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As income levels increase, numerous households will consider investing in risky assets. Credit availability, especially for high-income households, is playing an increasingly important role in enhancing households holdings of risky assets (HHRA). The purpose of this study is to investigate the impact of credit availability on HHRA. In this study, the data from the China Household Finance Survey in 2017 is utilized, and the approach of logit regression is employed to produce more accurate estimates. Meanwhile, this study also explores the heterogeneous roles of household income. The results show that the impact of credit availability on HHRA varies by household income. As household income increases from low to high, the effect of credit availability on HHRA transfers from negative to positive. Besides, the results also suggest that for high-income households, credit availability moderated with the attention to financial and economic information positively contributes to HHRA. Thus, it implies that policymakers and financial institutions are encouraged to expand access for households to invest in risky assets, enhance households’ availability of credit, and build more financing channels.

Hyperlipidemia (HLP) plays an important role in the pathogenesis of Alzheimer’s disease (AD). However, its pathological molecular mechanism remained unclear. 3β-hydroxysterol Δ24- reductase (DHCR24), a key enzyme in the last step of cholesterol synthesis, has been reported to decrease in the affected areas in the brain of AD patients. In this study, hyperlipidemic mouse model was established to study the effect of high blood lipid on brain. The data obtained from HPLC analysis demonstrated that the cholesterol level in brain of mice with hyperlipidemia was noticeably elevated compared to the control conditions. While the pathological damages were observed in both cerebral cortex and hippocampus in the brain of hyperlipidemic mice. Furthermore, the protein level of DHCR24 was downregulated accompanied by elevated ubiquitination level in the hyperlipidemic mice brain. The mouse neuroblastoma cells N2a were exposed to the excess cholesterol loading, the cells underwent apoptosis and the gene and protein of DHCR24 in cholesterol-loaded N2a cells were significantly reduced. In addition, the golden indexes of endoplasmic reticulum stress, BOP and ROP, increased significantly in response to the cholesterol loading. More importantly, overexpression of DHCR24 in N2a reversed neuronal apoptosis induced by the cholesterol loading. Conclusively, these findings suggested that hyperlipidemia could cause brain tissue injuries via down-regulating DHCR24, and overexpression of DHCR24 may alleviate hyperlipidemia-induced neuronal cells damage by reversing the endoplasmic reticulum stress-mediated apoptosis.

Acetaminophen (APAP), an over the counter (OTC) medication, is widely used in antipyretic treatment. Although the risk of dose-dependent cytotoxicity has been known, the potential effect of perinatal exposure to acetaminophen on metabolic function in offspring remains uninvestigated. Therefore, we established a prenatally APAP-exposed pregnancy mouse model to assess the possible adverse effect on liver metabolic function in offspring. Biochemical assays were applied in analysis of basic metabolic parameters in postnatal mice. Further, immunoblotting assay was used to assess the expressions of insulin receptor β (IRβ), insulin receptor substrate 1 (IRS1), phospho-Akt and phospho-GSK-3β proteins in liver cells. In addition, hepatic glucose transporter 2 (GLUT2) immunoactivity was determined by using immunohistochemistry staining. Compared with untreated postnatal mice, APAP-exposed offspring induced impaired glucose metabolism, increased plasma insulin level, and reduced liver glycogen content. In addition, APAP exposure decreased the expressions of IRS1 and phospho-GSK-3β, phospho-AKT proteins and down-regulated the level of glucose-import regulator GLUT2 in the liver. Taken together, our preliminary findings indicate that perinatal APAP exposure-impaired hepatic glucose metabolism in offspring may be associated with disturbance of insulin-dependent AKT signaling in the liver.