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Kiyoshi Tamaki

Publications and source records attributed to Kiyoshi Tamaki.

12 recordsLinked to original sources
PubMed2006

Carbonic-adsorbent AST-120 reduces overload of indoxyl sulfate and the plasma level of TGF-beta1 in patients with chronic renal failure.

BACKGROUND: We previously reported a significant increase in plasma TGF-beta1 in patients with chronic renal failure (CRF). Progression of CRF may be caused by persistent renal production of TGF-beta1. In CRF rat models, an oral carbonic absorbent (AST-120) reduces the expression of the TGF-beta1 gene in the kidney, and delays the progression of CRF, in part by alleviating the overload of indoxyl sulfate. The aim of this study was to evaluate the effect of AST-120 on plasma levels of indoxyl sulfate and TGF-beta1 in CRF patients. METHODS: Ten CRF patients (aged 59.3 +/- 9.5 years, 5 men, serum creatinine 4.37 +/- 1.72 mg/dl) were enrolled in this study. All patients maintained a regular dietary therapy and the same medication throughout the study. AST-120 was added at a dose of 6 g/day. Parameters including the slope of the reciprocal of the serum creatinine-time plot, plasma indoxyl sulfate level, and plasma and urinary levels of TGF-beta1 were compared before and after the treatment with AST-120. The mean observation periods before and after the treatment were 9.7 +/- 2.8 and 6.5 +/- 2.9 months, respectively. RESULTS: Administration of AST-120 significantly reduced the plasma levels of indoxyl sulfate (1.42 +/- 1.50 vs. 1.26 +/- 1.40 mg/dl, P < 0.05) and TGF-beta1 (17.9 +/- 7.2 vs. 10.6 +/- 4.7 ng/ml, P < 0.05) and improved the slope of the reciprocal of serum creatinine (-0.061 +/- 0.041 vs. -0.032 +/- 0.055 dl/mg/year, P < 0.05). CONCLUSIONS: These results support the notion that indoxyl sulfate and TGF-beta1 may be involved in the progression of CRF, and that the oral adsorbent AST-120 may suppress the progression, at least in part, by reducing overproduction of TGF-beta1.

Adsorption↗
PubMed2005

[Case of traditional herbal medicine-induced aristolochic acid nephropathy developing to end-stage renal failure].

A 48-year-old male was referred to our university hospital for severe azotemia with muscle cramp. He had been taking Chinese herbs as a traditional medicine to reduce hyperuricemia for about 9 months. Urinalysis showed trace proteinuria and hematuria without any casts. Renal glucosuria was also observed. In addition to azotemia, hyperchloremic metabolic acidosis and severe anemia were revealed. Hemodialysis was conducted and his general condition improved. A renal biopsy specimen revealed severe interstitial fibrosis and tubular atrophy with cellular degeneration. No remarkable glomerular changes were observed except for wrinkling of the basement membrane in a few glomeruli. Aristolochic acid was detected in the Chinese herbs, leading to the diagnosis of aristolochic acid nephropathy (AAN). His renal dysfunction was considered to be irreversible and he underwent maintenance hemodialysis. In Japan, AAN or Chinese herbs nephropathy decreased after an outbreak from 1995 to 2000. The public should be warned again that Chinese herbs, which are not permitted by the Japanese government, may contain aristolochic acid.

Aristolochic Acids↗
PubMed2005

[Steroid pulse therapy combined with tonsillectomy in a patient with IgA nephropathy complicated with tuberculous pleurisy].

We report a case of IgA nephropathy with tuberculous pleurisy that was treated with steroid pulse therapy combined with tonsillectomy. A 27-year-old female was referred to our hospital because of hematuria and proteinuria. Her urinalysis showed mild proteinuria (0.7 to 0.9 g/day) with dysmorphic red blood cells and cellular casts. Her serum creatinine level was within the normal range. Renal biopsy specimens revealed mild mesangial proliferation with cellular crescent and adhesion of glomeruli to the Bowman's capsule. Tubulointerstitial changes including mononuclear cell infiltration and tubular atrophy were also observed. Immunohistochemical staining of IgA and C3 was detected in the mesangial area, leading to the diagnosis of IgA nephropathy. She had a past history of tuberculous pleurisy at 13 years of age and had taken antituberculosis drug for one and a half year. Although treatment with angiotensin receptor antagonist was started, the amount of proteinuria was not changed. Steroid pulse therapy with tonsillectomy followed by oral prednisolone 20 mg/day was conducted. Proteinuria and hematuria gradually decreased. Her respiratory status and chest X-ray had been closely followed up by her respiratory physician. After one and a half years of treatment with low-dose prednisolone, her urinalysis became almost normal. Recurrence of tuberculosis was not observed during the follow-up period. The successful outcome of this case encouraged us to treat IgA nephropathy with a past history of tuberculosis using interventions including steroid pulse therapy.

Adult↗
PubMed2004

AGEs activate mesangial TGF-beta-Smad signaling via an angiotensin II type I receptor interaction.

BACKGROUND: The renin-angiotensin system (RAS) and the accumulation of advanced glycation end products (AGEs) have been implicated in the pathogenesis of diabetic nephropathy. Whether there is a functional interaction between the RAS and AGEs in diabetic nephropathy is not known. In this study, we investigated whether AGEs could activate autocrine angiotensin II (Ang II) signaling and subsequently induce transforming growth factor-beta (TGF-beta)-Smad signaling in cultured rat mesangial cells. METHODS: The intracellular formation of reactive oxygen species (ROS) was detected using the fluorescent probe CM-H2DCFDA. Ang II was measured by radioimmunoassay. TGF-beta released into media was quantitatively analyzed in an enzyme-linked immunosorbent assay (ELISA). Smad2, p27(Kip1) (p27), fibronectin, and receptor for AGEs (RAGE) protein expression were determined by Western blot analysis. TGF-beta-inducible promoter activity was analyzed by a luciferase assay. DNA synthesis was evaluated by 5-bomo-2'-deoxyuridine (BrdU) incorporation and de novo protein synthesis was determined by [3H]leucine incorporation. RESULTS: AGEs increased intracellular ROS generation in mesangial cells, and this effect was significantly inhibited by an antiserum against RAGE. AGEs also were found to stimulate Ang II production in a time- and dose-dependent manner, which was completely prevented by an antioxidant, N-acetylcysteine (NAC). AGE-induced TGF-beta overproduction was completely blocked by candesartan, an Ang II type 1 receptor (AT1R) antagonist. Both candesartan and neutralizing antibody against TGF-beta completely prevented AGEs-induced Smad2 phosphorylation and TGF-beta-inducible promoter activity. Furthermore, AGEs were found to inhibit DNA synthesis and to stimulate de novo protein synthesis and fibronectin production in association with up-regulation of p27. All of these phenomena were completely prevented by candesartan or a polyclonal antibody against TGF-beta. CONCLUSION: The present study suggests that AGE-RAGE-mediated ROS generation activates TGF-beta-Smad signaling and subsequently induces mesangial cell hypertrophy and fibronectin synthesis by autocrine production of Ang II. This pathway may provide an important link between metabolic and haemodynamic factors in promoting the development and progression of diabetic nephropathy.

Angiotensin II↗
PubMed2003

Unconditionally secure key distribution based on two nonorthogonal states.

We prove the unconditional security of the Bennett 1992 protocol, by using a reduction to an entanglement distillation protocol initiated by a local filtering process. The bit errors and the phase errors are correlated after the filtering, and we can bound the amount of phase errors from the observed bit errors by an estimation method involving nonorthogonal measurements. The angle between the two states shows a trade-off between accuracy of the estimation and robustness to noises.

Journal Article↗
PubMed2003

Smad protein and TGF-beta signaling in vascular smooth muscle cells.

Transforming growth factor-beta1 (TGF-beta1) plays a role in vascular remodeling by stimulating vascular smooth muscle cell (SMC) growth and matrix-protein synthesis at sites of vascular injury. Smad proteins have been shown to mediate intracellular signaling of this growth factor. We investigated the expression and phosphorylation of Smads in cultured rat aortic smooth muscle cells. In addition, we evaluated the effects of overexpression of Smad proteins on TGF-beta signal transduction by adenovirus-mediated gene transfer. In rat SMC, Smad1, Smad2, Smad3, Smad4 and Smad5 were detected by immunoprecipitation. Using antisera against phosphorylated Smad2, we showed that TGF-beta1-induced Smad2 phosphorylation in a concentration- and time-dependent manner. Using adenovirus-mediated transfection method, we demonstrated that overexpression of Smad2 or Smad4 was associated with an increased production of TGF-beta1-induced plasminogen activator inhibitor-1 (PAI-1). However, the most prominent expression of PAI-1 was observed upon cotransfection of both Smad2 and Smad4. Both the proliferative effect of TGF-beta1 under serum-free conditions and its anti-proliferative effect under serum-rich conditions were suppressed by the adenovirus-mediated overexpression of Smad7. These results indicated that Smads proteins were expressed in vascular SMC and that they mediated TGF-beta signaling in those cells.

Adenoviridae↗
PubMed2000

Locally activated renin-angiotensin system associated with TGF-beta1 as a major factor for renal injury induced by chronic inhibition of nitric oxide synthase in rats.

Chronic inhibition of nitric oxide synthase (NOS) is known to cause renal parenchymal injury with systemic hypertension. To elucidate the pathogenetic mechanism in renal damage induced by NOS inhibition, N(omega)-nitro-L-arginine methyl ester (L-NAME) was given orally for 12 wk in Wistar rats, and the roles of tissue renin-angiotensin system and transforming growth factor-beta1 (TGF-beta1) were investigated. BP and urinary protein excretion increased significantly in L-NAME rats compared with control rats, and glomerulosclerosis and interstitial fibrosis developed. In L-NAME rats, the cortical tissue levels of angiotensin-converting enzyme activity and angiotensin II were significantly higher than those in control rats. The cortical mRNA expressions of both TGF-beta1 and fibronectin were significantly elevated in L-NAME rats. Immunohistochemically, increased expressions of both fibronectin and alpha-smooth muscle actin were also revealed in L-NAME rats. In L-NAME rats, these histologic injuries and the increased expression of TGF-beta1 were equally ameliorated by either angiotensin-converting enzyme inhibitor or angiotensin II type 1 receptor antagonist, but not by hydralazine. In conclusion, the locally activated renin-angiotensin system in connection with the increased TGF-beta1 expression is a major pathogenetic feature of renal injury in chronically NOS-inhibited rats.

Actins↗