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Biomedical subjects

Tsugiyasu Kanda

Publications and source records attributed to Tsugiyasu Kanda.

10 recordsLinked to original sources
PubMed2003

Disaccharide analysis of glycosaminoglycans synthesized by cardiac myxoma cells in tumor tissues and in cell culture.

We analyzed the main disaccharide units of glycosaminoglycans synthesized by cardiac myxoma cells in vivo and in cell culture using high-performance liquid chromatography after 1-phenyl-3-methyl-5-pyrasolone labeling. Cardiac myxoma tissues contained large amounts of chondroitin-6-sulfate (46%) and hyaluronic acid (32%), along with some chondroitin-4-sulfate (13%), chondroitin (6%), and much less dermatan sulfate (3%). Cultured cardiac myxoma cells synthesized mainly chondroitin-6-sulfate. The abundant glycosaminoglycans in myxoma tissues may make up the characteristic friable gelatinous matrix which is favorable for embolism and tumor cell growth.

Adult↗
PubMed2003

Hormone replacement therapy causes a decrease in hepatocyte growth factor in hypertensive women.

OBJECTIVE: Serum hepatocyte growth factor (HGF) is associated with blood pressure. We investigated whether the serum HGF level differs between hypertensive and normotensive postmenopausal women (PMW) and whether hormone replacement therapy (HRT) alters the serum HGF level and blood pressure in hypertensive and normotensive PMW. DESIGN: Prospective observational study. METHODS: A total of 33 PMW with mild to moderate essential hypertension controlled by antihypertensive treatment (mean age, 57 +/- 6 years) and 23 normotensive PMW (mean age, 57 +/- 7 years) received continuous HRT (0.625 mg of conjugated equine estrogen combined with 2.5 mg of medroxyprogesterone acetate) once a day orally for 12 months, and we measured serum HGF levels and blood pressure before and 12 months after the start of HRT. RESULTS: The baseline serum HGF level was significantly higher in hypertensive PMW than in normotensive PMW. HRT significantly decreased the serum HGF level in hypertensive subjects, from 2.85 +/- 0.64 pmol/l to 2.49 +/- 0.65 pmol/l (P < 0.001), but not in normotensive subjects. HRT did not change blood pressure in either group. CONCLUSIONS: Serum HGF level before the start of HRT was higher in the hypertensive PMW than in the normotensive PMW. Furthermore, HRT decreases serum HGF without decreasing blood pressure in hypertensive PMW. The HRT-induced decrease in serum HGF was greater in hypertensive PMW than in normotensive PMW, and the decrease was independent of blood pressure changes.

Aged↗
PubMed2003

Hormone replacement therapy decreases insulin resistance and lipid metabolism in Japanese postmenopausal women with impaired and normal glucose tolerance.

OBJECTS: To investigate the effect of combined estrogen and progesterone therapy on insulin resistance (IR) and carbohydrate and lipid metabolism in postmenopausal women (PMW) with impaired (IGT) and normal glucose tolerance (NGT). METHODS: Sixteen Japanese PMW with IGT and 33 with NGT received daily oral hormone replacement therapy (HRT; 0.625 mg of conjugated equine estrogen plus 2.5 mg of medroxyprogesterone acetate) for 12 months. As controls, 13 Japanese PMW with IGT and 31 with NGT were enrolled and not treated by HRT. Fasting plasma glucose (FPG), fasting immunoreactive insulin (IRI), and IR were measured in each subject at study initiation and 12 months later. We used homeostasis model assessment (HOMA) to determine IR. RESULTS: FPG and HOMA IR were decreased in both HRT groups, and fasting IRI was reduced in the HRT-NGT group. In controls, FPG, fasting IRI, and HOMA IR were unaltered. Total and low-density lipoprotein cholesterol were decreased and high-density lipoprotein cholesterol was increased in both HRT groups, but triglyceride was unchanged. In controls, lipid metabolism was unaltered. CONCLUSION: HRT decreased IR and improved carbohydrate and lipid metabolism in Japanese PMW with IGT and NGT. These beneficial effects argue for the use of HRT in PMW with IGT as well as NGT.

Asian People↗
PubMed2003

Effects of hormone replacement therapy on office and ambulatory blood pressure in Japanese hypertensive postmenopausal women.

No study has demonstrated that hormone replacement therapy (HRT) affects blood pressure (BP) measured by 24-h ambulatory blood pressure monitoring (ABPM) in Japanese postmenopausal women (PMW) with normotension or mild-to-moderate essential hypertension. In the present study, we examined the effects of HRT on office BP and 24-h ambulatory blood pressure (ABP) in Japanese hypertensive or normotensive PMW. Thirty-one hypertensive (HT-HRT group) and 17 normotensive PMW (NT-HRT group) received HRT (0.625 mg of conjugated equine estrogen combined with 2.5 mg of medroxyprogesterone acetate) orally for 12 months, and 30 hypertensive (HT-Control group) and 19 normotensive PMW (NT-Control group) did not receive HRT. In all of the hypertensive PMW, BP was controlled by a variety of antihypertensive drugs before starting HRT. The hypertensive PMW were divided into two groups according to the results of ABP before HRT: nondippers (those without a diurnal change in BP) and dippers (those with a diurnal change in BP). In all patients, office BP measurements and 24-h ABPM were performed before and 12 months after the start of HRT. HRT did not change either the office or the 24-h ambulatory systolic, diastolic, or mean BP in any of the groups. Therefore, HRT did not significantly alter the proportion of nondippers. We conclude that with respect to BP, HRT might not be harmful in hypertensive PMW whose BP has been well-controlled prior to the initiation of HRT, as well as in normotensive PMW.

Antihypertensive Agents↗
PubMed2003

Effects of angiotensin II receptor antagonists on insulin resistance syndrome and leptin in sucrose-fed spontaneously hypertensive rats.

In order to investigate the usefulness of angiotensin II type 1 receptor (AT1) antagonists (ARA) in the treatment of hypertension with insulin resistance syndrome, we studied the effects of a high dose sucrose diet and ARA on insulin sensitivity, plasma lipids, and leptin in spontaneous hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). SHR and WKY were divided into three groups and treated for 12 weeks: those fed a standard chow, those given a sucrose-rich chow or those given a sucrose-rich chow and ARA. While in SHR the weight of both subcutaneous and mesenteric adipose tissue was greater in the sucrose-rich chow fed animals than in the standard chow fed animals, ARA treatment significantly decreased the weights of both subcutaneous and mesenteric adipose tissue. ARA treatment decreased free fatty acid and triglyceride in SHR, and increased high density lipoprotein cholesterol in SHR and WKY. Homeostasis model assessment-insulin resistance (HOMA-IR) index, plasma levels of leptin, and leptin mRNA in mesenteric adipose tissue were significantly greater in the sucrose-rich chow fed animals than in the standard chow fed animals, and significantly lower in the ARA-treated sucrose-rich chow fed animals than in the sucrose-rich chow fed animals in both SHR and WKY. ARA improved insulin resistance, and reduced plasma leptin and leptin mRNA in adipose tissue. These results suggest that the improvement of insulin resistance by ARA may be attributed, at least in part, to the reduction of adipose tissue weight. It is concluded that ARA is useful in the treatment of patients with hypertension and concomitant insulin resistance syndrome.

Adipose Tissue↗
PubMed2003

Effects of hormone replacement therapy on serum angiotensin-converting enzyme activity and plasma bradykinin in postmenopausal women according to angiotensin-converting enzyme-genotype.

An insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme (ACE) gene determines serum ACE levels. The D allele is associated with increased ACE activity and is linked to cardiovascular disease. Hormone replacement therapy (HRT) in postmenopausal women (PMW) decreases serum ACE activity and concomitantly increases plasma bradykinin. We investigated the effect of HRT on these parameters in PMW according to ACE-genotype. We assessed 68 PMW during 12-month oral HRT (0.625 mg conjugated estrogen +2.5 mg medroxyprogesterone acetate). ACE genotype was determined at baseline, and serum ACE activity and plasma bradykinin were measured at baseline and after 3-, 6-, and 12-month HRT. We divided the PMW into three groups according to ACE genotype: groups I/I (n = 26), I/D (n = 33), and D/D (n = 9). HRT resulted in a significant reduction in the genotype-associated increase in ACE activity in the ACE I/D and D/D groups after 6-month (p < 0.001 and p < 0.05, respectively) and 12-month HRT (p < 0.001 and p < 0.01, respectively), but not in the I/I group. While the reduction of ACE activity was expected to increase bradykinin in the ACE I/D and D/D groups, HRT significantly increased the bradykinin levels not only in these two groups but also in the ACE I/I group at both 6 months (p < 0.01, p < 0.05, and p < 0.001, respectively) and 12 months after the start of HRT (p < 0.01, p < 0.01, and p < 0.01, respectively). These results suggest that the increased plasma bradykinin of PMW by HRT might not be induced solely by the reduction in serum ACE activity.

Aged↗
PubMed2003

Effects of hormone replacement therapy on circulating docosahexaenoic acid and eicosapentaenoic acid levels in postmenopausal women.

Hormone replacement therapy (HRT) has antiatherosclerotic effects of which the mechanism remains unclear. The ingestion of fish oil or other sources of n-3 polyunsaturated fatty acids has been included in comprehensive strategies to prevent atherosclerosis. Many epidemiologic studies have shown that the dietary intake of docosahexaenoic acid and eicosapentaenoic acid has antiatherosclerotic effects. We investigated the effect of HRT on plasma docosahexaenoic acid and eicosapentaenoic acid concentrations in postmenopausal women. Fifty-nine postmenopausal women, who received conjugated estrogens (0.625 mg/day) and medroxyprogesterone (2.5 mg/day) for 12 months, and 45 control postmenopausal women, who did not receive HRT, volunteered to participate in this study. Plasma docosahexaenoic acid and eicosapentaenoic acid concentrations were measured at baseline and at 6 and 12 months after the start of HRT. HRT significantly increased the plasma docosahexaenoic acid and eicosapentaenoic acid concentrations from 134 +/- 5 microg/ml and 69 +/- 4 microg/ml at baseline to 156 +/- 7 microg/ml and 85 +/- 7 microg/ml after 12 months (both p<0.01). However, the control group showed no significant change in their plasma docosahexaenoic acid and eicosapentaenoic acid levels during the study. HRT increased plasma docosahexaenoic acid and eicosapentaenoic acid levels in postmenopausal women. We propose that the increase in docosahexaenoic acid and eicosapentaenoic acid may be partially responsible for the beneficial mechanisms by which HRT induces an antiatherosclerotic effect in postmenopausal women.

Adult↗
PubMed2002

Improved myocardial ischemia/reperfusion injury in mice lacking tumor necrosis factor-alpha.

OBJECTIVES: This study sought to assess the role of tumor necrosis factor-alpha (TNF-alpha) in myocardial ischemia/reperfusion (I/R) injury using TNF-alpha knockout (KO) mice. BACKGROUND: Tumor necrosis factor-alpha is thought to be involved in the pathogenesis of myocardial I/R injury by promoting leukocyte infiltration of the myocardium. However, the precise role of TNF-alpha in I/R injury is still unknown. METHODS: The hearts in TNF-alpha KO and wild-type (WT) mice were exposed by left lateral thoracotomy, and the left coronary artery was occluded for 30 min then reperfused for 120 min. RESULTS: The infarct size in TNF-alpha KO mice was significantly reduced compared with WT mice. The frequency of arrhythmia was decreased, and cardiac function during reperfusion was significantly improved in TNF-alpha KO mice compared with WT mice. The activation of nuclear factor-kappaB (NF-kappaB), the expression of chemokines and adhesion molecules and the infiltration of leukocytes were also significantly reduced in TNF-alpha KO mice, compared with WT mice. These findings provide evidence that TNF-alpha aggravates I/R injury. CONCLUSIONS: Tumor necrosis factor-alpha exacerbates myocardial I/R injury at an early stage of reperfusion by activating NF-kappaB, thereby inducing chemokines and adhesion molecules and facilitating leukocyte infiltration.

Animals↗
PubMed2002

Effects of hormone replacement therapy on left ventricular hypertrophy and growth-promoting factors in hypertensive postmenopausal women.

We investigated the effects of hormone replacement therapy (HRT) on left ventricular hypertrophy (LVH) and growth-promoting factors in hypertensive postmenopausal women (PMW) with LVH. Twenty-one Japanese hypertensive PMW (age 55.3+/-0.8 years) with LVH who had never received HRT volunteered to participate in this study. Eleven subjects received a daily dose of HRT (0.625 mg conjugated equine estrogen, 2.5 mg medroxyprogesterone acetate) orally for 12 months. Ten PMW who refused HRT were enrolled as controls. Blood pressure and serum angiotensin-converting enzyme (ACE) activity, plasma aldosterone, and insulin resistance were measured. M-mode echocardiography and blood pressure measurements were performed in all patients. Data obtained before and after 12 months of HRT were compared. No significant differences in blood pressure were observed between the two groups after 12 months of HRT. In the HRT group, the LV mass index (p<0.01), serum ACE activity (p<0.01), and plasma aldosterone (p<0.01) levels were reduced after 12 months of treatment. The changes in serum ACE activity and plasma aldosterone were not correlated with the change in LV mass index in the HRT group. No significant changes in blood pressure, LV mass index, serum ACE activity, plasma aldosterone, or insulin resistance were observed in the control group. HRT contributed to the reduction of LV mass in hypertensive PMW. However, the effect of HRT on LVH did not appear to be associated with changes in growth-promoting factors, such as blood pressure, serum ACE activity, plasma aldosterone, and insulin resistance.

Aldosterone↗