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Activating transcription factor 1 (ATF1) may be involved in essential hypertension (EH) by induction of NADPH oxidase 1 (NOX1) and radical oxygen species (ROSs) production. Abnormal expression of ATF1 was found in EH in previous microarray analysis. Here we tested whether a single nucleotide polymorphism (SNP) located in the 3′-untranslated region (3′UTR) of ATF1 was associated with EH susceptibility by affecting microRNA (miRNA) binding. In silico analysis indicated that rs11169571 (T > C) was a candidate SNP to modulate miRNA: ATF1 mRNA complex, with the greatest changed energy for hsa-miR-1283, and the luciferase reporter analysis showed that miR-1283 inhibited the activity of the reporter vector carrying –T allele, but not the –C allele. In addition, inhibition of miR-1283 in HA-VSMCs enhanced the expression of ATF1 mRNA as well as the ROS levels. Further case-control study showed that rs11169571 was significantly associated with increased risk of EH. Finally, we observed an increased ATF1 protein level in peripheral blood of EH patients with CC carriers compared to TT carriers of rs11169571, with an intermediate ATF1 level in TC carriers. These results suggested that rs11169571 of ATF1 gene may be associated with EH, and the SNP-modified posttranscriptional gene regulation by miRNAs could be a potentially pathogenetic mechanism of EH. [ABSTRACT FROM AUTHOR]

China has recently reformed its system of collective forest tenure to allow commercial logging, increased collection of firewood and nontimber forest products by outside enterprises, unmanaged tourism, and certain types of industrial development to occur in collective forests where these activities were previously restrained. The reform would also allow private or public agencies to buy back certain development rights from communities for conservation purposes ('eco-compensation'). We examine the impacts that the tenure reform could have on the survival of the giant panda, with or without eco-compensation in place. We estimate that $1,229 million in effective eco-compensation payments could prevent an estimated 15% decline in the giant panda population, whereas an additional $3,707 million for effective eco-compensation and restoration of potential habitat could restore the giant panda population to an estimated 40% above current levels. Specifically, we identify 14 key areas that link fragmented panda populations and habitats, and where approximately $779 million is needed for eco-compensation, matched with an additional investment of $131 million for the restoration of native forest habitat. [ABSTRACT FROM AUTHOR]

A series of high‐molecular‐weight terpolymers named PTG‐b‐LG and PT‐b‐LG were synthesized based on the macroinitiators of PTG copolymers and PTMC, respectively. In vitro degradation of PTG‐b‐LG and PT‐b‐LG was carried out by immersing into PBS, in comparison with that of PLLA. Mass loss, water uptake, GPC, DSC, WAXD, and 1H NMR were examined for the degradation study. It was found that PTG‐b‐LG degraded faster than PT‐b‐LG and PLLA due to the Di‐random block structure, which had lower regularity of chain and lower crystallinity. The compositional changes appeared to be more complex, but the molar mass decreased owing to chain fragmentation caused by hydrolysis. Moreover, morphological changes were also observed during the degradation in all situations with the crystallization of by‐products and a preferential degradation of amorphous domains. Specifically, PTG‐b‐LG presented an adjustable degradation rate and may be used for the fabrication of totally biodegradation stents in the future. © 2019 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 2019, 136, 47887. [ABSTRACT FROM AUTHOR]

Background: We recently demonstrated that acute administration of ibrutinib, a Bruton's tyrosine kinase inhibitor used in chemotherapy for blood malignancies, increases ventricular arrhythmia (VA) vulnerability. A pathway of ibrutinib-induced vulnerability to VA that can be modulated for cardioprotection remains unclear., Methods and Results: The effects of ibrutinib on cardiac electrical activity and Ca 2+ dynamics were investigated in Langendorff-perfused hearts using optical mapping. We also conducted Western blotting analysis to evaluate the impact of ibrutinib on various regulatory and Ca 2+ -handling proteins in rat cardiac tissues. Treatment with ibrutinib (10 mg/kg per day) for 4 weeks was associated with an increased VA inducibility (72.2%±6.3% versus 38.9±7.0% in controls, P <0.002) and shorter action potential durations during pacing at various frequencies ( P <0.05). Ibrutinib also decreased heart rate thresholds for beat-to-beat duration alternans of the cardiac action potential ( P <0.05). Significant changes in myocardial Ca 2+ transients included lower amplitude alternans ratios ( P <0.05), longer times-to-peak ( P <0.05), and greater spontaneous intracellular Ca 2+ elevations ( P <0.01). We also found lower abundance and phosphorylation of myocardial AMPK (5'-adenosine monophosphate-activated protein kinase), indicating reduced AMPK activity in hearts after ibrutinib treatment. An acute treatment with the AMPK activator 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside ameliorated abnormalities in action potential and Ca 2+ dynamics, and significantly reduced VA inducibility (37.1%±13.4% versus 72.2%±6.3% in the absence of 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside, P <0.05) in hearts from ibrutinib-treated rats., Conclusions: VA vulnerability inflicted by ibrutinib may be mediated in part by an impairment of myocardial AMPK activity. Pharmacological activation of AMPK may be a protective strategy against ibrutinib-induced cardiotoxicity.