bluuebunny/crossref_metadata_2025_split huggingface dataset:
Banking efficiency in emerging economies: Does foreign banks entry matter in the Ghanaian context?
Authors: Ofori‐Sasu Daniel , Mensah Lord , Akuma John Kwame , Doku Isaac 
Published: October 2018

AbstractThis study empirically examines the effect of foreign banks entry on banking efficiency scores, using the truncated regression data envelopment analysis model for 25s banks in Ghana, over a 6‐year period (2010–2015). We decompose the efficiency scores into three (technical, cost, and allocative efficiency), and the results indicate that banks in Ghana are marginally inefficient in operating closer to their optimal capacity. The findings show that the input‐oriented model slacks are needed to push an inefficient bank closer to where an efficient bank is positioned. From the results, an immediate and a short‐term entry of foreign banks have a consistent negative relationship with both technical‐ and cost‐efficiency scores whereas long‐term entry of foreign banks shows an inconsistent relationship with the three banking efficiency scores. Thus, the drive towards a positive impact of foreign banks entry on the three efficiency scores is dependent on the form of banking efficiency considered and the interaction term between competitive banking environment (competition) and foreign banks' entry. The study suggests that policymakers and managers in emerging markets should improve on their bank efficiencies in both a competitive banking environment and during periods of foreign bank entry. Moreover, managers of banks should make adjustment to their input resources in order to cope with new banking technologies from foreign bank entry—thereby improving banking efficiencies.
Effect of early “quilting” sutures on morbidity in postpartum hemorrhage
Authors: Stein Werner , Spätling Ludwig 
Published: October 2018

AbstractObjectiveTo examine whether “quilting” sutures are safe and effective in preventing hysterectomy among women with postpartum hemorrhage (PPH) and whether early application might reduce the incidence of transfusion.MethodsData were reviewed from women treated via quilting sutures after cesarean delivery at a university hospital between 2007 and 2016. Objective and subjective data were collected by analyzing medical records and performing telephone interviews. To observe trends during the study period, data from the first 50% of women treated were compared with those from the second 50%.ResultsOverall, 26 cesareans with quilting sutures were performed. Two hysterectomies could not be avoided. During 2012–2106, 18 quilting sutures were performed as compared with 8 in 2007–2011, pointing to a more liberal indication. Intensive care was required twice as frequently among the first 13 procedures than among the second 13 procedures (10 vs 5, respectively). A similar observation was made for the use of blood transfusions or clotting activation (9 vs 4, respectively). Three women who desired to have a child subsequently delivered a newborn.ConclusionQuilting sutures were found to be a safe and simple technique to prevent hysterectomies in PPH. Morbidity was reduced when the decision to perform sutures was taken early.
Identification of six miRNAs serving as predictive biomarkers in coronary artery disease
Authors: Ren Fei , Gao Wen‐Chuang , Ke Zun‐Ping , Xu Yong , Liu Yu 
Published: October 2018

AbstractCoronary artery disease (CAD) is quite a common disease with high risk. It was reported that microRNAs (miRNAs) had significant effect on the occurrence of CAD. The previously published results are inconsistent due to the parameters, such as sequencing platform, samples selection, and the filter conditions. Here we aimed to explore the critical miRNAs in the occurrence of CAD, which may function as the potential biomarkers. A total of 12 representative datasets of miRNAs related to the occurrence of miRNAs were finally selected, and the critical miRNAs were determined by the comparison of the overlap relations. TargetScan software was used to predict the target genes of these critical miRNAs. Besides, DAVID and Tfacts dataset were used to analyze the functional enrichment and the transcriptional factors analysis. At last, a total of six signature miRNAs were identified, among which five were significantly upregulated and one was downregulated. The target gene of upregulated miRNAs was mostly enriched in the process of RNA Polymerase II promoter and the transcription of DNA template, whereas the target genes of downregulated miRNAs were mostly enriched in the regulation of transcription, DNA‐templated. Besides, the result of the transcriptional factor analysis showed that there were 43 factors coexisting in two kinds of target genes. In summary, six critical miRNAs, as well as the corresponding target genes and transcriptional factors, were identified in the occurrence of CAD by bioinformatics analysis. These identified miRNAs may function as potential biomarkers in the clinical management of CAD.
Knockdown of PSMC3IP suppresses the proliferation and xenografted tumorigenesis of hepatocellular carcinoma cell
Authors: Ding Jingli , Li Yang , Fan Huxiong , Xu Weichang , Gao Rifeng , Bai Shuheng , Zhu Zhigang , Yang Wei , Gong Yi , Yang Juesheng , Zhou Jianliang 
Published: October 2018

AbstractHepatocellular carcinoma (HCC) is the fifth most frequent malignancy and the second leading cause of cancer‐related death worldwide. Proteasome 26S subunit ATPase 3 interacting protein (PSMC3IP) is an oncogene in breast cancer, while its role in HCC remains unclear. Here, we found that PSMC3IP was critical for the cell proliferation and tumorigenic capacity of HCC cells. Upregulation of PSMC3IP was observed in HCC specimens, and high PSMC3IP expression predicted poor overall survival of HCC patients. In vitro, knockdown of PSMC3IP blunted the proliferation and colony formation of BEL‐7404 and SMMC‐7721 cells. Likewise, PSMC3IP silencing suppressed the xenografted tumor development of BEL‐7404 cells. Mechanistically, apoptosis was enhanced after PSMC3IP knockdown in both BEL‐7404 and SMMC‐7721 cells. At the molecular level, TP53 and GNG4 were upregulated and eukaryotic translation initiation factor 4E (EIF4E) and insulin like growth factor 1 receptor (IGF1R) were downregulated in shPSMC3IP compared with shCtrl BEL‐7404 cells. Therefore, targeting PSMC3IP maybe a promising strategy for HCC.
RSPO2 enhances cell invasion and migration via the WNT/β‐catenin pathway in human gastric cancer
Authors: Zhang Haibo , Han Xiaoyan , Wei Bo , Fang Jiafeng , Hou Xuerui , Lan Tianyun , Wei Hongbo 
Published: October 2018

AbstractR‐spondins comprise a group of secreted WNT agonists. R‐spondin2 (RSPO2) plays a crucial role in the activation of the WNT/β‐catenin pathway and oncogenesis, though its specific role in human gastric cancer (GC) remains unclear. In the current study, RSPO2 expression levels were upregulated in cancer specimens and cell lines (AGS and BGC‐823). Inhibition of RSPO2 expression levels had distinct effects on cell invasion, migration, and epithelial‐mesenchymal transition (EMT) in AGS and BGC‐823 cells in vitro. Furthermore, RSPO2 positively correlated with leucine‐rich repeat‐containing G‐protein‐coupled receptor 5 (LGR5), the receptor of RSPO2. Silencing RSPO2 reduced the expression of LGR5 and WNT/β‐catenin effector molecule β‐catenin together with downstream targets TCF‐4 and Cyclin‐D1. These observations demonstrate that upregulation of RSPO2 in GC specimens and cell lines is closely related to tumor invasion and migration and that RSPO2 promotes EMT in gastric cancer cells by activating WNT/β‐catenin signaling.
Loss of miR‐146b‐5p promotes T cell acute lymphoblastic leukemia migration and invasion via the IL‐17A pathway
Authors: Tu Zhenbo , Xiong Jie , Xiao Ruijing , Shao Liang , Yang Xiangyong , Zhou Lu , Yuan Wen , Wang Meng , Yin Qian , Wu Yingjie , Pan Shan , Leng Jun , Jiang Daozi , He Chunjiang , Zhang Qiuping 
Published: October 2018

AbstractMetastatic disease remains the primary cause of death for individuals with T cell acute lymphoblastic leukemia (T‐ALL). microRNAs (miRNAs) play important roles in the pathogenesis of T‐ALL by inhibiting gene expression at posttranscriptional levels. The goal of the current project is to identify any significant miRNAs in T‐ALL metastasis. We observed miR‐146b‐5p to be downregulated in T‐ALL patients and cell lines, and bioinformatics analysis implicated miR‐146b‐5p in the hematopoietic system. miR‐146b‐5p inhibited the migration and invasion in T‐ALL cells. Interleukin‐17A (IL‐17A) was predicted to be a target of miR‐146b‐5p; this was confirmed by luciferase assays. Interestingly, T‐ALL patients and cell lines secreted IL‐17A and expressed the IL‐17A receptor (IL‐17RA). IL‐17A/IL‐17RA interactions promoted strong T‐ALL cell migration and invasion responses. Gene set enrichment analysis (GSEA) and quantitative polymerase chain reaction (qPCR) analysis indicated that matrix metallopeptidase‐9 (MMP9), was a potential downstream effector of IL‐17A activation, and nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB) signaling was also implicated in this process. Moreover, IL‐17A activation promoted T‐ALL cell metastasis to the liver in IL17A
−/− mouse models. These results indicate that reduced miR‐146b‐5p expression in T‐ALL may lead to the upregulation of IL‐17A, which then promotes T‐ALL cell migration and invasion by upregulating MMP9 via NF‐κB signaling.
P2X4R silence suppresses glioma cell growth through BDNF/TrkB/ATF4 signaling pathway
Authors: Huo Jun‐Feng , Chen Xiao‐Bing 
Published: October 2018

AbstractPurinergic receptor P2X 4 (P2X4R), a member of purinergic channels family and a subtype of ionotropic adenosine triphosphate receptors, plays a critical role in tumorigenesis. Evidence suggested that P2X4R is expressed in rat C6 glioma model, however, its role and the underlying mechanism of action are still unclear in human glioblastoma multiforme (GBM). In the current study, our aim is to examine the function and the molecular basis of P2X4R in GBM. We first observed that GBM cells, U251, T98, U87, U373, and A172 were all high expressed P2X4R, when compared with the normal human astrocytes (NHA) cells. To gain the function of P2X4R, P2X4R silence cells were constructed by transfection with P2X4R small interfering RNA (siRNA). We found that P2X4R deletion impeded T98 and U87 cell viability and proliferation, and further studies indicated that cell apoptosis and caspase‐3 activity was increased in T98 and U87 cell transfected with P2X4R siRNA. Subsequently, we confirmed that P2X4R silence suppressed brain‐derived neurotrophic factor (BDNF), Trk receptor tyrosine kinases (TrkB), and activating transcription factor 4 (ATF4) expression in T98 and U87 cells. And P2X4R siRNA–induced ATF4‐expression inhibition dependent on BDNF/TrkB signaling pathway. The impact of P2X4R silence on T98 and U87 cell growth and apoptosis was reversed by ATF4 overexpression. In summary, this study provides the first evidence that P2X4R plays important roles in GBM cell growth and apoptosis.
The roles of FOX proteins in virus‐associated cancers
Authors: Ramezani Ali , Nikravesh Hojatolla , Faghihloo Ebrahim 
Published: October 2018

AbstractForkhead box (FOX) proteins play a crucial role in regulating the expression of genes involved in multiple biological processes, such as metabolism, development, differentiation, proliferation, apoptosis, migration, invasion, and longevity. Deregulation of FOX proteins is commonly associated with cancer initiation, progression, and chemotherapeutic drug resistance in many human tumors. FOX proteins deregulate through genetic events and the perturbation of posttranslational modification. The purpose of the present review is to describe the deregulation of FOX proteins by oncoviruses. Oncoviruses utilize various mechanisms to deregulate FOX proteins, including alterations in posttranslational modifications, cellular localization independently of posttranslational modifications, virus‐encoded miRNAs, activation or suppression of a series of cell signaling pathways. This deregulation can affect proliferation, metastasis, chemotherapy resistance, and immunosuppression in virus‐induced cancers and help to chronic viral infection, development of gluconeogenic responses, and inflammation. Since the PI3K/Akt/mTOR signaling pathway is the upstream FOXO, suppressing it can cause FOXO function to return, and this can be one of the reasons for patients to recover from the infection of the viruses used to treat these inhibitors. Hence, FOX proteins could serve as prognosis markers and target therapy specifically in cancers caused by oncoviruses.
Involvement of H19/miR‐326 axis in hepatocellular carcinoma development through modulating TWIST1
Authors: Wei Li‐Qing , Li Li , Lu Chi , Liu Juan , Chen Yanhao , Wu Hongbin 
Published: October 2018

AbstractOverexpression of long noncoding RNA (lncRNA) H19 has been observed in various cancers, which indicates that H19 exert important roles in the progression of carcinogenesis. MiR‐326 has been reported to play tumor suppressive roles in multiple tumors. Recently, the competing endogenous RNA (ceRNA) hypothesis has implied that lncRNAs might function as molecular sponges for microRNAs in various cancers. However, the roles of H19/miR‐326 in human hepatocellular carcinoma (HCC) still remain unclear. The aim of our study was to determine H19/miR‐326 expression in HCC cells and investigate their roles in HCC development. We found that H19 was significantly elevated and miR‐326 was decreased in HCC cells including Hep3B, HepG2, MHCC‐97L, SK‐hep1, Hun7, SMCC‐7721 compared with LO2 cells, respectively. In the subsequent experiments, we observed that inhibition of H19 can repress HCC cell growth, migration, and invasion in vitro. H19 downregulation can increase miR‐326 expression in HCC cells. Meanwhile, miR‐326 mimics can also inhibit HCC progression, whereas miR‐326 inhibitors exhibited a reverse phenomenon by modulating H19 expression. In addition, a negative association between H19 and miR‐326 was predicted and confirmed. Furthermore, the transcription factor TWIST1 has been recognized as a significant regulator in tumor progression. Here, by performing bioinformatics analysis, TWIST1 was identified as a downstream target of miR‐326. The findings of our study implied that lncRNA H19 can serve as a ceRNA to sponge miR‐326 and modulate TWIST1 levels in HCC pathogenesis. Taken these together, these findings indicated that H19/miR‐326/TWIST1 axis was involved in HCC development and can indicate a novel HCC target.
Contriving multiepitope subunit vaccine by exploiting structural and nonstructural viral proteins to prevent Epstein–Barr virus‐associated malignancy
Authors: Ojha Rupal , Nandani Raj , Prajapati Vijay Kumar 
Published: October 2018

AbstractCancer is one of the common lifestyle diseases and is considered to be the leading cause of death worldwide. Epstein–Barr virus (EBV)‐infected individuals remain asymptomatic; but under certain stress conditions, EBV may lead to the development of cancers such as Burkitt’s and Hodgkin’s lymphoma and nasopharyngeal carcinoma. EBV‐associated cancers result in a large number of deaths in Asian and African population, and no effective cure has still been developed. We, therefore, tried to devise a subunit vaccine with the help of immunoinformatic approaches that can be used for the prevention of EBV‐associated malignancies. The epitopes were predicted through B‐cell, cytotoxic T lymphocytes (CTL), and helper T lymphocytes (HTL) from the different oncogenic proteins of EBV. A vaccine was designed by combining the B‐cell and T‐cell (HTL and CTL) epitopes through linkers, and for the enhancement of immunogenicity, an adjuvant was added at the N‐terminal. Further, homology modeling was performed to generate the 3D structure of the designed vaccine. Moreover, molecular docking was performed between the designed vaccine and immune receptor (TLR‐3) to determine the interaction between the final vaccine construct and the immune receptor complex. In addition, molecular dynamics was performed to analyze the stable interactions between the ligand final vaccine model and receptor TLR‐3 molecule. Lastly, to check the expression of our vaccine construct, we performed in silico cloning. This study needed experimental validation to ensure its effectiveness and potency to control malignancy.
The role of SDF1 in prostate epithelial morphogenesis
Authors: Barbosa Guilherme Oliveira , Augusto Taize Machado , Bruni‐Cardoso Alexandre , Carvalho Hernandes F. 
Published: October 2018

AbstractAndrogens induce rat prostate induction from the urogenital sinus epithelium at embryonic day 17.5. Subsequent morphogenesis, including epithelial cord growth, branching, and canalization, results from concerted paracrine interactions with the stroma. A significant number of paracrine factors bind heparan sulfate (HS). We hypothesized that interfering with overall sulfation could disrupt the signaling mediated by HS‐binding factors and that the undersulfated environment would allow investigation of individual exogenous morphogens. First, we investigated whether acinar morphogenesis involved HS‐proteoglycan expression and found that syndecans 1 and 3 were upregulated in RWPE1 cells in the transition from two‐ to three‐dimensional (3D) Matrigel, capable of promoting spheroid formation. We then investigated whether sodium chlorate, a general sulfation inhibitor, interfered with spheroid formation by RWPE1 cells and acinar morphogenesis in ex vivo ventral prostate (VP) organ culture. As expected, treatment with sodium chlorate inhibited spheroid formation by RWPE1 cells in 3D culture. Chlorate also inhibited ex vivo VP epithelial branching and canalization, resulting in long branchless epithelial structures. We then investigated whether the HS‐binding factors, FGF10, TGFβ1, and SDF1, could reverse the effect of sodium chlorate. Although no effect was seen in the FGF10‐ and TGFβ1‐treated samples, SDF1 promoted epithelial canalization in the low sulfated environment, highlighting its specific role in lumen formation. Altogether, the results show that sodium chlorate perturbed prostate morphogenesis and allowed investigation of factors involved in branching and/or canalization, implicating SDF1 signaling in epithelial canalization.
Immunological biomarkers of tolerance in human kidney transplantation: An updated literature review
Authors: Mirzakhani Mohammad , Shahbazi Mehdi , Oliaei Farshid , Mohammadnia‐Afrouzi Mousa 
Published: October 2018

AbstractThe half‐life of transplanted kidneys is <10 years. Acute or chronic rejections have a negative impact on transplant outcome. Therefore, achieving to allograft tolerance for improving long‐term transplant outcome is a desirable goal of transplantation field. In contrast, there are evidence that distinct immunological characteristics lead to tolerance in some transplant recipients. In contrast, the main reason for allograft loss is immunological responses. Various immune cells including T cells, B cells, dendritic cells, macrophages, natural killer, and myeloid‐derived suppressor cells damage graft tissue and, thereby, graft loss happens. Therefore, being armed with the comprehensive knowledge about either preimmunological or postimmunological characteristics of renal transplant patients may help us to achieve an operational tolerance. In the present study, we are going to review and discuss immunological characteristics of renal transplant recipients with rejection and compare them with tolerant subjects.
CXCL8 gene silencing promotes neuroglial cells activation while inhibiting neuroinflammation through the PI3K/Akt/NF‐κB‐signaling pathway in mice with ischemic stroke
Authors: Lv Hui , Li Jie , Che Yu‐Qin 
Published: October 2018

AbstractObjectiveIschemic stroke is known as a neurodegenerative disorder, which induces long‐period tissue damage. Chemokine (C–X–C motif) ligand 8 (CXCL8) is involved in acute inflammation and tumor progression through the phosphoinositide‐3‐kinase/protein kinase B/nuclear factor‐κB (PI3K/Akt/NF‐κB)‐signaling pathway. In this study, we aimed to explore the mechanism of CXCL8 in ischemic stroke in relation to the PI3K/Akt/NF‐κB‐signaling pathway.MethodsMicroarray‐based gene expression profiling of peripheral blood mononuclear cells was used to identify ischemic stroke‐related differentially expressed genes and explore role of CXCL8 in ischemic stroke. Next, the ischemic mice model was successfully established, with transfection efficiency detected. After that, deflection index, recovery of nervous system, infarct sizes, ischemia‐induced apoptosis, and neuroinflammatory response in ischemic stroke were measured. At last, the content of inflammatory factors as well as the expression of CXCL8, caspase‐3, caspase‐9, Bad, interleukin‐6 (IL‐6), IL‐1β, tumor necrosis factor‐α (TNF‐α), Akt, PI3K, and NF‐κB were determined.ResultsComprehensive gene expression profiling analysis identified that CXCL8 might affect the development of ischemic stroke through regulating the PI3K/Akt/NF‐κB‐signaling pathway. CXCL8 silencing significantly reduced deflection index and infarct size, improved neurological function, and suppressed neuroglial cell loss and apoptosis index. In addition, glial fibrillary acidic portein (GFAP) and ionized calcium‐binding adapter molecule 1 (IBA‐1) expressions were decreased following CXCL8 suppression, suggesting CXCL8 affected neuroglial activation. Importantly, we also found that CXCL8 silencing activated neuroglial cell and suppressed inflammatory cytokine production in ischemic stroke mice.ConclusionTaken together, these findings highlight that functional suppression of CXCL8 promotes neuroglial activation and inhibits neuroinflammation by regulating the PI3K/Akt/NF‐κB‐signaling pathway in mice with ischemic stroke, which might provide new insight for ischemic stroke treatment.
Meldonium improves Huntington’s disease mitochondrial dysfunction by restoring peroxisome proliferator‐activated receptor γ coactivator 1α expression
Authors: Di Cristo Francesca , Finicelli Mauro , Digilio Filomena Anna , Paladino Simona , Valentino Anna , Scialò Filippo , D’Apolito Maria , Saturnino Carmela , Galderisi Umberto , Giordano Antonio , Melone Mariarosa Anna Beatrice , Peluso Gianfranco 
Published: October 2018

AbstractMitochondrial dysfunction seems to play a fundamental role in the pathogenesis of neurodegeneration in Huntington’s disease (HD). We assessed possible neuroprotective actions of meldonium, a small molecule affecting mitochondrial fuel metabolism, in in vitro and in vivo HD models. We found that meldonium was able to prevent cytotoxicity induced by serum deprivation, to reduce the accumulation of mutated huntingtin (mHtt) aggregates, and to upregulate the expression of peroxisome proliferator‐activated receptor γ coactivator 1α (PGC‐1α) in mHTT‐expressing cells. The PGC‐1α increase was accompanied by the increment of mitochondrial mass and by the rebalancing of mitochondrial dynamics with a promotion of the mitochondrial fusion. Meldonium‐induced PGC‐1α significantly alleviated motor dysfunction and prolonged the survival of a transgenic HD Drosophila model in which mHtt expression in the nervous system led to progressive motor performance deficits. Our study strongly suggests that PGC‐1α, as a master coregulator of mitochondrial biogenesis, energy homeostasis, and antioxidant defense, is a potential therapeutic target in HD.