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Title III of the Older Americans Act requires congregate nutrition sites (CNSs) to provide nutrition education. In 2015, we assessed 19 CNSs in Appalachian South Carolina for nutrition education readiness. Nutrition education readiness and general education readiness were both low. Overall, the CNSs were not ready to deliver education interventions due to lack of training/education, funds, drivers, and communication technologies. Addressing these problems could improve the likelihood that education would be effective. The readiness concepts described here can be used by Extension educators to determine whether delivery sites are ready to effectively provide education programs.

The use of focus groups to formatively evaluate community-based curricula after development and before pilot testing is not highlighted in the literature. In the study discussed in this article, research with four focus groups, composed of 46 women aged 65 years and older and belonging to eight South Carolina Family and Community Leaders clubs, was conducted to evaluate the Cooking Healthy, Eating Smart (CHES) curriculum. The CHES curriculum was tailored based on suggestions from the older adults. Extension professionals can better prepare a curriculum for pilot testing in the community by conducting a formative evaluation using focus groups with community members at this particular stage of development.

Neutrophil recruitment to the lung after lipopolysaccharide (LPS; endotoxin) inhalation is primarily dependent on Toll-like receptor 4 (Tlr4) signaling, because it is virtually absent in mice deficient in Tlr4. However, among strains wild type for Tlr4, the magnitude of neutrophil recruitment to the lung after LPS inhalation is variable, suggesting the involvement of genes other than Tlr4. To identify genes associated with the inflammatory response to inhaled LPS, we evaluated the transcriptional response in lungs of 12 inbred strains of mice, 8 which are wild type for Tlr4 and 4 of which lack functional Tlr4. Using the promoter integration in microarray analysis algorithm, we scanned our gene list for transcription factor-binding sites significantly overrepresented among Tlr4 wild-type strains with high neutrophil influx in the lung after LPS inhalation. This analysis identified the interferon (IFN)-stimulated response element (ISRE) as the most overrepresented transcription factor (present in 24% of the promoters) associated with the neutrophil influx to the lower respiratory tract. To test the validity of this observation, we evaluated IFN-γ-deficient mice and found that the presence of lFN-γ is essential for robust neutrophil recruitment to the lower respiratory tract and modulation of key regulatory cytokines and chemokines after LPS inhalation. In conclusion, using a genomic approach, we identified the ISRE as a transcriptional element associated with the neutrophil response to inhaled LPS and demonstrated for the first time that lFN-γ plays a critical role in LPS-induced neutrophil recruitment to the lower airways. [ABSTRACT FROM AUTHOR]

Phosphorylation of mouse p53 at Ser[sup 18] occurs after DNA damage. To determine the physiological roles of this phosphorylation event in p53-dependent DNA damage responses, a Ser[sup 18] to Ala missense mutation was introduced into the germline of mice. Thymocytes and fibroblasts from the knock-in mice show reduced transactivation of many p53 target genes following DNA damage. p53 protein stabilization and DNA binding are similar in knock-in and wild type mice, but C-terminal acetylation was defective, consistent with a role for Ser[sup 18] in the recruitment of transcriptional co-activators. The apoptotic response of knock-in thymocytes to ionizing radiation is intermediate between that of wild type and p53 null thymocytes. Despite impaired transcriptional and apoptotic responses, the knock-in mice are not prone to spontaneous tumorigenesis. This indicates that neither phosphorylation of p53 on Ser[sup 18] by ATM nor a full transcriptional response is essential to prevent spontaneous tumor formation in mice. [ABSTRACT FROM AUTHOR]

Intervertebral disc degeneration is a degenerative disease where inflammation and immune responses play significant roles. Macrophages, as key immune cells, critically regulate inflammation through polarization into different phenotypes. In recent years, the role of macrophages in inflammation-related degenerative diseases, such as intervertebral disc degeneration, has been increasingly recognized. Macrophages construct the inflammatory microenvironment of the intervertebral disc and are involved in regulating intervertebral disc cell activities, extracellular matrix metabolism, intervertebral disc vascularization, and innervation, profoundly influencing the progression of disc degeneration. To gain a deeper understanding of the inflammatory microenvironment of intervertebral disc degeneration, this review will summarize the role of macrophages in the pathological process of intervertebral disc degeneration, analyze the regulatory mechanisms involving macrophages, and review therapeutic strategies targeting macrophage modulation for the treatment of intervertebral disc degeneration. These insights will be valuable for the treatment and research directions of intervertebral disc degeneration. [ABSTRACT FROM AUTHOR]

Introduction: The salinization of coastal soils is a primary cause of global land degradation. The aim of this study was to evaluate the effect of organic amendment on the soil microbial community within a saline gradient. Methods: The study was designed with five levels of electrical conductivity (EC): 0.33, 0.62, 1.13, 1.45 and 2.04 ds m−1. By conducting indoor potted plant experiments, determine the effects of applying microbial organic fertilizer on the physicochemical properties of soil and the structure of soil microbial communities under different salinity concentrations. Results: Compared with the control, higher OM content, total N, and higher crop biomass were observed in samples with organic amendment at the same salinity level. At the same salinity levels, the mean bacterial activity (AUC) and the mean number of substrates were higher than in the soil without organic amendment according to analyses by means of Biolog ECO MicroPlate. The results of canonical correspondence analysis indicate that after the application of organic amendments, the composition of loam and clay replaces soil pH, and aboveground biomass replaces root biomass as key indicators closely monitoring Community level physiological profiling (CLPP). In soil with the same salinity level, the application of microbial organic fertilizer led to an increase in the proportion of Actinobacteriota and a decrease in the proportion of Chloroflexi. In 0.3dS m-1 soil, the abundance of actinomycetes increased from 23% to 27% after application of microbial organic fertilizer, while the abundance of basidiomycetes decreased from 20% to 6%. In addition, after the application of microbial organic fertilizer, RB41, blastococcus and solirubrobacter significantly increased, while Melothermus and Herpetosiphon significantly decreased. Discussion: This study provides a strong theoretical basis for using microbial organic fertilizers to improve saline-alkali soil. [ABSTRACT FROM AUTHOR]

Simple Summary: Cancer signatures are very popular and support inference when reproducible and generalizable. However, every approach derives them differently, often in a context-specific way. Depending on the available experiments and data, computational methods used to obtain the signatures may vary. A few relevant questions motivated this research, one being the significance of collating signatures in terms of the outcomes, another being the synergistic meaning of a meta or super signature, and finally, whether some effective operational strategy exists to reduce the complexity of a signature set. There are numerous ways of portraying cancer complexity based on combining multiple types of data. A common approach involves developing signatures from gene expression profiles to highlight a few key reproducible features that provide insight into cancer risk, progression, or recurrence. Normally, a selection of such features is made through relevance or significance, given a reference context. In the case of highly metastatic cancers, numerous gene signatures have been published with varying levels of validation. Then, integrating the signatures could potentially lead to a more comprehensive view of the connection between cancer and its phenotypes by covering annotations not fully explored in individual studies. This broader understanding of disease phenotypes would improve the predictive accuracy of statistical models used to identify meaningful associations. We present an example of this approach by reconciling a great number of published signatures into meta-signatures relevant to Osteosarcoma (OS) metastasis. We generate a well-annotated and interpretable interactome network from integrated OS gene expression signatures and identify key nodes that regulate essential aspects of metastasis. While the connected signatures link diverse prognostic measurements for OS, the proposed approach is applicable to any type of cancer. [ABSTRACT FROM AUTHOR]

Low back pain caused by intervertebral disc degeneration (IDD) has emerged as a significant global public health concern, with far-reaching consequences for patients' quality of life and healthcare systems. Although previous research have revealed that the mechanisms of intervertebral disc cell apoptosis, pyroptosis and necroptosis can aggravate IDD damage by mediating inflammation and promoting extracellular matrix degradation, but they cannot explain the connection between different cell death mechanisms and ion metabolism disorders. The latest study shows that cell death mechanisms such as cellular senescence, ferroptosis, and cuproptosis, and PANopotosis have similar roles in the progression of intervertebral disc degeneration, but not exactly the same damage mechanism. This paper summarizes the effects of various cell death patterns on the disease progression of IDD, related molecular mechanisms and signaling pathways, providing new perspectives and potential clinical intervention strategies for the prevention and treatment of IDD. [ABSTRACT FROM AUTHOR]

This study aimed to evaluate the therapeutic properties of the traditional Chinese medicine Xuesanqi (XSQ, from the rhizome of Polygonum amplexicaule D. Don) in treating ulcerative colitis. We hypothesized that its many active components can alleviate symptoms of colitis by regulating the gut microbiota, its metabolites, and various signaling pathways. To test our hypotheses, we designed a DSS- induced colitis model in C57BL/6 male mice. Apparent metrics were evaluated in each group of mice and performed histological analysis of relevant tissues. The gut microbial composition was analyzed by 16S rRNA sequencing of bacteria. Simultaneously, the SCFAs content was detected by gas chromatography, inflammatory factor secretion was evaluated by ELISA or western-blot, the expression of tight junction protein and key proteins of the MAPK signaling pathway were analyzed by western-blot. Our result showed that the treatment with XSQ alleviated significant various symptoms such as weight loss, blood in stool, and shortening of colon. In addition, XSQ treatment restored the dysregulated gut microbiota in colitis mice, increased short chain fatty acids (SCFAs) and normalized the MAPK/ERK/JNK signaling pathways, promoted expression of tight junction protein Occludin, Claudin-1, and E-cadherin proteins. Furthermore, we also observed a dose-dependent pattern in these treatment responses. These findings demonstrated the active components of XSQ is a promising new treatment platform for ulcerative colitis. [ABSTRACT FROM AUTHOR]

Intervertebral discs (IVDs) are rhythmic tissues that experience daily low‐load recovery. Notably, aging and abnormal mechanical stress predispose IVDs to degeneration due to dysrhythmia‐induced disordered metabolism. Meanwhile, Rev‐erbα acts as a transcriptional repressor in maintaining biorhythms and homeostasis; however, its function in IVD homeostasis and degeneration remains unclear. This study assessed the relationship between low Rev‐erbα expression levels and IVD degeneration. Rev‐erbα deficiency accelerated needle puncture or aging‐induced IVD degeneration, characterized by increased extracellular matrix (ECM) catabolism and nucleus pulposus (NP) cell apoptosis. Mechanistically, Rev‐erbα knockdown in NP cells aggravated rhIL1β‐induced NOD‐like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation, exacerbating the imbalanced ECM and NP cell apoptosis. Meanwhile, blocking NLRP3 inflammasome activation mitigated Rev‐erbα deficiency and needle puncture‐induced IVD degeneration. Particularly, Rev‐erbα mediated the transcriptional repression of the NLRP3 inflammasome via the ligand heme‐binding of nuclear receptor co‐repressor (NCoR) and histone deacetylase 3 (HDAC3) complex. Thus, the increased expression of Rev‐erbα in NP cells following short‐term rhIL1β treatment failed to inhibit NLRP3 transcription in vitro owing to heme depletion. Pharmacological activation of Rev‐erbα in vivo and in vitro alleviated IVD degeneration by altering the NLRP3 inflammasome. Taken together, targeting Rev‐erbα may be a potential therapeutic strategy for alleviating IVD degeneration and its related diseases. [ABSTRACT FROM AUTHOR]

In this study, a novel lightweight Fe-Mn-Al-C steel composition and thermomechanical processing route was developed to produce a fully austenitic microstructure with a uniform intragranular dispersion of B2-NiAl precipitation in order to overcome the significant challenge of strengthening hot-rolled Fe-Mn-Al-C steels while retaining toughness. The new composition and processing methods allow for the processing of ultrahigh-strength Fe-Mn-Al-C steel containing nickel as thicker gauge plate for a multitude of new automotive and structural applications where lightweighting is critical. The composition investigated in this study was a fully austenitic Fe-21Mn-9Al-1C-8Ni wt% steel. Two hot rolling methods were investigated: the first procedure involved lower temperature rolling cycles to precipitate B2-NiAl during hot rolling and reheating. The second method involved higher temperature rolling to precipitate B2-NiAl after thermomechanical processing during a short isothermal treatment. The lower temperature rolling produced plate with an ultimate tensile strength of 1120 MPa and a Charpy V-Notch (CVN) toughness of 24 J at −40 °C. After the high temperature rolling procedure, precipitation of B2-NiAl through a subsequent precipitation hardening step resulted in reduced B2-NiAl size and improved the ultimate tensile strength above 1300 MPa. The two novel processing routes of a single composition can be performed with current manufacturing capabilities to produce hot rolled plate strengthened by B2-NiAl precipitation to various hardness (ranging from 33 to 41 HRC) and strength levels (ranging from 1100 to 1320 MPa ultimate tensile strength) while retaining 22–27% elongation. [ABSTRACT FROM AUTHOR]

Using e+e− collision data collected with the BESIII detector at seven energy points ranging from 3.68 to 3.71 GeV and corresponding to an integrated luminosity of 652.1 pb−1, we present an energy-dependent measurement of the transverse polarization, relative phase and modulus ratio of the electromagnetic form factors of the Σ+ hyperon in the e+e− → Σ + Σ ¯ − reaction. At each energy point, no evident polarization is observed. These results are helpful to understand the production mechanism of the Σ+- Σ ¯ − pairs. [ABSTRACT FROM AUTHOR]

We search for the radiative decays D+ → γρ+ and D+ → γK*+ using 20.3 fb−1 of e+e− annihilation data collected at the center-of-mass energy s = 3.773 GeV by the BESIII detector operating at the BEPCII collider. No significant signals are observed, and the upper limits on the branching fractions of D+→ γρ+ and D+→ γK*+ at 90% confidence level are set to be 1.3 × 10−5 and 1.8 × 10−5, respectively. [ABSTRACT FROM AUTHOR]

We search for the radiative decays D+ → γρ+ and D+ → γK*+ using 20.3 fb−1 of e+e− annihilation data collected at the center-of-mass energy s = 3.773 GeV by the BESIII detector operating at the BEPCII collider. No significant signals are observed, and the upper limits on the branching fractions of D+→ γρ+ and D+→ γK*+ at 90% confidence level are set to be 1.3 × 10−5 and 1.8 × 10−5, respectively. [ABSTRACT FROM AUTHOR]

Dark matter direct detection experiments are approaching the neutrino floor, with a significant probability of measuring coherent elastic neutrino-nucleus scattering (CEνNS) and exploring potential neutrino-related new physics (νNP). In the present study, the simultaneous presence of dark matter and νNP is emphatically investigated, revealing a response similar to Standard Model neutrino backgrounds in Xenon-based dark matter experiments. Through analyses of three U(1) extension models, it is determined that dark matter signals can be differentiated from an excess or a depletion of neutrino contributions from νNP by applying a statistically defined distinction method to nuclear and electronic recoil spectra. Additionally, an investigation is conducted into how νNP affects the exclusion limits for spin-independent dark matter-nucleon interactions. The present findings could facilitate the identification of new physics in future dark matter experiments. [ABSTRACT FROM AUTHOR]

Intervertebral disc degeneration (IVDD) stands as a prevalent chronic orthopedic ailment, profoundly impacting patients' well‐being due to incapacitating low back pain. Studies have highlighted a close correlation between IVDD and the programmed cell death of nucleus pulposus (NP) cells orchestrated by interleukin‐1 beta (IL‐1β), tumor necrosis factor‐alpha (TNF‐α), and caspase‐3 (CASP3). Puerarin, renowned for its anti‐inflammatory attributes and its influence on IL‐1β and TNF‐α, emerges as a promising candidate for IVDD treatment. However, the precise mechanism by which it regulates apoptosis via these pathways remains ambiguous. This investigation utilizes bioinformatics to unveil the molecular intricacies of puerarin‐mediated apoptosis regulation in IVDD, substantiated by preliminary in vitro experiments. Analysis exposes aberrant expression of pivotal apoptosis‐associated proteins (IL‐1β, TNF‐α, CASP3, CASP8, and BCL2) in IVDD patients, with network pharmacology indicating puerarin's potential efficacy in IVDD treatment by modulating apoptosis and cellular senescence pathways. Further experiments elucidate puerarin's capacity to stimulate NP cell proliferation while inhibiting apoptosis, potentially contributing to IVDD mitigation. Western blot and PCR outcomes reveal escalated expression of apoptosis‐related proteins (IL‐1β, TNF‐α, and CASP3) in lipopolysaccharide‐treated NPCs, ameliorated by puerarin intervention. Molecular docking simulations demonstrate favorable binding properties of puerarin with apoptotic proteins, while flow cytometry analysis indicates its ability to diminish NPC apoptosis. These discoveries imply that puerarin might alleviate NPC apoptosis by modulating key targets, thereby potentially ameliorating IVDD. In summary, this study unveils the intrinsic mechanism of puerarin in regulating NPC apoptosis to alleviate IVDD, underscoring its therapeutic promise. [ABSTRACT FROM AUTHOR]

Background: Intervertebral disc degeneration (IDD) is a progressive age‐related disorder characterized by the reduction in the number of nucleus pulposus cells (NPCs) and degradation of extracellular matrix (ECM), thereby leading to chronic pain and disability. The pathogenesis of IDD is multifaceted, and current therapeutic strategies remain limited. The nucleus pulposus (NP), primarily composed of NPCs, proteoglycans, and type II collagen, constitutes essential components for maintaining intervertebral disc (IVD) function and spinal motion. The disturbed homeostasis of NPCs is closely associated with IDD. Accumulating evidence increasingly suggests the crucial role of programmed cell death (PCD) in regulating the homeostasis of NPCs. Aims: This review aimed to elucidate various forms of PCD and their respective roles in IDD, and investigate diverse strategies targeting the cell death of NPCs for IDD treatment. Materials & Methods: We collected the relevant literature regarding PCD and their roles in the development of IDD. Subsequently, we comprehensively summarized the intricate association between PCD and IDD, and also explored the potential and application of cell therapy and traditional Chinese medicine (TCM) in the prevention and treatment of IDD. Results: Current literature indicated that the PCD of NPCs was closely associated with the pathogenesis of IDD. Additionally, the development of targeted pharmaceuticals based on the mechanisms of PCD could effectively impede the loss of NPCs. Conclusion: This review demonstrated that targeting the PCD of NPCs may be a promising strategy for the treatment of IDD. [ABSTRACT FROM AUTHOR]

Scutellarin (SCU), a flavonoid glucuronide derived from Scutellaria barbata and Erigeron breviscapus , exhibits broad pharmacological effects with promising therapeutic potential in treating various chronic diseases. It has demonstrated efficacy in modulating multiple biological pathways, including antioxidant, anti-inflammatory, anti-apoptotic, and vasodilatory mechanisms. These protective roles make SCU a valuable compound in treating chronic diseases such as cerebrovascular diseases, cardiovascular diseases, neurodegenerative disorders, and metabolic diseases. Despite its multi-targeted effects, SCU faces challenges such as low bioavailability and limited clinical data, which hinder its widespread therapeutic application. Current research supports its potential to prevent oxidative stress, reduce inflammatory responses, and enhance cell survival in cells and rats. However, more comprehensive studies are required to clarify its molecular mechanisms and to develop strategies that enhance its bioavailability for clinical use. SCU could emerge as a potent therapeutic agent for the treatment of chronic diseases with complex pathophysiological mechanisms. This review examines the current literature on Scutellarin to provide a comprehensive understanding of its pharmacological activity, mechanisms of action, and therapeutic potential in treating chronic diseases. [ABSTRACT FROM AUTHOR]

Using 7.33 fb−1 of e+e− collision data samples collected with the BESIII detector at center-of-mass energies between 4.128 and 4.226 GeV, we search for the radiative decay D s + → γρ 770 + for the first time. A hint of D s + → γρ 770 + is observed with a statistical significance of 2.5σ. The branching fraction of D s + → γρ 770 + is measured to be (2.2 ± 0.9stat. ± 0.2syst.) × 10−4, corresponding to an upper limit of 6.1 × 10−4 at the 90% confidence level. [ABSTRACT FROM AUTHOR]

Using e+e− collision data collected by the BESIII detector at BEPCII corresponding to an integrated luminosity of 30 fb−1, we measure Born cross sections and effective form factors for the process e + e − → Ξ 0 Ξ ¯ 0 at forty-five center-of-mass energies between 3.51 and 4.95 GeV. The dressed cross section is fitted, assuming a power-law function plus a charmonium(-like) state, i.e., ψ(3770), ψ(4040), ψ(4160), ψ(4230), ψ(4360), ψ(4415) or ψ(4660). No significant charmonium(-like) state decaying into Ξ 0 Ξ ¯ 0 is observed. Upper limits at the 90% confidence level on the product of the branching fraction and the electronic partial width are provided for each decay. In addition, ratios of the Born cross sections and the effective form factors for e + e − → Ξ 0 Ξ ¯ 0 and e + e − → Ξ − Ξ ¯ + are also presented to test isospin symmetry and the vector meson dominance model. [ABSTRACT FROM AUTHOR]

The great gerbil (Rhombomys opimus) is a gregarious rodent in Central Asia and is one of the major pests found in desert forest and grassland areas. The distribution changes and migration routes of R. opimus in Central Asia under climate change remain unexplored. This study employed multi‐model ensemble, correlation analysis, jackknife method, and minimum cumulative resistance (MCR) model to simulate the potential habitat of R. opimus under current and future (2030 and 2050) climate scenarios and estimate its possible migration routes. The results indicate that the ensemble model integrating Random Forest (RF), Gradient Boosting Machine (GBM), and Maximum Entropy Model (MaxEnt) performed best within the present climate context. The model predicted the potential distribution of R. opimus in Central Asia with an area under the curve (AUC) of 0.986 and a True Skill Statistic (TSS) of 0.899, demonstrating excellent statistical accuracy and spatial performance. Under future climate scenarios, northern Xinjiang and southeastern Kazakhstan will remain the core areas of R. opimus distribution. However, the optimal habitat region will expand relative to the current one. This expansion will increase with the rising CO2 emission levels and over time, potentially enlarging the suitable area by up to 39.49 × 104 km2. In terms of spatial distribution, the suitable habitat for R. opimus is shifting toward higher latitudes and elevations. For specific migration routes, R. opimus tends to favor paths through farmland and grassland. This study can provide guidance for managing and controlling R. opimus under future climate change scenarios. [ABSTRACT FROM AUTHOR]

One of the fundamental goals of particle physics is to gain a microscopic understanding of the strong interaction. Electromagnetic form factors quantify the structure of hadrons in terms of charge and magnetization distributions. While the nucleon structure has been investigated extensively, data on hyperons are still scarce. It has recently been demonstrated that electron-positron annihilations into hyperon-antihyperon pairs provide a powerful tool to investigate their inner structure. We present a method useful for hyperon-antihyperon pairs of different types which exploits the cross section enhancement due to the effect of vacuum polarization at the J/ψ resonance. Using the 10 billion J/ψ events collected with the BESIII detector, this allows a precise determination of the hyperon structure function. The result is essentially a precise snapshot of the Λ ¯ Σ 0 (Λ Σ ¯ 0 ) transition process, encoded in the transition form factor ratio and phase. Their values are measured to be R = 0.860 ± 0.029(stat.) ± 0.015(syst.), Δ Φ Λ ¯ Σ 0 = (1.011 ± 0.094 (stat.) ± 0.010 (syst.)) r a d and Δ Φ Λ Σ ¯ 0 = (2.128 ± 0.094 (stat.) ± 0.010 (syst.)) r a d . Furthermore, charge-parity (CP) breaking is investigated in this reaction and found to be consistent with CP symmetry. Investigating the inner structure of baryons is important to further our understanding of the strong interaction. Here, the BESIII Collaboration extracts the absolute value of the ratio of the electric to magnetic form factors and its relative phase for e + e − → J/ψ → ΛΣ decays, enhancing the signal thanks to the vacuum polarisation effect at the J/ψ peak. [ABSTRACT FROM AUTHOR]

Activities such as childbirth and breastfeeding can cause severe oxidative stress and inflammatory damage to the mother during early lactation, and can affect animal milk production, and the growth and development of offspring. Trehalose alleviates damage to the body by endowing it with stress resistance. In this study, we used trehalose combined with Lactobacillus plantarum, Bifidobacterium longum, Bacillus subtilis, and Saccharomyces cerevisiae to explore whether dietary intervention can alleviate oxidative stress and inflammatory damage in early lactation and to evaluate the growth ability, acid production ability, antioxidant ability, non-specific adhesion ability, antibacterial ability, and other parameters to determine the optimal combinations and proportions. The results showed that the synbiotics composed of 2.5% trehalose and 1 × 107 cfu/g of Bifidobacterium longum could regulate the gut microbiota, and promote mammary gland development in dams by reducing progesterone (PROG) content in the blood, increasing prolactin (PRL) and insulin-like growth factor-1 (IGF-1) content, enhancing their antioxidant and immune abilities, and effectively increasing the weight and lactation of early lactating dams. In addition, it can also affect the growth of offspring and the development of the intestinal barrier. These results indicate that trehalose synbiotics have great potential in alleviating oxidative stress and inflammatory damage in early lactation. [ABSTRACT FROM AUTHOR]

Intervertebral disc degeneration (IDD) is a major cause of discogenic pain, and is attributed to the dysfunction of nucleus pulposus, annulus fibrosus, and cartilaginous endplate (CEP). Osteopontin (OPN), a glycoprotein, is highly expressed in the CEP. However, little is known on how OPN regulates CEP homeostasis and degeneration, contributing to the pathogenesis of IDD. Here, we investigate the roles of OPN in CEP degeneration in a mouse IDD model induced by lumbar spine instability and its impact on the degeneration of endplate chondrocytes (EPCs) under pathological conditions. OPN is mainly expressed in the CEP and decreases with degeneration in mice and human patients with severe IDD. Conditional Spp1 knockout in EPCs of adult mice enhances age-related CEP degeneration and accelerates CEP remodeling during IDD. Mechanistically, OPN deficiency increases CCL2 and CCL5 production in EPCs to recruit macrophages and enhances the activation of NLRP3 inflammasome and NF-κB signaling by facilitating assembly of IRAK1-TRAF6 complex, deteriorating CEP degeneration in a spatiotemporal pattern. More importantly, pharmacological inhibition of the NF-κB/NLRP3 axis attenuates CEP degeneration in OPN-deficient IDD mice. Overall, this study highlights the importance of OPN in maintaining CEP and disc homeostasis, and proposes a promising therapeutic strategy for IDD by targeting the NF-κB/NLRP3 axis. [ABSTRACT FROM AUTHOR]

By analyzing e+e− annihilation data corresponding to an integrated luminosity of 2.93 fb−1 collected at a center-of-mass energy of 3.773 GeV with the BESIII detector, the first observation of the semileptonic decays D 0 → K S 0 π − π 0 e + ν e and D + → K S 0 π + π − e + ν e is reported. In the hypothesis that all events correspond to K1(1270) decays, the branching fractions are measured to be B D 0 → K 1 1270 − → K S 0 π − π 0 e + ν e = 1.69 − 0.46 + 0.53 ± 0.15 × 10 − 4 and B D + → K ¯ 1 1270 0 → K S 0 π + π − e + ν e = 1.47 − 0.40 + 0.45 ± 0.14 × 10 − 4 with statistical significance of 5.4σ and 5.6σ, respectively. When combined with measurements of the K1(1270) → K+π−π decays, the absolute branching fractions are determined to be B D 0 → K 1 1270 − e + ν e = 1.08 − 0.13 − 0.10 + 0.14 + 0.08 ± 0.21 × 10 − 3 and B D + → K ¯ 1 1270 0 e + ν e = 1.70 − 0.23 + 0.26 ± 0.13 ± 0.35 × 10 − 3 . The first and second uncertainties are statistical and systematic, respectively, and the third uncertainties originate from the assumed branching fractions of the K1(1270) → Kππ decays. [ABSTRACT FROM AUTHOR]

Using e+e− annihilation data sets corresponding to an integrated luminosity of 4.5 fb−1, collected with the BESIII detector at center-of-mass energies between 4.600 and 4.699 GeV, we report the first measurements of the absolute branching fractions B Λ c + → p K L 0 = (1.67 ± 0.06 ± 0.04)%, B Λ c + → p K L 0 π + π − = (1.69 ± 0.10 ± 0.05)%, and B Λ c + → p K L 0 π 0 = (2.02 ± 0.13 ± 0.05)%, where the first uncertainties are statistical and the second systematic. Combining with the known branching fractions of Λ c + → p K S 0 , Λ c + → p K S 0 π + π − , and Λ c + → p K S 0 π 0 , we present the first measurements of the K S 0 - K L 0 asymmetries R Λ c + K S , L 0 X = B Λ c + → K S 0 X − B Λ c + → K L 0 X B Λ c + → K S 0 X + B Λ c + → K L 0 X in charmed baryon decays: R Λ c + p K S , L 0 = − 0.025 ± 0.031 , R Λ c + p K S , L 0 π + π − = − 0.027 ± 0.048 and R Λ c + p K S , L 0 π 0 = − 0.015 ± 0.046 . No significant asymmetries with statistical significance are observed. [ABSTRACT FROM AUTHOR]

Degenerative disc disease (DDD) represents a significant global health challenge, yet its underlying molecular mechanisms remain elusive. This study aimed to investigate the role of type 1 phosphatidylinositol 4‐phosphate 5‐kinase (Pip5k1) in intervertebral disc (IVD) homeostasis and disease. All three Pip5k1 isoforms, namely Pip5k1α, Pip5k1β, and Pip5k1γ, were detectable in mouse and human IVD tissues, with Pip5k1γ displaying a highest expression in nucleus pulposus (NP) cells. The expression of Pip5k1γ was significantly down‐regulated in the NP cells of aged mice and patients with severe DDD. To determine whether Pip5k1γ expression is required for disc homeostasis, we generated a Pip5k1γfl/fl; AggrecanCreERT2 mouse model for the conditional knockout of the Pip5k1γ gene in aggrecan‐expressing IVD cells. Our findings revealed that the conditional deletion of Pip5k1γ did not affect the disc structure or cellular composition in 5‐month‐old adult mice. However, in aged (15‐month‐old) mice, this deletion led to several severe degenerative disc defects, including decreased NP cellularity, spontaneous fibrosis and cleft formation, and a loss of the boundary between NP and annulus fibrosus. At the molecular level, the absence of Pip5k1γ reduced the anabolism of NP cells without markedly affecting their catabolic or anti‐catabolic activities. Moreover, the loss of Pip5k1γ significantly dampened the activation of the protective Ampk pathway in NP cells, thereby accelerating NP cell senescence. Notably, Pip5k1γ deficiency blunted the effectiveness of metformin, a potent Ampk activator, in activating the Ampk pathway and mitigating lumbar spine instability (LSI)‐induced disc lesions in mice. Overall, our study unveils a novel role for Pip5k1γ in promoting anabolism and maintaining disc homeostasis, suggesting it as a potential therapeutic target for DDD. [ABSTRACT FROM AUTHOR]

The processes hc→ γP (P = η′, η, π0) are studied with a sample of (27.12 ± 0.14) × 108ψ(3686) events collected by the BESIII detector at the BEPCII collider. The decay hc→ γη is observed for the first time with the significance of 9.0 σ, and the branching fraction is determined to be (3.77 ± 0.55 ± 0.13 ± 0.26) × 10−4, while B (hc→ γη′) is measured to be (1.40 ± 0.11 ± 0.04 ± 0.10) × 10−3, where the first uncertainties are statistical, the second systematic, and the third from the branching fraction of ψ(3686) → π0hc. The combination of these results allows for a precise determination of R h c = B h c → γη B h c → γ η ′ , which is calculated to be (27.0 ± 4.4 ± 1.0)%. The results are valuable for gaining a deeper understanding of η − η′ mixing, and its manifestation within quantum chromodynamics. No significant signal is found for the decay hc → γπ0, and an upper limit is placed on its branching fraction of B (hc → γπ0) < 5.0 × 10−5, at the 90% confidence level. [ABSTRACT FROM AUTHOR]

Skeletal muscle metabolism has implications for swine feed efficiency (FE); however, it remains unclear if the metabolic profile of skeletal muscle changes during postnatal growth. To assess the metabolic changes, samples were collected from the longissimus dorsi (LD, glycolytic muscle), latissimus dorsi (LAT, mixed muscle), and masseter (MS, oxidative muscle) at 20, 53, 87, 120, and 180 days of age from barrows. Muscles were assessed to determine the abundance of several metabolic enzymes. Lactate dehydrogenase (LDHα) decreased in all muscles from 20 to 87 d (p < 0.01), which may be attributed to the muscles being more glycolytic at weaning from a milk-based diet. Pyruvate carboxylase (PC) increased in all muscles at 53 d compared to the other time points (p < 0.01), while pyruvate dehydrogenase α 1 (PDHα1) increased at 87 and 180 d in MS compared to LD (p < 0.05), indicating that potential changes occur in pyruvate entry into the tricarboxylic acid (TCA) cycle during growth. Isolated mitochondria from each muscle were incubated with 13C-labeled metabolites to assess isotopomer enrichment patterns of TCA intermediates. Citrate M + 2 and M + 4 derived from [13C3]-pyruvate increased at 87 d in LAT and MS mitochondria compared to LD mitochondria (p < 0.05). Regardless of the muscle, citrate M+3 increased at 87 d compared to 20, 53, and 120 d, while 180 d showed intermediate values (p < 0.01). These data support the notion that pyruvate metabolism is dynamic during growth. Our findings establish a metabolic fingerprint associated with postnatal muscle hypertrophy. [ABSTRACT FROM AUTHOR]

Electricity markets are struggling. Unprecedented energy price shocks, a deeply entrenched cost-of-living crisis, and the imperatives of decarbonization are challenging the ability of current market arrangements to deliver clean, affordable electricity at the scale and pace necessary to avoid widespread climate disruption. Over the last several years, mass protests around the world have put a vision of electricity as a primary social good and system of provisioning squarely on the public agenda for the first time in a generation. Regulators have responded with emergency packages of support and longer-term efforts to rethink and reform the basic design of electricity markets. In all of this, it is increasingly clear that the forty-year global experiment with neoliberal electricity has failed to deliver on even the most basic metrics and, more importantly, is no longer fit for purpose as electricity becomes the chief instrument of decarbonization for most economies around the world. This Article explains how and why electricity markets have failed and offers a series of prescriptions for where we go from here. The Article starts with a brief global history of neoliberal electricity that shows how the project of privatization and restructuring emerged and spread around the world and the consequences this entailed. It then discusses how these markets have struggled with persistent problems of market power, chronic underinvestment, high prices, and an inability to support renewable energy at scale. Finally, the Article offers some provisional thoughts on what an alternative, decommodified approach to electricity might look like as the clean energy transition accelerates, focusing specifically on the relationship between capital and infrastructure, the need for "social ratemaking" to ensure access and affordability, and the potential for a more cooperative approach to balancing the system as intermittent renewables come to dominate the supply of electricity. The Article draws on recent work in law and political economy as well as some of its precursors in legal realism and institutional economics. It also engages with a specific set of questions and concerns that have long preoccupied the fields of public utility and regulated industries law but have recently been revived and updated in the context of a new cross-sectoral approach to economic regulation known as networks, platforms, and utilities law. The key objective is to understand how law, politics, and economics have together structured distributional struggles over the design and maintenance of electricity markets and how they might be recombined in new ways to realize a vision of electricity as a key system of provisioning and vital infrastructure for the clean energy future. [ABSTRACT FROM AUTHOR]

With a sample of (10087 ± 44) × 106J/ψ events accumulated with the BESIII detector, we analyze the decays η′ → π+π−l+l−(l = e, μ) via the process J/ψ → γη′. The branching fractions are measured to be B (η′ → π+π−e+e−) = (2.45 ± 0.02(stat.) ± 0.08(syst.)) × 10−3 and B (η′ → π+π−μ+μ−) = (2.16 ± 0.12(stat.) ± 0.06(syst.)) × 10−5, and the ratio is B η ′ → π + π − e + e − B η ′ → π + π − μ + μ − = 113.4 ± 0.9 stat. ± 3.7 syst. . In addition, by combining the η′ → π+π−e+e− and η′ → π+π−μ+μ− decays, the slope parameter of the electromagnetic transition form factor is measured to be bη′ = 1.30 ± 0.19 (GeV/c2)−2, which is consistent with previous measurements from BESIII and theoretical predictions from the VMD model. The asymmetry in the angle between the π+π− and l+l− decay planes, which has the potential to reveal the CP-violation originating from an unconventional electric dipole transition, is also investigated. The asymmetry parameters are determined to be A CP η ′ → π + π − e + e − = − 0.21 ± 0.73 stat. ± 0.01 syst. % and A CP η ′ → π + π − μ + μ − = 0.62 ± 4.71 stat. ± 0.08 syst. % , implying that no evidence of CP-violation is observed at the present statistics. Finally, an axion-like particle is searched for via the decay η′ → π+π−a, a → e+e−, and upper limits of the branching fractions are presented for the mass assumptions of the axion-like particle in the range of 0 − 500 MeV/c2. [ABSTRACT FROM AUTHOR]

We measured the Born cross sections for the process e+e− → ωη′ at 22 center-of-mass energies from 2.000 to 3.080 GeV with the BESIII detector at the BEPCII collider. We observed a resonant structure with a statistical significance of 9.6σ. A Breit-Wigner fit determines its mass to be MR = (2153 ± 30 ± 31) MeV/c2 and its width to be ΓR = (167 ± 77 ± 7) MeV, where the first uncertainties are statistical and the second are systematic. [ABSTRACT FROM AUTHOR]

Using e+e− collision data collected with the BESIII detector at the BEPCII collider at center-of-mass energies between 3.510 and 4.914 GeV, corresponding to an integrated luminosity of 25 fb−1, we measure the Born cross sections for the process e + e − → K − Ξ ¯ + Λ / Σ 0 at thirty-five energy points with a partial-reconstruction strategy. By fitting the dressed cross sections of e + e − → K − Ξ ¯ + Λ / Σ 0 , evidence for ψ 4160 → K − Ξ ¯ + Λ is found for the first time with a significance of 4.4σ, including systematic uncertainties. No evidence for other possible resonances is found. In addition, the products of electronic partial width and branching fraction for all assumed resonances decaying into K − Ξ ¯ + Λ / Σ 0 are determined. [ABSTRACT FROM AUTHOR]