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Background Adolescents may experience stressful life events and associated physical and psychological symptoms of stress. Physical activity has a buffering effect on stress. However, whether physical activity attitudes modulate stress, and the relationship between physical activity attitudes, physical activity, and stress symptoms is unclear. The present study focuses on whether adolescent stress events predict stress symptoms, whether physical activity buffers stress, and whether this stress-buffering effect is enhanced when attitudes toward physical activity are positive. Methods A stratified and cluster sampling method was used to select 2420 junior high school students from nine provinces from each of the three economic zones (with high GDP level, medium GDP level, and low GPD level) of eastern, western, and central China and the Adolescent Self-Rating Life Events Checklist, the Calgary Symptoms of Stress Inventory, the Physical Activity Rating Scale, and the behavioral attitude dimension of the Physical Activity Attitude Scale were used to investigate adolescent stress events, stress symptoms, physical activity, and physical activity attitudes respectively. There are 1,190 boys and 1,230 girls from seventh to ninth grade 12–15 years old. Results Adolescents’ stress events and stress symptoms showed a significant positive correlation ( r  = 0.479, P  < 0.01). The more stressful events adolescents have, the more pronounced stress symptoms become. The interaction term between the total amount of physical activity and stress events was not influential on stress symptoms ( P  = 0.461), and neither was the distinction between high and moderate physical activity levels ( P h = 0.248, P m = 0.245). There was a moderating effect of physical activity attitudes on stress buffering for moderate physical activity levels ( P  < 0.01). The moderating effect was stronger when adolescents had positive attitudes toward physical activity. Conclusions Adolescent physical activity can buffer the effects of stress events on stress symptoms when physical activity attitudes are positive, revealing that stimulating adolescents’ physical activity initiative can promote physical activity to buffer stress.

Long noncoding RNAs (lncRNAs) are emerging as key regulators in cancer initiation and progression. TP53TG1 is a recently identified lncRNA and several studies have shown that TP53TG1 may play the role of tumor suppressor gene or oncogene in different tumors. Nevertheless, the involvement of TP53TG1 in carcinogenesis of pancreatic ductal adenocarcinoma (PDAC) has not been characterized. In our studies, we identified that TP53TG1 was highly expressed in PDAC and was a novel regulator of PDAC development. Knockdown of TP53TG1 inhibited proliferation, induced apoptosis, and decreased migration and invasion in PDAC cells, whereas enhanced expression of TP53TG1 had the opposite effects. Mechanistically, TP53TG1 could directly bind to microRNA (miR)‐96 and effectively function as a sponge for miR‐96, thus antagonizing the functions of miR‐96 and leading to derepression of its endogenous target KRAS, which is a core oncogene in the initiation and maintenance of PDAC. Taken together, these observations imply that TP53TG1 contributes to the growth and progression of PDAC by acting as a competing endogenous RNA (ceRNA) to competitively bind to miR‐96 and regulate KRAS expression, which highlights the importance of the complicated miRNA‐lncRNA network in modulating the progression of PDAC. TP53TG1 contributes to the growth and progression of PDAC by acting as a competing endogenous RNA to upregulate KRAS expression through competitive combination with miR‐96, which highlights the importance of the complicated miRNA‐lncRNA network in modulating the progression of PDAC.

With the discovery of research, many properties of carbon dots are getting better and better. People have taken advantage of this and utilized them interspersed in various fields. In the present study, water-soluble nitrogen-doped carbon dots (N-CDs) with excellent optical and fluorescence thermal properties were prepared by the hydrothermal method using 4-dimethylaminopyridine and N,N′-methylenebisacrylamide as precursors. Co2+ has a selective bursting effect on the fluorescence of N-CDs. The fluorescence of N-CDs is selectively burst by Co2+, and the high sensitivity is good in the range of 0–12 μM with a detection limit of 74 nM. In addition, the good temperature response (reversible and recoverable fluorescence in the temperature range of 20~90 °C) and excellent optical properties of the N-CDs also make them new potentials in the field of fluorescent inks and temperature sensing.

Background Tailoring gene expression to balance metabolic fluxes is critical for the overproduction of metabolites in yeast hosts, and its implementation requires coordinated regulation at both transcriptional and translational levels. Although synthetic minimal yeast promoters have shown many advantages compared to natural promoters, their transcriptional strength is still limited, which restricts their applications in pathway engineering. Results In this work, we sought to expand the application scope of synthetic minimal yeast promoters by enhancing the corresponding translation levels using specific Kozak sequence variants. Firstly, we chose the reported UAS F-E-C -Core1 minimal promoter as a library template and determined its Kozak motif (K 0 ). Next, we randomly mutated the K 0 to generate a chimeric promoter library, which was able to drive green fluorescent protein (GFP) expression with translational strengths spanning a 500-fold range. A total of 14 chimeric promoters showed at least two-fold differences in GFP expression strength compared to the K 0 control. The best one named K 528 even showed 8.5- and 3.3-fold increases in fluorescence intensity compared with UAS F-E-C -Core1 and the strong native constitutive promoter P TDH3 , respectively. Subsequently, we chose three representative strong chimeric promoters (K 540 , K 536 , and K 528 ) from this library to regulate pathway gene expression. In conjunction with the tHMG1 gene for squalene production, the K 528 variant produced the best squalene titer of 32.1 mg/L in shake flasks, which represents a more than 10-fold increase compared to the parental K 0 control (3.1 mg/L). Conclusions All these results demonstrate that this chimeric promoter library developed in this study is an effective tool for pathway engineering in yeast.

Sepsis is a common and life-threatening syndrome resulting from systemic and dysregulated immune response to severe infection, which contributes to morbidity and mortality in critically ill patients. This work aimed to evaluate the regulatory function of Breg cells in sepsis-associated pancreatic injury. We established mice model of sepsis-associated pancreatic injury by cecal ligation and puncture (CLP). Pancreatic injury was assessed by measuring the levels of amylase activity and histologic pancreatic injury scores. The proportions of Breg cells and T cell subsets were analyzed by flow cytometry, their secreted cytokines were detected by ELISA. The expressions of T-bet, RORγt and Foxp3 in spleen were determined by RT-PCR. The apoptosis of pancreatic cells was examined by LDH assay and Tunel, and the cell viability was detected by MTT assay. Compared to the sham group, a significantly lower percentage of Breg cells was observed in model mice. Anti-CD22 treatment exacerbated pancreatic injury, and significantly increased the percentages of Th1, Th17 cells along with the levels of IFN-γ, IL-17 in CLP-induced sepsis model, but did not affect the differentiation of Treg cells and expression of IL-10. Anti-CD22 administration promoted the expressions of T-bet and RORγt, but did not affect the Foxp3 expression. Adoptive transfer Breg cells remarkably alleviated pancreatic injury, and significantly decreased the percentages of Th1, Th17 cells along with the levels of IFN-γ, IL-17 and further promoted the percentage of Treg cells and expression of IL-10 in CLP-induced sepsis model. Moreover, adoptive transfer Breg cells inhibited the expressions of T-bet and RORγt, and promoted Foxp3 expression in model mice. Lipopolysaccharide (LPS) promoted the apoptosis in pancreatic acinar cells, which was inhibited after culturing with Breg cells in vitro. LPS remarkably upregulated the differentiation of Th1 and Th17 cells, and downregulated the differentiation of Treg cells, which could be significantly reversed by Breg cells in vitro. In conclusion, Breg cells may exhibit the protective effects by modulating T cell responses along with the cytokines in sepsis-associated pancreatic injury.

Background CB-1 and K326 are closely related tobacco cultivars; however, their cold tolerance capacities are different. K326 is much more cold tolerant than CB-1. Results We studied the transcriptomes and metabolomes of CB-1 and K326 leaf samples treated with cold stress. Totally, we have identified 14,590 differentially expressed genes (DEGs) in CB-1 and 14,605 DEGs in K326; there was also 200 differentially expressed metabolites in CB-1 and 194 in K326. Moreover, there were many overlapping genes (around 50%) that were cold-responsive in both plant cultivars, although there were also many differences in the cold responsive genes between the two cultivars. Importantly, for most of the overlapping cold responsive genes, the extent of the changes in expression were typically much more pronounced in K326 than in CB-1, which may help explain the superior cold tolerance of K326. Similar results were found in the metabolome analysis, particularly with the analysis of primary metabolites, including amino acids, organic acids, and sugars. The large number of specific responsive genes and metabolites highlight the complex regulatory mechanisms associated with cold stress in tobacco. In addition, our work implies that the energy metabolism and hormones may function distinctly between CB-1 and K326. Conclusions Differences in gene expression and metabolite levels following cold stress treatment seem likely to have contributed to the observed difference in the cold tolerance phenotype of these two tobacco cultivars.

With the significant and rapid growth in the number of remote-sensing images, deep hash methods have become a research topic. The main work of deep hash method is to build a discriminate embedding space through the similarity relation between sample pairs and then map the feature vector into Hamming space for hashing retrieval. We demonstrate that adding a binary classification label as a kind of semantic cue could further improve the retrieval performance. In this work, we propose a new method, which we called deep hashing, based on classification label (DHCL). First, we propose a network architecture, which can classify and retrieve remote-sensing images under a unified framework, and the classification labels are further utilized as the semantic cues to assist in network training. Second, we propose a hash code structure, which can integrate the classification results into the hash-retrieval process to improve accuracy. Finally, we validate the performance of the proposed method on several remote-sensing image datasets and show the superiority of our method.

Background To explore the efficacy and clinical significance of exchange transfusion (ET) therapy in infants with severe pertussis, and provide a basis for the diagnosis and treatment of severe pertussis. Methods 45 infants diagnosed with severe pertussis and receiving ET treatment in the intensive care unit of Hunan Children’s Hospital from January 1, 2019 to June 30, 2024 were selected as the study subjects. According to the prognosis, they were divided into surviving group ( n  = 35) and mortality group ( n  = 10), and the clinical manifestations and biochemical indicators of the two groups were compared. The comparison between groups of count data was conducted using the chi square test. The t -test is used to compare between groups whose measurement data conforms to a normal distribution; The Mann Whitney U test is used to compare between groups that do not follow a normal distribution. Results The mortality of 45 infants with severe pertussis who received ET treatment was 22.2% (10/45). The incidences of oliguria, bradycardia, and pleural effusion in the mortality group were higher than those in the surviving group, and the differences were statistically significant ( P  < 0.05). The white blood cells (WBC) and neutrophils (NE) in mortality group were significantly higher than those in surviving group before ET treatment. After 24 h and 48 h of ET treatment, the WBC and NE in mortality group were still higher than those in surviving group ( P  < 0.05). There were no statistically significant differences in WBC and NE between the two groups 72 h after ET treatment ( P  > 0.05). The levels of C-reactive protein (CRP), procalcitonin (PCT), N-terminal B-type natriuretic peptide precursor (NT-BNP), creatinine (Cr), lactate dehydrogenase (LDH), creatine kinase (CK), and myoglobin (MYO) in mortality group were all higher than those in surviving group before ET therapy ( P  < 0.05). The PH and PO 2 levels in the blood gas analysis of mortality group were lower than those of surviving group before ET treatment, while PCO 2 and lactate (Lac) levels were higher than those of mortality group ( P  < 0.05). The incidences of pulmonary hypertension, heart failure, cardiogenic shock, acute kidney injury, and pertussis encephalopathy in mortality group were higher than those in surviving group, and the differences were statistically significant ( P  < 0.05). The usage rates of hormones and vasoactive drugs in mortality group were higher than those in surviving group ( P  < 0.05). Conclusions ET is an important treatment for improving the prognosis of infants with severe pertussis. Infants with severe pertussis who undergo ET have a higher peak WBC count, and those with concomitant pulmonary arterial hypertension, cardiac, renal, neurological dysfunction have a poorer prognosis. Early intervention and active treatment are necessary.

Some articles have examined perfluorooctanoic acid (PFOA) exposure in early life in relation to risk of childhood adiposity. Nevertheless, the results from epidemiological studies exploring the associations remain inconsistent and contradictory. We thus conducted an analysis of data currently available to examine the association between PFOA exposure in early life and risk of childhood adiposity. The PubMed, EMBASE, and Web of Science databases were searched to identify studies that examined the impact of PFOA exposure in early life on childhood adiposity. A random-effects meta-analysis model was used to pool the statistical estimates. We identified ten prospective cohort studies comprising 6076 participants with PFOA exposure. The overall effect size (relative risk or odds ratio) for childhood overweight was 1.25 (95% confidence interval (CI): 1.04, 1.50; I2 = 40.5%). In addition, exposure to PFOA in early life increased the z-score of childhood body mass index (β = 0.10, 95% CI: 0.03, 0.17; I2 = 27.9%). Accordingly, exposure to PFOA in early life is associated with an increased risk for childhood adiposity. Further research is needed to verify these findings and to shed light on the molecular mechanism of PFOA in adiposity.

This study aims to systematically investigate the multi-target mechanisms of cobalamin in the treatment of ischemic stroke using network pharmacology and molecular docking approaches. We screened databases to identify the targets of cobalamin and performed intersected with with ischemic stroke-related targets to construct a “drug-target-disease” interaction network. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were conducted to identify key biological processes and signaling pathways. Additionally, molecular docking simulations were performed to assess the binding affinity between cobalamin and hub proteins. Molecular dynamics (MD) simulations were used to assess the stability of the protein–ligand complexes over a 500 ns simulation period. Additionally, ADME (Absorption, Distribution, Metabolism, Excretion) and blood–brain barrier (BBB) permeability predictions were made using ADMETlab 3.0 and admetSAR 3.0. A total of 95 therapeutic targets of cobalamin for ischemic stroke were identified. Network analysis and molecular docking highlighted eight core targets—ALB, TIMP1, PLG, FN1, AGT, SERPINE1, APOE, and SPP1—with high binding affinities to cobalamin. GO analysis suggested that cobalamin regulates inflammatory responses, post-translational modifications, complement binding, and lipoprotein particle binding. KEGG analysis identified complement and coagulation cascades, the PI3K/AKT pathway, and inflammation-related signaling as central to its therapeutic effects. Molecular docking showed strong binding to ALB and TIMP1, which was further confirmed by MD simulations, with minimal conformational changes. The PLG-cobalamin complex exhibited more fluctuations. ADME analysis revealed low passive permeability, particularly across the blood–brain barrier, but moderate distribution and high plasma protein binding. This study provides evidence that cobalamin may offer neuroprotective effects in ischemic stroke by interacting with key target proteins involved in coagulation, inflammation, and lipid metabolism. The findings highlight the potential of cobalamin as a therapeutic agent, although its limited ability to cross the blood–brain barrier may restrict its oral use. Further experimental validation and development of suitable delivery methods are needed to fully realize cobalamin’s potential in stroke therapy.