Explore the vast range of titles available.

The immunology of pregnancy is complex and poorly defined. During the complex process of pregnancy, macrophages secrete many cytokines/chemokines and play pivotal roles in the maintenance of maternal-fetal tolerance. Here, we summarized the current knowledge of macrophage polarization and the mechanisms involved in physiological or pathological pregnancy processes, including miscarriage, preeclampsia, and preterm birth. Although current evidence provides a compelling argument that macrophages are important in pregnancy, our understanding of the roles and mechanisms of macrophages in pregnancy is still rudimentary. Since macrophages exhibit functional plasticity, they may be ideal targets for therapeutic manipulation during pathological pregnancy. Additional studies are needed to better define the functions and mechanisms of various macrophage subsets in both normal and pathological pregnancy.

AbstractObjectiveTo assess the prevalence of diabetes and its risk factors.DesignPopulation based, cross sectional study.Setting31 provinces in mainland China with nationally representative cross sectional data from 2015 to 2017.Participants75 880 participants aged 18 and older—a nationally representative sample of the mainland Chinese population.Main outcome measuresPrevalence of diabetes among adults living in China, and the prevalence by sex, regions, and ethnic groups, estimated by the 2018 American Diabetes Association (ADA) and the World Health Organization diagnostic criteria. Demographic characteristics, lifestyle, and history of disease were recorded by participants on a questionnaire. Anthropometric and clinical assessments were made of serum concentrations of fasting plasma glucose (one measurement), two hour plasma glucose, and glycated haemoglobin (HbA1c).ResultsThe weighted prevalence of total diabetes (n=9772), self-reported diabetes (n=4464), newly diagnosed diabetes (n=5308), and prediabetes (n=27 230) diagnosed by the ADA criteria were 12.8% (95% confidence interval 12.0% to 13.6%), 6.0% (5.4% to 6.7%), 6.8% (6.1% to 7.4%), and 35.2% (33.5% to 37.0%), respectively, among adults living in China. The weighted prevalence of total diabetes was higher among adults aged 50 and older and among men. The prevalence of total diabetes in 31 provinces ranged from 6.2% in Guizhou to 19.9% in Inner Mongolia. Han ethnicity had the highest prevalence of diabetes (12.8%) and Hui ethnicity had the lowest (6.3%) among five investigated ethnicities. The weighted prevalence of total diabetes (n=8385) using the WHO criteria was 11.2% (95% confidence interval 10.5% to 11.9%).ConclusionThe prevalence of diabetes has increased slightly from 2007 to 2017 among adults living in China. The findings indicate that diabetes is an important public health problem in China.

Collaborative carbon regulation in Karst mountains critically reconciles socio-ecological conflicts. While intercity linkages drive spatial carbon heterogeneity, prior studies have focused on administrative-scale accounting, neglecting systematic spatial association network (SAN) analysis. Integrating SAN and geospatial detector models, we reveal county-level carbon balance dynamics in Guizhou, China (2000–2020). The key findings show the following: provincial carbon emissions rose 53% (0.96 to 1.47 × 108 t) against a 15% sequestration decline (0.67 to 0.57 × 108 t); emission networks shifted from single-core clustering to the axial Liupanshui–Guiyang–Tongren corridor, while sequestration networks retained peripheral ecological dominance; carbon balance capacity (CBC) exhibited an inverted C-shaped pattern (higher in the southeast, lower in the central–west) with westward centroid migration; and electricity consumption dominated spatial heterogeneity, with synergistic nighttime light–PM2.5 interactions showing strongest nonlinear enhancement. Notably, Jianhe County maintained peak CBC (16.5) via forest carbon sinks, whereas Shiqian County suffered the steepest decline due to industrial encroachment. This work pioneers dynamic carbon coupling analysis in fragile ecosystems, offering transdisciplinary tools for global “dual-carbon” governance.

Metformin, the first-line therapy for type 2 diabetes (T2D), decreases hepatic glucose production and reduces fasting plasma glucose levels. Dorzagliatin, a dual-acting orally bioavailable glucokinase activator targeting both the pancreas and liver glucokinase, decreases postprandial glucose in patients with T2D. In this randomized, double-blind, placebo-controlled phase 3 trial, the efficacy and safety of dorzagliatin as an add-on therapy to metformin were assessed in patients with T2D who had inadequate glycemic control using metformin alone. Eligible patients with T2D ( n  = 767) were randomly assigned to receive dorzagliatin or placebo (1:1 ratio) as an add-on to metformin (1,500 mg per day) for 24 weeks of double-blind treatment, followed by 28 weeks of open-label treatment with dorzagliatin for all patients. The primary efficacy endpoint was the change in glycated hemoglobin (HbA1c) levels from baseline to week 24, and safety was assessed throughout the trial. At week 24, the least-squares mean change from baseline in HbA1c (95% confidence interval (CI)) was −1.02% (−1.11, −0.93) in the dorzagliatin group and −0.36% (−0.45, −0.26) in the placebo group (estimated treatment difference, −0.66%; 95% CI: −0.79, −0.53; P  < 0.0001). The incidence of adverse events was similar between groups. There were no severe hypoglycemia events or drug-related serious adverse events in the dorzagliatin and metformin combined therapy group. In patients with T2D who experienced inadequate glycemic control with metformin alone, dorzagliatin resulted in effective glycemic control with good tolerability and safety profile ( NCT03141073 ). The DAWN study is a phase 3 clinical trial that demonstrates effective glycemic control of dorzagliatin as an add-on therapy to metfomin in patients with type 2 diabetes.

Exploring the spatiotemporal characteristics and spatial correlation structure of the coupling and coordination relationship between urban economic development and ecological resilience is of great significance for optimizing the regional coordinated development strategies of urban agglomerations and building high-quality economic development regions. Taking 33 counties (cities, districts) in the Qianzhong Urban Agglomeration as the research objects, this study adopts the analytical paradigm of “mechanism exploration—level measurement—relationship evolution—spatial correlation”, expands and constructs a four-dimensional ecological resilience evaluation index system based on the “risk resistance—adaptation—recovery” framework, and systematically analyzes the spatiotemporal dynamics and spatial correlation characteristics of the coupling and coordination between economic development and ecological resilience from 2005 to 2020 by combining the coupling coordination model, trend surface analysis, and spatial gravity model. The research results show that the overall coupling coordination degree between economic development and ecological resilience in the Qianzhong Urban Agglomeration presents an upward trend, and the key to optimizing the coupling coordination lies in improving the level of urban economic development. The spatial correlation of regional coupling coordination degree is increasingly close, and its spatial connection structure shows the characteristics of “core polarization, edge collapse and multi-center germination”. The research results provide important enlightenment for formulating differentiated sustainable development strategies for urban agglomerations in ecologically fragile areas.

N 1 -methyladenosine (m 1 A) is one of the important post-transcriptional modifications in RNA and plays an important role in promoting translation or decay of m 1 A-methylated messenger RNA (mRNA), but the “reader” protein and the exact biological role of m 1 A remain to be determined. Here, we identified that nine potential m 1 A “reader” proteins including YTH domain family and heterogeneous nuclear ribonucleoprotein by mass spectrometry, and among them, YTH domain-containing protein 3 (YTHDF3), could bind directly to m 1 A-carrying RNA. YTHDF3 was then identified to negatively regulate invasion and migration of trophoblast. Mechanistically, we found that the m 1 A “reader” YTHDF3 bound to certain m 1 A-methylated transcripts, such as insulin-like growth factor 1 receptor (IGF1R), with the combination of iCLIP-seq (individual-nucleotide resolution ultraviolet crosslinking and immunoprecipitation high-throughput sequencing) and m 1 A-seq. Furthermore, YTHDF3 could promote IGF1R mRNA degradation and thus inhibit IGF1R protein expression along with its downstream matrix metallopeptidase 9 signaling pathway, consequently decreasing migration and invasion of trophoblast. Thus, we demonstrated that YTHDF3 as an m 1 A reader decreased invasion and migration of trophoblast by inhibiting IGF1R expression. Our study outlines a new m 1 A epigenetic way to regulate the trophoblast activity, which suggests a novel therapeutic target for trophoblast-associated pregnancy disorders.

Background and aims Iodine is one of the most important trace elements in the human body. It is not only the main component of thyroid hormones but also has extrathyroid biological functions. To date, there have been no large-scale epidemiological studies on the relationship between hyperuricemia and iodine intake, although both are closely related to health. A population-based epidemiological survey in China offers such an opportunity. Methods This population-based cross-sectional study recruited 75,653 adults aged ≥ 18 years from 2015 to 2017 with a randomized, multistage, stratified sampling strategy. Serum uric acid levels and urinary iodine concentrations (UICs) were measured. Results Stratified by UIC, the prevalence of hyperuricemia was 17.8%, 18.8%, 16.0% and 13.7% in the UIC < 100, 100–199, 200–299, and ≥ 300 μg/L groups, respectively; the prevalence of gout was 4.0%, 3.4%, 2.4% and 1.7%, respectively. The prevalence of gout decreased significantly as the UIC increased. The prevalence of hyperuricemia and gout were markedly higher in postmenopausal females than in the premenopausal population (hyperuricemia: 15.9% vs. 8.3%, X 2  = 520.072, p  < 0.001; gout: 3.6% vs. 1.3%, X 2  = 219.889, p  < 0.001), and the prevalence decreased as the UIC increased. Subjects in the more than adequate and excessive iodine groups had lower likelihoods of having hyperuricemia [aOR = 0.81 (95% CI 0.77–0.85), aOR = 0.68 (95% CI 0.64–0.72)] and lower odds of having gout than subjects in the adequate iodine (AI) group [aOR = 0.77 (95% CI 0.68–0.86), aOR = 0.59 (95% CI 0.51–0.68)]. Conclusions UIC was inversely associated with the occurrence of hyperuricemia and gout. More in-depth research and prospective studies are needed to explore the molecular mechanisms and confirm the observed association.

Studies have shown that metabolic abnormalities influence the immune system. Because the prevalence of metabolic and autoimmune thyroid diseases has increased synchronously, the correlation between them was worth exploring. The study objective was to investigate the relationship between metabolic disorders and thyroid autoantibodies in euthyroid subjects. Data were obtained from a TIDE project survey of 55,891 subjects from 31 provinces in China. The body mass index(BMI), waist circumference(WC), blood pressure(BP), TPOAb, TgAb, TSH, UIC, blood glucose, lipid profile, uric acid(UA) levels were evaluated. FT4 and FT3 levels were measured in patients with abnormal serum TSH levels. In males, the BMI, WC, SBP, DBP, and OGTT2hPG of the TPOAb/TgAb-positive groups were significantly higher than those of the TPOAb/TgAb-negative groups. In females, the BMI, WC, SBP, DBP, TC, and LDL-C in the TPOAb/TgAb-positive groups were significantly increased compared to those in the TPOAb/TgAb-negative groups. Multivariate analysis showed that, in males, the OR of positive TgAb in the abdominal obesity group was 1.175 (95% CI 1.016-1.359, P for difference= 0.03), and the OR of positive TPOAb in the hyperuricemia group was 1.195 (95% CI 1.041-1.372, P for difference = 0.011). In females, the OR of positive TgAb was 1.19 (95% Cl 1.068-1.326, P for difference= 0.002) in the high LDL-C group. Obesity, high LDL-C and hyperuricemia were positively correlated with the prevalence of positive thyroid autoantibodies in euthyroid subjects in a gender-dependent manner. This cross-sectional survey showed that metabolic disorders are associated with increased positive thyroid autoantibody levels in euthyroid subjects in a gender-dependent manner.

N -methyladenosine (m A) is one of the important post-transcriptional modifications in RNA and plays an important role in promoting translation or decay of m A-methylated messenger RNA (mRNA), but the \"reader\" protein and the exact biological role of m A remain to be determined. Here, we identified that nine potential m A \"reader\" proteins including YTH domain family and heterogeneous nuclear ribonucleoprotein by mass spectrometry, and among them, YTH domain-containing protein 3 (YTHDF3), could bind directly to m A-carrying RNA. YTHDF3 was then identified to negatively regulate invasion and migration of trophoblast. Mechanistically, we found that the m A \"reader\" YTHDF3 bound to certain m A-methylated transcripts, such as insulin-like growth factor 1 receptor (IGF1R), with the combination of iCLIP-seq (individual-nucleotide resolution ultraviolet crosslinking and immunoprecipitation high-throughput sequencing) and m A-seq. Furthermore, YTHDF3 could promote IGF1R mRNA degradation and thus inhibit IGF1R protein expression along with its downstream matrix metallopeptidase 9 signaling pathway, consequently decreasing migration and invasion of trophoblast. Thus, we demonstrated that YTHDF3 as an m A reader decreased invasion and migration of trophoblast by inhibiting IGF1R expression. Our study outlines a new m A epigenetic way to regulate the trophoblast activity, which suggests a novel therapeutic target for trophoblast-associated pregnancy disorders.

N -methyladenosine (m A) is one of the important post-transcriptional modifications in RNA and plays an important role in promoting translation or decay of m A-methylated messenger RNA (mRNA), but the \"reader\" protein and the exact biological role of m A remain to be determined. Here, we identified that nine potential m A \"reader\" proteins including YTH domain family and heterogeneous nuclear ribonucleoprotein by mass spectrometry, and among them, YTH domain-containing protein 3 (YTHDF3), could bind directly to m A-carrying RNA. YTHDF3 was then identified to negatively regulate invasion and migration of trophoblast. Mechanistically, we found that the m A \"reader\" YTHDF3 bound to certain m A-methylated transcripts, such as insulin-like growth factor 1 receptor (IGF1R), with the combination of iCLIP-seq (individual-nucleotide resolution ultraviolet crosslinking and immunoprecipitation high-throughput sequencing) and m A-seq. Furthermore, YTHDF3 could promote IGF1R mRNA degradation and thus inhibit IGF1R protein expression along with its downstream matrix metallopeptidase 9 signaling pathway, consequently decreasing migration and invasion of trophoblast. Thus, we demonstrated that YTHDF3 as an m A reader decreased invasion and migration of trophoblast by inhibiting IGF1R expression. Our study outlines a new m A epigenetic way to regulate the trophoblast activity, which suggests a novel therapeutic target for trophoblast-associated pregnancy disorders.