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There is a scarcity of data on how the lipid composition of oily seeds changes in response to biotic stress. Yellow peach moth (Conogethes punctiferalis) has caused massive economic losses on the pecan (Carya illinoinensis) industry. Lipidomics is used in this study to determine the lipid composition of pecan and how it changes in response to insect attack. Pecan had 167 lipids, including 34 glycerolipids (GL), 62 glycerophospholipids (GP), 17 fatty acyls (FA), 41 sphingolipids (SP), and 13 saccharolipids (SL). The effects of biotic stress on lipids, particularly GL and GP, were significant. Biotic stress significantly reduced the lipid content of chains longer than 48. Forty-four significantly different lipids were discovered as potential biomarkers for distinguishing non-infected pecans from infested pecans. In addition, we used bioinformatics to identify the five most important metabolic pathways in order to investigate the processes underlying the changes. Our discoveries may offer valuable insights for enhancing pecan production in the future and contribute novel perspectives towards enhancing the nutritional value of pecans. [ABSTRACT FROM AUTHOR]

Background Skin barrier dysfunction may both initiate and aggravate skin inflammation. However, the mechanisms involved in the inflammation process remain largely unknown. Objectives We sought to determine how skin barrier dysfunction enhances skin inflammation and molecular mechanisms. Methods Skin barrier defect mice were established by tape stripping or topical use of acetone on wildtype mice, or filaggrin deficiency. RNA-Seq was employed to analyse the differentially expressed genes in mice with skin barrier defects. Primary human keratinocytes were transfected with formylpeptide receptor (FPR)1 or protein kinase R-like endoplasmic reticulum (ER) kinase (PERK) small interfering RNA to examine the effects of these gene targets. The expressions of inflammasome NOD-like receptor (NLR)C4, epidermal barrier genes and inflammatory mediators were evaluated. Results Mechanical (tape stripping), chemical (acetone) or genetic (filaggrin deficiency) barrier disruption in mice amplified the expression of proinflammatory genes, with transcriptomic profiling revealing overexpression of formylpeptide receptor (Fpr1) in the epidermis. Treatment with the FPR1 agonist fMLP in keratinocytes upregulated the expression of the NLRC4 inflammasome and increased interleukin-1β secretion through modulation of ER stress via the PERK-eIF2α-C/EBP homologous protein pathway. The activation of the FPR1-NLRC4 axis was also observed in skin specimens from old healthy individuals with skin barrier defect or elderly mice. Conversely, topical administration with a FPR1 antagonist, or Nlrc4 silencing, led to the normalization of barrier dysfunction and alleviation of inflammatory skin responses in vivo. Conclusions In summary, our findings show that the FPR1-NLRC4 inflammasome axis is activated upon skin barrier disruption and may explain exaggerated inflammatory responses that are observed in disease states characterized by epidermal dysfunction. Pharmacological inhibition of FPR1 or NLRC4 represents a potential therapeutic target. [ABSTRACT FROM AUTHOR]

Background: Osteoporosis, which is a bone disease, is characterized by low bone mineral density and an increased risk of fractures. The heel bone mineral density is often used as a representative measure of overall bone mineral density. Lipid metabolism, which includes processes such as fatty acid metabolism, glycerol metabolism, inositol metabolism, bile acid metabolism, carnitine metabolism, ketone body metabolism, sterol and steroid metabolism, etc., may have an impact on changes in bone mineral density. While some studies have reported correlations between lipid metabolism and heel bone mineral density, the overall causal relationship between metabolites and heel bone mineral density remains unclear. Objective: to investigate the causal relationship between lipid metabolites and heel bone mineral density using two-sample Mendelian randomization analysis. Methods: Summary-level data from large-scale genome-wide association studies were extracted to identify genetic variants linked to lipid metabolite levels. These genetic variants were subsequently employed as instrumental variables in Mendelian randomization analysis to estimate the causal effects of each lipid metabolite on heel bone mineral density. Furthermore, metabolites that could potentially be influenced by causal relationships with bone mineral density were extracted from the KEGG and WikiPathways databases. The causal associations between these downstream metabolites and heel bone mineral density were then examined. Lastly, a sensitivity analysis was conducted to evaluate the robustness of the results and address potential sources of bias. Results: A total of 130 lipid metabolites were analyzed, and it was found that acetylcarnitine, propionylcarnitine, hexadecanedioate, tetradecanedioate, myo-inositol, 1-arachidonoylglycerophosphorine, 1-linoleoylglycerophoethanolamine, and epiandrosterone sulfate had a causal relationship with heel bone mineral density (p < 0.05). Furthermore, our findings also indicate an absence of causal association between the downstream metabolites associated with the aforementioned metabolites identified in the KEGG and WikiPathways databases and heel bone mineral density. Conclusion: This work supports the hypothesis that lipid metabolites have an impact on bone health through demonstrating a causal relationship between specific lipid metabolites and heel bone mineral density. This study has significant implications for the development of new strategies to osteoporosis prevention and treatment. [ABSTRACT FROM AUTHOR]

In this study, the crystal structure analysis by particle swarm optimization (CALYPSO) was used to search the structure of negative LiBn− (n = 2–12) clusters, and the corresponding ground-state structures and low energy isomers were determined. Based on the predicted ground state structures, the doped Li atom has little modification on Bn− skeleton, which can be seen from the charge analysis that it is caused by the transfer of electron from dopant to Bn− part. The photoelectron spectroscopy (PES) simulations were conducted using time-dependent density functional theory (TD-DFT). By analyzing the stability, we find LiB8− cluster with high symmetry C7V with ideal stability, and it has a classic umbrella structure. Deep analysis of the bonding characteristics of the LiB8− cluster shows that the B–B covalent bonds in the B8− part and the electrostatic interaction between the B8− wheel and the Li atom stabilize the LiB8− cluster. [ABSTRACT FROM AUTHOR]

The Sunyaev Zel'dovich (SZ) effect is sensitive to the pressure of ionized gas inside galaxy clusters, which is in turn controlled largely by the gravitational potential of the cluster. Changing the concentration parameter describing the cluster mass distribution impacts the gravitational potential and thus the cluster SZ signal, with implications for cosmological and other analyses of SZ-selected clusters. We investigate the concentration–SZ relation in theory and simulations. We find that the impact of concentration on the inner SZ profile (R ≲ 0.75 R 200 c ) can be captured with standard polytropic gas models. However, we find that such models do a poor job of reproducing the outer SZ profiles (R ≳ 0.75 R 200 c ) and the relation between the integrated SZ signal, Y , and concentration. This disagreement results from a sharp truncation of the gas pressure profile near the splashback radius, likely caused by virial shocks. We develop a simple description of the truncation that leads to a good match with the simulated SZ profiles out to several R 200 c for clusters of varying mass and concentration, and that also accurately predicts the concentration– Y relationship. Finally, we determine how inference of the linear bias parameter and splashback radius for SZ-selected clusters can be biased by ignoring the concentration dependence of the SZ signal, finding that bias to the former is essentially negligible, while bias to the latter can be as much as 2 per cent. [ABSTRACT FROM AUTHOR]