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Articles by T Noda
Total Records ( 5 ) for T Noda
  K Iskandar , Y Cao , Y Hayashi , M Nakata , E Takano , T Yada , C Zhang , W Ogawa , M Oki , S Chua , H Itoh , T Noda , M Kasuga and J. Nakae
 

Both insulin and leptin signaling converge on phosphatidylinositol 3-OH kinase [PI(3)K]/3-phosphoinositide-dependent protein kinase-1 (PDK-1)/protein kinase B (PKB, also known as Akt) in proopiomelanocortin (POMC) neurons. Forkhead box-containing protein-O1 (FoxO1) is inactivated in a PI(3)K-dependent manner. However, the interrelationship between PI(3)K/PDK-1/Akt and FoxO1, and the chronic effects of the overexpression of FoxO1 in POMC neurons on energy homeostasis has not been elucidated. To determine the extent to which PDK-1 and FoxO1 signaling in POMC neurons was responsible for energy homeostasis, we generated POMC neuron-specific Pdk1 knockout mice (POMCPdk1–/–) and mice selectively expressing a constitutively nuclear (CN)FoxO1 or transactivation-defective (256)FoxO1 in POMC neurons (CNFoxO1POMC or 256FoxO1POMC). POMCPdk1–/– mice showed increased food intake and body weight accompanied by decreased expression of Pomc gene. The CNFoxO1POMC mice exhibited mild obesity and hyperphagia compared with POMCPdk1–/– mice. Although expression of the CNFoxO1 made POMCPdk1–/– mice more obese due to excessive suppression of Pomc gene, overexpression of 256FoxO1 in POMC neurons had no effects on metabolic phenotypes and Pomc expression levels of POMCPdk1–/– mice. These data suggest a requirement for PDK-1 and FoxO1 in transcriptional regulation of Pomc and food intake.

  S Kamakura , T Ohe , K Nakazawa , Y Aizawa , A Shimizu , M Horie , S Ogawa , K Okumura , K Tsuchihashi , K Sugi , N Makita , N Hagiwara , H Inoue , H Atarashi , N Aihara , W Shimizu , T Kurita , K Suyama , T Noda , K Satomi , H Okamura , H Tomoike and for the Brugada Syndrome Investigators in Japan
 

Background— The prognosis of patients with saddleback or noncoved type (non–type 1) ST-elevation in Brugada syndrome is unknown. The purpose of this study was to clarify the long-term prognosis of probands with non–type 1 ECG and those with coved (type 1) Brugada-pattern ECG.

Methods and Results— A total of 330 (123 symptomatic, 207 asymptomatic) probands with a coved or saddleback ST-elevation ≥1 mm in leads V1–V3 were divided into 2 ECG groups—type 1 (245 probands) and non–type 1 (85 probands)—and were prospectively followed for 48.7±15.0 months. The absence of type 1 ECG was confirmed by drug provocation test and multiple recordings. The ratio of individuals with a family history of sudden cardiac death (14%) was lower than previous studies. Clinical profiles and outcomes were not notably different between the 2 groups (annual arrhythmic event rate of probands with ventricular fibrillation; type 1: 10.2%, non–type 1: 10.6%, probands with syncope; type 1: 0.6%, non–type 1: 1.2%, and asymptomatic probands; type 1: 0.5%, non–type 1: 0%). Family history of sudden cardiac death at age <45 years and coexistence of inferolateral early repolarization with Brugada-pattern ECG were independent predictors of fatal arrhythmic events (hazard ratio, 3.28; 95% confidence interval, 1.42 to 7.60; P=0.005; hazard ratio, 2.66; 95% confidence interval, 1.06 to 6.71; P=0.03, respectively, by multivariate analysis), although spontaneous type 1 ECG and ventricular fibrillation inducibility by electrophysiological study were not reliable parameters.

Conclusions— The long-term prognosis of probands in non–type 1 group was similar to that of type 1 group. Family history of sudden cardiac death and the presence of early repolarization were predictors of poor outcome in this study, which included only probands with Brugada-pattern ST-elevation.

  T. a Matsuyama , T Kurita , K Suyama , H Okamura , T Noda , K Satomi , W Shimizu , N Aihara , Y Ikeda , S Inoue , S Kamakura and H. Ishibashi Ueda
 

A 68-year-old woman with idiopathic dilated cardiomyopathy suffered from drug-resistant monomorphic ventricular tachycardia (VT). Electrophysiological study revealed a re-entrant VT circuit located just beneath the inferior mitral valve annulus. The VT was considered to be related to the mitral valve isthmus and was abolished by radiofrequency ablation. The patient died 2 years after the ablation due to worsening of heart failure and an autopsy was performed. Pathological examination revealed ablation scar tissue on the localized myocardial bundle running parallel to the mitral valve annulus. Therefore, this bundle appeared to comprise the slow conduction area of the re-entrant VT in this case.

  T Noda and T. Yoshimori
 

Autophagy is a catabolic process by which cells degrade their own cytoplasmic constituents. Cells respond to the stress response of nutrient deficiency by degrading a portion of their cellular components to produce amino acids and energy. Recently, it became evident that the autophagic machinery is also involved in a kind of innate immune system. Some bacteria that invade mammalian cells are eventually entrapped in an autophagic membrane structure. In this review, we describe the current understanding of three of the basic components of the canonical autophagy machinery—LC3, the Atg16L complex and phosphatidylinositol 3-phosphate (PI3P)—which are dynamically associated with the autophagic structure. LC3 is proposed to function in autophagosome closure, whereas the Atg16L complex functions as an E3-like protein in ubiquitination-like reactions in the LC3 lipidation system. PI3P is a key determinant of the autophagic membrane. Further, their relation to bactericidal autophagy (i.e. xenophagy) will be introduced.

  K Matsunaga , E Morita , T Saitoh , S Akira , N. T Ktistakis , T Izumi , T Noda and T. Yoshimori
 

Generation of PI3P in the normally PI3P-deficient ER membrane makes the organelle a platform for autophagosome formation.

 
 
 
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