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The concept of precision nutrition was first proposed almost a decade ago. Current research in precision nutrition primarily focuses on comprehending individualized variations in response to dietary intake, with little attention being given to other crucial aspects of precision nutrition. Moreover, there is a dearth of comprehensive review studies that portray the landscape and framework of precision nutrition. This review commences by tracing the historical trajectory of nutritional science, with the aim of dissecting the challenges encountered in nutrition science within the new era of disease profiles. This review also deconstructs the field of precision nutrition into four key components: the proposal of the theory for individualized nutritional requirement phenotypes; the establishment of precise methods for measuring dietary intake and evaluating nutritional status; the creation of multidimensional nutritional intervention strategies that address the aspects of what, how, and when to eat; and the construction of a pathway for the translation and integration of scientific research into healthcare practices, utilizing artificial intelligence and information platforms. Incorporating these four components, this review further discusses prospective avenues that warrant exploration to achieve the objective of enhancing health through precision nutrition.

As people live longer, the burden of aging-related brain diseases, especially dementia, is increasing. Brain aging increases the risk of cognitive impairment, which manifests as a progressive loss of neuron function caused by the impairment of synaptic plasticity via disrupting lipid homeostasis. Therefore, supplemental dietary lipids have the potential to prevent brain aging. This review summarizes the important roles of dietary lipids in brain function from both structure and mechanism perspectives. Epidemiological and animal studies have provided evidence of the functions of polyunsaturated fatty acids (PUFAs) in brain health. The results of interventions indicate that phospholipids—including phosphatidylcholine, phosphatidylserine, and plasmalogen—are efficient in alleviating cognitive impairment during aging, with plasmalogen exhibiting higher efficacy than phosphatidylserine. Plasmalogen is a recognized nutrient used in clinical trials due to its special vinyl ether bonds and abundance in the postsynaptic membrane of neurons. Future research should determine the dose-dependent effects of plasmalogen in alleviating brain-aging diseases and should develop extraction and storage procedures for its clinical application.

Objectives This study aimed to explore the temporal relationship between blood glucose, lipids and body mass index (BMI), and their impacts on atherosclerosis (AS).Design A prospective cohort study was designed.Setting and participants A total of 2659 subjects from Harbin Cohort Study on Diet, Nutrition and Chronic Non-communicable Diseases, and aged from 20 to 74 years were included.Primary and secondary outcome measures Body weight, height, fasting blood glucose (FBG) and 2-hour postprandial glucose (2-h PG), blood lipids including total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-c) and high-density lipoprotein cholesterol (HDL-c) were measured at baseline and follow-up. Brachial ankle pulse wave velocity (baPWV) was examined at follow-up as a marker of AS risk. Logistic regression analysis, cross-lagged path analysis and mediation analysis were performed to explore the temporal relationships between blood glucose, lipids and BMI, and their impacts on AS risk.Results Logistic regression analysis indicated that increased FBG, 2-h PG, TC, TG, LDL-c and BMI were positively associated with AS risk, while increased HDL-c was negatively associated with AS risk. The path coefficients from baseline blood parameters to the follow-up BMI were significantly greater than those from baseline BMI to the follow-up blood parameters. Mediation analysis suggested that increased FBG, 2-h PG, TC, TG and LDL-c could increase AS risk via increasing BMI, the effect intensity from strong to weak was LDL-c>TC>TG>FBG>2 h PG, while increased HDL-c could decrease AS risk via decreasing BMI.Conclusions Changes in blood glucose and lipids could cause change in BMI, which mediated the impacts of blood glucose and lipids on AS risk. These results highlight the importance and provide support for the early and comprehensive strategies of AS prevention and control.

Abstract Background This study aims to investigate potential interactions between maternal smoking around birth (MSAB) and type 2 diabetes (T2D) pathway-specific genetic risks in relation to the development of T2D in offspring. Additionally, it seeks to determine whether and how nutritional factors during different life stages may modify the association between MSAB and risk of T2D. Methods This study included 460,234 participants aged 40 to 69 years, who were initially free of T2D from the UK Biobank. MSAB and breastfeeding were collected by questionnaire. The Alternative health eating index(AHEI) and dietary inflammation index(DII) were calculated. The polygenic risk scores(PRS) of T2D and pathway-specific were established, including β-cell function, proinsulin, obesity, lipodystrophy, liver function and glycated haemoglobin(HbA1c). Cox proportion hazards models were performed to evaluate the gene/diet-MSAB interaction on T2D. The relative excess risk due to additive interaction (RERI) were calculated. Results During a median follow-up period of 12.7 years, we identified 27,342 cases of incident T2D. After adjustment for potential confounders, participants exposed to MSAB had an increased risk of T2D (HR=1.11, 95%CI:1.08-1.14), and this association remained significant among the participants with breastfeeding (HR= HR=1.10, 95%CI: 1.06-1.14). Moreover, among the participants in the highest quartile of AHEI or in the lowest quartile of DII, the association between MSAB and the increased risk of T2D become non-significant (HR=0.94, 95%CI: 0.79-1.13 for AHEI; HR=1.09, 95%CI:0.99-1.20 for DII). Additionally, the association between MSAB and risk of T2D became non-significant among the participants with lower genetic risk of lipodystrophy (HR=1.06, 95%CI:0.99-1.14), and exposed to MSAB with a higher genetic risk for β-cell dysfunction or lipodystrophy additively elevated the risk of T2D(RERI=0.18, 95%CI:0.06-0.30 for β-cell function; RERI=0.16, 95%CI:0.04-0.28 for lipodystrophy). Conclusions This study indicates that maintaining a high dietary quality or lower dietary inflammation in diet may reduce the risk of T2D associated with MSAB, and the combination of higher genetic risk of β-cell dysfunction or lipodystrophy and MSAB significantly elevate the risk of T2D in offspring.

To address the larger numbers of small objects and the issues of occlusion and clustering in UAV aerial photography, which can lead to false positives and missed detections, we propose an improved small object detection algorithm for UAV aerial scenarios called YOLOv8 with tiny prediction head and Space-to-Depth Convolution (HSP-YOLOv8). Firstly, a tiny prediction head specifically for small targets is added to provide higher-resolution feature mapping, enabling better predictions. Secondly, we designed the Space-to-Depth Convolution (SPD-Conv) module to mitigate the loss of small target feature information and enhance the robustness of feature information. Lastly, soft non-maximum suppression (Soft-NMS) is used in the post-processing stage to improve accuracy by significantly reducing false positives in the detection results. In experiments on the Visdrone2019 dataset, the improved algorithm increased the detection precision mAP0.5 and mAP0.5:0.95 values by 11% and 9.8%, respectively, compared to the baseline model YOLOv8s.

This paper primarily studies the path planning problem for UAV formations guided by semantic map information. Our aim is to integrate prior information from semantic maps to provide initial information on task points for UAV formations, thereby planning formation paths that meet practical requirements. Firstly, a semantic segmentation network model based on multi-scale feature extraction and fusion is employed to obtain UAV aerial semantic maps containing environmental information. Secondly, based on the semantic maps, a three-point optimization model for the optimal UAV trajectory is established, and a general formula for calculating the heading angle is proposed to approximately decouple the triangular equation of the optimal trajectory. For large-scale formations and task points, an improved fuzzy clustering algorithm is proposed to classify task points that meet distance constraints by clusters, thereby reducing the computational scale of single samples without changing the sample size and improving the allocation efficiency of the UAV formation path planning model. Experimental data show that the UAV cluster path planning method using angle-optimized fuzzy clustering achieves an 8.6% improvement in total flight range compared to other algorithms and a 17.4% reduction in the number of large-angle turns.

This study primarily studies the shortest-path planning problem for unmanned aerial vehicle (UAV) formations under uncertain target sequences. In order to enhance the efficiency of collaborative search in drone clusters, a compensation look-ahead algorithm based on optimizing the four-point heading angles is proposed. Building upon the receding-horizon algorithm, this method introduces the heading angles of adjacent points to approximately compensate and decouple the triangular equations of the optimal trajectory, and a general formula for calculating the heading angles is proposed. The simulation data indicate that the model using the compensatory look forward algorithm exhibits a maximum improvement of 12.9% compared to other algorithms. Furthermore, to solve the computational complexity and sample size requirements for optimal solutions in the Dubins multiple traveling salesman model, a path-planning model for multiple UAV formations is introduced based on the Euclidean traveling salesman problem (ETSP) pre-allocation. By pre-allocating sub-goals, the model reduces the computational scale of individual samples while maintaining a constant sample size. The simulation results show an 8.4% and 17.5% improvement in sparse regions for the proposed Euclidean Dubins traveling salesman problem (EDTSP) model for takeoff from different points.

Surface α-particle emissivity testing and spectral characterization of two leaded tin spheres (Sn10%Pb90%, Sn63%Pb37%) and one lead-free tin sphere (Sn96.5%Ag3.0%Cu0.5%, SAC305) were carried out. The results show that Sn10%Pb90% Sn spheres have the highest α-particle emissivity; Sn63%Pb37% Sn spheres are the next highest, which is an order of magnitude lower than the α-particle emissivity of Sn10%Pb90% Sn spheres; and SAC305 Sn spheres have the lowest emissivity, which is reduced by about 55.6% compared to the emissivity of Sn63%Pb37% Sn spheres. All three types of tin spheres, after purification treatment, achieved the grade of ultra-low alpha particle emissivity (2·h)). The internal radionuclide traceability of the tin sphere, combined with the energy spectrum, reveals that the emission spectrum of the tin sphere exhibits an obvious “single peak” characteristic, with the peak energy in the interval of 5 MeV~5.5 MeV. Comparative analyses revealed that 210Po is the main nuclide that produces alpha particles, and 210Po originates from the decay of 210Pb. Further Monte Carlo simulations show that α-particles with energies greater than 4.1 MeV in the measured energy spectrum all come from the contribution of radionuclides within 5 μm of the surface layer of the tin sphere, which accounts for 60% of the total radioactivity. Combining the experimental and simulation results, it is found that the internal radionuclides of the tin sphere are characterized by more surface layer and less internal layer. The above results are of great significance for the establishment of α-particle mitigation methods for tin spheres.

Ensemble methods are a reliable way to combine several models to achieve superior performance. However, research on the application of ensemble methods in the remote sensing object detection scenario is mostly overlooked. Two problems arise. First, one unique characteristic of remote sensing object detection is the oriented bounding boxes (OBB) of the objects and the fusion of multiple OBBs requires further research attention. Second, the widely used deep learning object detectors provide a score for each detected object as an indicator of confidence, but how to use these indicators effectively in an ensemble method remains a problem. Trying to address these problems, this article proposes OBBStacking, an ensemble method that is compatible with OBBs and combines the detection results in a learned fashion. This ensemble method helps take first place in the Challenge Track Fine-Grained Object Recognition in High-Resolution Optical Images, which was featured in 2021 Gaofen Challenge on Automated High-Resolution Earth Observation Image Interpretation. The experiments on DOTA dataset and FAIR1M dataset demonstrate the improved performance of OBBStacking and the features of OBBStacking are analyzed.

Background Chronic exposure to elevated levels of saturated fatty acids results in pancreatic β-cell senescence. However, targets and effective agents for preventing stearic acid-induced β-cell senescence are still lacking. Although melatonin administration can protect β-cells against lipotoxicity through anti-senescence processes, the precise underlying mechanisms still need to be explored. Therefore, we investigated the anti-senescence effect of melatonin on stearic acid-treated mouse β-cells and elucidated the possible role of microRNAs in this process. Methods β-Cell senescence was identified by measuring the expression of senescence-related genes and senescence-associated β-galactosidase staining. Gain- and loss-of-function approaches were used to investigate the involvement of microRNAs in stearic acid-evoked β-cell senescence and dysfunction. Bioinformatics analyses and luciferase reporter activity assays were applied to predict the direct targets of microRNAs. Results Long-term exposure to a high concentration of stearic acid-induced senescence and upregulated miR-146a-5p and miR-8114 expression in both mouse islets and β-TC6 cell lines. Melatonin effectively suppressed this process and reduced the levels of these two miRNAs. A remarkable reversibility of stearic acid-induced β-cell senescence and dysfunction was observed after silencing miR-146a-5p and miR-8114. Moreover, V-maf musculoaponeurotic fibrosarcoma oncogene homolog A (Mafa) was verified as a direct target of miR-146a-5p and miR-8114. Melatonin also significantly ameliorated senescence and dysfunction in miR-146a-5pand miR-8114-transfected β-cells. Conclusion These data demonstrate that melatonin protects against stearic acid-induced β-cell senescence by inhibiting miR-146a- 5p and miR-8114 and upregulating Mafa expression. This not only provides novel targets for preventing stearic acid-induced β-cell dysfunction, but also points to melatonin as a promising drug to combat type 2 diabetes progression.

In recent years, neural networks have made pioneering achievements in the field of medical imaging. In particular, deep neural networks based on U-shaped structures are widely used in different medical image segmentation tasks. In order to improve the early diagnosis and clinical decision-making system of lung diseases, it has become a key step to use the neural network for lung segmentation to assist in positioning and observing the shape. There is still the problem of low precision. For the sake of achieving better segmentation accuracy, an optimized pure Transformer U-shaped segmentation is proposed in this article. The optimization segmentation network adopts the method of adding skip connections and performing special splicing processing, which reduces the information loss in the encoding process and increases the information in the decoding process, so as to achieve the purpose of improving the segmentation accuracy. The final experiment shows that our improved network achieves 97.86% accuracy in segmentation of the “Chest Xray Masks and Labels” dataset, which is better than the full convolutional network or the combination of Transformer and convolution.

Although the formation control of multi-agent systems has been widely investigated from various aspects, the problem is still not well resolved, especially for the case of distributed output-feedback formation controller design without input information exchange among neighboring agents. Using relative output information, this paper presents a novel distributed reduced-order estimation of the formation error at a predefined time. Based on the proposed distributed observer, a neural-network-based formation controller is then designed for multi-agent systems with connected graphs. The results are verified by both theoretical demonstration and simulation example.

Sonchus arvensisL. (SA) is a traditional Chinese food and medicine termed “Ju Mai Cai”. The aim of this study was to investigate the protective effects of an aqueous extract of SA on dextran sulfate sodium (DSS) - induced colitis in mice by adjusting the diversity of gut microbiota. Male C57BL/6 mice were randomly divided into four groups: CL (control group); ML group (DSS only); SA group (SA extract); and MS group (SA extract + DSS). The protective effect of SA on ulcerative disease was estimated by several analyses (i.e., body weight loss, diarrhea, bloody stools, disease activity index scores, and hematoxylin and eosin staining). The effect of SA on gut microbiota was determined by analysis of the 16S ribosomal RNA gene sequences. The results indicated that MS significantly attenuated the body weight loss. The disease activity index scores were markedly lower in the MS group versus in the ML group. Moreover, the length of the colon was significantly improved in the MS groups versus in the ML group. Pathological changes were markedly improved following the administration of SA to mice with DSS-induced ulcerative disease. The results of Beta diversity analysis revealed that the composition of gut microbiota was significantly different between groups. Taken together, the results indicated that SA extract may prevent ulcerative colitis.

Objectives This study aimed to explore the vitamin D status of children in northern China and the association between vitamin D and glucose metabolism.Design Cross-sectional study was conducted among child participants and retrospective study designs were conducted among adult participants.Setting and participants Both studies were recruited from Harbin, 326 children were included in children’s study, 8469 adults were included in adult study.Primary and secondary outcome measures Physical examination, lifestyle and dietary habit data were recorded in all the participants. Serum insulin, glucose, 25(OH)D3 concentrations in children and serum glucose and lipids levels in adults were measured. Rickets history was also investigated in adults, which was used to define vitamin D deficiency in childhood. The associations were tested by linear regression and binary logistic regression.Result In the children’s study, only 10.7% of participants were vitamin D sufficient (≥30 ng/mL). Inverse correlations between serum 25(OH)D3 concentration and fasting insulin and homeostasis model assessment - insulin resistance (HOMA-IR) were found, and children with lower serum 25(OH)D3 concentrations were likely to have insulin resistance (IR) (OR: 0.955, 95% CI: 0.917 to 0.995, p value: 0.027). In an adult study, rickets in childhood increased the risk of type 2 diabetes in male participants (OR=1.414, 95% CI=1.013 to 1.972; p value=0.042), but this result was not observed in female participants.Conclusion Our findings suggest that vitamin D deficiency is widespread in northern China. Vitamin D deficiency in childhood was associated with IR and increased the risk of type 2 diabetes in male adults.

Although growing evidence suggests that N,N-diethyl-m-toluamide (DEET) has adverse effects on public health, the relationship of DEET with cardiovascular disease (CVD) is still largely unknown. The purpose of this study was, therefore, to evaluate the association between DEET exposure and total and specific CVD among the US adults. In this cross-sectional study, a total of 5,972 participants were selected from the National Health and Nutrition Examination Survey (NHANES) 2007–2014. CVD was defined as a combination of congestive heart failure (CHF), coronary heart disease (CHD), angina, heart attack, or stroke. Logistic regression models were used to evaluate the association between DEET metabolites and the risks of total and specific CVD. Compared to the lowest quartile, 3-(diethylcarbamoyl) benzoic acid (DCBA) in the highest quartile was associated with the increased risks of CVD (odds ratio [OR]: 1.32, 95% CI: 1.03–1.68, P for trend = 0.025) and CHD (OR: 1.57, 95% CI: 1.10–2.25, P for trend = 0.017), after adjustment for potential covariates. Nevertheless, exposure to DCBA was not significantly associated with heart attack, CHF, angina, and stroke. Further studies are required to confirm these findings and identify the underlying mechanisms.

Background: A long-term consumption of saturated fat significantly increases the concentration of saturated fatty acids in serum, which accelerates the appearance of senescence markers in β-cells and leads to their dysfunction. An understanding of the mechanisms underlying β-cell senescence induced by stearic acid and the exploration of effective agents preventing it remains largely unclear. Here, we aimed to investigate the protective effect of metformin against stearic acid-treated β-cell senescence and to assess the involvement of miR-297b-5p in this process. Methods: To identify senescence, we measured senescence-associated β-galactosidase activity and the expression of senescence-related genes. Gain and loss of function approaches were applied to explore the role of miR-297b-5p in stearic acid-induced β-cell senescence. Bioinformatics analysis and a luciferase activity assay were used to predict the downstream targets of miR-297b-5p. Results: Stearic acid markedly induced senescence and suppressed miR-297b-5p expression in mouse β-TC6 cells, which were significantly alleviated by metformin. After transfection of miR-297b-5p mimics, stearic acid-evoked β-cell senescence was remarkably prevented. Insulin-like growth factor-1 receptor was identified as a direct target of miR-297b-5p. Inhibition of the insulin-like growth factor-1 receptor prevented stearic acid-induced β-cell senescence and dysfunction. Moreover, metformin alleviates the impairment of the miR-297b-5p inhibitor in β-TC6 cells. Additionally, long-term consumption of a high-stearic-acid diet significantly increased senescence and reduced miR-297b-5p expression in mouse islets. Conclusions: These findings imply that metformin alleviates β-cell senescence by stearic acid through upregulating miR-297b-5p to suppress insulin-like growth factor-1 receptor expression, thereby providing a potential target to not only prevent high fat-diet-induced β-cell dysfunction but also for metformin therapy in type 2 diabetes.

Abstract Background Intake time of diet has recently been demonstrated to be associated with the internal clock and circadian pattern. However, whether and how the intake time of minerals would influence the natural course of cancer was largely unknown. Methods This study aimed to assess the association of mineral intake at different periods with cancer and all-cause mortality. A total of 27,455 participants aged 18–85 years old in the National Health and Nutrition Examination Survey were recruited. The main exposures were the mineral intakes in the morning, afternoon and evening, which were categorized into quintiles, respectively. The main outcomes were mortality of cancer and all causes. Results During the 178,182 person-years of follow-up, 2680 deaths, including 601 deaths due to cancer, were documented. After adjusting for potential confounders, compared to the participants who were in the lowest quintile(quintile-1) of mineral intakes at dinner, the participants in the highest quintile intake(quintile-5) of dietary potassium, calcium and magnesium had lower mortality risks of cancer (HRpotassium = 0.72, 95% CI:0.55–0.94, P for trend = 0.023; HRcalcium = 0.74, 95% CI:0.57–0.98, P for trend = 0.05; HRmagnesium = 0.75, 95% CI:0.56–0.99, P for trend = 0.037) and all-cause (HRpotassium = 0.83, 95% CI:0.73–0.94, P for trend = 0.012; HRcalcium = 0.87, 95% CI:0.76–0.99, P for trend = 0.025; HRmagnesium = 0.85, 95% CI:0.74–0.97, P for trend = 0.011; HRcopper = 0.80, 95%CI: 0.68–0.94, P for trend = 0.012). Further, equivalently replacing 10% of dietary potassium, calcium and magnesium consumed in the morning with those in the evening were associated with lower mortality risk of cancer (HRpotassium = 0.94, 95%CI:0.91–0.97; HRcalcium = 0.95, 95%CI:0.92–0.98; HRmagnesium = 0.95, 95%CI: 0.92–0.98). Conclusions This study demonstrated that the optimal intake time of potassium, calcium and magnesium for reducing the risk of cancer and all-cause mortality was in the evening.

Dietary carbohydrate consumption was related to cognitive function. Whereas, there was no study investigate the association of dietary carbohydrate consumption with cognitive function modification by daily fasting duration. This study aims to examine the association between dietary carbohydrate consumption and cognitive function among participants with different daily fasting duration. In this cross-sectional study, 2485 adults aged over 60 years from the nationally representative data of the National Health and Nutrition Examination Survey (NHANES, 2011–2014) were enrolled. Percentage energy from carbohydrates was present in both quartiles and continuous forms. Daily fasting duration = 24 – (timing for dinner – breakfast). Cognitive function was assessed by the Consortium to Establish a Registry for Alzheimer’s Disease Word List Learning (CERAD-WL), CERAD Word List Delayed Recall (CERAD-DR), Animal Fluency (AF), and Digit Symbol Substitution (DSST) Test. Multiple logistic regression and linear regression models were developed to examine the association of dietary carbohydrates with cognitive function among participants with different daily fasting duration. Restricted cubic spline models were also applied. Compared with the lowest quartile of percentage energy from carbohydrates, the highest quartile had higher ORs of poor cognitive performance among total participants [(ORCERAD-WL 1.84 95% CI 1.25–2.71); (ORCERAD-DR 1.45 95% CI 1.10–1.91)] and participants with daily fasting duration fewer than 16 h [(ORCERAD-WL 2.14 95% CI 1.29–3.55); (ORCERAD-DR 1.51 95% CI 1.05–2.17)] but not in participants with daily fasting duration of more than 16 h. Further, the negative associations between percentage energy from carbohydrates and CERAD-WL score were still significant in addition to participants whose daily fasting duration was more than 16 h. Additionally, dose-response associations were detected between dietary carbohydrates and cognitive decline, while “U” curves were observed among participants whose daily fasting duration was more than 16 h. This study indicated that dietary carbohydrates consumption was associated with poor cognitive performance, but not in participants whose daily fasting duration was more than 16 h among US older adults. The current analysis provides evidence that a longer daily fasting duration may improve the harmful effect of dietary carbohydrates on cognitive function.

BackgroundCurrent studies on the protective effects of dietary spermidine (SPD) on cardiovascular disease (CVD) are mainly limited to animal studies, and the relationship between dietary SPD and CVD mortality remains inconclusive.ObjectiveThis study aims to evaluate the association between dietary SPD intake and CVD and all-cause mortality.MethodsA total of 23,894 people enrolled in the National Health and Nutrition Examination Survey (NHANES) from 2003 to 2014 were recruited for this study. The dietary intake of SPD from 11 specific food origins and total SPD was categorized into tertiles or quartiles. Cox proportional hazard regression models were developed to evaluate the association of SPD intake with CVD and all-cause mortalities.ResultsAmong the 23,894 participants, 2,365 deaths, including 736 deaths due to CVD, were documented. After adjustment for potential confounders, compared with participants in the lowest quartile, participants in the highest quartile of total SPD had a significantly lower risk of CVD mortality (HR = 0.68, 95% CI: 0.51–0.91) and all-cause mortality (HR = 0.70, 95% CI: 0.60–0.82); participants in the highest tertiles or quartiles of vegetable-derived SPD, cereal-derived SPD, legume-derived SPD, nut-derived SPD, and cheese-derived SPD had a lower risk of CVD mortality (HR vegetable − derivedSPD = 0.68, 95% CI: 0.54–0.86; HR cereal − derivedSPD = 0.75, 95% CI: 0.57–0.97; HR legume − derivedSPD = 0.68, 95% CI: 0.52–0.88; HR nut − derivedSPD = 0.66, 95% CI: 0.53–0.80; HR cheese − derivedSPD = 0.68, 95% CI: 0.52–0.88) and all-cause mortality (HR vegetable − derivedSPD = 0.73, 95% CI: 0.64–0.84; HR cereal − derivedSPD = 0.80, 95% CI: 0.69–0.93; HR legume − derivedSPD = 0.70, 95% CI: 0.60–0.80;HR nut − derivedSPD = 0.72, 95% CI: 0.64–0.81; HR cheese − derivedSPD = 0.70, 95% CI: 0.61–0.81) than those in the lowest tertiles or quartiles. Moreover, subgroup analysis showed consistent associations among the people with hypertension and hyperlipidemia.ConclusionHigher intake of dietary SPD is associated with decreased risk of CVD and all-cause mortality, and among specific food origin SPD, SPD derived from vegetables, cereals, legumes, nuts, and cheese was associated with reduced CVD and all-cause mortality.

The association between acrylamide (AA) and the development of cancer has been extensively discussed but the results remained controversial, especially in population studies. Large prospective epidemiological studies on the relationship of AA exposure with cancer mortality were still lacking. Therefore, we aimed to assess the association between AA biomarkers and cancer mortality in adult population from National Health and Nutrition Examination Survey (NHANES) 2003-2014. We followed 3717 participants for an average of 10.3 years. Cox regression models with multivariable adjustments were performed to determine the relationship of acrylamide hemoglobin adduct (HbAA) and glycidamide hemoglobin adduct (HbGA) with cancer mortality. Mediation analysis was conducted to demonstrate the mediated role of low-grade inflammation score (INFLA-score) in this correlation. Compared with the lowest quintile, participants with the highest quintile of HbAA, HbGA and HbAA+HbGA had increased cancer mortality risk, and the hazard ratios(HRs) were 2.07 (95%CI:1.04-4.14) for HbAA, 2.39 (95%CI:1.29-4.43) for HbGA and 2.48 (95%CI:1.28-4.80) for HbAA+HbGA, respectively. And there was a considerable non-linearity association between HbAA and cancer mortality (pfor non-linearity = 0.0139). We further found that increased INFLA-score significantly mediated 71.67% in the effect of HbGA exposure on increased cancer mortality risk. This study demonstrates that hemoglobin biomarkers of AA are positively associated with cancer mortality in adult American population and INFLA-score plays a mediated role in this process. Our findings can raise public awareness of environmental and dietary exposure to acrylamide and remind people to refrain from smoking or having acrylamide-rich foods.

BackgroundAcrylamide is a common environmental volatile organic compound that humans are frequently exposed to in their daily lives. However, whether exposure to acrylamide is associated with long-term survival in patients with hyperglycemia remains largely unknown.Methods and ResultsA total of 3,601 hyperglycemic people were recruited in this study, including 1,247 people with diabetes and 2,354 people with pre-diabetes, who enrolled in the National Health and Nutrition Examination survey (2003–2004, 2005–2006, and 2013–2014). The acrylamide exposure was measured by the serum hemoglobin adduct of acrylamide (HbAA) and glycidamide (HbGA), and the ratio of HbAA and HbGA (HbAA/HbGA) was calculated, which were all categorized into quintiles. The National Death Index was used to identify the participants' death information until 2015. Cox proportional hazards (CPHs) regression models were performed to examine the survival relationship between these biomarkers and mortality. During the 28,652 person-year follow-up, 268 deaths due to the cardiovascular disease (CVD) were documented. After adjustment for multiple confounders, compared with participants in the lowest quintile of HbAA/HbGA, the participants in the highest quintile were more likely to die due to CVD (hazard ratio [HR] = 1.61, 95% CI: 1.09–2.39) and all-cause (HR = 1.59, 95% CI: 1.25–2.01). Moreover, subgroup analysis showed that the highest quintile of HbAA/HbGA in the people with diabetes or pre-diabetes was related to mortalities risk of CVD (HRdiabetes = 1.92, 95% CI: 1.11–3.31; HRpre−diabetes = 1.78, 95% CI: 1.01–3.14) and all-cause mortality (HRdiabetes = 1.81, 95% CI: 1.27–2.58; HRpre−diabetes = 1.59, 95% CI: 1.14–2.20). Additionally, no significant association between the levels of HbAA or HbGA and CVD mortality was observed among people with diabetes or pre-diabetes.ConclusionHigher levels of HbAA/HbGA are associated with greater mortalities of CVD and all-cause among hyperglycemic people.

AbstractBackground Associations of dietary or supplementary intake of several unsaturated fatty acids and mortality have been widely studied but the results were still hitherto inconsistent or limited. It is still need to explore the effects of these fatty acids by using the objective biomarkers.Objective We aimed to investigate the relevancy of several serum n-3 and n-6 fatty acids with all-cause and disease-specific mortality to confirm their health effects and effects on the associations between dietary quality and all-cause mortality.Methods A total of 4132 people from NHANES 2003–2004 and 2011–2012 and the mortality information was confirmed from the NDI. CPH models adjusted for known risk factors were conducted to explore the associations between circulating n-3 and n-6 fatty acids and all-cause or CVD or cancer mortality under complex sampling. We further evaluated their effects on association between dietary quality and all-cause mortality.Results A total of 437 deaths occurred during the mean follow-up of 83.34 months, including 157 CVD death and 100 cancer death. Serum LA, ALA, EPA and DHA were associated with all-cause mortality (HR in quintile5: LA:0.584, 95%CI: 0.387–0.882, Ptrend = 0.011; ALA:0.626, 95%CI: 0.432–0.907, Ptrend = 0.008; EPA:0.535, 95%CI: 0.375–0.764, Ptrend = 0.001; DHA:0.669, 95%CI: 0.468–0.955, Ptrend = 0.031). Additionally, serum EPA and ALA were respectively related to CVD and cancer mortality (Q5 HR: EPA:0.450, 95%CI: 0.23–0.854, Ptrend = 0.009; ALA:0.387, 95%CI: 0.167–0.900, Ptrend = 0.022). Serum AA, GLA, DGLA and SDA were not associated with any risk of mortality. The effect on all-cause mortality of the lower AHEI scores can be improved by adherence to a higher serum LA, EPA and DHA (in the lowest AHEI strata, LA in tertile3 compared to tertile1 HR:0.596, 95%CI: 0.366–0.970; EPA:0.660, 95%CI: 0.454–0.959; DHA:0.666, 95%CI; 0.444–1.000).Conclusions Our results support the recent dietary recommendations to increase the intake of plant-derived and marine-derived n-6 and n-3 to improve the ability of primary and secondary prevention.

Abstract Background We previously identified the urinary biomarkers to diagnose calcium deficiency and nutritional rickets by ultra-performance liquid chromatography/quadrupole time-of-flight tandem mass spectrometry (UPLC/Q-TOF MS/MS). To find biomarkers of calcium deficiency and further confirm these biomarkers in serum, we performed serum metabolomics analysis of calcium-deficient rats. Methods A calcium-deficient rat model was established with a low-calcium diet for 12 weeks. Serum metabolomics based UPLC/Q-TOF MS/MS and multivariate statistical analysis was performed to identify the alterations in metabolites associated with calcium deficiency in rats. Results Bone mineral density, serum parathyroid hormone and alkaline phosphatase were significantly decreased in the low-calcium diet group (LCG) compared to the normal calcium diet group (NCG). Serum metabolic-profiling analysis could definitively distinguish between the LCG and NCG and identified 24 calcium-deficient biomarkers. Three metabolites (indoxyl sulfate, phosphate, and taurine) of the 24 biomarkers were found in our previous urinary metabolomics study of rats with a calcium deficiency and nutritional rickets. The areas under the curve (AUCs) of these three biomarkers were greater than 0.8, and the combination of any two biomarkers was higher than 0.95. Conclusion Dietary calcium deficiency induced the alterations of metabolites in the serum of rats, and the three identified biomarkers had relatively high diagnostic values for calcium deficiency in rats.

Breast cancer is one of the most common and deadliest cancers among women. Since histopathological images contain sufficient phenotypic information, they play an indispensable role in the diagnosis and treatment of breast cancers. To improve the accuracy and objectivity of Breast Histopathological Image Analysis (BHIA), Artificial Neural Network (ANN) approaches are widely used in the segmentation and classification tasks of breast histopathological images. In this review, we present a comprehensive overview of the BHIA techniques based on ANNs. First of all, we categorize the BHIA systems into classical and deep neural networks for in-depth investigation. Then, the relevant studies based on BHIA systems are presented. After that, we analyze the existing models to discover the most suitable algorithms. Finally, publicly accessible datasets, along with their download links, are provided for the convenience of future researchers.

The aims of this research are to elucidate whether serum retinol is associated with type 2 diabetes and to explore the underlying mechanisms of the association in a prospective cohort study. A total of 3,526 diabetes-free participants aged 40 years or older were enrolled at baseline in 2010–2012. Multivariable logistic regression was adopted to evaluate the associations of serum retinol and dietary vitamin A (VA) intake with type 2 diabetes. Mediation analyses were used to reveal potential mediators in their associations. After a mean follow-up of 5.3 years, 280 incident cases of type 2 diabetes occurred. Serum retinol was positively associated with the incidence of type 2 diabetes. The multivariable-adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for type 2 diabetes from the bottom to the top quintile of serum retinol were 1, 1.878 (1.202, 2.936), 2.110 (1.364, 3.263), 1.614 (1.027, 2.538), and 2.134 (1.377, 3.306) (p-trend = 0.009), respectively. Mediation analysis showed that increased homeostasis model assessment - insulin resistance HOMA-IR, triglycerides (TG), and serum xanthine oxidase (XO) activity could account for 8.5, 14.7, and 12.1% of the total effects of serum retinol on type 2 diabetes, respectively. Serum retinol concentration was not significantly associated with dietary VA intake (r = −0.010, p = 0.570). In addition, no significant relationship was observed between dietary VA intake and the risk of type 2 diabetes. Overall, elevated serum retinol might increase the risk of type 2 diabetes which is mainly mediated by increased insulin resistance, TG, or serum XO activity.

Fatty acid amides (FAAs) are endogenous lipid molecules that exhibit various physiological activities. FAAs are usually present at nanomolar levels in biological samples. In this study, a method for the qualitative and quantitative determination of six FAAs (linoleamide, linoleoyl ethanolamide, oleoyl ethanolamide, palmitic amide, oleamide, and octadecanamide) in edible vegetable oils was established. All six FAAs were detected in sesame, peanut, soybean (decolorized and non-decolorized), and blended oils; five in sunflower oil; four in rice oil; three in linseed and olive oils; and two in corn and canola oils. The total contents of FAAs were highest in sesame oil (104.88 ± 3.01 μg/mL), followed by peanut oil (34.96 ± 3.87 μg/mL), soybean oil (16.75 ± 1.27 μg/mL), and blended oil (13.33 ± 0.77 μg/mL), and the contents in the other edible vegetable oils were all

Although there has been increasing recognition that famine exposure in the fetal stage damages liver function in adulthood, this deteriorated effect could be extended to the next generation remains vague. This study aimed to explore whether famine exposure was associated with liver function in the two consecutive generations, and its association with the mediation role of inflammatory markers. We analyzed the data of 2,681 participants from Suihua rural area, Heilongjiang Province, China. According to the date of birth, the participants were classified as fetal exposed and nonexposed. The F2 subjects were classified as having no parents exposed to famine, maternal famine exposure, paternal famine exposure, or parental famine exposure. In the mixed-effect models, prenatal exposure to famine was associated with the elevation of Δ aspartate aminotransferase (ΔAST) (β: 0.22, 95% CI: 0.01, 0.43) and Δ alanine aminotransferase (ΔALT) (β: 0.42, 95% CI: 0.19, 0.66) levels in F1 adults. The mediation analysis showed that the inflammatory markers including serum C-reactive protein (CRP) and tumor necrosis factor-alpha (TNF-α) might mediate the famine-liver function association. This longitudinal data were consistent with the hypothesis that the inflammatory markers explained part of the influence of prenatal famine exposure on liver function injury, and the natal mechanism was needed to be elucidated in the future study.

Background: Calcium is an essential element in our diet and the most abundant mineral in the body. A high proportion of Chinese residents are not meeting dietary calcium recommendations. The purpose of this study was to investigate the relationship between calcium intake and the health of residents in two longitudinal studies of Chinese residents.Methods: This study used nationally representative data from the Harbin Cohort Study on Diet, Nutrition, and Chronic Non-communicable Disease Study (HDNNCDS) and China Health Nutrition Survey (CHNS), including 6,499 and 8,140 Chinese adults, respectively, who were free of chronic diseases at recruitment, with mean values of 4.2- and 5.3-year follow-up. Cox's proportional-hazards regression was conducted to explore the relationship between dietary calcium intake and the incidence of obesity, type 2 diabetes, hypertension, and cardiovascular disease (CVD) with adjustment for covariates.Results: Calcium intakes were 451.35 ± 203.56 and 484.32 ± 198.61 (mean ± SD) mg/day in HDNNCDS and CHNS. After adjusting the covariates, the relationship between dietary calcium intake and bone mineral density (BMD) was not statistically significant (p = 0.110). In the multivariate-adjusted Cox's proportional-hazards regression model, dietary calcium intakes were inversely associated with obesity incidence in both cohorts (HR [95% CI]: 0.61 [0.48–0.77] and p trend < 0.001 in fixed-effects model); nevertheless, there was no correlation between dietary calcium intake and the risk of type 2 diabetes (p trend = 0.442 and 0.759) and CVD (p trend = 0.826 and 0.072). The relationship between dietary calcium intake and the risk of hypertension in the two cohorts was inconsistent (p trend = 0.012 and 0.559). Additionally, after further adjusting the vegetable intake in the original multivariate model, both cohorts found no association between dietary calcium intake and the risk of developing obesity (p trend = 0.084 and 0.444).Conclusions: Our data suggest that the current calcium intake of Chinese residents was inversely associated with obesity, which may be related to consumption of vegetables. Meanwhile, the current calcium intake does not increase the risk of type 2 diabetes, CVD, and bone health burden. This research suggested that the Chinese current calcium intake level may have met the needs of the body.

Background: The health impacts of dietary fat-to-energy ratio (FER) compared to carbohydrate-to-energy ratio (CER) are widely discussed topics in public health. This study aimed to assess the health impacts of FER and CER by establishing trajectory-patterns of FER and CER over the course of adult life.Methods: This study used the weighted longitudinal data of the China Health and Nutrition Survey, including eight surveys from 1991 to 2011. The trajectories of FER and CER were determined via latent class trajectory modeling. The trajectories were then cross-grouped into different trajectory-patterns. Multivariate Cox regression models were used to assess the relationship between these trajectory-patterns and cardio-metabolic diseases and all-cause mortality. Ten thousand nine hundred and twenty-six adults with a total of 50,693 observations across eight surveys were included.Results: Compared to the trajectory-pattern of persistently low-FER (increased from 10 to 20%) and moderate-CER (stable and ranging from 55 to 65%) over the adult life-course, the two trajectory-patterns that showed changing to high-FER and low-CER were significantly associated with obesity [HR 1.83 [95% CI, 1.10–3.04]; HR 1.46 [95% CI, 1.02–2.17]], diabetes [HR 1.80 [95% CI, 1.03–3.16]; HR 1.49 [95% CI, 1.01–2.25]], and all-cause mortality [HR 2.29 [95% CI, 1.35–3.87]; HR 1.62 [95% CI, 1.18–2.22]]. In contrast, the trajectory-pattern of a persistently low-FER and high-CER diet was not associated with obesity [HR 1.19 [95% CI, 0.82–1.17]], diabetes [HR 1.41 [95% CI, 0.98–2.02]], cardiovascular-disease [HR 1.48 [95% CI, 0.91–2.39]], and all-cause mortality [HR 1.23 [95% CI, 0.94–1.61]].Conclusions: This study indicates that changing to a high-FER and low-CER diet over the course of adult life was significantly associated with obesity, diabetes, and all-cause mortality in the Chinese adult population. In addition, low-FER and high-CER were not associated with cardio-metabolic disease and all-cause mortality. These observations may provide insights into nutritional policy and dietary guidelines.

Objective This study aimed to investigate the association between the trajectories of energy consumption at dinner versus breakfast and the risk of type 2 diabetes (T2D).Design Cohort study.Setting The study was conducted in China.Participants A total of 10 727 adults, including 5239 men and 5488 women, with a mean age of 42.7±11.2 years and a mean follow-up time of 9.1 years, met the study criteria and completed a questionnaire about energy intake and diabetes status from the China Health and Nutrition Survey in 1997–2011.Primary outcome measures Participants were divided into subgroups based on the trajectories of the ratio of energy consumption at dinner versus breakfast. Cox multivariate regression models were used to explore the associations between different trajectories and the risk of T2D after adjustment for confounders and their risk factors. Mediation analysis was performed to explore the intermediary effect of triacylglycerol (TG), total cholesterol (TC), uric acid (UA) and apolipoprotein B (ApoB) between the trajectories and the risk of T2D.Results For energy consumption at dinner versus breakfast, compared with a low-stable trajectory, the adjusted HR of T2D in low-increasing from early-stage trajectory was 1.29 (95% CI 1.04 to 1.60). TG, TC, UA and ApoB were significantly higher in low-increasing from early-stage trajectory than other trajectories and play partial regulation roles between trajectories and T2D.Conclusions This study emphasised the harmful effect of a gradual increase in the ratio of energy consumption at dinner versus breakfast from early stage on the development of T2D and partially mediated by TG, TC, UA and ApoB, highlighting that it is necessary to intake more energy at breakfast compared with dinner to prevent T2D in adults.

Background Although accumulating evidence has demonstrated that consumption time of energy and macronutrients plays an important role in maintaining health, the association between consumption time of different foods and cardiovascular disease, cancer, and all‐cause mortalities is still largely unknown. Methods and Results A noninstitutionalized household population of the US 21 503 participants from National Health and Nutrition Examination Survey was included. Meal patterns and snack patterns throughout a whole day were measured using 24‐hour dietary recall. Principal component analysis was performed to establish dietary patterns. Cox proportional hazards models were used to evaluate the association between dietary patterns across meals and cardiovascular disease (CVD), cancer, and all‐cause mortalities. During the 149 875 person‐years of follow‐up, 2192 deaths including 676 deaths because of CVD and 476 because of cancer were documented. After adjusting for potential confounders, participants consuming fruit‐lunch had lower mortality risks of all‐cause (hazard ratio [HR], 0.82; 95% CI, 0.72–0.92) and CVD (HR, 0.66; 95% CI, 0.49–0.87); whereas participants who consumed Western‐lunch were more likely to die because of CVD (HR, 1.44; 95% CI, 1.10–1.89). Participants who consumed vegetable‐dinner had lower mortality risks of all‐cause, CVD, and cancer (HRall‐cause, 0.69; 95% CI, 0.60–0.78; HRCVD, 0.77; 95% CI, 0.61–0.95; HRcancer, 0.63; 95% CI, 0.48–0.83). For the snack patterns, participants who consumed fruit‐snack after breakfast had lower mortality risks of all‐cause and cancer (HRall‐cause, 0.78; 95% CI, 0.66–0.93; HRcancer, 0.55; 95% CI, 0.39–0.78), and participants who consumed dairy‐snack after dinner had lower risks of all‐cause and CVD mortalities (HRall‐cause, 0.82; 95% CI, 0.72–0.94; HRCVD, 0.67; 95% CI, 0.52–0.87). Participants who consumed a starchy‐snack after main meals had greater mortality risks of all‐cause (HRafter‐breakfast, 1.50; 95% CI, 1.24–1.82; HRafter‐lunch, 1.52; 95% CI, 1.27–1.81; HRafter‐dinner, 1.50; 95% CI, 1.25–1.80) and CVD (HRafter‐breakfast, 1.55; 95% CI, 1.08–2.24; HRafter‐lunch, 1.44; 95% CI, 1.03–2.02; HRafter‐dinner, 1.57; 95% CI, 1.10–2.23). Conclusions Fruit‐snack after breakfast, fruit‐lunch, vegetable‐dinner, and dairy‐snack after dinner was associated with lower mortality risks of CVD, cancer, and all‐cause; whereas Western‐lunch and starchy‐snack after main meals had greater CVD and all‐cause mortalities.

miR-29a-3p has been shown to be associated with cardiovascular diseases; however, the effect of miR-29a-3p on endothelial dysfunction is unclear. This study aimed to reveal the effects and mechanisms of miR-29a-3p on endothelial dysfunction. The levels of vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), and E-selectin were determined by real-time PCR and immunofluorescence staining to reveal the degree of tumor necrosis factor alpha (TNFα)-induced endothelial dysfunction. A luciferase activity assay and cell transfection with a miR-29a-3p mimic or an inhibitor were used to reveal the underlying mechanisms of miR-29a-3p action. Furthermore, the effects of miR-29a-3p on endothelial dysfunction were assessed in C57BL/6 mice injected with TNFα and/or a miR-29a-3p agomir. The results showed that the expression of TNFα-induced adhesion molecules in vascular endothelial cells (EA.hy926 cells, human aortic endothelial cells [HAECs], and primary human umbilical vein endothelial cells [pHUVECs]) and smooth muscle cells (human umbilical vein smooth muscle cells [HUVSMCs]) was significantly decreased following transfection with miR-29a-3p. This effect was reversed by cotransfection with a miR-29a-3p inhibitor. As a key target of miR-29a-3p, tumor necrosis factor receptor 1 mediated the effect of miR-29a-3p. Moreover, miR-29a-3p decreased the plasma levels of TNFα-induced VCAM-1 (32.62%), ICAM-1 (38.22%), and E-selectin (39.32%) in vivo. These data indicate that miR-29a-3p plays a protective role in TNFα-induced endothelial dysfunction, suggesting that miR-29a-3p is a novel target for the prevention and treatment of atherosclerosis. Keywords: miR-29a-3p, TNF-R1, adhesion molecules, endothelial dysfunction, atherosclerosis

Abstract Background Hepatic insulin resistance (IR) plays a crucial role in the development of many metabolic diseases, such as type 2 diabetes. MicroRNAs (miRNAs) are involved in the pathogenesis of IR and related diseases; however, studies of miRNAs in hepatic IR are limited. Method In this study, we adopted a high-throughput sequencing approach to construct small RNA libraries in the livers of normal mice and high-fat diet-induced hepatic IR mice. Results Through analysis of data, 107 known and 56 novel miRNAs were identified as differentially expressed miRNAs between the two groups. Additionally, bioinformatics methods were used to predict targets of the differentially expressed miRNAs and to explore the potential downstream Gene Ontology categories and Kyoto Encyclopedia of Genes and Genomes pathways. Meanwhile, some differentially expressed miRNAs (miR-34a-5p, miR-149-5p, miR-335-3p, miR-10b-5p, miR-1a-3p, miR-411-5p, and miR-592-5p) were validated by quantitative-time PCR, and their potential target genes related to IR or glycolipid metabolism were also predicted and presented in this study. Conclusion Taken together, our results defined miRNA expression signature that may lead to hepatic IR in mice, and the findings provided a foundation for future studies to further explore the effects and underlying mechanisms of the miRNAs and their target genes in the pathogenesis of hepatic IR and related diseases.

This paper investigates the problem of distributed constrained consensus of utilities for multiple networked nodes, which is essentially challenging in view of the fact that local constraints may hinder the global optimization across the network. Focusing on this problem, a generalized framework is developed via a self evaluation approach, in which each node uses utility evaluations to update individual states by interacting with neighbors only. Following the framework, the distributed constrained consensus algorithms is derived, with theoretical analyses presented to show the convergence and stability. In addition, an approximation method is proposed as well for ease of engineering implementation. Finally, illustrative examples are provided and analyzed to substantiate the efficacy of the proposed algorithm.

Dibromoacetic acid (DBA) is a by-product of disinfection in drinking water, which could cause many adverse effects in test animals. However, little research on its neurotoxicity has been conducted, and its mechanism has not been elucidated. In the present study, ninety Sprague−Dawley rats were administered DBA at doses of 0, 30, and 90 mg/kg body weight for 28 days via oral gavage. We found that DBA could induce obvious neurotoxicity in the pineal gland as indicated by histological changes and impaired rhythm of melatonin in pineal and serum. In the mechanism study, transcriptome data showed that DBA exposure could induce 732 differential expression genes. Besides, GO and KEGG analysis results indicated that these genes were enriched in circadian rhythms, among which CREB1 had the most significant fold change. And immunofluorescence staining (IF) and immunohistochemical staining (IHC) results showed that the number of amber-colored masculine neurons for the p-CREB1 in the 90 mg/kg group was markedly lower, and staining for the p-CREB1 was weaker. Moreover, the results of PCR and western blot showed that DBA exposure could down-regulate the expressions of CREB1 and p-CREB1, leading to the decreased expressions of gene and protein of arylalkylamine N-acetyltransferase (AANAT), and then resulting in the impaired melatonin synthesis in the pineal and serum. In conclusion, DBA exposure is associated with abnormal melatonin rhythm via inhibition of the p-CREB1-AANAT signalling pathway.

Abstract Introduction Dichloroacetic acid (DCA), a by‐product of disinfection in drinking water, is a multiple organ carcinogen in humans and animals. Still, little research on its neurotoxicity and its underlying mechanism has not been elucidated. Methods Sprague Dawley rats were intragastrically treated with DCA at 10, 30, 90 mg/kg body weight from pregnancy till delivery. At eight weeks of age of pups, we assessed cognitive performance using the standard behavioral tests. And the hippocampus structure and ultrastructure were evaluated using light and electron microscope. The oxidative stress indicators and neuroinflammation factors were measured with the corresponding kits. The mRNA and protein of synaptic factors were detected using RT‐PCR and Western blot. Results The results indicated that maternal weight gain and offspring birthweight were not significantly affected by DCA. However, behavioral tests, including morris water maze and step down, showed varying degrees of changes in DCA‐treated pups. Additionally, we found significant differences in hippocampal neurons by histomorphological observation. Biochemical analysis results indicated superoxide dismutase (SOD) and catalase (CAT) activities, as well as reactive oxygen species (ROS), nitric oxide (NO), and reduced glutathione (GSH) levels, were affected by DCA accompanying with DNA damage. Moreover, the results showed that the neuroinflammation factors (TNF‐α, IL‐6, IL‐1β) in DCA treatment groups increased significantly compared with the control pups. And we also found that DCA treatment caused a differential modulation of proteins (BDNF, cAMP‐response element‐binding protein1 (CREB1), p‐CREB1, postsynaptic density‐95 (PSD‐95), synapsin I, p‐synapsin I), and mRNA (BDNF, PSD‐95). Conclusions Taken together, these results above showed that oxidative stress, neuroinflammation response, and weakened synaptic plasticity in pups hippocampus induced by fetal exposure to DCA could damage the function of memory and cognition in the adulthood.

The relationship between soy intake (SI) and breast cancer (BC) has been widely investigated with limited information on the significance of hormone receptor status of BC on the association. This study assessed the relationship between SI and BC risk in the context of oestrogen receptor (ER) status of BC. We meta-analyzed data from published studies on SI and BC after a methodical search of EMBASE, PubMed and Cochrane Library through December 2019. Summary estimates with 95% confidence intervals (CI) were presented using a random-effects model. Eighteen (5 cohorts and 13 case-control) studies, were included in this meta-analysis and SI was inversely associated with BC risk [OR (95%) for highest vs. lowest soy food intake = 0.88 (0.84–0.92), P < 0.001, I2 = 76.1%, Egger's p-value = 0.425] among all women. The inverse relationship was stronger among premenopausal women [OR (95%) = 0.79 (0.71–0.87), P < 0.001, I2 = 77.3%, Egger's p-value = 0.644]. In addition, SI was inversely associated with BC risk among ER-negative (–) BC women [OR (95%) = 0.71 (0.57–0.90), P = 0.013, I2 = 72.0%, Egger's p-value = 0.355] and among ER-positive (+) BC women [OR (95%) = 0.87 (0.79–0.96), P = 0.008 I2 = 74.6%, Egger's p-value = 0.061]. SI appears inversely associated with BC risk, with a stronger inverse association among pre-menopausal and ER-negative BC women.

For large-scale wireless sensor networks, the nonlinear localization problem where only neighboring distances are available to each individual sensor nodes have been attracting great research attention. In general, distributed algorithms for this problem are likely to suffer from the failures that localizations are trapped in local minima. Focusing on this issue, this article considers a fully distributed algorithm by introducing a novel mechanism, where each individual node is allowed to computationally interact with a random subset of its neighbors, for helping localizations escape from local minima. Theoretical analyses reveal that with the proposed algorithm, any local minimum of the localization will be unstable, and the global optimum would finally be achieved with probability 1 after enough time of iterations. Numerical simulations are given as well to demonstrate the effectiveness of the algorithm.

Background/Aims: Ovarian cancer (OC) is a malignant neoplasm of the female reproductive system with a high mortality rate. Identifying useful biomarkers and clarifying the molecular pathogenesis of OC are critical for early diagnosis and treatment. The aim of the study was to identify candidate biomarkers and explore metabolic changes of OC. Methods: A two-stage design was used in our study, with a discovery cohort of OC cases (n = 30) and controls (n = 30) and an independent cohort of cases (n = 17) and controls (n = 18) for validation. The serum metabolic profiling was investigated by ultra-performance liquid chromatography and quadrupole time-of-fight mass spectrometry with positive electrospray ionization. Results: A total of 18 metabolites closely related to OC were identified in the discovery stage, of which 12 were confirmed in the validation cohort. Metabolic pathways in OC related to these biomarkers included fatty acid β-oxidation, phospholipid metabolism, and bile acid metabolism, which are closely related to the proliferation, invasion, and metastasis of cancer cells. Multiple logistic regression analysis of these metabolites showed that 2-piperidinone and 1-heptadecanoylglycerophosphoethanolamine were potential biomarkers of OC, with high sensitivity (96.7%), specificity (66.7%), and area under the receiver operating characteristic curve value (0.894). Conclusion: These findings provide insight into the pathogenesis pathogenesis of OC and may be useful for clinical diagnosis and treatment.

Abstract Background The aims of the current study were to assess the nutritional status of 25OHD3 and retinol in a northern Chinese population using our established reliable method for the simultaneous determination of serum 25OHD3 and retinol. Method We established a reliable method for the simultaneous determination of 25OHD3 and retinol using SPE and UPLC/PDA; measured the serum levels of 25OHD3 and retinol in elementary school students, middle school students, and adults (n = 1181) in northern China; and assessed their nutritional status. Results Our method had good precision, detection limit, and linear quantitative range and could process 100 samples within 12 h. The average levels of 25OHD3 and retinol were 16.1 ± 6.7 ng/ml and 328.1 ± 117.1 ng/ml, respectively, in all samples. VD deficiency was common, with a prevalence > 60% in all three age groups, and the high prevalence of VA deficiency (26.1%) was observed only in the elementary school students. Conclusions Vitamin A supplementation should be considered for elementary school students, and vitamin D supplementation is highly recommended for all age groups in Harbin. Our method could be widely adopted in population-based studies and clinical practice.

4-Hydroxynonenal (4-HNE) is a critical lipid peroxidation product induced by oxidative stress that has been implicated in the pathophysiology of non-alcoholic fatty liver disease (NAFLD). We previously reported that histidine ameliorated oxidative stress in both obese women and high-fat diet (HFD)-induced rats. However, the mechanism of histidine against liver injury in NAFLD remains unclear. This study aimed to investigate the effect of histidine supplementation on alleviating HFD-induced liver injury. Histidine relieved both HFD-induced liver injury and 4-HNE-induced hepatotoxicity. Histidine acted partly by inhibiting both c-Jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) pathways in paralle, while the reactive oxygen species-mediated MAPKs axes were also implicated in the protective role of histidine. Histidine reversed 4-HNE-protein adducts formation in both rat liver and hepatocytes. These findings suggest that increased histidine intake may be a potential therapeutic choice for NAFLD.

Abstract We conducted a comprehensive and in-depth assessment of body mass index (BMI) or waist circumference (WC) related to blood pressure (BP) and determined whether the association is mediated by the possible potential mediators in the cross-sectional survey of the Harbin Cohort Study on Diet, Nutrition and Chronic Non-communicable Diseases of 7094 participants aged 20–74 years, and validated the significant findings in the US National Health and Nutrition Examination Survey four cross-sectional cohorts (2005–2006, 2007–2008, 2009–2010, and 2011–2012) and the cohort data of the Harbin People’s Health Study (a median of 4.2 follow-up years). We observed that BMI or WC was positively associated with BP (all P-values

Background/Aims: Atherosclerosis is a multifactorial chronic disease and is the main cause of death and impairment in the world. Endothelial injury and apoptosis play a crucial role in the onset and development of atherosclerosis. MicroRNAs (miRNAs) have been proven to be involved in the pathogenesis of atherosclerosis. However, studies of the functional role of apoptosis-related miRNAs in the endothelium during atherogenesis are limited. Methods: Cell injury and apoptosis were measured in five types of cells transfected with miR-1185 or co-transfected with miR-1185 and its inhibitor. Bioinformatics analysis and a luciferase reporter assay were used to confirm the targets of miR-1185. The effects of the targets of miR-1185 on endothelial apoptosis were determined using small-interfering RNA. Results: In this study, we first report that miR-1185 significantly promoted apoptosis in endothelial cells but not in vascular smooth muscle cells and macrophages. A mechanistic analysis showed that ultraviolet irradiation resistance-associated gene (UVRAG) and krev1 interaction trapped gene 1 (KRIT1), targets of miR-1185, mediated miR-1185-induced endothelial cell apoptosis. Conclusion: The results revealed the impact of miR-1185 on endothelial apoptosis, suggesting that miR-1185 may be a potential target for the prevention and treatment of atherosclerosis.

Serratia marcescens, a gram-negative bacterium, found in a wide range of ecological niches can produce several high-value products, including prodigiosin, althiomycin, and serratamolide. Among them, prodigiosin has attracted attention due to its immunosuppressive, antimicrobial, and anticancer properties. However, the regulatory mechanisms behind prodigiosin synthesis in Serratia marcescens remains limited. Here, a transposon mutant library was constructed to identify the genes related to prodigiosin synthesis, and BVG90_02415 gene encoding a peptidoglycan synthesizing enzyme D-Ala-D-Ala carboxypeptidase DacA was found to negatively regulates prodigiosin synthesis. Quantitative measurements revealed that disruption of dacA increased prodigiosin production 1.46-fold that of the wild-type strain JNB5-1 in fermentation medium. By comparing differences in cell growth, pigA gene expression level, cell morphology, membrane permeability, and intracellular prodigiosin concentration between wild-type strain JNB5-1 and dacA mutant SK4-72, results revealed that the mechanism for hyper-producing of prodigiosin by the dacA mutant was probably that dacA disruption enhanced prodigiosin leakage, which in turn alleviated feedback inhibition of prodigiosin and increased expression of pig gene cluster. Collectively, this work provides a novel insight into regulatory mechanisms of prodigiosin synthesis and uncovers new roles of DacA protein in regulating cell growth, cell morphology, and membrane permeability in Serratia marcescens. Finally, this study offers a new strategy for improving production of high-value compounds in Serratia marcescens.

Background The temporal sequence between serum calcium and insulin resistance (IR) and their effects on hypertension are unclear. We studied the association between serum calcium and IR, with risk of hypertension events in a longitudinal cohort conducted in China. Methods and Results Data from 8653 subjects aged 20 to 74 years with an average follow‐up of 5.3 years were analyzed. Serum calcium, and fasting and 2‐hour serum glucose and insulin were measured at baseline and follow‐up. Cross‐lagged panel and mediation analysis were used to examine the temporal relationship between serum calcium and IR and its impact on hypertension incidence. The conjoint effects of serum calcium and IR at baseline on hypertension at follow‐up were observed (P=0.029 for HOMA_IR [hepatic IR] and P=0.009 for Gutt index [peripheral IR]). The cross‐lagged path coefficient (β2) from baseline serum calcium to follow‐up peripheral IR were significantly greater than path coefficient (β1) from baseline peripheral insulin resistance to follow‐up serum calcium (β2 =−0.354 versus β1=−0.005; P=0.027). However, no directional relationships were observed in the serum calcium↔hepatic IR analysis. The mediation effect of peripheral IR on the association of serum calcium at baseline with hypertension at follow‐up was estimated at 16.4% (P

Ursolic acid is a naturally occurring pentacyclic triterpenoid in many plants, such as medicinal herbs and food, and was previously found to be an effective phytochemical that protected against high-fat diet-induced hepatic steatosis and liver injury. However, the molecular mechanisms are not fully determined. The present study examined the protective role of ursolic acid against saturated fatty acid-induced lipotoxicity. We found that ursolic acid protected HepG2 (hepatocellular carcinoma, human) cells against palmitate-induced cell death and mitochondrial dysfunction. The protective activity was the result of ursolic acid-induced autophagy, and an autophagy inhibitor prevented this protective effect. Ursolic acid activated/phosphorylated adenosine monophosphate-activated protein kinase (AMPK) and reduced phosphorylation of mammalian target of rapamycin. AMPK gene knockdown by siRNA transfection abolished the protective effect of ursolic acid. Ursolic acid induced autophagy in HepG2 cells to protect against palmitate-induced cell death via an AMPK/mTOR pathway.

Despite growing interest in the protective role that dietary antioxidant vitamins may have in the development of type 2 diabetes (T2D), little epidemiological evidence is available in non-Western populations especially about the possible mediators underlying in this role. The present study aimed to investigate the association of vitamin C and vitamin E intakes with T2D risk in Chinese adults and examine the potential mediators. 178 incident T2D cases among 3483 participants in the Harbin People Health Study (HPHS), and 522 newly diagnosed T2D among 7595 participants in the Harbin Cohort Study on Diet, Nutrition and Chronic Non-communicable Diseases (HDNNCDS) were studied. In the multivariable-adjusted logistics regression model, the relative risks (RRs) were 1.00, 0.75, and 0.76 (Ptrend = 0.003) across tertiles of vitamin C intake in the HDNNCDS, and this association was validated in the HPHS with RRs of 1.00, 0.47, and 0.46 (Ptrend = 0.002). The RRs were 1.00, 0.72, and 0.76 (Ptrend = 0.039) when T2D diagnosed by haemoglobin A1c in the HDNNCDS. The mediation analysis discovered that insulin resistance (indicated by homeostasis model assessment) and oxidative stress (indicated by plasma total antioxidative capacity) partly mediated this association. But no association was evident between vitamin E intake and T2D. In conclusion, our research adds further support to the role of vitamin C intake in reducing the development of T2D in the broader population studied. The results also suggested that this association was partly mediated by inhibiting or ameliorating oxidative stress and insulin resistance.

There is no diabetes risk model that includes dietary predictors in Asia. We sought to develop a diet-containing noninvasive diabetes risk model in Northern China and to evaluate whether dietary predictors can improve model performance and predictive ability. Cross-sectional data for 9,734 adults aged 20-74 years old were used as the derivation data, and results obtained for a cohort of 4,515 adults with 4.2 years of follow-up were used as the validation data. We used a logistic regression model to develop a diet-containing noninvasive risk model. Akaike's information criterion (AIC), area under curve (AUC), integrated discrimination improvements (IDI), net classification improvement (NRI) and calibration statistics were calculated to explicitly assess the effect of dietary predictors on a diabetes risk model. A diet-containing type 2 diabetes risk model was developed. The significant dietary predictors including the consumption of staple foods, livestock, eggs, potato, dairy products, fresh fruit and vegetables were included in the risk model. Dietary predictors improved the noninvasive diabetes risk model with a significant increase in the AUC (delta AUC = 0.03, P

A prospect of increasing penetration of uncoordinated electric vehicles (EVs) together with intermittent renewable energy generation in microgrid systems has motivated us to explore an effective strategy for safe and economic operation of such distributed generation systems. This paper presents a robust economic dispatch strategy for grid-connected microgrids. Uncertainty from wind power and EV charging loads is modeled as an uncertain set of interval predictions. Considering the worst case scenario, the proposed strategy can help to regulate the EV charging behaviors, and distributed generation in order to reduce operation cost under practical constraints. To address the issue of over-conservatism of robust optimization, a dispatch interval coefficient is introduced to adjust the level of robustness with probabilistic bounds on constraints, which gradually improves the system's economic efficiency. In addition, in order to facilitate the decision-making strategies from an economic perspective, this paper explores the relationship between the volatility of uncertain parameters and the economy based on the theory of interval forecast. Numerical case studies demonstrate the feasibility and robustness of the proposed dispatch strategy.