Boundary-Layer Disruption and Heat-Transfer Enhancement in Convection Turbulence by Oscillating Deformations of Boundary.

In this Letter, we propose a novel strategy for significantly enhancing the heat transfer in convection turbulence. By introducing a boundary deformation of the standing-wave type, flow modulation can be realized when the amplitude is comparable or larger than the boundary-layer thickness. For a fixed moderate frequency, the entire fluid layer follows the boundary motion at small wave numbers, while only the near-wall regions are affected by the boundary deformation at large wave numbers.

Risk assessment of airborne transmission of COVID-19 by asymptomatic individuals under different practical settings.

The lack of quantitative risk assessment of airborne transmission of COVID-19 under practical settings leads to large uncertainties and inconsistencies in our preventive measures. Combining measurements and computational fluid dynamics simulations, we quantify the exhaled particles from normal respiratory behaviors and their transport under elevator, small classroom, and supermarket settings to evaluate the risk of inhaling potentially virus-containing particles. Our results show that the design of ventilation is critical for reducing the risk of particle encounters.

Risk assessment of airborne transmission of COVID-19 by asymptomatic individuals under different practical settings.

The lack of quantitative risk assessment of airborne transmission of COVID-19 under practical settings leads to large uncertainties and inconsistencies in our preventive measures. Combining in situ measurements and numerical simulations, we quantify the exhaled particles from normal respiratory behaviors and their transport under elevator, small classroom and supermarket settings to evaluate the risk of inhaling potentially virus-containing particles. Our results show that the design of ventilation is critical for reducing the risk of particle encounters.

KLF15 is a protective regulatory factor of heart failure induced by pressure overload.

The aim of the present study was to investigate the protective effect of Kruppel‑like factor 15 (KLF15) overexpression on heart failure (HF) induced by left ventricular (LV) pressure overload in mice. Wild‑type (WT) mice and cardiac‑specific KLF15‑overexpressed transgenic (TG) mice were selected as research subjects, and an LV pressure overload model was constructed by ascending aortic constriction surgery. Changes in cardiac morphology and function, and ultrastructure and molecular expression were observed via M‑mode echocardiography, histological and immunohistochemical staining, ELISA and western blotting at 2 and 6 weeks of LV overload.

[Impacts and mechanisms of kruppel like factor 15 in pressure overload induced cardiac remodeling and angiogenesis in rats].

Objective: To explore the impact of kruppel like factor 15 (KLF15) on cardiac fibroblasts on angiogenesis in a pressure overload rat model.

Methods: Pressure overload was induced in female rats by aortic constriction for 3 and 6 weeks. After 6 weeks aortic banding, rats underwent aortic debanding for 3 or 6 weeks.