Biomedical subjects

Tetsuro Miyata

Publications and source records attributed to Tetsuro Miyata.

23 records · Page 2Linked to original sources

PubMed2003

Long-term survival after surgical treatment of patients with Takayasu's arteritis.

BACKGROUND: Surgical interventions have been performed to ameliorate the complications of Takayasu's arteritis. However, the efficacy of surgery to increase long-term survival has not been established. METHODS AND RESULTS: A retrospective review was performed on the survival of 106 consecutive patients with Takayasu's arteritis who underwent surgical treatment during the past 40 years. Their ages ranged from 5 to 69 years (mean+/-SEM, 31.7+/-1.3 years). Survival was compared with the reported results of medically treated patients according to Ishikawa's prognostic classification. There were 12 hospital deaths, and the remaining 94 patients were followed up from 8 months to 41.8 years (mean, 19.8 years). A serious long-term complication was anastomotic aneurysm, with a cumulative incidence at 20 years of 13.8%. Thirty-one late deaths were observed, and the major cause was congestive heart failure. The overall cumulative survival rate at 20 years was 73.5%. The prognostic classification by Ishikawa had little influence on the survival of surgically treated patients. For stage 3 patients, surgery seemed to increase survival; however, surgery-related complications conversely decreased the survival of stage 1 patients. CONCLUSIONS: Surgery seems to increase the long-term survival of patients with stage 3 Takayasu's arteritis, whereas conservative treatment is recommended for those with stage 1 or 2 disease. An anastomotic aneurysm may occur at any time after surgery, and regular follow-up using imaging modalities such as multi-detector CT, MRI, or ultrasonography at least once every several years for the rest of the patient's life is mandatory for the early detection of anastomotic aneurysm.

Adolescent↗

PubMed2002

Cell replication induces in-stent lesion growth in rabbit carotid artery with preexisting intimal hyperplasia.

This study examined the responses of rabbit carotid artery with a preexisting intimal lesion, to stent implantation and balloon dilation. Rabbit carotid arteries were injured with a Fogarty catheter, and 28 days later the same arteries were subjected to implantation of a Palmaz-Schatz stent or balloon dilation angioplasty. Intimal size was significantly increased after stent implantation and balloon dilation, and no significant difference was detected between the two procedures. After stent implantation, replicating intimal cells were increased mainly in the inner intima, and the increase of cell replication was prolonged until day 28. In contrast, a significant increase of intimal cell replication was detected only at 2 days after balloon dilation. Intimal cell number after stent implantation was significantly higher than that after balloon dilation from day 7. Abundant leukocytes adhered to the luminal surface until 14 days after stent implantation, and significant infiltration of macrophages was observed in the mid-intima. Activation of proteases was prolonged, and obvious accumulation of proteoglycans was detected after stent implantation as compared with balloon dilation. These findings suggest that, an increase in cell replication is critical in the development of in-stent restenosis, and that inflammatory responses represent a unique property after stent implantation.

Angioplasty, Balloon↗

PubMed2002

A lipoprotein lipase activator, NO-1886 prevents impaired endothelium-dependent relaxation of aorta caused by exercise in aged rats.

Exercise decreases plasma total cholesterol and triglycerides, and simultaneously, increases high density lipoprotein (HDL) cholesterol. As a result, exercise is believed to aid in preventing atherosclerosis. However, we do not know whether exercise protects against the development of atherosclerosis in the elderly. The aim of this study was to ascertain whether the lipoprotein lipase activator NO-1886 had an effect on the prevention of atherosclerosis in aged rats which undergo exercise. Exercise for 3 months did not affect plasma lipids but decreased the accumulation of visceral fat in 2-year-old rats (aged rat). Exercise also resulted in an elevation of plasma lipid peroxide (LPO) levels and impaired the endothelium-dependent relaxation of the thoracic aorta caused by acetylcholine in aged rats. On the other hand, NO-1886 decreased plasma triglycerides and increased HDL cholesterol and suppressed the elevation of plasma LPO levels caused by exercise. Furthermore, NO-1886 prevented impaired endothelium-dependent relaxation caused by exercise. In summary, the results of our study indicate that exercise may cause impaired endothelium-dependent relaxation by elevation of LPO in aged rats, and that NO-1886 prevents this impaired endothelium-dependent relaxation of aorta by reducing plasma triglycerides, elevating HDL cholesterol, and suppressing the elevation of plasma LPO caused by exercise.

Aging↗

PubMed2002

Correlation between lipid and glycogen contents in liver and insulin resistance in high-fat-fed rats treated with the lipoprotein lipase activator NO-1886.

Insulin resistance results in accumulation of triglyceride content and reduction of glycogen content in skeletal muscle. However, very few studies have measured lipid content and glycogen content in liver associated with insulin resistance. We studied the relationship between liver lipid content, liver glycogen, and insulin resistance in high-fat-fed rats, which are animal models of insulin resistance. High-fat-fed rats were hyperlipidemic, hyperglycemic, and hyperinsulinemic. Furthermore, the glucose infusion rates (GIR) were lower (normal rats, 10.35 +/- 1.66; high-fat-fed rats, 4.86 +/- 0.93 mg/kg/min; P <.01) and the triglyceride and cholesterol contents in liver were higher in the high-fat-fed rats than in normal rats. On the other hand, the glycogen content in liver was lower than in normal rats. There was an inverse relationship between liver triglyceride content and liver glycogen content. When the lipoprotein lipase (LPL) activator NO-1886 was administered to the high-fat-fed rats at a daily dose of 50 mg/kg body weight for 10 weeks, GIR (9.87 +/- 3.76 mg/kg/min, P <.05 v high-fat-fed control group) improved, causing an improvement of the hyperlipidemia, hyperglycemia, and hyperinsulinemia. Furthermore, NO-1886 decreased triglyceride and cholesterol concentrations and increased glycogen content in liver of the high-fat-fed rats. In this study, we found that insulin resistance caused fatty liver and reduced glycogen content in liver. Administration of the LPL activator NO-1886 improved the insulin resistance, resulting in an improvement in the relationship between triglyceride and glycogen content in liver of high-fat-fed rats.

Animals↗

PubMed2002

Pathogenetic heterogeneity of in-stent lesion formation in human peripheral arterial disease.

PURPOSE: Intimal hyperplasia is known to promote in-stent restenosis after vascular stent implantation. Although previous studies have presented a variety of evidence that suggests the mechanisms of intimal lesion formation, it is still controversial which factor(s) predominantly contribute to the development of in-stent restenosis. In this study, we hypothesized that heterogeneous mechanisms coexist in the same lesion and then assessed the validity with resected whole arteries with in-stent lesions. METHODS: Whole arterial specimens with in-stent lesions were surgically resected from five patients who had undergone implantation of a Palmaz-Schatz stent 7 to 19 months previously and were histologically analyzed. For assessment of the pathogenetic heterogeneity of in-stent lesions, we divided each cross section into three parts: the inner intima within 250 microm from the luminal surface (zone A), the area surrounding the stent struts within 250 microm from the strut hole (zone B), and the remaining part of the intimal layer (zone C). We then evaluated cell density, cell replication, and cellular composition in each zone. Cell replication and cellular composition were analyzed with immunohistologic staining with antibodies against proliferating cell nuclear antigen and cell-specific antibodies. Each section was also stained with Alcian blue or Elastica van Gieson method for detection of matrix components. RESULTS: In all samples, the cell density of zone A was significantly higher than that of zone B (P <.05). Proliferating cell nuclear antigen staining results showed significantly higher cell replication in zone A as compared with that in other zones (P <.05). To the contrary, cell-specific immunostaining results revealed marked accumulation of leukocytes, macrophages, and T lymphocytes in zone B (P <.05). Regarding matrix components, proteoglycan was predominantly stained around stent struts and in the inner intima. CONCLUSION: The data of this study showed that two different pathogenetic processes in different zones possibly contributed to in-stent lesion formation at the same time. One process was an increase of cell number in the inner intima, which was the result of a prolonged increase of cell replication. The other process was accumulation of matrix around stent struts, which was suggested to be linked to infiltration of inflammatory cells in the same zone.

Aged↗