Erratum:Randomized double-blind placebo-controlled trial of perhexiline in heart failure with preserved ejection fraction syndrome (Future Cardiology (2014) 10:6 (693-698))

Following publication of the Clinical Trial Protocol by Satnam Singh, Roger Beadle, Donnie Cameron, Amelia Rudd, Maggie Bruce, Baljit Jagpal, Konstantin Schwarz, Gemma Brindley, Fergus McKiddie, Chim Lang, Dana Dawson and Michael Frenneaux, titled ‘Randomized double-blind placebo-controlled trial of perhexiline in heart failure with preserved ejection fraction syndrome’, which appeared in the December 2014 issue of Future Cardiology (Future Oncol. 10[6], 693–698 [2014]), it has been brought to our attention that the author names were presented incorrectly as:Satnam Singh, Roger Beadle, Donnie Cameron, Amelia Rudd, Maggie Bruce, Baljit Jagpal, Konstantin Schwarz, Gemma Brindley, Fergus Mckiddie, Peter Nightingale, Chim Lang, Dana Dawson and Michael Frenneaux.The correct presentation should be:Satnam Singh, Roger Beadle, Donnie Cameron, Amelia Rudd, Maggie Bruce, Baljit Jagpal, Konstantin Schwarz, Gemma Brindley, Fergus Mckiddie, Chim Lang, Dana Dawson and Michael Frenneaux.The authors and editors of Future Cardiology would like to sincerely apologize for any inconvenience or confusion this may have caused our readers.<br/

The role of cardiac neural crest cells in the development of the outflow tract of the heart

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Randomized double-blind placebo-controlled trial of perhexiline in heart failure with preserved ejection fraction syndrome

Recently heart failure with preserved ejection fraction (HFpEF) has emerged as a huge epidemic. Increasing evidence shows the role of energy deficiency in the pathophysiology of HFpEF. In the current study, we hypothesize that the use of metabolic modulator perhexiline would correct myocardial energy deficiency and improve exercise capacity and diastolic abnormalities in patients with this syndrome

Deletion of SIRT1 From Hepatocytes in Mice Disrupts Lipin-1 Signaling and Aggravates Alcoholic Fatty Liver

BACKGROUND&AIMS: Sirtuin (SIRT1) is a NAD(+)-dependent protein deacetylase that regulates hepatic lipid metabolism by modifying histones and transcription factors. Ethanol exposure disrupts SIRT1 activity and contributes to alcoholic liver disease (ALD) in rodents, but the exact pathogenic mechanism is not clear. We compared mice with liver-specific deletion of Sirt1 (Sirt1LKO) mice with their LOX littermates (controls). METHODS: We induced alcoholic liver injury in male Sirt1LKO and control mice, placing them on Lieber-DeCarli ethanol-containing diets for 10 days and then administering a single dose of ethanol (5 g/kg body weight) via gavage. Liver and serum samples were collected. We also measured mRNA levels of SIRT1, SFRS10, and lipin-1β and lipin-1α in liver samples from patients with alcoholic hepatitis (AH) and individuals without AH (controls). RESULTS: On the ethanol-containing diet, livers of Sirt1LKO mice accumulated larger amounts of hepatic lipid and expressed higher levels of inflammatory cytokines than control mice; serum of Sirt1LKO mice had increased levels of alanine aminotransferase and aspartate aminotransferase. Hepatic deletion of SIRT1 exacerbated ethanol-mediated defects in lipid metabolism, mainly by altering the function of lipin-1, a transcriptional regulator of lipid metabolism. In cultured mouse AML-12 hepatocytes, transgenic expression of SIRT1 prevented fat accumulation in response to ethanol exposure, largely by reversing the aberrations in lipin-1 signaling induced by ethanol. Liver samples from patients with AH had reduced levels of SIRT1 and a higher ratio of Lpin1β:α mRNAs than controls. CONCLUSIONS: In mice, hepatic deletion of Sirt1 promotes steatosis, inflammation, and fibrosis in response to ethanol challenge. Ethanol-mediated impairment of hepatic SIRT1 signaling via lipin-1 contributes to development of alcoholic steatosis and inflammation. Reagents designed to increase SIRT1 regulation of lipin-1 might be developed to treat patients with alcoholic fatty liver disease