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Machine learning (ML) is becoming a new paradigm for scientific research in various research fields due to its exciting and powerful capability of modeling tools used for big-data processing tasks. In this review, we first briefly introduce the different methodologies used in ML algorithms and techniques. As a snapshot of many applications by ML, some selected applications are presented, especially for low- and intermediate-energy nuclear physics, which include topics on theoretical applications in nuclear structure, nuclear reactions, properties of nuclear matter, and experimental applications in event identification/reconstruction, complex system control, and firmware performance. Finally, we present a summary and outlook on the possible directions of ML use in low-intermediate energy nuclear physics and possible improvements in ML algorithms.

Vascular calcification is common in chronic kidney disease (CKD) and contributes to cardiovascular disease (CVD) without any effective therapies available up to date. The expression of soluble epoxide hydrolase (sEH) is different in patients with and without vascular calcification. The present study investigates the role of sEH as a potential mediator of vascular calcification in CKD. Both Ephx2 − /− and wild-type (WT) mice fed with high adenine and phosphate (AP) diet were used to explore the vascular calcification in CKD. Compared with WT, deletion of sEH inhibited vascular calcification induced by AP. sEH deletion also abolished high phosphorus (Pi)-induced phenotypic transition of vascular smooth muscle cells (VSMCs) independent of its epoxyeicosatrienoic acids (EETs) hydrolysis. Further gene expression analysis identified the potential role of Sirtuin 3 (Sirt3) in the sEH-regulated VSMC calcification. Under high Pi treatment, sEH interacted with Sirt3, which might destabilize Sirt3 and accelerate the degradation of Sirt3. Deletion of sEH may preserve the expression of Sirt3, and thus maintain the mitochondrial adenosine triphosphate (ATP) synthesis and morphology, significantly suppressing VSMC calcification. Our data supported that sEH deletion inhibited vascular calcification and indicated a promising target of sEH inhibition in vascular calcification prevention.

Objective The triglyceride–glucose (TyG) index has been shown to be a new alternative measure for insulin resistance. However, no study has attempted to investigate the association of the TyG index with incident atrial fibrillation (AF) in the general population without known cardiovascular diseases. Methods Individuals without known cardiovascular diseases (heart failure, coronary heart disease, or stroke) from the Atherosclerosis Risk in Communities (ARIC) cohort were recruited. The baseline TyG index was calculated as the Ln [fasting triglycerides (mg/dL) × fasting glucose (mg/dL)/2]. The association between the baseline TyG index and incident AF was examined using Cox regression. Results Of 11,851 participants, the mean age was 54.0 years; 6586 (55.6%) were female. During a median follow-up of 24.26 years, 1925 incidents of AF cases (0.78/per 100 person-years) occurred. An increased AF incidence with a graded TyG index was found by Kaplan‒Meier curves ( P  < 0.001). In multivariable-adjusted analysis, both < 8.80 (adjusted hazard ratio [aHR] = 1.15, 95% confidence interval [CI] 1.02, 1.29) and > 9.20 levels (aHR 1.18, 95% CI 1.03, 1.37) of the TyG index were associated with an increased risk of AF compared with the middle TyG index category (8.80–9.20). The exposure-effect analysis confirmed the U-shaped association between the TyG index and AF incidence ( P  = 0.041). Further sex-specific analysis showed that a U-shaped association between the TyG index and incident AF still existed in females but not in males. Conclusions A U-shaped association between the TyG index and AF incidence is observed in Americans without known cardiovascular diseases. Female sex may be a modifier in the association between the TyG index and AF incidence. Graphical Abstract

The chiral magnetic effect (CME) induces an electric charge separation in a chiral medium along the magnetic field that is mostly produced by spectator protons in heavy-ion collisions. The experimental searches for the CME, based on the charge-dependent angular correlations ( γ ), however, have remained inconclusive, because the non-CME background contributions are not well understood. Experimentally, the γ correlators have been measured with respect to the second-order ( Ψ 2 ) and the third-order ( Ψ 3 ) symmetry planes, defined as γ 112 and γ 123 , respectively. The expectation was that with a proper normalization, γ 123 would provide a data-driven estimate for the background contributions in γ 112 . In this work, we calculate different harmonics of the γ correlators using a charge-conserving version of a multiphase transport (AMPT) model to examine the validity of the said assumption. We find that the pure-background AMPT simulations do not yield an equality in the normalized γ 112 and γ 123 , quantified by κ 112 and κ 123 , respectively. Furthermore, we test another correlator, γ 132 , within AMPT, and discuss the relation between different γ correlators.

Purpose Coronary artery calcification (CAC) progression is a strong predictor of cardiovascular disease (CVD) morbidity and mortality. However, the association between whole milk and CAC progression remains unknown. Recent studies highlighted beneficial effects of short chain fatty acids (SCFA) from whole milk on CVD. In this study, we attempted to investigate the relationship between whole milk consumption and CAC progression, and the potential effect of SCFA in it. Methods We analyzed a population-based cohort with 5273 participants from the Multi-Ethnic Study of Atherosclerosis (MESA) who completed a dietary questionnaire at baseline. CAC was measured at baseline and subsequent follow-up examinations by multi-detector computed tomography (MDCT) scans with Agatston scores. CAC progression was defined as increased CAC scores in the follow-up from the baseline exam. Results Participants consuming whole milk exhibited lower baseline CAC and CAC progression than those who never/rarely consumed whole milk ( P  < 0.001 and P  = 0.010, respectively). Moreover, multivariable logistic regression analysis demonstrated that whole milk intake was independently associated with lower CAC progression (OR 0.765; 95% CI 0.600–0.977; P  = 0.032), especially in males, participants with age ≤ 64 years and with body mass index (BMI) ≤ 25 kg/m 2 . Mediation analysis further showed that caproic acid, one kind of SCFA, partly mediated protective effects of whole milk on CAC progression. Conclusions Self-reported whole milk consumption was inversely associated with CAC progression in community-dwelling participants, especially in those at relatively low cardiovascular risks. The beneficial effect was partially mediated by SCFA. Therefore, whole milk can be incorporated into part of a cardio-protective diet. Regarding this, future studies may target SCFA to provide insight into more mechanistic views.

Background Commencing work at an early age has been linked to various risk factors for coronary heart disease (CHD), such as shift work and intensive job strain. However, the relationship between starting work too early and CHD risk remains largely unclear. We examined the association between age at job initiation and the risk of CHD. Methods UK Biobank participants aged 38 to 70 years without cardiovascular disease who provided data on their age at job initiation were included. The primary outcome was CHD, which was ascertained using hospital and death records. The hazard ratios (HRs) and 95% confidence interval (CIs) for the association between age at job initiation and CHD were calculated using multivariable Cox regression. Results Of the 501,971 participants, 114,418 eligible participants were included in the final analysis. The median age at job initiation was 19.0 years. During the mean follow-up of 12.6 years, 6,130 (5.4%) first CHD events occurred. We observed that age at job initiation was inversely associated with CHD (HR 0.98, 95% CI 0.97–0.99), and the association was potentially J-shaped. The HRs for the < 17-year, 17–18-year, and 19–21-year age groups were 1.29 (95%CI 1.18–1.41), 1.12 (95% CI 1.03–1.22) and 1.05 (95% CI 0.97–1.14), respectively, compared with those of the ≥ 22-year group. Conclusions Age at job initiation was associated with incident CHD, which was independent of socioeconomic status. Participants who commenced employment before the age of 19 years exhibited a higher risk of developing CHD later in adulthood.

Microvascular complications are prevalent in patients with type 2 diabetes mellitus (T2DM), resulting in increased risk of cardiovascular mortality. However, it is unclear whether above-knee artery calcification relates to microvascular complications. This study was aimed to investigate the role of calcification in superficial femoral arteries (SFA), the major above-knee artery, compared with anterior tibial arteries (ATA) and posterior tibial arteries (PTA), in T2DM-related microvascular complications and explore its risk factors. A single-center and observational study involving 359 T2DM patients was conducted. Clinical and laboratory data were collected. SFA calcification was evaluated by ultrasonography. Compared with ATA and PTA calcification, operating characteristics curve analysis showed that SFA calcification was the strongest predictor (63.1% sensitivity and 69.2% specificity) for T2DM-related microvascular complications (diabetic neuropathy, diabetic nephropathy and diabetic retinopathy). With the severity of SFA calcification increased, age, duration of T2DM, and SBP were significantly elevated, but triglyceride and glucose index and estimated glomerular filtration rate (eGFR) were significantly reduced (all P  < 0.05). Multivariate logistic analysis showed that eGFR (OR 0.953; 95% CI 0.931–0.976; P  < 0.001) was an independent risk factor of SFA calcification, especially in young patients with HbA1c > 7.0. We identified SFA calcification as a good predictor of microvascular complications in T2DM patients. Reduced eGFR was significantly associated with increased SFA calcification prevalence, especially in young T2DM patients with bad controlled hyperglycemia.

Aim Non‐alcoholic fatty liver disease (NAFLD)‐related advanced liver fibrosis (Stage 3 or 4) was reported to be linked to worse prognosis in patients with heart failure with preserved ejection fraction (HFpEF). This study aims to assess the relationship between liver fibrosis scores and new‐onset atrial fibrillation (AF) incidence in patients with HFpEF in the Treatment of Preserved Cardiac Function Heart Failure with an Aldosterone Antagonist (TOPCAT) trial. Methods and results Baseline liver fibrosis levels, assessed by NAFLD fibrosis score (NFS) or Fibrosis‐4 index (FIB‐4), with AF incidence were expressed as hazard ratios (HRs) using the Cox proportional hazard model. The risk for advanced fibrosis was estimated to be 21.5% (447/2072) as assessed by FIB‐4 (>3.25) and 4.2% (88/2072) as assessed by NFS (>0.676) in HFpEF patients without baseline AF. After a median follow‐up of 3.11 years, 106 new‐onset AF cases occurred. In multivariate analysis, elevated NFS [NFS = −1.455–0.676: HR 2.44, 95% confidence interval (CI) 1.27–4.68; NFS > 0.676: HR 3.36, 95% CI 1.27–6.80; per 1 unit increase: HR 1.15, 95% CI 1.01–1.32], not FIB‐4 (FIB‐4 = 1.45–3.25: HR 1.02, 95% CI 0.67–1.55; FIB‐4 > 3.25: HR 1.69, 95% CI 0.76–3.79; per 1 unit increase: HR 1.13, 95% CI 0.93–1.37), was associated with increased AF incidence. The NFS (C‐index 0.662), not FIB‐4 (C‐index 0.531), had a moderate predictive ability in predicting incident AF. Conclusions Among patients with HFpEF, the risk of advanced liver fibrosis is associated with an increased incidence of new‐onset AF and may be a novel predictor for new‐onset AF. Additional studies are needed to confirm our results.

ObjectivesWe aimed to develop an effective tool for predicting severe acute kidney injury (AKI) in patients admitted to the cardiac surgery recovery unit (CSRU).DesignA retrospective cohort study.SettingData were extracted from the Medical Information Mart for Intensive Care (MIMIC)-III database, consisting of critically ill participants between 2001 and 2012 in the USA.ParticipantsA total of 6271 patients admitted to the CSRU were enrolled from the MIMIC-III database.Primary and secondary outcomeStages 2–3 AKI.ResultAs identified by least absolute shrinkage and selection operator (LASSO) and logistic regression, risk factors for AKI included age, sex, weight, respiratory rate, systolic blood pressure, diastolic blood pressure, central venous pressure, urine output, partial pressure of oxygen, sedative use, furosemide use, atrial fibrillation, congestive heart failure and left heart catheterisation, all of which were used to establish a clinical score. The areas under the receiver operating characteristic curve of the model were 0.779 (95% CI: 0.766 to 0.793) for the primary cohort and 0.778 (95% CI: 0.757 to 0.799) for the validation cohort. The calibration curves showed good agreement between the predictions and observations. Decision curve analysis demonstrated that the model could achieve a net benefit.ConclusionA clinical score built by using LASSO regression and logistic regression to screen multiple clinical risk factors was established to estimate the probability of severe AKI in CSRU patients. This may be an intuitive and practical tool for severe AKI prediction in the CSRU.

Background: Vascular calcification (VC) is a landmark of aging, while β-hydroxybutyric acid (BHB) induced by calorie restriction has been identified as a promising factor to extend the lifespan. However, the effect of BHB on VC and the potential mechanism remain unknown. Methods: A total of 160 subjects with or without metabolic abnormalities (MAs) were assigned to four groups according to different calcification severities. The association between BHB, MAs, and VC was investigated via mediation analysis. Then, with high phosphate-induced calcification models, the effect of BHB on arterial ring calcification and osteogenic phenotypic differentiation of vascular smooth muscle cells (VSMCs) was investigated. Hereafter the expressions of autophagy biomarkers, autophagy flux, and effects of autophagy inhibitors on VC were detected. Results: Severe VC was observed in the elderly, accompanied with a higher proportion of hypertension, chronic kidney disease, and lower estimated glomerular filtration rate. The serum BHB level was an independent influencing factor of VC severities. With mediation analysis, BHB was determined as a significant mediator in the effects of MAs on VC, and the indirect effect of BHB accounted for 23% of the total effect. Furthermore, BHB directly inhibited arterial ring calcification and osteogenic phenotypic differentiation in VSMCs, accompanied with autophagy enhancement in VSMCs. In accordance, the inhibition of autophagy counteracted the protective effect of BHB on VC. Conclusion: The present study demonstrated that BHB mediated the effects of MAs on VC; then, it further elucidated that BHB could inhibit arterial and VSMC calcification via autophagy enhancement.