bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sleep‐competing behaviours among Australian school‐attending youth: Associations with sleep, mental health and daytime functioning
Authors: Mellor David , Hallford David J. , Tan Jeretine , Waterhouse Monique 
Published: December 2018

Sleep problems are highly prevalent among school‐attending youth, and impact on school performance and outcomes. Sleep‐competing behaviours are likely factors in the inadequate sleep time and related functional outcomes observed in this population. We examined a range of sleep‐competing behaviours and their associations with sleep variables in Australian school‐attending youth. We also assessed whether these behaviours indirectly affected mental health and daytime functioning through poorer sleep quality. A total of 353 school‐attending youth (mean age = 14.6 years, 53% female) were recruited from high schools in Australia, and completed a range of self‐report measures. Approximately 50% of the youth obtained sub‐optimal levels of sleep and reported having a problematically long sleep onset latency. Sleep competing behaviours, related and unrelated to electronic media use, were reported as occurring frequently, and were associated with a range of sleep variables. These behaviours were also related to poorer mental health and daytime sleepiness, with this association explained by indirect effects through sleep quality. Sleep‐competing behaviours are prevalent on school nights in Australian youth, and may have adverse associations with mental health and functioning. Prevention and intervention programs might address the risk factors identified in the current study.
A Comparison of US and Canadian Osteoporosis Screening and Treatment Strategies in Postmenopausal Women
Authors: Crandall Carolyn J , Larson Joseph , Manson JoAnn E , Cauley Jane A , LaCroix Andrea Z , Wactawski-Wende Jean , Datta Mridul , Sattari Maryam , Schousboe John T , Leslie William D , Ensrud Kristine E 
Published: December 2018

ABSTRACT

The optimal approach to osteoporosis screening and treatment in postmenopausal women is unclear. We compared (i) the United States Preventive Services Task Force (USPSTF) and Osteoporosis Canada osteoporosis screening strategies; and (ii) the National Osteoporosis Foundation (NOF) and Canadian treatment strategies. We used data from the prospective Women's Health Initiative Observational Study and Clinical Trials of women aged 50 to 79 years at baseline (n = 117,707 followed for self-reported fractures; n = 8134 in bone mineral density [BMD] subset). We determined the yield of the screening and treatment strategies in identifying women who experienced major osteoporotic fractures (MOFs) during a 10-year follow-up. Among women aged 50 to 64 years, 23.1% of women were identified for BMD testing under the USPSTF strategy and 52.3% under the Canadian strategy. For women ≥65 years, 100% were identified for testing under the USPSTF and Canadian strategies, 35% to 74% were identified for treatment under NOF, and 16% to 37% were identified for treatment under CAROC (range among 5-year age subgroups). Among women who experienced MOF during follow-up, the USPSTF strategy identified 6.7% of women 50 to 54 years-old and 49.5% of women 60 to 64 years-old for BMD testing (versus 54.4% and 60.6% for the Canadian strategy, respectively). However, the specificity of the USPSTF strategy was higher than that of the Canadian strategy among women 50 to 64 years-old. Among women who experienced MOF during follow-up, sensitivity for identifying women as treatment candidates was lowest for both strategies in women aged 50 to 64 (NOF 10% to 38%; CAROC 1% to 15%) and maximal in 75-year-old to 79-year-old women (NOF 82.8%; 51.6% CAROC); specificity declined with advancing age and was lower with the NOF compared to the CAROC strategy. Among women aged 50 to 64 years, the screening and treatment strategies examined had low sensitivity for identifying those who subsequently experience MOF; sensitivity was higher among women ≥65 years than among younger women. New screening and treatment algorithms are needed. © 2018 American Society for Bone and Mineral Research.
Molecular docking and two‐dimensional quantitative structure‐activity relationship studies of synthetic flavonoids on horseradish peroxidase compounds (I, II, and III)
Authors: Mahfoudi Reguia , Tahri Djilali , Djeridane Amar , Yousfi Mohamed , Gaydou Emile M. 
Published: December 2018

AbstractFor the first time, the enzymatic inhibition activity of 13 synthetic flavonoids was assessed by quantitative structure‐activity relationship (QSAR) modeling and molecular docking with the three states of the enzyme horseradish peroxidase (HRP). The results show that apigenin, quercetin, kaempferol, fisetin, tricetin, and luteolin exerted a high competitive inhibition on HRP (Ki between 0.14 and 1.74 mM) compared with other flavonoids. The QSAR model of enzymatic activity (R2 = 0.95, RMSE = 5.48) showed that Ghose‐Crippen octanol‐water partition coefficient (Alog P) and lowest unoccupied molecular orbital’s energy (εlumo) correlated with 0.65 and 0.17, respectively, with Ki values. According to the docking results using Molegro Virtual Docker program, all the flavonoids have shown great binding affinity towards peroxidase. Apigenin has the largest MolDock score in the three states of HRP noting an increased affinity of these flavonoids between compound I and compound II by 2.26%. However, these affinities strongly decrease between compound II and compound III by 28.43% especially for luteolin whose MolDock score decreased by 74.7%. With the results of docking, the affinities of the flavonoids tested and translated by their Ki values are much more presentative of the inhibition of the first reaction states of HRP because their inhibitory effect is important.
Retracted: miR‐145 modulates epithelial‐mesenchymal transition and invasion by targeting ZEB2 in non–small cell lung cancer cell lines
Authors: Liu Qun , Chen Jianhui , Wang Baolan , Zheng Yulong , Wan Yufeng , Wang Yi , Zhou Liyang , Liu Shu , Li Gang , Yan Yi 
Published: December 2018

AbstractLung cancer is the leading cause of cancer‐related deaths worldwide. Epithelial‐mesenchymal transition (EMT) is a major event that drives cancer progression. Here we aim to investigate the role of microRNA, miR‐145, in regulating EMT of the highly invasive non–small cell lung cancer (NSCLC). Quantitative real‐time polymerase chain reaction analysis indicated that miR‐145 was downregulated in cancer tissue compared with that in adjacent normal tissue. NSCLC cell lines, namely H1299, PC7, and SPCA‐1, also demonstrated miR‐145 downregulation, which is correlated well with their invasive ability, assessed by the Matrigel invasion assay. miR‐145 overexpression resulted in downregulation of N‐cadherin, and downregulation of vimentin and E‐cadherin, suggesting a decreased EMT activity. TargetScan analysis predicted that a binding site exists between miR‐145 and an oncogene, ZEB2, which was verified using the dual‐luciferase assay. Alteration of miR‐145 expression also induced inverse effects on ZEB2 expression, and a negative correlation exists between ZEB2 and miR‐145 in human tissues. ZEB2 and miR‐145 also exerted antagonizing effects on the invasion of NSCLC cells. Therefore, miR‐145 is an important molecule in NSCLC that regulates cancer EMT through targeting ZEB2.
Construction and analysis of dysregulated lncRNA‐associated ceRNA network in colorectal cancer
Authors: Zhu Yiping , Bian Yinzhu , Zhang Qun , Hu Jing , Li Li , Yang Mi , Qian Hanqing , Yu Lixia , Liu Baorui , Qian Xiaoping 
Published: December 2018

AbstractColorectal cancer (CRC) is one of the most frequently diagnosed digestive system cancer. The aim of the present study was to investigate the interactions among messenger RNAs (mRNAs), microRNAs (miRNAs), and long noncoding RNAs (lncRNAs) in CRC to reveal the mechanisms of CRC. Differentially expressed genes (DEGs) were identified from public gene expression data sets. One thousand eighty‐one common dysregulated mRNAs in two data sets were identified. Gene function analysis and protein‐protein interaction network analysis indicated that these DEGs might play important roles in CRC. LINC00365 was selected through coding‐ noncoding network analysis and its expression was validated upregulated in 22 paired clinical samples and four CRC cell lines. A competing endogenous RNA network composed of 70 miRNAs, nine mRNAs, and LINC00365 was constructed. Eight of nine mRNAs were validated upregulated in The Cancer Genome Atlas data set. Our results suggested that LINC00365 was an oncogene in CRC and it could regulate the expression of several mRNAs through sponging miRNAs.
Acetylation drives hepatocyte nuclear factor 1β stability by blocking proteasome‐mediated degradation
Authors: Lopes‐Coelho Filipa , Silva Fernanda , Hipólito Ana , Cardoso Bruno A. , Serpa Jacinta 
Published: December 2018

AbstractHepatocyte nuclear factor 1β (HNF1β) is mostly expressed in the liver, but is also expressed in other organs, like kidney, pancreas and genitourinary tract. In fact, HNF1β, a member of the superfamily of homeodomain‐containing transcription factors, has been described as a hallmark in clear cell carcinomas. However, its role as an oncogene or as tumor suppressor gene remains controversial. Here, we disclose a mechanism of HNF1β stabilization and degradation, using human HNF1β‐expressing cell lines of ovarian clear cell carcinoma (ES2), hepatocellular carcinoma (HEPG2), and normal immortalized kidney tubular cells (HK2). We show that increased levels of HNF1β is concomitant with an increase in the acetylation load and protein stabilization by interfering with the ubiquitin‐proteasome degradation system. This study reinforces that acetylation, besides their role in regulating chromatin conformation and gene expression, could also act in the action, turnover and stability of proteins essential for the survival and progression of certain cancer types.
Lack of Association between IL‐6 Polymorphisms and Haplotypes with Gastric Cancer
Authors: dos Santos Mônica Pezenatto , Sallas Mayara Luciana , Zapparoli Diana , Orcini Wilson Aparecido , Chen Elizabeth , Smith Marilia de Arruda Cardoso , Payão Spencer L. Marques , Rasmussen Lucas Trevizani 
Published: December 2018

AbstractThe process of combating neoplasms and mononuclear cells, and during H. pylori infection, several pro‐inflammatory and anti‐inflammatory cytokines are synthesized. In view of the involvement of the IL‐6 law and the presence of H. pylori in the development of gastric diseases, the present study aimed to characterize the promoter‐region polymorphism −597 (G/A) (rs1800797), −572 (C/G) (rs1800796), and −174 (G/C) (rs1800795) by PCR‐RFLP in 375 gastric biopsy specimens from patients with peptic symptoms. A total of 375 samples were analyzed: 87 patients (without lesion without gastric tissue); 236 patients with gastritis and 52 patients with gastric cancer analyzed the PCR‐RFLP techniques. All the results were normalized in relation to the presence of H. pylori. The frequencies of the three polymorphisms were compared in the Control vs Gastritis groups and a statistically significant test observed: −174 (G/C) (OR: 1.27; 95% CI: 0.84–1.93; P = 0.26), 572 (C/G) (OR: 1.42; 95% CI: 0.78–2.59; P = 0.25), and 597 (G/A) (OR: 0.98; 95% CI, 0.64–1.52; P = 0.94). Similar results were obtained when the gastric cancer group was compared to the control group: −174 (G/C) (OR: 1.27; 95% CI: 0.66–2.47; P = 0.47), −572 (C/G) (OR: 1.07; 95% CI: 0.43–2.68; P = 0.88), and −597 (G/A) (OR: 1.01; 95% CI, 0.5–0.9; P = 0.99). The haplotypes were and were not observed statistically significant differences. In conclusion, we found no correlations between any of the three polymorphisms in the IL‐6 gene analyzed in this study and a higher risk of gastritis or gastric cancer.
Molecular mechanism of miR‐153 inhibiting migration, invasion and epithelial‐mesenchymal transition of breast cancer by regulating transforming growth factor beta (TGF‐β) signaling pathway
Authors: Wang Jingwei , Liang Shuhang , Duan Xiuqing 
Published: December 2018

AbstractObjectiveTo investigate the role and mechanism of action of miR‐153 in the migration, invasion, and epithelial‐mesenchymal transition (EMT) of breast cancer cells.MethodsQuantitative real time polymerase chain reaction (qRT‐PCR) was used to detect the expression of miR‐153 and transforming growth factor beta receptor 2 (TGFBR2) in tissue specimens and cells. miR‐153 overexpression in breast cancer cells was achieved by miR‐153 mimic transfection. Mobility and invasiveness of breast cancer cells were evaluated by transwell assay. EMT was evaluated by Western blot detecting the protein level of E‐cadherin and Vimentin. Interaction of miR‐153 and 3′‐untranslated region (UTR) of TGFBR2 messenger RNA (mRNA) was investigated by luciferase reporter assay.ResultsThe expression of miR‐153 in breast cancer tissue specimens and MDA‐MB‐231 cells was significantly lower than that in nonmalignant counterparts, inversely correlating with that of TGFBR2 mRNA. Transfection with miR‐153 mimic significantly increased miR‐153 level in MDA‐MB‐231 cells while inhibiting its migration, invasion, and EMT in vitro, which could be mimicked by TGFBR2 knockdown. Luciferase reporter assay confirmed two targets of miR‐153 on the 3′‐UTR of TGFBR2 mRNA. Restoring TGFBR2 protein level by transient overexpression largely rescued migration, invasion, and EMT of MDA‐MB‐231 cells that were repressed by miR‐153 mimic transfection.ConclusionmiR‐153 inhibits breast cancer cell migration, invasion, and EMT by targeting TGFBR2.
Association between polymorphisms of VKORC1 and CYP2C9 genes with warfarin maintenance dose in a group of warfarin users in Birjand city, Iran
Authors: Fereidouni Mohammad , Moossavi Maryam , Kazemi Touba , Nouranihassankiade Shaghayeghsadat , Asghari Arghavan 
Published: December 2018

AbstractWarfarin is the cardinal anticoagulant drug prescribed around the world. Due to stochastic bleeding in patients, it is essential to adjust the dose for every individual. The aim of the present study was to evaluate the frequency of CYP2C9 and VKORC1 gene polymorphisms and their association with warfarin maintenance dose in a sample of cardiovascular patients in Birjand, South‐Khorasan province of Iran. Patients with a history of cardiovascular disorders who take warfarin daily were selected. CYP2C9 and VKORC1 gene polymorphisms were detected by polymerase chain reaction‐restriction fragment length polymorphism in all participants. A total of 114 patients (mean age: 52.7 ± 14.9 years, M/F ratio: 0.76) participated in this study. Regarding CYP2C9 gene polymorphisms, the most frequent genotype was 1*/1* (80.4% in females and 62.5% in males). The frequency of 1*/2* and 2*/2* variants was 13% and 6.5% in females and 25% and 12.5% in males, respectively. The frequency of VKORC1 gene (1639 G > A), was 31.5%, 39.5%, and 29% for GG, GA, and AA in males, respectively. Besides, the mentioned genotype frequencies for females were 50%, 40.5%, and 9.5%, respectively. Moreover, there was a statistically significant correlation between VKORC1 gene −1639 G > A variant and warfarin maintenance dose (P < 0.001) but not for CYP2C9 variants. The results of the current study confirmed that the mutant variants of CYP2C9 are not frequent and do not have any impact on warfarin dose. In the case of VKORC1, the mutant allele (A) showed a positive correlation with warfarin dose adjustment.
4‐Deoxyraputindole C induces cell death and cell cycle arrest in tumor cell lines
Authors: Vital Wagner D. , Torquato Heron F. V. , Jesus Larissa de Oliveira Passos , Judice Wagner Alves de Souza , Silva Maria Fátima das G. F. da , Rodrigues Tiago , Justo Giselle Zenker , Veiga Thiago A. M. , Paredes‐Gamero Edgar J. 
Published: December 2018

AbstractSeveral molecules extracted from natural products exhibit different biological activities, such as ion channel modulation, activation of signaling pathways, and anti‐inflammatory or antitumor activity. In this study, we tested the antitumor ability of natural compounds extracted from the Raputia praetermissa plant. Among the compounds tested, an alkaloid, here called compound S4 (4‐Deoxyraputindole C), showed antitumor effects against human tumor lineages. Compound S4 was the most active against Raji, a lymphoma lineage, promoting cell death with characteristics that including membrane permeabilization, dissipation of the mitochondrial potential, increased superoxide production, and lysosomal membrane permeabilization. The use of cell death inhibitors such as Z‐VAD‐FMK (caspase inhibitor), necrostatin‐1 (receptor‐interacting serine/threonine‐protein kinase 1 inhibitor), E‐64 (cysteine peptidases inhibitor), and
N‐acetyl‐
L‐cysteine (antioxidant) did not decrease compound S4‐dependent cell death. Additionally, we tested the effect of cellular activity on adherent human tumor cells. The highest reduction of cellular activity was observed in A549 cells, a lung carcinoma lineage. In this lineage, the effect on the reduction of the cellular activity was due to cell cycle arrest, without plasma membrane permeabilization, loss of the mitochondrial potential or lysosomal membrane permeabilization. Compound S4 was able to inhibit cathepsin B and L by a nonlinear competitive (negative co‐operativity) and simple‐linear competitive inhibitions, respectively. The potency of inhibition was higher against cathepsin L. Compound S4 promoted cell cycle arrest at G
0 and G
2 phase, and increase the expression of p16 and p21 proteins. In conclusion, compound S4 is an interesting molecule against cancer, promoting cell death in the human lymphoma lineage Raji and cell cycle arrest in the human lung carcinoma lineage A549.
Identification of core genes and outcomes in hepatocellular carcinoma by bioinformatics analysis
Authors: Shen Shu , Kong Junjie , Qiu Yiwen , Yang Xianwei , Wang Wentao , Yan Lvnan 
Published: December 2018

AbstractHepatocellular carcinoma (HCC) is the most common malignant liver disease in the world. However, the mechanistic relationships among various genes and signaling pathways are still largely unclear. In this study, we aimed to elucidate potential core candidate genes and pathways in HCC. The expression profiles GSE14520, GSE25097, GSE29721, and GSE62232, which cover 606 tumor and 550 nontumour samples, were downloaded from the Gene Expression Omnibus (GEO) database. Furthermore, HCC RNA‐seq datasets were also downloaded from the Cancer Genome Atlas (TCGA) database. The differentially expressed genes (DEGs) were filtered using R software, and we performed gene ontology (GO) and Kyoto Encyclopedia of Gene and Genome (KEGG) pathway analysis using the online databases DAVID 6.8 and KOBAS 3.0. Furthermore, the protein‐protein interaction (PPI) network complex of these DEGs was constructed by Cytoscape software, the molecular complex detection (MCODE) plug‐in and the online database STRING. First, a total of 173 DEGs (41 upregulated and 132 downregulated) were identified that were aberrantly expressed in both the GEO and TCGA datasets. Second, GO analysis revealed that most of the DEGs were significantly enriched in extracellular exosomes, cytosol, extracellular region, and extracellular space. Signaling pathway analysis indicated that the DEGs had common pathways in metabolism‐related pathways, cell cycle, and biological oxidations. Third, 146 nodes were identified from the DEG PPI network complex, and two important modules with a high degree were detected using the MCODE plug‐in. In addition, 10 core genes were identified, TOP2A, NDC80, FOXM1, HMMR, KNTC1, PTTG1, FEN1, RFC4, SMC4, and PRC1. Finally, Kaplan‐Meier analysis of overall survival and correlation analysis were applied to these genes. The abovementioned findings indicate that the identified core genes and pathways in this bioinformatics analysis could significantly enrich our understanding of the development and recurrence of HCC; furthermore, these candidate genes and pathways could be therapeutic targets for HCC treatment.
Pulmonary vein reconnection mapping with Advisor HD Grid demonstrating local EGM which were not visible on Tacticath ablation catheter
Authors: Yeo Colin , Tan Vern Hsen , Wong Kelvin Cheok Keng 
Published: December 2018

AbstractWe present a case of redo atrial fibrillation (AF) ablation for pulmonary vein reconnection. In mapping of posterior wall of left upper pulmonary vein (LUPV) with HD grid, a new and unique multipolar mapping catheter, it demonstrated presence of local electrocardiogram signals (EGM). But during mapping with the Tacticath ablation catheter, these signals were not visible. Nevertheless, ablation at this point resulted in isolation of LUPV. The unique mapping technology offered by HD grid mapping catheter may enable us to discover local EGM not otherwise visible in conventional bipole parallel recordings, to have more accurate maps and deliver for effective therapies.
Efficient Cholera Toxin B Subunit‐Based Nanoparticles with MRI Capability for Drug Delivery to the Brain Following Intranasal Administration
Authors: Chen Yiming , Fan Huimin , Xu Chen , Hu Wenli , Yu Bingran 
Published: December 2018

AbstractAlzheimer's disease (AD) is an incurable neurodegenerative brain disorder that exhibits clear pathologic changes in the hippocampus. Traditional drug delivery systems are ineffective due to the existence of the blood–brain barrier (BBB). In this study, an efficient, stable, and easily constructed nanosystem (CB‐Gd‐Cy5.5) based on the cholera toxin B subunit (CB) is designed to improve the efficiency of drug delivery to the brain, especially the hippocampus. Through intranasal administration, CB‐Gd‐Cy5.5 is easily delivered to the brain without intervention by the BBB. The CB in CB‐Gd‐Cy5.5 is used for specifically combining with the monosialoganglioside GM1, which is widely found in the hippocampus. This nanosystem exhibits impressive performance in accumulating in the hippocampus. In addition, the good magnetic resonance imaging (MRI) capability of CB‐Gd‐Cy5.5 can satisfy the monitoring of AD in the different stages.