Unstandardized path estimates for structural model with latent interaction effects.

<p>Age, gender, primary caregiver, and family location were included as covariates in this model, but are not shown in this figure. Dashed lines represent nonsignificant latent interaction paths at <i>p</i> < .05. Curved arrows among latent variables represent correlated errors. **<i>p</i> < .01, ***<i>p</i> < .001.</p

Resilience as a moderator between negative parenting and externalizing problems that illustrates the protective-reactive pattern.

<p>Resilience as a moderator between negative parenting and externalizing problems that illustrates the protective-reactive pattern.</p

Family Material Hardship and Chinese Adolescents’ Problem Behaviors: A Moderated Mediation Analysis

<div><p>In the current study, we examined a moderated mediation model using the risk and resilience framework. Specifically, the impact of family material hardship on adolescent problem behaviors was examined in a Chinese sample; we used the family stress model framework to investigate parental depression and negative parenting as potential mediators of the relation between family material hardship and adolescents’ problem behaviors. In addition, based on resilience theory, we investigated adolescents’ resilience as a potential protective factor in the development of their internalizing and externalizing problems. Participants included 1,419 Chinese adolescents (mean age = 15.38 years, <i>SD</i> = 1.79) and their primary caregivers. After controlling for covariates (age, gender, location of family residence, and primary caregiver), we found that parental depression and negative parenting mediated the association between family material hardship and adolescents’ problem behaviors. Furthermore, the adolescent resilience moderated the relationship between negative parenting and internalizing problems in a protective-stabilizing pattern; in addition, a protective-reactive pattern also emerged when adolescent resilience was examined as a moderator of the relationship between negative parenting and externalizing problems. These findings contribute to a comprehensive understanding of the mechanisms of risk and resilience in youth development. Moreover, the findings have important implications for the prevention of adolescent problem behaviors.</p></div

The Measurement Model: Latent Variable Factor Loadings.

<p><i>Note</i>.</p><p>***<i>p</i> < .001.</p><p>The Measurement Model: Latent Variable Factor Loadings.</p

The Correlations Between the Study Variables.

<p>Note. N = 1,419. Gender was dummy coded: 0 = female and 1 = male. Primary caregiver was dummy coded into mother (= 1) and other (= 1), with father (= 0) as the reference category. Family location was dummy coded into suburban (= 1) and rural (= 1), with urban (= 0) as the reference category. Correlations were significant at the p < .05; the italicized values indicate that the correlations were no-significant at (p > .05).</p><p>The Correlations Between the Study Variables.</p

Resilience as a moderator between negative parenting and internalizing problems that illustrates the protective-stabilizing pattern.

<p>Resilience as a moderator between negative parenting and internalizing problems that illustrates the protective-stabilizing pattern.</p

DataSheet1_The RNA-binding protein RBM24 regulates lipid metabolism and SLC7A11 mRNA stability to modulate ferroptosis and inflammatory response.PDF

Lipids play a critical role in many cellular processes by serving as structural components of cell membranes or functioning as energy fuel and signaling molecules. The RNA-binding proteins RBM24 and RBM38 share an identical RNA-binding domain and thereby, regulate a group of same targets, such as p21. However, it is not certain whether RBM24 and RBM38 participates in lipid homeostasis. Here, lipidomic analysis showed that a deficiency in RBM24 or RBM38 leads to altered lipid metabolism, with more profound alteration by loss of RBM24 in MCF7 cells. We also showed that mice deficient in RBM24 were prone to chronic inflammation and liver steatosis, but not spontaneous tumors. These data let us speculate whether RBM24 regulates ferroptosis, a programmed cell death that links inflammation and liver steatosis via lipid peroxidation. Indeed, we found that over-expression of RBM24 protected, whereas knockout of RBM24 sensitized, cells to Erastin-induced ferroptosis by modulating the mRNA stability of SLC7A11, a ferroptosis inhibitor. Moreover, we showed that knockdown of SLC7A11 reversed the effect of RBM24 on ferroptosis. Together, our study revealed that RBM24 regulates lipid metabolism and SLC7A11 mRNA stability to modulate ferroptosis and inflammatory response.</p

Table4_Combined analysis of differentially expressed lncRNAs and miRNAs in liver tissues of high-fat fed rabbits by transcriptome sequencing.XLS

High-fat diet could lead to a series of metabolic diseases, including obesity, and its mechanism is not clear. In this study, the rabbit individuals were fed with high-fat diet, the liver tissues were collected, high-throughput sequencing technology was used to reveal the expression of lncRNA and miRNA difference, and the molecular regulation mechanism of lncRNA-miRNA. A total of 24,615 DE lncRNAs and 52 DE miRNAs were identified, including 15 novel discovered DE miRNAs (5 upregulated and 10 downregulated). Furthermore, five miRNAs and three mRNAs were verified by qRT-PCR, and the results showed that the expression of the DE miRNAs and DE lncRNAs in the two groups was consistent with our sequencing results. GO and KEGG analyzed 7,57,139 target genes respectively, enriching the pathways related to lipid metabolism, including mucin O-glycan biosynthesis pathway, insulin resistance and glucagon signaling pathway. Moreover, 65 targeting relationships were obtained. Among them, LOC103348122/miR-450a-5p, LOC103350359/miR-450a-3p and LOC103350429/miR-148a-5p were proposed the first time. Significantly, LOC103348122/miR-450a-5p and LOC103350429/miR-148a-5p were related to lipid metabolism in the liver. This study is of great significance to the CeRNA regulatory network related to lipid metabolism in the liver of rabbits, and provides a basis for understanding hepatic steatosis in rabbits.</p

Table9_Combined analysis of differentially expressed lncRNAs and miRNAs in liver tissues of high-fat fed rabbits by transcriptome sequencing.XLSX

High-fat diet could lead to a series of metabolic diseases, including obesity, and its mechanism is not clear. In this study, the rabbit individuals were fed with high-fat diet, the liver tissues were collected, high-throughput sequencing technology was used to reveal the expression of lncRNA and miRNA difference, and the molecular regulation mechanism of lncRNA-miRNA. A total of 24,615 DE lncRNAs and 52 DE miRNAs were identified, including 15 novel discovered DE miRNAs (5 upregulated and 10 downregulated). Furthermore, five miRNAs and three mRNAs were verified by qRT-PCR, and the results showed that the expression of the DE miRNAs and DE lncRNAs in the two groups was consistent with our sequencing results. GO and KEGG analyzed 7,57,139 target genes respectively, enriching the pathways related to lipid metabolism, including mucin O-glycan biosynthesis pathway, insulin resistance and glucagon signaling pathway. Moreover, 65 targeting relationships were obtained. Among them, LOC103348122/miR-450a-5p, LOC103350359/miR-450a-3p and LOC103350429/miR-148a-5p were proposed the first time. Significantly, LOC103348122/miR-450a-5p and LOC103350429/miR-148a-5p were related to lipid metabolism in the liver. This study is of great significance to the CeRNA regulatory network related to lipid metabolism in the liver of rabbits, and provides a basis for understanding hepatic steatosis in rabbits.</p

Table1_Combined analysis of differentially expressed lncRNAs and miRNAs in liver tissues of high-fat fed rabbits by transcriptome sequencing.XLSX

High-fat diet could lead to a series of metabolic diseases, including obesity, and its mechanism is not clear. In this study, the rabbit individuals were fed with high-fat diet, the liver tissues were collected, high-throughput sequencing technology was used to reveal the expression of lncRNA and miRNA difference, and the molecular regulation mechanism of lncRNA-miRNA. A total of 24,615 DE lncRNAs and 52 DE miRNAs were identified, including 15 novel discovered DE miRNAs (5 upregulated and 10 downregulated). Furthermore, five miRNAs and three mRNAs were verified by qRT-PCR, and the results showed that the expression of the DE miRNAs and DE lncRNAs in the two groups was consistent with our sequencing results. GO and KEGG analyzed 7,57,139 target genes respectively, enriching the pathways related to lipid metabolism, including mucin O-glycan biosynthesis pathway, insulin resistance and glucagon signaling pathway. Moreover, 65 targeting relationships were obtained. Among them, LOC103348122/miR-450a-5p, LOC103350359/miR-450a-3p and LOC103350429/miR-148a-5p were proposed the first time. Significantly, LOC103348122/miR-450a-5p and LOC103350429/miR-148a-5p were related to lipid metabolism in the liver. This study is of great significance to the CeRNA regulatory network related to lipid metabolism in the liver of rabbits, and provides a basis for understanding hepatic steatosis in rabbits.</p