In February 2018, we completed a follow-on public offering of 9,660,000 shares of common stock, including the full exercise of the underwriters’ option to purchase an additional 1,260,000 shares, at $6.00 per share and received aggregate net proceeds of $54.1 million, after deducting $3.5 million of underwriting discounts and commissions and approximately $0.4 million of offering expenses.

        The Company’s consolidated financial statements reflect its financial statements and those of its subsidiaries in which the Company holds a controlling financial interest, including Cosmix, Ra Europe Limited, and Ra Pharmaceuticals Security Corporation. Intercompany balances and transactions are eliminated in consolidation.

Qu, Y. L. et al. Heat-treated membranes with bioelectricity promote bone regeneration. J. Biomater. Sci-Polym. Ed. 25, 211–223 (2014).

The primary endpoint of the study was the change from baseline to end of study in liver triglycerides ratio as measured by magnetic resonance spectroscopy, or MRS (Aramchol 600mg vs. placebo). Secondary endpoints, demonstrated through biopsy, included fibrosis improvement by at least one stage or more without worsening of NASH (defined by an increase of inflammation and or ballooning) and NASH resolution (defined by ballooning score 0 and inflammation score 0-1 at termination) without worsening of fibrosis. Other secondary endpoints included improvement (2 points or more) in NASH activity index, as measured by NAS or SAF, without worsening fibrosis and change in baseline to week 52/termination in ALT (U/L).

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So we’re going to have to think about the way that synthetic routes in the generic API business are monitored, it would seem. People seem to have missed that changing the chemistry for the sartans could lead to this problem, so what else are we missing? It’ll be tricky – generic drug synthesis is generally a low-margin business where people compete at least partially on price, so the companies are always looking for new routes that will give them an advantage. And as the present example illustrates, there can be many different manufacturing sources scattered over several different countries. But no one wants to see this sort of thing happening again, either. . .

There were no changes in our internal control over financial reporting that occurred during the year ended December 31, 2018 that have materially affected, or are reasonably likely to materially affect, our internal control over financial reporting.

U.S. Holders who fail to report required information could become subject to substantial penalties. U.S. Holders should consult their tax advisors regarding the possible implications of these reporting requirements arising from their investment in our ordinary shares.

In renal fibrogenesis, matrix-producing cells integrate various fibrogenic signals and regulate ECM production and assembly. These fibrogenic factors include TGF-β1, platelet-derived growth factor, fibroblast growth factor, connective tissue growth factor and angiotensin II15. Among these cytokines, TGF-β1 is the key contributor to EMT in tubular epithelial cells29. In the kidneys of patients with IgA nephropathy, P311 protein expression correlates with TGF-β expression and proteinuria30. Thus, we next examined whether TGF-β1 was involved in EMT related to P311-mediated renal fibrogenesis. As predicted, obstructed kidneys from P311−/− mice showed impaired TGF-β1 protein expression. Interestingly, there was no difference in TGF-β1 mRNA levels between the P311−/− and P311+/+ groups. These results differ from our previous observations in human fibroblasts, which showed that P311 transfection induces TGF-β1 mRNA expression and that interfering with P311 expression in fibroblasts decreases TGF-β1 mRNA expression10. The different models (in vivo versus in vitro) and different cell types (human fibroblasts versus mouse tubular epithelial cells) might be responsible for the discrepancy. P311 binds to latency-associated proteins to regulate TGF-β1 expression31. Recently, P311 was reported to bind to eukaryotic translation initiation factor 3 subunit b to promote TGF-β translation and to be the first pan-regulator of TGF-β expression under steady-state conditions8,32. These findings may explain our results.

Mark-to-Market Election. Alternatively, if our ordinary shares are treated as “marketable stock,” a U.S. Holder would be allowed to make a “mark-to-market” election with respect to our ordinary shares, provided the U.S. Holder completes and files IRS Form 8621 in accordance with the relevant instructions and related Treasury Regulations. If that election is made, the U.S. Holder generally would include as ordinary income in each taxable year the excess, if any, of the fair market value of our ordinary shares at the end of the taxable year over such holder’s adjusted tax basis in such ordinary shares. The U.S. Holder would also be permitted an ordinary loss in respect of the excess, if any, of the U.S. Holder’s adjusted tax basis in our ordinary shares over their fair market value at the end of the taxable year, but only to the extent of the net amount previously included in income as a result of the mark-to- market election. A U.S. Holder’s tax basis in our ordinary shares would be adjusted to reflect any such income or loss amount. Gain realized on the sale, exchange or other disposition of our ordinary shares would be treated as ordinary income, and any loss realized on the sale, exchange or other disposition of our ordinary shares would be treated as ordinary loss to the extent that such loss does not exceed the net mark-to-market gains previously included in income by the U.S. Holder, and any loss in excess of such amount will be treated as capital loss. Amounts treated as ordinary income will not be eligible for the favorable tax rates applicable to qualified dividend income or long-term capital gains.

Yes, I agree! Since others have mentioned Einstein as the greatest scientist ever (I wont debate that), we know that he denied that black holes were possible as late as 1939, 78 years ago. He changed his mind later of course, when he had more “facts”/data.

How to cite this article: Zeng, Y. et al. Hypoxia inducible factor-1 mediates expression of miR-322: potential role in proliferation and migration of pulmonary arterial smooth muscle cells. Sci. Rep. 5, 12098; doi: 10.1038/srep12098 (2015).