Genome-wide identification of quantitative trait loci and candidate genes for seven carcass traits in a four-way intercross porcine population.

BACKGROUND: Carcass traits are essential economic traits in the commercial pig industry. However, the genetic mechanism of carcass traits is still unclear. In this study, we performed a genome-wide association study (GWAS) based on the specific-locus amplified fragment sequencing (SLAF-seq) to study seven carcass traits on 223 four-way intercross pigs, including dressing percentage (DP), number of ribs (RIB), skin thinkness (ST), carcass straight length (CSL), carcass diagonal length (CDL), loin eye width (LEW), and loin eye thickness (LET). RESULTS: A total of 227,921 high-quality single nucleotide polymorphisms (SNPs) were detected to perform GWAS. A total of 30 SNPs were identified for seven carcass traits using the mixed linear model (MLM) (p < 1.0 × 10- 5), of which 9 SNPs were located in previously reported quantitative trait loci (QTL) regions. The phenotypic variation explained (PVE) by the significant SNPs was from 2.43 to 16.32%. Furthermore, 11 candidate genes (LYPLAL1, EPC1, MATN2, ZFAT, ZBTB10, ZNF704, INHBA, SMYD3, PAK1, SPTBN2, and ACTN3) were found for carcass traits in pigs. CONCLUSIONS: The GWAS results will improve our understanding of the genetic basis of carcass traits. We hypothesized that the candidate genes associated with these discovered SNPs would offer a biological basis for enhancing the carcass quality of pigs in swine breeding.

Prognostic value of plasma microRNAs for non-small cell lung cancer based on data mining models.

BACKGROUND: As biomarkers, microRNAs (miRNAs) are closely associated with the occurrence, progression, and prognosis of non-small cell lung cancer (NSCLC). However, the prognostic predictive value of miRNAs in NSCLC has rarely been explored. In this study, the value in prognosis prediction of NSCLC was mined based on data mining models using clinical data and plasma miRNAs biomarkers. METHODS: A total of 69 patients were included in this prospective cohort study. After informed consent, they filled out questionnaires and had their peripheral blood collected. The expressions of plasma miRNAs were examined by quantitative polymerase chain reaction (qPCR). The Whitney U test was used to analyze non-normally distributed data. Kaplan-Meier was used to plot the survival curve, the log-rank test was used to compare with the overall survival curve, and the Cox proportional hazards model was used to screen the factors related to the prognosis of lung cancer. Data mining techniques were utilized to predict the prognostic status of patients. RESULTS: We identified that smoking (HR = 2.406, 95% CI = 1.256-4.611), clinical stage III + IV (HR = 5.389, 95% CI = 2.290-12.684), the high expression group of miR-20a (HR = 4.420, 95% CI = 1.760-11.100), the high expression group of miR-197 (HR = 3.828, 95% CI = 1.778-8.245), the low expression group of miR-145 ( HR = 0.286, 95% CI = 0.116-0.709), and the low expression group of miR-30a (HR = 0.307, 95% CI = 0.133-0.706) was associated with worse prognosis. Among the five data mining models, the decision trees (DT) C5.0 model performs the best, with accuracy and Area Under Curve (AUC) of 93.75% and 0.929 (0.685, 0.997), respectively. CONCLUSION: The results showed that the high expression level of miR-20a and miR-197, the low expression level of miR-145 and miR-30a were strongly associated with poorer prognosis in NSCLC patients, and the DT C5.0 model may serve as a novel, accurate, method for predicting prognosis of NSCLC.

In Addition to Damaging the Plasma Membrane, Phenolic Monoterpenoid Carvacrol Can Bind to the Minor Groove of DNA of Phytopathogenic Fungi to Potentially Control Tea Leaf Spot Caused by Lasiodiplodia theobromae.

Carvacrol expresses a wide range of biological activities, but the studies of its mechanisms focused on bacteria, mainly involving the destruction of the plasma membrane. In this study, carvacrol exhibited strong activities against several phytopathogenic fungi and demonstrated a novel antifungal mechanism against Lasiodiplodia theobromae. RNA sequencing indicated that many genes of L. theobromae hyphae were predominately induced by carvacrol, particularly those involved in replication and transcription. Hyperchromic, hypsochromic, and bathochromic effects in the UV-visible absorption spectrum were observed following titration of calf thymus DNA (ctDNA) and carvacrol, which indicated the formation of a DNA-carvacrol complex. Circular dichroism (CD) spectroscopy indicated that the response of DNA to carvacrol was similar to that of 4',6-diamidino-2-phenylindole (DAPI) but different from that of ethidium bromide (EB), implying the ionic bonds between carvacrol and ctDNA. Fluorescence spectrum (FS) analysis indicated that carvacrol quenched the fluorescence of double-stranded DNA (dsDNA) more than single-stranded DNA, indicating that carvacrol mainly bound to dsDNA. A displacement assay showed that carvacrol reduced the fluorescence intensity of the DNA-DAPI complex through competition with DAPI, but this did not occur for DNA-EB. The FS assay revealed that carvacrol bound to the AAA sequence on the minor groove of ds-oligonucleotides. The hydroxyl of carvacrol was verified to bind to ctDNA through a comparative test in which structural analogs of carvacrol, including thymol and 4-ethyl-1,2-dimethyl, were analyzed. The current study indicated carvacrol can destruct plasma membranes and bind to the minor groove of DNA, inhibiting fungal proliferation by disturbing the stability of dsDNA.

Causal effects of sleep traits on metabolic syndrome and its components: a Mendelian randomization study.

PURPOSE: Previous observational studies have suggested an association between sleep disturbance and metabolic syndrome (MetS). However, it remains unclear whether this association is causal. This study aims to investigate the causal effects of sleep-related traits on MetS using Mendelian randomization (MR). METHODS: Single-nucleotide polymorphisms strongly associated with daytime napping, insomnia, chronotype, short sleep, and long sleep were selected as genetic instruments from the corresponding genome-wide association studies (GWAS). Summary-level data for MetS were obtained from two independent GWAS datasets. Univariable and multivariable MR analyses were conducted to investigate and verify the causal effects of sleep traits on MetS. RESULTS: The univariable MR analysis demonstrated that genetically predicted daytime napping and insomnia were associated with increased risk of MetS in both discovery dataset (OR daytime napping = 1.630, 95% CI 1.273, 2.086; OR insomnia = 1.155, 95% CI 1.108, 1.204) and replication dataset (OR daytime napping = 1.325, 95% CI 1.131, 1.551; OR insomnia = 1.072, 95% CI 1.046, 1.099). For components, daytime napping was positively associated with triglycerides (beta = 0.383, 95% CI 0.160, 0.607) and waist circumference (beta = 0.383, 95% CI 0.184, 0.583). Insomnia was positively associated with hypertension (OR = 1.101, 95% CI 1.042, 1.162) and waist circumference (beta = 0.067, 95% CI 0.031, 0.104). The multivariable MR analysis indicated that the adverse effect of daytime napping and insomnia on MetS persisted after adjusting for BMI, smoking, drinking, and another sleep trait. CONCLUSION: Our study supported daytime napping and insomnia were potential causal factors for MetS characterized by central obesity, hypertension, or elevated triglycerides.

Chest CT radiomics is feasible in evaluating bone changes in chronic kidney diseases.

BACKGROUND: Non-invasive imaging methods are still lacking for evaluating bone changes in chronic kidney diseases (CKD). PURPOSE: To investigate the feasibility of chest CT radiomics in evaluating bone changes caused by CKD. MATERIAL AND METHODS: In total, 75 patients with stage 1 CKD (CKD1) and 75 with stage 5 CKD (CKD5) were assessed using the chest CT radiomics method. Radiomics features of bone were obtained using 3D Slicer software and were then compared between CKD1 and CKD5 cases. The methods of maximum correlation minimum redundancy (mRMR) and least absolute shrinkage and selection operator (LASSO) were used to establish a prediction model to determine CKD. The receiver operating characteristic (ROC) curve was used to determine the performance of the model. RESULTS: Cases of CKD1 and CKD5 differed in 40 radiomics features (P <0.05). Using the mRMR and LASSO methods, five features were finally selected to establish a predication model. The area under the receiver operating characteristic curve of the model in the determination of CKD1 and CKD5 was 0.903 and 0.854, respectively, for the training and validation cohorts. CONCLUSION: Chest CT radiomics is feasible in evaluating bone changes caused by CKD.

Investigating the shared genetic architecture between breast and ovarian cancers.

High heritability and strong correlation have been observed in breast and ovarian cancers. However, their shared genetic architecture remained unclear. Linkage disequilibrium score regression (LDSC) and heritability estimation from summary statistics (ρ-HESS) were applied to estimate heritability and genetic correlations. Bivariate causal mixture model (MiXeR) was used to qualify the polygenic overlap. Then, stratified-LDSC (S-LDSC) was used to identify tissue and cell type specificity. Meanwhile, the adaptive association test called MTaSPUsSet was performed to identify potential pleiotropic genes. The Single Nucleotide Polymorphisms (SNP) heritability was 13% for breast cancer and 5% for ovarian cancer. There was a significant genetic correlation between breast and ovarian cancers (rg=0.21). Breast and ovarian cancers exhibited polygenic overlap, sharing 0.4 K out 2.8 K of causal variants. Tissue and cell type specificity displayed significant enrichment in female breast mammary, uterus, kidney tissues, and adipose cell. Moreover, the 74 potential pleiotropic genes were identified between breast and ovarian cancers, which were related to the regulation of cell cycle and cell death. We quantified the shared genetic architecture between breast and ovarian cancers and shed light on the biological basis of the co-morbidity. Ultimately, these findings facilitated the understanding of disease etiology.

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Further evidence is needed to explore the impact of high-altitude environments on the neurologic function of neonates. Non-invasive techniques such as cerebral near-infrared spectroscopy and amplitude-integrated electroencephalography can provide data on cerebral oxygenation and brain electrical activity. This study will conduct multiple cerebral near-infrared spectroscopy and amplitude-integrated electroencephalography monitoring sessions at various time points within the first 3 days postpartum for healthy full-term neonates at different altitudes. The obtained data on cerebral oxygenation and brain electrical activity will be compared between different altitudes, and corresponding reference ranges will be established. The study involves 6 participating centers in the Chinese High Altitude Neonatal Medicine Alliance, with altitude gradients divided into 4 categories: 800 m, 1 900 m, 2 400 m, and 3 500 m, with an anticipated sample size of 170 neonates per altitude gradient. This multicenter prospective cohort study aims to provide evidence supporting the impact of high-altitude environments on early brain function and metabolism in neonates.

Identification of exosomes-related lncRNAs in clear cell renal cell carcinoma based on Bayesian spike-and-slab lasso approach.

Exosomes-related long non-coding RNAs (lncRNAs) have been reported to play significant roles in clear cell renal cell carcinoma (ccRCC). However, there is little known about the relationship between exosomes-related lncRNAs and ccRCC. This study aimed to select optimal prognostic model based on exosomes-related lncRNAs to provide a methodological reference for high-dimensional data. Based on the Cancer Genome Atlas (TCGA) database of 515 ccRCC patients, two risk score models were generated underlying Bayesian spike-and-slab lasso and lasso regression. The optimal model was determined by calculating the area of time-dependent receiver-operating characteristic (ROC) curves in the TCGA and ArrayExpress databases. The immune patterns and sensitivity of immunotherapy between the high and low groups were further explored. Initially, we constructed two risk score models containing 11 and 7 exosomes-related lncRNAs according to Bayesian spike-and-slab lasso and lasso regression respectively. ROC curves revealed that the model constructed by Bayesian spike-and-slab lasso regression was more reliable in predicting survival at 1, 3, and 5 years, yielding an area under the curves (AUCs) of 0.796, 0.732, and 0.742, respectively. Kaplan-Meier (K-M) curves presented that prognosis was poorer in the high-risk score group (P < 0.001). Additionally, the high-risk score group patients were enriched in immune-activating phenotypes and more sensitive to immunotherapy. The exosomes-related lncRNAs model constructed with Bayesian spike-and-slab lasso regression has higher predictive power for ccRCC patients' prognosis, which provides methodological reference for the analysis of high-dimensional data in bioinformatics and guides the tailored treatment of ccRCC patients.

Association of solid fuel use with a risk score capturing dementia risk among middle-aged and older adults: A prospective cohort study.

OBJECTIVES: Whether household air pollution is associated with dementia risk remains unknown. This study examined the associations between solid fuel use for cooking and heating (the main source of household air pollution) and dementia risk. METHODS: This analysis included data on 11,352 participants (aged 45+ years) from the 2011 wave of China Health and Retirement Longitudinal Study, with follow-up to 2018. Dementia risk was assessed by a risk score using the Rotterdam Study Basic Dementia Risk Model (BDRM), which was subsequently standardized for analysis. Household fuel types of cooking and heating were categorized as solid (e.g., coal and crop residue) and clean (e.g., central heating and solar). Multivariable analyses were performed using generalized estimating equations. Moreover, we examined the joint associations of solid fuel use for cooking and heating with the BDRM score. RESULTS: After adjusting for potential confounders, we found an independent and significant association of solid (vs. clean) fuel use for cooking and heating with a higher BDRM score (e.g., ß = 0.17 for solid fuel for cooking; 95% confidence interval [CI]: 0.15-0.19). Participants who used solid (vs. clean) fuel for both cooking and heating had the highest BDRM score (ß = 0.32; 95% CI: 0.29-0.36). Subgroup analysis suggested stronger associations in participants living in rural areas. CONCLUSIONS: Solid fuel use for cooking and heating was independently associated with increased dementia risk in Chinese middle-aged and older adults, particularly among those living in rural areas. Our findings call for more efforts to facilitate universal access to clean energy for dementia prevention.

Spatial distribution and driving factors of the associations between temperature and influenza-like illness in the United States: a time-stratified case-crossover study.

BACKGROUND: Several previous studies investigated the associations between temperature and influenza in a single city or region without a national picture. The attributable risk of influenza due to temperature and the corresponding driving factors were unclear. This study aimed to evaluate the spatial distribution characteristics of attributable risk of Influenza-like illness (ILI) caused by adverse temperatures and explore the related driving factors in the United States. METHODS: ILI, meteorological factors, and PM2.5 of 48 states in the United States were collected during 2011-2019. The time-stratified case-crossover design with a distributed lag non-linear model was carried out to evaluate the association between temperature and ILI at the state level. The multivariate meta-analysis was performed to obtain the combined effects at the national level. The attributable fraction (AF) was calculated to assess the ILI burden ascribed to adverse temperatures. The ordinary least square model (OLS), spatial lag model (SLM), and spatial error model (SEM) were utilized to identify driving factors. RESULTS: A total of 7,716,115 ILI cases were included in this study. Overall, the temperature was negatively associated with ILI risk, and lower temperature gave rise to a higher risk of ILI. AF ascribed to adverse temperatures differed across states, from 49.44% (95% eCI: 36.47% ~ 58.68%) in Montana to 6.51% (95% eCI: -6.49% ~ 16.46%) in Wisconsin. At the national level, 29.08% (95% eCI: 27.60% ~ 30.24%) of ILI was attributable to cold. Per 10,000 dollars increase in per-capita income was associated with the increment in AF (OLS: ß = -6.110, P = 0.021; SLM: ß = -5.496, P = 0.022; SEM: ß = -6.150, P = 0.022). CONCLUSION: The cold could enhance the risk of ILI and result in a considerable proportion of ILI disease burden. The ILI burden attributed to cold varied across states and was higher in those states with lower economic status. Targeted prevention programs should be considered to lower the burden of influenza.

Effect and interaction of TNKS genetic polymorphisms and environmental factors on telomere damage in COEs-exposure workers.

Coke oven emissions (COEs) contain many carcinogenic polycyclic aromatic hydrocarbons (PAHs). Telomere damage is an early biological marker reflecting long-term COEs-exposure. Whereas, whether the genetic variations of telomere-regulated gene TNKS have an effect on the COEs-induced telomere damage is unknown. So we detected the environmental exposure levels, relative telomere length (RTL), and TNKS genetic polymorphisms among 544 COEs-exposure workers and 238 healthy participants. We found that the RTL of the wild homozygous GG genotype in rs1055328 locus was statistically shorter compared with the CG+CC genotype for the healthy participants using covariance analysis(P = 0.008). In the Generalized linear model (GLM) analysis, TNKS rs1055328 GG could accelerate telomere shortening (P = 0.011); and the interaction between TNKS rs1055328 GG and COEs-exposure had an effect on RTL (P = 0.002). In conclusion, this study was the first to discover the role of TNKS rs1055328 locus in COEs-induced telomere damage, and proved that chromosomal damage was a combined consequence of environmental and genetic factors.

The global burden of colorectal cancer attributable to high plasma glucose in 204 countries and territories, 1990-2019: an analysis of the Global Burden of Disease Study.

OBJECTIVES: This study aimed to estimate the burden of colorectal cancer (CRC) attributable to high plasma glucose from 1990 to 2019. STUDY DESIGN AND METHODS: Data on the disease burden were retrieved from the Global Burden of Disease online database. Estimated average percentage change (EAPC) was used to quantify the age-standardized mortality rate (ASMR) and age-standardized disability-adjusted life years (DALYs) rate (ASDR) of high plasma glucose-related CRC trends by sex and location between 1990 and 2019. RESULTS: Globally, the death number and DALYs of CRC attributable to high plasma glucose remained a steady increase at global level from 1990 to 2019, and similar trends have been reported in age-standardized rate. The country with the largest number of death cases and DALYs of high plasma glucose-related CRC in 2019 was China, followed by the United States of America and India. Nearly three-quarters of total countries experienced an increase in the ASMR and ASDR, and the greatest increase of ASMR and ASDR was found in Uzbekistan (EAPC = 5.32) and Equatorial Guinea (EAPC = 4.65), respectively. A negative correlation was found between sociodemographic indices and the EAPC of ASMR and ASDR (rASMR = -0.259, p < 0.001; rASDR = -0.282, p < 0.001). CONCLUSIONS: A significant increase in mortality and DALYs of CRC attributable to high plasma glucose was observed in global and most countries, especially in the developing countries. Public health policies and targeted programs are needed to reduce the burden of disease.

The polymorphisms in cGAS-STING pathway are associated with mitochondrial DNA copy number in coke oven workers.

OBJECTIVE: To evaluate the interaction effects of Polycyclic aromatic hydrocarbons (PAHs) exposure and variants in cGAS-STING genes on mitochondrial DNA copy number (mtDNAcn) in workers. METHODS: The mtDNAcn was determined by real-time quantitative polymerase-chain reaction in 544 PAHs-exposed workers and 238 office workers. The polymorphisms were detected by flight mass spectrometry. RESULTS: The mtDNAcn in PAHs exposure group was significantly lower than non-occupational exposure population (P < 0.00). The cGAS rs610913 CA+AA had significant interaction effects with STING rs11554776 GG+GA (P = 0.035), rs7380824 CC+CT (P = 0.026), and rs78233829 GC+CC (P = 0.034) on mtDNAcn. The generalized linear model results showed that the influencing factors of mtDNAcn include PAHs exposure (P < 0.001) and the interaction of PAHs exposure and cGAS rs 311678 AA+AG (P = 0.047). CONCLUSION: The influencing factors of mtDNAcn include PAHs exposure and the interaction of PAHs exposure and cGAS rs 311678 AA+AG.

Association of Genetic Polymorphisms of TERT with Telomere Length in Coke Oven Emissions-Exposed Workers.

We explored the association between variations in the telomere maintenance genes and change in telomere length (TL) in workers. The TL of peripheral blood leukocytes from 544 coke oven workers and 238 controls were detected using the Real-time PCR method. Variations in four genes were then detected using the PCR based restriction fragment length polymorphism. The effects of environmental and genetic factors on TL were subsequently analyzed through covariance analysis and a generalized linear model .The TL of subjects with GG genotypes were longer than those with AG genotype in the TERT rs2736098 locus amongst the controls (P = .032). The combined effect of COEs exposure and AG+AA genotypes had a significant effect on TL (P < .001). The interaction between the COEs exposure factor and the rs2736098AG+AA genotypes had a significant effect on the TL (P < .05). The TL in coke oven workers is associated with the interactions between TERT rs2736098 AG+AA and COEs exposure.

Association between cardiorespiratory fitness and risk of all-cause and cause-specific mortality.

OBJECTIVE: The association of cardiorespiratory fitness (CRF) with all-cause and cause-specific mortality remains unclear in Chinese population. This study aimed to evaluate the risk of all-cause, cardiovascular disease (CVD), cancer and other-cause mortality in Chinese adults using estimated CRF (eCRF). PATIENTS AND METHODS: We analysed data for 15,566 participants aged ≥20 years recruited in The Rural Chinese Cohort Study during 2007 to 2008 and followed for mortality during 2013 to 2014. eCRF was calculated with sex-specific longitudinal non-exercise algorithms. Cox proportional-hazards models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause and cause-specific mortality risk according to baseline eCRF. RESULTS: During a median of 6.01 years of follow-up, 859 deaths occurred, including 359 from CVD, 221 from cancer, and 279 from other causes. Each 1 metabolic equivalent increment in eCRF was associated with decreased risk of all-cause mortality (men: HR 0.70, 95% CI [0.66-0.74]; women: 0.59, [0.54-0.64]); CVD mortality (men: 0.70 [0.64-0.77]; women: 0.55, [0.48-0.62]); and other-cause mortality (men: 0.68 [0.62-0.75]; women: 0.57, [0.49-0.66]). The area under receiver operating characteristic curve was significantly higher for eCRF than its modifiable components (waist circumference, body mass index and resting heart rate) in predicting all-cause and cause-specific mortality incidence (all p < .001). CONCLUSION: eCRF was inversely associated with all-cause, CVD and other-cause mortality.

Comparison of six surrogate insulin resistance indexes for predicting the risk of incident stroke: The Rural Chinese Cohort Study.

BACKGROUND AND PURPOSE: Some cheap and easily used operated indexes of insulin resistance (IR) were currently available. We aimed to evaluate the association of six surrogate indexes of IR with incident stroke and to compare their predictive capacity. METHODS: We analysed data from 14,595 eligible study participants from the Rural Chinese Cohort Study. Modified Poisson regression models were used to estimate relative risks (RRs) and 95% confidence intervals (95% CIs) of incident stroke associated with the visceral adiposity index (VAI), the Chinese visceral adiposity index (CVAI), lipid accumulation product (LAP), triglyceride-glucose (TyG), TyG-body mass index, and TyG-waist circumference. The receiver operator characteristic curve was used to compare the ability of the abovementioned IR indexes to predict stroke. RESULTS: During a median follow-up of 6 years, 786 newly diagnosed stroke cases were identified. The levels of six surrogate indexes of IR were all significantly higher in the stroke population than in the non-stroke population (p < 0.001). Compared with quartile 1, the multivariable adjusted RRs (95% CIs) of incident stroke for quartile 4 were 2.01 (1.47-2.76), 1.62 (1.28, 2.04), 1.64 (1.28-2.09), and 1.92 (1.50-2.45) for CVAI, VAI, LAP, and TyG, respectively. Significant dose-response associations were also found between surrogate IR indexes and risk of stroke. The area under the curves|areas under the curves for CVAI (0.674) was significantly greater than for other indexes (TyG-WC:0.622, TyG:0.614, LAP:0.606, TyG-BMI:0.598, and VAI:0.577) (p < 0.001). CONCLUSIONS: Six surrogate indexes of IR were independently associated with incident stroke. The CVAI may be the most suitable index for stroke prediction.

Trends and influence factors in the prevalence, intervention, and control of metabolic syndrome among US adults, 1999-2018.

AIM: We aimed to describe the trends in the prevalence, intervention, and control of metabolic syndrome (MetS) among US adults through 1999-2018. Additionally, the influence factors of MetS and its control were further explored. METHODS: We included participants older than 20 using the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2018 (n = 22,114). The rate of prevalence, intervention, and control of MetS were caculated by survey weights. Joinpoint regression and survey-weighted generalized linear models were used to analyze trends and influence factors, respectively. RESULTS: The prevalence of MetS increased from 28.23 to 37.09% during 1999-2018 (P for trend < 0.05). The former smoker (OR = 1.20, 95%CI: 1.07, 1.36) and current smoker (OR = 1.27, 95%CI: 1.11, 1.45) increased the prevalence of MetS. While vigorous activity (OR = 0.53, 95%CI: 0.47, 0.61) decreased it. Among MetS components, the prevalence of elevated blood-glucose (from 21.18 to 34.68%) and obesity (from 44.81 to 59.06%) raised (P for trend < 0.05), with an uptrend in the use of antidiabetic (from 9.87 to 28.63%) and a downtrend of vigorous activity (from 23.79 to 16.53%) (P for trend < 0.05). Decreased trends were observed in the control of Hb1Ac (< 7%) (from 87.13 to 84.06%) and BMI (<25 kg/m2) (from 11.36 to 7.49%). Among MetS underwent antidiabetic, 45-64 years old and male decreased the control of Hb1Ac (< 7%). The control of BMI (<25 kg/m2) among individuals with physical activity was reduced mainly in the population of younger (aged 20-44 years old), male, non-Hispanic black, middle income and smoker (former and current). CONCLUSIONS: The prevalence of MetS increased significantly through 1999-2018. Elevated blood glucose and obesity were the main causes of MetS burden. Quitting smoking and increasing physical activity may decrease the prevalence of MetS. In the control of blood-glucose and obesity, we should screen out the focus population to modify treatment and improve lifestyle.

Cardiorespiratory fitness and mortality from all causes, cardiovascular disease and cancer: dose-response meta-analysis of cohort studies.

OBJECTIVE: Current evidence of the associations between cardiorespiratory fitness (CRF) and mortality is limited. We performed a meta-analysis to assess the dose-response association of CRF with mortality from all causes, cardiovascular disease (CVD) and cancer in healthy population. METHODS: PubMed, EMBASE and Web of Science were searched up to 26 December 2019 for reports of cohort studies giving risk estimates for all-cause, CVD and cancer mortality by level of CRF. Cohort studies were included if CRF was assessed by an exercise stress test and reported as at least three levels or per incremental increase, and the association of CRF with all-cause, CVD and cancer mortality was evaluated. Generalised least-squares regression models were used to assess the quantitative relation of CRF with all-cause, CVD and cancer mortality. RESULTS: 34 cohort studies were eligible for the meta-analysis. The pooled relative risks (RRs) for all-cause, CVD and cancer mortality per one-metabolic equivalent increase in CRF were 0.88 (95% CI 0.83 to 0.93), 0.87 (95% CI0.83 to 0.91) and 0.93 (95% CI 0.91 to 0.96), respectively. As compared with lowest CRF, with intermediate CRF, the summary RRs for all-cause, CVD and cancer mortality were 0.67 (95% CI 0.61 to 0.74), 0.60 (95% CI 0.51 to 0.69) and 0.76 (95% CI 0.69 to 0.84), respectively, and with highest CRF were 0.47 (95% CI 0.39 to 0.56), 0.49 (95% CI 0.42 to 0.56) and 0.57 (95% CI 0.46 to 0.70), respectively. CONCLUSION: Our analysis showed inverse dose-response associations of CRF with all-cause, CVD and cancer mortality, which provides evidence for public health recommendations for preventing all-cause, CVD and cancer mortality. PROSPERO REGISTRATION NUMBER: CRD42020208883.

Does healthy lifestyle attenuate the detrimental effects of urinary polycyclic aromatic hydrocarbons on phenotypic aging? An analysis from NHANES 2001-2010.

Existing evidence has showed that exposure to polycyclic aromatic hydrocarbons (PAHs) increases the risk of many chronic diseases. Given the close connection between aging (a major risk factor) and chronic diseases, however, very few studies have evaluated the association between PAHs and aging. Furthermore, whether modifiable healthy lifestyle could attenuate the detrimental effect of PAHs on aging remains unknown. Therefore, we conducted this study, aiming to: (1) examine the associations of urinary monohydroxy polycyclic aromatic hydrocarbons (OH-PAHs) and lifestyle with Phenotypic Age Acceleration (PhenoAge.Accel), a novel aging measure that captures morbidity and mortality risk; and (2) evaluate the potential interaction effects of OH-PAHs and lifestyle on PhenoAge.Accel. Cross-sectional data of 2,579 participants (aged 20-84 years, n = 1,292 females) from the National Health and Nutrition Examination Survey for years 2001-2010 were analyzed. A lifestyle index was constructed based on five components (drinking, smoking, body mass index, physical activity, and diet), ranging from 0 to 5. We calculated PhenoAge.Accel using algorithms developed previously. General linear regression models were used to examine the associations. We observed strong associations of OH-PAHs and lifestyle with PhenoAge.Accel. For instance, one unit increase in ∑NAP (sum of 1- and 2-hydroxynaphthalene) was associated with 0.37 year (95% confidence interval [CI]: 0.26, 0.48) increase in PhenoAge.Accel. We did not observe statistically significant interaction effects between OH-PAHs and lifestyle on PhenoAge.Accel. After stratified by sex, we observed strong associations as well as statistically significant interactions of OH-PAHs and lifestyle with PhenoAge.Accel among females. In conclusion, both OH-PAHs and lifestyle were independently associated with phenotypic aging and there were statistically significant interactions between OH-PAHs and lifestyle on phenotypic aging among females. The findings highlight the importance of adherence to a healthy lifestyle to attenuate the detrimental effects of exposures to PAHs on phenotypic aging among females.

Genetic variants in telomerase-associated protein 1 are associated with telomere damage in PAH-exposed workers.

Telomeres are functional complexes at the ends of linear chromosomes, and telomerase aids in their maintenance and replication. Additionally, accumulating evidence suggests that telomerase-associated protein 1 (TEP1) is a component of the telomerase ribonucleoprotein complex and is responsible for catalyzing the addition of new synthetic telomere sequences to chromosome ends. In our previous study, we found that genetic variants of the TERT gene participated in the regulation of telomere length. Exposure to particulate matter, environmental pollutants, oxidative stress, and pesticides is associated with shortening of telomere length. However, it is unknown whether genetic variants in the TEP1 gene may affect telomere length (TL) in polycyclic aromatic hydrocarbon (PAH)-exposed workers. Therefore, we measured the peripheral leukocyte TL and genotyped the polymorphism loci in the TEP1 gene among 544 PAH-exposed workers and 238 healthy controls. Covariance analysis showed that the individuals carrying TEP1 rs1760903 CC and TEP1 rs1760904 TT had longer TL in the control group (P < 0.05). In the generalized linear model, we found that rs1760903 CC was a protective factor against TL shortening, and PAH exposure could promote telomere shortening (P < 0.05). Thus, this study reinforces the roles of environmental factors and genetic variations in telomere damage, and provides a theoretical foundation for the early detection of susceptible populations and the establishment of occupational standards.