Recognition and detection technology for microplastic, its source and health effects.

Microplastic (MP) is ubiquitous in the environment which appeared as an immense intimidation to human and animal health. The plastic fragments significantly polluted the ocean, fresh water, food chain, and other food items. Inadequate maintenance, less knowledge of adverse influence along with inappropriate usage in addition throwing away of plastics items revolves present planet in to plastics planet. The present study aims to focus on the recognition and advance detection technologies for MPs and the adverse effects of micro- and nanoplastics on human health. MPs have rigorous adverse effect on human health that leads to condensed growth rates, lessened reproductive capability, ulcer, scrape, and oxidative nervous anxiety, in addition, also disturb circulatory and respiratory mechanism. The detection of MP particles has also placed emphasis on identification technologies such as scanning electron microscopy, Raman spectroscopy, optical detection, Fourier transform infrared spectroscopy, thermo-analytical techniques, flow cytometry, holography, and hyperspectral imaging. It suggests that further research should be explored to understand the source, distribution, and health impacts and evaluate numerous detection methodologies for the MPs along with purification techniques.

Global air pollution exposure and congenital anomalies: an updated systematic review and meta-analysis of epidemiological studies.

A systematic review and meta-analysis was conducted to evaluate recent epidemiological evidence on the association of air pollution with congenital anomalies (CAs). Of 11,014 records, 49 were finally included in this meta-analysis. Per 10 µg/m3 increase in air pollutant, PM10 exposure during the 1st month of pregnancy and at the first trimester (T1) was associated with increased overall CAs. Further, exposure to PM10 was associated with congenital heart disease (OR = 1.055, 95% CI: 1.035, 1.074) and patent ductus arteriosus (OR = 1.094, 95% CI: 1.020, 1.168) at T1, with chromosomal anomalies during the entire pregnancy and with nervous system anomalies when exposure occurred 3 months prior to pregnancy, during the 1st, 2nd months of pregnancy and at T1. Besides, a significant association with overall CAs was observed for a combined exposure of PM10 and SO2 during the 1st month of gestation (OR: 1.101, 95% CI: 1.023, 1.180). A combined exposure of PM10 and CO was also associated with tetralogy of Fallot during 3-8 weeks of gestation (OR: 1.016, 95% CI: 1.005, 1.027). No significant associations were observed between PM2.5, NO2, and O3 exposure and CAs.

The association between retinol-binding protein 4 and risk of type 2 diabetes: A systematic review and meta-analysis.

Retinol-binding protein 4 (RBP4) was controversially associated with type 2 diabetes mellitus (T2DM). This meta-analysis aimed at evaluating the association between RBP4 level and T2DM risk. MEDLINE and EMBASE were searched to identify relevant studies up to 3 December 2022. Random effects model was used to pool multivariate-adjusted odds ratios (ORs) and 95% confidence intervals (CIs). Publication bias was estimated by Funnel plot and Egger's test, it was considered to be significant when P < 0.05. Eight studies including 8087 participants were finally included. Compared to those with the lowest level, subjects with the highest level of RBP4 have a higher risk of T2DM (OR = 1.47, 95% CI: 1.16-1.78, P < 0.001, I2 = 86.9%). No publication bias among the included studies was found (t = 0.94, P = 0.377). This meta-analysis indicated that high RBP4 level was associated with increasing risk of T2DM.

The effect of China's birth policy changes on birth defects-A large hospital-based cross-sectional study.

A retrospective analysis of birth data hospital-based obtained from 14 monitoring areas in the Huaihe River Basin from 2009 to 2019 was conducted. Trend in the total prevalence of birth defects (BDs) and subgroups were analyzed using the Joinpoint Regression model. The incidence of BDs increased gradually from 118.87 per 10,000 in 2009 to 241.18 per 10,000 in 2019 (AAPC = 5.91, P < 0.001). Congenital heart diseases were the most common subtype of BDs. The proportion of maternal age younger than 25 decreased but the age 25-40 years increased significantly (AAPC<20=-5.58; AAPC20-24=-6.38; AAPC25-29 = 5.15; AAPC30-35 = 7.07; AAPC35-40 = 8.27; All P < 0.05). Compared with the one-child policy period, the risk of BDs was greater for groups among maternal age younger than 40 years during the partial and universal two-child policy period (P < 0.001). The incidence of BDs and the proportion of women with advanced maternal age in Huaihe River Basin is increasing. There was an interaction between changes in birth policy and the mother's age on the risk of BDs.

Upregulated LncRNA-Meg3 modulates the proliferation and survival of MEPM cells via interacting with Smad signaling in TCDD-induced cleft palate.

Exposure to the environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in utero can result in high rates of cleft palate (CP) formation, yet the underlying mechanisms remain to be characterized. In vivo, the lncRNA Meg3 was upregulated following TCDD treatment in CP-associated murine embryonic palatal tissue, with concomitant changes in proliferative and apoptotic activity in these murine embryonic palatal mesenchymal (MEPM) cells. Meg3 can modulate the TGF-ß/Smad to control the proliferation, survival, and differentiation of cells. Accordingly, TCCD and TGF-ß1 were herein used to treat MEPM cells in vitro, revealing that while TCDD exposure altered the proliferative activity and apoptotic death of these cells, exogenous TGF-ß1 exposure antagonized these effects via TGF-ß/Smad signaling. TCDD promoted Meg3 upregulation, whereas TGF-ß1 suppressed TCDD-driven upregulation of this lncRNA. Meg3 was additionally determined to directly interact with Smad2, with significant Meg3 enrichment in Smad2-immunoprecipitates following TCDD treatment. When Meg3 was silenced, the impact of TCDD on Smad signaling, proliferative activity, and apoptosis were ablated, while the effects of exogenous TGF-ß1 were unchanged. This supports a model wherein Meg3 is upregulated in TCDD-exposed palatal tissue whereupon it can interact with Smad2 to suppress Smad-dependent signaling, thus controlling MEPM cell proliferation and apoptosis, contributing to TCDD-induced CP, which provides a theoretical support for the precautions of cleft palate induced by TCDD.

Cadmium-induced reproductive toxicity combined with a correlation to the oogenesis process and competing endogenous RNA networks based on a Caenorhabditis elegans model.

Accumulation of the heavy metal Cadmium (Cd) in the ovaries and placenta can affect the structure and function of these organs and induce female reproductive toxicity. This toxicity may be due to Cd's similarity to estrogen and its ability to disrupt endocrine systems. However, the exact molecular mechanism by which Cd causes reproductive toxicity at the transcriptome level remains poorly understood. Hence, this study aimed to observe Cd-induced reproductive damage at the gene level, scrutinize the repercussions of Cd exposure on oogenesis, and explicate the putative pathogenesis of Cd-induced oogenesis based on Caenorhabditis elegans (C. elegans) as an in vivo model. The results showed that Cd exposure significantly decreased the number of offspring and prolonged the reproductive span of C. elegans. Cd exposure also reduced the number of cells in mitosis and the pachytene and diakinesis stages of meiosis, thereby disrupting oogenesis. Combined with transcriptional sequencing and bioinformatics analysis, a total of 3167 DEmRNAs were identified. Regarding gene expression, cul-6, mum-2, and vang-1 were found to be related to Cd-induced reproductive toxicity, and their competing endogenous RNA networks were constructed. We observed that mutations of mom-2 and vang-1 in the Wnt pathway could induce susceptibility to Cd-caused meiosis injury. In conclusion, the results indicated that Cd could impair the oogenesis of C. elegans and the Wnt pathway might serve as a protective mechanism against Cd reproductive toxicity. These findings contribute to a better understanding of the damaging effects and molecular biological mechanisms of Cd on the human reproductive system.

Associations between the proliferation of palatal mesenchymal cells, Tgfß2 promoter methylation, Meg3 expression, and Smad signaling in atRA-induced cleft palate.

All-trans retinoic acid (atRA) is a teratogen that can induce cleft palate formation. During palatal development, murine embryonic palate mesenchymal (MEPM) cell proliferation is required for the appropriate development of the palatal frame, with Meg3 serving as a key regulator of the proliferative activity of these cells and the associated epithelial-mesenchymal transition process. DNA methylation and signaling via the TGFß/Smad pathway are key in regulating embryonic development. Here, the impact of atRA on MEPM cell proliferation and associations between Tgfß2 promoter methylation, Meg3, and signaling via the Smad pathway were explored using C57BL/6 N mice treated with atRA (100 mg/kg) to induce fetal cleft palate formation. Immunohistochemistry and BrdU assays were used to detect MEPM proliferation and DNA methylation assays were performed to detect Tgfß2 promoter expression. These analyses revealed that atRA suppressed MEPM cell proliferation, promoted the upregulation of Meg3, and reduced the levels of Smad2 and Tgfß2 expression phosphorylation, whereas Tgfß2 promoter methylation was unaffected. RNA immunoprecipitation experiments indicated that the TgfßI receptor is directly targeted by Meg3, suggesting that the ability of atRA to induce cleft palate may be mediated through the Tgfß/Smad signaling pathway.

Dynamic changes in ambient PM2.5 and body mass index among old adults: a nationwide cohort study.

Outdoor air pollution has been considered as a severe environmental health issue that almost affecting everyone in the world, and intensive actions were launched. However, little is known about the association between dynamic changes in ambient fine particulate matter (PM2.5) exposure and body mass index (BMI) among old adults. To investigate the dynamic changes in ambient PM2.5 and body mass index among the elderly, we included a total of 7204 participants from 28 provinces of China during 2011-2015 in the China Health and Retirement Longitudinal Study (CHARLS). Ambient fine particle matter (PM2.5) was estimated using a well-validated space-time extremely randomized trees model. Change in PM2.5 and BMI (ΔPM2.5 and ΔBMI) were calculated as the value at a follow-up visit minus value at baseline. Linear mixed-effects models were applied to quantify the associations, controlling for sociodemographic factors. We found that per 1 µg/m3 increase in PM2.5 exposure was associated with a 0.031-0.044 kg/m2 increase in BMI among the elderly. We observed an approximate linear concentration-response relationship of PM2.5 and BMI in each visit. Each 1 µg/m3 increase in ΔPM2.5 exposure was associated with an increase in ΔBMI (ß = 0.040, 95% CI 0.030, 0.049), while per 1 µg/m3 decrease in the ΔPM2.5 exposure level was associated with a decrease in ΔBMI (ß = -0.016, 95% CI -0.027, -0.004). Our findings suggest that dynamic changes in ambient PM2.5 was positively associated with changes in BMI among old Chinese population.

Ambient particulate matter, maternal thyroid function, and birth weight: A mediation analysis.

BACKGROUND: Birth weight (BW) is an indicator of fetal growth and development. Previous studies showed inconsistent results on the association of ambient particulate matter (PM) exposure with BW, and the role of maternal thyroid function has not been clarified. METHODS: We recruited 1711 gravidas between 2017 and 2019 in Henan, China. All participants were followed up until delivery. Daily concentrations of PM, including PM2.5 and PM10, were evaluated by using the spatial-temporal model. Maternal thyroid hormone (TH) levels were quantified by electrochemiluminescent microparticle immunoassay. Linear regression models were employed to examine the association among PM, BW, and maternal TH. Mediating effects of maternal TH interrelated with PM exposure on BW were investigated by causal mediation analyses. RESULTS: A total of 1049 gravidas were identified. We found that per 10 µg/m3 increase in PM2.5 and PM10 were associated with a decreased BW of 9.941 g, and 7.758 g (PM2.5: 95 %CI: -18.184, -1.698; PM10: 95 %CI: -14.436, -1.080). An inverse correlation of maternal FT4 levels with BW was found, with the pooled ß of -319.983 g (95 %CI: -483.216, -156.750). We found a prominent positive correlation between gestational FT4 and PM exposure (PM2.5: ß = 0.004, 95 %CI: 0.001, 0.007; PM10: ß = 0.003, 95 %CI: 0.000, 0.006). Mediation analysis found that FT4 levels mediated the relationship between maternal PM exposure and BW, ranging from 5.55 % to 15.86 %. CONCLUSIONS: Maternal PM exposure may induce a reduction in newborn BW by affecting the maternal TH concentrations.

Association of greenspace with hypertension in adult: a systematic review and meta-analysis of epidemiological studies.

BACKGROUND: Several studies have investigated the relationship of greenspace with blood pressure (BP) and hypertension, but the results were inconsistent. We aimed to assess the relationship of greenspace with BP/hypertension. METHODS: We searched PubMed, Embase and Web of Science on greenspace and BP/hypertension published before 5 April 2023. The methodological quality and risk of bias were evaluated. RESULTS: Twenty-seven articles were included. Our results suggested that higher normalized difference vegetation index (NDVI) was associated with lower odds of hypertension and levels of SBP [for every 10% increase of NDVI 500-m and NDVI 1000-m, the ORs were 0.95 (95% CI: 0.90-0.99) and 0.95 (95% CI: 0.90-0.99), the ꞵwas -1.32 (95% CI: -2.18, -0.45) and -1.41 (95% CI: -2.57, -0.25), respectively]. CONCLUSION: This study indicated that higher exposure to greenspace might be associated with lower levels of BP and risk of hypertension. Increase green spaces should be regarded as an important public health intervention..

Sex Specificity in the Mixed Effects of Blood Heavy Metals and Cognitive Function on Elderly: Evidence from NHANES.

The way that males and females react to environmental exposures and negative impacts on their neurological systems is often different. Although previous research has examined the cognitively impairing effects of solitary metal exposures, the relationship between metal mixtures and cognitive function, particularly when considering an individual's sex, remains elusive. This study aimed to investigate the sex differences in the association between multiple metal combinations and cognitive function in older Americans. This research employed the 2011-2014 NHANES survey of elderly Americans. The association between five mixed metals and four cognitive tests (the animal fluency test (AFT), the digit symbol substitution test (DSST), the instant recall test (IRT), and the delayed recall test (DRT)) were investigated with generalized linear regression model (GLM), Bayesian kernel machine regression model (BKMR), weighted quantile sum regression model (WQS), and quantile g-computation regression model (Qgcomp). A total of 1833 people, including 883 males and 950 females, enrolled in this cross-sectional study. We discovered that blood lead and blood cadmium were negatively associated with cognitive performance, while blood selenium demonstrated a positive association with cognitive function in older people. The negative relationship of heavy metal combinations on cognitive function might be somewhat reduced or even reversed via selenium. The IRT, AFT, and DSST are three of the four cognitive tests where men had more dramatic positive or negative results. There was a sex-specific connection between blood metal ratios and cognitive function among older Americans, as evidenced by the more significant relationship between mixed metals and cognitive performance in men (either positively or negatively). These results emphasize the impacts of ambient heavy metal exposure on cognitive function by employing sex-specific methods.

Atopic dermatitis and chronic kidney disease: a bidirectional Mendelian randomization study.

Background: A bidirectional association between atopic dermatitis and chronic kidney disease (CKD) has been revealed in observational studies, whereas the causality of this association was unclear. We conducted a Mendelian randomization study to determine the bidirectional causal association between atopic dermatitis and CKD. Methods: Independent genetic instruments associated with atopic dermatitis and CKD at the genome-wide significance level were chosen from corresponding meta-analyses of genome-wide association studies. Summary-level data for atopic dermatitis were obtained from the EAGLE Eczema consortium (30,047 cases and 40,835 controls) and FinnGen consortium (7,024 cases and 198,740 controls). Summary-level data for CKD were derived from CKDGen consortium (64,164 cases and 625,219 controls) and FinnGen consortium (3,902 cases and 212,841 controls). The inverse-variance weighted method was used in the main analysis and supplemented with three sensitivity analyses. Results: Genetic predisposition to atopic dermatitis was associated with an increased risk of CKD. For a one-unit increase in the prevalence of atopic dermatitis, the odds ratio of CKD was 1.07 (95% confidence interval: 1.01-1.12). In the reverse Mendelian randomization analysis, the odds ratio of atopic dermatitis was 1.14 (95% confidence interval: 1.03-1.26) for a one-unit increase in the prevalence of CKD. The associations persisted in sensitivity analyses and no pleiotropy was detected. Conclusion: This Mendelian randomization study suggests a bidirectional positive association between atopic dermatitis and CKD.

Ambient fine particulate matter and pregnancy outcomes: An umbrella review.

The available evidence on the effects of ambient fine particulate matter (PM2.5) and pregnancy outcomes (birth outcomes and pregnancy complications) has increased substantially. The purpose of this umbrella review is to refine the evidence of the association between birth outcome (birth defects) and PM2.5; and summarize the credibility of existing research on the association between pregnancy complications and PM2.5. We searched PubMed, Web of Science, Embase, and Cochrane databases for relevant systematic reviews and meta-analyses up to March 16, 2022 in accordance with PRISMA guidelines. Two independent investigators conducted data extraction. AMSTAR 2 and GRADE assessment criteria were used to evaluate the methodological and evidence quality. We performed subgroup analyses by trimesters of pregnancy. The review protocol for this study has been registered in PROSPERO (CRD42022325550). This umbrella review identified a total of 41 systematic reviews, including 28 articles evaluating the influence of PM2.5 on birth outcomes and 13 on pregnancy complications. Positive associations between perinatal PM2.5 exposure and adverse birth outcomes were found, including low birth weight, preterm birth, stillbirth, small for gestational age, and birth defects. Pregnant women exposed to PM2.5 had a significantly higher risk of developing hypertensive disorder of pregnancy, gestational diabetes mellitus, gestational hypertension, and preeclampsia. The findings of subgroup analysis demonstrated that the effects of ambient PM2.5 exposure on pregnancy outcomes varied by trimesters. The findings of this extensive umbrella review provide convincing proof that exposure to ambient PM2.5 raises the risks of unfavorable birth outcomes and pregnancy complications. Some associations show considerable disparity between trimesters. These findings have implications for strengthen perinatal health care on air pollution and improving intergenerational equity.

Spatiotemporal Trends of Stroke Burden Attributable to Ambient PM2.5 in 204 Countries and Territories, 1990-2019: A Global Analysis.

BACKGROUND AND OBJECTIVES: Previous studies suggested that long-term exposure to ambient fine particulate matter (PM2.5) is associated with increased risk of stroke. However, limited studies evaluated the stroke burden attributable to ambient PM2.5 globally, especially comprising across different regions, countries, and social-economic levels. We thus conducted this study to estimate the spatial and temporal trends of ambient PM2.5-related stroke burden by sex, age, and subtypes from 1990 to 2019 at global, regional, and national levels. METHODS: Information on the ambient PM2.5-related stroke burden from 1990 to 2019 was obtained from the Global Burden of Disease study 2019. The burdens of stroke attributable to ambient PM2.5 (i.e., age-standardized mortality rate [ASMR] and age-standardized disability-adjusted life-year rate [ASDR]) were estimated by sex, age, and subtypes from 1990 to 2019 at global, regional, and national levels. The estimated annual percentage change (EAPC) was used to evaluate the changing trends of ASDR and ASMR attributable to ambient PM2.5 from 1990 to 2019. The Spearman correlation coefficient was used to examine the correlation between sociodemographic index (SDI) and EAPC of ASMR and ASDR at the national level. RESULTS: In 2019, the global ambient PM2.5-related stroke mortality and disability-adjusted life years were 1.14 million and 28.74 million, respectively, with the corresponding ASDR and ASMR of 348.1 and 14.3 per 100,000 population, respectively. The ASDR and ASMR increased with age and were highest among male patients, in the middle SDI regions, and for intracerebral hemorrhage (ICH). From 1990 to 2019, the absolute death number of stroke attributable to ambient PM2.5 and the corresponding ASMR and ASDR were both in an increasing trend. The corresponding EAPCs in ASMR and ASDR were 0.09 (95% CI -0.05 to 0.24) and 0.31 (95% CI 0.18-0.44), respectively. The significant increases of ASMR and ASDR were observed in the low, low-middle, and middle SDI regions, and for ICH. However, a decreasing trend was observed in high and middle-high SDI regions, and for subarachnoid hemorrhage. DISCUSSION: The global burden of stroke attributable to ambient PM2.5 showed an increasing trend over the past 30 years, especially in male patients, low-income countries, and for ICH. Continued efforts on reducing the level of ambient PM2.5 are necessary to reduce the burden of stroke.

The mechanisms governing mouse embryonic palate mesenchymal cells' proliferation associated with atRA-induced cleft palate in mice: insights from integrated transcriptomic and metabolomic analyses.

While exposure to high levels of all-trans retinoic acid (atRA) during pregnancy is known to suppress murine embryonic palate mesenchymal (MEPM) cells proliferation and to result in cleft palate (CP) development, the underlying mechanisms are poorly understood. Accordingly, this study was designed with the goal of clarifying the etiological basis for atRA-induced CP. A murine model of CP was established via the oral administration of atRA to pregnant mice on gestational day (GD) 10.5, after which transcriptomic and metabolomic analyses were performed with the goal of clarifying the critical genes and metabolites associated with CP development through an integrated multi-omics approach. MEPM cells proliferation was altered by atRA exposure as expected, contributing to CP incidence. In total, 110 genes were differentially expressed in the atRA treatment groups, suggesting that atRA may influence key biological processes including stimulus, adhesion, and signaling-related activities. In addition, 133 differentially abundant metabolites were identified including molecules associated with ABC transporters, protein digestion and absorption, mTOR signaling pathway, and the TCA cycle, suggesting a link between these mechanisms and CP. Overall, combined analyses of these transcriptomic and metabolomic results suggested that the MAPK, calcium, PI3K-Akt, Wnt, and mTOR signaling pathways are particularly important pathways enriched in the palatal cleft under conditions of atRA exposure. Together, these integrated transcriptomic and metabolomic approaches provided new evidence with respect to the mechanisms underlying altered MEPM cells proliferation and signal transduction associated with atRA-induced CP, revealing a possible link between oxidative stress and these pathological changes.

The Role of Protein Arginine Methyltransferases in Pathogenesis and Treatment of Digestive System Carcinoma.

Posttranslational modification of proteins increases their diversity and maintains the stability of the intracellular environment. Protein arginine methyltransferases (PRMT) are an important family of epigenetic modification enzymes, which play a critical role in posttranslational modification. In recent years, with the in-depth study of the role of epigenetics, the structure and function of PRMTs have been gradually understood. PRMT enzymatic activity is related to a variety of cellular processes in digestive system malignancies, such as inflammation and immune response, activation of cell cycle and proliferation, inhibition of apoptosis, DNA damage repair, and epithelial-mesenchymal transition. A variety of chemical tools are developed to inhibit PRMT activity, which have been verified by tumor models and clinical trials. This review summarizes the structure and functions of PRMTs as a prelude to our further studies on their role in tumors. The involvement of different PRMTs in the pathogenesis of gastrointestinal tumors is then reviewed. In addition, the application of PRMT inhibitors as therapeutic agents for digestive system cancers is highlighted. In conclusion, PRMTs play an important role in the pathogenesis of gastrointestinal tumors, and their prognostic and therapeutic potential warrants further investigation.

Nutritional supplements improve cardiovascular risk factors in overweight and obese patients: A Bayesian network meta-analysis.

Background: Overweight and obesity are considered as one of the major risk factors for cardiovascular diseases (CVD). At present, many studies have proved that multiple nutritional supplements play an active role in metabolic diseases. However, the comparative efficacy of different nutritional supplements in improving indicators of cardiometabolic risk in obese and overweight patients is uncertain. Methods: Cochrane Library, PubMed, Embase, and Web of Science were searched for the period from January 1990 to March 2022. A random-effect model was built in the Bayesian network meta-analysis. The surface under the cumulative ranking analysis (SUCRA) and clustering rank analysis was performed for ranking the effects. Results: The study included 65 RCTs with 4,241 patients. In terms of glucose control, probiotic was more conductive to improve FBG (MD: -0.90; 95%CrI: -1.41 to -0.38), FINS (MD: -2.05; 95%CrI: -4.27 to -0.02), HOMA-IR (MD: -2.59; 95%CI -3.42 to -1.76). Probiotic (MD: -11.15, 95%CrI -22.16 to -1.26), omega-3 (MD: -9.45; 95%CrI: -20.69 to -0.93), VD (MD: -17.86; 95%CrI: -35.53 to -0.27), and probiotic +omega-3 (MD: 5.24; 95%CrI: 0.78 to 9.63) were beneficial to the improvement of TGs, TC and HDL-C, respectively. The SUCRA revealed that probiotic might be the best intervention to reduce FBG, FINS, HOMA-IR; Simultaneously, α-lipoic acid, VD, and probiotic + omega-3 might be the best intervention to improve TGs, TC, and HDL-C, respectively. Cluster-rank results revealed probiotic had the best comprehensive improvement effect on glucose metabolism, and probiotic + omega-3 may have a better comprehensive improvement effect on lipid metabolism (cluster-rank value for FBG and FINS: 3290.50 and for TGs and HDL-C: 2117.61). Conclusion: Nutritional supplementation is effective on CVD risk factors in overweight and obese patients. Probiotic supplementation might be the best intervention for blood glucose control; VD, probiotic + omega-3 have a better impact on improving lipid metabolism. Further studies are required to verify the current findings.

The spread of antibiotic resistance to humans and potential protection strategies.

Antibiotic resistance is currently one of the greatest threats to human health. Widespread use and residues of antibiotics in humans, animals, and the environment can exert selective pressure on antibiotic resistance bacteria (ARB) and antibiotic resistance gene (ARG), accelerating the flow of antibiotic resistance. As ARG spreads to the population, the burden of antibiotic resistance in humans increases, which may have potential health effects on people. Therefore, it is critical to mitigate the spread of antibiotic resistance to humans and reduce the load of antibiotic resistance in humans. This review briefly described the information of global antibiotic consumption information and national action plans (NAPs) to combat antibiotic resistance and provided a set of feasible control strategies for the transmission of ARB and ARG to humans in three areas including (a) Reducing the colonization capacity of exogenous ARB, (b) Enhancing human colonization resistance and mitigating the horizontal gene transfer (HGT) of ARG, (c) Reversing ARB antibiotic resistance. With the hope of achieving interdisciplinary one-health prevention and control of bacterial resistance.

Naringin Alleviates Glucose-Induced Aging by Reducing Fat Accumulation and Promoting Autophagy in Caenorhabditis elegans.

Naringin (Nar) is a dihydroflavonoid compound, widely found in citrus fruit and used in Chinese herbal medicine. As a phytochemical, it acts as a dietary supplement that can delay aging and prevent aging-related disease, such as obesity and diabetes. However, its exact mechanism remains unclear. In this study, the high-glucose-induced (HGI) Caenorhabditis elegans model was used to evaluate the anti-aging and anti-obesity effects of Nar. The mean lifespan and fast movement span of HGI worms were extended roughly 24% and 11%, respectively, by Nar treatment. Oil red O staining revealed a significant reduction in fat accumulation and dFP::LGG-labeled worms showed the promotion of autophagy. Additionally, whole transcriptome sequencing and gene set variation analysis suggested that Nar upregulated the lipid biosynthesis and metabolism pathways, as well as the TGF-ß, Wnt and longevity signaling pathways. Protein-protein interaction (PPI) network analysis identified hub genes in these pathways for further analysis. Mutant worms and RNA interference were used to study mechanisms; the suppression of hlh-30, lgg-1, unc-51, pha-4, skn-1 and yap-1 disabled the fat-lowering, lifespan-prolonging, and health-promoting properties of Nar. Collectively, our findings indicate that Nar plays an important role in alleviating HGI-aging and anti-obesity effects by reducing fat accumulation and promoting autophagy.