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Microwave curing has emerged as a promising technique to accelerate the hydration process in ultra-high-performance concrete (UHPC), yet its effects on the material dielectric properties and molecular-level polarization remain insufficiently understood. This study investigates the impact of microwave curing on the dielectric properties and molecular polarization behavior of UHPC. UHPC samples were cured under both standard curing (SC) and microwave curing (MC) conditions for 28 days, with an analysis of the dielectric properties throughout the curing period. The correlation between the degree of hydration and the dielectric constant (ε) was explored to understand the influence of microwave curing on the material performance. A molecular dynamics (MD) simulation was employed to model the effect of 2.45 GHz microwave fields on the dielectric properties of calcium-silicate-hydrate (C-S-H), complemented by grey correlation and multi-scale analyses. Results show that microwave time and temperature significantly affect the dielectric constant of UHPC, with the most optimal acceleration effect observed at 30 °C for 0.25 h. A linear relationship between dielectric constants and hydration degrees was established for both SC and MC specimens, indicating that microwaves uniquely influence hydration processes. Molecular dynamics simulations revealed that microwave irradiation enhances the orientational polarization of interlayer molecules in C-S-H, increasing the polarization rate by 1.19 × 10⁻³ D/ų under a 0.4 V/nm field strength. This study provides valuable insights into the macroscopic and microscopic effects of microwaves on UHPC, offering theoretical support for advancing microwave curing technology in construction materials.

Background: Cold environments pose serious threats on human health, with increased risk for myocardial infarction, stroke, frostbite, and hypothermia. Acquired cold acclimation is required to minimize cold-induced injures and to improve metabolic health. However, the underlying mechanisms remain to be fully elucidated. Objective: We aimed to identify critical amino acids involved in cold acclimation and unmask the regulatory mechanisms. Methods: A total of twenty male participants were recruited and followed up after 3 months’ natural cold exposure. Cold-induced vasodilation (CIVD) tests and clinical biochemical analysis were performed at baseline and after 3-months cold exposure, whilst blood samples were collected, and plasma amino acids were analyzed by targeted metabolomics. To further confirm the effect of lysine on cold tolerance and explain the latent mechanism, mice were challenged with chronic cold exposure for 7 days with lysine supplement, then core and local surface temperature as well as thermogenesis activity were detected. Results: Continuous cold exposure shortened the CIVD onset time and increased the average finger temperature. Levels of the plasma lysine and glycine were decreased in both humans and mice. Venn analysis from three datasets revealed that lysine was the only significantly changed plasma amino acid, which strongly correlated with the altered CIVD. Moreover, mice sustained a relatively higher core temperature and surface temperature in the back, tail and paws upon lysine supplementation. Furthermore, lysine supplementation increased the level of histone H3K18cr and promoted the gene and protein expression of Cpt1a, Cpt2 and Cyp27a1 in liver. Conclusion: Our work identified lysine as a critical amino acid for the remodeling of hepatic histone crotonylation that facilitates cold acclimation.

Summary: Background: Since the initial identification of the Severe Fever with Thrombocytopenia Syndrome (SFTS) in ticks in rural areas of China in 2009, the virus has been increasingly isolated from a diverse array of hosts globally, exhibiting a rising trend in incidence. This study aims to conduct a systematic analysis of the temporal and spatial distribution of SFTS cases, alongside an examination of the infection rates across various hosts, with the objective of addressing public concerns regarding the spread and impact of the disease. Methods: In this systematic review and meta-analysis, an exhaustive search was conducted across multiple databases, including PubMed, Web of Science, Embase, and Medline, CNKI, WanFang, and CQVIP. The literature search was confined to publications released between January 1, 2009, and May 29, 2023. The study focused on collating data pertaining to animal infections under natural conditions and human infection cases reported. Additionally, species names were unified using the National Center for Biotechnology Information (NCBI) database. The notification rate, notification death rate, case fatality rate, and infection rates (or MIR) were assessed for each study with available data. The proportions were pooled using a generalized linear mixed-effects model (GLMM). Meta-regressions were conducted for subgroup analysis. This research has been duly registered with PROSPERO, bearing the registration number CRD42023431010. Findings: We identified 5492 studies from database searches and assessed 238 full-text studies for eligibility, of which 234 studies were included in the meta-analysis. For human infection data, the overall pooled notification rate was 18.93 (95% CI 17.02–21.05) per ten million people, the overall pooled notification deaths rate was 3.49 (95% CI 2.97–4.10) per ten million people, and the overall pooled case fatality rate was 7.80% (95% CI 7.01%–8.69%). There was an increasing trend in notification rate and deaths rate, while the case fatality rate showed a significant decrease globally. Regarding animal infection data, among 94 species tested, 48 species were found to carry positive nucleic acid or antibodies. Out of these, 14 species were classified under Arthropoda, while 34 species fell under Chordata, comprising 27 Mammalia and 7 Aves. Interpretation: This systematic review and meta-analysis present the latest global report on SFTS. In terms of human infections, notification rates and notification deaths rates are on the rise, while the case fatality rate has significantly decreased. More SFTSV animal hosts have been discovered than before, particularly among birds, indicating a potentially broader transmission range for SFTSV. These findings provide crucial insights for the prevention and control of SFTS on a global scale. Funding: None.

The present study was aimed to verify whether an integrating of wearable activity tracker device and a social media intervention strategy would be better than a standalone social media intervention for improving physical activity (PA) and reducing sedentary time for Chinese postgraduate population. A total of 42 full-time postgraduate students participated in this study, which were randomized to receive a 4-week social media intervention through WeChat either with (Wearable Device group) or without (control group) a wearable activity tracker device. Energy expenditure, step counts, moderate to vigorous physical activity time (MVPA) and sedentary time were assessed before and after the intervention. Besides, anthropometric parameters of body weight, body mass index, body fat rate, waist-to-hip ratio, as well as self-reported quality of life were also evaluated. It was found that both energy expenditure and step counts were significantly increased, while sedentary time was significantly reduced during the post-intervention test compared to the baseline test for Wearable Device group. No significant difference of PA was found for the control group. The results demonstrated that the integrating of wearable activity tracker device and a social media intervention was effective in promoting PA, while a standalone social media intervention may have no effect on the influence of PA for Chinese postgraduates.

As increasing number of people migrated to high altitude, highland encephalopathy and hypoxia-induced cognitive impairment arouse public attention. Yet, its underlying mechanisms remain unclear. Emerging evidence has implied neuroinflammation and neuronal loss may be involved. In the present study, we investigated the neuroinflammation and neuronal loss in mice after hypoxic insult. Our reports showed hypobaric hypoxia exposure for 3 weeks led to impaired spatial exploration and short-term memory in mice, concomitant with neuron loss. In addition, hypoxia induced neuroinflammation and NLRP3 inflammasome activation. Besides, to explore the role of the inflammasome in hypoxia-induced cognitive dysfunction, NLRP3 knockout mice were applied and the results showed that NLRP3 could negatively regulate GPX4 to modify antioxidant capacity. In summary, our work demonstrated that hypoxia exposure led to neuroinflammation and neuronal-deletion, which may be the key events in the process of hypoxia induced cognitive impairment. NLRP3 inflammasome promoted antioxidant deficiency by negatively regulating GPX4.

Background: Cadmium is the most prevalent form of heavy metal contaminant globally and its exposure rises serious health concern. Chronic exposure to cadmium causes immune disturbances. However, few studies have addressed how it affects circulating immune cells, one of the most essential elements for the host defense system, at both population and molecular level. Therefore, this is the first single-cell transcriptomic analysis of the response of the human circulating immune system to plasma cadmium level. Methods: We conducted a cross-sectional study in Hunan province, which has the highest level of cadmium land contamination in China. A total of 3283 individuals were eligible for analyzing the association between plasma cadmium levels and the monocyte counts and its subgroups. Another 780 individuals were assigned for validation. Thirty propensity-matched individuals without chronic disease from the lowest- and highest-quartile groups according to serum cadmium levels were selected for single-cell RNA sequencing (scRNA-seq) and flow cytometry analyses. Moreover, the monocyte phenotypic alterations in the heavy metal-exposed population were validated with a cecal ligation and puncture sepsis mouse model. Results: From August 2016 to July 2017, we conducted a cross-sectional study to identify phenotypic alterations in peripheral immune cells in cadmium polluted areas in China. Monocyte percentages were negatively associated with plasma cadmium levels in multivariable linear regression analysis. Peripheral blood mononuclear cell scRNA-seq revealed that the CD14+ monocyte subset was dramatically reduced in the highest-quartile cadmium-exposed group. Moreover, we assessed different hallmarks of immune cell dysfunction—such as host defense capability, apoptotic signaling, cellular diversity and malignant gene expression in monocytes. Importantly, cadmium induced phenotypic alterations in the immune system were validated in the cecal ligation and puncture sepsis mouse model, in which chronic exposure to cadmium not only increased the death rate but also decreased monocyte numbers and the ability to clear bacterial infections. Conclusion: This transcriptomic analysis provides molecular information about how the most important hallmarks of immune cell dysfunction are affected by plasma cadmium level. The significant phenotypic alterations in monocytes serving as early indicators of increased susceptibility to infectious and malignant diseases.

Objective: Several heavy metals have been reported to be associated with metabolic syndrome(MetS) in general population, while effects of multiple metals exposure on MetS in residents living in heavy metal polluted regions have not been investigated. We aimed to assess the association of 23 metal levels and MetS among population living in China’s heavy metal polluted regions. Methods: From August 2016 to July 2017, a total of 2109 eligible participants were consecutively enrolled in our study in Hunan province, China. The levels of plasma and urine metals were measured by inductively coupled plasma mass spectrometer (ICP-MS). MetS was defined by the criteria of the International Diabetes Federation. Multivariable regression models were applied to analysis the potential relationship. Results: In the overall population, crude model showed positive relationship of plasma titanium (Ti) with MetS and negative association of urine vanadium, iron, and selenium with MetS. After adjusted for potential confounders, only plasma Ti was positive associated with MetS (adjusted OR for Q4 versus Q1: 1.46; 95% CI: 1.06–1.99), and this positive correlation was explained by abdominal obesity (OR = 1.84, 95% CI: 1.41–2.39) and high triglycerides (OR = 2.23, 95% CI: 1.68–2.96). Further linear regression analysis revealed significant association of plasma Ti levels with waist circumference (β = 0.0056, 95% CI: 0.0004–0.0109, P = 0.036) and triglycerides (β = 0.0012, 95% CI: 0.0006–0.0019, P

Background: Statins are the cornerstone of low-density lipoprotein cholesterol (LDL-C)-lowering therapy; however, the therapeutic efficacy of statins in countering atherosclerotic cardiovascular disease (ASCVD) is compromised by the concurrent elevation of proprotein convertase subtilisin/kexin type 9 (PCSK9), a pivotal molecule that increases LDL-C levels. Aerobic exercise lowers PCSK9 levels, but the underlying mechanism remains unclear. Therefore, we investigated how aerobic exercise can ameliorate statin-induced increases in PCSK9 levels. Methods: Three-week-old male American Institute of Cancer Research (ICR) mice were fed a high-fat-cholesterol diet (HFD) for 12 weeks and then administered atorvastatin alone or atorvastatin combined with aerobic exercise (Statin + Ex). Moreover, a total of 165 participants with stable coronary heart disease (CHD) enrolled at the Inpatient and Outpatient Departments of the Second Xiangya Hospital of Central South University, China, from January 2018 to July 2020 were randomized into the Statin group (male/female = 51/33) and Statin + Ex group (male/female = 52/29). Patients in the Statin + Ex group underwent treadmill exercise of 45–60 min/day for 7 days. Results: Aerobic exercise effectively alleviated statin-induced PCSK9 upregulation in human patients with CHD and hypercholesterolemic ICR mice (all p < 0.05). Mechanistically, our findings revealed that aerobic exercise induced elevated epoxyeicosatrienoic acids (EETs) plasma levels while concurrently reducing the activity of soluble epoxide hydrolase (sEH) (all p < 0.05), an enzyme responsible for EETs degradation. Further, EETs significantly suppressed PCSK9 expression, subsequently reducing the LDL-C levels (all p < 0.05); this effect was mediated via the activation of the forkhead box O3a–silent mating type information regulation 2 homolog 6 (FoxO3a–Sirt6) axis, with no impact on the sterol regulatory element binding protein 2 and 3-hydroxy-3-methylglutaryl-CoA reductase (SREBP2-HMGCR) pathway. Conclusion: Our study sheds light on the paradigm of “Exercise is Medicine”, providing evidence to support the use of statins combined with exercise in reducing LDL-C levels, and unveils potential avenues for clinical applications of sEH inhibitors, presenting novel prospects for therapeutic interventions in ASCVD.