Ultra-high molecular weight polyethylene (UHMWPE) is used as a bearing surface of joint prostheses and has been reported to absorb lipids such as squalene (SQ) and cholesterol esters in vivo. These lipids have been suggested by in vitro studies using SQ as a model lipid to have the potential to induce polymer degradation. However, the impact of lipid-induced degradation on the strength and wear resistance of UHMWPE is unknown. In this study, lipid-induced degradation was simulated by SQ absorption and subsequent accelerated aging, and its influence on the strength and wear resistance of UHMWPE was investigated using wear, fatigue crack growth, and delamination testing. Lipid-induced degradation was found to have little impact on fatigue crack growth rates and delamination resistance. These results were consistent with previous reports that lipid-induced degradation is localized near the surface. However, we also found that lipid-induced degradation increased the wear rate of both non-crosslinked and crosslinked UHMWPE by a factor of 2.5 and 14, respectively. These results indicate that lipid-induced degradation may affect the durability and long-term clinical outcome of joint replacements due to increased wear of UHMWPE.
Background: Non-alcoholic fatty liver disease (NAFLD), which is a significant liver condition associated with metabolic syndrome, is the leading cause of liver diseases globally and its prevalence is on the rise in most nations. The protective impact of vitamin D on NAFLD and its specific mechanism remains unclear.
Aim: To examine the role of vitamin D in NAFLD and how vitamin D affects the polarization of hepatic macrophages in NAFLD through the vitamin D receptor (VDR)-peroxisome proliferator activated receptor (PPAR)γ pathway.
Mechanical stiffness of liver organoid is a key indicator for the progress of hepatic steatosis. Probe indentation is a noninvasive methodology to measure Young's modulus (YM); however, the inhomogeneous nature of the liver organoid induces measurement uncertainty requiring a large number of indentations covering a wide scanning area. Here, we demonstrate that lipid-stained fluorescence imaging-assisted probe indentation significantly reduces the number of measurements by specifying the highly lipid-induced area.
Harbin Medical University, Harbin 150001, PR China; Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, Harbin 150001, PR China; Key Laboratory of Myocardial Ischemia, Ministry of Education, Harbin 150001, PR China. Electronic address:
C1q/TNF-related protein 13 (CTRP13) is a secreted adipokine that has been shown to play an important role in a variety of cardiovascular diseases. However, the effect of CTRP13 on ferroptosis of endothelial cells and its underlying mechanism remain unclear. In the present study, we analyzed the effects of CTRP13 on endothelial dysfunction in high-lipid-induced ApoE mice and ox-LDL-induced mouse aortic endothelial cells (MAECs).
Objective: Apolipoprotein A4 (APOA4) is synthesized by the small intestine in response to dietary lipids. Chronic exposure to a high-fat diet (HFD) desensitizes lipid-induced APOA4 production and attenuates brown adipose tissue (BAT) thermogenesis. We hypothesized that exogenous APOA4 could increase BAT thermogenesis and energy expenditure in HFD-fed mice, resulting in decreased obesity and improved glucose tolerance.
Hepatic insulin resistance (IR) is often said to be "pathway-selective" with preserved insulin stimulation of lipogenesis (DNL) despite attenuated insulin signaling toward glucose metabolism. However, DNL has not been assessed in models of liver-specific IR. We studied mice with differential tissue-specific lipid-induced IR achieved by different durations of high-fat diet (HFD) feeding.
