Gaps in Framing and Naming: Commentary to "A Viewpoint on Accent Services".

Purpose: In this commentary, we offer a critique of "A Viewpoint on Accent Services: Framing and Terminology Matter" (Grover et al., 2022). We argue that the authors' proposal to rename and reframe accent modification lacks criticality, which actually hinders-rather than advances-the movement toward equitable, culturally sustaining, and emancipatory practices.

First Bignoniaceae liana from the Miocene of South America and its evolutionary significance.

Premise: Two Bignoniaceae stems with the distinctive anatomy of a liana are described from the Miocene of South America. They are the first fossil evidence of climbing habit in Bignoniaceae.

Methods: The fossil lianas are siliceous permineralizations.

PDE5 inhibition improves cardiac morphology and function in SHR by reducing NHE1 activity: Repurposing Sildenafil for the treatment of hypertensive cardiac hypertrophy.

Previously, we have shown that an increased cGMP-activated protein Kinase (PKG) activity after phosphodiesterase 5 (PDE5) inhibition by Sildenafil (SIL), leads to myocardial Na/H exchanger (NHE1) inhibition preserving its basal homeostatic function. Since NHE1 is hyperactive in the hypertrophied myocardium of spontaneous hypertensive rats (SHR), while its inhibition was shown to prevent and revert this pathology, the current study was aimed to evaluate the potential antihypertrophic effect of SIL on adult SHR myocardium. We initially tested the inhibitory capability of SIL on NHE1 in isolated cardiomyocytes of SHR by comparing H efflux during the recovery from an acid load.

Silencing of epidermal growth factor receptor reduces Na/H exchanger 1 activity and hypertensive cardiac hypertrophy.

Pathological cardiac hypertrophy (PCH) can be triggered by epidermal growth factor receptor (EGFR) transactivation. Progression of PCH can be prevented by inhibition of hyperactive Na/H exchanger isoform 1 (NHE1). We first aimed, to limit PCH of spontaneously hypertensive rats (SHR) by specific and localized silencing of cardiac EGFR, and second to study the connection of its activation pathway with cardiac NHE1 activity.