Slow dynamics of phospholipid monolayers at the air/water interface

Phospholipid monolayers at the air-water interface serve as model systems for various biological interfaces, e.g. lung surfactant layers and outer leaflets of cell membranes. Although the dynamical (viscoelastic) properties of these interfaces may play a key role in stability, dynamics and function, the relatively weak rheological properties of most such monolayers have rendered their study difficult or impossible. A novel technique to measure the dynamical properties of fluid-fluid interfaces have developed accordingly. We microfabricate micron-scale ferromagnetic disks, place them on fluid-fluid interfaces, and use external electromagnets to exert torques upon them. By measuring the rotation that results from a known external torque, we compute the rotational drag, from which we deduce the rheological properties of the interface. Notably, our apparatus enable direct interfacial visualization while the probes are torqued. In this fluid dynamics video, we directly visualize dipalmitoylphosphatidylcholine(DPPC) monolayers at the air-water interface while shearing. At about 9 mN/m, DPPC exhibits a liquid condensed(LC) phase where liquid crystalline domains are compressed each other, and separated by grain boundaries. Under weak oscillatory torque, the grain boundaries slip past each other while larger shear strain forms a yield surface by deforming and fracturing the domains. Shear banding, which is a clear evidence of yield stress, is visualized during steady rotation. Remarkably slow relaxation time was also found due to slow unwinding of the stretched domains.Comment: 1 page, no figures, gallery of fluid motion 200

Yield Stress Fluids Solidifying in Capillary Imbibition

When subjected to an external stress that exceeds the yield stress ($\sigma_\mathrm{Y}$), yield stress fluids (YSFs) undergo a solid-to-liquid transition. Despite the extensive studies, there has been limited attention to the process of liquid-to-solid transition. This work examines the solidification of YSFs through capillary imbibition, easily observed in the processes of wetting, coating, spreading, and wicking. During gradual deceleration of the capillary rise, YSFs display an unexpected flowing behavior, even when subjected to stresses below the $\sigma_\mathrm{Y}$. We propose a model with numerical solutions based on rheological properties of YSFs and slip to capture this unusual, yet universal behavior

Collagen microarchitecture mechanically controls myofibroblast differentiation.

Altered microarchitecture of collagen type I is a hallmark of wound healing and cancer that is commonly attributed to myofibroblasts. However, it remains unknown which effect collagen microarchitecture has on myofibroblast differentiation. Here, we combined experimental and computational approaches to investigate the hypothesis that the microarchitecture of fibrillar collagen networks mechanically regulates myofibroblast differentiation of adipose stromal cells (ASCs) independent of bulk stiffness. Collagen gels with controlled fiber thickness and pore size were microfabricated by adjusting the gelation temperature while keeping their concentration constant. Rheological characterization and simulation data indicated that networks with thicker fibers and larger pores exhibited increased strain-stiffening relative to networks with thinner fibers and smaller pores. Accordingly, ASCs cultured in scaffolds with thicker fibers were more contractile, expressed myofibroblast markers, and deposited more extended fibronectin fibers. Consistent with elevated myofibroblast differentiation, ASCs in scaffolds with thicker fibers exhibited a more proangiogenic phenotype that promoted endothelial sprouting in a contractility-dependent manner. Our findings suggest that changes of collagen microarchitecture regulate myofibroblast differentiation and fibrosis independent of collagen quantity and bulk stiffness by locally modulating cellular mechanosignaling. These findings have implications for regenerative medicine and anticancer treatments

Relationship between sleep and obesity among U.S. and South Korean college students

Background Little is known about the relationship between sleep and obesity in young adults, particularly college students. This study examined the relationship between sleep (i.e., sleep duration and quality) and obesity in a large and diverse binational sample of college students. Methods Analyses were based on a 40-item paper survey from 2016/2017 to 2017/2018 academic years, with a 72% response rate. The samples were 1578 college students aged 18–25 years from five universities (two in the U.S. and three in South Korea). Weight and height were measured objectively; other measures (e.g., health behaviors) were self-reported. Multinomial logistic regression was used to assess the association between sleep duration and independent variables (race/nationality, gender, and BMI). Poisson regression was used to examine the relationship between sleep quality and independent variables. Results Overall, blacks had a higher adjusted odds ratio (AOR) of short sleep (\u3c 7 h/night) than whites (AOR = 1.74, P \u3c .01); overweight participants had a higher AOR of short sleep than normal weight participants (AOR = 1.52, P \u3c .01); and obese participants had a higher AORs of both short and long sleep (\u3e 9 h/night) (AOR = 1.67, P \u3c .01; AOR = 1.79, P \u3c .05, respectively). Among men, being black, overweight, and obesity were associated with short sleep (P \u3c .05), whereas only obesity was related to short sleep among women (P \u3c .05). In analyses stratified by race and nationality, overweight and obesity were related to short sleep among blacks only (P \u3c .05). Overall, sleep quality (getting enough sleep to feel rested in the morning in the past 7 days) was worse in blacks and South Koreans than whites (P \u3c .05), worse in women than men (P \u3c .05), and worse in participants with obesity than normal weight participants (P \u3c .05). Conclusions Obesity was associated with both short (\u3c 7 h/night) and long sleep duration (\u3e 9 h/night) and poor sleep quality among all participants. In comparison with whites, blacks were more like to have short sleep, and blacks and South Koreans had worse sleep quality. Further investigations using a larger sample of college students in multiple countries may be helpful to identify target populations who are at a greater risk of obesity and sleep problems

Obesity-dependent changes in interstitial ECM mechanics promote breast tumorigenesis.

Obesity and extracellular matrix (ECM) density are considered independent risk and prognostic factors for breast cancer. Whether they are functionally linked is uncertain. We investigated the hypothesis that obesity enhances local myofibroblast content in mammary adipose tissue and that these stromal changes increase malignant potential by enhancing interstitial ECM stiffness. Indeed, mammary fat of both diet- and genetically induced mouse models of obesity were enriched for myofibroblasts and stiffness-promoting ECM components. These differences were related to varied adipose stromal cell (ASC) characteristics because ASCs isolated from obese mice contained more myofibroblasts and deposited denser and stiffer ECMs relative to ASCs from lean control mice. Accordingly, decellularized matrices from obese ASCs stimulated mechanosignaling and thereby the malignant potential of breast cancer cells. Finally, the clinical relevance and translational potential of our findings were supported by analysis of patient specimens and the observation that caloric restriction in a mouse model reduces myofibroblast content in mammary fat. Collectively, these findings suggest that obesity-induced interstitial fibrosis promotes breast tumorigenesis by altering mammary ECM mechanics with important potential implications for anticancer therapies

Relationship between sleep and obesity among U.S. and South Korean college students

Background Little is known about the relationship between sleep and obesity in young adults, particularly college students. This study examined the relationship between sleep (i.e., sleep duration and quality) and obesity in a large and diverse binational sample of college students. Methods Analyses were based on a 40-item paper survey from 2016/2017 to 2017/2018 academic years, with a 72% response rate. The samples were 1578 college students aged 18–25 years from five universities (two in the U.S. and three in South Korea). Weight and height were measured objectively; other measures (e.g., health behaviors) were self-reported. Multinomial logistic regression was used to assess the association between sleep duration and independent variables (race/nationality, gender, and BMI). Poisson regression was used to examine the relationship between sleep quality and independent variables. Results Overall, blacks had a higher adjusted odds ratio (AOR) of short sleep ( 9 h/night) (AOR = 1.67, P < .01; AOR = 1.79, P < .05, respectively). Among men, being black, overweight, and obesity were associated with short sleep (P < .05), whereas only obesity was related to short sleep among women (P < .05). In analyses stratified by race and nationality, overweight and obesity were related to short sleep among blacks only (P < .05). Overall, sleep quality (getting enough sleep to feel rested in the morning in the past 7 days) was worse in blacks and South Koreans than whites (P < .05), worse in women than men (P < .05), and worse in participants with obesity than normal weight participants (P < .05). Conclusions Obesity was associated with both short ( 9 h/night) and poor sleep quality among all participants. In comparison with whites, blacks were more like to have short sleep, and blacks and South Koreans had worse sleep quality. Further investigations using a larger sample of college students in multiple countries may be helpful to identify target populations who are at a greater risk of obesity and sleep problems

Obesity-dependent changes in interstitial ECM mechanics promote breast tumorigenesis

Obesity and extracellular matrix (ECM) density are considered independent risk and prognostic factors for breast cancer. Whether they are functionally linked is uncertain. We investigated the hypothesis that obesity enhances local myofibroblast content in mammary adipose tissue and that these stromal changes increase malignant potential by enhancing interstitial ECM stiffness. Indeed, mammary fat of both diet- and genetically induced mouse models of obesity were enriched for myofibroblasts and stiffness-promoting ECM components. These differences were related to varied adipose stromal cell (ASC) characteristics because ASCs isolated from obese mice contained more myofibroblasts and deposited denser and stiffer ECMs relative to ASCs from lean control mice. Accordingly, decellularized matrices from obese ASCs stimulated mechanosignaling and thereby the malignant potential of breast cancer cells. Finally, the clinical relevance and translational potential of our findings were supported by analysis of patient specimens and the observation that caloric restriction in a mouse model reduces myofibroblast content in mammary fat. Collectively, these findings suggest that obesity-induced interstitial fibrosis promotes breast tumorigenesis by altering mammary ECM mechanics with important potential implications for anticancer therapies

Elevated IFNA1 and suppressed IL12p40 associated with persistent hyperinflammation in COVID-19 pneumonia

IntroductionDespite of massive endeavors to characterize inflammation in COVID-19 patients, the core network of inflammatory mediators responsible for severe pneumonia stillremain remains elusive. MethodsHere, we performed quantitative and kinetic analysis of 191 inflammatory factors in 955 plasma samples from 80 normal controls (sample n = 80) and 347 confirmed COVID-19 pneumonia patients (sample n = 875), including 8 deceased patients. ResultsDifferential expression analysis showed that 76% of plasmaproteins (145 factors) were upregulated in severe COVID-19 patients comparedwith moderate patients, confirming overt inflammatory responses in severe COVID-19 pneumonia patients. Global correlation analysis of the plasma factorsrevealed two core inflammatory modules, core I and II, comprising mainly myeloid cell and lymphoid cell compartments, respectively, with enhanced impact in a severity-dependent manner. We observed elevated IFNA1 and suppressed IL12p40, presenting a robust inverse correlation in severe patients, which was strongly associated with persistent hyperinflammation in 8.3% of moderate pneumonia patients and 59.4% of severe patients. DiscussionAberrant persistence of pulmonary and systemic inflammation might be associated with long COVID-19 sequelae. Our comprehensive analysis of inflammatory mediators in plasmarevealed the complexity of pneumonic inflammation in COVID-19 patients anddefined critical modules responsible for severe pneumonic progression