Publications (6)10.03 Total impact
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Article: Direct renin inhibitor prevents and ameliorates insulin resistance, aortic endothelial dysfunction and vascular remodeling in fructose-fed hypertensive rats.
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ABSTRACT: Angiotensin-converting enzyme inhibitors and angiotensin II type 1 receptor blockers can improve insulin resistance and vascular dysfunction in insulin-resistant rats; however, there are few reports on the effects of direct renin inhibitors on these conditions. We investigated the effects of a direct renin inhibitor, aliskiren, on insulin resistance, aortic endothelial dysfunction and vascular remodeling in fructose-fed hypertensive rats. Male Wistar-Kyoto rats were divided into four groups (n=6 per group) and studied for 8 weeks: Group Con: standard chow diet; group Fru: high-fructose diet (60% fructose); Group FruA: high-fructose diet with concurrent aliskiren treatment (100 mg kg(-1) per day); and Group FruB: high-fructose diet with subsequent aliskiren treatment 4 weeks later. Blood was collected for biochemical assays, and isolated rings of the thoracic aorta were obtained for analysis of vascular reactivity, vascular structure and lipid peroxide. Rats fed with high-fructose diets developed significant systolic hypertension, decreased plasma nitrite (NO(2); nitric oxide metabolite) levels and increased plasma glucose, insulin, triglyceride, total cholesterol and aortic lipid peroxide levels, and aortic wall thickness compared with control rats. Aliskiren treatment, either concurrent or subsequent, elevated plasma NO(2) levels and reduced systolic hypertension, insulin resistance, dyslipidemia, aortic lipid peroxide levels and aortic wall hypertrophy in FHR. The peak endothelium-dependent aortic relaxations were significantly higher in rats that received aliskiren treatment than in those that did not. In conclusion, our findings suggest that aliskiren prevents and ameliorates insulin resistance, aortic endothelial dysfunction and oxidative vascular remodeling in fructose-fed hypertensive rats.Hypertension Research advance online publication, 16 August 2012; doi:10.1038/hr.2012.124.Hypertension Research 08/2012; · 2.58 Impact Factor -
Article: Aliskiren prevents and ameliorates metabolic syndrome in fructose-fed rats.
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ABSTRACT: The renin-angiotensin system plays a major role in the pathogenesis of metabolic syndrome. The objective of this study was to examine the effects of aliskiren, a direct renin inhibitor, on the metabolic syndrome of fructose-fed rats. Male Sprague-Dawley rats were divided into 4 groups (n = 6 for each group). Group Con: rats were fed a standard chow diet for 8 weeks, group Fru: rats were fed a high fructose diet (60% fructose) for 8 weeks, group FruA: rats were fed a high fructose diet and were co-infused with aliskiren (100 mg/kg/day), and group FruB: rats were treated as group Fru, but aliskiren was administered 4 weeks later. Systolic blood pressure (SBP), homeostasis model assessment-insulin resistance (HOMA-IR), and blood profiles were measured. By the end of week 4 and 8 of a high fructose diet, SBP had increased significantly from 111 ±5 to 142 ±4 and 139 ±5 mmHg (p < 0.05), respectively. A high fructose diet significantly increased HOMA-IR from baseline (6.15 ±1.59) to 21.25 ±2.08 and 21.28 ±3.1 (p < 0.05) at week 4 and 8, respectively, and significantly induced metabolic syndrome. Concurrent aliskiren treatment prevented the development of hypertension and metabolic syndrome in fructose-fed rats. When fructose-induced hypertension was established, subsequent aliskiren treatment for 4 weeks reversed the elevated SBP and ameliorated metabolic syndrome. There were no significant differences in food, water intake, urine flow or body weight gain among groups. Aliskiren not only prevents but also ameliorates metabolic syndrome in fructose-fed rats.Archives of medical science : AMS. 10/2011; 7(5):882-8. -
Article: Increased risk of cancer in chronic dialysis patients: a population-based cohort study in Taiwan.
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ABSTRACT: An increased incidence of cancer in chronic dialysis patients has not been confirmed in the Chinese population. The aim of this population-based study was to examine the risk of various types of cancers in chronic dialysis patients in Taiwan. Data of 92 348 chronic dialysis patients extracted from the National Health Institutes Research Database during 1997-2008 were analyzed. Patients newly diagnosed with end-stage renal disease, free of cancer and receiving dialysis for >3 months were eligible for inclusion in the study. After a mean follow-up of 4.4 years, a new cancer was diagnosed in 4328 chronic dialysis patients. The standardized incidence ratio (SIR) of chronic dialysis patients was 1.4 [95% confidence interval (CI): 1.3-1.4] and annual incidence of cancer was 1.1%. A trend of an increased SIR of cancer was observed in young patients and within the first year of dialysis. Bladder cancer carried the highest SIR (SIR: 8.2, 95% CI: 6.7-9.9) and had the highest frequency (21.2%). Importantly, the frequency (15.3%) of liver cancer was the second highest and the SIR (SIR: 1.4, 95% CI: 1.2-1.5) of liver cancer in chronic dialysis patients was higher than that of their healthy counterparts. Unexpectedly, chronic dialysis patients had a significantly reduced risk of developing lung cancer. Increased risk of cancer in chronic dialysis patients is confirmed in the Taiwanese population and it is necessary to develop different strategies for cancer screening in chronic dialysis patients among different ethnicities.Nephrology Dialysis Transplantation 08/2011; 27(4):1585-90. · 3.40 Impact Factor -
Article: RC-RNase-induced cell death in estrogen receptor positive breast tumors through down-regulation of Bcl-2 and estrogen receptor.
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ABSTRACT: RC-RNase exerts anti-cancer effects on many tumors. However, the mechanisms by which RC-RNase induces cytotoxicity in different tumor cells are unclear. Currently, estrogen receptor (ER)-positive and negative breast tumors are treated with RC-RNase. Our data demonstrate that RC-RNase induces cell death on ER-positive but not on ER-negative breast tumors. This study also shows that down-regulation of ER and Bcl-2 is found on RC-RNase-treated ER-positive breast tumors. Additionally, Bcl-2 overxpression can prevent ER-positive breast tumors from cell death treated with RC-RNase. In summary, this study demonstrates that RC-RNase-induced cell death of ER-positive breast tumors is through regulation of ER and Bcl-2.Oncology Reports 03/2011; 25(3):849-53. · 1.84 Impact Factor -
Article: Baclofen-induced neurotoxicity in chronic renal failure patients with intractable hiccups.
Southern Medical Journal 12/2006; 99(11):1308-9. · 0.83 Impact Factor -
Article: Acquired bartter-like syndrome associated with gentamicin administration.
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ABSTRACT: Although acute nonoliguric renal failure is a well-known nephrotoxic effect of aminoglycoside antibiotics, less recognized is acquired Bartter-like syndrome. Herein, we describe four female patients who presented with marked paresthesia, muscle weakness, and tetany following gentamicin therapy with total dose ranging from 1.2 g to 2.6 g. All were normotensive. Biochemical abnormalities included hypokalemia (K+ 1.8-2.3 mmol/L), metabolic alkalosis (HCO(3-) 31.9-34.2 mmol/L), hypomagnesemia (Mg2+ 0.9-1.2 mg/dL), hypermagnesiuria (fractional excretion of Mg 3-6%), hypocalcemia (free Ca2+ 2.0-4.1 mg/dL), and hypercalciuria (molar ratio of Ca2+/creatinine 0.23-0.53), all consistent with Bartter-like syndrome. Serum immunoreactive parathyroid hormone concentration was low despite the hypocalcemia. The Bartter-like syndrome lasted for 2 to 6 weeks after cessation of gentamicin, coupled with supplementation of K+, Ca2+, and Mg2+. These biochemical abnormalities resembled those seen in patients with gain-of-function mutations in the calcium-sensing receptor. We hypothesize that gentamicin, a polyvalent cationic molecule, induces the action of calcium-sensing receptor on the thick ascending loop of Henle and distal convoluted tubule to cause renal wasting of Na+, K+, Cl-, Ca2+, and Mg2+.The American Journal of the Medical Sciences 04/2005; 329(3):144-9. · 1.39 Impact Factor
Top co-authors
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Institutions
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2012
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Buddhist Tzu Chi General Hospital
Taipei, Taipei, Taiwan
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2011
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Tzu Chi University
- Institute of Medical Sciences
Hualian, Taiwan, Taiwan
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2005
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National Defense Medical Center
- Tri-Service General Hospital
Taipei, Taipei, Taiwan
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