It’s certainly a complicated picture. Here we learn that MTOR inhibition (or AMPK activation) is actually preserving telomeres by unregulating the shelterin protein TERRA.

(a) Schematic diagram of cloned rat putative promoter region of miR-322, stretching from upstream 1000 bp. The position of the putative HRE matching the core sequence (A/G)CGTG is labeled in box, between two functional CACAG elements (P1k). A mutant promoter was constructed with the sequence as shown below (P1k-m). (b) Luciferase reporter assays of miR-322 promoter activity with both wild (pGL4-P1k) and mutant constructs (pGl4-P1k-m) in the presence or absence of CoCl2 (200μM) (left panel); Under these conditions, the protein levels of HIF-1α and HIF-2α were stabilized after CoCl2 treatment in the cells as determined by western blot analysis and normalized to β-actin levels (right panel). (c) miR-322 promoter activity assessed by luciferase reporter assay after CoCl2 treatment was diminished by HIF-1α knockdown. Cells were transduced with shRNA targeting HIF-1α (shHIF-1α) or HIF-2α (shHIF-2α) and miR-322 promoter activity was determined in the luciferase reporter assay after transfection of wild type and mutant constructs and CoCl2 treatment (left panel) as described under Methods; Control (sh-Con) or HIF-1α/-2α shRNA-transfected cells were harvested for protein analysis by western blot to determine knockdown specificity (right panel); *p < 0.05 compared with sh-Con. (d & e) A7r5 cells were transfected with recombinant adenoviruses expressing oxygen-dependent degradation domains (ODDD-wt) or mutated ODDD (ODDD-mut) under normoxic conditions. The influence on the miR-322 promoter reporter activity (d) and the endogenous expression levels (e) of miR-322 were determined by real-time PCR. All the bar plots represent means ± SD. *p < 0.05, **p < 0.01,compared with ODDD-mut. (f) Western blot for HIF-1α and HIF-2α in ODDD–transfected A7r5 cells after 24 hours. β-actin served as loading control. The full-length blots with these antibodies were presented in supplementary Figure S3. All gels have been run simultaneously under the same experimental conditions. (g) HIF-1α dynamic binding on the HRE site (−797 to −793) on the miR-322 promoter. ChIP assays were performed with indicated antibodies in the absence or presence of CoCl2 (left), or transfected with ODDD-wt or ODDD-mut (right) as described under Methods. Representative gel with input lanes showing products after PCR amplification and before immunoprecipitation.

Ding, Y., Chen, M. Wang, M., Li, Y. & Wen, A. Posttreatment with 11-Keto-beta-Boswellic Acid Ameliorates Cerebral Ischemia-Reperfusion Injury: Nrf2/HO-1 Pathway as a Potential Mechanism. Mol Neurobiol. (2014). 10.1007/s12035-014-8929-9.

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There is an exceptionally wide range of estimates regarding the potential commercial market for NASH. This uncertainty stems from (i) the overall size of the patient population, (ii) the percentage of the addressable market that will be diagnosed and, subsequently, seek treatment, (iii) the ultimate cost of the therapies, (iv) the number of approved drugs for NASH and their profile. Some of these factors cannot be known until NASH drugs begin to hit the market, which based on analysts’ estimates, will likely be 2020 or 2021 at the earliest or biomarkers replacing the biopsy diagnosis are validated. Independent estimates generally estimate a commercial multi billion market in developed countries, though we do not endorse any estimates, which are based on a number of different underlying assumptions.

        In September 2018, based on FDA feedback, as well as advice provided by MHRA and Health Canada, we announced the design of a single-arm Phase 3 study in treatment-naïve PNH patients. In January 2019, we concluded scientific advice and protocol design discussions with the EMA. The EMA was not receptive to a single-arm study design to support approval of zilucoplan in PNH. We do not plan to alter the design of the Phase 3 PNH program, but are reassessing the likelihood of obtaining marketing authorization for PNH in the E.U.

First China Pharmaceutical Group, Inc. (OTCBB:FCPG) aims to develop a high growth pharmaceutical distribution company generating significant revenue from the sale of healthcare products in China. As part of its business strategy, the Company has acquired the assets of Kun Ming Xin Yuan Tang Pharmacies Co. Ltd. (XYT), which includes a strategic advantage over its competitors as it is one of a handful of pharmaceutical distribution companies in Yunnan Province that has obtained government approval to market and fill orders using the internet. First China Pharmaceutical Group plans to continue the rapid growth of the company from its current position as a provider of approximately 7,100 drugs to more than 4,700 pharmacies, hospitals and clinics in China’s Yunnan Province.

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For another example of how a little stress (in the form of infection) could be good for you (with excellent clinical evidence) — see https://luysii.wordpress.com/2018/12/05/is-a-little-infection-good-for-you-if-so-what-about-radiation/

Bachem has extended its product offering with custom manufacturing of cytostatic and cytotoxic peptides and complex organic molecules. These substances are used as active ingredients for cancer therapy and have to be manufactured according to the strictest safety requirements for both staff and the environment.