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Background: Shortening retention time and minimizing relapse rates are ongoing challenges in orthodontics. This study investigated the effects of natural fulvic acids (FAs) and low-level laser therapy (LLLT) on orthodontic retention in rats. Methods: Seventy-two male Sprague-Dawley rats underwent mesial movement of the left maxillary first molar using a 50 g force via a nickel-titanium tension spring. After three weeks of movement, the rats entered the retention phase with retainer wires and were divided into four groups: Control (no intervention), FAs (80 mg/kg orally daily), LLLT (808 nm laser twice weekly), and FAs + LLLT (both treatments). Retainers were removed on days 7, 14, and 21 for a 3-day relapse assessment. Maxillary impressions were analyzed for relapse rates using 3Shape software, alongside histological and immunohistochemical evaluations of bone morphogenetic protein-2 (BMP-2) expression in periodontal tissues, with differences among groups analyzed using an ordinary two-way analysis of variance (ANOVA). Results: The relapse rate decreased over time, particularly at 10, 17, and 24 days (p < 0.001). The FAs group did not significantly affect relapse rates compared to the control group (p = 0.084). In contrast, both the LLLT and FAs + LLLT groups significantly reduced relapse rate (p < 0.001), with no significant difference between these groups (p = 0.555). Histological examination revealed active osteoclasts on day 10, decreasing by days 17 and 24. The LLLT and FAs + LLLT groups showed less local cementum resorption and better periodontal fiber arrangement. All treatment groups significantly increased BMP-2 expression (P < 0.05) compared to controls. with LLLT and FAs + LLLT differing significantly from FAs (P < 0.001), though no difference was observed between LLLT and FAs + LLLT (P = 0.578). Conclusions: FAs did not significantly reduce relapse rate with retainers, while LLLT effectively reduced relapse rates, showing no additional benefit from combining FAs with LLLT. Both FAs and LLLT increased BMP-2 expression in PDL fibroblasts but with no synergistic effect. [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]

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]

To understand the prevalence of avian methicillin-resistant Staphylococcus aureus (MRSA) and the current status of drug resistance in Qingdao, a comprehensive molecular epidemiological investigation and analysis of evolutionary relationships of MRSA isolates from broiler and layer chickens and waterfowl was conducted. One hundred and two avian MRSA strains were identified by multi-locus sequence typing, staphylococcal protein A (spa) and staphylococcal cassette chromosome mec (SCCmec) typing, and whole-genome sequencing. The sequence type (ST) 9-t899-SCCmec IVb type represented the highest proportion of avian-derived MRSA strains (71.57%), with ST398 type strains occasionally observed in broilers and waterfowl. The poultry-derived MRSA strains were all resistant to eight or more antimicrobials. Avian-derived MRSA strains carried 20 resistance genes, 109 virulence genes and 10 plasmids. Strains carrying the cfr oxazolidinone resistance gene were occasionally seen in broiler- and layer-derived MRSA. Single nucleotide polymorphism (SNP) core genome evolution and locus difference analysis showed that the closest strains were all of ST9-t899 type (to which also affiliated the highest number of strains) and this type occurred on all three kinds of poultry farm, but the SNP difference loci between strains of the same type ranged from 0 to 1472. The dominant type of MRSA from different poultry sources in Qingdao is ST9-t899-SCCmec IVb, which is commonly resistant to a variety of antimicrobial drugs and carries a variety of resistance genes and a large number of virulence genes. Sequence type 9-t899 type is widely spread among the three kinds of poultry investigated, but there are differences in affiliations. [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]

This paper examines the effects of mobile payment (m-payment) adoption on household savings decline in China. Using data from the 2017 China Household Finance Survey, we employ an instrumental variable approach with multiple robustness checks to evaluate the impact of m-payment adoption on household savings rate. Our study discovers that m-payment usage decreases the household savings rate by about 20% points. We also find that, relative to that of rural and older households, the savings of urban and younger households are more significantly influenced by m-payment adoption. The main channels through which m-payment usage affects the household saving rate likely include improved risk sharing, alleviated credit constraint, and enhanced risk tolerance. This paper provides important insights about m-payment adoption and the ongoing household savings decline in China. [ABSTRACT FROM AUTHOR]

Pork is one of the most common foods causing microbial foodborne diseases. Since pork directly enters the market after slaughtering, the control of microbial contamination in the slaughtering processes is the key to ensuring the quality and safety of pork. The contamination level of Escherichia coli , a health-indicator bacterium, can reflect the risk level of potential pathogens. In order to assess the E. coli exposure risk of pork during slaughtering and to identify the key control points, we established an E. coli quantitative exposure assessment model for swine-slaughtering processes in slaughterhouses of different sizes. The model simulation data indicated the E. coli contamination pattern on the surfaces of swine carcasses during slaughtering. The changes in E. coli contamination were analyzed according to the simulation data of each slaughtering process. It was found that the number of E. coli after trimming in big and small slaughterhouses increased to the maximum values for the whole processes, which were 3.63 and 3.52 log10 CFU/100 cm2, respectively. The risk contribution of each slaughtering process to the E. coli contamination on the surface of terminal swine carcasses can be determined by correlation analysis. Because the absolute value of correlation coefficient during the trimming process was maximum (0.49), it was regarded as the most important key control point. This result can be further proved via the multilocus sequence typing of E. coli. The dominant sequence type before trimming processes was ST10. ST1434 began to appear in the trimming process and then became the dominant sequence type in the trimming and pre-cooling processes. The model can provide a theoretical basis for microbial hygiene supervision and risk control in swine-slaughtering processes. [ABSTRACT FROM AUTHOR]

Melasma is an acquired and chronic hyperpigmentation disorder which is recognized as one of the most psychologically distressing and difficult to cure forms of skin hyperpigmentation. It is associated with substantial quality of life impairments. Treatments of melasma include local application, oral medication, physical laser therapy and program combination therapy. However, routine treatment usually leads to the damage of skin barrier function, resulting in adverse reactions such as erythema, pruritus, post-inflammatory pigmentation and even scar. Skin care products contain a variety of active ingredients, which are widely concerned by cosmetic dermatologists because of high safety, good tolerance and the effect of improving the damaged skin barrier. Using skin care products alone or in combination with routine treatment not only can improve the curative effect for melasma, reduce side effects and recurrence rate, but also improve patient satisfaction. This article mainly describes the application of skin care products in the treatment of melasma. [ABSTRACT FROM AUTHOR]

Resident adipocytes under a hypoxic tumor microenvironment exert an increasingly important role in cell growth, proliferation, and invasion in cancers. However, the communication between adipocytes and cancer cells during nasopharyngeal carcinoma (NPC) progression is poorly understood. Here, we demonstrate that hypoxic adipocyte‐derived exosomes are key information carriers that transfer low expression of miR‐433‐3p into NPC cells. In addition, luciferase reporter assays detected that hypoxia inducible factor‐1α (HIF‐1α) induced miR‐433‐3p transcription through five binding sites at its promoter region. Concordantly, the low expression of miR‐433‐3p promoted proliferation, migration, and lipid accumulation in NPC cells via targeting stearoyl‐CoA desaturase 1 (SCD1) are suggested by functional studies. Consistent with these findings, in tumor‐bearing mice, NPC cells with low HIF‐1α expression, high miR‐433‐3p expression, and low SCD1 expression were equally endowed with remarkably reduced potential of tumorigenesis. Collectively, our study highlights the critical role of the HIF‐1α‐miR‐433‐3p‐SCD1 axis in NPC progression, which can serve as a mechanism‐based potential therapeutic approach. [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]

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]

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]

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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]

Background: Kawasaki disease (KD) is a common, yet unknown etiology disease in Asian countries, which causes acquired heart disease in childhood. It is characterized by an inflammatory acute febrile vasculitis of medium-sized arteries, particularly the coronary arteries. High-mobility group box-1 protein (HMGB1) is a non-histone chromosomal-binding protein present in the nucleus of eukaryotic cells, which contains 215 amino acid residues. Although the cellular signal transduction mechanisms of HMGB1 are currently unclear, the important role of the receptor for advanced glycation end-products (RAGE), the main receptor for HMGB1 has been reported in detail. The purpose of our study was to verify the mechanism and clinical significance of HMGB1-RAGE in coronary artery injury of Kawasaki disease. Methods: 52 blood samples of patients in KD were collected, and the coronary artery Z score was calculated according to the echocardiographic results. The Z score ≥ 2.0 was classified as coronary artery lesions (CAL); otherwise, it was no-coronary artery lesions (NCAL). In addition, the fever group and control group were set. Among them, the fever group were children with fever due to respiratory tract infection at the same time period as KD (heat peak ≥ 38.5 ℃). The normal group were children at a routine physical examination in the outpatient clinic of Nantong University and the physical examination center of the child care insurance, and there were no infectious diseases and heart diseases. The serum levels of HMGB1, RAGE, and NF-κB in each group were detected by ELISA. The animal model of KD was established using the New Zealand young rabbits. We used RT-qPCR/H&E staining/immunohistochemistry/ELISA and western blot to detect the level of HMGB1/RAGE and NF-κB. Results: In this study, we found that the HMGB1/RAGE/NF-κB axis was elevated in the serum of children with KD. In addition, an animal model of KD was subsequently prepared to examine the pathological changes of the coronary arteries. We found that the serum levels of HMGB1/RAGE/NF-κB in rabbits with KD were significantly higher than those of the control group. Moreover, the lumen diameter of the coronary artery was slightly enlarged, and the wall of the tube became thinner and deformed. In addition, the HMGB1/RAGE/NF-κB levels in the coronary artery were higher in the rabbits with KD in the acute phase. Conclusions: On the whole, the findings of this study demonstrate that the expression of HMGB1/RAGE/NF-κB is altered at different stages of KD, suggesting that the HMGB1/RAGE/NF-κB signaling pathway plays an important role in vascular injury in KD. The results of this study may have important implications for the early warning of coronary artery lesions in KD. [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]

Competing endogenous RNAs (ceRNAs) represent a novel mechanism of gene regulation that may mediate key subpathway regions and contribute to the altered activities of pathways. However, the classical methods used to identify pathways fail to specifically consider ceRNAs within the pathways and key regions impacted by them. We proposed a powerful strategy named ce‐Subpathway for the identification of ceRNA‐mediated functional subpathways. It provided an effective level of pathway analysis via integrating ceRNAs, differentially expressed (DE) genes and their key regions within the given pathways. We respectively analysed one pulmonary arterial hypertension (PAH) and one myocardial infarction (MI) data sets and demonstrated that ce‐Subpathway could identify many subpathways whose corresponding entire pathways were ignored by those non‐ceRNA‐mediated pathway identification methods. And these pathways have been well reported to be associated with PAH/MI‐related cardiovascular diseases. Further evidence showed reliability of ceRNA interactions and robustness/reproducibility of the ce‐Subpathway strategy by several data sets of different cancers, including breast cancer, oesophageal cancer and colon cancer. Survival analysis was finally applied to illustrate the clinical application value of the ceRNA‐mediated functional subpathways using another data sets of pancreatic cancer. Comprehensive analyses have shown the power of a joint ceRNAs/DE genes and subpathway strategy based on their topologies. [ABSTRACT FROM AUTHOR]

Abstract: This paper investigates the effects of house price appreciation on homeowners' labour force participation (LFP). Although economic theories predict that housing capital gains will reduce labour supply, empirical evidence from urban China revealed that house price appreciation significantly boosts homeowners' LFP. Heterogeneous analyses indicate that LFP behaviour is more likely to be affected by house price appreciation for female and younger homeowners. Furthermore, homeowners living in provinces with greater house price appreciation tend to be more active in job participation than those living in provinces with lower price appreciation. [ABSTRACT FROM AUTHOR]

Abstract: Cardiac hypertrophy (CH) is a common disease that originates from long‐term heart pressure overload and finally leads to heart failure. Recently, long non‐coding RNAs (lncRNAs) have attracted attention because they have broad and crucial functions in regulating complex biological processes. Some studies had found that lncRNAs play vital roles in complex cardiovascular diseases. However, the function and mechanism of lncRNAs in CH have not been elucidated. In our study, to investigate the potential roles of lncRNAs in CH, the Cardiac Hypertrophy‐associated LncRNAs‐Protein coding genes Network (CHLPN) was constructed by integrating gene microarray re‐annotation and subpathway enrichment analyses. After performing random walking with restart in CHLPN, we predicted 21 significant risk lncRNAs, of which 7 (Kis2, 1700110K17Rik, Gm17501, E330017L17Rik, C630043F03Rik, Gm9866 and Ube4bos1) formed a close module with their co‐expressed protein‐coding genes (PCGs). We found that the module might play crucial roles in the development of CH. In particular, 44 PCGs that were co‐expressed with six lncRNAs were enriched in CH‐related biological processes and pathways. We also found that some lncRNAs participated in the competitive endogenous RNA cross‐talk that might be involved in CH. These results indicate that the functional lncRNAs are related to post‐transcriptional regulation and could shed light on a new molecular diagnostic target of CH. [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]

The widespread environmental contaminant, 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD), is considered one of the most toxic dioxin-like compounds. Although epidemiological studies have shown that TCDD exposure is linked to some neurological and neurophysiological disorders, the underlying mechanism of TCDD-mediated neurotoxicity has remained unclear. Astrocytes are the most abundant cells in the nervous systems, and are recognized as the important mediators of normal brain functions as well as neurological, neurodevelopmental and neurodegenerative brain diseases. In this study, we investigated the role of TCDD in regulating the expression of glutamate transporter GLT-1 in astrocytes. TCDD, at concentrations of 0.1-100 n m, had no significantly harmful effect on the viability of C6 glioma cells. However, the expression of GLT-1 in C6 glioma cells was downregulated in a dose- and time-dependent manner. TCDD also caused activation of protein kinase C (PKC), as TCDD induced translocation of the PKC from the cytoplasm or perinuclear to the membrane. The translocation of PKC was inhibited by one Ca2+ blocker, nifedipine, suggesting that the effects are triggered by the initial elevated intracellular concentration of free Ca2+. Finally, we showed that inhibition of the PKC activity reverses the TCDD-triggered reduction of GLT-1. In summary, our results suggested that TCDD exposure could downregulate the expression of GLT-1 in C6 via Ca2+/PKC pathway. The downregulation of GLT-1 might participate in TCDD-mediated neurotoxicity. Copyright © 2016 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

ABSTRACT The environmental toxicant TCDD may elicit cytotoxic effects by inducing reactive oxygen species (ROS) generation. Autophagy is one of the first lines of defense against oxidative stress damage. Herein, we investigated whether autophagy played a regulatory role in TCDD-induced neurotoxicity. Here, we showed that TCDD exposure caused marked autophagy in SH-SY5Y cells, whose dose range was close to that inducing apoptosis. Electron microscopic and Western blot analyses revealed that TCDD induced autophagy at a starting dose of approximate 100 nM. Interestingly, 100-200 nM TCDD exposure resulted in obviously decreased cell viability and evident apoptotic phenotype. Furthermore, the levels of pro-apoptotic molecules, Bax and cleaved-PARP, increased significantly, whereas Bcl2 declined after exposed to 100 nM TCDD. In addition, the apoptosis was verified using flow cytometrical analysis. These data strongly suggested that TCDD induced both autophagy and apoptosis at a similar dose range in SH-SY5Y cells. Interestingly, pretreatment with ROS scavenger, N-acetyl-cysteine (NAC), could effectively block both TCDD-induced apoptosis and autophagy. More surprisingly, inhibition of autophagy with 3-methyladenine (3MA), remarkably augmented TCDD-induced apoptosis. The findings implicated that the onset of autophagy might serve as a protective mechanism to ameliorate ROS-triggered cytotoxic effects in human SH-SY5Y neuronal cells under TCDD exposure. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1068-1079, 2016. [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 ubiquitination is a dynamic two-way process that can be reversed or regulated by deubiquitinating enzymes (DUB). USP11, located on the X chromosome, 6 is a member of USP subclass of the DUB family. Here, we demonstrate that USP11 may be involved in neuronal apoptosis in the processes of intracerebral hemorrhage (ICH). From the results of Western blot, immunohistochemistry, and immunofluorescence, we obtained a significant up-regulation of USP11 in neurons adjacent to the hematoma following ICH. Increasing USP11 level was found to be accompanied by the up-regulation of active caspase-3, Fas receptor (Fas), Fas ligand (FasL), and active caspase-8. Besides, USP11 co-localized well with active caspase-3 in neurons, indicating its potential role in neuronal apoptosis. What is more, knocking down USP11 by RNA-interference in PC12 cells reduced active caspase-3 expression. Thus, USP11 may play a role in promoting the brain secondary damage following ICH. [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]

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]

Purpose -- The purpose of this paper is to evaluate the effects of access to formal credit on rural household technical efficiency in China. Design/methodology/approach -- Based on the rural household survey data in Weifang city, Shandong province in northern China, the authors apply recent developed bootstrapped DEA approach to investigate rural technical efficiency at the household level under the consideration of off-farm activities. Rural households are then identified as credit constrained and classified as supply-side and demand-side credit constraints by applying direct elicitation method. Finally, the authors apply a tobit regression to examine the effects of credit constraints on household technical efficiency. Findings -- Rural households in China not only suffer supply-side credit constraints, but also demand-side credit constraints resulted from the transaction costs and risk rationing. The tobit regression discloses that demand-side credit constraints impose significant negative impacts on household technical efficiency. Originality/value -- The authors clarify the definition of credit constraints and classify the credit constraints into supply-side and demand-side credit constraints. The results of this paper have significant policy implications for rural finance policies in China. [ABSTRACT FROM AUTHOR]

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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]

Inflammatory infiltration has been recently emphasized in the demyelinating diseases of the central nervous system including multiple sclerosis. β-1,4-Galactosyltransferase I (β-1,4-GalT-I) is a major galactosyltransferase responsible for selectin-ligand biosynthesis, mediating rolling of the inflammatory lymphocytes. In the present study, Western blot showed that expression of β-1,4-GalT-I was low in normal or complete Freund's adjuvant (CFA) control rats' spinal cords, and it began to increase since early stage and peaked at E4 stage of experimental autoimmune encephalomyelitis (EAE) and restored approximately at normal level in the recovery stage. Immunohistochemisty revealed that upregulation of β-1,4-GalT-I was predominantly distributed in the white matter of spinal cord , while there was also some increased staining of β-1,4-GalT-I in the grey matter. Meanwhile, the expression of E-selectin, the substrate of β-1,4-GalT-I, was significantly increased, with a peak at E4 stage of EAE, and gradually decreased thereafter. Lectin blot showed that the protein bands with molecular weights of 65-25 kDa reacted a remarkable increase at the peak stage of EAE when compared with the normal and CFA control. Ricinus Communis Agglutinin-I (RCA-I) histochemistry revealed that RCA-Ι-positive signals were most intense in white matter of lumbosacral spinal cord at the peak stage of EAE (E4). Immunohistochemistry showed that β-1,4-GalT-I and CD62E, a marker for E-selectin stainings located in a considerable number of ED1 (+) macrophages in perivascular or in the white matter in EAE lesions, and a good co-localization of ED1 (+) cells with CD62E was observed. All these results suggest that β-1,4-GalT-I might serve as an inflammatory mediator regulating adhesion and migration of inflammatory cells in EAE, possibly through influencing the modification of galactosylated carbohydrate chains to modulate selectin-ligand biosynthesis and interaction with E-selectin. [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]

This article identifies the level of the expected utility (EU) risk aversion and Value-at-Risk (VaR) confidence level that yield the same choice from a given distribution of outcomes, and thus allow for consistent application of the two criteria. The result for a given distribution is an explicit mapping between risk aversion under EU and VaR, for both normal and nonnormal distributions. The Cornish–Fisher expansion is used to establish adjusted mean-deviates for nonnormal outcome distributions and the investor's preference function is expanded to include elements for variance, skewness, and excess kurtosis. A farm-level application with nonnormal revenue distribution illustrates these approaches. [ABSTRACT FROM AUTHOR]

The extant literature regarding the effects of housing on stock investment shows inconsistent findings, either positive or negative effects have been reported. This paper investigates the mechanisms by which housing affects household stock investment through a structure equation model (SEM). Applying the data from the China Household Finance Survey (CHFS), we confirm and quantify the magnitudes of contemporaneous "wealth effects" and "crowd-out effects" of housing on household equity investment. Overall, the combined effect of housing on stock investment is positive in the context of urban China. [ABSTRACT FROM AUTHOR]