Full-field Strain Measurements for Microstructurally Small Fatigue Crack Propagation Using Digital Image Correlation Method.

A novel measurement approach is used to reveal the cumulative deformation field at a sub-grain level and to study the influence of microstructure on the growth of microstructurally small fatigue cracks. The proposed strain field analysis methodology is based on the use of a unique pattering technique with a characteristic speckle size of approximately 10 µm. The developed methodology is applied to study the small fatigue crack behavior in body centered cubic (bcc) Fe-Cr ferritic stainless steel with a relatively large grain size allowing a high spatial measurement accuracy at the sub-grain level.

β-adrenergic signaling inhibits Gq-dependent protein kinase D activation by preventing protein kinase D translocation.

Rationale: Both β-adrenergic receptor (β-AR) and Gq-coupled receptor (GqR) agonist-driven signaling play key roles in the events, leading up to and during cardiac dysfunction. How these stimuli interact at the level of protein kinase D (PKD), a nodal point in cardiac hypertrophic signaling, remains unclear.

Objective: To assess the spatiotemporal dynamics of PKD activation in response to β-AR signaling alone and on coactivation with GqR-agonists.

Spatiotemporally distinct protein kinase D activation in adult cardiomyocytes in response to phenylephrine and endothelin.

Protein kinase D (PKD) is a nodal point in cardiac hypertrophic signaling. It triggers nuclear export of class II histone deacetylase (HDAC) and regulates transcription. Although this pathway is thought to be critical in cardiac hypertrophy and heart failure, little is known about spatiotemporal aspects of PKD activation at the myocyte level.