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T-2 toxin can induce bone and cartilage development disorder, and oxidative stress plays an important role in it. It is well known that selenomethionine (Se-Met) has antioxidative stress properties and promotes the repair of cartilage lesion, but it remains unclear whether Se-Met can relieve damaged cartilage exposure to T-2 toxin. Here, the oxidative stress and ferroptosis of chondrocytes exposure to T-2 toxin were observed. Mechanistically, T-2 toxin increased ROS, lipid ROS, MDA and Fe2+ contents in chondrocytes, decreased GSH and GPX4 activity, and inhibited the system Xc−/GSH/GPX4 antioxidant axis. In addition, the mitochondria of chondrocytes shrunk and the mitochondrial crest decreased or disappeared. However, Fer-1 (Ferrostatin-1) inhibited ferroptosis induced by T-2 toxin in chondrocytes. The Se-Met alleviated lipid peroxidation, oxidative stress, and damaged mitochondrial in T-2 toxin-infected chondrocytes, enhanced antioxidant enzyme activity, and activated the system Xc−/GSH/GPX4 axis, thereby antagonizing ferroptosis of chondrocytes and alleviating articular cartilage damage. In conclusion, our findings highlight the essentiality of ferroptosis in chondrocyte caused by T-2 toxin, elucidate how Se-Met offers protection against this injury and provide research evidence for the drug treatment target of Kashin-Beck disease.

Osteoarticular degeneration (OAD) is an important issue. Excessive fluoride can damage osteoarticular health. Besides, personal susceptibility (including genetic factors, physiological characteristics, and lifestyle) also contributes to osteoarticular development significantly. However, little evidence focused on the comprehensive modification of fluoride exposure and personal susceptibility on osteoarticular health. Thus, this study explored the relationships among fluoride exposure, genetic factors, physiological characteristics, lifestyle, and OAD risk, as well as the potential interactions among contributors in 593 adults from a cross-sectional study conducted in 2017. We observed that the OAD (n = 175) risk was increased with increasing urinary fluoride (UF) levels (OR=1.484; 95 %CI: 1.043, 2.111), age (OR=1.065; 95 %CI: 1.033, 1.098), and hip circumference (OR=1.069; 95 %CI: 1.014, 1.127), as well as a poor night sleep quality (OR=1.818; 95 %CI: 1.072, 3.084). More fruit consumption (>350 g/d) was beneficial to OAD prevention (OR=0.102; 95 %CI: 0.012, 0.850). Genetic susceptibility analysis showed that the CG genotype of calcitonin related polypeptide alpha (CALCA) rs1553005 loci was related to higher OAD risk (OR=1.959; 95 %CI: 1.003, 3.825), whereas higher methylation status of GNAS complex locus (GNAS) (OR=0.617; 95 %CI: 0.410, 0.929) and TC genotype of rs7121 loci (OR=0.569; 95 %CI: 0.371, 0.871) showed protective effect on OAD. Additionally, OAD risk was related to the interaction of fluoride-rs1553005 polymorphism-rs7121 polymorphism-GNAS methylation, fluoride-age-fruits, age-fruits, and rs1553005 polymorphism-GNAS methylation-rs7121 polymorphism-age-hip circumference-fruits-UF. Findings suggested that the OAD susceptibility might be modified by the interactions between fluoride and personal susceptibility.

AbstractThe associations between multiple sleep characteristics and smoking behavior are inconsistent, and it is unclear which sleep characteristics are most crucial for tobacco prevention. This study aimed to explore the associations between smoking status/intensity and multiple sleep characteristics and to identify the potential core domain of smoking-related sleep using network analysis. Data were obtained from a survey of cancer-related risk factors among Chinese adults. Logistic regression models were used to quantify the associations between sleep characteristics and smoking status/intensity. Network analyses were employed to identify the core sleep characteristics. A total of 5,228 participants with a median age of 44 years old were included in the study. Current smoking was significantly positively associated with long nap time, difficulty falling asleep, late bedtime, getting up after 7 am, and waking up earlier than expected. There was significant positive association between current smoking and short sleep duration in young adults under 45 years old. Late bedtime and getting up after 7 am were only associated with current heavy smoking, but not current light smoking. Network analyses showed that multiple smoking-related sleep characteristics were interconnected, with difficulty falling asleep and late bedtime as central characteristics in the network. The study found that the associations between sleep characteristics and smoking varied by age and smoking intensity and highlights the potential benefits of sleep health promotion in smoking cessation, with a particular focus on difficulty falling asleep and late bedtime.

Abstract Background Silica-induced pulmonary fibrosis (silicosis) is a diffuse interstitial fibrotic disease characterized by the massive deposition of extracellular matrix in lung tissue. Fibroblast to myofibroblast differentiation is crucial for the disease progression. Inhibiting myofibroblast differentiation may be an effective way for pulmonary fibrosis treatment. Methods The experiments were conducted in TGF-β treated human lung fibroblasts to induce myofibroblast differentiation in vitro and silica treated mice to induce pulmonary fibrosis in vivo. Results By quantitative mass spectrometry, we revealed that proteins involved in mitochondrial folate metabolism were specifically upregulated during myofibroblast differentiation following TGF-β stimulation. The expression level of proteins in mitochondrial folate pathway, MTHFD2 and SLC25A32, negatively regulated myofibroblast differentiation. Moreover, plasma folate concentration was significantly reduced in patients and mice with silicosis. Folate supplementation elevated the expression of MTHFD2 and SLC25A32, alleviated oxidative stress and effectively suppressed myofibroblast differentiation and silica-induced pulmonary fibrosis in mice. Conclusion Our study suggests that mitochondrial folate pathway regulates myofibroblast differentiation and could serve as a potential target for ameliorating silica-induced pulmonary fibrosis.

Abstract. Background:. Excessive exposure to fluoride can reduce intelligence. Methylenetetrahydrofolate dehydrogenase, cyclohydrolase, and formyltetrahydrofolate synthetase 1 (MTHFD1) polymorphisms have important roles in neurodevelopment. However, the association of MTHFD1 polymorphisms with children's intelligence changes in endemic fluorosis areas has been rarely explored. Methods:. A cross-sectional study was conducted in four randomly selected primary schools in Tongxu County, Henan Province, from April to May in 2017. A total of 694 children aged 8 to 12 years were included in the study with the recruitment by the cluster sampling method. Urinary fluoride (UF) and urinary creatinine were separately determined using the fluoride ion-selective electrode and creatinine assay kit. Children were classified as the high fluoride group and control group according to the median of urinary creatinine-adjusted urinary fluoride (UFCr) level. Four loci of MTHFD1 were genotyped, and the Combined Raven's Test was used to evaluate children's intelligence quotient (IQ). Generalized linear model and multinomial logistic regression model were performed to analyze the associations between children's UFCr level, MTHFD1 polymorphisms, and intelligence. The general linear model was used to explore the effects of gene-environment and gene-gene interaction on intelligence. Results:. In the high fluoride group, children's IQ scores decreased by 2.502 when the UFCr level increased by 1.0 mg/L (β = −2.502, 95% confidence interval [CI]:−4.411, −0.593), and the possibility for having “excellent” intelligence decreased by 46.3% (odds ratio = 0.537, 95% CI: 0.290, 0.994). Children with the GG genotype showed increased IQ scores than those with the AA genotype of rs11627387 locus in the high fluoride group (P

Dental fluorosis (DF) is a widely prevalent disease caused by excessive fluoride with limited awareness of its underlying pathogenesis. Here, a pilot population study was conducted to explore the pathogenesis of DF from the perspective of intestinal microbiome changes, and verified it in animal experiments combining intestinal microbiome and metabolomics. A total of 23 children were recruited in 2017 in China and divided into DF (n = 9) and control (n = 14) groups (DFG and CG, respectively). The SD rat model was established by drinking water containing sodium fluoride (NaF). Gut microbiome profiles of children and rats were analyzed by16S rDNA V3-V4 sequencing, and the intestinal metabolomics analysis of rats was performed by LC-MS methods. The 16 S rDNA sequencing revealed that the gut microbiome composition was significantly perturbed in children in DFG compared to that in CG. Acidobacteria and Thermi were specifically observed in DFG and CG, respectively. Besides, 15 fecal microbiotas were significantly altered at the genus level in DFG. Furthermore, only the expression of annotated genes for pentose and glucuronate interconversion pathway was significant lower in DFG than that in CG (P = 0.04). Notably, in NaF-treated rats, we also observed the changes of some key components of pentose and glucuronate interconversion pathway at the level of microorganisms and metabolites. Our findings suggested that the occurrence of DF is closely related to the alteration of intestinal microorganisms and metabolites annotated in the pentose and glucuronate interconversion pathway.

Abstract Background The intellectual loss induced by fluoride exposure has been extensively studied, but the association between fluoride exposure in different susceptibility windows and children’s intelligence is rarely reported. Hence, we conducted a cross-sectional study to explore the association between fluoride exposure in prenatal and childhood periods and intelligence quotient (IQ). Methods We recruited 633 local children aged 7–13 years old randomly from four primary schools in Kaifeng, China in 2017. The children were divided into four groups, of which included: control group (CG, n = 228), only prenatal excessive fluoride exposure group (PFG, n = 107), only childhood excessive fluoride exposure group (CFG, n = 157), both prenatal and childhood excessive fluoride exposure group (BFG, n = 141). The concentrations of urinary fluoride (UF) and urinary creatinine (UCr) were determined by fluoride ion-selective electrode assay and a creatinine assay kit (picric acid method), respectively. The concentration of UCr-adjusted urinary fluoride (CUF) was calculated. IQ score was assessed using the second revision of the Combined Raven’s Test-The Rural in China (CRT-RC2). Threshold and saturation effects analysis, multiple linear regression analysis and logistic regression analysis were conducted to analyze the association between fluoride exposure and IQ. Results The mean IQ score in PFG was respectively lower than those in CG, CFG and BFG (P

Bioaerosols containing pathogens released from wastewater treatment plants (WWTP) may pose potential health risks to workers on-site and residents downwind. In this study, sampling points were set up in the wastewater treatment facility to investigate the generation pattern of bioaerosols in the aeration tank section. High-throughput sequencing was utilized to assay the intestinal bacteria population, while the health risks associated with airborne bacteria were estimated based on average daily dose rates. The contribution of wastewater to bioaerosols was evaluated using the traceability analysis. As the rotational speed increased from 200 rpm to 800 rpm, the concentration of culturable bacteria increased from 397 CFU/m3 to 1611 CFU/m3, the proportion of bacteria attached to particles with an aerodynamic diameter larger than 4.7 µm increased from 30.41% to 48.44%, and the Shannon index of air samples increased from 1.032485 to 1.282065. Microbial composition, sources, and health risks of bioaerosols also changed as the rotational speed increased. The results showed that the predominant bacteria in the air at 200 rpm were Bacillus (78.78%), Paenibacillus (11.77%) and Lysinibacillus (1.40%). When the rotating speed reached 800 rpm, the dominant bacteria became Bacillus (55.50%), Acinetobacter (31.01%), and Paenarthrobacter (13.17%). The contribution of the wastewater to bioaerosols increased from 46.49% to 65.10%, in which surface water was the main source of bioaerosols (34.64% on average). Although the contribution of bottom water was lower than that of surface water, its contribution increased more, from 15.36% to 29.31%. The health risk of bioaerosols was 1.28 × 10−2 on average, which increased with the increase of rotational speed. At the same exposure concentration, children (2.31 × 10−2) have a higher exposure risk than adults (7.67 × 10−3). This study is aimed at exploring the variation law of bioaerosols discharged from WWTP with oxidation ditch process and providing preliminary data for reducing its risk.

The main etiological mechanism for Kashin-Beck disease (KBD) is deep chondrocyte necrosis induced by environmental risk factors (ERFs). The scholars have conducted several epidemiological, cellular, and animal model studies on ERFs. Gradually, four etiological hypotheses have been formed, including water of organic poisoning hypothesis represented by fulvic acid (FA), biogeochemical hypothesis represented by selenium (Se) deficiency, food mycotoxin poisoning hypothesis represented by T-2 toxin poisoning and compound etiology theory hypothesis. The animal models of KBD have been replicated based on the previous etiological hypotheses. The different species of animals (monkey, rat, dog, pig, chicken, and rabbit) were treated with different ERFs interventions, and the clinical manifestations and pathological changes of articular cartilages were observed. The animals in the experimental group were fed with endemic water, endemic grain, low nutrition, thallium sulfate, FA, Se, T-2 toxin, and iodine. The dose of thallium sulfate was 1154 μg/d; the doses range of FA were 5, 50, 150, 200, and 211 mg/kg; the doses range of Se were 0.00035, 0.00175, 0.005, 0.02, 0.031, 0.1, 0.15, 0.314, 0.5, and 10 mg/kg; the doses range of T-2 toxin were 40, 100, 200, 600, 1000, 1500, 3000, 6000, and 9000 ng/g; and the doses range of iodine were 0.04, 0.18, and 0.4–0.5 μg/g. The sample size ranged from 9 to 230 depending on the interventions and grouping; the follow-up duration ranged from 1 week to 18 months. Moreover, the methods and comparisons of different animal models of KBD had been summarized to provide a useful basis for studying the pathogenesis of KBD. In conclusion, the rhesus monkeys administrated endemic water and grain were susceptible animals to replicate KBD. The rats treated with T-2 toxin combined with Se/nutrition deficiency could be a suitable and widely used animal model.

To identify the role of the Hippo signaling pathway in the extracellular matrix degradation of chondrocytes induced by fluoride exposure. Environmental response genes (ERGs) of bone injury induced by fluoride exposure were obtained from the Comparative Toxicogenomics Database, and annotated by STRING for KEGG pathway enrichment analysis. The CCK-8 kit was used to measure the proliferation of ATDC5 cells. The malondialdehyde (MDA), total antioxidant capacity (T-AOC), total superoxide dismutase (T-SOD), and glutathione peroxidase (GSH-PX) levels in ATDC5 cells were measured using oxidative stress detection kit. Western blot analysis was used to measure the p-MST1/2, p-LATS1/2, and p-YAP/YAP1 expression levels in the Hippo pathway and the COL2A1, ACAN and MMP13 expression levels in the cartilage matrix. Localizations of YAP1 and COL2A1 proteins in chondrocytes were performed using cell immunofluorescence. Continuous data from the multiple groups were compared using one-way analysis of variance, and then the differences between groups were tested with Dunnett's t-test, with the test level α = 0.05. The 145 ERGs of bone injury induced by fluoride exposure were identified, and KEGG enrichment analysis revealed Hippo signaling pathways significantly related to bone injury. A CCK-8 assay revealed that the viability of the ATDC5 cells was significantly decreased with increased fluorine concentration. The MDA content in 20 mg/L sodium fluoride (NaF) exposure group was significantly higher than that in the control group, the T-SOD, T-AOC and GSH-PX activities in 15 and 20 mg/L NaF exposure groups were significantly lower than those in the control group (P

Excessive fluoride exposure and epigenetic change can induce numerous adverse health outcomes, but the role of epigenetics underneath the harmful health effects induced by fluoride exposure is unclear. In such gap, we evaluated the associations between fluoride exposure and genome-wide DNA methylation, and identified that novel candidate genes associated with fluoride exposure. A total of 931 school-age children (8–12 years) in Tongxu County of Henan Province (China) were recruited in 2017. Urinary fluoride (UF) concentrations were measured using the national standardized ion selective electrode method. Participants were divided into a high fluoride-exposure group (HFG) and control group (CG) according to the UF concentrations. Candidate differentially methylated regions (DMRs) were screened by Infinium-Methylation EPIC BeadChip of DNA samples collected from 16 participants (eight each from each group). Differentially methylated genes (DMGs) containing DMRs associated with skeletal and neuronal development influenced by fluoride exposure were confirmed using MethylTarget™ technology from 100 participants (fifty each from each group). DMGs were verified by quantitative methylation specific PCR from 815 participants. Serum levels of hormones were measured by auto biochemical analyzer. The mediation analysis of methylation in the effect of fluoride exposure on hormone levels was also performed. A total of 237 differentially methylated sites (DMSs) and 212 DMRs were found in different fluoride-exposure groups in the epigenome-wide phase. Methylation of the target sequences of neuronatin (NNAT), calcitonin-related polypeptide alpha (CALCA) and methylenetetrahydrofolate dehydrogenase 1 showed significant difference between the HFG and CG. Each 0.06% (95% CI: −0.11%, −0.01%) decreased in NNAT methylation status correlated with each increase of 1.0 mg/L in UF concentration in 815 school-age children using QMSP. Also, each 1.88% (95% CI: 0.04%, 3.72%) increase in CALCA methylation status correlated with each increase of 1.0 mg/L in UF concentration. The mediating effect of NNAT methylation was found in alterations of ACTH levels influenced by fluoride exposure, with a β value of 11.7% (95% CI: 3.4%, 33.4%). In conclusion, long-term fluoride exposure affected the methylation pattern of genomic DNA. NNAT and CALCA as DMGs might be susceptible to fluoride exposure in school-age children.

This study examined the neuroprotective properties of resveratrol (Res) and its target sirtuin1 (SIRT1) against lead (Pb)-mediated toxicity and discovered that both resveratrol treatment and SIRT1 overexpression restored blocked autophagic flux as well as reduced β-amyloid (Aβ) contents. Four-week-old male C57BL/6 mice were employed to consumed 0.2% Pb(Ac)2 solution or deionized water for 3 months followed by 12 months of Res (50 mg/kg BW) or vehicle gavage. In in vitro study, SH-SY5Y cells were pretreated with the SIRT1 activator SRT1720 (2 μM) or the inhibitor EX527 (2 μM) for 2 h, then 25 μM of Pb(Ac)2 was added and incubated for 48 h. Western blotting, RT-qPCR, enzyme-linked immunosorbent assay (ELISA), and Lyso-Tracker Red Staining were next used to estimate the potential alterations of the autophagic pathway as well as BACE1-mediated amyloid processing in response to Pb exposure, respectively. Our data revealed that Res treatment or SIRT1 activation resisted the induction of autophagy by Pb exposure through inhibition of LC3 and Beclin-1 expression and promoted the degradation of Aβ and Tau phosphorylation. Besides, the SIRT1 activator (SRT1720) downregulated the expression of BACE1, the rate-limiting enzyme for Aβ production, by inhibiting the activation of nuclear factor-κB (NF-κB) in Pb-treated SH-SY5Y cells, which resulted in reduced Aβ production. Collectively, we verified the role of Res-SIRT1-autophagy as well as the SIRT1-NF-κB-BACE1 pathway in Pb-induced neuronal cell injury by in vivo or in vitro models. Our findings further elucidate the important role of SIRT1 and Res in counteracting Pb neurotoxicity, which may provide new interventions and targets for the subsequent treatment of neurodegenerative diseases.

Abstract Background Evidence shows that low serum vitamin D concentrations account for an increased risk of obesity by inducing vitamin D receptor (VDR) hypofunction. Although the correlation between single nucleotide polymorphisms (SNPs) of VDR gene and obesity-related anthropometric measures (such as body mass index [BMI] and waist circumference[WC]) has already been tested, there are only few studies on the association between direct measures of body fat percentage (BFP) and triceps skinfold thickness and the SNPs of VDR. The aim of the present study was to evaluate the effect of VDR gene polymorphism on multiple obesity indexes in Han Chinese, including BMI, WC, BFP and triceps skinfold thickness. Methods In this cross-sectional study, five hundred and seventeen healthy Chinese adults were enrolled in the trial. Four loci in VDR gene (rs2228570 [FokI], rs2189480, rs2239179 and rs7975232[ApaI]) were genotyped by TaqMan probe assays. Obesity indexes including BMI, WC, BFP and triceps skinfold thickness were used to evaluate the relationship to the VDR SNPs. Multiple logistic regression, linear regression and general multifactor dimensionality reduction (GMDR) were performed to analyze the correlation of VDR gene and obesity indexes. Results None of the VDR SNPs were associated with BMI and WC, the C allele of FokI and the T allele of ApaI were associated with an increase in BFP (β = 0.069,P = 0.007; β = 0.087, P = 0.022 respectively); the G allele of rs2239179 and the T allele of ApaI were associated with an increase in triceps skin fold thickness (β = 0.074, P = 0.001; β = 0.122, P

This article has been retracted. Please see the Retraction Notice for more detail: https://doi.org/10.1186/s12889-020-09765-4.

Objective: This study is aimed to explore the potential association among the estrogen receptor alpha (ESRα) promoter methylation, lipid metabolism and the risk of type 2 diabetes mellitus (T2DM).Methods: A total of 1143 rural residents were recruited randomly from Henan Province, China. The circulating methylation levels in ESRα promoter region were determined by quantitative methylation-specific polymerase chain reaction. Serum high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), triglyceride (TG), total cholesterol (TC) and fasting plasma-glucose (FPG) were measured.Results: The ESRα promoter methylation levels were negatively associated with HDL-C levels whether gender stratification was performed (P < 0.05) and positively correlated with LDL-C in men (P < 0.05). Each unit standard deviation (SD) increment in TG was associated with a 43% increase (95% CI: 1.25, 1.64) in the risks of T2DM in all participants, a 36% increase (95% CI: 1.13, 1.64) in the risks of T2DM in men and a 49% increase (95% CI: 1.21, 1.83) in the risks of T2DM in women. Furthermore, each SD increment in HDL-C was associated with a reduction of 25% (OR = 0.75, 95% CI: 0.58, 0.97) in the risks of T2DM in men, and the risk of T2DM in men may be more susceptible to HDL-C than that in women (P for interaction < 0.05). Additionally, we found that the risk of T2DM in participants with lower methylation levels (≤4.07%) were more susceptible to HDL-C (P for interaction < 0.05).Conclusions: These findings suggested that lipid metabolism was associated with ESRα promoter methylation levels and the risk of T2DM. Besides, the levels of ESRα promoter methylation and gender can modify the association of HDL-C and T2DM.

Circulating water is used as the working medium in water-based chillers. Salt ions, such as calcium in circulating water, may precipitate during long-term operation, resulting in the attenuation of heat transfer performance. The application of small-diameter tubes in heat exchangers may lead to more prominent fouling problems. This study developed an accelerated fouling method to evaluate water fouling risk. The most typical operating conditions for water-based chillers were selected as the experimental conditions. The test samples included small diameter (5 mm) smooth tubes, with 7 mm smooth tubes selected for the control experiment. The experimental conditions include a circulating water inlet temperature of 60 ℃, a flow rate of 1 m/s, a foulant mass concentration of 800 mg/L, and a test time of 0-400 h. The results revealed that the total fouling mass was 39.5% higher and required fouling time was 17.6% shorter when comparing the 5 mm and 7 mm smooth tubes; the small diameter tubes had a larger total fouling mass and higher fouling rate. The heat transfer coefficients of the 5 mm and 7 mm tubes after fouling decreased by 12.5% and 9.7%, respectively, and the pressure drops increased by 50.6% and 10.4%, respectively, demonstrating a more severe heat transfer performance deterioration of small diameter tubes after fouling. The microscopic observation results of the fouling layer morphology demonstrated that the fouling layer in 5 mm tubes is a form of compact lamellar scaling, which is more difficult to remove compared with the 7 mm tube; therefore, the fouling risk should be considered when promoting the application of small diameter tubes in chillers.

Abstract Background Coronary Artery Spasm (CAS) often presents in the epicardial coronary arteries. The anterior septal branch is distributed within the myocardium, and occurrences of spasms are rare. Currently, there is no available literature on this topic, and the onset of symptoms remains elusive, potentially leading to misdiagnosis. Case presentation We present a case of acute myocardial infarction (AMI) caused by spasm in the anterior septal branch, accompanied by transient right bundle branch block (RBBB). The administration of nitroglycerin via intracoronary injection resulted in the alleviation of spasm in the anterior septal branch and the disappearance of RBBB. After the administration of anti-coronary spasm medications, the patient exhibited favorable recovery outcomes. No episodes of myocardial ischemia were observed during the six-month follow-up. Conclusions The presence of new RBBB in patients may warrant consideration of anterior septal coronary artery spasm, which necessitates urgent coronary angiography to clarify the underlying cause and facilitate the prompt initiation of anti-spasm treatment.

Abstract Considering a universal deep neural network organized as a series of nested qubit rotations, accomplished by adjustable data re-uploads we analyze its expressivity. This ability to approximate continuous functions in regression tasks is quantified making use of a partial Fourier decomposition of the generated output and systematically benchmarked with the aid of a teacher-student scheme. While the maximal expressive power increases with the depth of the network and the number of qubits, it is fundamentally bounded by the data encoding mechanism. However, we show that the measurement of the network generated output drastically modifies the attainability of this bound. Global-entangling measurements on the network can saturate the maximal expressive bound leading to an enhancement of the approximation capabilities of the network compared to local readouts of the individual qubits in non-entangling networks. We attribute this enhancement to a larger survival set of Fourier harmonics when decomposing the output signal.

Abstract Exploring the ground state properties of many-body quantum systems conventionally involves adiabatic processes, alongside exact diagonalization, in the context of quantum annealing or adiabatic quantum computation. Shortcuts to adiabaticity by counter-diabatic driving serve to accelerate these processes by suppressing energy excitations. Motivated by this, we develop variational quantum algorithms incorporating the auxiliary counter-diabatic interactions, comparing them with digitized adiabatic algorithms. These algorithms are then implemented on gate-based quantum circuits to explore the ground states of the Fermi-Hubbard model on honeycomb lattices, utilizing systems with up to 26 qubits. The comparison reveals that the counter-diabatic inspired ansatz is superior to traditional Hamiltonian variational ansatz. Furthermore, the number and duration of Trotter steps are analyzed to understand and mitigate errors. Given the model’s relevance to materials in condensed matter, our study paves the way for using variational quantum algorithms with counterdiabaticity to explore quantum materials in the noisy intermediate-scale quantum era.

The extremely thick dark mudstone of the Permian Linxi Formation in the Kundu-Taohaiyingzi area of northeastern China is a promising potential area for shale gas prospecting in the periphery of the Songliao Basin. This study involved a geological field survey, outcrop sample collection, and comprehensive geochemical analysis to conduct an in-depth analysis of the organic matter enrichment and hydrocarbon generation potential of the dark mudstone of the target zone, using organic petrology and organic geochemistry. The results show that the thermal maturity of the dark mudstone of the Linxi Formation is in the mature to high-mature stage. The organic matter is dominated by type II kerogen and supplemented by type III kerogen, and the average total organic carbon content is 0.76%, classifying it as a medium-good source rock. The main peak of carbon numbers is primarily distributed between nC17 and nC19, with a smaller amount at nC21. The distribution of n-alkanes follows a pre-peak pattern characterized by medium and low carbon numbers, suggesting that the organic matter originates from aquatic plants, bacteria, and algae. Combined with the fact that the ratios of pristine and phytane (Pr/Ph) are mainly distributed in the range of 0.99â1.33, the sedimentary environment is a weakly reduced to weakly oxidized lacustrine bay. The systematic analysis of the source rocks of the Upper Permian Linxi Formation in the Kundu-Taohaiyingzi area indicates favorable prospects for shale gas exploration. Utilizing a comprehensive superposition method of geological information, this article identified the Yamen GachaâSaihan Tala area as a potential area for shale gas exploration.

BackgroundAnemia is considered a risk factor for cardiovascular disease. However, there is little evidence regarding the relationship between hemoglobin (HB) and cerebral infarction after revascularization in patients with moyamoya disease (MMD). This study aimed to explore the relationship between postoperative cerebral infarction and HB in patients with MMD and to establish a predictive model.MethodsDemographic information and different HB levels (the preoperative and postoperative HB, highest and lowest HB, and mean HB during hospitalization) of 112 patients with MMD were collected, of which 11 had cerebral infarction after revascularization.ResultsIn the binomial logistic regression analysis, low HB levels were an independent risk factor for cerebral infarction after revascularization, which also led to a worse long-term prognosis in patients with MMD. The risk factors, including Pre-HB, Post-HB, type of MMD, and hypertension (HTN), were incorporated into the receiver operating characteristic curve, which yielded an area under the curve (AUC) of 0.83.ConclusionThe prediction model was visualized using a nomogram, and a clinical decision curve was drawn to evaluate the net benefit of clinical decisions.

Abstract One of the key applications of near-term quantum computers has been the development of quantum optimization algorithms. However, these algorithms have largely been focused on qubit-based technologies. Here, we propose a hybrid quantum-classical approximate optimization algorithm for photonic quantum computing, specifically tailored for addressing continuous-variable optimization problems. Inspired by counterdiabatic protocols, our algorithm reduces the required quantum operations for optimization compared to adiabatic protocols. This reduction enables us to tackle non-convex continuous optimization within the near-term era of quantum computing. Through illustrative benchmarking, we show that our approach can outperform existing state-of-the-art hybrid adiabatic quantum algorithms in terms of convergence and implementability. Our algorithm offers a practical and accessible experimental realization, bypassing the need for high-order operations and overcoming experimental constraints. We conduct a proof-of-principle demonstration on Xanadu’s eight-mode nanophotonic quantum chip, successfully showcasing the feasibility and potential impact of the algorithm.

Abstract Background and aims Numerous research have focused on the relationship of metabolic markers and stroke risk, yet limited research has focused on the triglyceride glucose-waist circumference (TyG-WC) index. This study explored the possible association of TyG-WC and stroke among moderately aged and old Chinese adults over 45 years of age. Methods This observational cohort analysis involved 9054 participants from the Chinese Longitudinal Study of Health and Retirement and employed a standardized questionnaire administered via in-person interviews. Cox proportional hazard model, smoothed curve fitting, and threshold effect analysis were conducted for examining the potential nonlinear relationships among TyG-WC and stroke risk. Results Within an average follow-up period of six years, 463 new strokes occurred, representing 5.11% of the total number of patients. After adjusting for possible confounding factors, a nonlinear association between TyG-WC and stroke risk was identified, with a significant dose–response relationship (P = 0.023 for the log-likelihood ratio test). A turning point was identified at the TyG-WC level of 554.48, beyond that the likelihood of stroke increased markedly (HR = 1.323, 95% CI = 1.098–1.594, P = 0.003). Conclusion This study revealed a specific curvilinear association with the TyG-WC score and stroke risk, identifying a key threshold value. This study focused on Chinese middle-aged and senior adults over the age of 45, emphasizing that increased stroke risk is linked to higher TyG-WC levels.