4000 units/ml). Moreover, SOD, Cp, catalase and Hp.Hb (but not Hp) partially prevented oxygen-dependent reduction in growth in an aerobic environment when added to sample A HSA-supplemented medium. These results suggest that Cp and Hp.Hb act as an antioxidants in culture.

Blood Protein Electrophoresis↗

The effects of the oral administration of fish oil concentrate on the release and the metabolism of [14C]arachidonic acid and [14C]eicosapentaenoic acid by human platelets.

It has been suggested by several investigators that eicosapentaenoic acid (C20:5 omega 3, EPA) might have anti-thrombotic effects. In this experiment, the effect of the oral administration of EPA rich fish oil concentrate on platelet aggregation and the release and the metabolism of [1-14C]arachidonic acid and [(U)-14C]eicosapentaenoic acid by human platelets was studied. Eight healthy male subjects ingested 18 capsules of fish oil concentrate (EPA 1.4 g) per day for 4 weeks. Plasma and platelet concentrations of EPA markedly increased, while those of arachidonic acid (C20:4 omega 6, AA) and docosahexaenoic acid (C22:6 omega 3, DHA) did not change. Platelet aggregation induced by collagen and ADP was reduced. Collagen induced [14C]thromboxane B2 (TXB2) formation from [14C]AA prelabeled platelets decreased. There was no detectable formation of [14C]TXB3 from [14C]EPA prelabeled platelets, and the conversion of exogenous [14C]EPA to [14C]TXB3 was lower than that of [14C]AA to [14C]TXB2. The release of [14C]AA from [14C]AA prelabeled platelets by collagen was significantly decreased. These observations raise the possibility that the release of arachidonic acid from platelet lipids might be affected by the alteration of EPA content in platelets.

Adenosine Diphosphate↗

Effects of orally administered ethyl ester of eicosapentaenoic acid (EPA; C20:5, omega-3) on PGI2-like substance production by rat aorta.

A highly purified ethyl ester of EPA (EPAEE) (74%) was manufactured from sardine oil. Sixty mg/kg/day of EPAEE was given orally to male Wistar rats for 8 weeks. No side effect or toxicity from the administration of EPAEE was observed. Plasma EPA concentration and the ratio of EPA to arachidonic acid were significantly increased, compared with control Wistar rats. An enhancement of PGI2-like substance production by aortas obtained from rats fed EPAEE was noted. Conversion of EPA to delta 17-6-keto-PGF1 alpha, a stable metabolite of PGI3, could not be detected by an incubation study of 14C-EPA and aortas either from rats fed EPAEE or from control rats. Therefore, PGI2-like substance produced by rat aorta is most likely to be PGI2 itself and not PGI3.

6-Ketoprostaglandin F1 alpha↗

Nosocomial septicemias due to methicillin-resistant staphylococcus aureus and Pseudomonas aeruginosa in a university hospital over a 12-year period--the same intractable infections.

Clinical features of nosocomial bacteremias due to methicillin-resistant Staphylococcus aureus (MRSA) (M group, n = 71) and Pseudomonas aeruginosa (P group, n = 25) in a university hospital during 1982-1993 were retrospectively analyzed. The majority of these patients had an underlying disease, and bacteremia occurred in hospital. There were no differences in the male to female ratio and the mean age of the patients between the two groups. The ratio of medical wards to surgical wards was higher in the P group (18/7 = 2.6) than for the M group (38/33 = 1.2). P. aeruginosa was more frequently isolated from patients with hematological malignancies and MRSA with solid tumors. The percentage of MRSA among gram-positive bacteremia and of P. aeruginosa among gram-negative bacteria has shown a tendency to increase in recent years, and antibiotic sensitivity of these two organisms showed, on a whole, a tendency to decrease. Attention should be called to the increase of these two pathogens.

Adolescent↗

Cooperative induction of 15-lipoxygenase in rheumatoid synovial cells by IL-4 and proinflammatory cytokines.

OBJECTIVE: To clarify the role of interleukin-4 (IL-4) in the expression of 15-lipoxygenase (15-LOX), whose metabolities are known to suppress the inflammatory reaction, in freshly prepared rheumatoid synovial cells. METHODS: Adherent synovial cells were prepared by enzymatic digestion of synovia obtained from patients with rheumatoid arthritis (RA). Protein expression of 15-LOX was determined by Western blot analysis. The messenger RNAs of 15-LOX were determined by reverse transcription and the polymerase chain reaction (RT-PCR). RESULTS: Freshly prepared rheumatoid synovial cells did not express 15-LOX at either the mRNA or protein levels. IL-4 induced the protein expression of 15-LOX after 24 hours of culture. Although interleukin-1 alpha (IL-1 alpha) and tumor necrosis factor alpha (TNF alpha), major inflammatory cytokines in rheumatoid synovia, did not induce the expression of 15-LOX, IL-4 and these inflammatory cytokines synergistically enhanced the protein expression of 15-LOX. The synergistic effect was also observed at the level of mRNA. CONCLUSIONS: We demonstrate that IL-4 cooperated with the inflammatory cytokines IL-1 alpha and TNF alpha to enhance the expression of 15-LOX in rheumatoid synovial cells. Since 15-LOX metabolites have potent anti-inflammatory actions, our data suggest that IL-4 might downregulate rheumatoid inflammation via the induction of 15-LOX and its metabolites.

Alprostadil↗

Chylopericardium following right thoracotomy for lung cancer.

A 69-year-old woman underwent the right upper lobectomy, a partial resection of right segment 6 (rt S6) and removal of mediastinal lymph nodes (LN) for adenocarcinoma of the lung (rt S2), stage IIIA (T2N2M0). A chest computerized tomography (CT) taken one month after the operation revealed a pericardial effusion which was milky in color, and contained high levels of triglycerides (TG) of 615 mg/dl (serum, 217 mg/dl). Cytology of effusion for malignant cells was negative. The pericardial effusion gradually decreased in one month by restriction of her fat intake. Chylopericardium following right thoracotomy for lung cancer is extremely rare.

Adenocarcinoma↗

Effects of eicosapentaenoic acids on remnant-like particles, cholesterol concentrations and plasma fatty acid composition in patients with diabetes mellitus.

Remnant lipoproteins are transient metabolites from chylomicron and/or very low density lipoproteins (VLDL), and remnant hyperlipoproteinemia has recently been reported to be a risk factor for atherosclerosis. Eicosapentaenoic acid (EPA), a major component of fish oil, has the following effects: anti-platelet aggregation, vaso-dilation, anti-inflammation, hypotriglyceridemia, and therefore has potential anti-atherosclerotic effects. We measured serum of remnant-like particle cholesterol (RLP-C) concentrations, and investigated the effects of EPA on serum RLP-C concentrations in patients with diabetes mellitus. Ten patients with non-insulin dependent diabetes mellitus were treated with 900-1800 mg EPA ethyl-ester daily for 3 months. We investigated serum RLP-C concentrations and plasma fatty acid composition before and after the administration of EPA. Serum RLP-C concentrations were significantly decreased 3 months after the administration of EPA (from 14.5 +/- 5.3 mg/dL to 3.3 +/- 0.8 mg/dL, P < 0.01). Plasma EPA concentrations and the ratios of EPA to arachidonic acids (AA) were significantly increased during the same period (from 86.2 +/- 12.4 mg/L to 194.6 +/- 27.3 mg/L, P < 0.01, from 0.571 +/- 0.074 to 1.242 +/- 0.163. P < 0.01, respectively). Serum RLP-C concentrations were inversely correlated with the ratios of EPA to AA in plasma (r = -.516, P < 0.05). These results suggested that administration of EPA was effective on remnant hyperlipoproteinemia which was a risk factor for atherosclerosis.

Aged↗