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BackgroundNutritional support has been identified as a potential intervention for cognitive frailty; however, the association between 25-hydroxyvitamin D [25-(OH)D], vitamin B12, and cognitive frailty remains ambiguous.MethodsThis study utilized data from two cycles (2011–2012, 2013–2014) of the National Health and Nutrition Examination Survey (NHANES) to investigate this relationship. The researchers constructed a 41-item frailty index encompassing diverse aspects of physical functioning, psychological evaluation, and medical conditions, and evaluated each participant individually. The study utilized Spearman's rank correlation coefficient and univariate ordered logistic regression to assess the relationships between variables and cognitive frailty. Recursive feature elimination and cross-validation methods were employed to identify the most influential variables for building and optimizing multivariate ordered logistic regression models. Subgroup analyses and interaction tests were further conducted to validate the identified correlations.ResultsThe findings of this study confirm a negative linear correlation between 25-(OH)D levels and cognitive frailty in older adults. Specifically, a one-unit increase in 25-(OH)D levels was associated with a 12% reduction in the risk of cognitive frailty. The result was further supported by subgroup analyses and interaction tests.ConclusionThe existence of a negatively correlated linear association between 25-(OH)D levels and cognitive frailty in older adults is plausible, but further rigorously designed longitudinal studies are necessary to validate this relationship.

Objective To investigate the effect of salidroside (SAL) on the proliferation, apoptosis and epithelial mesenchymal transformation (EMT) of non-small cell lung cancer (NSCLC) cell line and to clarify the molecular mechanism. Methods The cancer tissues from 22 lung cancer patients and adjecent tissues were collected, and the different lung cancer cell lines (A549, H358, H1299, H1650) were cultured in vitro. RT-qPCR was used to detect the expression of transforming acidic coiled-coid protein 2(TACC2) in cancer tissues and the lung cancer cell lines. After cells (A549 and H1299) were treated with SAL at different concentrations, the apoptosis and proliferation rates were analyzed by flow cytometry and CCK-8, respectively. The expression of E-cadherin, N-cadherin, TACC2 and the phosphorylation level of P38/MAPK in NSCLC cell were detected by Western blot. Plasmid (pcDNA3.0-TACC2) was transfected into A549 and H1299 cell to detect the effects of TACC2 over-expression on the levels of apoptosis, proliferation and EMT. Results The relative expression of TACC2 in lung cancer tissue significantly increased as compared with adjecent tissues.Meanwhile, the expression of TACC2 in NSCLC cell was also markedly higher than human lung fibroblasts cell line(HFL-1)(P＜0.05). Different concentrations of SAL can significantly inhibit the proliferation and increase the apoptosis of cells(P＜0.05). Western blot results showed that the expression of TACC2 and N-cadherin was significantly down-regulated, while E-cadherin expression was up-regulated in A549 and H1299 cells after treatment with SAL. Transfection with pcDNA3.0-TACC2 plasmid could significantly reduced the inhibited effect of SAL on the proliferation and EMT of A549 and H1299 cells (P＜0.05). In addition, the phosphorylation of intracellular p38/MAPK was significantly reduced after treatment with various SAL concentrations (P＜0.05). Conclusions SAL can inhibit the levels of proliferation and EMT in NSCLC cell by negatively regulates the expression of TACC2, which may be related to the inhibition of p38/MAPK signaling pathway.

In a Poynting-flux-dominated jet that exhibits an ordered magnetic field, a transition toward turbulence and magnetic disorder follows after magnetic reconnection and energy dissipation during the prompt emission phase. In this process, the configuration of the magnetic field evolves with time, rendering it impossible to entirely categorize the magnetic field as ordered. Therefore, we assumed a crude model that incorporates a random magnetic field and an ordered magnetic field, and takes into account the proportionality of the random magnetic field strength to the ordered magnetic field, in order to compute the polarization degree (PD) curve for an individual pulse. It has been discovered that the random magnetic field has a significant impact on the PD results of the low-energy X-ray. In an ordered magnetic field, the X-ray segment maintains a significant PD compared to those in the hundreds of keV and MeV ranges even after electron injection ceases, making PD easier to detect by polarimetry. However, when the random magnetic field is introduced, the low-energy and high-energy PDs exhibit a similar trend, with the X-ray PD being lower than that of the high-energy segment. Of course, this is related to the rate of disorder in the magnetic field. Additionally, there are two rotations of the polarization angles (PAs) that were not present previously, and the rotation of the PA in the high-energy segment occurs slightly earlier. These results are unrelated to the structure of the ordered magnetic field.

According to the characteristics of the actual service environment of inner cavity of automobile, the damp heat test, salt spray test and electrochemical AC impedance technology were used to evaluate the coating and establish the aging kinetic equation. Results showed that under the accelerated aging test, the coating was intact within 600 h of the damp heat test and 360 h of the salt spray test. The failure aging of the inner cavity coating in 3.5% (mass fraction) NaCl solution at 25 ℃ could be divided into three stages: the initial stage , the middle stage and the late stage of aging; the initial stage of aging (the 0th to 2nd cycle) had good corrosion resistance, and low frequency electrochemical impedance|Z| 0.01 Hz was on the order of 109 Ω·cm2 or more; in the middle stage (the 4th to 6th cycle), |Z|0.01 Hz was on the order of 105～108 Ω·cm2, the size and quantity of internal micropores increased, and the corrosion resistance was obviously attenuated; in the late stage (8th cycle), local bulges appeared on the surface, |Z|0.01 Hz was on the order of 105 Ω·cm2 and below, and the coating failed. Based on this, establishing the aging kinetic equation could predict and evaluate the service life and protective performance of the inner cavity anti-corrosive coatings.

The primary traffic-based indicators for identifying critical links account for travel time, transportation efficiency, and traffic demand. These indicators are seldom applied to scenarios in which link capacity degradation occurs across the entire network. In addition, the commonly used traffic demand-based indicator, known as unsatisfied demand, can only work when there are disconnected origin–destination (OD) pairs in the network. In this context, this study incorporates the concept of a degradable road network to represent such scenarios and introduces a new network-wide traffic demand-based indicator, defined as late arrival demand (LAD), to identify critical links. Specifically, we built a late arrival rate (LAR)-based user equilibrium (UE) model to capture travel behavior and estimate the LAD in degradable road networks. Then, LAD and four other indicators were introduced to identify critical links in the framework of the LAR-based UE model. Finally, the Nguyen–Dupuis and Sioux Falls networks were employed for numerical experiments. The results, under various levels of traffic demand and degradation, demonstrate that LAD is a flexible and effective network-wide traffic demand-based indicator. This new approach provides insights that can help managers assess link criticality in degradable road networks from the perspective of traffic demand. [ABSTRACT FROM AUTHOR]

Meiosis is a specialized cell division process that generates gametes for sexual reproduction. However, the factors and underlying mechanisms involving meiotic progression remain largely unknown, especially in humans. Here, it is first showed that HSF5 is associated with human spermatogenesis. Patients with a pathogenic variant of HSF5 are completely infertile. Testicular histologic findings in the patients reveal rare postmeiotic germ cells resulting from meiotic prophase I arrest. Hsf5 knockout (KO) mice confirms that the loss of HSF5 causes defects in meiotic recombination, crossover formation, sex chromosome synapsis, and sex chromosome inactivation (MSCI), which may contribute to spermatocyte arrest at the late pachytene stage. Importantly, spermatogenic arrest can be rescued by compensatory HSF5 adeno‐associated virus injection into KO mouse testes. Mechanistically, integrated analysis of RNA sequencing and chromatin immunoprecipitation sequencing data revealed that HSF5 predominantly binds to promoters of key genes involved in crossover formation (e.g., HFM1, MSH5 and MLH3), synapsis (e.g., SYCP1, SYCP2 and SYCE3), recombination (TEX15), and MSCI (MDC1) and further regulates their transcription during meiotic progression. Taken together, the study demonstrates that HSF5 modulates the transcriptome to ensure meiotic progression in humans and mice. These findings will aid in genetic diagnosis of and potential treatments for male infertility. [ABSTRACT FROM AUTHOR]

Di (2-ethyl-hexyl) phthalate (DEHP) is a wildly used plasticizer. Maternal exposure to DEHP during pregnancy blocks the placental cell cycle at the G2/M phase by reducing the efficiency of the DNA repair pathways and affects the health of offsprings. However, the mechanism by which DEHP inhibits the repair of DNA damage remains unclear. In this study, we demonstrated that DEHP inhibits DNA damage repair by reducing the activity of the DNA repair factor recruitment molecule PARP1. NAD+ and ATP are two substrates necessary for PARP1 activity. DEHP abated NAD+ in the nucleus by reducing the level of NAD+ synthase NMNAT1 and elevated NAD+ in the mitochondrial by promoting synthesis. Furthermore, DEHP destroyed the mitochondrial respiratory chain, affected the structure and quantity of mitochondria, and decreased ATP production. Therefore, DEHP inhibits PARP1 activity by reducing the amount of NAD+ and ATP, which hinders the DNA damage repair pathways. The supplement of NAD+ precursor NAM can partially rescue the DNA and mitochondria damage. It provides a new idea for the prevention of health problems of offsprings caused by DEHP injury to the placenta.

In order to understand the concentration decay law of sulfuryl fluoride fumigation in warehouses with different airtightness,five warehouses were selected in this experiment.Through the concentration monitoring during the fumigation process,the correlation between the decay half-life of the gas concentration and the air tightness of the warehouses is analyzed and compared.The results show that when the airtightness of the warehouse is 143 s,the maximum concentration half-life is 8.5 d,while with the airtightness of 53 s and 46 s,the maximum concentration half-life are 2.7 d and 4.6 d,respectively.The half-life of gas concentration in warehouses where air-tightness cannot be detected is about 2～3 d.The higher the concentration of sulfuryl fluoride gas,the faster the decay speed,however the concentration decay process does not show a certain connection with the air tightness of the warehouses.

The control region (CR) regulates the replication and transcription of the mitochondrial genome (mitogenome). Some avian mitogenomes possess two CRs, and the second control region (CR2) may enhance replication and transcription; however, the CR2 in lark mitogenome appears to be undergoing loss and is accompanied by tandem repeats. Here, we characterized six lark mitogenomes from Alaudala cheleensis, Eremophila alpestris, Alauda razae, and Calandrella cinerea and reconstructed the phylogeny of Passerida. Through further comparative analysis among larks, we traced the evolutionary process of CR2. The mitochondrial gene orders were conserved in all published lark mitogenomes, with Cytb-trnT-CR1-trnP-ND6-trnE-remnant CR2 with tandem repeat-trnF-rrnS. Phylogenetic analysis revealed Alaudidae and Panuridae are sister groups at the base of Sylvioidea, and sporadic losses of CR2 may occur in their common ancestor. CR sequence and phylogeny analysis indicated CR2 tandem repeats were generated within CR2, originating in the ancestor of all larks, rather than inherited from CR1. The secondary structure comparison of tandem repeat units within and between species suggested slipped-strand mispairing and DNA turnover as suitable models for explaining the origin and evolution of these repeats. This study reveals the evolutionary process of the CR2 containing tandem repeat in Alaudidae, providing reference for understanding the evolutionary characteristics and dynamics of tandem repeats. [ABSTRACT FROM AUTHOR]

Background Bronchopneumonia is a disease of the respiratory tract. It leads to other complications and endangers life and health. Long non-coding RNA (lncRNA) participates in the occurrence and development of bronchopneumonia. Nuclear paraspeckle assembly transcript 1 (NEAT1) plays a key role in inflammatory diseases, but the function of NEAT1 in bronchopneumonia remains unclear. Methods RT-qPCR and Western blotting were performed to determine genes and proteins expressions. MTT was applied to test cell viability. Cell apoptosis was detected by flow cytometry. RIP was used to investigate the correlation between NEAT1 and miR-155-5p. The interaction between miR-155-5p and NEAT1 or MyD88 was evaluated by the dual-luciferase reporter gene. Results NEAT1 and MyD88 were upregulated in BEAS-2B cells by LPS, while miR-155-5p was downregulated. Knockdown of NEAT1 inhibited LPS-induced BEAS-2B cells growth inhibition by inhibiting the apoptosis. In addition, NEAT1 silencing suppressed LPS-induced inflammatory responses in BEAS-2B cells via suppression of TNF-α, IL-1β, IL-6, and IL-18. Meanwhile, NEAT1 is directly bound to miR-155-5p to regulate MyD88/NF-κB axis, and overexpression of miR-155-5p increased cell proliferation and suppressed inflammatory factors expression levels and cell apoptosis. Furthermore, sh-NEAT1-induced inhibition of BEAS-2B cells injury was partially reversed by miR-155-5p inhibitor or MyD88 overexpression. Conclusion NEAT1 silencing suppressed LPS-induced BEAS-2B cells injury and inflammation by the mediation of miR-155-5p/MyD88/NF-κB axis. Thus, our study might shed new light on exploring the new strategies for the treatment of bronchopneumonia.