JMJD6 protects against isoproterenol-induced cardiac hypertrophy via inhibition of NF-κB activation by demethylating R149 of the p65 subunit.

Histone modification plays an important role in pathological cardiac hypertrophy and heart failure. In this study we investigated the role of a histone arginine demethylase, Jumonji C domain-containing protein 6 (JMJD6) in pathological cardiac hypertrophy. Cardiac hypertrophy was induced in rats by subcutaneous injection of isoproterenol (ISO, 1.

Faster State Preparation across Quantum Phase Transition Assisted by Reinforcement Learning.

An energy gap develops near quantum critical point of quantum phase transition in a finite many-body (MB) system, facilitating the ground state transformation by adiabatic parameter change. In real application scenarios, however, the efficacy for such a protocol is compromised by the need to balance finite system lifetime with adiabaticity, as exemplified in a recent experiment that prepares three-mode balanced Dicke state near deterministically [Y.-Q.

Beating the classical precision limit with spin-1 Dicke states of more than 10,000 atoms.

Interferometry is a paradigm for most precision measurements. Using N uncorrelated particles, the achievable precision for a two-mode (two-path) interferometer is bounded by the standard quantum limit (SQL), [Formula: see text], due to the discrete (quanta) nature of individual measurements. Despite being a challenging benchmark, the two-mode SQL has been approached in a number of systems, including the Laser Interferometer Gravitational-Wave Observatory and today's best atomic clocks.

C33(S), a novel PDE9A inhibitor, protects against rat cardiac hypertrophy through upregulating cGMP signaling.

Phosphodiesterase-9A (PDE9A) expression is upregulated during cardiac hypertrophy and heart failure. Accumulating evidence suggests that PDE9A might be a promising therapeutic target for heart diseases. The present study sought to investigate the effects and underlying mechanisms of C33(S), a novel selective PDE9A inhibitor, on cardiac hypertrophy in vitro and in vivo.

Synthesis of the novel PARP-1 inhibitor AG-690/11026014 and its protective effects on angiotensin II-induced mouse cardiac remodeling.

We previously identified AG-690/11026014 (6014) as a novel poly(ADP-ribose) polymerase-1 (PARP-1) inhibitor that effectively prevented angiotensin II (Ang II)-induced cardiomyocyte hypertrophy. In the present study, we reported a new synthesis route for 6014, and investigated its protective effects on Ang II-induced cardiac remodeling and cardiac dysfunction and the underlying mechanisms in mice. We designed a new synthesis route to obtain a sufficient quantity of 6014 for this in vivo study.