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Triglycerides, phospholipids, and cholesterol are prominent lipid types that serve diverse biological functions. These lipids act as vital structural components of cell membranes, provide energy for the body, and serve as signaling molecules that regulate physiological and pathological processes, including regulated cell death (RCD). While the initiation signals, biochemical pathways, and effector molecules may differ, increased membrane permeabilization from plasma membranes or organelles is a shared characteristic of RCD. This process involves alterations in lipid species and functions, along with autophagic degradation. Thus, the lipid hypothesis presents a novel perspective that complements other theories elucidating the features of cell survival and cell death. In this review, we present a comprehensive summary of the latest findings on the role and potential mechanisms of diverse lipids in influencing RCD processes, encompassing apoptosis, necroptosis, pyroptosis, ferroptosis, and autophagy. ACSL: acyl-CoA synthetase long chain family; DISC: death-inducing signaling complex; DAMPs: danger/damage-associated molecular patterns; Dtgn: dispersed trans-Golgi network; FAR1: fatty acyl-CoA reductase 1; GPX4: glutathione peroxidase 4; LPCAT3: lysophosphatidylcholine acyltransferase 3; LPS: lipopolysaccharide; MUFAs: monounsaturated fatty acids; MOMP: mitochondrial outer membrane permeabilization; MLKL, mixed lineage kinase domain like pseudokinase; oxPAPC: oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine; OxPCs: oxidized phosphatidylcholines; PUFAs: polyunsaturated fatty acids; POR: cytochrome p450 oxidoreductase; PUFAs: polyunsaturated fatty acids; RCD: regulated cell death; RIPK1: receptor interacting serine/threonine kinase 1; SPHK1: sphingosine kinase 1; SOAT1: sterol O-acyltransferase 1; SCP2: sterol carrier protein 2; SFAs: saturated fatty acids; SLC47A1: solute carrier family 47 member 1; SCD: stearoyl-CoA desaturase; VLCFA: very long chain fatty acids [ABSTRACT FROM AUTHOR]

Fat storage-inducing transmembrane protein 2 (FITM2) plays an important role in regulating lipid storage and could be regarded as a candidate gene for intramuscular fat deposition in pigs. The aim of this study was to clone the coding domain sequence (CDS) of FITM2 gene, to compare the nucleotide acid and deduced amino acid sequences between breeds and species, to analyze the structure and characteristics of protein and to detect the expression profile of gene. The results exhibited that the CDS of FITM2 gene was 789 bp in length. The mutation of nucleotide acids led to the mutation of deduced amino acids between Banna miniature inbred pigs and other two breeds (Yorkshire × Landrace pigs and Duroc × (Landrace × Yorkshire) pigs). It was indicated that high identities of nucleotide acid and deduced amino acid sequences between Banna miniature inbred pigs and other species. The deduced amino acids were composed of loops and alpha helices in the structure. FITM2 protein may be a 30 kDa hydrophobic protein with 26 phosphorylation sites and one potential N-glycosylated site. FITM2 gene was widely expressed in various tissues, and the highest expression level was in adipose tissue. [ABSTRACT FROM AUTHOR]

In this paper, the effects of partial replacement of cement by metakaolin (MK) and different supplementary cementitious materials (SCMs) were investigated on the compressive strength and elasticity modulus of ultra-high-performance concrete (UHPC) at different ages, and the laws of the effects of MK alone, MK and conventional SCMs on the mechanical properties of UHPC were quantitatively analyzed at the macroscopic level. The results showed that the compressive strength of UHPC reached the maximum value when the MK doping amount reached 10%, and its compressive strength at 7, 28 and 90 days increased by 21%, 28% and 18.2%, respectively. Furthermore, the elasticity modulus of UHPC also showed a similar trend. When MK and Blast furnace slag or Fly ash were compounded, the mechanical properties (compressive strength and elasticity modulus) of UHPC were significantly enhanced in the later stage, showing sound synergistic effects. Based on the experimental test data, a model for predicting the elasticity modulus of UHPC based on the change of time and SCMs was proposed with good reliability. [ABSTRACT FROM AUTHOR]

Growth performance and meat quality are important traits for pig production. The aim of the present study was to investigate the molecular mechanisms underlying growth performance and meat quality, and to identify novel target molecules for predicting the growth performance and meat quality. The differentially expressed genes (DEGs) in Diannan small ears pigs (DSP) and Landrace pigs (LP) were assessed by RNA-sequencing analyzing technology. A total of 339 DEGs were obtained between DSP and LP. 146 DEGs were upregulated in LP compared with DSP and 193 DEGs were upregulated in DSP compared with LP. The DEGs were significantly enriched in 26 GO and 3 KEGG pathways. The protein–protein interaction (PPI) network with 201 nodes and 382 edges was constructed and 5 modules were extracted from the entire network. The identified upregulated expression of genes involved in glycolysis and myogenesis as well as extracellular matrix may be associated with fast body and muscle deposition rates in LP. Increased expression of genes involved in PPAR signaling pathway and fatty acid metabolism as well as oxidative phosphate processes could be related to the intramuscular fat deposition and meat quality in DSP. The present study may provide an improved understanding of the growth performance and meat quality. [ABSTRACT FROM AUTHOR]

In this article, we consider Nernst–Planck–Poisson system with generalized dissipation. First, we prove the Gevrey class regularity of local solutions to system with large rough initial data in modulation spaces. Secondly, applying so-called Gevrey estimates, which is motivated by the works of Foias and Temam, we establish Gevrey class regularity of solutions to the system with initial data in a certein critical Fourier–Besov spaces. The results of us particularly imply that the solution is analytic in the spatial variable and obtain temporal decay rates of higher Fourier–Besov norms of solutions. [ABSTRACT FROM PUBLISHER]

Autophagy has recently attracted increasing attention for its role in conferring resistance to various commonly used anticancer therapies. Whereas its activities are known primarily to be under regulation of the high mobility group box-1 (HMGB1) gene, the expression of HMGB1 and its function in leukemia cells still remain unclear. In this study, we found that HMGB1 was expressed abundantly in various kinds of both leukemia and non-blood cancer cell-lines, and its expression was positively correlated with clinical status in childhood leukemia. In leukemia cells, when endogenous HMGB1 increased starvation-induced autophagy, this reaction was inhibited by the suppression of HMGB1. While the use of autophagy inhibitor, 3-methyladenine (3-MA), blocked the autophagic reaction and increased leukemia cell sensitivity to chemotherapy, enhancing HMGB1 expression decreased this sensitivity. Notably, suppressing HMGB1 expression also increased leukemia cell chemosensitivity. Furthermore, the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin complex 1 (mTORC1) pathway was found to be functionally connected with HMGB1. HMGB1 gene transfection increased the LC3-II level and inhibited phosphorylation of Akt and p70S6K levels. Knockdown of HMGB1 expression blocked the association between mTOR and raptor in the setting of enhanced autophagy. When class I PI3K was inhibited by PI3K-I shRNA, it decreased the PI3K-I expression level. Knockdown of HMGB1 expression had no further effects on LC3-II. These results suggest that endogenous HMGB1 is an intrinsic regulator of autophagy in leukemia cells and it enhances leukemia cell chemoresistance likely through the PI3K/Akt/mTORC1 pathway. [ABSTRACT FROM AUTHOR]

The objective of this work is to assess two novel controlled-release nitrendipine formulations, i.e., sustained-release nitrendipine microspheres having solid dispersion structure and a novel pH-dependent gradient-release delivery system for nitrendipine in healthy male volunteers, which were prepared by current authors. Domestic commercial nitrendipine tablets and Baypress™ nitrendipine tablets were employed as reference formulations. In a randomized, single-dose, fasting-state, crossover study design with a 1-week washout period, each subject received a 40-mg nitrendipine formulation. Plasma samples were collected over a 25-hour period after oral administration and were analyzed by a validated method using high performance liquid chromatography with ultraviolet detection. Pharmacokinetic parameters were determined using a noncompartmental analysis. The results provided evidence that the time to maximum plasma concentration of two novel controlled-release nitrendipine formulations were statistically significant prolonged in comparison with that of Baypress™ nitrendipine tablets. The relative bioavailabilities of test formulations were intensively improved compared with the domestic nitrendipine tablets, while the ratio is in a range of 80–120% in comparison with Baypress™ nitrendipine tablets. It is concluded that the two types of controlled-release systems are feasible for improving the dissolution rate of nitrendipine and obtaining a long-acting in vivo as well. [ABSTRACT FROM AUTHOR]

Immunogenic cell death (ICD) is a type of cell death that is accompanied by the release of damage-associated molecular patterns (DAMPs) and results in a dead-cell antigen-specific immune response. Here, we report that spautin-1, an inhibitor of ubiquitin-specific peptidases, triggers immunogenic cancer cell death in vitro and in vivo. The anticancer activity of spautin-1 occurs independent of autophagy inhibition, but depends on the intrinsic mitochondrial apoptosis pathway. Spautin-1 causes mitochondrial oxidative injury, which results in JUN transcription factor activation in a JNK-dependent manner. Mechanistically, activation of JUN by spautin-1 leads to apoptosis by upregulation of pro-apoptotic BAD expression. Importantly, the release of TFAM, a mitochondrial DAMP, by apoptotic cells may contribute to spautin-1-induced ICD via its action on the receptor AGER. Indeed, cancer cells treated with spautin-1 in vitro were able to elicit an anticancer immune response when inoculated in vivo, in the absence of any adjuvant. This immunogenic effect of spautin-1-treated cancer cells was lost when TFAM or AGER were neutralized by specific antibodies. Altogether, our results suggest that spautin-1 may stimulate an apoptotic pathway that results in ICD, in TFAM- and AGER-dependent fashion. [ABSTRACT FROM AUTHOR]