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The tubular epithelium, which undergoes EMT, is an important source of matrix-producing cells and contributes to renal fibrogenesis. During EMT, tubular epithelial cells express vimentin, a fibroblast marker, and α-SMA, a myofibroblast marker17. To determine whether P311 regulates renal fibrogenesis via EMT, we examined vimentin and α-SMA expression. We found that vimentin protein levels as well as α-SMA mRNA and protein expression were significantly down-regulated in obstructed kidneys from P311−/− mice. Furthermore, α-SMA-positive regions and acidophilic degeneration seem to be co-localized with P311-positive areas in some tubular epithelial cells. Our previous study also showed that transfecting P311 into human fibroblasts stimulated α-SMA expression10. Moreover, P311 transfection into two murine fibroblast cells induced α-SMA expression. P311 and α-SMA co-localize in myofibroblasts during wound healing, and P311 expression occurs upstream of α-SMA expression9. These findings support our hypothesis that P311 is involved in renal fibrogenesis EMT.

DYNAMIC ALERT Limited ( OTCBB: DYMC ) works with World Authorities on phytocannabinoid science targeting critical illnesses. Adhering to scientific methodologies to develop, produce, and commercialize phytocannabinoid based pharmaceutical products.

Hogman, M., Frostell, C., Arnberg, H. & Hedenstierna, G. Bleeding time prolongation and NO inhalation. Lancet. 341, 1664–1665 (1993).

A foreign corporation’s PFIC status is an annual determination that is based on tests that are factual in nature, and our status for any year will depend on our income, assets, and activities for such year. Based upon our review of our financial data, we believe that we were not a PFIC for our 2018 taxable year and we expect to be a PFIC for the 2019 taxable year. Because the PFIC determination is highly fact intensive, there can be no assurance that we will be a PFIC in 2019 or for any other taxable year.

I appreciate your input. Thank you for the information about the optimal IGF -1 levels. Very helpful to know.

        As of March 1, 2019, we had 10 stockholders of record. The number of holders is based upon the actual number of holders registered in our records at such date and excludes holders in "street name" or persons, partnerships, associations, corporations, or other entities identified in security positions listings maintained by depository trust companies.

Hi Your points are interesting and deserving of further research. I wasn’t aware of the sirt1 issue until now, so perhaps as you suggest when I take rapamycin on a Sunday I should wait until Tuesday or Wednesday to hit the resveratrol/ pterostilbene. That’s certainly a consideration. Will look into it.

        The weighted average assumptions used to estimate the grant date fair value of the stock options using the Black-Scholes option pricing model were as follows:

Additional clinical trials may divert a significant amount of Company resources and may ultimately be unsuccessful.

All references to “we,” “us,” “our,” “the Company” and “our Company”, in this Annual Report on Form 20-F, or our annual report, are to Galmed Pharmaceuticals Ltd. and its subsidiaries, unless the context otherwise requires. All references to “shares” or “ordinary shares” are to our ordinary shares, NIS 0.01 nominal par value per share. All references to “Israel” are to the State of Israel. “U.S. GAAP” means the generally accepted accounting principles of the United States. Unless otherwise stated, all of our financial information presented in this annual report has been prepared in accordance with U.S. GAAP. Any discrepancies in any table between totals and sums of the amounts listed are due to rounding. Unless otherwise indicated, or the context otherwise requires, references in this annual report to financial and operational data for a particular year refer to the fiscal year of our company ended December 31 of that year.

        There are numerous potential therapeutic targets in the complement cascade, and inhibiting the cascade at different points may be beneficial to treat different conditions depending on the disease biology. Inhibition of C5 cleavage effectively blocks generation of C5a and MAC regardless of the specific pathway involved in complement activation. This approach of inhibiting C5 cleavage is most relevant to diseases with significant MAC deposition resulting in tissue injury, as is the case for gMG and PNH. In other conditions, the tissue injury is related to activation of a specific pathway of complement, such as kidney diseases like C3 glomerulopathies, in which tissue injury may be mediated by deposition of complement component 3 following uncontrolled activation of the alternative pathway. In this case, selective inhibition of the alternative pathway by targeting a key enzyme in the alternative pathway, Factor D, may block C3 deposition while preserving the capacity of the classical and lectin pathways of complement to continue to fight infection. The classical pathway is activated when an antibody binds to the surface of a pathogen and recruits a complex of C1q, C1r, and C1s, and we believe that inhibition of C1 may be efficacious for treatment of certain autoimmune and CNS diseases.