Evidence of h_{b}(2P)→ϒ(1S)η Decay and Search for h_{b}(1P,2P)→ϒ(1S)π^{0} with the Belle Detector.

We report the first evidence for the h_{b}(2P)→ϒ(1S)η transition with a significance of 3.5 standard deviations. The decay branching fraction is measured to be B[h_{b}(2P)→ϒ(1S)η]=(7.

Downregulation of RhoA/ROCK1/YAP/F-actin causing decreased aortic smooth muscle cell stiffness promotes aortic dissection formation.

Downregulated RhoA/ROCK1/YAP/F-actin axis leads to decreased AoSMC stiffness and promotes AD formation.

HMOX1 as a potential drug target for upper and lower airway diseases: insights from multi-omics analysis.

Background: Oxidative stress is key in inflammatory airway diseases. Heme oxygenase 1 (HMOX1) regulates oxidative stress, but its role in airway diseases needs exploration.

Methods: Differentially expressed genes (DEGs) between healthy nasal mucosa and chronic rhinosinusitis with nasal polyps (CRSwNP) were identified from Gene Expression Omnibus (GEO).

Electrophysiological characterization of human KCNT1 channel modulators and the therapeutic potential of hydroquinine and tipepidine in KCNT1 mutation-associated epilepsy mouse model.

Patients suffering epilepsy caused by the gain-of-function mutants of the hKCNT1 potassium channels are drug refractory. In this study, we cloned a novel human KCNT1B channel isoform using the brain cDNA library and conducted patch-clamp and molecular docking analyses to characterize the pharmacological properties of the hKCNT1B channel using thirteen drugs. Among cinchona alkaloids, we found that hydroquinine exerted the strongest blocking effect on the hKCNT1B channel, especially the F313L mutant.