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Noise pollution is reported to be associated with diabetes, but few studies have elucidated the associations between noise frequency characteristics. We aimed to evaluate the relationships between different noise frequency components and incident hyperglycaemia. An industry-based cohort of 905 volunteers was enrolled and followed up to 2012. Octave-band frequencies of workstation noise and individual noise levels were measured in 2012 to classify subjects’ exposures retrospectively. We applied Cox regression models to estimate the relative risk (RR) of hyperglycaemia. An increased RR for hyperglycaemia of 1.80 (95% confidence interval [CI]: 1.04, 3.10) was found among subjects exposed to ≥ 85 A-weighted decibels (dBA) compared with those exposed to < 70 dBA. The high-exposure groups at frequencies of 31.5, 63, 125, 250, 500, 1000, and 2000 Hz had a significantly higher risk of hyperglycaemia (all p values < 0.050) than the low-exposure groups. A 5-dB increase in noise frequencies at 31.5, 63, 125, 250, 500 Hz, and 1000 Hz was associated with an elevated risk of hyperglycaemia (all p values < 0.050), with the highest value of 1.27 (95% CI: 1.10, 1.47) at 31.5 Hz (p = 0.001). Occupational noise exposure may be associated with an increased incidence of hyperglycaemia, with the highest risk observed at 31.5 Hz.

Selenium (Se) is one of the essential trace elements in animal organisms with good antioxidant and immune-enhancing abilities. In this study, we investigated the effect and mechanism of Se deficiency on skeletal muscle cell differentiation. A selenium-deficient skeletal muscle model was established. The skeletal muscle tissue and blood Se content were significantly reduced in the Se deficiency group. HE staining showed that the skeletal muscle tissue had a reduced myofiber area and nuclei and an increased myofascicular membrane with Se deficiency. The TUNEL test showed massive apoptosis of skeletal muscle cells in Se deficiency. With Se deficiency, reactive oxygen species (ROS) and malondialdehyde (MDA) increased, and the activities of glutathione peroxidase (GSH-Px), total antioxidant capacity (T-AOC), superoxide dismutase (SOD), and catalase (CAT) were inhibited. In in vitro experiments, microscopic observations showed that the low-Se group had reduced C2C12 cell fusion and a reduced number of differentiated myotubes. In addition, qPCR results showed that differentiation genes (Myog, Myod, Myh2, Myh3, and Myf5) were significantly reduced in the low Se group. Meanwhile, Western blot analysis showed that the levels of differentiation proteins (Myog, Myod, and Myhc) were significantly reduced in the low-Se group. This finding indicates that Se deficiency reduces the expression of skeletal muscle cell differentiation factors. All the above data suggest that Se deficiency can lead to oxidative stress in skeletal muscle, resulting in a reduction in the differentiation capacity of muscle cells.

Gliomas are the most common central nervous system tumors. They show malignant characteristics indicating rapid proliferation and a high invasive capacity and are associated with a poor prognosis. In our previous study, p68 was overexpressed in glioma cells and correlated with both the degree of glioma differentiation and poor overall survival. Downregulating p68 significantly suppressed proliferation in glioma cells. Moreover, we found that the p68 gene promoted glioma cell growth by activating the nuclear factor‐κB signaling pathway by a downstream molecular mechanism that remains incompletely understood. In this study, we found that dual specificity phosphatase 5 (DUSP5) is a downstream target of p68, using microarray analysis, and that p68 negatively regulates DUSP5. Upregulating DUSP5 in stably expressing cell lines (U87 and LN‐229) suppressed proliferation, invasion, and migration in glioma cells in vitro, consistent with the downregulation of p68. Furthermore, upregulating DUSP5 inhibited ERK phosphorylation, whereas downregulating DUSP5 rescued the level of ERK phosphorylation, indicating that DUSP5 might negatively regulate ERK signaling. Additionally, we show that DUSP5 levels were lower in high‐grade glioma than in low‐grade glioma. These results suggest that the p68‐induced negative regulation of DUSP5 promoted invasion by glioma cells and mediated the activation of the ERK signaling pathway. We found that the function of the DUSP5 gene is to act as the downstream signaling pathway of p68 using global microarray gene expression analysis, and revealed that p68 negatively regulated the DUSP5 gene. Our discovery provides novel insight into the mode of negative regulation in cancer cells and represents a new facet in the complexities of p68 gene tumor‐promoting function.

It is being debated whether prostate-specific antigen (PSA)-based screening effectively reduces prostate cancer mortality. Some of the uncertainty could be related to deficiencies in the age-based PSA cut-off thresholds used in screening. Current study considered 2779 men with prostate cancer and 1606 men without a cancer diagnosis, recruited for various studies in New Zealand, US, and Taiwan. Association of PSA with demographic, lifestyle, clinical characteristics (for cases), and the aldo–keto reductase 1C3 ( AKR1C3 ) rs12529 genetic polymorphisms were analysed using multiple linear regression and univariate modelling. Pooled multivariable analysis of cases showed that PSA was significantly associated with demographic, lifestyle, and clinical data with an interaction between ethnicity and age further modifying the association. Pooled multivariable analysis of controls data also showed that demographic and lifestyle are significantly associated with PSA level. Independent case and control analyses indicated that factors associated with PSA were specific for each cohort. Univariate analyses showed a significant age and PSA correlation among all cases and controls except for the US-European cases while genetic stratification in cases showed variability of correlation. Data suggests that unique PSA cut-off thresholds factorized with demographics, lifestyle and genetics may be more appropriate for prostate cancer screening.

Apical-basal cell polarity must be tightly controlled for epithelial cyst and tubule formation, and these are important functional units in various epithelial organs. Polarization is achieved through the coordination of several molecules that divide cells into an apical domain and a basolateral domain, which are separated from tight and adherens junctions. Cdc42 regulates cytoskeletal organization and the tight junction protein ZO-1 at the apical margin of epithelial cell junctions. MST kinases control organ size through the regulation of cell proliferation and cell polarity. For example, MST1 relays the Rap1 signal to induce cell polarity and adhesion of lymphocytes. Our previous study showed that MST3 was involved in E-cadherin regulation and migration in MCF7 cells. In vivo , MST3 knockout mice exhibited higher ENaC expression at the apical site of renal tubules, resulting in hypertension. However, it was not clear whether MST3 was involved in cell polarity. Here, control MDCK cells, HA-MST3 and HA-MST3 kinase-dead (HA-MST3-KD) overexpressing MDCK cells were cultured in collagen or Matrigel. We found that the cysts of HA-MST3 cells were fewer and smaller than those of control MDCK cells; ZO-1 was delayed to the apical site of cysts and in cell-cell contact in the Ca 2+ switch assay. However, HA-MST3-KD cells exhibited multilumen cysts. Intensive F-actin stress fibers were observed in HA-MST3 cells with higher Cdc42 activity; in contrast, HA-MST3-KD cells had lower Cdc42 activity and weaker F-actin staining. In this study, we identified a new MST3 function in the establishment of cell polarity through Cdc42 regulation.

Atomic magnetometers based on the spin-exchange relaxation-free (SERF) regime have broad applications in bio-magnetic measurement due to their high sensitivity and miniaturized size. In this paper, we propose a SERF-based magnetometer using 1 × 2 polarization-maintaining fiber (PMF) with single-beam parameter optimization. The impacts of temperature, pumping laser power, and modulation amplitude on the magnetometer’s response signal at the SERF regime are examined. Moreover, through the simulation of zero-field resonance, the compensation accuracy is optimized. To further improve the compensation stability and accuracy, a novel finite state machine (FSM)-assisted iterative optimization magnetic field compensation algorithm is proposed. A pT-level compensation resolution with an error below 1.6% is achieved, which lays the foundation for the subsequent application of biomagnetic measurement arrays.

The Comment of Riaza is acknowledged. In response, it is argued that by establishing the complete corresponding relations between the voltage-current relation and the constitutive relation of memristors, the conclusions in the original Letter are appropriate. It is further illustrated that if the voltage-current model is used, the memristor is regarded as a dynamic element, whereas if the flux–charge model is utilised, the memristor is treated as a non-dynamic element. The results indicate that the memristor initial conditions described by the constitutive relation should be assigned in the modelling of memristive circuits, and the dynamic nature of memristors is related with the memristive circuit model.

Genetic susceptibility to prostate cancer (PCa) varies across populations, yet East Asian men remain underrepresented in genome-wide association studies (GWAS). This study aimed to identify genetic variants associated with PCa in a Taiwanese cohort and to explore their potential biological relevance using integrative annotation approaches. We analyzed 961 PCa patients and 3792 age-matched controls from the Taiwan Biobank. Genotyping and imputation were performed using the Taiwan Biobank 2.0 array and the 1000 Genomes East Asian reference panel. Association testing was conducted using logistic regression adjusted for age and population structure. Gene-based analysis using Multi-marker Analysis of GenoMic Annotation (MAGMA), functional annotation using HaploReg, and prostate tissue cis-expression quantitative trait loci (cis-eQTL) and splicing QTL (sQTL) evaluation using the Genotype-Tissue Expression project (GTEx) were performed to explore functional relevance. We identified 371 genome-wide significant variants and 47 independent risk loci, including established regions (8q24.21, ZNF365, NCOR2, and PRKCB) as well as loci not previously reported in major GWAS (CCDC36, RAB6B, TTLL3, and PARD3B). MAGMA analysis identified 80 PCa-associated genes, and pathway analysis highlighted sphingolipid metabolism and leukocyte transendothelial migration. Integrative annotation indicated that several variants are located in regulatory elements and are associated with prostate-specific eQTL and sQTL effects. Additional analyses showed that several variants were associated with clinical indicators of disease aggressiveness, and age-stratified sensitivity analyses demonstrated consistent associations across age groups. Sensitivity analyses using alternative modeling approaches yielded comparable results. This study identifies both established and putatively novel genetic loci associated with PCa in a Taiwanese cohort and provides functional insights through integrative annotation. These findings contribute to understanding the genetic architecture of PCa in East Asian populations and highlight candidate loci that require independent validation in future studies.

Respiratory signals are basic indicators of human life and health that are used as effective biomarkers to detect respiratory diseases in clinics, including cardiopulmonary function, breathing disorders, and breathing system infections. Therefore, it is necessary to continuously measure respiratory signals. However, there is still a lack of effective portable electronic devices designed to meet the needs of daily respiratory monitoring. This study presents an intelligent, portable, and wireless respiratory monitoring system for real-time evaluation of human respiratory behaviors. The system consists of a triboelectric respiratory sensor; circuit board hardware for data acquisition, preprocessing, and wireless transmission; a machine learning algorithm for enhancing recognition accuracy; and a mobile terminal app. The triboelectric sensor—fabricated by the screen-printing method—is lightweight, non-invasive, and biocompatible. It provides a clear response to the frequency and intensity of respiratory airflow. The portable circuit board is reusable and cost-effective. The decision tree model algorithm is used to identify the respiratory signals with an average accuracy of 97.2%. The real-time signal and statistical results can be uploaded to a server network and displayed on various mobile terminals for body health warnings and advice. This work promotes the development of wearable health monitoring systems.

Our study showed that total urinary arsenic concentrations were positively correlated with renal cell carcinoma (RCC). Chronic inflammation is a key player in the development of RCC. This study explored the association between nucleotide-binding domain-like receptor protein 3 ( NLRP3 ) genotypes and the development of RCC. We also investigated whether any of the NLRP3 genotypes modified the risk between arsenic and RCC. We recruited 350 RCC patients and 700 age-sex matched controls. RCC was confirmed by pathological assessment following surgical resection or image-guided biopsy of a renal tumor. Fifteen sites of N LRP3 gene polymorphisms were identified using the Agena Bioscience MassARRAY platform. The concentrations of the urinary arsenic species were determined by HPLC-HG-AAS. There was a significant dose-dependent association between arsenic and RCC. In addition, six of thirteen NLRP3 alleles, including rs12239046 C, rs10925025 G, rs1539019 C, rs10925026 A, rs10157379 T, and rs12143966 A, had increased odds ratios (ORs) for RCC than other NLRP3 alleles. Among these sites, we found the novel haplotype of five tag-SNPs (C-A-A-A-A) was significantly related to RCC, the OR and 95% confidence interval was 1.44 (1.08–1.92). Furthermore, participants with high total urinary arsenic levels and the NLRP3 rs1539019 C allele had significantly multiplicative and additive interactions for the risk of RCC (p interaction  = 0.012). This study is the first to identify the modified effects of NLRP3 risk alleles involved in the association between arsenic and RCC risk in a population with low arsenic exposure.