ABSTRACT
Circulating tumor cells (CTCs) shed from primary tumors must overcome the cytotoxicity of immune cells, particularly natural killer (NK) cells, to cause metastasis. The tumor microenvironment (TME) protects tumor cells from the cytotoxicity of immune cells, which is partially executed by cancer-associated mesenchymal stromal cells (MSCs). However, the mechanisms by which MSCs influence the NK resistance of CTCs remain poorly understood. This study demonstrates that MSCs enhance the NK resistance of cancer cells in a gap junction-dependent manner, thereby promoting the survival and metastatic seeding of CTCs in immunocompromised mice. Tumor cells crosstalk with MSCs through an intercellular cGAS-cGAMP-STING signaling loop, leading to increased production of interferon-ß (IFNß) by MSCs. IFNß reversely enhances the type I IFN (IFN-I) signaling in tumor cells and hence the expression of human leukocyte antigen class I (HLA-I) on the cell surface, protecting the tumor cells from NK cytotoxicity. Disruption of this loop reverses NK sensitivity in tumor cells and decreases tumor metastasis. Moreover, there are positive correlations between IFN-I signaling, HLA-I expression, and NK tolerance in human tumor samples. Thus, the NK-resistant signaling loop between tumor cells and MSCs may serve as a novel therapeutic target.
Subject(s)
Interferon-beta , Killer Cells, Natural , Mesenchymal Stem Cells , Neoplastic Cells, Circulating , Nucleotidyltransferases , Signal Transduction , Tumor Microenvironment , Mesenchymal Stem Cells/immunology , Mesenchymal Stem Cells/metabolism , Animals , Killer Cells, Natural/immunology , Mice , Interferon-beta/metabolism , Interferon-beta/immunology , Nucleotidyltransferases/metabolism , Nucleotidyltransferases/genetics , Humans , Neoplastic Cells, Circulating/immunology , Neoplastic Cells, Circulating/metabolism , Tumor Microenvironment/immunology , Membrane Proteins/metabolism , Disease Models, Animal , Cell Line, TumorABSTRACT
Environmental arsenic exposure is a significant global public health concern. Previous studies have demonstrated the association between arsenic-induced liver injury and oxidative stress as well as ferroptosis. However, the knowledge of the interactions among these mechanisms remains limited. Moreover, there is a lack of research on potential therapeutic interventions for liver injury resulting from arsenic exposure. To address these limitations, we established a rat model with liver injury caused by arsenic exposure and investigated the impact of the nuclear factor E2-related factor 2 (Nrf2)/glutathione peroxidase 4 (GPx4) signaling pathway and ferroptosis on arsenic-induced liver injury. Our findings revealed that arsenic increased Nrf2 expression and decreased GPx4 expression in the rat liver. This was accompanied by a substantial generation of reactive oxygen species and disruption of the antioxidant defense system, ultimately promoting liver injury through ferroptosis. Subsequently, we conducted intervention experiments using Rosa roxburghii Tratt (RRT) in rats exposed to arsenic. The results showed that the detrimental effects mentioned earlier were partially alleviated following RRT intervention. This study offers preliminary evidence that persistent activation of Nrf2 by arsenic triggers an adaptive antioxidant response, leading to liver injury through the promotion of ferroptosis. Additionally, we discovered that RRT inhibits Nrf2-mediated adaptive antioxidant responses by reducing hepatic ferroptosis, thereby mitigating liver injury caused by arsenic exposure in rats. Our study contributes to a deeper understanding of the molecular mechanisms underlying liver injury resulting from arsenic exposure. Furthermore, our findings may facilitate the identification of a potential edible and medicinal plant extracts that could be utilized to develop a more effective adjunctive treatment approach.
Subject(s)
Arsenic , Chemical and Drug Induced Liver Injury, Chronic , Animals , Rats , Antioxidants , NF-E2-Related Factor 2ABSTRACT
Metastasis is an important contributor to increased mortality rates in non-small cell lung cancer (NSCLC). The TGF-ß signalling pathway plays a crucial role in facilitating tumour metastasis through epithelial-mesenchymal transition (EMT). Glycolysis, a key metabolic process, is strongly correlated with NSCLC metastasis. Pirfenidone (PFD) has been shown to safely and effectively inhibit TGF-ß1 in patients with lung diseases. Furthermore, TGF-ß1 and glycolysis demonstrate an interdependent relationship within the tumour microenvironment. Our previous study demonstrated that PFD effectively inhibited glycolysis in NSCLC cells, prompting further investigation into its potential antitumour effects in this context. Therefore, the present study aims to investigate the potential antitumour effect of PFD in NSCLC and explore the relationship among TGF-ß1, glycolysis and EMT through further experimentation. The antitumour effects of PFD were evaluated using five different NSCLC cell lines and a xenograft tumour model. Notably, PFD demonstrated a significant antitumour effect specifically in highly glycolytic H1299 cells. To elucidate the underlying mechanism, we compared the efficacy of PFD after pretreatment with either TGF-ß1 or a TGF-ß receptor inhibitor (LY2109761). The energy metabolomics analysis of tumour tissue demonstrated that PFD, a chemosensitizing agent, reduced lactate and ATP production, thereby inhibiting glycolysis and exerting synergistic antineoplastic effects. Additionally, PFD combined with cisplatin targeted TGF-ß1 to inhibit glycolysis during EMT and enhanced the chemosensitization of A549 and H1299 cells. The magnitude of the anticancer effect exhibited by PFD was intricately linked to its metabolic properties.
Subject(s)
Carcinoma, Non-Small-Cell Lung , Lung Neoplasms , Pyridones , Humans , Carcinoma, Non-Small-Cell Lung/pathology , Cell Line, Tumor , Cell Movement , Epithelial-Mesenchymal Transition , Lung Neoplasms/pathology , Metabolic Reprogramming , Transforming Growth Factor beta1/metabolism , Tumor Microenvironment , AnimalsABSTRACT
BACKGROUND: The prevalence of metabolic dysfunction-associated fatty liver disease (MAFLD) has been rising rapidly in western China. Diet acts as an effective therapy for MAFLD. However, there has been scarce research on the association between a posteriori diet patterns (DPs) and MAFLD in this region. METHOD: We identified three a posteriori DPs which were "Sichuan Basin pattern" characterized by a high intake of fish/seafood, poultry, fresh fruit and vegetables, indicating a balanced and modern DP; the "Yunnan-Guizhou Plateau dietary pattern" characterized mainly by a high intake of animal oil and salt, indicating an agricultural and poor DP; and the "Qinghai-Tibet Plateau dietary pattern" characterized by a high intake of coarse grains, wheat products, tubers and tea, respectively, indicating a high-altitude DP. Then, we performed marginal structural models that combined logistic regression and inverse probability exposure weighting (IPEW) to examine the associations between MAFLD and these a posteriori DPs. RESULT: We found the "Yunnan-Guizhou Plateau dietary pattern" revealed stronger positive association (OR = 1.50, 95% CI 1.40-1.60) with MAFLD than that of the "Qinghai-Tibet Plateau dietary pattern" (OR = 1.21, 95% CI 1.14-1.30). In contrast, the "Sichuan Basin dietary pattern" showed no significant association with MAFLD. In the further stratified analysis, we found those above associations were stronger in ethnic minorities and rural residents than their counterparts. CONCLUSION: Our study implied the unfavourable effects of "Yunnan-Guizhou Plateau dietary pattern" on MAFLD and provided evidence that reducing the intake of oil and sodium may be optimal for MAFLD control in the multi-ethnic region in western China.
Subject(s)
Liver Diseases , Humans , China/epidemiology , Diet/adverse effects , VegetablesABSTRACT
Arsenic exposure is a public health concern worldwide. Skin damage, as a typical lesion of arsenic exposure, the mechanism is still unknown. Studies have found that cellular senescence plays a key role in arsenic-induced skin damage, and the previous research found that the ERK/CEBPB signaling pathway may be an important molecular event of arsenic-induced skin cell senescence, but its specific mechanism is unknown. In this study, genetic engineering technology was used to construct stable HaCaT cell lines, and the role and mechanism of ERK/CEBPB signaling pathway in arsenic-induced HaCaT cell senescence were verified by knockdown and overexpression of ERK and CEBPB in both forward and backward. It was found that knockdown of CEBPB or ERK can downregulate the ERK/CEBPB signaling pathway and reduce arsenic-induced skin cell senescence. In contrast to knockdown, overexpression of CEBPB or ERK can upregulate the ERK/CEBPB signaling pathway and aggravate the senescence of skin cells caused by arsenic. These findings suggest that sodium arsenite can further promote SASP secretion and the expression of p53, p21 and p16 INK4a by activating the ERK/CEBPB signaling pathway, induce cell cycle arrest and trigger cellular senescence.
ABSTRACT
Risk assessment of arsenic-induced skin damage has always received significant global attention. Theories derived from arsenic exposure in drinking water may not be applicable to the coal-burning type to arsenic-exposed area. Furthermore, very few studies have successfully determined the reference value of cumulative arsenic (CA) exposure that leads to specific skin lesions. In this study, we conducted a 22-year follow-up investigation to assess the risk of skin lesions and cancer resulting from long-term, multi-channel arsenic exposure from hazard identification, dose-response assessment, exposure assessment, and risk characterization. The results show that the arsenic exposure can significantly increase the prevalence of skin lesions. For each interquartile range increase of hair arsenic (HA) and CA, the risk of skin damage increased by 1.91 and 3.90 times, respectively. The lower confidence limit of the benchmark dose of HA of arsenic-induced various skin lesions ranged from 0.07 to 0.12 µg·g-1, and 932.57 to 1368.92 mg for CA. The chronic daily intake, lifetime average daily dose in the arsenic-exposed area after the comprehensive prevention and control measures have decreased significantly, but remained higher than the daily baseline level of 3.0 µg·kg-1·d-1. Even as recently as 2020, the hazard quotients and hazard index still exceeded 1, measuring 155.33 and 55.20, and the lifetime excess risk of skin cancer (2.80 × 10-3) remains significantly higher than the acceptable level of 10-6. Our study underscores the effectiveness of comprehensive prevention and control measures in managing high arsenic exposure in coal-burning arsenic poisoning areas. However, it is crucial to acknowledge that the risk of both non-carcinogenic and carcinogenic effects on the skin remains substantially higher than the acceptable level. We recommend setting reference limits for monitoring skin damage among individuals exposed to arsenic, with a recommended upper limit of 0.07 µg·g-1 for HA and a maximum acceptable level of 935.57 mg for CA.
Subject(s)
Arsenic Poisoning , Arsenic , Skin Diseases , Humans , Arsenic/toxicity , Arsenic/analysis , Follow-Up Studies , Coal/toxicity , Environmental Exposure , Arsenic Poisoning/epidemiology , Skin Diseases/chemically induced , Skin Diseases/epidemiology , China/epidemiologyABSTRACT
Arsenic exposure is a major environmental public health challenge worldwide. As typical manifestations for arsenic exposure, the pathogenesis of arsenic-induced skin lesions has not been fully elucidated, as well as the lack of effective control measures. In this study, we first determined the short-term and high-dose arsenic exposure can increase the apoptosis rates, while long-term low-dose arsenic exposure decrease the apoptosis rates. Then, the HaCaT cells with knockdown and overexpression of CCAAT-enhancer-binding protein ß (CEBPB) and extracellular signal-regulated kinase (ERK) were constructed. The results demonstrate that knockdown of CEBPB and ERK can reduce NaAsO2 -induced cell apoptosis by inhibiting ERK/CEBPB signaling pathway and vice versa. Further cells were treated with Kaji-Ichigoside F1 (KF1). The results clearly show that KF1 can decrease the arsenic-induced cell apoptosis rates and the expression of ERK/CEBPB signaling pathway-related genes. These results provide evidence that ERK/CEBPB signaling pathway acts as a double-edged sword in arsenic-induced skin damage. Another interesting finding was that KF1 can alleviate arsenic-induced skin cell apoptosis by inhibiting the ERK/CEBPB signaling pathway. This study will contribute to a deeper understanding of the mechanisms of arsenic-induced skin cell apoptosis, and our findings will help to identify a potential food-borne intervention in arsenic detoxification.
Subject(s)
Arsenic , Extracellular Signal-Regulated MAP Kinases , Extracellular Signal-Regulated MAP Kinases/genetics , Extracellular Signal-Regulated MAP Kinases/metabolism , Arsenic/toxicity , Signal Transduction , Apoptosis , CCAAT-Enhancer-Binding Proteins/metabolism , CCAAT-Enhancer-Binding Proteins/pharmacologyABSTRACT
Background: Anemia leads to a lower cure rate and poor prognosis in tuberculosis patients. Effective predictors for the prognosis of tuberculosis with anemia (A-TB) are urgently needed. Monocyte has been proven to be a prognostic biomarker of many lung diseases. Whether monocyte that the predominant innate immune cell as early defense against tuberculosis can predict A-TB is not known. Methods: Data for A-TB patients with initial treatment in Shanghai Pulmonary Hospital were retrospectively collected and analyzed. Logistics regression analysis was used to study the correlation between peripheral blood cells and treatment outcomes. The receiver operating characteristic (ROC) curve was used to determine the cut-off value. We estimated a 12-month prognosis using Kaplan-Meier techniques. The Cox proportional hazards model was used for the univariate and multivariate analyses to analyze the predictors of poor prognosis of A-TB. Results: Of 181 patients analyzed, 94 were cured and 87 non-cured. Logistic regression analysis identified monocyte as an independent immune-related risk factor for the prognosis of A-TB (OR: 7.881, 95% CI: 1.675-37.075, P = 0.009). The ROC curve analysis proved that the most discriminative cut-off value of monocyte was 0.535 × 10^9/L. K-M analysis demonstrated that the cumulative cure rates of A-TB were significantly higher in A-TB with monocyte < 0.535 × 10^9/L (69.62%) than that in those with monocyte ≥ 0.535 × 10^9/L (38.24%) (Log-rank, χ2 = 16.530, P < 0.0001). On univariate and multivariable analysis, monocyte was an independent predictor of poor prognosis in A-TB. Similarly, monocyte was also an independent predictor of poor pulmonary cavity closure in A-TB (HR: 3.614, 95% CI: 1.335-9.787, P = 0.011). Conclusion: In A-TB patients, elevated monocyte was associated with poor prognosis and poor cavity pulmonary closure. Monocyte may provide a simple and inexpensive prognostic biomarker in A-TB.
ABSTRACT
Breast cancer (BC) is one of the major public health challenges worldwide. Studies that address the new evidence on trends of BC are of great importance for preventing and controlling the occurrence and development of diseases and improving health. The aim of this study was to analyze the outcomes for the global burden of disease (GBD), incidence, deaths, and risk factors for BC from 1990 to 2019, and predict the GBD of BC until 2050 to inform global BC control planning efforts. In this study, the results show that the regions with low levels of socio-demographic index (SDI) will have the largest disease burden of BC in the future. The leading global risk factor for death attributable to BC in 2019 was metabolic risks, followed by behavioral risks. This study supports the worldwide urgent need for comprehensive cancer prevention and control strategies to reduce exposure, early screening, and improve treatment to effectively reduce the GBD of BC.
Subject(s)
Breast Neoplasms , Humans , Female , Quality-Adjusted Life Years , Breast Neoplasms/epidemiology , Incidence , Risk Factors , Global Burden of DiseaseABSTRACT
This study examined the potential of hyperspectral techniques for the rapid detection of characteristic indicators of yak meat freshness during the oxidation of yak meat. TVB-N values were determined by significance analysis as the characteristic index of yak meat freshness. Reflectance spectral information of yak meat samples (400-1000 nm) was collected by hyperspectral technology. The raw spectral information was processed by 5 methods and then principal component regression (PCR), support vector machine regression (SVR) and partial least squares regression (PLSR) were used to build regression models. The results indicated that the full-wavelength based on PCR, SVR, and PLSR models were shown greater performance in the prediction of TVB-N content. In order to improve the computational efficiency of the model, 9 and 11 characteristic wavelengths were selected from 128 wavelengths by successive projection algorithm (SPA) and competitive adaptive reweighted sampling (CARS), respectively. The CARS-PLSR model exhibited excellent predictive power and model stability.
ABSTRACT
Grifola frondosa is an edible medicinal mushroom that has been proven to have a variety of health benefits. The main active ingredients of this mushroom are polysaccharides. In this study, ultrasonic-assisted extraction was used to obtain crude Grifola frondosa polysaccharides (GFPs). Then, purified GFP was obtained after purification. The optimum extraction conditions were an extraction time of 71 min, an extraction temperature of 90°C in a solid-to-liquid ratio of 1:37 g/mL, and an ultrasonic power of 500 W. GFP was purified using DEAE-52 and Sephadex G-100. The structural characterization of GFP was performed using Fourier transform infrared spectroscopy (FT-IR), X-ray diffraction (XRD), ion chromatography (IC), and ultraviolet (UV) visible photometry. The morphology of GFP was analyzed by scanning electron microscopy (SEM), thermogravimetric differential scanning calorimetry (TG-DSC), and Congo red testing. In addition, the administration of GFP in oxazolone (OXZ)-induced ulcerative colitis (UC) in mice was found to prevent weight loss. Different doses of GFP (80, 160, and 320 mg/kg body weight) were used, and sulfapyridine (SASP) was used as a positive control (370 mg/kg body weight) for the treatment of OXZ-induced UC. After treatment, the mice were killed, and blood and colon tissue samples were collected. GFP was found to prevent decreases in colon length and the levels of leukocytes, platelets, and neutrophils in UC mice. Moreover, GFP also decreased the expression of pro-inflammatory cytokines [tumor necrosis factor (TNF)-α and interleukin (IL)-1 ß], increased IL-10, and reduced colon injury in UC mice. The results showed that Under these conditions, the predicted polysaccharide yield was 21.72%, and the actual extraction rate was 21.13%. The polysaccharide composition (molar ratio) was composed of fucose (0.025), glucosamine hydrochloride (0.004), galactose (0.063), glucose (0.869), and mannose (0.038). GFP was also found to have a typical absorption peak, and the GFP extracted using the ultrasound-assisted extraction protocol was mainly ß-glucan. These results indicate that ultrasound-assisted extraction of GFP could reduce OXZ-induced intestinal inflammation as a promising candidate for the treatment of UC, with the potential for development as a food supplement to improve intestinal diseases.
ABSTRACT
BACKGROUND: Exposure to build environments, especially residential greenness, offers benefits to reduce the development of atherosclerotic cardiovascular diseases (ASCVD). The 10-year ASCVD risk is a useful indicator for long-term ASCVD risk, but the evidence on the association and potential pathway of residential greenness in mitigating its development remains unclear. OBJECTIVES: This study aimed to investigate the associations between residential greenness and the 10-year predicted ASCVD risks, and potentially mediation effect on this association by air pollution, body mass index (BMI) and physical activity (PA). METHODS: The baseline of the China Multi-Ethnic Cohort (CMEC) study, enrolling 99,556 adults during 2018-2019, was used in this cross-sectional study. The participants' 10-year ASCVD risks were predicted as low-, moderate-, and high-risk groups, based on the six risk factors: age, smoking, hypertension, low-density lipoprotein cholesterol (LDL-C), high high-density lipoprotein cholesterol (HDL-C), and high total cholesterol (TC). The 3-year mean value within the circular buffer of 500 m and 1000 m of Enhanced Vegetation Index (EVI500m and EVI1000m) were used to assess greenness exposure. Multiple logistic regression was used to evaluate the association between residential greenness and the 10-year ASCVD risks. Stratified analyses by sex, age and smoking status were performed to identify susceptible populations. Causal mediation analysis was used to explore the mediation effects of air pollution, BMI and PA. RESULTS: A total of 75,975 participants were included, of which 17.9 % (n = 13,614) and 5.6 % (n = 4253) had the moderate and high 10-year ASCVD risks, respectively. Compared to the low-risk group, each interquartile increase in EVI500m and EVI1000m reduced the ASCVD risk of the moderate-risk group by 4 % (OR = 0.96 [0.94, 0.98]) and 4 % (OR = 0.96 [0.94, 0.98]), respectively; and reduced the risk of the high-risk group by 8 % (OR = 0.92 [0.90, 0.96]) and 7 % (OR = 0.93 [0.90, 0.97]), respectively. However, the increased greenness did not affect the ASCVD risk of the high-risk group when compared to the moderate-risk group. Effects of residential greenness on the ASCVD risk were stronger in women than in men (p < 0.05), and were not observed in those aged ≥55. PA and BMI partially mediated the association between greenness and the 10-year ASCVD risk. CONCLUSIONS: ASCVD prevention strategies should be tailored to maximize the effectiveness within the groups with different ASCVD risks, better at early stages when the ASCVD risk is low.
Subject(s)
Air Pollution , Cardiovascular Diseases , Residence Characteristics , Adult , Female , Humans , Male , Air Pollution/analysis , Cardiovascular Diseases/prevention & control , China , Cholesterol , Cross-Sectional Studies , East Asian People , Parks, RecreationalABSTRACT
OBJECTIVE: To estimate and compare sex-specific differences between metabolically healthy overweight/obesity (MHOO) and the risk of hypertension among Dong, Bouyei, and Miao adults in southwest China. METHODS: MHOO was diagnosed when the patient had a body mass index ≥24 kg/m2 and the presence of ≤1 component of metabolic syndrome. The main outcome was the occurrence of hypertension after the diagnosis or measurement by a physician at the baseline survey. Multivariate logistic regression models were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) between MHOO and the risk of hypertension. RESULTS: We enrolled 16,433 Chinese Dong, Bouyei, and Miao adults. Using the metabolically healthy normal weight (MHNW) as a reference and after adjusting for confounders, the association between MHOO and the risk of hypertension was stronger in Dong (OR = 1.46, 95% CI: 1.07-2.00) and Miao (OR = 2.05, 95% CI: 1.48-2.85) men and did not exist in Bouyei men (OR = 1.14, 95% CI: 0.81-1.60). After adjusting for the age, the association between MHOO and the risk of hypertension was stronger in men than in women among Dong adults aged 30-59 years (OR = 1.64, 95% CI: 1.12-2.40) and did not differ between men and women among Dong adults aged 60-79 years or among Miao or Bouyei adults. CONCLUSION: The results of this study demonstrated sex-specific differences in the association between MHOO and the risk of hypertension and that sex-specific differences further differed among Dong, Bouyei, and Miao adults.
Subject(s)
Hypertension , Obesity, Metabolically Benign , Adult , Female , Humans , Male , Middle Aged , Body Mass Index , China/epidemiology , East Asian People , Ethnic and Racial Minorities , Hypertension/epidemiology , Obesity/complications , Obesity/epidemiology , Obesity/metabolism , Overweight/complications , Overweight/epidemiology , Risk Factors , AgedABSTRACT
Ferroptosis is a unique form of programmed cell death driven by iron-dependent phospholipid peroxidation that was proposed in recent years. It plays an important role in processes of various trace element-related diseases and is regulated by redox homeostasis and various cellular metabolic pathways (iron, amino acids, lipids, sugars), as well as disease-related signaling pathways. Some limited pioneering studies have demonstrated ferroptosis as a mechanism for the health effects of essential trace elements and potentially toxic trace elements, with crosstalk among them. The aim of this review is to bring together research articles and identify key direct and indirect evidence regarding essential trace elements (iron, selenium, zinc, copper, chromium, manganese) and potentially toxic trace elements (arsenic, aluminum, mercury) and their possible roles in ferroptosis. Our review may help determine future research priorities and opportunities.
Subject(s)
Ferroptosis , Selenium , Trace Elements , Copper , Iron , Trace Elements/metabolism , Trace Elements/toxicity , ZincABSTRACT
BACKGROUND: Little is known about the association between a plant-based diet and the risk of gallstone disease (GD), especially in developing counties. We tested the hypothesis that shifting dietary patterns would be related to the risk of GD, and that the Mediterranean diet (MED) adjusted for China would be beneficial for lowering risk of GD. METHODS: Data were extracted from the baseline survey of the China Multi-Ethnic Cohort study. An alternative Mediterranean diet (aMED) score was assessed based on a food frequency questionnaire, and three posteriori dietary patterns (the modern dietary pattern, the coarse grain dietary pattern, and the rice dietary pattern) were identified using factor analysis. Multivariable logistic regression models were developed to evaluate the association between dietary patterns and GD risks. RESULTS: A total of 89,544 participants were included. The prevalence of GD was 7.5%. Comparing the highest with lowest quintiles, aMED was associated with an increased risk of GD (OR 1.13; 95% CI, 1.04-1.24; Ptrend = 0.003), whereas the rice dietary pattern was inversely related to GD risk (OR 0.79; 95% CI, 0.71-0.87; Ptrend < 0.001). In stratified analysis, the rice dietary pattern had a stronger inverse association in the subgroups of females, older, urban, and overweight participants, and those with diabetes-factors associated with higher rates of GD in previous studies. CONCLUSION: Higher adherence to the rice dietary pattern was associated with a lower risk of GD. For high-risk populations, making some shift to a traditional agricultural diet might help with primary prevention of GD.
Subject(s)
Diet, Mediterranean , Gallstones , Adult , Humans , China/epidemiology , Cohort Studies , Cross-Sectional Studies , Diet , East Asian People , Gallstones/epidemiology , Japan , Risk FactorsABSTRACT
Cataracts are an ailment representing the leading cause of blindness in the world. The pathogenesis of cataracts is not clear, and there is no effective treatment. An increasing amount of evidence shows that oxidative stress and autophagy in lens epithelial cells play a key role in the occurrence and development of cataracts. Buddleja officinalis Maxim flavonoids (BMF) are natural antioxidants and regulators that present anti-inflammatory and anti-tumor effects, among others. In this study, we optimized the extraction method of BMFs and detected three of their main active monomers (luteolin, apigenin, and acacetin). In addition, a model of oxidative damage model using rabbit lens epithelial cells induced by hydrogen peroxide (H2O2). By detecting the levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), and OH (OH), the expression of autophagosomes and autolysosomes were observed after MRFP-GFP-LC3 adenovirus was introduced into the cells. Western blotting was used to detect the expression of Beclin-1 and P62. Our research results showed that the optimal extraction parameters to obtain the highest yield of total flavonoids were a liquid−solid ratio of 1:31 g/mL, an ethanol volume fraction of 67%, an extraction time of 2.6 h, and an extraction temperature of 58 °C. Moreover, the content of luteolin was 690.85 ppb, that of apigenin was 114.91 ppb, and the content of acacetin was 5.617 ppb. After oxidative damage was induced by H2O2, the cell survival rate decreased significantly. BMFs could increase the levels of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and decrease the levels of malondialdehyde (MDA) and OH (OH). After the MRFP-GFP-LC3 virus was introduced into rabbit lens epithelial cells and detecting the expression of P62 and Beclin-1, we found that the intervention of BMF could promote the binding of autophagosomes to lysosomes. Compared with the model group, the level of P62 in the low-, middle-, and high-dose groups of BMF was significantly down-regulated, the level of Beclin-1 was significantly increased, and the difference was statistically significant (p < 0.05). In other words, the optimized extraction method was better than others, and the purified BMF contained three main active monomers (luteolin, apigenin, and acacetin). In addition, BMFs could ameliorate the H2O2-induced oxidative damage to rabbit lens cells by promoting autophagy and regulating the level of antioxidation.
Subject(s)
Buddleja , Cataract , Animals , Rabbits , Hydrogen Peroxide/pharmacology , Flavonoids/pharmacology , Beclin-1/metabolism , Apigenin/pharmacology , Luteolin/pharmacology , Oxidative Stress , Antioxidants/pharmacology , Antioxidants/metabolism , Superoxide Dismutase/metabolism , Autophagy , Malondialdehyde/metabolism , Glutathione Peroxidase/metabolismABSTRACT
Exposure to coal-burning arsenic leads to an increased risk of cancer, multi-systems damage and chronic diseases, with DNA methylation one potential mechanism of arsenic toxicity. There are few studies on genome-wide methylation in the coal-burning arsenic poisoning population. Illumina 850 K methylation beadchip is the most suitable technology for DNA methylation of epigenome-wide association analysis. This study used 850 K to detect changes in Genome-wide DNA methylation in whole blood samples of 12 patients with coal-burning arsenic poisoning ( Arsenic poisoning group) and four healthy control participants (Healthy control group). There is clearly abnormal genome-wide DNA methylation in coal-burning arsenic poisoning, with 647 significantly different methylation positions, 524 different methylation regions and 335 significantly different methylation genes in arsenic poisoning patients compared with healthy controls. Further functional analysis of Gene ontology (GO) and Kyoto encyclopedia of genes (KEGG) found 592 GO items and 131 KEGG pathways between patients of coal-burning arsenic poisoning and healthy control. Then, analysis of gene degree and combined-score identified NAPRT1, NT5C3B, NEDD4L, SLC22A3 and RAB11B as target genes. Further validation by qRT-PCR indicates that mRNA expression of five genes changes significantly in the arsenic poisoning group (n = 72) compared to the healthy control group (n = 72). These results showed the genome-wide methylation pattern and highlighted five critical genes within the coal-burning arsenic poisoning population that involve Nicotinate and nicotinamide metabolism, Choline metabolism in cancer, and Ubiquitin mediated proteolysis. Next, the methylation profile of coal burning arsenic poisoning will be further excavation and the mechanism of coal burning arsenic poisoning will be further explored from five genes related pathways and functions.
Subject(s)
Arsenic Poisoning , Arsenic , Humans , DNA Methylation/genetics , Arsenic Poisoning/genetics , Coal , DNAABSTRACT
BACKGROUND: Studies that address the changing characteristics of diseases are of great importance for preventing and controlling the occurrence and development of diseases and for improving health. However, studies of the epidemiological characteristics of noncommunicable diseases (NCDs) and malignant tumors (MTs) of the residents in Guiyang, China, are lacking. OBJECTIVE: The aim of this study was to evaluate the prevalences of NCDs and MTs in residents of Guiyang, Guizhou Province, China, and analyze differences among ages, genders, and regions. METHODS: A multistage stratified cluster sampling method was used. Based on the inclusion and exclusion criteria, 81,517 individuals were selected for the study. Of these, 77,381 (94.9%) participants completed the study. Structured questionnaires were used to collect information on demographic characteristics, NCDs, and MTs. The chi-square test (with 95% confidence intervals) was used to analyze differences in disease prevalence among genders, ages, and geographical regions. RESULTS: The major chronic NCDs of Guiyang residents are obesity, hypertension, and diabetes. MTs in women are mostly breast cancer, cervical cancer, and endometrial cancer, whereas in men, MTs are mainly lung cancer, rectal cancer, and gastric cancer. The prevalences of hypertension and diabetes in women are higher than in men, but the prevalences of lung cancer and gastric cancer in men are higher than in women. The epidemiological characteristics of individuals in different life stages are dissimilar. In terms of regional distribution, the prevalences of the above diseases in the Baiyun and Yunyan districts of Guiyang are relatively high. CONCLUSIONS: Several NCDs (obesity, hypertension, and diabetes) and MTs (women: breast cancer, cervical cancer, and endometrial cancer; men: lung cancer, rectal cancer, and gastric cancer) should be the focus for the prevention and control of chronic diseases in the future. In particular, the Baiyun and Yunyan districts of Guiyang are the important regions to emphasize.
Subject(s)
Breast Neoplasms , Diabetes Mellitus , Endometrial Neoplasms , Hypertension , Noncommunicable Diseases , Rectal Neoplasms , Stomach Neoplasms , Uterine Cervical Neoplasms , Female , Humans , Male , Noncommunicable Diseases/epidemiology , Cross-Sectional Studies , Stomach Neoplasms/epidemiology , China/epidemiology , Diabetes Mellitus/epidemiology , Hypertension/epidemiology , Obesity/epidemiologyABSTRACT
Greenly synthesized silver nanoparticles (AgNPs) on different cellulosic materials show tremendous potential for colorful, biocidal, and reasonably strong products by replacing the traditional chemical-based synthesis protocols. This study reports on a novel in situ synthesis protocol for synthesizing green and sustainable AgNPs over cellulosic kraft paper substrates using a bio-based stabilizing agent (Cephalotaxus harringtonia fruit extract). The protocol could play a significant role in packaging industries. The aqueous extracts of Cephalotaxus harringtonia fruits have been used to synthesize the metallic silver. The deposited AgNPs values were investigated through XRF (X-ray fluorescence) analysis. The number of deposited nanoparticles (NPs) was 268 ± 7, 805 ± 14, and 1,045 ± 16 PPM, respectively for 0.5, 1.5, and 2.5 mm silver precursors. The developed products were tested with SEM (scanning electron microscopy), SEM-mediated elemental mapping, EDX (energy disruptive X-ray), FTIR (Fourier transform infrared spectroscopy), and XRD (X-Ray diffraction). XRD analysis further confirmed the presence of peaks for elemental AgNP on the deposited papers. Colorimetric values were measured to confirm the colorful appearances of the developed metallic silvers. Mechanical properties were tested in terms of the tensile index and bursting index. Moreover, the statistical analysis of coefficient of variations (R2) and a post-hoc ANOVA test that adopted the Newman-Keul methodology also confirm the significance of developed nanoparticles in the papers. The shielding capacity against UV light was also investigated; all the AgNPs-treated products provided values higher than 40, demonstrating the strong UV resistance capability of the kraft paper material. Overall, the study confirms a successful development of green AgNPs on paper materials.
ABSTRACT
Previous studies assessing adverse health have traditionally focused on a single environmental exposure, failing to reflect the reality of various exposures present simultaneously. Air pollution, ambient temperature and greenness have been proposed as critical environmental factors associated with metabolic syndrome (MetS). However, evidence exploring their joint relationships with MetS is needed for identifying interactive factors and developing more targeted public health interventions. The baseline data was obtained from China Multi-Ethnic Cohort (CMEC). Environmental data of air pollutants (PM2.5, O3) and NDVI for greenness was calculated from satellites data. Ambient temperature data were obtained from European Center for Medium-Range Weather Forecasts (ECMWF). MetS was classified based on National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) using anthropometric measures and biomarkers. Logistic regression models were utilized to examine the combined relationship of MetS with three-year exposure to air pollutants, temperature and NDVI. Relative excess risk due to interaction (RERI) was calculated to evaluate interaction on an additive scale. We found associations between prevalent MetS and interquartile range (IQR) increases in PM2.5 (OR: 1.38; 95% confidence interval [95% CI]: 1.23, 1.55) and O3 (OR: 1.15; 95% CI: 1.09, 1.22). Additive and multiplicative interactions were observed between air pollutants and temperature exposure. Compared to low-temperature level, the relationship between PM2.5 and MetS attenuated (RERI: 0.22, 95% CI: 0.44, -0.04) at high-temperature level, while the relationship between O3 and MetS enhanced (RERI: 0.05, 95% CI: 0.02, 0.11). At low NDVI 250 m, the association between PM2.5 and MetS was stronger (RERI: 0.13, 95% CI: 0.05, 0.19) with high NDVI 250 m as the reference group. Our findings showed that ambient temperature and residential greenness could affect the relationship between air pollutants and MetS.