bluuebunny/crossref_metadata_2025_split huggingface dataset:
Flow alteration impacts on Hudson Bay river discharge
Authors: Déry Stephen J. , Stadnyk Tricia A. , MacDonald Matthew K. , Koenig Kristina A. , Guay Catherine 
Published: September 2018

AbstractThis study explores flow regulation controls on daily river discharge variations and trends into Hudson Bay from four highly regulated and 17 moderately regulated/unregulated systems over 1960–2016. These 21 rivers contribute ~70% of the total annual riverine freshwater export to Hudson Bay, with highly regulated and moderately regulated/unregulated rivers accounting for 47% and 53% of the discharge, respectively. Daily observed streamflow data from the Water Survey of Canada, Manitoba Hydro, Ontario Power Generation, and Hydro‐Québec are used. Decadal hydrographs of the mean and coefficient of variation of daily river discharge are developed to assess the changing hydrological regimes in both systems. Decadal spectral analyses reveal the dominant controls on daily river discharge input to Hudson Bay from the regulated and unregulated systems. Apart from expected peaks in spectral power on annual timescales arising from the nival regimes in both systems, a strong secondary peak emerges at weekly timescales from flow regulation due to hydropower production. Hydrographs that consider the day of the week reveal distinct weekly cycles in regulated rivers with ~10% declines in daily river discharge during weekends and statutory holidays relative to weekday averages, demonstrating the importance of regulation on the timing of freshwater into Hudson Bay.
Acute inhalation co‐exposure to 1,2‐dichloropropane and dichloromethane cause liver damage by inhibiting mitochondrial respiration and defense ability in mice
Authors: Wang Hufei , Chen Jiamin , Suda Megumi , Yanagiba Yukie , Weng Zuquan , Wang Rui‐Sheng 
Published: September 2018

Abstract1,2‐Dichloropropane (1,2‐DCP) is used as an industrial solvent, insecticide fumigant and household dry cleaning product. Carcinogenicity caused by long‐term exposure to 1,2‐DCP is well established. However, the possible liver damage and related toxic mechanisms associated with acute inhalation exposure to 1,2‐DCP are rarely reported. In this study, we investigated the effects of individual and combined exposure to 1,2‐DCP and dichloromethane (DCM) on mice liver. The results showed that 1,2‐DCP significantly caused liver necrosis, possibly due to 1,2‐DCP‐induced inhibition of the mitochondrial respiratory chain complex I‐IV activities, resulting in mitochondrial dysfunction and extreme ATP consumption. Moreover, 1,2‐DCP also decreased mitochondrial defense ability by inhibiting the mitochondrial glutathione S‐transferase 1 (MGST1) activity, further aggravating liver damage. Additionally, we found that DCM co‐exposure potentially enhanced 1,2‐DCP toxicity. Our findings suggest that inhibition of mitochondrial function and MGST1 activity play critical roles in modulating 1,2‐DCP‐induced liver damage. Furthermore, our results contribute to study the new mechanism of mitochondria‐dominated signaling pathways underlying liver injury induced by 1,2‐DCP and DCM.
Cardiomyogenic differentiation of human bone marrow‐derived mesenchymal stem cell spheroids within electrospun collagen nanofiber mats
Authors: Joshi Jyotsna , Brennan David , Beachley Vince , Kothapalli Chandrasekhar R. 
Published: September 2018

AbstractCollagen is the major structural protein in myocardium and contributes to tissue strength and integrity, cellular orientation, and cell–cell and cell‐matrix interactions. Significant post‐myocardial infarction related loss of cardiomyocytes and cardiac tissue, and their subsequent replacement with fibrous scar tissue, negatively impacts endogenous tissue repair and regeneration capabilities. To overcome such limitations, tissue engineers are working toward developing a 3D cardiac patch which not only mimics the structural, functional, and biological hierarchy of the native cardiac tissue, but also could deliver autologous stem cells and encourage their homing and differentiation. In this study, we examined the utility of electrospun, randomly‐oriented, type‐I collagen nanofiber (dia = 789 ± 162 nm) mats on the cardiomyogenic differentiation of human bone marrow‐derived mesenchymal stem cells (BM‐MSC) spheroids, in the presence or absence of 10 μM 5‐azacytidine (aza). Results showed that these scaffolds are biocompatible and enable time‐dependent evolution of early (GATA binding protein 4: GATA4), late (cardiac troponin I: cTnI), and mature (myosin heavy chain: MHC) cardiomyogenic markers, with a simultaneous reduction in CD90 (stemness) expression, independent of aza‐treatment. Aza‐exposure improved connexin‐4 expression and sustained sarcomeric α‐actin expression, but provided only transient improvement in cardiac troponin T (cTnT) expression. Cell orientation and alignment significantly improved in these nanofiber scaffolds over time and with aza‐exposure. Although further quantitative in vitro and in vivo studies are needed to establish the clinical applicability of such stem‐cell laden collagen nanofiber mats as cardiac patches for cardiac tissue regeneration, our results underscore the benefits of 3D milieu provided by electrospun collagen nanofiber mats, aza, and spheroids on the survival, cardiac differentiation and maturation of human BM‐MSCs. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 106A: 3303–3312, 2018.
Retracted: CRNDE promotes cell tongue squamous cell carcinoma cell growth and invasion through suppressing miR‐384
Authors: Ren Yixiong , He Wenting , Chen Wenge , Ma Chao , Li Yun , Zhao Zhenyan , Gao Tao , Ni Qianwei , Chai Juan , Sun Moyi 
Published: September 2018

AbstractTongue squamous cell carcinoma (TSCC) is the most common type of oral cancer and is an aggressive head and neck malignancy. Increasing studies have demonstrated that long noncoding RNAs (lncRNAs) play important roles in diverse biological cell processes, such as cell development, fate decisions, cell differentiation, cell migration, and invasion. In our study, we showed that long noncoding RNA colorectal neoplasia differentially expressed (CRNDE) expression was upregulated in TSCC cell lines and tissues. Overexpression of CRNDE increased the TSCC cell proliferation, cell cycle, and cell invasion. Moreover, ectopic expression of CRNDE inhibited the miR‐384 expression in the SCC1 cell and increased the Kirsten Ras (KRAS), cell division cycle 42, and insulin receptor substrate 1 expression, which were the direct target genes of miR‐384. We demonstrated that the miR‐384 expression was downregulated in the TSCC samples compared with the paired adjacent nontumor samples. The expression of CRNDE was negatively correlated with the expression of miR‐384 in the TSCC samples. Overexpression of miR‐384 suppressed TSCC cell proliferation, cell cycle, and invasion. Furthermore, we demonstrated that CRNDE promoted TSCC cell proliferation and invasion through inhibiting miR‐384 expression. These results suggested that CRNDE acts as an oncogene in the development of TSCC, which partially occurs through inhibiting miR‐384 expression.
Minor allele of rs1057317 polymorphism in TLR4 is associated with increased risk of Helicobacter pylori ‐induced gastric cancer
Authors: Wang Yi‐Wei , Zhang Cai‐Hong , He Xiang 
Published: September 2018

AbstractBackgroundHelicobacter pylori (HP) plays a significant role in the carcinogenesis of gastric cancer (GC), the second leading cause of cancer‐related death worldwide. The aim of this study was to investigate the effect of rs1057317 polymorphism on the interaction between microRNA‐034a (miR‐034a) and toll‐like receptor 4 (TLR4), and their involvement in the HP‐associated GC.MethodsComputation analyses, real‐time polymerase chain reaction, enzyme‐linked immunosorbent assay, 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide, and luciferase assays were performed to identify potential miRNAs involved in the carcinogenesis of HP‐induced GC. Subsequently, the effect of miR‐34a and recombinant TNFα‐interacting protein α (rTip‐α) on the expression of TLR4, interleukin (IL)‐6, and tumor necrosis factor α (TNF‐α) was measured.ResultsThree hundred and twelve HP‐positive GC patients (HP+ GC) and 380 HP‐negative GC patients (HP− GC) were enrolled into this study. It was found that, in HP‐positive patient, the AA genotype of the rs1057317 polymorphism was closely associated with the risk of GC (95% confidence interval, 1.12 to 2.70; odds ratio, 1.74; P = 0.0129). Furthermore, between the HP+ GC and HP− GC groups, miR‐34a was the only miRNA showing a significantly different expression. Subsequently, TLR4 was identified as a target gene of miR‐34a. Interestingly, miR‐34a evidently reduced the expression of TLR4 3′‐untranslated region (3′‐UTR) containing the C allele of the rs1057317 polymorphism, but the TLR4 3′‐UTR containing the A allele in the rs1057317 was not affected by miR‐34a. In addition, the expression of IL‐6 and TNF‐α was significantly downregulated by miR‐34a, but increased by rTip‐α. Both miR‐34a and rTip‐α could enhance the viability of cells, although the effect of rTip‐α was stronger.ConclusionThe data of this study suggested that the rs1057317 polymorphism in the miR‐34a binding site of TLR4 may predict the risk of HP‐induced GC.
Retracted: Curcumin derivative L6H4 inhibits proliferation and invasion of gastric cancer cell line BGC‐823
Authors: Mu Jianfeng , Wang Xiaodong , Dong Lihua , Sun Pengda 
Published: September 2018

AbstractCurcumin and its chalcone derivatives have well‐known, explicit biological antitumor properties, such as instance antiproliferative and apoptotic effects via multiple molecular targets. In this study, we investigated the anticancer activity of curcumin derivative L6H4 (curcumin L6H4) on gastric cancer cells. Inhibitory effects of curcumin L6H4 on gastric cancer cells (BGC‐823) were studied by the diphenyltetrazolium (MTT) assay, and cell apoptosis was detected by Annexin‐V/propidium iodide (PI) staining and then analyzed by flow cytometry. A mouse xenotransplant gastric tumor model was established to detect the role of curcumin L6H4 in vivo. The apoptosis‐related proteins p53, p21, Bax, and Bcl‐2 in BGC‐823 cells and mouse xenotransplant models treated with curcumin L6H4 were determined by Western blot analysis. Curcumin L6H4 can significantly inhibit the proliferation and induce the apoptosis of BGC‐823 cells, thus enhancing the expression levels of p53, p21, Bax, and Bcl‐2 noticeably in vivo and in vitro. Meanwhile, curcumin L6H4 can remarkably suppress the growth of tumor cells in animal models. These results suggest that curcumin derivative L6H4 has potent of antitumor properties in vitro or in vivo.
Ulinastatin protects rats from sepsis‐induced acute lung injury by suppressing the JAK‐STAT3 pathway
Authors: Wu Jian , Yan Xin , Jin Guoqiang 
Published: September 2018

AbstractSepsis is usually accompanied by pulmonary inflammations, leading to acute lung injury. During this process, endogenous factors that play a regulatory role could be exploited to therapeutically alleviate such lethal tissue injury. Here, we showed that ulinastatin (UTI) administration could reduce lung tissue necrosis and swelling during sepsis in rats. UTI treatment also decreased the levels of inflammatory mediators both in the lung and in the serum. Mechanistically, we showed that the phosphorylation levels of JAK2 and STAT3 in the lung of UTI‐treated rats were lower than control rats and were correlated with the decreased levels of inflammatory mediators. Taken together, these results demonstrate the protective role of UTI in sepsis‐induced acute lung injury.
Exosomes and their importance in metastasis, diagnosis, and therapy of colorectal cancer
Authors: Cheshomi Hamid , Matin Maryam M. 
Published: September 2018

AbstractExtracellular vesicles are known as actual intermediaries of intercellular communications, such as biological signals and cargo transfer between different cells. A variety of cells release the exosomes as nanovesicular bodies. Exosomes contain different compounds such as several types of nucleic acids and proteins. In this study, we focused on exosomes in colorectal cancer as good tools that can be involved in various cancer‐related processes. Furthermore, we summarize the advantages and disadvantages of exosome extraction methods and review related studies on the role of exosomes in colorectal cancer. Finally, we focus on reports available on relations between mesenchymal stem cell–derived exosomes and colorectal cancer. Several cancer‐related processes such as cancer progression, metastasis, and drug resistance of colorectal cancer are related to the cargoes of exosomes. A variety of molecules, especially proteins, microRNAs, and long noncoding RNAs, play important roles in these processes. The microenvironment features, such as hypoxia, also have very important effects on the properties of the origin cell–derived exosomes. On the other hand, exosomes derived from colorectal cancer cells also interfere with cancer chemoresistance. Furthermore, today it is known that exosomes and their contents can likely be very effective in noninvasive colorectal cancer diagnosis and therapy. Thus, exosomes, and especially their cargoes, play different key roles in various aspects of basic and clinical research related to both progression and therapy of colorectal cancer.
The lncRNA small nucleolar RNA host gene 5 regulates trophoblast cell proliferation, invasion, and migration via modulating miR‐26a‐5p/N‐cadherin axis
Authors: Yang Yang , Xi Lan , Ma Yuan , Zhu Xiaoming , Chen Rui , Luan Lixia , Yan Jiajia , An Ruifang 
Published: September 2018

AbstractPre‐eclampsia (PE) is a pregnancy‐specific disease characterized by the occurrence of hypertension and proteinuria after two weeks of gestation. Long noncoding RNAs (lncRNAs) are emerging as key regulators in PE development. This study aims to investigate the role of lncRNA, small nucleolar RNA host gene 5 (SNHG5), in the pathogenesis of PE. The expression of SNHG5 was significantly downregulated in placental tissues from patients with severe PE compared normal controls. Overexpression of SNHG5 promoted trophoblast (HTR‐8/SVneo) cell proliferation, invasion, and migration, and flow cytometry results showed that SNHG5 overexpression inhibited apoptosis and caused a decrease of cell population at the G
0/G
1 phase and an increase of cell population at the S phase, while knockdown of SNHG5 had the opposite effects. The interaction between SNHG5 and miR‐26a‐5p was predicted by bioinformatics analysis and confirmed by luciferase reporter assay and RNA immunoprecipitation, and miR‐26a‐5p was negatively regulated by SNHG5; miR‐26a‐5p expression was upregulated in PE placental tissues and was inversely correlated with SNHG5 expression. Furthermore, miR‐26a‐5p was predicted to target the 3′ untranslated region of N‐cadherin, which was confirmed by luciferase reporter assay, and miR‐26a‐5p overexpression suppressed N‐cadherin expression in HTR‐8/SVneo cells. N‐cadherin mRNA expression was downregulated in PE placental tissues and was positively correlated with SNHG5 expression. Both overexpression of miR‐26a‐5p and knockdown of N‐cadherin suppressed HTR‐8/SVneo cell invasion and migration, and also attenuated the effects of SNHG5 on the cellular functions of HTR‐8/SVneo cells. In conclusion, our study suggested that SNHG5 promotes trophoblast cell proliferation, invasion, and migration at least partly via regulating the miR‐26a‐5p/N‐cadherin axis.
Improvement of membranous nephropathy by inhibition of miR‐193a to affect podocytosis via targeting WT1
Authors: Li Jiao , Chen Yi , Shen Lianli , Deng Yueyi 
Published: September 2018

AbstractThe objective of this paper was to explore the role and molecular mechanism of miR‐193a in membranous nephropathy (MN). Experimental rats and podocytes were randomly divided into four groups: control, MN, miR‐NC, and miR‐193a inhibitor groups. The relative mRNA level of miR‐193a was determined. The mRNA level and protein expression of PODXL, NPHS1, and Notch1 were determined by real‐time polymerase chain reaction (RT‐PCR) and Western blot analysis, respectively. The mRNA level and protein expression of WT1 in podocytes were also determined by RT‐PCR and Western blot analysis. The relative mRNA level of miR‐193a in the MN group was significantly higher than that in the control group, and inhibition of miR‐193a inhibited the increase successfully. Inhibition of miR‐193a inhibited renal injury, podocyte injury, and tissue cell apoptosis resulting from MN. The expression of PODXL, NPHS1, and Notch1 was decreased in the MN group, while the expression was increased in the miR‐193a inhibitor group. WT1 was verified as a target gene of miR‐193a and the expression of WT1 increased after inhibition of miR‐193a. Inhibition of miR‐193a by targeting WT1 could inhibit renal function injury, renal tissue cell apoptosis, and podocytosis.
Scaffolding role of TcpB in disrupting TLR4‐Mal interactions: Three to tango
Authors: Saqib Uzma , Baig Mirza S 
Published: September 2018

AbstractToll/interleukin‐1 like receptors (TLRs) are membrane‐spanning proteins crucially involved in innate immunity. On activation, the cytoplasmic toll/interleukin‐1 receptor (TIR) domains of these receptors undergo homo‐ or heterodimerization.
Brucella sp. are bacterial pathogens that affect the immune system by suppressing the TLR signaling pathway. They enact this by encoding a TIR domain–containing protein, TcpB, which suppresses NF‐κB activation and proinflammatory cytokine secretion mediated by TLR4 receptors. TcpB has been shown to target the Mal‐mediated pathway to suppress TLR signaling. The recent identification of its mechanism of interference with TLR4 signaling involving Mal prompted us to further study the structural aspects of TcpB binding with TLR4 and Mal. Our triprotein model displays the overall scaffolding role of TcpB in anchoring TLR4 and Mal thereby inhibiting their interaction leading to the attenuation of the TLR4 pathway.
mTOR/STAT‐3 pathway mediates mesenchymal stem cell–secreted hepatocyte growth factor protective effects against lipopolysaccharide‐induced vascular endothelial barrier dysfunction and apoptosis
Authors: Meng Shan‐Shan , Guo Feng‐Mei , Zhang Xi‐Wen , Chang Wei , Peng Fei , Qiu Hai‐Bo , Yang Yi 
Published: September 2018

AbstractMesenchymal stem cells (MSCs) protect the endothelial barrier complex and survival, implicated in the pathogenesis of acute lung injury (ALI) via paracrine hepatocyte growth factor (HGF). However, the mechanism of HGF in endothelial regulation remains unclear. Here, we introduced a coculture protocol of pulmonary microvascular endothelial cells (PMVECs) and overexpression of the HGF gene of MSCs (MSC‐HGF). Immunofluorescence and endothelial permeability analysis revealed that MSC‐HGF protected endothelial tight junction protein occludin expression and attenuated cellular permeability as well as endothelial apoptosis. To investigate the novel mechanism mammalian TOR (mTOR)/ signal transducer and activator of transcription 3 (STAT‐3) signaling in HGF protective effects against endothelial barrier and apoptosis, we used recombinant mouse HGF in endothelial cells. In addition, we used mTOR inhibitor rapamycin to inhibit the mTOR pathway. Our study demonstrated that rapamycin decreased the protective effects of HGF on the endothelium by decreasing tight junction protein occludin expression and cell proliferation, and raising lipopolysaccharide (LPS)‐induced endothelial permeability, endothelial cell injury factors ET‐1 and vWF. Similarly, the protective effects of HGF on reducing endothelial barrier and apoptosis were weakened when PMVECs were treated with the STAT‐3 inhibitor S3I‐201. Moreover, mTOR/STAT‐3 were activated by HGF demonstrated as raising mTOR (Ser2448) and STAT3 (Ser727) phosphorylation proteins, leading to endothelial barrier improvement and survival. Reversely, rapamycin or S3I‐201 inhibited mTOR/STAT‐3 activation. Taken together, our findings highlight that the activation of the mTOR/STAT‐3 pathway provides novel mechanistic insights into MSC‐secreted HGF protection against LPS‐induced vascular endothelial permeability dysfunction and apoptosis, which contributes to decreasing microvascular loss and lung injury.
A 4‐microRNA signature for survival prognosis in pediatric and adolescent acute myeloid leukemia
Authors: Zhu Ruiqi , Lin Wenyi , Zhao Weiwei , Fan Fengjuan , Tang Liang , Hu Yu 
Published: September 2018

AbstractAcute myeloid leukemia (AML) is a hematologic malignancy with significant molecular heterogeneity. MicroRNAs (miRNAs) play a critical role in AML diagnosis, pathogenesis, and prognosis of AML. Little has been done to identify a miRNA signature in pediatric and adolescent patients for predicting overall survival. This study aims to identify a panel of miRNA signature that could predict the prognosis of all younger AML patients with all subtypes of AML by analyzing data from The Cancer Genome Atlas (TCGA). A total of 229 patients under 23 years with miRNA data and corresponding clinical data from TCGA database were enrolled in this study. Through conducting multivariate analysis in the training test, it was identified that the high expression of hsa‐miR‐509 and hsa‐miR‐542 were independent poor prognostic factors, whereas that of hsa‐miR‐146a and hsa‐miR‐3667 had a trend to be favorable factors. A 4‐miRNA signature was constructed by these miRNAs considering the weight of each. In testing group and all 229 patients’ cohort as well as 59 cytogenetically normal AML (CN‐AML) patients’ cohort, higher risk score was associated with shorter overall survival (OS). All results were confidential by using powerful statistical analysis. Gene ontology and Kyoto Encyclopedia of Genes and Genomes analysis were carried out to further develop leukemia‐relevant mechanisms supporting the model. The results indicate that the 4‐miRNA‐based signature is a reliable prognostic biomarker for pediatric and adolescent AML patients.
Blood routine test is a good indicator for predicting premature rupture of membranes
Authors: Zhan Fengxia , Zhu Shuzhen , Liu Haiying , Wang Qian , Zhao Guanghui 
Published: September 2018

ObjectiveTo assess the value of blood routine test (blood RT) in order to predict the occurrence of premature rupture of membranes (PROM).MethodsA retrospective study was conducted to collect blood RT data from 100 cases of preterm premature rupture of membranes (pPROM), 70 cases of full‐term premature rupture of membranes (fPROM), and 100 cases of full‐term pregnancy (Normal). Nonparametric tests were performed for each blood routine parameter, the ROC curve was established for the parameters with significant difference, and the sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), positive likelihood ratios (+LR), and negative likelihood ratios (−LR) were further calculated.ResultsThe statistical results showed that WBC, NE.%, LY.%, EO.%, BA.%, NE.#, EO.#, RBC, HGB, HCT, and NLR were significantly different between pPROM and fPROM (P < 0.05). There was a significant difference in WBC, NE.%, LY.%, NE.#, MO.#, RBC, HGB, HCT, and NLR between the pPROM and Normal groups (P < 0.05). Between the fPROM and Normal groups, only WBC was statistically significant (P < 0.05). By establishing ROC curve, the results showed that when the cutoff value of WBC was 9.63 and NEU# was 7.12, their combined detection had the best predictive value with a sensitivity of 73% and a specificity of 81%. In addition, Its PPV was 79.3%, NPV was 75%, +LR was 3.84, and ‐LR was 0.33.ConclusionThe patient's blood RT results can be used to predict the risk of premature rupture of membranes, and in order to improve the sensitivity and specificity, multiple parameters can be combined.