The H&E staining revealed that blood vessel endothelium in the normal group was integrated, but was not integrated in the model group. β-BA protected endothelium from the injury (Fig. 2). In addition, counts of circulating endothelial cells was performed. The results clearly showed that β-BA treatment significantly diminished circulating endothelial cells (CEC) count in blood compare to model (see Supplementary Fig. S1 online). The levels of NO and cGMP were determined in rats’ carotid aortas. β-BA significantly increased both the product of NO and cGMP in a dose-dependent manner (Fig. 3a,b). Moreover, NO production was directly investigated in cultured HUVECs by referring to NO indicator DAF-FM DA (Fig. 3c,d). Application of β-BA triggered a progressive rise in intracellular NO production in cultured HUVECs, as reflected by the increase of fluorescence intensity. The present results strongly indicate that β-BA could dose-dependently elevate the NO production in HUVECs.
The carrying amounts of cash and cash equivalents, short-term bank deposits, other accounts receivables, trade payables and other trade payables approximate their fair value due to the short-term maturity of such instruments.
Antisoma (LSE:ASM.L) is a biotechnology company specialising in the development of novel drugs for the treatment of cancer. Antisoma has a diverse portfolio of drugs in development
Study design had to meet the following criteria: (1) randomized, placebo-controlled parallel or cross-over trial, (2) population enrolled: adults ≥ 18 years, and, (3) plasma ADMA levels at baseline and after statin administration were available.
The best example is the famous J curve for alcohol in which small amounts are beneficial at low doses for the heart and huge amounts are horrible (although a recent meta-analysis has challenged this [ Lancet vol. 392 pp. 1015 – 1035 ’18 ], but I don’t trust them — for why see http://science.sciencemag.org/content/sci/361/6408/1184.full.pdf.
In May 2018, we entered into a sales agreement (the "Sales Agreement") with Stifel, Nicolaus & Company, Incorporated ("Stifel"), which permitted us to sell, from time to time, at our option, up to an aggregate of $50.0 million of shares of our common stock through Stifel, as sales agent. In December 2018, we terminated the Sales Agreement. Prior to termination, we had not sold any Shares pursuant to the Sales Agreement.
We rely on consultants and advisors, including scientific and clinical advisors, to assist us in formulating our research and development and commercialization strategy. Our consultants and advisors may be employed by other entities and may have commitments under consulting or advisory contracts with those entities that may limit their availability to us. If we are unable to continue to attract and retain highly qualified personnel, our ability to develop and commercialize our product candidates will be limited.
Ghosh et al. have reported that human miR-424, the homolog of rodent miR-322, stabilizes HIF-1α leading to its accumulation in the nucleus in human umbilical vein endothelial cells (HUVEC)23. Therefore, we determined whether manipulating miR-322 expression could affect the levels of HIF-1α in rat PASMCs. Cells were transfected with recombinant lentivirus expressing miR-322 (miR-322), or no miRNA sequence as a negative control (miR-Con). Stably transfected cells were generated by puromycin selection. As shown in Fig. 4a, exposure to hypoxia induced HIF-1α accumulation in the nucleus of PASMCs. qRT-PCR revealed an over 12-fold increase in miR-322 in the cells overexpressing miR-322 compared with control cells (Fig. 4b). Western blot showed that the accumulation of HIF-1α increased in the nucleus when overexpressing miR-322 in normoxia (Fig. 4c). Cells were also transfected with dTud constructs for miR-322 knockdown studies. As shown in Fig. 4b, cells with miR-322 inhibition (anti-322) exhibited significantly reduced expression in miR-322 compared to its control cells (anti-Con). Knockdown of miR-322 abolished the stabilization of HIF-1α in PASMCs under hypoxic condition (Fig. 4c). Taken together these results indicate that hypoxia-induced miR-322 is involved in regulating the stability of HIF-1α in PASMCs.
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