Valuation of the significant hypoglycemic activity of black currant anthocyanin extract by both starch structure transformation and glycosidase activity inhibition.

The objective of this study was to investigate the impact of anthocyanin-rich black currant extract (BCE) on the structural properties of starch and the inhibition of glycosidases, gathering data and research evidence to support the use of low glycemic index (GI) foods. The BCE induced a change in the starch crystal structure from A-type to V-type, resulting in a drop in digestibility from 81.41 % to 65.57 %. Furthermore, the inhibitory effects of BCE on glycosidases activity (α-glucosidase: IC50 = 0.13 ± 0.05 mg/mL and α-amylase: IC50 = 2.67 ± 0.16 mg/mL) by inducing a change in spatial conformation were confirmed through in vitro analysis. The presence of a 5'-OH group facilitated the interaction between anthocyanins and receptors of amylose, α-amylase, and α-glucosidase. The glycosyl moiety enhanced the affinity for amylose yet lowered the inhibitory effect on α-amylase. The in vivo analysis demonstrated that BCE resulted in a reduction of 3.96 mM·h in blood glucose levels (Area Under Curve). The significant hypoglycemic activity, particularly the decrease in postprandial blood glucose levels, highlights the potential of utilizing BCE in functional foods for preventing diabetes.

Low ankle-brachial index is associated with higher cardiovascular mortality in individuals with nonalcoholic fatty liver disease.

BACKGROUND AND AIMS: Ankle brachial index (ABI) is a risk factor for cardiovascular mortality, but it is unclear whether ABI is associated with cardiovascular mortality in patients with nonalcoholic fatty liver disease (NAFLD). The current study aimed to evaluate the association between ABI with cardiovascular and all-cause mortality in patients with NAFLD. METHODS: We performed a cohort study using the data of the1999-2004 National Health and Nutrition Examination Survey data of adults. Mortality data were followed up to December 2015. NAFLD was defined by the hepatic steatosis index or the US fatty liver index. ABI was classified into three groups: ABI ≤ 0.9 (low value); 0.9 < ABI ≤ 1.1 (borderline value); ABI greater than 1.1 (normal value). RESULTS: We found that low ABI was associated with an increased risk of cardiovascular mortality in patients with NAFLD (HR: 2.42, 95% CI 1.10-5.33 for low value ABI vs normal value ABI, P for trend = 0.04), and the relationship was linearly and negatively correlated in the range of ABI < 1.4. However, low ABI was not associated with all-cause mortality in patients with NAFLD. Stratified by cardiovascular disease, ABI remains inversely correlated with cardiovascular mortality in NAFLD patients without cardiovascular disease. Stratified by diabetes, ABI is inversely correlated with cardiovascular mortality in NAFLD patients regardless of diabetes status. CONCLUSIONS: Low ABI is independently associated with higher cardiovascular mortality in NAFLD cases. This correlation remains significant even in the absence of pre-existing cardiovascular disease or diabetes.

Predictive models for lymph node metastasis in endometrial cancer: A systematic review and bibliometric analysis.

BACKGROUND: Lymph node metastasis is associated with a poorer prognosis in endometrial cancer. OBJECTIVE: The objective was to synthesize and critically appraise existing predictive models for lymph node metastasis risk stratification in endometrial cancer. DESIGN: This study is a systematic review. DATA SOURCES AND METHODS: We searched the Web of Science for articles reporting models predicting lymph node metastasis in endometrial cancer, with a systematic review and bibliometric analysis conducted based upon which. Risk of bias was assessed by the Prediction model Risk Of BiAS assessment Tool (PROBAST). RESULTS: A total of 64 articles were included in the systematic review, published between 2010 and 2023. The most common articles were "development only." Traditional clinicopathological parameters remained the mainstream in models, for example, serum tumor marker, myometrial invasion and tumor grade. Also, models based upon gene-signatures, radiomics and digital histopathological images exhibited an acceptable self-reported performance. The most frequently validated models were the Mayo criteria, which reached a negative predictive value of 97.1%-98.2%. Substantial variability and inconsistency were observed through PROBAST, indicating significant between-study heterogeneity. A further bibliometric analysis revealed a relatively weak link between authors and organizations on models predicting lymph node metastasis in endometrial cancer. CONCLUSION: A number of predictive models for lymph node metastasis in endometrial cancer have been developed. Although some exhibited promising performance as they demonstrated adequate to good discrimination, few models can currently be recommended for clinical practice due to lack of independent validation, high risk of bias and low consistency in measured predictors. Collaborations between authors, organizations and countries were weak. Model updating, external validation and collaborative research are urgently needed. REGISTRATION: None.

Introduction to predictive models for lymph node metastasis in endometrial cancerLymph node metastasis of endometrial cancer is associated with a poor prognosis. There are currently many predictive models. We summarized and evaluated them in this article.

Distributed Robust Fault Estimation for Multiagent Systems Based on Transition Variable Estimator.

This article investigates the distributed robust fault estimation for a class of multiagent systems with actuator faults and nonlinear uncertainties. To estimate the actuator faults and system states simultaneously, a novel transition variable estimator is constructed. Compared with existing similar results, the fault estimator existing condition is not necessary for designing the transition variable estimator. Furthermore, the bounds of the faults and their derivatives can be unknown in designing the estimator for each agent in the system. The parameters of the estimator are calculated by using Schur decomposition and linear matrix inequality algorithm. Finally, the performance of the proposed method is demonstrated through experiments of wheeled mobile robots.

Effect of Zinc Amino Acid Complexes on Growth Performance, Tissue Zinc Concentration, and Muscle Development of Broilers.

The present study aimed to evaluate the effects of zinc amino acid complexes on growth performance, tissue zinc concentration, and muscle development in broilers. A total of 504 day-old male arbor acres broilers were randomly divided into seven treatments (fed with a basal diet or a basal diet supplemented with 120 mg kg-1 Zn as ZnSO4, 30, 60, 90 or 120 mg kg-1 Zn as ZnN, or 30 mg kg-1 Zn as ZnA separately). Each group had six replicates, with 12 birds per replicate. The results showed that the addition of 60 mg kg-1 ZnN significantly increased (P < 0.05) the average daily gain (ADG) and breast muscle percentage of broilers. Zinc concentration of ZnN and ZnA added groups were higher than (P < 0.05) that in the Zn sulfate group under the same addition dose. Except for the 30 mg kg-1 ZnN group, the muscle fiber diameter and cross-sectional area (CSA) were significantly increased (P < 0.05) in the ZnN addition groups. Compared with the basal diet group, adding ZnN significantly increased (P < 0.05) the expression of MTOR, MYOD, and MYOG at day 21 and decreased (P < 0.05) the expression of Atrogin-1. The expression levels of AKT, MTOR, P70S6K, and MYOD were increased at day 42, while the expression levels of MuRF1 and Atrogin-1 were decreased. Adhesion, backbone regulation of actin, MAPK, mTOR, and AMPK were significantly enriched as indicated by KEGG pathway enrichment analysis. In conclusion, zinc amino acid complexes could improve growth performance, tissue zinc concentration, and regulate breast muscle development.

Ginsenoside RK3 promotes neurogenesis in Alzheimer's disease through activation of the CREB/BDNF pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: In the ancient book "Shen Nong's Herbal Classic," Panax ginseng CA Mey was believed to have multiple benefits, including calming nerves, improving cognitive function, and promoting longevity. Ginsenosides are the main active ingredients of ginseng. Ginsenoside RK3 (RK3), a rare ginsenoside extracted from ginseng, displays strong pharmacological potential. However, its effect on neurogenesis remains insufficiently investigated. AIM OF THE STUDY: This study aims to investigate whether RK3 improves learning and memory by promoting neurogenesis, and to explore the mechanism of RK3 action. MATERIALS AND METHODS: The therapeutic effect of RK3 on learning and memory was determined by the Morris water maze (MWM) and novel object recognition test (NORT). The pathogenesis and protective effect of RK3 on primary neurons and animal models were detected by immunofluorescence and western blotting. Protein expression of cAMP response element-binding protein (CREB)/brain-derived neurotrophic factor (BDNF) signaling pathway was detected by western blotting. RESULTS: Our results showed that RK3 treatment significantly improved cognitive function in APPswe/PSEN1dE9 (APP/PS1) mice and C57BL/6 (C57) mice. RK3 promotes neurogenesis and synaptogenesis in the mouse hippocampus. In vitro, RK3 prevents Aß-induced injury in primary cultured neurons and promotes the proliferation of PC12 as well as the expression of synapse-associated proteins. Mechanically, the positve role of RK3 on neurogenesis was combined with the activation of CREB/BDNF pathway. Inhibition of CREB/BDNF pathway attenuated the effect of RK3. CONCLUSION: In conclusion, this study demonstrated that RK3 promotes learning and cognition in APP/PS1 and C57 mice by promoting neurogenesis and synaptogenesis through the CREB/BDNF signaling pathway. Therefore, RK3 is expected to be further developed into a potential drug candidate for the treatment of Alzheimer's disease (AD).

Isolinderalactone Ameliorates the Pathology of Alzheimer's Disease by Inhibiting the JNK Signaling Pathway.

Neuronal cell damage is a major cause of cognitive impairment in Alzheimer's disease (AD). Multiple factors, such as amyloid deposition, tau hyperphosphorylation, and neuroinflammation, can lead to neuronal cell damage. Therefore, the development of multi-target drugs with broad neuroprotective effects may be an effective strategy for the treatment of AD. Natural products have become an important source of drug discovery because of their good pharmacological activity, multiple targets, and low toxicity. In this study, we screened a natural compound library and found that the fat-soluble sesquiterpene natural compound isolinderalactone (Iso) extracted from the dried root pieces of Lindera aggregata had the ability to alleviate cellular damage induced by ß-amyloid-1-42 (Aß1-42). The role and mechanism of Iso in AD have not yet been reported. Herein, we demonstrated that Iso significantly reduced the level of apoptosis in PC12 cells. Besides, Iso treatment reduced amyloid deposition, neuron apoptosis, and neuroinflammation, ultimately improving the cognitive dysfunction of APP/PS1 (APPswe/PSEN 1dE9) mice. Notably, Iso-10 mg/kg showed superior improved effects in APP/PS1 mice compared with the positive control drug donepezil-5 mg/kg. Mechanistically, the results of RNA sequencing combined with Western blots showed that Iso exerted its therapeutic effect by inhibiting the c-Jun N-terminal kinase (JNK) signaling pathway. Taken together, our findings suggest that Iso is a potential drug candidate for the treatment of AD.

Parthenolide alleviates cognitive dysfunction and neurotoxicity via regulation of AMPK/GSK3ß(Ser9)/Nrf2 signaling pathway.

Alzheimer's disease (AD) stands as the predominant age-related neurodegenerative disorder, for which efficacious treatment remains elusive. An auspicious avenue for this disease lies in natural compounds sourced from tranditional medicine and plant origins. Parthenolide (PTN) is a natural product with multiple biological functionsand. Recent investigations have illuminated PTN's protective properties against neurological maladies; however, its potential therapeutic role against AD remains uncharted. This study aims to explore the role of PTN in treating AD. Our in vitro findings underscore PTN's bioactivity, as evidenced by its capacity to curtail apoptosis, reduce reactive oxygen species (ROS) production, and restore mitochondrial membrane potential in PC12 cells. Moreover, PTN treatment demonstrates a capacity to ameliorate deficits in spatial learning and memory in the 3 ×Tg-AD murine model. Notably, PTN's therapeutic efficacy surpasses that of a clinical agent, donepezil. Mechanistically, PTN's neuroprotective effects stem from its adept regulation of the AMPK/GSK3ß(ser9)/Nrf2 signaling pathway and protection on neuronal cells from ROS-related apoptosis. Although the molecular target and the pre-clinical evaluations of PTN need to be further explored, this study indicates PTN as a potential agent or lead compound for the drug development against AD.

The CD2v protein of African swine fever virus inhibits macrophage migration and inflammatory cytokines expression by downregulating EGR1 expression through dampening ERK1/2 activity.

African swine fever virus (ASFV) is a highly contagious and deadly virus that leads to high mortality rates in domestic swine populations. Although the envelope protein CD2v of ASFV has been implicated in immunomodulation, the molecular mechanisms underlying CD2v-mediated immunoregulation remain unclear. In this study, we generated a stable CD2v-expressing porcine macrophage (PAM-CD2v) line and investigated the CD2v-dependent transcriptomic landscape using RNA-seq. GO terms enrichment analysis and gene set enrichment analysis revealed that CD2v predominantly affected the organization and assembly process of the extracellular matrix. Wound healing and Transwell assays showed that CD2v inhibited swine macrophage migration. Further investigation revealed a significant decrease in the expression of transcription factor early growth response 1 (EGR1) through inhibiting the activity of extracellular signal-regulated kinase 1 and 2 (ERK1/2). Notably, EGR1 knockout in swine macrophages restricted cell migration, whereas EGR1 overexpression in PAM-CD2v restored the ability of macrophage migration, suggesting that CD2v inhibits swine macrophage motility by downregulating EGR1 expression. Furthermore, we performed chromatin immunoprecipitation and sequencing for EGR1 and the histone mark H3K27 acetylation (H3K27ac), and we found that EGR1 co-localized with the activated histone modification H3K27ac neighboring the transcriptional start sites. Further analysis indicated that EGR1 and H3K27ac co-occupy the promoter regions of cell locomotion-related genes. Finally, by treating various derivatives of swine macrophages with lipopolysaccharides, we showed that depletion of EGR1 decreased the expression of inflammatory cytokines including TNFα, IL1α, IL1ß, IL6, and IL8, which play essential roles in inflammation and host immune response. Collectively, our results provide new insights into the immunomodulatory mechanism of ASFV CD2v.

PGAM5 degrades PDCoV N protein and activates type I interferon to antagonize viral replication.

IMPORTANCE: As a member of the δ-coronavirus family, porcine deltacoronavirus (PDCoV) is a vital reason for diarrhea in piglets, which can contribute to high morbidity and mortality rates. Initially identified in Hong Kong in 2012, the virus has rapidly spread worldwide. During PDCoV infection, the virus employs evasion mechanisms to evade host surveillance, while the host mounts corresponding responses to impede viral replication. Our research has revealed that PDCoV infection down-regulates the expression of PGAM5 to promote virus replication. In contrast, PGAM5 degrades PDCoV N through autophagy by interacting with the cargo receptor P62 and the E3 ubiquitination ligase STUB1. Additionally, PGAM5 interacts with MyD88 and TRAF3 to activate the IFN signal pathway, resulting in the inhibition of viral replication.

Advances in research on cell models for skeletal muscle atrophy.

Skeletal muscle, the largest organ in the human body, plays a crucial role in supporting and defending the body and is essential for movement. It also participates in regulating the processes of protein synthesis and degradation. Inhibition of protein synthesis and activation of degradation metabolism can both lead to the development of skeletal muscle atrophy, a pathological condition characterized by a decrease in muscle mass and fiber size. Many physiological and pathological conditions can cause a decline in muscle mass, but the underlying mechanisms of its pathogenesis remain incompletely understood, and the selection of treatment strategies and efficacy evaluations vary. Moreover, the early symptoms of this condition are often not apparent, making it easily overlooked in clinical practice. Therefore, it is necessary to develop and use cell models to understand the etiology and influencing factors of skeletal muscle atrophy. In this review, we summarize the methods used to construct skeletal muscle cell models, including hormone, inflammation, cachexia, genetic engineering, drug, and physicochemical models. We also analyze, compare, and evaluate the various construction and assessment methods.

Expression of ASFV p17 in CHO cells and identification of one novel epitope using a monoclonal antibody.

As a highly pathogenic large DNA virus, African swine fever virus (ASFV) has huge particles and numerous encoded proteins. At present, few of the existing studies on ASFV proteins have investigated the function of p17. Specific antibodies against p17 to promote the development of prevention techniques against African swine fever (ASF) are urgently needed. Herein, we successfully expressed ASFV p17 in CHO cells using a suspension culture system and generated a monoclonal antibody (mAb) against p17. The mAb recognized a novel linear epitope (8LLSHNLSTREGIK20) and exhibited specific reactivity, which was conducive to the identification of ectopically expressed p17, the recombinant porcine reproductive and respiratory syndrome virus expressing p17, and the ASFV-SY18. The epitope was conservative among genotype I and genotype II ASFV strains. Overall, the mAb against p17 revealed efficient detection and promising application prospects, making it a useful tool for future vaccine research on ASF. Determination of the conserved linear epitope of p17 would contribute to the in-depth exploration of the biological function of ASFV antigen protein.

Inhibitory Effect of PPARδ Agonist GW501516 on Proliferation of Hypoxia-induced Pulmonary Arterial Smooth Muscle Cells by Regulating the mTOR Pathway.

OBJECTIVE: This study aimed to investigate the effects of the peroxisome proliferator-activated receptor δ (PPARδ) agonist GW501516 on the proliferation of pulmonary artery smooth muscle cells (PASMCs) induced by hypoxia, in order to search for new drugs for the treatment and prevention of pulmonary vascular remodeling. METHODS: PASMCs were incubated with different concentrations of GW501516 (10, 30, 100 nmol/L) under the hypoxic condition. The proliferation was determined by a CCK-8 assay. The cell cycle progression was analyzed by flow cytometry. The expression of PPARδ, S phase kinase-associated protein 2 (Skp2), and cell cycle-dependent kinase inhibitor p27 was detected by Western blotting. Then PASMCs were treated with 100 nmol/ L GW501516, 100 nmol/L mammalian target of rapamycin (mTOR) inhibitor rapamycin and/or 2 µmol/L mTOR activator MHY1485 to explore the molecular mechanisms by which GW501516 reduces the proliferation of PASMCs. RESULTS: The presented data demonstrated that hypoxia reduced the expression of PPARδ in an oxygen concentration- and time-dependent manner, and GW501516 decreased the proliferation of PASMCs induced by hypoxia by blocking the progression through the G0/G1 to S phase of the cell cycle. In accordance with these findings, GW501516 downregulated Skp2 and upregulated p27 in hypoxia-exposed PASMCs. Further experiments showed that rapamycin had similar effects as GW501516 in inhibiting cell proliferation, arresting the cell cycle, regulating the expression of Skp2 and p27, and inactivating mTOR in hypoxia-exposed PASMCs. Moreover, MHY1485 reversed all the beneficial effects of GW501516 on hypoxia-stimulated PASMCs. CONCLUSION: GW501516 inhibited the proliferation of PASMCs induced by hypoxia through blocking the mTOR/Skp2/p27 signaling pathway.

BST2 negatively regulates porcine reproductive and respiratory syndrome virus replication by restricting the expression of viral proteins.

Porcine reproductive and respiratory syndrome virus (PRRSV) has seriously affected the viability of swine industries worldwide, and effective measures to control PRRSV are urgently required. Understanding the mechanisms of action of antiviral proteins is crucial for developing antiviral strategies. Interferon-induced bone marrow stromal cell antigen 2 (BST2) can inhibit the replication of various viruses via different pathways. However, little is known about the effects of BST2 on PRRSV. Therefore, this study aimed to evaluate whether the interferon-induced BST2 can inhibit PRRSV replication. We used western blotting and RT-qPCR techniques to analyze the effect of BST2 overexpression and knockdown on PRRSV replication. Overexpression of BST2 inhibited the replication of PRRSV, whereas knockdown of BST2 by small interfering RNA promoted PRRSV replication. Additionally, the expression of BST2 was upregulated during the early phase of PRRSV infection in porcine alveolar macrophages. Analysis of PRRSV proteins showed that BST2 restricted the expression of several non-structural viral proteins. BST2 downregulated the expression of Nsp12 through a proteasome-dependent pathway and downregulated the expression and transcription of E protein. These findings demonstrate the potential of BST2 as a critical regulator of PRRSV replication.

ß-amyloid binds to microglia Dectin-1 to induce inflammatory response in the pathogenesis of Alzheimer's disease.

Microglia-mediated neuroinflammation is closely related to the development of Alzheimer's disease (AD). In the early stages of the inflammation response, pattern recognition receptors (PRRs) play a key role in clearing damaged cells and defending against infection by recognizing endogenous and exogenous ligands. However, the regulation of pathogenic microglial activation and its role in AD pathology remains poorly understood. Here we showed that a pattern recognition receptor called Dectin-1, expressed on microglia, mediates the pro-inflammatory responses of beta-amyloid (Aß). Knockout of Dectin-1 reduced Aß1-42 (Aß42)-induced microglial activation, inflammatory responses, and synaptic and cognitive deficits in Aß42-infused AD mice. Similar results were obtained in the BV2 cell model. Mechanistically, we showed that Aß42 could directly bind to Dectin-1, causing Dectin-1 homodimerization and activating downstream spleen tyrosine kinase (Syk)/nuclear factor-κB (NF-κB) signaling pathway to induce the expression of inflammatory factors and, in turn, AD pathology. These results suggest the important role of microglia Dectin-1 as a new direct receptor for Aß42 in microglial activation and AD pathology and provide a potential therapeutic strategy for neuroinflammation in AD.

Wolfberry water extract attenuates blue light-emitting diode damage to ARPE-19 cells and mouse retina by activating the NRF2 signaling pathway.

The wolfberry is believed to improve eyesight in traditional Chinese medicine. Soaking wolfberry in thermos cups has become a common health-preserving practice. The object of this paper was to research the protective effects of wolfberry water extract (WWE) on oxidative injury induced by blue light-emitting diodes (LEDs) in ARPE-19 cells and C57BL/6J mice. Wolfberry water extract significantly increased cell viability, reduced ROS production, stabilized mitochondrial membrane potential, and inhibited apoptosis in blue LED-induced cells (P < 0.05). The protective effects of WWE against blue LED-induced cytotoxicity and ROS accumulation in cells were abolished by transfection with Nrf2 siRNA. In blue LED-exposed C57BL/6J mice, WWE treatment markedly increased the amplitudes of electroretinogram (ERG) waves a and b, increased the thickness of retinal outer nuclear layer (ONL), activated endogenous antioxidant enzymes, and decreased MDA levels in the retina and lens. WWE also promoted NRF2 translocation and the expression of the downstream genes Ho-1, Nqo1, Gclc, and Gclm in the retina. The protection of WWE in ERG a and b wave amplitudes and ROS levels were abrogated in Nrf2 knockout mice. These results suggested that WWE has beneficial effects on retinal injury induced by blue LED, and mechanisms of action at least partly via the NRF2 signaling pathway.

The rPRRSV-E2 strain exhibited a low level of potential risk for virulence reversion.

Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) and Classical Swine Fever Virus (CSFV) are two important pathogens, which cause serious impact on swine industry worldwide. In our previous research, rPRRSV-E2, the recombinant PRRSV expressing CSFV E2 protein, could provide sufficient protection against the lethal challenge of highly pathogenic PRRSV and CSFV, and could maintained genetically stable in vitro. Here, to evaluate the virulence reversion potential risk, rPRRSV-E2 had been continuously passaged in vivo, the stability of E2 expression and virulence of the passage viruses were analyzed. The results showed that no clinical symptoms or pathological changes could be found in the inoculated groups, and there were no significant differences of viraemia among the test groups. Sequencing and IFA analysis showed that the coding gene of exogenous CSFV E2 protein existed in the passaged viruses without any sequence mutations, deletions or insertions, and could expressed steadily. It could be concluded that the foreign CSFV E2 gene in the genome of rPRRSV-E2 could be maintained genetically stable in vivo, and rPRRSV-E2 strain had relatively low level of potential risk for virulence reversion.

Expression of EMT-related genes in lymph node metastasis in endometrial cancer: a TCGA-based study.

BACKGROUND: Endometrial cancer (EC) with metastasis in pelvic/para-aortic lymph nodes suggests an unsatisfactory prognosis. Nevertheless, there is still rare literature focusing on the role of epithelial-mesenchymal transition (EMT) in lymph node metastasis (LNM) in EC. METHODS: Transcriptional data were derived from the TCGA database. Patients with stage IA-IIIC2 EC were included, constituting the LN-positive and LN-negative groups. To evaluate the extent of EMT, an EMT signature composed of 315 genes was adopted. The EMT-related genes (ERGs) were obtained from the dbEMT2 database, and the differentially expressed ERGs (DEERGs) between these two groups were screened. On the basis of DEERGs, pathway analysis was carried out. We eventually adopted the logistic regression model to build an ERG-based gene signature with predictive value for LNM in EC. RESULTS: A total of 498 patients were included, with 75 in the LN-positive group. Median EMT score of tumor tissues from LN-negative group was - 0.369, while that from the LN-positive group was - 0.296 (P < 0.001), which clearly exhibited a more mesenchymal phenotype for LNM cases on the EMT continuum. By comparing expression profiles, 266 genes were identified as DEERGs, in which 184 were upregulated and 82 were downregulated. In pathway analysis, various EMT-related pathways were enriched. DEERGs shared between molecular subtypes were comparatively few. The ROC curve and logistic regression analysis screened 7 genes with the best performance to distinguish between the LN-positive and LN-negative group, i.e., CIRBP, DDR1, F2RL2, HOXA10, PPARGC1A, SEMA3E, and TGFB1. A logistic regression model including the 7-gene-based risk score, age, grade, myometrial invasion, and histological subtype was built, with an AUC of 0.850 and a favorite calibration (P = 0.074). In the validation dataset composed of 83 EC patients, the model exhibited a satisfactory predictive value and was well-calibrated (P = 0.42). CONCLUSION: The EMT status and expression of ERGs varied in LNM and non-LNM EC tissues, involving multiple EMT-related signaling pathways. Aside from that, the distribution of DEERGs differed among molecular subtypes. An ERG-based gene signature including 7 DEERGs exhibited a desirable predictive value for LNM in EC, which required further validation based upon clinical specimens in the future.

[Pollution Characteristics and Health Risk Assessment of Heavy Metals in PM2.5 of Different Air Masses During Heating Season in Tianjin].

In order to explore the pollution characteristics and health risks of heavy metals in PM2.5 in Tianjin, heavy metal samples (Pb, Cd, Cr, As, Zn, Mn, Co, Ni, Cu, and V) in PM2.5 were analyzed from November 2020 to March 2021 using the Xact-625 heavy metal online analyzer. The spatial and temporal distribution characteristics were analyzed using the HYSPLIT model, and the health risks of heavy metals were analyzed using the US EPA risk assessment model. The results indicated that the average total concentration of the 10 heavy metal elements was (261.56±241.74) ng·m-3, among which the concentrations of Cr ï¼»converted Cr(Ⅵ)ï¼½ and As were higher than the annual average limit of the National Ambient Air Quality Standard (GB 3095-2012). According to the back trajectory results, the medium-distance transmissions from northwest areas (NO.1), the long-distance transmissions from northwest areas (NO.2), the transmissions from southwest areas (NO.3), and the transmissions from northeast areas (NO.4) were the major sources in Tianjin City. The heavy metals of different air masses presented different pollution characteristics and health risks; the concentration of PM2.5, the total concentration of the 10 heavy metal elements, and the total carcinogenic risk of the five heavy metal elements of the NO.3 air mass were the highest, whereas the total non-carcinogenic risk of the 10 heavy metal elements of the NO.2 air mass was higher than that of the other two air mass. The health risk assessment showed that Mn posed non-carcinogenic risks to children, and Cr and As presented carcinogenic risk. Meanwhile, Cd of the NO.3 air masses also presented carcinogenic risk.