Aging is associated with a progressive decline of muscle mass, strength, and quality, a condition described as sarcopenia of aging. Despite the significance of skeletal muscle atrophy, the mechanisms responsible for the deterioration of muscle performance are only partially understood. The purpose of this review is to highlight cellular, molecular and biochemical changes that contribute to age-related muscle weakness.

The pretilt angles for the optically compensated bend (OCB) mode liquid crystals have been improved using novel patterned dual alignment coating structures in this study. The transition from the splay configuration to the bend configuration can thus be effectively reduced. The dual alignment coating structures consisted of a horizontal alignment polyimide (PI) and a patterned vertical alignment liquid crystal polymer (LCP). Three patterning masks were designed for the photolithography process. The pretilt angles were demonstrated to be increased to 34 degrees for the triangle lattice array-patterned cells. It became 31 degrees for the square lattice array-patterned cells, and 24 degrees for the honeycomb lattice array-patterned cells. The improved pretilt angles were illustrated by the force balance model that can be predicted by the LCP area ratio. The effective control over the pretilt angle could improve the response time to 2 ms when the voltage was ramped up to 5.5 V for the OCB mode liquid crystal devices.

The phenotype of vascular smooth muscle cells (SMCs) play important roles in atherogenesis. We studied roles of extracellular matrix (ECM) and platelet‐derived growth factor (PDGF)‐BB/interleukin (IL)‐1b in modulating SMC phenotype. Human aortic SMCs on monomeric collagen (MC) showed lower expression of contractile markers, with a higher percentage in the S‐phase, than the cells on polymerized collagen (PC). SMCs on PC had lower expressions of cyclin A, D1, and E, cyclin‐dependent protein kinase (Cdk) 2, 4, and 6, and higher expressions of p27 and p21, as compared with the cells on MC. PDGF‐BB/IL‐1b inhibited the contractile marker expression and induced cell cycle progression, with an increase in Cdk6 expression, in SMCs on PC. Transfection of SMCs with Cdk6‐siRNA inhibited the PDGF‐BB/IL‐1b‐induced cell cycle progression. Wortmannin and LY294002 inhibited the PDGF‐BB/IL‐1b‐induced Cdk6 expression in SMCs on PC. SMCs on MC showed higher levels of avb3 and lower levels of a2b1 integrins than the cells on PC. PDGF‐BB/IL‐1b inhibited the b1 and b3 expressions in SMCs on PC. Our findings provide insights into the molecular basis for the roles of ECM and PDGF‐BB/IL‐1b in modulating SMC phenotype.