Acute kidney injury in hospitalized patients with nonmalignant pleural effusions: a retrospective cohort study.

BACKGROUND: Nonmalignant pleural effusion (NMPE) is common and remains a definite health care problem. Pleural effusion was supposed to be a risk factor for acute kidney injury (AKI). Incidence of AKI in NMPE patients and whether there is correlation between the size of effusions and AKI is unknown. OBJECTIVE: To assess the incidence of AKI in NMPE inpatients and its association with effusion size. STUDY DESIGN AND METHOD: We conducted a retrospective cohort study of inpatients admitted to the Chinese PLA General Hospital with pleural effusion from 2018-2021. All patients with pleural effusions confirmed by chest radiography (CT or X-ray) were included, excluding patients with diagnosis of malignancy, chronic dialysis, end-stage renal disease (ESRD), community-acquired AKI, hospital-acquired AKI before chest radiography, and fewer than two serum creatinine tests during hospitalization. Multivariate logistic regression and LASSO logistic regression models were used to identify risk factors associated with AKI. Subgroup analyses and interaction tests for effusion volume were performed adjusted for the variables selected by LASSO. Causal mediation analysis was used to estimate the mediating effect of heart failure, pneumonia, and eGFR < 60 ml/min/1.73m2 on AKI through effusion volume. RESULTS: NMPE was present in 7.8% of internal medicine inpatients. Of the 3047 patients included, 360 (11.8%) developed AKI during hospitalization. After adjustment by covariates selected by LASSO, moderate and large effusions increased the risk of AKI compared with small effusions (moderate: OR 1.47, 95%CI 1.11-1.94 p = 0.006; large: OR 1.86, 95%CI 1.05-3.20 p = 0.028). No significant modification effect was observed among age, gender, diabetes, bilateral effusions, and eGFR. Volume of effusions mediated 6.8% (p = 0.005), 4.0% (p = 0.046) and 4.6% (p < 0.001) of the effect of heart failure, pneumonia and low eGFR on the development of AKI respectively. CONCLUSION: The incidence of AKI is high among NMPE patients. Moderate and large effusion volume is independently associated with AKI compared to small size. The effusion size acts as a mediator in heart failure, pneumonia, and eGFR.

POLR3-related leukodystrophy caused by biallelic POLR3A and 1C pathogenic variants: a single-center experience.

Objectives: This study aimed to investigate the clinical, radiological, and genetic features of POLR3-related leukodystrophy caused by mutations in POLR3A or POLR1C. Methods: Fourteen Chinese patients with POLR3-related leukodystrophy were enrolled in this cross-sectional observational study. The clinical manifestations, brain MRI and genetic tests of the patients were evaluated. Results: Thirteen patients had biallelic variants in POLR3A (92.9%), and one had biallelic variants in POLR1C (7.1%). The median age at disease onset was 9 months. A total of 85.7% of the patients presented with motor delay, abnormal gait, and intelligence disability in the first 2 years of life. Intellectual disability can be categorized based on its severity. It varied from mild (which involves difficulty concentrating) to very severe (with no smiling or laughing or never being able to speak since birth). Short stature was observed in all patients, and delayed dentition was observed in 64.3% of them. Furthermore, three out of 14 patients had myopia. Hypomyelination was invariably present in all patients, whereas myelination of the basal ganglia was preserved in only six out of 14 patients. All the mutations were compound heterozygous and included missense (n = 25), deletion (n = 1), and splice site variants (n = 2). A total of 78.6% of the patients with POLR3A were identified as carrying the c.1771-6C>G variant or the c.1771-7C>G variant. Conclusion: The phenotypic diversity of POLR3-HLD associated with pathogenic variants ranges from mild to very severe for neurological and non-neurological symptoms. Most patients presented symptoms in the first 2 years of life. The c.1771-6C>G or c.1771-7C>G variant is the most frequent mutation site in POLR3A in Chinese individuals.

A Luminescent Cd-MOF Used as a Chemosensor for High-Efficiency Sensing of Fe3+, Cr(IV), Trinitrophenol, and Colchicine.

A Cd-MOF was constructed based on 3,5-bis(4-carboxyphenyl) pyridine under solvothermal conditions. Its structure and phase purity were verified by single-crystal X-ray diffraction. Thereafter, some studies on the morphology, structure, and luminescent properties of the compound were carried out. The compound exhibited a highly sensitive response to Fe3+, Cr(IV), trinitrophenol (TNP), and colchicine based on the fluorescence-quenching mechanism. The possible mechanism of luminescence quenching was discussed in detail.

CT-based radiomics for differentiating peripherally located pulmonary sclerosing pneumocytoma from carcinoid.

BACKGROUND: Pulmonary sclerosing pneumocytoma (PSP) and pulmonary carcinoid (PC) are difficult to distinguish based on conventional imaging examinations. In recent years, radiomics has been used to discriminate benign from malignant pulmonary lesions. However, the value of radiomics based on computed tomography (CT) images to differentiate PSP from PC has not been well explored. PURPOSE: We aimed to investigate the feasibility of radiomics in the differentiation between PSP and PC. METHODS: Fifty-three PSP and fifty-five PC were retrospectively enrolled and then were randomly divided into the training and test sets. Univariate and multivariable logistic analyses were carried to select clinical predictor related to differential diagnosis of PSP and PC. A total of 1316 radiomics features were extracted from the unenhanced CT (UECT) and contrast-enhanced CT (CECT) images, respectively. The minimum redundancy maximum relevance and the least absolute shrinkage and selection operator were used to select the most significant radiomics features to construct radiomics models. The clinical predictor and radiomics features were integrated to develop combined models. Two senior radiologists independently categorized each patient into PSP or PC group based on traditional CT method. The performances of clinical, radiomics, and combined models in differentiating PSP from PC were investigated by the receiver operating characteristic (ROC) curve. The diagnostic performance was also compared between the combined models and radiologists. RESULTS: In regard to differentiating PSP from PC, the area under the curves (AUCs) of the clinical, radiomics, and combined models were 0.87, 0.96, and 0.99 in the training set UECT, and were 0.87, 0.97, and 0.98 in the training set CECT, respectively. The AUCs of the clinical, radiomics, and combined models were 0.84, 0.92, and 0.97 in the test set UECT, and were 0.84, 0.93, and 0.98 in the test set CECT, respectively. In regard to the differentiation between PSP and PC, the combined model was comparable to the radiomics model, but outperformed the clinical model and the two radiologists, whether in the test set UECT or CECT. CONCLUSIONS: Radiomics approaches show promise in distinguishing between PSP and PC. Moreover, the integration of clinical predictor (gender) has the potential to enhance the diagnostic performance even further.

Causal effects of inflammatory bowel disease on risk of type 2 diabetes: a two-sample multivariable Mendelian randomization study.

AIM: This study aimed to explore the causal association between inflammatory bowel disease (IBD) and the risk of type 2 diabetes (T2D) based on a two-sample Mendelian randomization (MR) study. METHODS: Summary single nucleotide polymorphism (SNP)-phenotype association data were obtained from published two genome-wide association studies (GWAS) including SNPs related to IBD, UC, or CD in European participants (n = 71,997) and East Asian participants (n = 16,805). Two GWAS including SNPs associated with T2D included 655,666 Europeans and 433,540 East Asians. A series of screening processes were performed to select qualified instrumental SNPs strongly related to exposure. We applied the inverse variance weighted (IVW), the MR-Egger regression, and the weighted median to estimate the causal effects of IBD, ulcerative colitis (UC) or Crohn' disease (CD) on T2D. Cochran's Q test was conducted to evaluate the statistical heterogeneity between SNPs in the IVW method. The leave-one-out analysis was employed to assess whether the results were caused by any single SNP associated with IBD, UC, or CD. Odds ratio (OR) and 95% confidence interval (CI) were calculated. RESULTS: The IVW results demonstrated that IBD could increase the risk of T2D in the European population (OR = 1.0230, 95%CI: 1.0073-1.0390). UC was positively associated with the risk of T2D according to the weighted median (OR = 1.0274, 95%CI: 1.0009-1.0546) and IVW (OR = 1.0244, 95%CI: 1.0071-1.0421) results in the European population. The IVW results indicated that the CD was positively associated with the risk of T2D in the European population (OR = 1.0187, 95%CI: 1.0045-1.0330). In the East Asian population, there are no associations between the IBD, UC, or CD and the risk of T2D (all P > 0.05). MVMR results revealed that the causal effect UC on T2D was still statistically significant after including body mass index (BMI) or low-density lipoprotein (LDL). CONCLUSION: IBD, UC, or CD had causal effects on the risk of T2D in the European population, which might provide evidence for the prevention of T2D in patients with IBD, UC, or CD.

Progress in the study of aging marker criteria in human populations.

The use of human aging markers, which are physiological, biochemical and molecular indicators of structural or functional degeneration associated with aging, is the fundamental basis of individualized aging assessments. Identifying methods for selecting markers has become a primary and vital aspect of aging research. However, there is no clear consensus or uniform principle on the criteria for screening aging markers. Therefore, we combine previous research from our center and summarize the criteria for screening aging markers in previous population studies, which are discussed in three aspects: functional perspective, operational implementation perspective and methodological perspective. Finally, an evaluation framework has been established, and the criteria are categorized into three levels based on their importance, which can help assess the extent to which a candidate biomarker may be feasible, valid, and useful for a specific use context.

Characterization of tomato autophagy-related SlCOST family genes.

Autophagy is a eukaryote-specific cellular process that can engulf unwanted targets with double-membrane autophagosomes and subject them to the vacuole or lysosome for breaking down and recycling, playing dual roles in plant growth and environmental adaptions. However, perception of specific environmental signals for autophagy induction is largely unknown, limiting its application in agricultural usage. Identification of plant-unique DUF641 family COST1 (Constitutively Stressed 1) protein directly links drought perception and autophagy induction, shedding light on manipulating autophagy for breeding stress tolerant crops. In this study, we performed a genome-wide analysis of DUF641/COST family in tomato, and identified five SlCOST genes SlCOST1, -2, -3, -4, and -5. SlCOST genes show both overlapping and distinct expression patterns in plant growth and stress responding. In addition, SlCOST1, -3, -4, -5 proteins demonstrate co-localization with autophagy adaptor protein ATG8e, and all five SlCOST proteins show interactions ATG8e in planta. However, only SlCOST1, the closest ortholog of Arabidopsis AtCOST1, can restore cost1 mutant to WT level, suggesting conserved role of COST1 and functional diversification of SlCOST family in tomato. Our study provides clues for future investigation of autophagy-related COST family and its promising implementations in breeding crops with robust environmental plasticity.

Arterial stiffness is associated with handgrip strength in relatively healthy Chinese older adults.

Background: Increased arterial stiffness and low handgrip strength (HGS) are associated with poor health outcomes and are a severe health risk for older adults. However, there is limited evidence and mixed results on whether there is an association between them. Therefore, this study focused on the association between arterial stiffness and HGS in relatively healthy older adults in Beijing, China. Methods: In 2016, 2,217 adult volunteers were recruited in Beijing. Brachial-ankle pulse wave velocity (baPWV) and the ankle-brachial index were measured using an automatic vascular profiling system. Carotid artery intima-media thickness and common carotid artery-internal diameter (CCAID) were evaluated using Doppler ultrasound, and HGS was measured with a dynamometer. Low HGS was determined using the Asian Sarcopenia Working Group 2019 criteria. Multivariate linear and logistic regressions evaluated the relationship between arterial stiffness and HGS. Results: Ultimately, 776 relatively healthy older adults (mean age 69.05 ± 6.46 years) were included. Based on the AWGS2019 criteria, 137 participants were defined as having low HGS. Compared to the normal HGS group, the low HGS group was older and had higher baPWV (p < 0.001) but lower CCAID, body mass index (BMI) and hemoglobin (Hb) (p < 0.05). The multiple linear regression analysis revealed that baPWV was negatively correlated with HGS (ß = -0.173, t = -2.587, p = 0.01). Multivariate logistic regression analysis showed that baPWV and CCAID were associated with an increased risk of low HGS (odds ratio (OR) per SD increase: 1.318, p = 0.007; OR per SD increase: 0.541, p < 0.001). Conclusion: Arterial stiffness and HGS were significantly negatively correlated in relatively healthy Chinese older adults. Low HGS is associated with increased arterial stiffness. Encouraging exercise training to improve HGS, thereby reducing arterial stiffness and the risk of cardiovascular events, may be a simple and effective intervention.

Enhanced TRPC3 transcription through AT1R/PKA/CREB signaling contributes to mitochondrial dysfunction in renal tubular epithelial cells in D-galactose-induced accelerated aging mice.

Aging-associated renal dysfunction promotes the pathogenesis of chronic kidney disease. Mitochondrial dysfunction in renal tubular epithelial cells is a hallmark of senescence and leads to accelerated progression of renal disorders. Dysregulated calcium profiles in mitochondria contribute to aging-associated disorders, but the detailed mechanism of this process is not clear. In this study, modulation of the sirtuin 1/angiotensin II type 1 receptor (Sirt1/AT1R) pathway partially attenuated renal glomerular sclerosis, tubular atrophy, and interstitial fibrosis in D-galactose (D-gal)-induced accelerated aging mice. Moreover, modulation of the Sirt1/AT1R pathway improved mitochondrial dysfunction induced by D-gal treatment. Transient receptor potential channel, subtype C, member 3 (TRPC3) upregulation mediated dysregulated cellular and mitochondrial calcium homeostasis during aging. Furthermore, knockdown or knockout (KO) of Trpc3 in mice ameliorated D-gal-induced mitochondrial reactive oxygen species production, membrane potential deterioration, and energy metabolism disorder. Mechanistically, activation of the AT1R/PKA pathway promoted CREB phosphorylation and nucleation of CRE2 binding to the Trpc3 promoter (-1659 to -1648 bp) to enhance transcription. Trpc3 KO significantly improved the renal disorder and cell senescence in D-gal-induced mice. Taken together, these results indicate that TRPC3 upregulation mediates age-related renal disorder and is associated with mitochondrial calcium overload and dysfunction. TRPC3 is a promising therapeutic target for aging-associated renal disorders.

Unlocking digital potential: Exploring the drivers of employee dynamic capability on employee digital performance in Chinese SMEs-moderation effect of competitive climate.

While dynamic capabilities have been described as crucial for achieving organizational performance in dynamic environments, there has been limited scholarly distinction between dynamic capabilities and employee dynamic capabilities (EDC), especially in the digital era. Consequently, a knowledge gap has emerged. To address this void, this paper aims to investigate the driving factors of EDC and their impact on employee digital performance (EDP). Simultaneously, incorporating the competitive climate (CC) as a moderating variable between employee dynamic capabilities and employee digital performance addresses theoretical gaps in specific regions in China, particularly in small and medium-sized enterprises (SMEs). This study utilizes survey data from SMEs in four Chinese provinces: Shanghai, Guizhou, Guangdong, and Anhui. It employs CB-SEM (AMOS) to analyze the new conceptual framework. Firstly, the research uncovers that the positive relationship between digital capabilities and employee digital performance necessitates employee dynamic capabilities as a mediator. Secondly, there exists a direct and indirect relationship between organizational learning and employee digital performance. Finally, this study discerns that the competitive climate moderates the relationship between employee dynamic capabilities and employee digital performance. This finding demonstrates remarkable alignment with the competitive culture in specific regions of China. The research results encourage SMEs to seize the opportunities presented by emerging digital technologies and industry digitization trends. They should commit to embracing new digital technologies, enhancing digital capability, strengthening organizational learning, fostering a positive competitive climate, and focusing on the development of employee dynamic capability to enhance their competitive edge. The findings of this research contribute not only to academic inquiry but also furnish pertinent decision-making references for relevant departments.

A bibliometric analysis of research on the health impacts of ozone air pollution.

Ground-level ozone (O3) is one of the major air pollutants. A large body of literature has linked O3 air pollution to various adverse human health effects. The objective of this study is to attain a comprehensive and in-depth understanding of the progress and frontiers of research on O3 and human health. We used bibliometric methods to summarize publications on O3 air pollution and public health between 1990 and 2022 obtained from the Web of Science Core Collection database. VOSviewer and R software were used for bibliometric analysis and visualization. A total of 4501 relevant papers were included in the analysis. There has been a significant increase in the number of publications since 2013, with the USA being the major contributor, followed by China and England. Harvard University was the most prolific research institution, followed by the US Environmental Protection Agency and the University of North Carolina System. Professor Joel Schwartz was the most published author and has established a complex network of national and international collaborations. Co-occurrence analysis of keywords suggested evolving research hotspots, from toxicological studies to population-based epidemiological studies and from the respiratory system to the extra-pulmonary system. Research on O3 and its human health effects has progressed rapidly over the past few decades, but academic disparities still persist between developed and developing countries. There is an urgent need to strengthen international cooperation to address the public health challenges posed by rising O3 air pollution in the future.

Genotype and phenotype correlation of PHACTR1-related neurological disorders.

BACKGROUND: PHACTR1 (phosphatase and actin regulators) plays a key role in cortical migration and synaptic activity by binding and regulating G-actin and PPP1CA. This study aimed to expand the genotype and phenotype of patients with de novo variants in PHACTR1 and analyse the impact of variants on protein-protein interaction. METHODS: We identified seven patients with PHACTR1 variants by trio-based whole-exome sequencing. Additional two subjects were ascertained from two centres through GeneMatcher. The genotype-phenotype correlation was determined, and AlphaFold-Multimer was used to predict protein-protein interactions and interfaces. RESULTS: Eight individuals carried missense variants and one had CNV in the PHACTR1. Infantile epileptic spasms syndrome (IESS) was the unifying phenotype in eight patients with missense variants of PHACTR1. They could present with other types of seizures and often exhibit drug-resistant epilepsy with a poor prognosis. One patient with CNV displayed a developmental encephalopathy phenotype. Using AlphaFold-Multimer, our findings indicate that PHACTR1 and G-actin-binding sequences overlap with PPP1CA at the RPEL3 domain, which suggests possible competition between PPP1CA and G-actin for binding to PHACTR1 through a similar polymerisation interface. In addition, patients carrying missense variants located at the PHACTR1-PPP1CA or PHACTR1-G-actin interfaces consistently exhibit the IESS phenotype. These missense variants are mostly concentrated in the overlapping sequence (RPEL3 domain). CONCLUSIONS: Patients with variants in PHACTR1 can have a phenotype of developmental encephalopathy in addition to IESS. Moreover, our study confirmed that the variants affect the binding of PHACTR1 to G-actin or PPP1CA, resulting in neurological disorders in patients.

Short-term exposure to ozone may trigger the onset of Kawasaki disease: An individual-level, case-crossover study in East China.

Kawasaki disease (KD) is an acute, systemic vasculitis that primarily affects children aged under the age of 5. While environmental factors have been linked to the development of KD, the specific role of ozone (O3) pollution in triggering the disease onset remains uncertain. This study aimed to examine the associations between short-term O3 exposure and KD onset in children. Utilizing a satellite-based model with a spatial resolution of 1 × 1 km, we matched 1808 KD patients (out of a total of 6115 eligible individuals) to pre-onset ozone exposures based on their home addresses in East China between 2013 and 2020. Our findings revealed a significant association of O3 exposure with KD onset on the day of onset (lag 0 day). However, this association attenuated and became statistically insignificant on lag 1 and lag 2 days. Each interquartile range (52.32 µg/m3) increase in O3 concentration at lag 0 day was associated with a 16.2% (95% CI: 3.6%, 30.3%) increased risk of KD onset. The E-R curve for O3 exhibited a plateau at low concentrations and then increased rapidly at concentrations ≥75 µg/m3. Notably, these associations were stronger in male children, younger children (<2 years of age) and patients experiencing KD onset during the warm season. This study provides novel epidemiological evidence indicating that short-term O3 exposure is associated with an increased risk of childhood KD onset. These findings emphasized the importance of considering this environmental risk factor in KD prevention strategies.

Unraveling the link between dietary factors and cardiovascular metabolic diseases: Insights from a two-sample Mendelian Randomization investigation.

BACKGROUND: When specific nutrients are inadequate, vulnerability to cardiovascular and metabolic illnesses increases. The data linking dietary nutrition with these illnesses, however, has been sparse in the past observational research and randomized controlled trials. OBJECTIVES: A Mendelian randomization (MR) analysis was performed to assess the influence of macronutrients (fat, protein, sugar, and carbohydrates) and micronutrients (ß-carotene, folate, calcium, iron, copper, magnesium, phosphorus, selenium, zinc, vitamin C, vitamin D, vitamin B, and vitamin B12) on the susceptibility to cardiovascular metabolic disorders, including coronary artery disease, heart failure, ischemic stroke, and type 2 diabetes. METHODS: We employed a two-sample Mendelian randomization (MR) analysis, utilizing inverse variance weighting and conducting comprehensive sensitivity assessments. We obtained publicly accessible summary data from separate cohorts comprising individuals of European ancestry. The level of statistical significance was established at a threshold of P < 0. 00074. RESULTS: Based on our research findings, we have established a causal association between the consumption of circulating fat and the development of cardiovascular and metabolic diseases. The study found that an increase of one standard deviation in fat consumption was associated with a decreased risk of heart failure, with an odds ratio of 0. 56 (95 % CI: 0. 40-0. 79; p = 0. 0007). Notably, various sensitivity analyses confirmed the robustness of this association. Conversely, we did not find any significant correlation between other dietary components and the risk of cardiovascular and metabolic disorders. CONCLUSION: Our research findings demonstrate a conspicuous impact of dietary fat consumption on the susceptibility to heart failure, independent of coronary artery disease, diabetes, and stroke. Consequently, it is indicated that dietary factors are unrelated to the predisposition to cardiovascular metabolic disorders.

Actin-depolymerizing factors 8 and 11 promote root hair elongation at high pH.

A root hair is a polarly elongated single-celled structure that derives from a root epidermal cell and functions in uptake of water and nutrients from the surrounding environment. Previous reports have demonstrated that short periods of high pH inhibit root hair extension; but the effects of long-term high-pH treatment on root hair growth are still unclear. Here, we report that the duration of root hair elongation is significantly prolonged with increasing external pH, which counteracts the effect of decreasing root hair elongation rate and ultimately produces longer root hairs, whereas loss of actin-depolymerizing factor 8 and 11 (ADF8/11) function causes shortening of root hair length at high pH (pH 7.4). Accumulation of ADF8/11 at the tips of root hairs is inhibited by high pH, and increasing environmental pH affects the actin filament (F-actin) meshwork at the root hair tip. At high pH, the tip-focused F-actin meshwork is absent in root hairs of the adf8/11 mutant, actin filaments are disordered at the adf8/11 root hair tips, and actin turnover is attenuated. Secretory and recycling vesicles do not aggregate in the apical region of adf8/11 root hairs at high pH. Together, our results suggest that, under long-term exposure to high extracellular pH, ADF8/11 may establish and maintain the tip-focused F-actin meshwork to regulate polar trafficking of secretory/recycling vesicles at the root hair tips, thereby promoting root hair elongation.

Epigenome-wide association study on short-, intermediate- and long-term ozone exposure in Han Chinese, the NSPT study.

Epidemiological and epigenetic studies have acknowledged ambient ozone exposure associated with inflammatory and cardiovascular disease. However, the molecular mechanisms still remained unclear, and epigenome-wide analysis in cohort were lacking, especially in Chinese. We included blood-derived DNA methylation for 3365 Chinese participants from the NSPT cohort and estimated individual ozone exposure level of short-, intermediate- and long-term, based on a validated prediction model. We performed epigenome-wide association studies which identified 59 CpGs and 30 DMRs at a strict genome-wide significance (P < 5 ×10-8). We also conducted comparison on the DNA methylation alteration corresponding to different time windows, and observed an enhanced differentiated methylation trend for intermediate- and long-term exposure, while the short-term exposure associated methylation changes did not retain. The targeted genes of methylation alteration were involved in mechanism related to aging, inflammation disease, metabolic syndrome, neurodevelopmental disorders, and oncogenesis. Underlying pathways were enriched in biological activities including telomere maintenance process, DNA damage response and megakaryocyte differentiation. In conclusion, our study is the first EWAS on ozone exposure conducted in large-scale Han Chinese cohort and identified associated DNA methylation change on CpGs and regions, as well as related gene functions and pathways.

The biological age model for evaluating the degree of aging in centenarians.

BACKGROUND: Biological age (BA) has been used to assess individuals' aging conditions. However, few studies have evaluated BA models' applicability in centenarians. METHODS: Important organ function examinations were performed in 1798 cases of the longevity population (80∼115 years old) in Hainan, China. Eighty indicators were selected that responded to nutritional status, cardiovascular function, liver and kidney function, bone metabolic function, endocrine system, hematological system, and immune system. BA models were constructed using multiple linear regression (MLR), principal component analysis (PCA), Klemera and Doubal method (KDM), random forest (RF), support vector machine (SVM), extreme gradient boosting (XGBoost), and light gradient boosting machine (lightGBM) methods. A tenfold crossover validated the efficacy of models. RESULTS: A total of 1398 participants were enrolled, of whom centenarians accounted for 49.21%. Seven aging markers were obtained, including estimated glomerular filtration rate, albumin, pulse pressure, calf circumference, body surface area, fructosamine, and complement 4. Eight BA models were successfully constructed, namely MLR, PCA, KDM1, KDM2, RF, SVM, XGBoost and lightGBM, which had the worst R2 of 0.45 and the best R2 of 0.92. The best R2 for cross-validation was KDM2 (0.89), followed by PCA (0.62). CONCLUSION: In this study, we successfully applied eight methods, including traditional methods and machine learning, to construct models of biological age, and the performance varied among the models.

Comparison of preoperative CT- and MRI-based multiparametric radiomics in the prediction of lymph node metastasis in rectal cancer.

Objective: To compare computed tomography (CT)- and magnetic resonance imaging (MRI)-based multiparametric radiomics models and validate a multi-modality, multiparametric clinical-radiomics nomogram for individual preoperative prediction of lymph node metastasis (LNM) in rectal cancer (RC) patients. Methods: 234 rectal adenocarcinoma patients from our retrospective study cohort were randomly selected as the training (n = 164) and testing (n = 70) cohorts. The radiomics features of the primary tumor were extracted from the non-contrast enhanced computed tomography (NCE-CT), the enhanced computed tomography (CE-CT), the T2-weighted imaging (T2WI) and the gadolinium contrast-enhanced T1-weighted imaging (CE-TIWI) of each patient. Three kinds of models were constructed based on training cohort, including the Clinical model (based on the clinical features), the radiomics models (based on NCE-CT, CE-CT, T2WI, CE-T1WI, CT, MRI, CT combing with MRI) and the clinical-radiomics models (based on CT or MRI radiomics model combing with clinical data) and Clinical-IMG model (based on CT and MRI radiomics model combing with clinical data). The performances of the 11 models were evaluated via the area under the receiver operator characteristic curve (AUC), accuracy, sensitivity, and specificity in the training and validation cohort. Differences in the AUCs among the 11 models were compared using DeLong's test. Finally, the optimal model (Clinical-IMG model) was selected to create a radiomics nomogram. The performance of the nomogram to evaluate clinical efficacy was verified by ROC curves and decision curve analysis (DCA). Results: The MRI radiomics model in the validation cohort significantly outperformed than CT radiomics model (AUC, 0.785 vs. 0.721, p<0.05). The Clinical-IMG nomogram had the highest prediction efficiency than all other predictive models (p<0.05), of which the AUC was 0.947, the sensitivity was 0.870 and the specificity was 0.884. Conclusion: MRI radiomics model performed better than both CT radiomics model and Clinical model in predicting LNM of RC. The clinical-radiomics nomogram that combines the radiomics features obtained from both CT and MRI along with preoperative clinical characteristics exhibits the best diagnostic performance.

0D van der Waals interfacial ferroelectricity.

The dimensional limit of ferroelectricity has been long explored. The critical contravention is that the downscaling of ferroelectricity leads to a loss of polarization. This work demonstrates a zero-dimensional ferroelectricity by the atomic sliding at the restrained van der Waals interface of crossed tungsten disufilde nanotubes. The developed zero-dimensional ferroelectric diode in this work presents not only non-volatile resistive memory, but also the programmable photovoltaic effect at the visible band. Benefiting from the intrinsic dimensional limitation, the zero-dimensional ferroelectric diode allows electrical operation at an ultra-low current. By breaking through the critical size of depolarization, this work demonstrates the ultimately downscaled interfacial ferroelectricity of zero-dimensional, and contributes to a branch of devices that integrates zero-dimensional ferroelectric memory, nano electro-mechanical system, and programmable photovoltaics in one.