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William Marth, a director of the Company since March 2014. Since April 2018, Mr. Marth has served as the President and Chief Executive Officer of North America and Europe for Heritage Pharma Holdings Inc., a wholly owned subsidiary of Emcure Pharmaceuticals Ltd. Mr. Marth previously served as President and Chief Executive Officer of Albany Molecular Research Inc. since January 2014 until January 2018. Previously, Mr. Marth served as a Director of Albany Molecular Research Inc. and as chairman of its board of directors from June to December 2013. Prior to this, he served as President and Chief Executive Officer of Teva Pharmaceutical Industries Ltd. in the Americas from June 2010 to November 2012 and Chief Executive Officer of Teva North America from January 2008 to June 2010  and CEO  of Teva USA from January 2005 to January 2008. In addition, Mr. Marth worked with several large equity firms providing guidance on their healthcare investments. He was a member of Teva’s global executive management team from 2007 to 2012. From July 1999 to January 2002, he was the Executive Vice President and Vice President of Sales and Marketing for Teva USA. Prior to joining Teva USA, he held various positions with the Apothecon division of Bristol-Myers Squibb. Mr. Marth is a pharmacist and is currently a director at the University of Illinois at Chicago College of Pharmacy (UIC). Previously, Mr. Marth served as the Chairman of the Board of Directors of Sorrento Therapeutics from 2014 to July 2017, the Chairman of the Board of the Generic Pharmaceutical Association (GPhA) in 2008 and 2009 and the American Society for Health-System Pharmacists (ASHP) in 2010, and various boards and committees, including the University of the Sciences in Philadelphia and the Board of Ambassadors for John Hopkins’ Project RESTORE. Mr. Marth earned his B.Sc. in Pharmacy from the University of Illinois in 1977 and his M.B.A. in 1989 from the Keller Graduate School of Management, DeVry University. 

How to cite this article: Chen, Y.-Y. et al. QiShenYiQi Pills, a compound in Chinese medicine, protects against pressure overload-induced cardiac hypertrophy through a multi-component and multi-target mode. Sci. Rep. 5, 11802; doi: 10.1038/srep11802 (2015).

        (b)   Any fraud, whether or not material, that involves management or other employees who have a significant role in the registrant’s internal control over financial reporting.

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Reducing IGF-1 with metformin doesn’t need to involve AMPK,. Mice mutations with low IGF-1 live 25-60% longer than controls. Brown-Borg Nature 1996 384:33 and Flurkey. Mech Aging Dev 2002 123 (2-3) 121-130

We are slowly gaining an appreciation for the regulation of ion channels and membrane proteins by the lipids in which they are embedded. We have demonstrated that cholesterol regulates the expression and function of the 3 main cardiac isoforms of HCN channels, HCN1, HCN2, and HCN4. Intriguingly, this regulation appears to be isoform specific. Further studies will be needed to address the molecular details and physiological consequences of cholesterol regulation in this family of channels.

Aramchol is a synthetic conjugate of cholic acid, or a type of bile acid, and arachidic acid, or a type of saturated fatty acid, both of which, in their non-synthetic forms, are naturally occurring. The conjugated molecule acts upon important metabolic pathways, reducing fat accumulation in the liver, improving fatty acid oxidation and regulating the transport of cholesterol. The ability of Aramchol to decrease liver fat content may also reduce the inflammation and fibrosis in the liver and the risk of cardiovascular complications associated with NASH. Pre-clinical studies suggest Aramchol effect on fibrosis is also direct via collagen production from human hepatic stellate cells. We believe that Aramchol’s ability to reduce liver fat and liver fibrosis and the safety profile observed to date will enable it to be a safe and effective treatment for all stages of NASH in patients who are overweight or obese and have pre diabetes or type II diabetes mellitus and prevent the hepatic complications associated therewith.

α-SMA is a key marker of myofibroblasts, which are be the interstitial cells that are responsible for fibrosis25. Therefore, we examined whether P311 induced α-SMA expression. We assessed α-SMA mRNA and protein levels in both P311+/+ and P311−/− kidneys after UUO or sham operation. As shown in Fig. 5A, α-SMA mRNA expression was low in both the P311+/+ and P311−/− Sham groups, but was induced by UUO. However, α-SMA mRNA expression was higher in obstructed kidneys from P311+/+ mice compared to P311−/− mice (Fig. 4A, 1.93-fold difference, P < 0.001). Immunohistochemical analyses revealed that α-SMA protein localized to the cytoplasm of some tubular epithelial cells and interstitial cells in obstructed kidneys from both P311+/+ and P311−/− mice (Fig. 4B). However, the intensity of α-SMA expression, as determined by morphometric quantification, was significantly higher in obstructed kidneys from P311+/+ mice compared to P311−/− mice (Fig. 4C, 3.05-fold difference, P = 0.014). Consistent with these observations, western blot analysis showed that α-SMA protein expression was significantly higher in obstructed kidneys from P311+/+ mice compared to P311−/− mice (Fig. 4D, 1.48-fold difference, P = 0.032). No α-SMA expression was detected in the Sham groups (Fig. 4D). These data implied that P311 is involved in EMT in renal fibrogenesis.

The SPSS version 18.0 (Chicago, IL, USA) software was used in the statistical analysis. The data were expressed as means ± SD and p < 0.05 was considered statistically significant. Tukey was used to determine differences between groups.

Nevertheless, under the Companies Law, a company may not indemnify, exculpate or insure an Office Holder against any of the following:

(2) Audit related services consist of services that were reasonably related to the performance of the audit or reviews of our financial statements and not included under “Audit Fees” above, including, principally, providing consents for registration statement filings.