Liquid-vapor transition on patterned solid surfaces in a shear flow.

Liquids on a solid surface patterned with microstructures can exhibit the Cassie-Baxter (Cassie) state and the wetted Wenzel state. The transitions between the two states and the effects of surface topography, surface chemistry as well as the geometry of the microstructures on the transitions have been extensively studied in earlier work. However, most of these work focused on the study of the free energy landscape and the energy barriers. In the current work, we consider the transitions in the presence of a shear flow. We compute the minimum action path between the Wenzel and Cassie states using the minimum action method [W. E, W. Ren, and E. Vanden-Eijnden, Commun. Pure Appl. Math. 57, 637 (2004)]. Numerical results are obtained for transitions on a surface patterned with straight pillars. It is found that the shear flow facilitates the transition from the Wenzel state to the Cassie state, while it inhibits the transition backwards. The Wenzel state becomes unstable when the shear rate reaches a certain critical value. Two different scenarios for the Wenzel-Cassie transition are observed. At low shear rate, the transition happens via nucleation of the vapor phase at the bottom of the groove followed by its growth. At high shear rate, in contrary, the nucleation of the vapor phase occurs at the top corner of a pillar. The vapor phase grows in the direction of the flow, and the system goes through an intermediate metastable state before reaching the Cassie state.

Electronic Interactive Games for Glycemic Control in Individuals With Diabetes: Systematic Review and Meta-Analysis.

BACKGROUND: Several electronic interventions have been used to improve glycemic control in patients with diabetes. Electronic interactive games specific to physical activity are available, but it is unclear if these are effective at improving glycemic control in patients with diabetes. OBJECTIVE: This study aimed to determine the effects of electronic game-based interventions on glycemic control in patients with diabetes. METHODS: Relevant studies that were published before April 1, 2023, were searched from 5 databases: PubMed, Embase, Web of Science, Scopus, and Cochrane Library. Eligibility criteria included prospective studies examining the relationship between electronic games with physical activities or diet education and glycemic control as the outcome. The risk of bias was assessed using the Cochrane risk-of-bias tool. All analyses were conducted using RevMan5.4.1. Depending on the heterogeneity across studies, the pooled effects were calculated using fixed-effects or random-effects models. RESULTS: Participants from 9 studies were included and assessed. Glycated hemoglobin (HbA1c) and fasting blood glucose improved in the intervention group, although the analysis revealed no significant reduction in HbA1c (-0.09%, 95% CI -0.29% to 0.10%) or fasting blood glucose (-0.94 mg/dL, 95% CI -9.34 to 7.46 mg/dL). However, the physical activity of individuals in the intervention group was significantly higher than that of those in the control group (standardized mean difference=0.84, 95% CI 0.30 to 1.38; P=.002). Other outcomes, such as weight and blood lipids, exhibited no significant improvement (all P>.05). CONCLUSIONS: Electronic games had a good impact on participants' physical activity and offered an advantage in glycemic control without reaching statistical significance. Electronic games are convenient for reminders and education. Low-intensity exercise games may not be considered a better adjuvant intervention to improve diabetes self-management care.

Macropinocytosis contributes to the macrophage foam cell formation in RAW264.7 cells.

The key event in the atherosclerosis development is the lipids uptake by macrophage and the formation of foam cell in subendothelial arterial space. Besides the uptake of modified low-density lipoprotein (LDL) by scavenger receptor-mediated endocytosis, macrophages possess constitutive macropinocytosis, which is capable of taking up a large quantity of solute. Macrophage foam cell formation could be induced in RAW264.7 cells by increasing the serum concentration in the culture medium. Foam cell formation induced by serum could be blocked by phosphoinositide 3-kinase inhibitor, LY294002 or wortmannin, which inhibited macropinocytosis but not receptor-mediated endocytosis. Further analysis indicated that macropinocytosis took place at the gangliosides-enriched membrane area. Cholesterol depletion by beta-methylcyclodextrin-blocked macropinocytosis without affecting scavenger receptor-mediated endocytosis of modified LDLs. These results suggested that macropinocytosis might be one of the important mechanisms for lipid uptake in macrophage. And it made significant contribution to the lipid accumulation and foam cell formation.

3T3-L1 adipocyte apoptosis induced by thiazolidinediones is peroxisome proliferator-activated receptor-gamma-dependent and mediated by the caspase-3-dependent apoptotic pathway.

Although thiazolidinediones (TZDs) are potent promoters of adipogenesis in the preadipocyte, they induce apoptosis in several other cell types, such as cancer cells, endothelial cells and T-lymphocytes. In this study, we investigated the proapoptotic effect of TZDs in mature 3T3-L1 adipocytes, which express high levels of the peroxisome proliferator-activated receptor-gamma (PPARgamma) protein. Apoptosis was induced in mature 3T3-L1 adipocytes by treatment with troglitazone, pioglitazone or prostaglandin J2, and could be blocked by the PPARgamma antagonist GW9662. Treatment with PPARgamma agonists also decreased Akt-1 protein and phosphorylation levels without affecting phosphoinositide 3-kinase and PTEN. Further analysis indicated that in troglitazone-treated 3T3-L1 adipocytes, Bad phosphorylation and Bcl-2 protein levels were reduced, and Bax translocation to the mitochondria was increased. Subsequently, cytochrome c release and caspase-3 cleavage were observed. TZD-induced adipocyte apoptosis could be blocked by the caspase-3 inhibitor Ac-DEVD-CHO or by overexpression of Bcl2. In cultured rat primary adipocytes, similar apoptosis-inducing effects of troglitazone were also observed. Thus, TZDs promote apoptosis in adipocytes through a PPARgamma-dependent pathway. This apoptosis is mediated by the inhibition of Akt-1, which decreases Bad phosphorylation and activates the mitochondrial apoptotic pathway.

Berberine promotes the development of atherosclerosis and foam cell formation by inducing scavenger receptor A expression in macrophage.

Berberine is identified to lower the serum cholesterol level in human and hamster through the induction of low density lipoproteins (LDL) receptor in hepatic cells. To evaluate its potential in preventing atherosclerosis, the effect of berberine on atherosclerosis development in apolipoprotein E-deficient (apoE(-/-)) mice was investigated. In apoE(-/-) mice, berberine induced in vivo foam cell formation and promoted atherosclerosis development. The foam cell formation induced by berberine was also observed in mouse RAW264.7 cells, as well as in mouse and human primary macrophages. By inducing scavenger receptor A (SR-A) expression in macrophages, berberine increased the uptake of modified LDL (DiO-Ac-LDL). Berberine-induced SR-A expression was also observed in macrophage foam cells in vivo and in the cells at atherosclerotic lesion. Analysis in RAW264.7 cells indicated that berberine induced SR-A expression by suppressing PTEN expression, which led to sustained Akt activation. Our results suggest that to evaluate the potential of a cholesterol-reducing compound in alleviating atherosclerosis, its effect on the cells involved in atherosclerosis development, such as macrophages, should also be considered. Promotion of foam cell formation could counter-balance the beneficial effect of lowering serum cholesterol.