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Telomere length is closely linked to biological aging, oxidative stress, and the development of cardiovascular diseases. This study aimed to assess the association between dietary selenium intake and telomere length in individuals with hypertension. Data on dietary selenium intake were captured through the National Health and Nutrition Examination Survey (NHANES) computer‐assisted dietary interview system (CADI). Telomere length determination entailed selecting blood samples from all participants in the NHANES database. The analysis was performed using Analysis System software, with Empower stats utilized for data analysis. Results showed that there was a significant association between dietary selenium intake and telomere length in hypertension, particularly within the female group. In female hypertension cases, a 1 mcg increase in dietary selenium intake corresponded to a telomere length increase of 1.19 bp, even after adjusting for age, race, BMI, marital status, physical activity, energy intake, and stroke history. The relationship between dietary selenium intake and telomere length exhibited a linear pattern in female hypertension patients. This study identified a positive association between dietary selenium intake and telomere length in hypertension, particularly within the female group. [ABSTRACT FROM AUTHOR]

The aim of this research was to assess the efficacy of different microbial strains in the decolorization of anthraquinone dyes. Strain R81 was obtained from a textile company's wastewater discharge for its remarkable ability to decolorize reactive blue 19 (RB19). By employing physiological and biochemical analyses, along with 16S rRNA gene sequencing, strain R81 was determined to be Brevibacillus laterosporus. After optimization, the decolorization rate achieved a peak of 86.24% over a 48‐h timeframe, utilizing an initial dye concentration of 100 mg L–1. The decolorization capacity of strain R81 was observed to be impeded by heightened levels of salt and temperature in culture solutions, yet remained unaltered when R81 cells were directly introduced into dye solutions. Furthermore, cells that were induced through prior cultivation in a medium containing RB19 demonstrated enhanced efficacy in decolorization compared to noninduced cells. Subsequent analysis indicated that the development of biofilms and the synthesis of polysaccharides by strain R81 were augmented in a concentration‐dependent fashion by RB19. Nevertheless, the decolorization efficacy of R81 was impeded by the existence of sodium dodecyl sulfate (SDS) and cetyltrimethylammonium bromide (CTAB), both of which possess the capacity to eliminate polysaccharides. The decolorization capabilities were reinstated by the SDS or CTAB eluent containing polysaccharides, suggesting a reliance on the presence of polysaccharides. The employment of stepwise diethylaminoethyl (DEAE)‐cellulose chromatography and decolorization experiments elucidated the importance of a specific polysaccharide in the decolorization process. This study proposes a bacteria‐derived polysaccharide as a promising remedy for treating dyeing wastewater contaminated with anthraquinones. [ABSTRACT FROM AUTHOR]

Cynanchum auriculatum Royle ex Wight (CA) is experiencing challenges with continuous cropping obstacle (CCO) due to soil-borne fungal pathogens. The leaf litter from CA is regularly incorporated into the soil after root harvesting, but the impact of this practice on pathogen outbreaks remains uncertain. In this study, a fungal strain D1, identified as Fusarium solani , was isolated and confirmed as a potential factor in CCO. Both leave extract (LE) and root extract (RE) were found to inhibit seed germination and the activities of plant defense-related enzymes. The combinations of extracts and D1 exacerbated these negative effects. Beyond promoting the proliferation of D1 in soil, the extracts also enhanced the hypha weight, spore number, and spore germination rate of D1. Compared to RE, LE exhibited a greater degree of promotion in the activities of pathogenesis-related enzymes in D1. Additionally, caffeic acid and ferulic acid were identified as potential active compounds. LE, particularly in combination with D1, induced a shift in the composition of fungal communities rather than bacterial communities. These findings indicate that the water extract of leaf litter stimulated the growth and proliferation of fungal strain D1, thereby augmenting its pathogenicity toward CA and ultimately contributing to the CCO process. [ABSTRACT FROM AUTHOR]

Esophageal Squamous Cell Carcinoma (ESCC) is a common malignant tumor of digestive tract, accounting for 90% of all pathological types of esophageal cancer. Despite the rapid development of multi-disciplinary treatment such as surgery, chemotherapy, radiotherapy and chemoradiotherapy, the prognosis of patients with ESCC is still poor. Regulators of G-protein signaling (RGSs) are involved in the processes of various cancers. The expression levels of its family member RGS16 are abnormally elevated in a variety of tumors, but its role in ESCC is still unclear. We found that RGS16 expression is aberrantly increased in ESCC tissues and correlated with poor prognosis of ESCC patients from The Cancer Genome Atlas (TCGA) database and our collected ESCC tissues. Moreover, knockdown of RGS16 in two ESCC cells could indeed inhibit their proliferation and migration. We further explored the molecular mechanism of RGS16 in ESCC, and the correlation analysis from TCGA database showed that the mRNA levels of RGS16 was positively correlated with that of CTGF and CYR61 , two target genes of Hippo-YAP signaling. Consistently, RGS16- knockdown significantly inhibited the expression of CTGF and CYR61 in ESCC cells. We found that the phosphorylation levels of LATS1 and YAP were significantly increased and YAP translocated into the cytoplasm after depletion of RGS16 in ESCC cells. Also, RGS16-knockdown promoted the interaction between LATS1 and upstream kinase MST1. In addition, reintroduction of a constitutive active YAP5A mutant significantly rescued CTGF expression and cell proliferation in RGS16-knockdown cells. Together, our work revealed that RGS16 promoted YAP activity through disrupting the interaction between LATS1 and MST1, thus promoting the proliferation and migration of ESCC cells. • RGS16 expression was elevated in ESCC tissues and correlated with poor prognosis of ESCC patients. • RGS16 inhibition suppressed cell proliferation and migration of ESCC cells. • RGS16 regulated YAP and LATS1 phosphorylation in ESCC cells. • RGS16 disrupted the interaction between LATS1 and upstream kinase MST1. [ABSTRACT FROM AUTHOR]

Background: Ventricular septal rupture (VSR) is a rare but well‐known mechanical consequence of an acute myocardial infarction (AMI). Even in the later stages of re‐perfusion therapy, the result of VSR remains poor. Our aim is to assess the site and size of VSR in relation to the severity of cardiac failure. Methods: From January 2016 to December 2022, a total of 71 patients with a diagnosis of post‐myocardial infarction VSR were admitted to the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. Data records were retrospectively included in this registry. In all patients, clinical and echocardiographic data were gathered, and statistical analyses were performed. Results: A total of 71 consecutive patients (mean age: 66.27 ± 8.88 years); 50.7% male, 49.3% female, with (M:F) ratio of almost (1:1). Left ventricular ejection fraction (LVEF) was (48.55 ± 10.44%) on echocardiography, and apical VSR was the most common site (69.0%). Overall, the VSD site was strongly related to the VSD size (p =.016), LVEF (p =.012), AMI site (p =.001), and affected coronary vessel (p =.004). Prodromal angina (p =.041), intra‐aortic balloon pump (p =.002), affected coronary vessels (p =.020), pro‐BNP (p =.000), and LVEF (p =.017) were predictors of the severity of heart failure. Conclusions: Diabetes mellitus is a common risk factor for post‐myocardial infarction VSR. VSR site and size had no relation to the severity of heart failure. A presentation with prodromal angina predicted severe heart failure and a worse prognosis. [ABSTRACT FROM AUTHOR]

Highly pathogenic avian influenza (HPAI) A(H5N1) virus is an ineradicable zoonotic virus that continues to mutate and reassort in nature and poses a serious threat to avian and human health. [...]

As an emerging communication technology, time-sensitive networking (TSN) promises the real time and deterministic interaction of massive data in Industrial Internet of Things. However, it is challenging to schedule the time-sensitive flows timely and superiorly through the mechanism analysis for current TSN scheduling models, especially in complex industrial scenarios. In this article, we propose an analysis approach of flow sequences based on divisibility theory to characterize the flow conflicts and dependencies, which derives the scheduling flexibility based on flow position diversity (PD) and the equivalent flow judgment conditions for slot occupancy. Integrating the abovementioned derivation, a parallel computing framework with the generalized slot length is established to lower the scheduling complexity. Within each computing unit, an incremental scheduling algorithm with the flow judgment conditions and PD-based search boundary is proposed. It reduces the scheduling complexity further while maintaining load balance for the mixed transmission of periodic and aperiodic flows. To achieve the optimality of runtime and load balance, two PD-based flow sorting strategies are designed, respectively. The evaluation results show that compared with the existing works, the runtime efficiency of scheduling at scale is increased by at least 1500 times in complex traffic scenarios while the load balance on the network links is also improved. [ABSTRACT FROM AUTHOR]

purpose of this study was to compare the efficacy and safety of them in HFrEF. Methods: Two hundred and thirty-three patients with HFrEF admitted to a tertiary hospital of Zhengzhou and commenced to take dapagliflozin 10 mg/d or empagliflozin 10 mg/d were retrospectively included and separated into the dapagliflozin group (n=105) and the empagliflozin group (n=128). Their cardiac function indices before and after therapy were compared, together with the ratios of adverse events during therapy. Results: After 6 months of therapy, left ventricular ejection fraction was higher, and the ratio of New York Heart Association functional class III or IV, left ventricular end-diastolic diameter, and N-terminal pro-B-type natriuretic peptide were lower in the empagliflozin group than the dapagliflozin group (P< 0.05). During 6 months of therapy, there were no statistically significant differences for the ratios of hypotension, deteriorating kidney function, and genitourinary infections between the dapagliflozin and empagliflozin groups (P> 0.05). Conclusion: Despite its many limitations, this study suggested that different SGLT2 inhibitors might have differences regarding efficacy in HFrEF. We look forward to future studies to verify our conjectures. [ABSTRACT FROM AUTHOR]

Cardiac hypertrophy and the resultant heart failure are among the most common causes of morbidity and mortality worldwide; thus, identifying the key factor mediating pathological cardiac hypertrophy is critically important for developing the strategy to protect against heart failure. Runx1 (Runt‐related transcription factor 1) acts as an essential transcription factor that functions in a variety of cellular processes including differentiation, proliferation, tissue growth and DNA damage response. However, relatively little is known about the role of Runx1 in heart, especially cardiac hypertrophy and heart failure. In the present study, we investigated the role of Runx1 in experimentally pathological cardiac hypertrophy. The in vitro model was induced by Ang II exposure to cultured neonatal rat cardiomyocytes, and the in vivo pathological cardiac hypertrophy models were induced by chronic pressure overload in mice. Runx1 expression is increased in heart tissues from mice with pressure overload–induced cardiac hypertrophy and in neonatal rat cardiomyocytes in response to Ang II stimulation. Moreover, knockdown of cardiac Runx1 alleviates the pressure overload–induced cardiac hypertrophy. Mechanistically, Runx1 activates the p53 signalling by binding to the p53 gene and promotes its transcription. Rescue experiments indicate that Runx1 promotes cardiac hypertrophy in a p53‐dependent manner. Remarkably, we demonstrated that Ro5‐3335 (a Runx1 inhibitor) acts as a potential therapeutic drug for treating pathological cardiac hypertrophy. In summary, we conclude that Runx1 is a novel mediator and therapeutic target for pathological cardiac hypertrophy. [ABSTRACT FROM AUTHOR]

Abstract Background Since its emergence in March 2009, the pandemic 2009 H1N1 influenza A virus has posed a serious threat to public health. To trace the evolutionary path of these new pathogens, we performed a selection-pressure analysis of a large number of hemagglutinin (HA) and neuraminidase (NA) gene sequences of H1N1 influenza viruses from different hosts. Results Phylogenetic analysis revealed that both HA and NA genes have evolved into five distinct clusters, with further analyses indicating that the pandemic 2009 strains have experienced the strongest positive selection. We also found evidence of strong selection acting on the seasonal human H1N1 isolates. However, swine viruses from North America and Eurasia were under weak positive selection, while there was no significant evidence of positive selection acting on the avian isolates. A site-by-site analysis revealed that the positively selected sites were located in both of the cleaved products of HA (HA1 and HA2), as well as NA. In addition, the pandemic 2009 strains were subject to differential selection pressures compared to seasonal human, North American swine and Eurasian swine H1N1 viruses. Conclusions Most of these positively and/or differentially selected sites were situated in the B-cell and/or T-cell antigenic regions, suggesting that selection at these sites might be responsible for the antigenic variation of the viruses. Moreover, some sites were also associated with glycosylation and receptor-binding ability. Thus, selection at these positions might have helped the pandemic 2009 H1N1 viruses to adapt to the new hosts after they were introduced from pigs to humans. Positive selection on position 274 of NA protein, associated with drug resistance, might account for the prevalence of drug-resistant variants of seasonal human H1N1 influenza viruses, but there was no evidence that positive selection was responsible for the spread of the drug resistance of the pandemic H1N1 strains.

Abstract Background A well-informed choice of genetic locus is central to the efficacy of DNA barcoding. Current DNA barcoding in animals involves the use of the 5' half of the mitochondrial cytochrome oxidase 1 gene (CO1) to diagnose and delimit species. However, there is no compelling a priori reason for the exclusive focus on this region, and it has been shown that it performs poorly for certain animal groups. To explore alternative mitochondrial barcoding regions, we compared the efficacy of the universal CO1 barcoding region with the other mitochondrial protein-coding genes in eutherian mammals. Four criteria were used for this comparison: the number of recovered species, sequence variability within and between species, resolution to taxonomic levels above that of species, and the degree of mutational saturation. Results Based on 1,179 mitochondrial genomes of eutherians, we found that the universal CO1 barcoding region is a good representative of mitochondrial genes as a whole because the high species-recovery rate (> 90%) was similar to that of other mitochondrial genes, and there were no significant differences in intra- or interspecific variability among genes. However, an overlap between intra- and interspecific variability was still problematic for all mitochondrial genes. Our results also demonstrated that any choice of mitochondrial gene for DNA barcoding failed to offer significant resolution at higher taxonomic levels. Conclusions We suggest that the CO1 barcoding region, the universal DNA barcode, is preferred among the mitochondrial protein-coding genes as a molecular diagnostic at least for eutherian species identification. Nevertheless, DNA barcoding with this marker may still be problematic for certain eutherian taxa and our approach can be used to test potential barcoding loci for such groups.

Abstract Background Explicit evolutionary models are required in maximum-likelihood and Bayesian inference, the two methods that are overwhelmingly used in phylogenetic studies of DNA sequence data. Appropriate selection of nucleotide substitution models is important because the use of incorrect models can mislead phylogenetic inference. To better understand the performance of different model-selection criteria, we used 33,600 simulated data sets to analyse the accuracy, precision, dissimilarity, and biases of the hierarchical likelihood-ratio test, Akaike information criterion, Bayesian information criterion, and decision theory. Results We demonstrate that the Bayesian information criterion and decision theory are the most appropriate model-selection criteria because of their high accuracy and precision. Our results also indicate that in some situations different models are selected by different criteria for the same dataset. Such dissimilarity was the highest between the hierarchical likelihood-ratio test and Akaike information criterion, and lowest between the Bayesian information criterion and decision theory. The hierarchical likelihood-ratio test performed poorly when the true model included a proportion of invariable sites, while the Bayesian information criterion and decision theory generally exhibited similar performance to each other. Conclusions Our results indicate that the Bayesian information criterion and decision theory should be preferred for model selection. Together with model-adequacy tests, accurate model selection will serve to improve the reliability of phylogenetic inference and related analyses.

Only when the interfacial charge separation is enhanced and the CO2 activation is improved, can the heterojunction nanocomposite photocatalyst be brought into full play for the CO2 reduction reaction (CO2RR). Here, Er3+ single atom composite photocatalysts were successfully constructed based on both the special role of Er3+ single atoms and the special advantages of the SrTiO3:Er3+/g-C3N4 heterojunction in the field of photocatalysis for the first time. As we expected, the SrTiO3:Er3+/g-C3N4 (22.35 and 16.90 μmol g−1 h−1 for CO and CH4) exhibits about 5 times enhancement in visible-light photocatalytic activity compared to pure g-C3N4 (4.60 and 3.40 μmol g−1 h−1 for CO and CH4). In particular, the photocatalytic performance of SrTiO3:Er3+/g-C3N4 is more than three times higher than that of SrTiO3/g-C3N4. From Er3+ fluorescence quenching measurements, photoelectrochemical studies, transient PL studies and DFT calculations, it is verified that a small fraction of surface doping of Er3+ formed Er single-atoms on SrTiO3 building an energy transfer bridge between the interface of SrTiO3 and g-C3N4, resulting in enhanced interfacial charge separation. Aberration-corrected high-angle annular dark-field scanning transmission electron microscopy (AC HAADF-STEM) and adsorption energy calculations demonstrated that the exposed Er single-atoms outside the interface on SrTiO3 preferentially activate the adsorbed CO2, leading to the high photoactivity for the CO2RR. A novel enhanced photocatalytic mechanism was proposed, in which Er single-atoms play dual roles of an energy transfer bridge and activating CO2 to promote charge separation. This provides new insights and feasible routes to develop highly efficient photocatalytic materials by engineering rare-earth single-atom doping. [ABSTRACT FROM AUTHOR]