Forensic Identification and Evaluation of 25 Obstetric Brachial Plexus Palsy Medical Damage Cases.

OBJECTIVES: To analyze the high risk factors of obstetric brachial plexus palsy (OBPP), and to explore how to evaluate the relationship between fault medical behavior and OBPP in the process of medical damage forensic identification. METHODS: A retrospective analysis was carried out on 25 cases of medical damage liability disputes related to OBPP from 2017 to 2021 in Beijing Fayuan Judicial Science Evidence Appraisal Center. The shortcomings of hospitals in birth weight assessment, delivery mode selection, labor process observation and shoulder dystocia management, and the causal relationship between them and the damage consequences of the children were summarized. RESULTS: Fault medical behavior was assessed as the primary cause in 2 cases, equal cause in 10 cases, secondary cause in 8 cases, minor cause in 1 case, no causal relationship in 1 case, and unclear causal force in 3 cases. CONCLUSIONS: In the process of forensic identification of OBPP, whether medical behaviors fulfill diagnosis and treatment obligations should be objectively analyzed from the aspects of prenatal evaluation, delivery mode notification, standardized use of oxytocin, standard operation of shoulder dystocia, etc. Meanwhile, it is necessary to fully consider the objective risk of different risk factors and the difficulty of injury prevention, and comprehensively evaluate the causal force of fault medical behavior in the damage consequences.

DDB2 and MDM2 genes are promising markers for radiation diagnosis and estimation of radiation dose independent of trauma and burns.

In the field of biodosimetry, the current accepted method for evaluating radiation dose fails to meet the need of rapid, large-scale screening, and most RNA marker-related studies of biodosimetry are concentrating on a single type of ray, while some other potential factors, such as trauma and burns, have not been covered. Microarray datasets that contain the data of human peripheral blood samples exposed to X-ray, neutron, and γ-ray radiation were obtained from the GEO database. Totally, 33 multi-type ray co-induced genes were obtained at first from the differentially expressed genes (DEGs) and key genes identified by weighted gene co-expression network analysis (WGCNA), and these genes were mainly enriched in DNA damage, cellular apoptosis, and p53 signaling pathway. Following transcriptome sequencing of blood samples from 11 healthy volunteers, 13 patients with severe burns, and 37 patients with severe trauma, 6635 trauma-related DEGs and 7703 burn-related DEGs were obtained. Through the exclusion method, a total of 12 radiation-specific genes independent of trauma and burns were identified. ROC curve analysis revealed that the DDB2 gene performed the best in diagnosis of all three types of ray radiation, while correlation analysis showed that the MDM2 gene was the best in assessment of radiation dose. The results of multiple-linear regression analysis indicated that such analysis could improve the accuracy in assessment of radiation dose. Moreover, the DDB2 and MDM2 genes remained effective in radiation diagnosis and assessment of radiation dose in an external dataset. In general, the study brings new insights into radiation biodosimetry.

A Common East Asian aldehyde dehydrogenase 2*2 variant promotes ventricular arrhythmia with chronic light-to-moderate alcohol use in mice.

Chronic heavy alcohol use is associated with lethal arrhythmias. Whether common East Asian-specific aldehyde dehydrogenase deficiency (ALDH2*2) contributes to arrhythmogenesis caused by low level alcohol use remains unclear. Here we show 59 habitual alcohol users carrying ALDH2 rs671 have longer QT interval (corrected) and higher ventricular tachyarrhythmia events compared with 137 ALDH2 wild-type (Wt) habitual alcohol users and 57 alcohol non-users. Notably, we observe QT prolongation and a higher risk of premature ventricular contractions among human ALDH2 variants showing habitual light-to-moderate alcohol consumption. We recapitulate a human electrophysiological QT prolongation phenotype using a mouse ALDH2*2 knock-in (KI) model treated with 4% ethanol, which shows markedly reduced total amount of connexin43 albeit increased lateralization accompanied by markedly downregulated sarcolemmal Nav1.5, Kv1.4 and Kv4.2 expressions compared to EtOH-treated Wt mice. Whole-cell patch-clamps reveal a more pronounced action potential prolongation in EtOH-treated ALDH2*2 KI mice. By programmed electrical stimulation, rotors are only provokable in EtOH-treated ALDH2*2 KI mice along with higher number and duration of ventricular arrhythmia episodes. The present research helps formulate safe alcohol drinking guideline for ALDH2 deficient population and develop novel protective agents for these subjects.

IRAS/Nischarin modulates morphine reward by glutamate receptor activation in the nucleus accumbens of mouse brain.

The I1 imidazoline receptor and its candidate protein imidazoline receptor antisera-selected (IRAS)/Nischarin are linked to µ opioid receptor (MOR) functions associated with MOR trafficking. We previously demonstrated that IRAS may play an important role in the development of morphine tolerance and physical dependence in vivo. However, the effects of IRAS on morphine psychological dependence are not fully understood. To extend these studies, we investigated the impact of IRAS on morphine dependence in conditioned place preference (CPP) experiments and explored the underlying mechanisms. Knockout of IRAS enhanced the acquisition and reinstatement of morphine-induced CPP. Conditional-knockout of IRAS in the nucleus accumbens (NAc) reproduced higher CPP, and overexpression of IRAS in the NAc rescued the increased morphine-induced CPP in IRAS-/- mice. IRAS-/- mice showed dramatic cAMP-dependent protein kinase (PKA) activation, upregulation of the phosphorylation of the AMPA receptor GluR1-S845 and NMDA receptor NR1-S897 in the NAc after CPP experiment. Moreover, knockout of IRAS induced an increase in spontaneous excitatory postsynaptic current (sEPSC) frequency and a decrease in the AMPA/NMDA ratio in the NAc after chronic morphine treatment. The selective AMPA receptor antagonist NBQX could inhibit morphine CPP in WT mice, while its effect was significantly reduced in IRAS-/- mice. Together, our results demonstrate that IRAS contributes to the regulation of morphine dependence and that the alteration of glutamatergic transmission in the NAc may participate in the effect of IRAS.

Aging Combined with High Waist-to-Hip Ratio Is Associated with a Higher Risk of Gastro-Esophageal Reflux Disease.

Background and Objective: To assess whether the combination of high waist-to-hip ratio (WHR) and elderly age is associated with higher risk of GERD. Material and Methods: A total of 16,996 subjects aged ≥20 years who received esophagogastroduodenoscopy (EGD) between January 2010 and December 2019. We evaluated the risk of GERD in different age groups and WHR groups in unadjusted analysis and multivariate logistic regression models for predictors of GERD. Results: There was a trend towards more participants with both age ≥65 years and WHR ≥ 1 (n = 129) (n = 66, 51%) than participants with age < 65 and WHR < 0.9 (n = 10,422) (n = 2814, 27%) presenting with GERD. Participants who had both age ≥ 65 years and high WHR ≥ 1 had the highest risk of any type of GERD (adjusted OR, 2.07; 95% CI, 1.44−2.96, p value < 0.05) based on multivariate logistic regression analysis. Conclusions: The combination of having a high WHR and being elderly was associated with a higher risk of GERD, and preventing central obesity in the elderly population reduced the risk of GERD and the requirement for medical resources.

Risk assessment indicators and brachial-ankle pulse wave velocity to predict atherosclerotic cardiovascular disease.

Brachial-ankle pulse wave velocity (baPWV) is used for predicting the severity of vascular damage and prognosis of atherosclerotic cardiovascular disease (ASCVD) in people with hypertension and diabetes mellitus. This correlation study aimed to compare the baPWV with other risk indicators for identification of subclinical vascular disease for primary prevention and to determine the clinical utility of baPWV-guided therapy in improving prognosis in high-risk subjects. We included 4881 subjects who underwent voluntary health examination at Mackay Memorial Hospital, Taiwan between 2014 and 2019. Participants were categorized into the low-risk (<5%), borderline-risk (5%-7.4%), intermediate-risk (7.5%-19.9%), and high-risk (≥20%) groups based on the 10-year risk for ASCVD. The predictive risk criteria, that is, the metabolic syndrome score, Framingham Risk Score, estimated glomerular filtration rate, and baPWV were compared among these groups. The chief cause of induced responses and the relationships between parameters were identified using principal component analysis. The participants' ages, body mass index, systolic, diastolic blood pressure, triglycerides, fasting glucose, hemoglobin A1c, creatinine, neutrophil-to-lymphocyte ratio, monocyte-to-lymphocyte ratio, metabolic syndrome, Framingham Risk Score, and age-related arterial stiffness (vascular age) increased significantly from the low-risk to high-risk groups (P < .001). The mean estimated glomerular filtration rate decreased significantly from the low- to high-risk groups (P < .001). The predicted vascular age and actual age differed significantly between the intermediate- and high-risk groups (P < .001). High-density lipoprotein levels plummeted significantly among the 4 groups (P < .001). The right and left baPWV and ankle brachial index differed significantly among the 4 groups (all P < .001) and increased from the low-risk to high-risk groups (P < .001). Carotid Doppler ultrasonography revealed a significant increase in plaque formation (23.5%, 35.4%, 46.3%, and 61.5% for the low-, borderline-, intermediate, and high-risk groups, respectively). The total explanatory variation was 61.9% for 2 principal variation factors (baPWV, 36.8% and creatinine, 25.1%). The vascular age predicted using baPWV greatly exceeded the chronological age. Plaque formation was significant even in the low-risk group, and its frequency increased with the predicted ASCVD risk. Risk indicators and baPWV are useful predictors of ASCVD, which in conjunction with conventional pharmacotherapy could be useful for primary prevention of plaque formation in subjects with cardiovascular comorbidities.

[Salidroside inhibits phenotypic transformation of rat pulmonary artery smooth muscle cells induced by hypoxia].

This study investigated the effect of salidroside on phenotypic transformation of rat pulmonary artery smooth muscle cells(PASMCs) induced by hypoxia. Rat pulmonary arteries were isolated by tissue digestion and PASMCs were cultured. The OD values of cells treated with salidroside at different concentrations for 48 hours were measured by cell counting kit-8(CCK-8) to determine the appropriate concentration range of salidroside. The cells were divided into a normal(normoxia) group, a model(hypoxia) group, and three hypoxia + salidroside groups(40, 60, and 80 µg·mL~(-1)). Quantitative real-time PCR(qRT-PCR) was used to detect the mRNA expression of cell contractile markers in each group, such as α-smooth muscle actin(α-SMA), smooth muscle 22(SM22), and calcium-binding protein(calponin), and synthetic marker vimentin. The expression levels of cell phenotypic markers and proliferating cell nuclear antigen(PCNA) were detected by Western blot. The proliferation of cells in each group was detected by the 5-ethynyl-2'-deoxyuridine(EdU) assay. Cell migration was measured by Transwell assay. As revealed by results, compared with the normal group, the model group showed decreased mRNA and protein expression of contractile phenotypic markers of PASMCs and increased mRNA and protein expression of synthetic markers. Compared with the conditions in the model group, salidroside could down-regulate the mRNA and protein expression of synthetic markers in PASMCs and up-regulated the mRNA and protein expression of contractile phenotypic markers. Compared with the normal group, the model group showed potentiated proliferation and migration. Compared with the model group, the hypoxia + salidroside groups showed blunted proliferation and migration of cells after phenotypic transformation. The results suggest that salidroside can inhibit the expression of synthetic markers in PASMCs and promote the expression of contractile markers to inhibit the hypoxia-induced phenotypic transformation of PASMCs. The mechanism of salidroside in inhibiting the proliferation and migration of PASMCs is related to the inhibition of the phenotypic transformation of PASMCs.

Prediction and identification of epitopes in the Echinococcus multilocularis thrombospondin 3 antigen.

BACKGROUND: Alveolar echinococcosis is an epidemic disease caused by the parasitism of Echinococcus multilocularis (Em) larvae in the intermediate or final host. OBJECTIVE: To identify and analyze B-cell and T-cell (Th1, Th2, and Th17) epitopes of the Em antigen protein thrombospondin 3 (TSP3). METHODS: The amino acid sequence of TSP3 was obtained, and the secondary structural characteristics of TSP3 were predicted using bioinformatics software to further predict its potential T-cell and B-cell epitopes. The spleen lymphocytes of BALB/c mice, which were immunized with the TSP3 protein, were collected for co-culture with B-cell and T-cell antigen small peptides. The B-cell epitopes and T-cell epitope subtypes Th1, Th2, and Th17 were identified as having good immunogenicity. RESULTS: After identification, it was found that the predominant epitopes of B cells existing in TSP3 were T18-33, T45-55, and T110-122. Furthermore, the predominant epitopes of T cells existing in TSP3 were T33-42, T45-55, T80-90, and T110-122 in the T1 subtype, T45-55, T68-77, and T92-104 in the Th2 subtype, and T53-63 and T80-90 in the Th17 subtype. CONCLUSIONS: Six T-cell and eight B-cell dominant epitopes of the TSP3 antigen were revealed; these results may be applied in the development of a dominant epitope vaccine.

Variant Aldehyde Dehydrogenase 2 (ALDH2*2) as a Risk Factor for Mechanical LA Substrate Formation and Atrial Fibrillation with Modest Alcohol Consumption in Ethnic Asians.

Aldehyde dehydrogenase 2 (ALDH2) rs671 polymorphism is a common genetic variant in Asians that is responsible for defective toxic aldehyde and lipid peroxidation metabolism after alcohol consumption. The extent to which low alcohol consumption may cause atrial substrates to trigger atrial fibrillation (AF) development in users with ALDH2 variants remains to be determined. We prospectively enrolled 249 ethnic Asians, including 56 non-drinkers and 193 habitual drinkers (135 (70%) as ALDH2 wild-type: GG, rs671; 58 (30%) as ALDH2 variants: G/A or A/A, rs671). Novel left atrial (LA) mechanical substrates with dynamic characteristics were assessed using a speckle-tracking algorithm and correlated to daily alcohol consumption and ALDH2 genotypes. Despite modest and comparable alcohol consumption by the habitual alcohol users (14.3 [8.3~28.6] and 12.3 [6.3~30.7] g/day for those without and with ALDH2 polymorphism, p = 0.31), there was a substantial and graded increase in the 4-HNE adduct and prolonged PR, and a reduction in novel LA mechanical parameters (including peak atrial longitudinal strain (PALS) and phasic strain rates (reservoir, conduit, and booster pump functions), p < 0.05), rather than an LA emptying fraction (LAEF) or LA volume index across non-drinkers, and in habitual drinkers without and with ALDH2 polymorphism (all p < 0.05). The presence of ALDH2 polymorphism worsened the association between increasing daily alcohol dose and LAEF, PALS, and phasic reservoir and booster functions (all Pinteraction: <0.05). Binge drinking superimposed on regular alcohol use exclusively further worsened LA booster pump function compared to regular drinking without binge use (1.66 ± 0.57 vs. 1.97 ± 0.56 1/s, p = 0.001). Impaired LA booster function further independently helped to predict AF after consideration of the CHARGE-AF score (adjusted 1.68 (95% CI: 1.06-2.67), p = 0.028, per 1 z-score increment). Habitual modest alcohol consumption led to mechanical LA substrate formation in an ethnic Asian population, which was more pronounced in subjects harboring ALDH2 variants. Impaired LA booster functions may serve as a useful predictor of AF in such populations.

Visceral adiposity index outperforms conventional anthropometric assessments as predictor of diabetes mellitus in elderly Chinese: a population-based study.

BACKGROUND: This study assessed the performance of visceral adiposity index and body shape index in predicting diabetes mellitus (DM) risk and compared their predictive ability to that of body mass index and waist circumference. METHODS: Among 8249 consecutive subjects who attended the Nationwide Health Check Up System for Senior Citizens (≥ 65 years) between 2008 and 2018, we examined the associations of several adiposity indices with DM risk and explored gender differences. RESULTS: Among all adiposity indicators, Chinese visceral adiposity index (CVAI) demonstrated the highest discriminatory ability for diabetes mellitus with area under receiver operating characteristic curves (AUC) of 0.65, 0.68, and 0.66 for men, women, and all participants, respectively, and optimal cut-offs set as 126.09 in men and 117.77 in women. Compared with body shape index (ABSI), both CVAI and VAI were strongly associated with baseline DM (adjusted OR: 4.85, 95% CI: 4.05-5.82 and 4.22, 95% CI: 3.53-5.05 for 4th vs 1st quartile groups by CVAI and VAI, P < 0.001), which was more pronounced in older adult women (Pinteraction < 0.05). Over a median of 5.25 years (IQR: 3.07-6.44 years) follow-up, Cox regression models showed higher predictive ability of CVAI and VAI compared to ABSI. Further, both CVAI and VAI independently predicted new-onset DM (adjusted HR: 1.29, 95% CI: 1.22-1.37 and 1.16, 95% CI: 1.11-1.21 by CVAI and VAI) and composite endpoint of new DM and death among those without baseline DM. CONCLUSIONS: Our population-based data demonstrated that Chinese visceral adiposity index may serve as a superior clinical indicator of diabetes when compared with conventional anthropometric indices among older adult Chinese, especially in women.

Thoracic Aortic Calcification and Pre-Clinical Hypertension by New 2017 ACC/AHA Hypertension Guidelines.

The recently revised 2017 American College of Cardiology/American Heart Association (ACC/AHA) hypertension (HTN) guidelines employ a lower blood pressure threshold to define HTN, aiming for earlier prevention of HTN-related cardiovascular diseases (CVD). Thoracic aortic calcification (TAC), a new surrogate marker of aging and aortic medial layer degeneration, and different stages of HTN, according to the 2017 ACC/AHA HTN guidelines, remain unknown. We classified 3022 consecutive asymptomatic individuals enrolled into four HTN categories using the revised 2017 ACC/AHA guidelines: normal blood pressure (NBP), elevated blood pressure (EBP), and stage 1 (S1) and stage 2 (S2) HTN. The coronary artery calcification score and TAC metrics (total Agaston TAC score, total plaque volume (mm3), and mean density (Hounsfield units, HU)) were measured using multi-detector computed tomography. Compared to NBP, a graded and significant increase in the TAC metrics was observed starting from EBP and S1 and S2 HTN, using the new 2017 ACC/AHA guidelines (NBP as reference; all trends: p < 0.001). These differences remained consistent after being fully adjusted. Older age (>50 years), S1 and S2 HTN, prevalent diabetes, and chronic kidney disease (<60 mL/min/1.73 m2) are all independently contributing factors to higher TAC risk using multivariate stepwise logistic regressions (all p ≤ 0.001). The optimal cutoff values of systolic blood pressure, diastolic blood pressure, and pulse pressure were 121, 74, and 45 mmHg, respectively, for the presence of TAC after excluding subjects with known CVD and ongoing HTN medication treatment. Our data showed that the presence of TAC starts at a stage of elevated blood pressure not categorized as HTN from the updated 2017 ACC/AHA hypertension guidelines.

Prediction and Identification of Epitopes in the Emy162 Antigen of Echinococcus multilocularis.

INTRODUCTION: Alveolar echinococcosis (AE) is a zoonotic disease caused by the parasitism of Echinococcus multilocularis larvae in the intermediate host or the final host. This study aims to identify and analyze the B-cell and T-cell (Th1, Th2 and Th17) epitopes of E. multilocularis antigen Emy162. METHODS: (1) The secondary structural characteristics of the Emy162 protein were predicted by bioinformatics software to further predict the potential T- and B-cell epitopes. (2) The dominant antigen epitopes were detected by ELISA through the reaction of patient serum with small B-cell antigen peptide and assessing the proliferation of splenic lymphocytes of mice immunized with Emy162. (3) The expression of cytokines in splenic lymphocytes of mice stimulated by small T-cell antigen peptides was detected by ELISA, ELISpot and flow cytometry to enable the identification of the T-cell epitopes. RESULTS: (1) The high-scored T-cell epitopes were located at positions E7-13, E36-41, E80-89, E87-96, E97-106 and E129-139, while B-cell epitopes were located at positions E7-13, E19-27, E28-36, E37-48, E78-83, E101-109, E112-121 and E129-139. (2) The three advanced antigen epitopes of Emy162 were E19-27, E112-121 and E129-139. (3) The four Th1 advanced antigen epitopes of Emy162 were E7-13, E36-41, E80-89 and E129-139. The three Th2 advanced antigen epitopes were E36-41, E87-96 and E97-106. The three Th17 advanced antigen epitopes were E36-41, E87-96 and E97-106. CONCLUSION: (1) The Emy162 protein has advanced antigenicity and numerous potential epitopes. Six T-cell and eight B-cell dominant epitopes were revealed using bioinformatics methods. (2) There are three dominant B-cell epitopes, four dominant Th1 epitopes, three dominant Th2 epitopes, and three dominant Th17 epitopes in the Emy162 antigen.

Circulating Monocyte Count as a Surrogate Marker for Ventricular-Arterial Remodeling and Incident Heart Failure with Preserved Ejection Fraction.

Among 2085 asymptomatic subjects (age: 51.0±10.7 years, 41.3% female) with data available on common carotid artery diameter (CCAD) and circulating total white blood cell (WBC) counts, higher circulating leukocytes positively correlated with higher high sensitivity C-reactive protein (hs-CRP).Higher WBC/segmented cells and monocyte counts were independently associated with greater relative wall thicknesses and larger CCADs,which in generalweremore pronounced in men and obese subjects (body mass index ≥ 25kg/m2) (all P interaction: < 0.05). Using multivariate adjusting models, only the monocyte count independently predicted theleft ventricularmass index (LVMi) (ß-Coef: 0.06, p = 0.01). Higher circulating WBC, segmented,and monocyte counts and a greater CCAD were all independently associated with a higher risk of heart failure (HF)/all-cause death during a median of 12.1 years of follow-up in fully adjusted models, with individuals manifesting both higher CCADs and monocyte countsincurring the highest risk of HF/death (adjusted hazard ratio: 2.81, 95% CI: 1.57. -5.03, p< 0.001; P interaction, 0.035; lower CCAD/lower monocyte as reference). We conclude that a higher monocyte count is associated with cardiac remodeling and carotid artery dilation.Both an elevated monocyte count and a larger CCAD may indicate a specific phenotype that confers the highest risk of HF, which likely signifies the role of circulating monocytes in the pathophysiology of heart failure with preserved ejection fraction (HFpEF).

Associations of cigarette smoking and burden of thoracic aortic calcification in asymptomatic individuals: A dose-response relationship.

Smoking is known as a powerful predictor of pathological coronary atherosclerosis. Thoracic aortic calcification (TAC), an alternative marker for pathological atherosclerosis, has also been shown to be associated unfavorable cardiovascular outcomes. We aimed to investigate the dose-response relationship between cigarette use and calcification burden in subjects free from clinical symptoms. Among 3109 patients enrolled in this analysis, we categorized study participants according to smoking exposure pattern as: non-smokers, ex-smokers and current smokers. Smoking dose (cigarette/day), duration (years) and pack-years were semi-quantified as smoking dose exposure variables. Thoracic aortic calcification burden (including TAC score, plaque volume and plaque density) were determined and related to smoking dose and pattern information. TAC burdens (including TAC score, plaque volume and density) were highest in current smoker compared to non-smoker group, with ex-smoker showing TAC burdens in-between (all ANOVA p<0.05). Linear regression models consistently demonstrated that TAC burdens as continuous variables were independently higher in a dose-dependent manner with smoking exposure, particularly in high-dose (> 10 cigarettes/day) and the long-duration (> 3 years) smokers, even after adjusting for baseline demographic differences (all p<0.05). By logistic regression, subjects who never smoke consistently demonstrated reduced risk of TAC existence (adjusted OR: 0.65 [95% CI: 0.48-0.86], P = 0.003) in contrary to those current smokers (adjusted OR: 1.47 [95% CI: 1.10-1.89], P = 0.009). A dose-response relationship between active cigarette use and TAC burden was observed, with those who never exposed to smoking or quitted demonstrating partial protective effects. Our data provided imaging-based evidence about the potential deleterious biological hazards of long-term and high-dose cigarette consumption.

Neutrophil-to-lymphocyte ratio as a predictive marker of metabolic syndrome.

Neutrophil-to-lymphocyte ratio (NLR) serves as a strong prognostic indicator for patients suffering from various diseases. Neutrophil activation promotes the recruitment of a number of different cell types that are involved in acute and chronic inflammation and are associated with cancer treatment outcome. Measurement of NLR, an established inflammation marker, is cost-effective, and it is likely that NLR can be used to predict the development of metabolic syndrome (MS) at an early stage. MS scores range from 1 to 5, and an elevated MS score indicates a greater risk for MS. Monitoring NLR can prevent the risk of MS.A total of 34,013 subjects were enrolled in this study. The subjects (score 0-5) within the 6 groups were classified according to the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) criteria, and all anthropometrics, laboratory biomarkers, and hematological measurements were recorded. For the 6 groups, statistical analysis and receiver operating characteristic (ROC) curves were used to identify the development of MS.Analysis of the ROC curve indicated that NLR served as a good predictor for MS. An MS score of 1 to 2 yielded an acceptable discrimination rate, and these rates were even higher for MS scores of 3 to 5 (P < .001), where the prevalence of MS was 30.8%.NLR can be used as a prognostic marker for several diseases, including those associated with MS.

Correction: Thoracic aortic calcification across the clinical dysglycemic continuum in a large Asian population free of cardiovascular symptoms.

[This corrects the article DOI: 10.1371/journal.pone.0207089.].

Helicobacter pylori infection combined with non-alcoholic fatty liver disease increase the risk of atherosclerosis: Focus in carotid artery plaque.

Atherosclerosis has severe consequences on human health. Carotid artery plaques are a condition typically caused by atherosclerosis. Previous studies showed that nonalcoholic fatty liver disease (NAFLD) and Helicobacter pylori (H pylori) are risks factors for carotid artery plaque formation. We hypothesize that the combination of NAFLD with H pylori infection increases the risk of carotid artery plaque formation.A total of 4669 subjects aged > 40 years who underwent routine health checkups between January 2006 and December 2015 were retrospectively reviewed. A serial examination, including abdominal ultrasound, carotid artery ultrasound and esophago-gastroduodenoscopy (EGD), and biopsy urease testing, was conducted.In total, 2402 subjects were enrolled. There were no differences in H pylori infection status among patients with or without NAFLD. There was a trend of more participants with both NAFLD and H pylori infection (number [N]=583) presenting carotid artery plaque (N = 187,32.08%) than participants without NAFLD and H pylori infection (N = 589) who presented plaque formation (N = 106, 18.00%). Participants who had both H pylori infection and NAFLD had the highest risk of any carotid artery plaque (odds ratio [OR], 1.93; 95% confidence interval [CI], 1.413-2.636) based on a multivariate logistic regression analysis. This analysis also showed that age >60 years, male sex, low-density lipoprotein (LDL) >130 mg/dL, and H pylori infection were independent risk factors for concomitant NAFLD and carotid artery plaque formation.The combination of H pylori infection and NAFLD increases carotid artery plaque formation. H pylori eradication and NAFLD control may be warranted to prevent carotid artery plaque formation.

Thoracic aortic calcification across the clinical dysglycemic continuum in a large Asian population free of cardiovascular symptoms.

Thoracic aortic calcification (TAC) is tightly linked to pathological atherosclerosis and associated with certain cardiovascular diseases. While diabetes mellitus (DM) is known as a coronary heart disease equivalent, we examined the presence of TAC across the dysglycemic spectrum of diabetes mellitus (DM). We consecutively studied 3003 asymptomatic ethnic Asians underwent annual cardiovacular health survey, and further categorized them into: 1) 1760 normo-glycemic, 2) 968 pre-diabetic, and 3) 274 overt DM based on dysglycemic indices and medical histories. Several TAC parameters were assessed using non-contrast multi-detector computed tomography (MDCT), and related to dysglycemic indices or diabetes mellitus status. A remarkably graded increases of adjusted total TAC calcium burden, volume and density were seen across Non-diabetes, Pre-diabetes, and diabetes mellitus categories and positively correlated with all dysglycemic profiles (all p<0.001). Multi-variate logistic and linear regression models demonstrated independent associations between greater TAC density and all dysglycemic indices (Coef: 2.5, 1.4, 6.8 for fasting, postprandial sugar and HbA1c) and diabetes mellitus status (all p<0.05). Furthermore, Receiver-operating characteristic curves (ROC) showed fasting sugar and postprandial sugar set at 103mg/dL and 111mg/dL, separately, with HbA1c set at 5.8% all predict the presence of aortic calcification. Dysglycemic status, even without overt diabetes mellitus, were tighly linked to subclinical, pathological thoracic aortic calcification.