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Ongoing rural depopulation is a serious concern in China and worldwide. Given the rapid development of e-commerce in rural China, this study examines the impact of e-commerce on rural depopulation and explores its underlying pathways. Employing a staggered difference-in-differences estimation using combined county-level panel data, our research reveals that e-commerce significantly mitigates rural depopulation, resulting in a 1.4 % increase in the population growth rate. Furthermore, this study identifies several pathways through which e-commerce counteracts rural depopulation, encompassing the creation of employment opportunities, the cultivation of rural entrepreneurship, the augmentation of rural income and its growth, as well as the enhancement of rural infrastructure and public services. The findings propose e-commerce as a potential solution to address the challenge of rural depopulation. • This study examines the effect of e-commerce development on rural depopulation in China. • This study reveals that e-commerce significantly counteracts rural depopulation. • This study identifies the multiple mechanisms through which e-commerce counteracts rural depopulation. • This research proposes a potential solution to combating the global issue of rural depopulation. [ABSTRACT FROM AUTHOR]

Acne is a kind of chronic inflammatory skin disease, which is common in the hair follicle and sebaceous gland of teenagers. It often recurs and affects the quality of life of patients. Acne itself can cause the damage of skin barrier function. On the other hand, common acne treatment methods, such as external drugs, systemic drugs, physical, and chemical treatment, can also lead to the damage of skin barrier function and affect the treatment effect. The application of skin care in the adjuvant treatment of acne has been widely concerned. Due to their high safety, good tolerance, and the effect of improving the damaged skin barrier, medical skin care products are a hot spot in the treatment of cosmetic skin diseases in recent years. It can not only increase the curative effect, reduce the side effects, but also increase the compliance of patients when combined with conventional acne treatment. In this article, skin care products and their application in acne treatment were reviewed. [ABSTRACT FROM AUTHOR]

With the increasing awareness of heterogeneity in cancers, better prediction of cancer prognosis is much needed for more personalized treatment. Recently, extensive efforts have been made to explore the variations in gene expression for better prognosis. However, the prognostic gene signatures predicted by most existing methods have little robustness among different datasets of the same cancer. To improve the robustness of the gene signatures, we propose a novel high-frequency sub-pathways mining approach (HiFreSP), integrating a randomization strategy with gene interaction pathways. We identified a six-gene signature (CCND1, CSF3R, E2F2, JUP, RARA and TCF7) in esophageal squamous cell carcinoma (ESCC) by HiFreSP. This signature displayed a strong ability to predict the clinical outcome of ESCC patients in two independent datasets (log-rank test, P  = 0.0045 and 0.0087). To further show the predictive performance of HiFreSP, we applied it to two other cancers: pancreatic adenocarcinoma and breast cancer. The identified signatures show high predictive power in all testing datasets of the two cancers. Furthermore, compared with the two popular prognosis signature predicting methods, the least absolute shrinkage and selection operator penalized Cox proportional hazards model and the random survival forest, HiFreSP showed better predictive accuracy and generalization across all testing datasets of the above three cancers. Lastly, we applied HiFreSP to 8137 patients involving 20 cancer types in the TCGA database and found high-frequency prognosis-associated pathways in many cancers. Taken together, HiFreSP shows higher prognostic capability and greater robustness, and the identified signatures provide clinical guidance for cancer prognosis. HiFreSP is freely available via GitHub: https://github.com/chunquanlipathway/HiFreSP. [ABSTRACT FROM AUTHOR]

In a society where financial market and insurance market are under-developed, social networks play an important role in risk sharing. Using data from the 2011 China Household Finance Survey, this paper examines the effect of siblings, which form strong ties in a social network, on household equity investment. We find that having one more sibling increases the probability of participation in stock market by 15–17% points and increases the fraction of total assets in stock investment by 2–3% points. We also find that sisters have a larger effect on equity investment than brothers. With the examination of the effects of siblings on social interaction, risk tolerance, saving, and borrowing behaviors, we argue that the main channel through which siblings affect household investment is risk sharing. [ABSTRACT FROM AUTHOR]

Developing countries often lack an adequate social security system, and elderly parents rely heavily on their children for support. Aging populations and low-fertility rates are an emerging trend in developing countries. In this paper, we examine the effects of sibship size on individuals' internal migration decisions in China. We find that the number of siblings has a positive effect on individual migration decisions, but this effect is non-linear and marginally increasing. Second, we find that having brothers has a more significant effect on migration decisions than having sisters. Finally, although of different magnitudes, the effects are persistent across genders, Hukou status, and education levels. [ABSTRACT FROM AUTHOR]

This article investigates the effectiveness of China's "Rural Appliance Rebate" (RAR) program in boosting rural appliance consumption during the latest economic recession. Based on two rounds of rural household survey data in China, we adopt a difference-in-difference matching approach to assess the extent to which these rebates induced greater rural appliance consumption than they otherwise would have. Our analysis finds that the RAR program boosted subsidized home appliance consumption, but its stimulus effects are driven mainly by cell phones, no significant impacts are detected on refrigerators and color TVs, and its impacts on aggregate home appliance consumption are not pronounced on the whole. Our investigation into the heterogeneity of these effects suggests that, for low income households, the RAR program prominently boost their aggregate home appliance consumption. [ABSTRACT FROM AUTHOR]

Purpose: As a member of the ubiquitin‐conjugating enzyme (E2) family, UBE2V2 demonstrates significant tumorigenicity in many cancers. However, the relationship between UBE2V2 expression and the morbidity of lung adenocarcinoma (LUAD) is still unknown. Methods: We detected the mRNA and protein expression of UBE2V2 and analyzed its relationship with clinical parameters as well as survival prognosis based on bioinformatic and immunohistochemistry (IHC) in LUAD. The signaling pathway of UBE2V2 in the development of LUAD was obtained by GSEA. The TIMER database was used to investigate the association between UBE2V2 expression and the level of infiltration of different immune cells. Finally, we explored the effects of UBE2V2 knockdown on the proliferation, apoptosis, and migration of LUAD cells. Results: The results showed that UBE2V2 was a potential oncogene and might be considered an independent prognostic molecule for LUAD patients based on TCGA prediction (HR: 1.497 p = 0.012) and IHC (HR:1.864 p = 0.044). IHC showed that UBE2V2 was related to the following clinicopathological factors: gender (p = 0.043), stage (p = 0.042), and lymph node metastasis (p = 0.002). Finally, knockdown of UBE2V2 reduced the migration of LUAD cells by regulating EMT‐related proteins. Knockdown of UBE2V2 induced LUAD cells to arrest in the G1 phase. Knockdown of UBE2V2 increased LUAD cell apoptosis and decreased proliferation, which might be related to the downregulation of PCNA and upregulation of P53 and ƳH2AX expression. Interestingly, UBE2V2 is negatively correlated with B cells, CD4+ T cells, macrophages, and dendritic cells. Conclusion: UBE2V2 may be a valuable therapeutic target for lung cancer. [ABSTRACT FROM AUTHOR]

This article examines how different patterns of farm-level diversification affect the income levels of rural households in China. Using quantile regression analysis of data from a rural household survey, the empirical results exhibit significant differences in diversification effects across rural income strata and various structural characteristics. Diversification, especially involving nonfarm employment and migration, brings a monetary premium to low-income rural families and an income discount to highincome families. The policy implications suggest the encouragement of labor-intensive enterprises in rural areas and improvement of labor quality through rural education and training programs. [ABSTRACT FROM AUTHOR]

Src-suppressed C kinase substrate (SSeCKS), an in vivo and in vitro protein kinase C substrate, is a major lipopolysaccharide (LPS) response protein which markedly upregulated in several organs, including brain, lung, heart, kidney etc., indicating a possible role of SSeCKS in inflammatory process. However, the expression and biological function of SSeCKS during neuronal inflammation remains to be elucidated, so we established an inflammatory model injected with LPS to investigate the gene expression patterns of SSeCKS in neural tissues by using TaqMan quantitative real-time PCR and immunohistochemistry in rat. Real-time PCR showed that LPS stimulated the expression of SSeCKS mRNA in a dose- and time-dependent manner in sciatic nerves, spinal cords and dorsal root ganglions. Immunohistochemistry showed that SSeCKS colocalized with nerve fibers in sciatic nerve after LPS administration, but there was no colocalization between SSeCKS and Schwann cells. In addition, SSeCKS colocalized with neurons which existed in dorsal root ganglions and spinal cords. These findings indicated that SSeCKS might play some important roles in sciatic nerve fibers and neurons in spinal cords and dorsal root ganglions after LPS injection. [ABSTRACT FROM AUTHOR]

This paper explores incentive effects of total central fiscal transfers and its components – tax rebates and equalization grants – on provincial tax efforts in China. Our theoretical model predicts negative impacts on provincial tax efforts from both total fiscal transfers and equalization grants, while the effects of tax rebates are theoretically unclear. Using Chinese provincial panel data from 1995 to 2007, our empirical study provides significant evidence that federal grants substitute for local taxes. [ABSTRACT FROM AUTHOR]

Background: Kawasaki disease (KD) is an immune vasculitis of unknown origin, characterized by transient inflammation. The activation of the cGAS-STING pathway, triggered by mitochondrial DNA (mtDNA) release, has been implicated in the onset of KD. However, its specific role in the progression of inflammation during KD's acute phase remains unclear. Methods: We measured mtDNA and 2'3'-cGAMP expression in KD patient serum using RT-qPCR and ELISA. A murine model of KD was induced by injecting Lactobacillus casei cell wall extract (LCWE), after which cGAS-STING pathway activation and inflammatory markers were assessed via immunohistochemistry, western blot, and RT-qPCR. Human umbilical vein endothelial cells (HUVECs) were treated with KD serum and modulators of the cGAS-STING pathway for comparative analysis. Mitochondrial function was evaluated using Mitosox staining, mPTP opening was quantified by fluorescence microscopy, and mitochondrial membrane potential (MMP) was determined with JC-1 staining. Results: KD patient serum exhibited increased mtDNA and 2'3'-cGAMP expression, with elevated levels of pathway-related proteins and inflammatory markers observed in both in vivo and in vitro models. TEM confirmed mitochondrial damage, and further studies demonstrated that inhibition of mPTP opening reduced mtDNA release, abrogated cGAS-STING pathway activation, and mitigated inflammation. Conclusion: These findings indicate that mtDNA released through the mPTP is a critical activator of the cGAS-STING pathway, contributing significantly to KD-associated inflammation. Targeting mtDNA release or the cGAS-STING pathway may offer novel therapeutic approaches for KD management. [ABSTRACT FROM AUTHOR]

Vascular endothelial inflammation and endothelial dysfunction are the main causes of endothelial injury in Kawasaki disease (KD). Human umbilical cord–derived mesenchymal stem cells (Huc-MSCs) have multiple functions in immune regulation. This study examined whether Huc-MSCs inhibited endothelial inflammation and improved endothelial function in KD through constructing cell and in vivo animal KD vasculitis models. The pyroptosis factor NOD-like receptor protein 3 (NLRP3) was involved in the inflammatory process in the acute phase of KD. After tail vein injection of Huc-MSCs, inflammatory cell infiltration and the expression of pyroptosis-related proteins in the LCWE-induced KD mouse vasculitis model were significantly reduced. In vitro, NLRP3-dependent pyroptosis successfully induced human umbilical vein endothelial cell (HUVEC) damage. Huc-MSCs effectively increased the abilities of impaired HUVECs to proliferate, migrate, invade, and form vessel-like tubes, while inhibiting their apoptosis, suggesting that Huc-MSCs can reduce inflammation and improve vascular endothelial function by inhibiting the NLRP3-dependent pyroptosis pathway in KD, providing a possibility and novel target for KD endothelial injury and dysfunction. [ABSTRACT FROM AUTHOR]

Purpose: Nasopharyngeal carcinoma (NPC) has characteristics of high invasion and early metastasis. Most NPC patients present with locoregionally advanced illness when first diagnosed. Therefore, it is urgent to discover NPC biomarkers. Fibroblast growth Factor 19 (FGF19) plays a role in various physiological or pathological processes, including cancer. In this research, we discovered the importance of FGF19 in NPC, and clarified its role in tumour angiogenesis. Methods: Western blotting, immunohistochemistry and ELISA were used to investigate FGF19 expression in NPC. Then we took CCK8, colony formation, Transwell and wound healing assays to identify the influence of FGF19 on NPC malignant behaviours. The proliferative and metastatic capacity of FGF19 were evaluated in nude mice and zebrafish. The role of FGF19 in angiogenesis was investigated by tube formation and Matrigel plug angiogenesis assays. We then evaluated the variation in Annexin A2(ANXA2) levels with the treatment of FGF19. Lastly, co-immunoprecipitation and ubiquitination assays were performed to identify the mechanisms involved. Results: FGF19 levels were elevated in tissues and serum of NPC patients and were associated with poor clinical stages. High expression of FGF19 promoted NPC malignant behaviours. In particular, FGF19 expression was correlated with microvessel density in tissues and NPC-derived FGF19 could accelerate angiogenesis in vitro and in vivo. Mechanistically, FGF19 influenced ANXA2 expression to promote angiogenesis. Moreover, tripartite motif-containing 21(TRIM21) interacted with ANXA2 and was responsible for ANXA2 ubiquitination. Conclusion: FGF19 promoted NPC angiogenesis by inhibiting TRIM21-mediated ANXA2 ubiquitination. It may serve as a noninvasive biomarker for NPC and provides new insights for therapy. [ABSTRACT FROM AUTHOR]

In recent years, high-throughput genomic technologies like chromatin immunoprecipitation sequencing (ChIp-seq) and transcriptome sequencing (RNA-seq) have been becoming both more refined and less expensive, making them more accessible. Many circular RNAs (circRNAs) that originate from back-spliced exons have been identified in various cell lines across different species. However, the regulatory mechanism for transcription of circRNAs remains unclear. Therefore, there is an urgent need to construct a database detailing the transcriptional regulation of circRNAs. TRCirc (http://www.licpathway.net/TRCirc) provides a resource for efficient retrieval, browsing and visualization of transcriptional regulation information of circRNAs. The current version of TRCirc documents 92 375 circRNAs and 161 transcription factors (TFs) from more than 100 cell types and together represent more than 765 000 TF–circRNA regulatory relationships. Furthermore, TRCirc provides other regulatory information about transcription of circRNAs, including their expression, methylation levels, H3K27ac signals in regulation regions and super-enhancers associated with circRNAs. TRCirc provides a convenient, user-friendly interface to search, browse and visualize detailed information about these circRNAs. [ABSTRACT FROM AUTHOR]

Eggs continue to be significant in terms of the world economy and human nutrition. The aim of this study was to estimate the prevalence of foodborne pathogens in a cross section of egg production types in China and to examine the virulence features of the isolated pathogens. Three hundred eggs from three provinces were tested for Salmonella, Escherichia coli, Staphylococcus aureus, and Campylobacter. Two eggs were positive for Salmonella, one was positive for both E. coli and S. aureus, and none were positive for Campylobacter. When comparing different egg laying systems, there were no significant differences in findings between packaged and unpackaged eggs and between battery cage and cage-free eggs, but there were significant differences in the findings among pathogens and among provinces. Other potential foodborne pathogens were identified in addition to the targeted pathogens. The virulence of Serratia marcescens was higher than that of the isolated Salmonella Typhimurium, and the virulence of Staphylococcus saprophyticus was comparable to that of the isolated S. aureus. These findings are important for local risk assessments concerning possible human foodborne infections via cross-contamination of eggs. [ABSTRACT FROM AUTHOR]

Arsenic is a widely distributed toxic metalloid in around the world. Inorganic arsenic species are deemed to affect astrocytes functions and to cause neuron apoptosis. Microglia are the key cell type involved in innate immune responses in CNS, and microglia activation has been linked to inflammation and neurotoxicity. In this study, using ELISA and reverse transcriptase PCR (RT-PCR), we showed that Arsenic trioxide up-regulated the expression and secretion of IL-6 in a dose-dependent manner and a time-dependent manner in cultured HAPI microglia cells. These pro-inflammatory responses were inhibited by the Akt blocker, LY294002. Further, Arsenic trioxide exposure could induce phospho rylationand degradation of IкBα, and the translocation of NF-κB p65 from the cytosol to the nucleus in this HAPI microglia cell line. Thus, the NF-кB signaling pathway can be activated after Arsenic trioxide treatment. Besides, Akt blocker LY294002 also obviously attenuated NF-кB activation and transnuclear induced by Arsenic trioxide. In concert with these results, we highlighted that the secretion of pro-inflammatory cytokine and NF-кB activation induced by Arsenic trioxide can be mediated by elevation of p-Akt in HAPI microglia cells. [ABSTRACT FROM AUTHOR]

To better guide microbial risk management and control, growth kinetic models of Salmonella with the coexistence of two other dominant background bacteria in pork were constructed. Sterilized pork cutlets were inoculated with a cocktail of Salmonella Derby (S. Derby), Pseudomonas aeruginosa (P. aeruginosa), and Escherichia coli (E. coli), and incubated at various temperatures (4–37 °C). The predictive growth models were developed based on the observed growth data. By comparing R2 of primary models, Baranyi models were preferred to fit the growth curves of S. Derby and P. aeruginosa, while the Huang model was preferred for E. coli (all R2 ≥ 0.997). The secondary Ratkowsky square root model can well describe the relationship between temperature and μmax (all R2 ≥ 0.97) or Lag (all R2 ≥ 0.98). Growth models were validated by the actual test values, with Bf and Af close to 1, and MSE around 0.001. The time for S. Derby to reach a pathogenic dose (105 CFU/g) at each temperature in pork was predicted accordingly and found to be earlier than the time when the pork began to be judged nearly fresh according to the sensory indicators. Therefore, the predictive microbiology model can be applied to more accurately predict the shelf life of pork to secure its quality and safety. [ABSTRACT FROM AUTHOR]

• MALAT1 is key for diabetic foot ulcer healing in rats. • High glucose reduces MALAT1 in stem cells, affecting ulcers. • MiR-142 regulates genes crucial for diabetic ulcer healing. • Studies show MALAT1′s role in age-related diabetic ulcers. • Stem cell therapy promising for elderly diabetic foot ulcers. Diabetic foot ulcer (DFU) is a serious diabetes complication, significantly impacting the quality of life, particularly in the elderly. Age-associated DFUs pose additional challenges due to impaired healing mechanisms. Our study aims to explore the role of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) as a miR-142 sponge in repairing diabetic rat foot ulcer tissue under age-associated diabetes, offering a new theoretical basis and therapeutic target for preventing and treating diabetic vascular disease in the elderly. Using qPCR, we analyzed MALAT1 and miR-142 expression in EPCs and hUC-MSCs. Targetscan predicted potential interaction targets for MALAT1 and miR-142, confirmed by dual luciferase reporter gene assay. An age-associated diabetic rat model was established using Streptozotocin (STZ) injection. Hypoxia, apoptosis, and angiogenesis-related proteins were assessed through Western Blot. In vitro, miR-142 inhibition and MALAT1 overexpression promoted foot ulcer healing in diabetic rats. MALAT1 acted as a miR-142 sponge, downregulated in hUC-MSCs under high glucose, relevant to age-associated diabetic foot ulcers. MiR-142 negatively regulated SIRT1 and Nrf2. In vitro experiments demonstrated potential significance for age-related DFU treatment. MALAT1 in human umbilical cord mesenchymal stem cells expedited foot ulcer healing in diabetic rats, particularly in age-associated diabetes, through miR-142 sponge activity. These findings offer insights for novel therapeutic strategies targeting elderly diabetic foot ulcers, emphasizing exogenous stem cell transplantation's potential in effective DFU treatment for the elderly. [Display omitted] [ABSTRACT FROM AUTHOR]

Long noncoding RNAs (lncRNAs) have been proven to play important roles in transcriptional processes and biological functions. With the increasing study of human diseases and biological processes, information in human H3K27ac ChIP-seq, ATAC-seq and DNase-seq datasets is accumulating rapidly, resulting in an urgent need to collect and process data to identify transcriptional regulatory regions of lncRNAs. We therefore developed a comprehensive database for human regulatory information of lncRNAs (TRlnc, http://bio.licpathway.net/TRlnc), which aimed to collect available resources of transcriptional regulatory regions of lncRNAs and to annotate and illustrate their potential roles in the regulation of lncRNAs in a cell type-specific manner. The current version of TRlnc contains 8 683 028 typical enhancers/super-enhancers and 32 348 244 chromatin accessibility regions associated with 91 906 human lncRNAs. These regions are identified from over 900 human H3K27ac ChIP-seq, ATAC-seq and DNase-seq samples. Furthermore, TRlnc provides the detailed genetic and epigenetic annotation information within transcriptional regulatory regions (promoter, enhancer/super-enhancer and chromatin accessibility regions) of lncRNAs, including common SNPs, risk SNPs, eQTLs, linkage disequilibrium SNPs, transcription factors, methylation sites, histone modifications and 3D chromatin interactions. It is anticipated that the use of TRlnc will help users to gain in-depth and useful insights into the transcriptional regulatory mechanisms of lncRNAs. [ABSTRACT FROM AUTHOR]

Salmonella developed drug-resistance under durative antibiotic pressures pressure. The widespread prevalence of Salmonella has been associated with not only drug-resistance but also pathogenicity. Outer membrane porin proteins (OMPs) are critical for the drug resistance of bacteria. Virulence genes in Salmonella pathogenicity islands (SPIs) play key roles in the virulence of bacteria. In this study, we analyzed the expression levels of three critical genes in ciprofloxacin-resistant strains and ciprofloxacin-susceptible strains of Salmonella, including outer membrane porin protein F (ompF), virulence genes invA and invE. In the clinical ciprofloxacin-resistant strains of Salmonella, the expression level of ompF was decreased. Meanwhile, the expression levels of invA and invE were decreased except for only one strain, indicating generally decreased virulence. These results were also verified with ciprofloxacin-induced resistant strains. Thus, it was informative for understanding the drug-resistance in Salmonella. Monitoring drug-resistance and virulence relevant genes would be significant in the prevention and control of salmonellosis. [ABSTRACT FROM AUTHOR]

Karyopherin α2 (KPNA2) plays a central role in nucleocytoplasmic transport. It is involved in controlling the flow of genetic information and the modulation of diverse cellular activities. Here we explored the KPNA2′s roles during the pathophysiological processes of intracerebral hemorrhage (ICH). An ICH rat model was built and evaluated according to behavioral testing. Using Western blot, immunohistochemistry, and immunofluorescence, significant upregulation of KPNA2 was found in neurons in brain areas surrounding the hematoma following ICH. Increasing KPNA2 level was found to be accompanied by the upregulation of active caspase-3, Bax, and decreased expression of Bcl-2. Besides, KPNA2 co-localized well with active caspase-3 in neurons, indicating its potential role in neuronal apoptosis. What's more, knocking down KPNA2 by RNA-interference in PC12 cells reduced active caspase-3 expression. Thus, KPNA2 may play a role in promoting the brain secondary damage following ICH. [ABSTRACT FROM AUTHOR]

Protein tyrosine phosphatase 1B (PTP1B), a member of the protein tyrosine phosphatase family, attaches to the endoplasmic reticulum (ER) via its C-terminal tail. Previous studies have reported that PTP1B participates in various signal transduction pathways in many human diseases, including diabetes, cancers, osteoporosis, and obesity. It also plays an important role in the ER stress. ER stress induced by spinal cord injury (SCI) was reported to result in cell apoptosis. Till now, the role of PTP1B in the injury of the central nervous system remains unknown. In the present study, we built an adult rat SCI model to investigate the potential role of PTP1B in SCI. Western blot analysis detected a notable alteration of PTP1B expression after SCI. Immunohistochemistry indicated that PTP1B expressed at a low level in the normal spinal cord and greatly increased after SCI. Double immunofluorescence staining revealed that PTP1B immunoreactivity was predominantly increased in neurons following SCI. In addition, SCI resulted in a significant alteration in the level of active caspase-3, caspase-12, and 153/C/EBP homologous transcription factor protein, which were correlated with the upregulation of PTP1B. Co-localization of PTP1B/active caspase-3 was also detected in neurons. Taken together, our findings elucidated the PTP1B expression in the SCI for the first time. These results suggested that PTP1B might be deeply involved in the injury response and probably played an important role in the neuro-pathological process of SCI. [ABSTRACT FROM AUTHOR]

The objective was to evaluate the expression levels of CD31+CD54+ and CD31+CD105+ endothelial microparticles (EMPs) before and after intravenous immunoglobulin (IVIG) treatment of Kawasaki disease (KD). To explore the role of human umbilical cord mesenchymal stem cells (hucMSCs) in inhibiting endothelial inflammation in KD, the effects of hucMSCs on the expression of CD54 and CD105 in endothelial cells in KD were analyzed in vivo and in vitro. The concentrations of IL-1β and VEGF in the peripheral blood of KD or healthy children were detected, and the distributions of CD31+CD54+ and CD31+CD105+ EMPs in platelet-poor plasma (PPP) were analyzed by flow cytometry. Human umbilical vein endothelial cells (HUVECs) were first cocultured with the patients' peripheral blood mononuclear cells (PBMCs). Next, HUVECs were cocultured with hucMSCs after stimulation with inactivated serum from patients. Cell proliferation and migration activities were assessed, and the expression of CD54, CD105 and IL-1β was analyzed. In an in vivo study, hucMSCs were transplanted into KD mice. The locations and expression levels of CD54, CD105 and IL-1β in the heart tissues of mice were analyzed. The levels of IL-1β and CD31+CD54+ EMPs were significantly higher before IVIG treatment and 2 weeks after treatment in KD patients (P < 0.01). However, the levels of VEGF and CD31+CD105+ EMPs increased significantly in KD only after IVIG treatment (P < 0.01). KD-inactivated serum stimulation combined with cocultivation of PBMCs can activate inflammation in HUVECs, leading to reduced cell proliferation and migration activities. Cocultivation also increased the expression of CD54 and decreased the expression of CD105 (P < 0.001). Cocultivation with hucMSCs can reverse these changes. Additionally, hucMSC transplantation downregulated the expression of IL-1β and CD54 and significantly upregulated the expression of CD105 in KD mice. The expression levels of CD31+CD54+ and CD31+CD105+ EMPs showed inconsistent changes at different KD statuses, providing potential markers for clinical application. HucMSCs suppress inflammation and regulate the expression levels of CD54 and CD105 in vascular endothelial cells in KD, possibly providing a new basis for stem cell therapy for KD. • CD31+CD54+ and CD31+CD105+ EMPs change inconsistently at different stages of KD, potentially reflect endothelial function. • HucMSCs suppress inflammation and regulate the expression levels of CD54 and CD105 in vascular endothelial cells in KD. • HucMSCs inhibit coronary artery inflammation while also promoting the repair of damaged tissues in KD mice. [ABSTRACT FROM AUTHOR]

In order to investigate enterobacteria presence involved in the secondary infections in Porcine Reproductive and Respiratory Syndrome (PRRS) pigs with different viral co-infections, we identified enterobacteria for guiding clinical treatment. Twenty-one diseased pigs were diagnosed with the PRRS virus (PRRSV) and other 7 virus primers by PCR/RT-PCR in the lung and spleen samples. Enterobacteria were isolated using MacConkey agar from 5 visceral samples of PRRS pigs, and identified by 16S rDNA sequencing. PRRSV was positive in 100% of the lung samples and 81.0% of the spleen samples. Seven diseased pigs were diagnosed with only PRRSV infection (33.3%), 7 pigs with PRRSV and 1 or 2 other viruses (33.3%) and 7 pigs with PRRSV and more than 2 types of other viruses (33.3%). PRRSV was more inclined to co-infect pigs with porcine group A rotavirus (PARV) with the co-infection rate of 52.4% (11/21). Approximately 13 types of bacteria were successfully isolated from lung, spleen, liver, kidney and lymph node samples of different PRRS pigs. Enterobacteria were isolated in 100% of lung, liver and lymph samples from pigs infected with PRRSV alone. However, the isolation rates were significantly decreased in the more than 3 viruses co-infection group. Escherichia coli was the most prevalent bacterium, followed by Morganella , Proteus , Shigella , Salmonella, Klebsiella and Aeromonas. Most of the isolated enterobacteria were opportunistic pathogens. Therefore, timely combination with antimicrobial agents is necessary for effective treatment of PRRS-infected pigs. • PRRSV was more inclined to co-infect with PARV. • Pigs co-infected with more virus, less enterobacteria were isolated from their viscera. • Enterobacteria isolated from viscera of PRRS pigs were opportunistic pathogens. • coli, Morganella and Proteus were the most prevalent enterobacteria. • Secondary infection of enterobacteria should be considered in PRRS treatment. [ABSTRACT FROM AUTHOR]