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Trace elements, though required only in minute quantities, are indispensable for the proper functioning of biological systems [...].Trace elements, though required only in minute quantities, are indispensable for the proper functioning of biological systems [...].

The rapid growth of internet health care (IH) offers older adults convenient medical services like remote consultations and health monitoring. However, its adoption among this group remains low, highlighting a significant digital divide. Understanding the behavioral patterns and determinants of IH use in the older population is crucial for optimizing digital health design and improving service accessibility. This study aimed to analyze the multidimensional influencing factors of Chinese older adults' use of IH services based on the integrated framework of the technology acceptance model and social ecological model, and explore their behavioral patterns and key driving factors. A cross-sectional study design was adopted to conduct a multistage stratified cluster random sampling survey in 3 cities in Shandong Province from May 2024 to July 2024, with a total of 1828 older adults aged 60 to 75 years included. The study uses latent category analysis to classify the use of IH service behaviors and employs multiple logistic regression, decision tree models, and structural equation modeling to analyze influencing factors and mediating pathways. Five distinct user groups were identified: nonusers (n=911), registration-dominant users (n=286), low-activity users (n=320), moderate comprehensive users (n=288), and full-service users (n=23). Multinomial logistic regression with nonusers as the reference group identified key determinants: individuals with below primary education had 96% lower odds of membership (odds ratios [OR] 0.039, 95% CI 0.012-0.084) compared to the reference group with junior college education or above in moderate comprehensive users, while male participants had higher odds of being full-service (OR 1.980, 95% CI 1.126-3.514) or moderate comprehensive (OR 1.310, 95% CI 1.012-1.705) users. Older age was consistently associated with lower adoption across all classes. Full-service users exhibited exceptionally high social support (OR 4.502, 95% CI 3.601-5.627), while moderate comprehensive users showed the highest technology acceptance (OR 2.803, 95% CI 2.355-3.342). The decision tree model (area under the curve of 0.94) found the optimal path: sufficient social support (≥2), good health status (>5), and high technical acceptance (≥30) yield the highest use probability (92%→96%). Mediation analysis indicated that social support influences usage willingness through both direct and indirect pathways. The direct effect was 0.712 (95% CI 0.552-0.972; P<.001). Among indirect pathways, technology availability and practicality accounted for the largest proportion of mediation (19.7%, 95% CI 16.8%-22.6%), followed by technology acceptance (13.7%, 95% CI 11.1%-16.3%) and social influence (8.9%, 95% CI 6.9%-10.9%). Optimizing age-friendly design, strengthening social support networks, and improving technological usability are keys to increasing the adoption of IH services among the older population. Future policies should develop targeted intervention strategies for different user groups to narrow the digital health divide.

To assess the combined effects of dyslipidemia, lipid parameters, non-traditional lipid markers, and body mass index (BMI) on hypertension incidence among petrochemical workers. This retrospective cohort study analyzed associations between lipid markers, BMI, and incident hypertension using multivariable logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Dose-response relationships were examined with restricted cubic spline models. Dyslipidemia was associated with increased hypertension risk, with stronger associations in men. Elevated TC, TG, and LDL-C were significantly associated with hypertension in men, whereas only TG was significant in women. High LDL-C independently increased hypertension risk in the total population and in men. Increasing quartiles of TC and TG showed clear linear dose-response relationships. In men, hypertension risk rose with the number of coexisting lipid abnormalities. Non-traditional lipid markers (non-HDL-C, TG/HDL-C ratio, and TyG index) were positively associated with hypertension and exhibited linear dose-response patterns. Overweight and obesity further increased risk, particularly when combined with dyslipidemia. Adverse lipid profiles, non-traditional lipid markers, and excess body weight are important determinants of hypertension risk in this occupational cohort.

Selenium, an essential trace element for human health, exerts an indispensable effect in maintaining physiological homeostasis and functions in the body. Selenium deficiency is associated with arthropathies, such as Kashin-Beck disease, rheumatoid arthritis, osteoarthritis, and osteoporosis. Selenium deficiency mainly affects the normal physiological state of bone and cartilage through oxidative stress reaction and immune reaction. This review aims to explore the role of selenium deficiency and its mechanisms existed in the pathogenesis of arthropathies. Meanwhile, this review also summarized various experiments to highlight the crucial functions of selenium in maintaining the homeostasis of bone and cartilage.

Bone mineral density (BMD) is a key parameter widely used in the assessment of bone health. Although many investigations have explored the relationship between trace elements and BMD, there are fewer studies focused on serum copper and BMD, especially for adolescents. Using data extracted from the National Health and Nutrition Examination Survey, we applied a multiple-linear regression and smooth curve fitting to assess the relationship between serum copper and BMD. A total of 910 participants were finally included in this study. After adjusting for relevant covariates, serum copper was negatively associated with lumbar spine BMD (β = −0.057, 95% CI: −0.109 to −0.005), trunk bone BMD (β = −0.068, 95% CI: −0.110 to −0.026), pelvis BMD (β = −0.085, 95% CI: −0.145 to −0.024), subtotal BMD (β = −0.072, 95% CI: −0.111 to −0.033), and total BMD (β = −0.051, 95% CI: −0.087 to −0.016) (p < 0.05). In quartile analysis, the highest level of serum copper was associated with decreased BMD when compared with those at the lowest quartile (p < 0.05). The stratified analysis revealed a significant interaction between age and the effects of serum copper on trunk bone BMD (p = 0.022) and pelvis BMD (p = 0.018). Meanwhile, the higher level of serum copper was negatively associated with BMD in males, and gender modified the relationship (p < 0.001). Future longitudinal studies will be necessary for a more definitive interpretation of our results.

Background: As a central organ of energy metabolism, the liver is closely related to selenium for its normal function and disease development. However, the underlying roles of mitochondrial energy metabolism and mitophagy in liver fibrosis associated with selenium remain unclear. Methods: 28 rats were randomly divided into normal, low-selenium, nano-selenium supplement-1, and supplement-2 groups for a 12-week intervention. We observed pathological and ultrastructural changes in the liver and analyzed the effects of selenium deficiency and nano-selenium supplementation on liver metabolic activities and crucial proteins expression of mammalian target of the rapamycin (mTOR) signaling pathway. Results: Selenium deficiency caused liver pathological damage and fibrosis with the occurrence of mitophagy by disrupting normal metabolic activities; meanwhile, the mTOR signaling pathway was up-regulated to enhance mitophagy to clear damaged mitochondria. Furthermore, nano-selenium supplements could reduce the severity of pathological damage and fibrosis in livers and maintain normal energy metabolic activity. With the increased concentrations of nano-selenium supplement, swelling mitochondria and mitophagy gradually decreased, accompanied by the higher expression of mTOR and phosphorylation-modified mTOR proteins and lower expression of unc-51 like autophagy activating kinase 1 (ULK1) and phosphorylation-modified ULK1 proteins. Conclusions: Mitophagy regulated by the mTOR signaling pathway plays a dual protective role on low-selenium inducing liver fibrosis and nano-selenium supplements preventing liver fibrosis. Mitochondrial energy metabolism plays an important role in these processes as well.

Increasing attention has recently been paid to the harm of polycystic ovary syndrome (PCOS) to women. However, due to the inconsistency of global clinical diagnostic standards and the differing allocation of medical resources among different regions, there is a lack of comprehensive estimation of the global incidence and disability-adjusted life years (DALYs) of PCOS. Thus, it is difficult to assess the disease burden. We extracted PCOS disease data from 1990 to 2019 from the Global Burden of Disease Study (GBD) 2019 and estimated the incidence, DALYs, and the corresponding age-standardized rates (ASRs) of PCOS, as well as the socio-demographic index (SDI) quintiles, to describe epidemiological trends at the global level, encompassing 21 regions and 204 countries and territories. Globally, the incidence and DALYs of PCOS have increased. Its ASR also shows an increasing trend. Among them, the high SDI quintile seems relatively stable, whereas other SDI quintiles are constantly rising over time. Our research has provided clues regarding the disease pattern and epidemic trend of PCOS and analyzed the possible causes of disease burden in some specific countries and territories, which may have some value in health resource allocation and health policy formulation and prevention strategies.

The single and combined effects of short-term selenium (Se) deficiency and T-2 toxin-induced kidney pathological injury through the MMPs/TIMPs system were investigated. Forty-eight rats were randomly divided into control, 10 ng/g T-2 toxin, 100 ng/g T-2 toxin, Se-deficient, 10 ng/g T-2 toxin and Se deficiency combined, and 100 ng/g T-2 toxin and Se deficiency combined groups for a 4-week intervention. The kidney Se concentration was measured to evaluate the construction of animal models of Se deficiency. Kidney tissues were analyzed by hematoxylin–eosin staining, Masson staining, and transmission electron microscope to observe the pathological changes, the severity of kidney fibrosis, and ultrastructural changes, respectively. Meanwhile, quantitative polymerase chain reaction and immunohistochemical staining were used to analyze the gene and protein expression levels of matrix metallopeptidase 2/3 (MMP2/3) and tissue inhibitor of metalloproteinase 1 (TIMP1). The results showed that short-term Se deficiency and T-2 toxin exposure can cause kidney injury through tubular degeneration and even lead to kidney fibrosis. And the combination of T-2 toxin and Se deficiency had a synergistic effect on the kidney. A dose–response effect of the T-2 toxin was also observed. At the gene and protein levels, the expression of MMP2/3 in the intervention group increased, while the expression of TIMP1 decreased compared with the control group. In conclusion, short-term Se deficiency and T-2 toxin exposure might lead to injury and even the development of fibrosis in the kidneys, and combined intervention can increase the severity with a dose-dependent trend. MMP2/3 and TIMP1 likely play a significant role in the development of kidney fibrosis.

The objective of this study was to investigate the effects of anthracene (Ant) with 3 rings, benzo[a]anthracene (BaA) with 4 rings and benzo[b]fluoranthene (BbF) with 5 rings in fine particulate matter (PM 2.5 ) at different exposure times (4 h and 24 h) and low exposure levels (0 pg/mL, 0.1 pg/mL, 1 pg/mL, 100 pg/mL and 10,000 pg/mL) on RAW264.7 cells. The changes of interleukin-6 (IL-6) and oxidative stress levels in RAW264.7 cells were investigated by methyl-thiazolyl-tetrazolium (MTT) and enzyme-linked immunosorbent assay (ELISA). Pearson correlation analysis was used to analyze the correlation between variables. Ant, BaA and BbF induced the secretion of IL-6 and the occurrence of oxidative stress in RAW264.7 cells. The inflammatory effect and oxidative damage were exacerbated with prolonged exposure time, increasing exposure concentration and increasing number of PAH rings. At the same time, IL-6 was found to have a certain correlation with the levels of ROS, MDA and SOD. Exposure to atmospheric PAHs at low concentrations can also produce toxic effects on cells, IL-6 and oxidative stress work together in cell damage. The study is expected to provide a theoretical and experimental basis for air pollution control and human health promotion.

The effects of short-term dietary selenium deficiency on the liver and protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway were evaluated. Fourteen growing rats were randomly divided into control and selenium deficiency groups and fed standard and selenium-deficient diets for 4 weeks, respectively. The serum and liver selenium concentrations were measured to evaluate the construction of animal models with selenium deficiency. Liver tissues were analyzed by transmission electron microscope, hematoxylin–eosin staining, and Masson staining to observe the ultrastructural changes, pathological changes, and severity of liver fibrosis, respectively. Besides, immunohistochemical staining (IHC) was used to analyze the effects of selenium deficiency on the expression of key proteins in the Akt/mTOR signaling pathway. The results showed that selenium concentrations in the serum and liver tissue were significantly lower in the selenium deficiency group than in the control group, and the selenium deficiency intervention could affect the morphology and structure of hepatocytes and mitochondria. Meanwhile, the liver tissue showed structural damage and fibrotic changes in the selenium deficiency group. The IHC results showed the positive staining rates of Akt, phosphorylation-modified protein kinase B (p-Akt), mTOR, and phosphorylation-modified mammalian target of the rapamycin (p-mTOR) in the liver of the selenium deficiency group which were significantly lower than that of the control group. In conclusion, short-term selenium deficiency dietary intervention could lead to liver fibrosis by inhibiting the Akt/mTOR signaling pathway.