Vibration analysis of the human radius of elderly men

Vibration analysis seldom has been used in detecting structural and mechanical changes in physiologic and pathologic bone conditions. We sought to correlate natural frequency of the radius measured by vibration analyses with bone mineral density measured by dual-energy xray absorptiometry and quantitative computed tomography (including cortical thickness). Sixty sedentary men between 50 and 70 years old were deemed osteopenic or healthy. A higher natural frequency of the dominant and nondominant radius was seen in the healthy men compared with the osteopenic men. Natural frequency was consistent with bone mineral density in dominant and nondominant radius in both groups. Moreover, there was a correlation between bone mineral density measured by dual-energy xray absorptiometry and natural frequency in the dominant and nondominant radius. Cortical thickness of the dominant and nondominant radius also correlated with natural frequency. We concluded natural frequency measured by vibration analysis is a precise method for the assessment of structural properties of bone and correlates with the bone mineral density of the radius

Mural cell SRF controls pericyte migration, vessel patterning and blood flow

Rationale Pericytes (PCs) and vascular smooth muscle cells (vSMCs), collectively known as mural cells (MCs), are recruited through PDGFB-PDGFRB signaling. MCs are essential for vascular integrity, and their loss has been associated with numerous diseases. Most of this knowledge is based on studies in which MCs are insufficiently recruited or fully absent upon inducible ablation. In contrast, little is known about the physiological consequences that result from impairment of specific MC functions. Objective Here, we characterize the role of the transcription factor serum response factor (SRF) in MCs and study its function in developmental and pathological contexts. Methods and Results We generated a mouse model of MC-specific inducible Srf gene deletion and studied its consequences during retinal angiogenesis. By postnatal day (P)6, PCs lacking SRF were morphologically abnormal and failed to properly co-migrate with angiogenic sprouts. As a consequence, PC-deficient vessels at the retinal sprouting front became dilated and leaky. By P12, also the vSMCs had lost SRF, which coincided with the formation of pathological arteriovenous (AV) shunts. Mechanistically, we show that PDGFB-dependent SRF activation is mediated via MRTF co-factors. We further show that MRTF-SRF signaling promotes pathological PC activation during ischemic retinopathy. RNA-sequencing, immunohistology, in vivo live imaging and in vitro experiments demonstrated that SRF regulates expression of contractile SMC proteins essential to maintain the vascular tone. Conclusions SRF is crucial for distinct functions in PCs and vSMCs. SRF directs PC migration downstream of PDGFRB signaling and mediates pathological PC activation during ischemic retinopathy. In vSMCs, SRF is essential for expression of the contractile machinery, and its deletion triggers formation of AV shunts. These essential roles in physiological and pathological contexts provide a rational for novel therapeutic approaches through targeting SRF activity in MCs