bluuebunny/crossref_metadata_2025_split huggingface dataset:
Changes in river networks and their storage and regulation capacities in the Rapidly Urbanized Taihu Basin, China
Authors: Xu Yu , Xu Youpeng , Wu Lei 
Published: August 2018

AbstractOwing to the crucial environmental and hydrological functions of river systems and intensive human disturbance, further investigations of their change patterns and flood control functions are urgently needed. The Rapidly Urbanized Taihu Basin (RUTB) was selected as the study region to investigate changes in the river networks, the relationship between changes in river systems and urbanization, and the changes in the static drainage storage capacity (SC) and regulation capacity (RC) from the 1980s to the 2010s. The results indicated that the total drainage density in RUTB decreased by 10.17%. For the first‐, second‐, and third‐order rivers, the changes are +7.61%, −14.35%, and −17.84%, respectively. Spatially, the change pattern of the third‐order river drainage density displayed significant spatial clustering. The ratio of main to tributary river length (Rmt) was increased from 0.31 in the 1980s to 0.39 in the 2010s. Spatially, the drastic increases were found in the south‐east of Wu–Cheng–Xi–Yu, the east of Yang–Cheng–Dian–Mao, and the central southern part of Hang–Jia–Hu. Results moreover show that urbanization has the greatest influence on the third‐order drainage density, especially around the secondary and rapidly developing cities. The demand for flood control has led to a slight increase in the density of main rivers. The values of SC and RC decreased by 0.69% and 40.61% in RUTB, respectively. These changes were mainly concentrated around the major cities and urban corridors. The decrease in SC was caused by the decay of the river system, and the reduction in RC was caused by a combination of river system degradation and increase in ordinary water levels.
Advanced Functional Materials Constructed from Pillar[n]arenes
Authors: Xiao Tangxin , Xu Lixiang , Zhong Weiwei , Zhou Ling , Sun Xiao‐Qiang , Hu Xiao‐Yu , Wang Leyong 
Published: August 2018

AbstractPillar[n]arenes are new generation of supramolecular macrocyclic host, which exhibit excellent host−guest recognition properties. In the last decade, functional materials constructed from pillar[n]arenes have been attracted more and more attention and displayed outstanding characteristics, such as stimuli‐responsiveness, self‐healing and adaptability. In this mini‐review, we provide a survey of the pillar[n]arene‐based literatures covering light‐harvesting systems, functional hydrogels, and solid materials. It is anticipated that more and more pillar[n]arenes‐based advanced materials with multi‐functional properties will appear in the near future.
Nonperforming loans in the euro area: Are core–periphery banking markets fragmented?
Authors: Anastasiou Dimitrios , Louri Helen , Tsionas Mike 
Published: August 2018

AbstractThe objectives of this study are, first, to examine the causes of nonperforming loans (NPLs) in the euro area for the period 2003Q1 to 2016Q1 and, second, to investigate if there is fragmentation between core and periphery banking markets. By employing both fully modified ordinary least squares (FMOLS) and Bayesian panel‐cointegration vector autoregression techniques, we estimate the long‐run effects of both bank‐specific and macroeconomic factors on NPLs. We find that NPLs in the euro area have performed an upward (much higher in the periphery) shift after 2008 and are mostly related to worsening macroeconomic conditions. A chi‐square test comparing the estimated coefficients for the core and periphery NPLs rejects the hypothesis of equality revealing another aspect of financial fragmentation in the euro area that leaves the periphery more vulnerable. Such findings can be helpful when designing macroprudential as well as NPL resolution policies.
PREGNANT WOMEN'S RECOLLECTIONS OF EARLY MATERNAL BONDING: ASSOCIATIONS WITH MATERNAL–FETAL ATTACHMENT AND BIRTH CHOICES
Authors: Handelzalts Jonathan E. , Preis Heidi , Rosenbaum Maya , Gozlan Miri , Benyamini Yael 
Published: August 2018

ABSTRACTRecollections of own maternal care measured by parental bonding were found to be important in the pregnant woman's construction of herself as a mother. Although these recollections were studied with regard to various variables, there is a dearth of studies associated with pregnancy and childbirth. In this cross‐sectional study, 341 pregnant women were recruited. Measures included a Sociodemographics–Obstetric History Questionnaire; the Childbirth Choices Questionnaire (H. Preis, M. Gozlan, U. Dan, & Y. Benyamini, 2018); the Parental Bonding Instrument (G. Parker, H. Tupling, & L.B. Brown, 1979); a question regarding the planned presence of the woman's mother at delivery; and the Maternal‐Fetal Attachment Scale (M.S. Cranley, 1981). Parental recollections of Care were associated with fewer natural birth choices (hence, a more “medicalized” delivery), lower maternal–fetal attachment, and a wish for the mother's mother to be present at the birth. Parental recollections of Encouragement of Behavioral Freedom in childhood were associated with more natural choices regarding childbirth. In addition, women with higher scores on the parental bonding Denial of Autonomy factor reported stronger maternal–fetal attachment. Thus, early recollections of experiences with caregivers as manifested in parental bonding may be a possible influence on the transition to motherhood, and working through possible difficulties associated with these recollections may improve adjustment to motherhood.
Governance lessons from an interorganizational health information system implementation in Ethiopia
Authors: Gebre‐Mariam Mikael 
Published: August 2018

AbstractThe paper investigates interorganizational health information system implementation in a developing country health sector and the influence of the sociopolitical context that constitutes the institutions of the global health system. It argues that a comprehensive understanding of interorganizational system (IOS) implementation should include the study of the institutional context and its stakeholders who exhibit complex social and political attributes that influences its implementation and trajectory. This paper charts this course by examining the key governance dimensions of coordination and alignment. Building on this, the study challenges the viability of the unstructured institutional arrangements and the ensuing development modalities for health information system implementation, which are largely facilitated by international nongovernmental organizations and leverage on information and communication technology. The paper concludes by discussing the implications of the study. These include (1) the influence of unstructured interorganizational relations, at both the organizational and sector levels, on IOS adoption, (2) how the social and political behaviors of opportunistic interorganizational participants are implicated in the IOS adoption process, and (3) the role of strategic alignment, largely driven by the informal interorganizational relationship and social dimensions, on the prioritization and fit between IOS technological and organizational components.
Improved oxidation and wear resistance of ultrahigh molecular weight polyethylene using cross‐linked powder reinforcement
Authors: Xu Jia‐Zhuang , Muratoglu Orhun K. , Oral Ebru 
Published: August 2018

AbstractRadiation crosslinking decreases the wear of ultrahigh molecular weight polyethylene (UHMWPE) used in total joint implants and creates residual free radicals, which are the precursors of oxidative degradation. It is desirable to obtain a simultaneously wear‐ and oxidation‐resistant UHMWPE in order to prolong the longevity of implants. In this study, we hypothesized that the oxidative stability of a vitamin E‐containing, wear resistant UHMWPE can be improved by limiting the exposure of the antioxidant to radiation to maximize its activity. We blended UHMWPE powder with 0.1 wt % vitamin‐E and irradiated these powder blends (XPE). We further blended and consolidated uncrosslinked 0.1 wt % vitamin E‐blended UHMWPE with XPE and assessed the effects of radiation dose used for XPE and XPE content in the formulation on pin‐on‐disk wear resistance, static mechanical properties, and squalene‐initiated accelerated thermal aging. The wear rate decreased significantly with increasing XPE content in UHMWPE/XPE and increasing radiation dose used in the XPE preparation. The UHMWPE/XPE blends displayed improved oxidation resistance in the presence of the pro‐oxidant squalene compared to vitamin E‐blended UHMWPE irradiated to 125 kGy after consolidation. Strength and toughness of the UHMWPE/XPE blends decreased with increasing radiation dose and increasing XPE content; and these were comparable to those measured with the consolidated and irradiated vitamin E‐blended UHMWPE. Blending UHMWPE with XPE is a feasible approach to create a wear resistant UHMWPE with more active vitamin E available for long‐term oxidative protection of the polymer as the radiation exposure of the vitamin‐E in the vitamin E‐blended UHMWPE matrix is minimized. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 107B: 716–723, 2019.
MiR‐125a‐5p functions as a tumour suppressor in breast cancer by downregulating BAP1
Authors: Yan Liang , Yu Meng‐Chao , Gao Guang‐Lei , Liang Hong‐Wei , Zhou Xin‐Yan , Zhu Zhou‐Ting , Zhang Chen‐Yu , Wang Ya‐Bing , Chen Xi 
Published: August 2018

AbstractMicroRNAs (miRNAs) play an important role in the regulation of human cancers, including breast cancer (BC). In the current study, we examined the expression pattern of the miRNA miR‐125a‐5p in human BC tissues, tumorigenesis of BC progression. We found that miR‐125a‐5p was significantly downregulated in human BC tissues. Overexpression of miR‐125a‐5p in a xenograft mouse model indicated that miR‐125a‐5p may function as a tumour suppressor during carcinogenesis. To explore the molecular mechanism by which miR‐125a‐5p contributes to BC progression, we predicted the target genes of miR‐125a‐5p and identified BC susceptibility gene 1–associated protein 1 (BAP1) as a direct target. Finally, we demonstrated that BAP1 had opposing effects to those of miR‐125a‐5p on BC cells, suggesting that miR‐125a‐5p may inhibit cell proliferation and promote cell apoptosis by negatively regulating BAP1. Taken together, our findings provide the first clues regarding the role of miR‐125a‐5p as a tumour suppressor in BC via the inhibition of BAP1 translation.
Analgesic and sedative agents used in the intensive care unit: A review
Authors: Panahi Yunes , Dehcheshmeh Hamid Sadeghi , Mojtahedzadeh Mojtaba , Joneidi‐Jafari Nosratollah , Johnston Thomas P. , Sahebkar Amirhossein 
Published: August 2018

AbstractPain is a common experience for most patients in the intensive care unit (ICU). In the current study, the advantages and disadvantages of analgesic and sedative drugs used in the ICU are reviewed. An ideal sedative and analgesic agent should have features such as rapid onset of action, rapid recovery after discontinuation, predictability, minimal accumulation of the agent and metabolites in the body, and lack of toxicity. None of the sedative and analgesic agents have all of these desired characteristics; nevertheless, clinicians must be familiar with these classes of drugs to optimize pharmacotherapy and ensure as few side‐effects as possible for ICU patients.
SPDEF is overexpressed in gastric cancer and triggers cell proliferation by forming a positive regulation loop with FoxM1
Authors: Wu Jing , Qin Wen , Wang Ying , Sadik Arsil , Liu Jilan , Wang Yangyang , Song Ping , Wang Xiaoyun , Sun Kaiyue , Zeng Jiping , Wang Lixiang 
Published: August 2018

AbstractThe SAM‐pointed domain‐containing ETS transcription factor (SPDEF) is an epithelial‐specific transcription factor of the E26 transformation‐specific (ETS) family, which binds the target gene through the high‐affinity sequence of GGAT. It is suggested that SPDEF targets the promoter activity of Forkhead Box M1 (FoxM1), which has been proven to be highly expressed in gastric cancer. We found that SPDEF was overexpressed both at the messenger RNA (mRNA) and at the protein level in human gastric cancer species. The gastric cancer cells transfected with the SPDEF expression plasmid or SPDEF small interfering RNA (siRNA) led to observations on the clone genetics assay that indicated the promotion or the inhibition of gastric cancer cell proliferation, respectively. Both mRNA and protein levels of FoxM1 were regulated by SPDEF in gastric cancer cells and FoxM1 was also overexpressed in the corresponding human gastric cancer species. The overexpression and inhibition of FoxM1 could upregulate and downregulate the mRNA and protein levels of SPDEF expression, respectively. The recovery experiments verified that the overexpression of FoxM1 could at least partially revert both the expression of SPDEF and the proliferation of the cell lines even with the siRNA inhibition of SPDEF. The result of the dual luciferase activity assay showed that SPDEF bound to the promoter of FoxM1 and activated it. FoxM1 might also bind to the promoter of SPDEF to affect its expression. The results were checked in vivo. In conclusion, SPDEF is overexpressed in gastric cancer, which can form a positive regulation loop with FoxM1 to promote gastric carcinogenesis.
DNA hydroxymethylation mediated traumatic spinal injury by influencing cell death–related gene expression
Authors: Sun Hao , Miao Zhigang , Wang Hua , Tao Yuping , Yang Jiandong , Cai Jun , Wang Jingcheng , Wang Yongxiang 
Published: August 2018

AbstractSpinal cord injury (SCI) is a serious neurological disease, often leading to segmental injury following severe limb dysfunction. Recent studies showed that epigenetic regulation is involved in the pathogenesis of SCI. In this study, we examined the change in 5‐hydroxymethylcytosine (5hmC), a mechanism of demethylation, and its role in SCI in rats. We found that global 5hmC modification significantly increased in traumatic spinal cord tissues. Ten‐eleven translocation (Tet) enzymes are the limiting‐rate enzyme to catalyze the conversion of 5‐methylcytosine to 5hmC. In our study, the data indicated that Tet2, but not Tet1 and Tet3, significantly increased in traumatic spinal cord tissues. Further, we treated rats with SC‐1, a Tet2 expression inhibitor. SC‐1 increased necrotic volume after SCI. To further demonstrate that the damage caused by SC‐1 was related to DNA 5hmC, we examined the messenger RNA (mRNA) expression of many genes that related to cell death and cell survival. Our data showed that the 5hmC levels were related to the mRNA levels of these genes. In conclusion, targeting Tet2 to cause change in 5hmC levels in cell death–related genes may be new therapeutic strategy for the treatment of SCI.
Stem cell‐ and gene‐based therapies as potential candidates in Alzheimer's therapy
Authors: Hosseini Seyede Atefe , Mohammadi Rezvan , Noruzi Somaye , Mohamadi Yousef , Azizian Mitra , Mousavy Seyed Mojta , Ghasemi Faezeh , Hesari AmirReza , Sahebkar Amirhossein , Salarinia Reza , Aghdam Arad Mobasher , Mirzaei Hamed 
Published: August 2018

AbstractAlzheimer's disease (AD) is a progressive neurodegenerative disorder, which is associated with impairments of memory, thinking, language, and reasoning. Despite extensive research aiming at the treatment of AD, durable and complete remissions are rare. Hence, new therapeutic approaches are required. Among various therapeutic approaches, stem cells (ie, neural stem cells, mesenchymal stem cells, and embryonic stem cells) and delivery of protective genes such as encoding nerve growth factor, APOE, and glial cell–derived neurotrophic factor have generated promise in AD therapy. Here, we summarized a variety of effective therapeutic approaches (ie, stem cells, and genes) in AD therapy.
Novel THRB mutation analysis in congenital hypothyroidism with thyroid dysgenesis
Authors: Zhou Zhixia , Yang Chengyu , Lv Fuyan , Liu Wenmiao , Yan Shengli , Zang Hongwei , Li Miaomiao , Wang Fang , Zang Yucui , Liu Shiguo 
Published: August 2018

AbstractThyroid dysgenesis (TD) accounts for most cases of congenital hypothyroidism. Although mutations in thyroid hormone receptor β (THRB) have been identified in TD, the mutational spectrum of THRB and phenotype‐genotype correlations have not been fully elucidated. In this study, we aimed to find mutations of THRB, examine the functions of these mutations, and attempt to elucidate the relationship between THRB and TD. Thus, we screened the exons of THRB in 280 patients with TD and 200 normal subjects in samples collected from China. We performed cell morphology assays, MTT assays, flow cytometric analyses, and a quantitative reverse‐transcription polymerase chain reaction in human thyroid follicular epithelial cells (Nthy‐ori cell line) to examine the impact of THRB mutations. In two unrelated patients, two novel missense mutations, c.76G>A (p.D26N) and c.107G>A (p.C36Y), were identified in THRB. Functional studies suggested that the C36Y mutant caused changes in morphology, inhibiting cell proliferation and promoting apoptosis in a human thyroid cell line. In addition, we found that messenger RNA expressions of thyroglobulin (TG) and the Na+/I− symporter (NIS) were decreased in a time‐dependent manner in mutant THRB compared with the wild type. To our knowledge, this is the first study to document the prevalence of THRB mutations and the genotype‐phenotype spectrum of TD in a Chinese population. We characterized the function of a C36Y mutation, which reduced cell proliferation and increased cell death in thyroid epithelial cells. This study provides further evidence for genetic THRB defects and disease mechanisms in TD.
Andrographolide protects chondrocytes from oxidative stress injury by activation of the Keap1–Nrf2–Are signaling pathway
Authors: Li Bo , Jiang Tongmeng , Liu Hui , Miao Zhikang , Fang Depeng , Zheng Li , Zhao Jinmin 
Published: August 2018

Recent studies have shown that andrographolide (AP) has the potential to be developed as a drug for therapy for osteoarthritis (OA). However, the role of AP in attenuating the progression of OA is still unknown. We hypothesized that its therapeutic effect may be associated with its antioxidant potential. In this study, we investigated the therapeutic effect of AP on chondrocytes injured by H2O2 and the association with the oxidation‐related signaling pathways through the detection of cell proliferation, cell viability, the expression of oxidative stress‐specific genes (Sod1, Cat, and malonaldehyde [Mda]) and proteins (superoxide dismutase [SOD], catalase [CAT]) after a culture period of 3 and 5 days, respectively. Further exploration of the expression of nuclear factor erythroid 2‐related factor 2 (Nrf2) messenger RNA and protein was also performed. The results showed that 0.625 µg/ml and 2.5 µg/ml of AP decreased oxidative stress injury of chondrocytes by increasing cell proliferation reduced by H2O2 and antioxidant enzyme activity, including SOD and CAT. Inflammation factors, such as matrix metallopeptidase 13 (Mmp13), tissue inhibitor of metalloproteinase 1 (Timp1), and interleukin‐6 (Il6), were downregulated in the H2O2 group with AP, demonstrating a decrease in the progression of OA. Pathway analyses identified that the kelch‐like ECH‐associated protein 1 (Keap1)–Nrf2–antioxidant response element (Are) pathway is an important mediator in AP therapy on H2O2‐induced OA. This study indicates that AP exerts protection effects on oxidative stress via activation of the Keap1–Nrf2–Are pathway in chondrocytes injured by H2O2, which may be promising for the therapy of OA.
Restoration of miR‐152 expression suppresses cell proliferation, survival, and migration through inhibition of AKT–ERK pathway in colorectal cancer
Authors: Ghazanchaei Ardavan , Mansoori Behzad , Mohammadi Ali , Biglari Alireza , Baradaran Behzad 
Published: August 2018

BackgroundMiR‐152 has been reported as a tumor suppressor microRNA that is downregulated in a number of cancers, including colorectal cancer (CRC). A recent study suggested that miR‐152 could be one of the key regulators of CRC. The aim of this study is to investigate the role of miR‐152 in CRC and its mechanisms.MethodsThe pCMV‐GPF‐miR‐152 vector was transfected into SW‐480 and HCT‐116 CRC cells via JetPEI transfection reagent. The stable miR‐152‐expressed cells were selected for the further experiment. To evaluate the effect of miR‐152 on cell proliferation, 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay was performed. Also, the effect of miR‐152 on the survival of CRC cells was analyzed using terminal deoxynucleotidyl transferase dUTP nick‐end labeling (TUNEL) assay. The inhibitory effect of miR‐152 on migration was assessed by wound healing scratch assay. Then, the proteins expression levels of protein kinase B (AKT), phosphorylated AKT (p‐AKT), extracellular signal–regulated kinase (ERK), and phosphorylated ERK (p‐ERK) were measured by the western blot analysis method.ResultsThe result of MTT assay represented miR‐152 could inhibit cell proliferation. The TUNEL assay showed miR‐152 could induce apoptosis in CRC cells. The wound healing scratch assay showed that miR‐152 replacement repressed cell migration in CRC cell lines compared to control groups. The result of protein expression by western blot analysis demonstrated that miR‐152 could reduce AKT–p‐AKT, and ERK–p‐ERK ratio compared to control cells.ConclusionOur results show that miR‐152 has new anticancer and antimetastatic effect in CRC tissue. The current study showed that miR‐152 could be a novel therapeutic small molecule to suppress CRC cell proliferation, survival, and migration by suppressing AKT–ERK signaling pathways.
Exogenous hydrogen sulfide attenuates the development of diabetic cardiomyopathy via the FoxO1 pathway
Authors: Ye Peng , Gu Yue , Zhu Yan‐Rong , Chao Yue‐Lin , Kong Xiang‐Quan , Luo Jie , Ren Xiao‐Min , Zuo Guang‐Feng , Zhang Dai‐Min , Chen Shao‐Liang 
Published: August 2018

BackgroundPrevious studies have suggested that exogenous hydrogen sulfide can alleviate the development of diabetic cardiomyopathy (DCM) by inhibiting oxidative stress, inflammation, and apoptosis. However, the underlying mechanism is not fully understood. Nuclear expression and function of the transcription factor Forkhead box protein O (FoxO1) have been associated with cardiovascular diseases, and thus, the importance of FoxO1 in DCM has gained increasing attention. This study was designed to investigate the interactions between hydrogen sulfide (H2S) and nuclear FoxO1 in DCM.MethodsDiabetes was induced in adult male C57BL/6J mice by intraperitoneal injection of streptozotocin and was treated with H2S donor sodium hydrosulfide for 12 weeks. The H9C2 cardiomyoblast cell line and neonatal rat cardiomyocytes (NRCMs) were treated with the slow‐releasing H2S donor GYY4137 before high‐glucose (HG) exposure with or without pretreatment with the Akt inhibitor MK‐2206 2HCl. Changes in FoxO1 protein phosphorylation and subcellular localization were determined in H9C2 cells, NRCMs, and cardiac tissues from normal and diabetic mice. Cardiac structure and function in the diabetic mice were evaluated by echocardiography and histological analysis and compared with those in control animals.ResultsThe echocardiographic and histopathological data indicated that exogenous H2S improved cardiac function and attenuated cardiac hypertrophy and myocardial fibrosis in diabetic mice. H2S also improved HG‐induced oxidative stress and apoptosis in cardiac tissue and NRCMs. In addition, H2S induced FoxO1 phosphorylation and nuclear exclusion in vitro and in vivo, and this function was not inhibited by MK‐2206 2HCl. Alanine substitution mutation of three sites in FoxO1‐enhanced FoxO1 transcriptional activity, and subsequent treatment with exogenous H2S could not prevent HG‐induced nuclear retention.ConclusionsOur data indicate that H2S is a novel regulator of FoxO1 in cardiac cells and provide evidence supporting the potential of H2S in inhibiting the progression of DCM.