bluuebunny/crossref_metadata_2025_split huggingface dataset:
An entropy based morphological variability assessment of a large braided river
Authors: Chembolu Vinay , Dutta Subashisa 
Published: June 2018

AbstractThe present paper utilizes entropy to investigate variability in the surface areas of sandbars distribution of the Brahmaputra River, India. The intensity entropy disorder index (IDI) was computed for the dry and the post‐monsoon season for a selected reach of the river. The planform disorder index (PDI) was computed to represent the annual scale planform change due to seasonal flood. Finally, annual monsoon and peak flood stream power were evaluated and related to PDI. The results showed that the intensity disorder index followed a decreasing trend in dry and post‐monsoon seasons; tending towards lower deviation from a uniform distribution. It was noted that except for extreme flood years the PDI trend correlated well with monsoonal stream power. Distinctive trends in stream power were also observed in the present study. © 2018 John Wiley & Sons, Ltd.
Sheet erosion rates and erosion control on steep rangelands in loess regions
Authors: Wang Dongdong , Wang Zhanli , Zhang Qingwei , Zhang Qilin , Tian Naling , Liu Jun'e 
Published: June 2018

AbstractNumerous steep rangelands have been restored from abandoned steep croplands, and sheet erosion has become the dominant erosion process on rangelands since the Grain‐to‐Green Project was launched in 1999 on the Loess Plateau. Quantifying sheet erosion rates and dynamics on steep rangelands may aid soil erosion management strategies and improve grassland health. Simulated rainfall experiments were conducted on a rangeland plot under five vegetation coverages (30%, 40%, 50%, 60% and 70%), five rainfall intensities (0.7, 1.0, 1.5, 2.0 and 2.5 mm min‐1) and five slopes (7°, 10°, 15°, 20° and 25°). The results show that the sheet erosion rate decreased as vegetation cover increased, as described by linear or logarithmic equations under different rainfall intensities or slopes. Herbaceous vegetation can reduce and control sheet erosion by reducing the effect of rainfall intensity or slope, especially under sufficiently high vegetation cover. The sheet erosion rate was accurately modelled by a linear equation that included the three factors, i.e. rainfall intensity, vegetation cover, and slope. Among the different hydrodynamic parameters (shear stress, stream power, unit stream power and unit energy), stream power resulted in the best model for the sheet erosion rate. Velocity measurements and calculations, water depth calculations, and aggregative indicators of herbaceous vegetation for sheet flow should be explored in future research, which will be important in improving experimental accuracy and sheet erosion modelling. © 2018 John Wiley & Sons, Ltd.
Modeling surface tension of a two‐dimensional droplet using smoothed particle hydrodynamics
Authors: Ehigiamusoe Nowoghomwenma Noel , Maxutov Samat , Lee Yeaw Chu 
Published: June 2018

SummarySurface tension plays a significant role at the dynamic interface of free‐surface flows especially at the microscale in capillary‐dominated flows. A model for accurately predicting the formation of two‐dimensional viscous droplets in vacuum or gas of negligible density and viscosity resulting from axisymmetric oscillation due to surface tension is solved using smoothed particle hydrodynamics composed of the Navier‐Stokes system and appropriate interfacial conditions for the free‐surface boundaries. The evolution of the droplet and its free‐surface interface is tracked over time to investigate the effects of surface tension forces implemented using a modified continuous surface force method and is compared with those performed using interparticle interaction force. The dynamic viscous fluid and surface tension interactions are investigated via a controlled curvature model and test cases of nonsteady oscillating droplets; attention is focused here on droplet oscillation that is released from an initial static deformation. Accuracy of the results is attested by demonstrating that (i) the curvature of the droplet that is controlled; (ii) uniform distribution of fluid particles; (iii) clean asymmetric forces acting on the free surface; and (iv) nonsteady oscillating droplets compare well with analytical and published experiment findings. The advantage of the proposed continuous surface force method only requires the use of physical properties of the fluid, whereas the interparticle interaction force method is restricted by the requirement of tuning parameters.
Visual hallucinations in dementia and Parkinson's disease: A qualitative exploration of patient and caregiver experiences
Authors: Renouf Sarah , ffytche Dominic , Pinto Rebecca , Murray Joanna , Lawrence Vanessa 
Published: June 2018

ObjectivesVisual hallucinations (VHs) can occur in several clinical conditions, of which the dementias, broadly defined, and Parkinson's disease rank among the most common. There is limited research on the lived experience of hallucinations among affected individuals and therefore a lack of evidence‐based management strategies. This study used qualitative methods to explore the VH experience of individuals with dementia or Parkinson's disease and their informal caregivers.MethodsIn‐depth interviews were conducted with 10 individuals with VHs and dementia and 11 informal caregivers, and 11 individuals with VHs and Parkinson's disease and 9 informal caregivers. Interviews were analysed using an inductive thematic approach.ResultsThree themes emerged from the data: “Insight and distress,” “Caregiver approach: challenging v reassurance,” and “Normality and stigma.” Insight appeared to affect whether hallucinations were perceived as threatening and whether acceptance occurred over time. Emotional reactions and management strategies varied as insight changed with disease progression. Concerns around stigmatisation negatively influenced help‐seeking and acceptance of the hallucinations.ConclusionsDegree of insight and cognitive ability appear fundamental to the lived experience of hallucinations. Irrespective of the clinical context, support in early stages should focus on raising awareness of VH, symptom disclosure, stigma reduction, and contact with others affected. In later stages, the focus shifts to informal caregiver needs and a flexible approach to reassuring those affected.
Pharmacogenetic evaluation of a DISP1 gene variant in antidepressant treatment of obsessive–compulsive disorder
Authors: Lisoway Amanda J. , Zai Gwyneth , Tiwari Arun K. , Zai Clement C. , Wigg Karen , Goncalves Vanessa , Zhang Danning , Freeman Natalie , Müller Daniel J. , Kennedy James L. , Richter Margaret A. 
Published: June 2018

AbstractObjectivesA recent genome‐wide association study (GWAS) in obsessive–compulsive disorder (OCD) reported a significant marker in the dispatched homolog 1 (Drosophila) gene (DISP1 gene) associated with serotonin reuptake inhibitor (SRI) antidepressant response (Qin et al., ). DISP1 has never been examined before in terms of association with SRI response until this GWAS. We attempt to replicate the GWAS finding by investigating the association of the DISP1 rs17162912 polymorphism with SRI response in our sample of 112 European Caucasian OCD patients.MethodsPatients were previously treated naturalistically with up to 6 different SRIs sequentially, including 5 selective SRIs (fluoxetine, fluvoxamine, sertraline, paroxetine, and citalopram) and 1 SRI (clomipramine). Each medication trial was evaluated retrospectively for response and was rated categorically as either responder or nonresponder using the Clinical Global Impression–Improvement scale. Fisher's exact test was used to investigate the relationship between the DISP1 rs17162912 genotype distribution and SRI response.ResultsWe did not observe a significant association between rs17162912 and SRI response (p = .32).ConclusionThis replication study did not support the role of DISP1 in predicting SRI response in OCD; however, methodological differences between the original GWAS and our study, as well as limited power and low minor allele frequency, may have hindered replication.
MicroRNA‐138 Inhibits Osteogenic Differentiation and Mineralization of Human Dedifferentiated Chondrocytes by Regulating RhoC and the Actin Cytoskeleton
Authors: Zheng Hongjun , Ramnaraign David , Anderson Britta A , Tycksen Eric , Nunley Ryan , McAlinden Audrey 
Published: June 2018

ABSTRACTMicroRNAs (miRNAs) are known to play critical roles in many cellular processes including those regulating skeletal development and homeostasis. A previous study from our group identified differentially expressed miRNAs in the developing human growth plate. Among those more highly expressed in hypertrophic chondrocytes compared to progenitor chondrocytes was miR‐138, therefore suggesting a possible role for this miRNA in regulating chondrogenesis and/or endochondral ossification. The goal of this study was to determine the function of miR‐ 138 in regulating osteogenesis by using human osteoarthritic dedifferentiated chondrocytes (DDCs) as source of inducible cells. We show that over‐expression of miR‐138 inhibited osteogenic differentiation of DDCs in vitro. Moreover, cell shape was altered and cell proliferation and possibly migration was also suppressed by miR‐138. Given alterations in cell shape, closer analysis revealed that F‐actin polymerization was also inhibited by miR‐138. Computational approaches showed that the small GTPase, RhoC, is a potential miR‐138 target gene. We pursued RhoC further given its function in regulating cell proliferation and migration in cancer cells. Indeed, miR‐138 over‐expression in DDCs resulted in decreased RhoC protein levels. A series of rescue experiments showed that RhoC over‐expression could attenuate the inhibitory actions of miR‐138 on DDC proliferation, F‐actin polymerization and osteogenic differentiation. Bone formation was also found to be enhanced within human demineralized bone scaffolds seeded with DDCs expressing both miR‐138 and RhoC. In conclusion, we have discovered a new mechanism in DDCs whereby miR‐138 functions to suppress RhoC which subsequently inhibits proliferation, F‐actin polymerization and osteogenic differentiation. To date, there are no published reports on the importance of RhoC in regulating osteogenesis. This opens up new avenues of research involving miR‐138 and RhoC pathways to better understand mechanisms regulating bone formation in addition to the potential use of DDCs as a cell source for bone tissue engineering. © 2018 The Authors. JBMR Plus is published by Wiley Periodicals, Inc. on behalf of the American Society for Bone and Mineral Research.
FGF9 modulates Schwann cell myelination in developing nerves and induces a pro‐inflammatory environment during injury
Authors: Deng Binbin , Lv Wenjing , Duan Weisong , Liu Yakun , Li Zhongyao , Song Xueqing , Cui Can , Qi Xiaoming , Wang Xiaoxiao , Li Chunyan 
Published: June 2018

AbstractMyelin sheath is critical for the proper functioning of the peripheral nervous system (PNS), which allows the effective conduction of nerve impulses. Fibroblast growth factor 9 (FGF9) is an autocrine and paracrine protein in the fibroblast growth factor family that regulates cell differentiation and proliferation. Fgf9 Schwann cell (SC) conditional knockout mice were developed to detect the role of FGF9 in the PNS. In our study, the absence of Fgf9 led to delayed myelination in early development. The expression of mature SC‐related genes decreased, and the expression of genes associated with immature SCs increased in the Fgf9 knockout mice. These data were consistent with the morphology and praxeology we observed during the development of the peripheral nerves. Extracellular‐regulated kinases 1/2 (ERK1/2) are key signals for myelination, and our results showed that Fgf9 ablation led to the inactivation of ERK1/2. Further research was performed to detect the role of FGF9 in peripheral nerve injury. In superoxide dismutase 1‐G93A mice with Fgf9 SC knockout, we found that Fgf9 ablation inhibited the expressions of Cd68, Il‐1β, and Cd86, which contributed to the degeneration of the axon and myelin sheath.
Long noncoding RNA GIHCG enhanced tongue squamous cell carcinoma progression through regulating miR‐429
Authors: Ma Long , Wang Qibao , Gong Zuode , Xue Lande , Zuo Zhibin 
Published: June 2018

AbstractLong noncoding RNAs play essential roles in cancer development and progression. Here, we tried to investigate the role of GIHCG in the progression and metastasis of tongue squamous cell carcinoma (TSCC). In our study, we showed that that the expression level of GIHCG was upregulated in TSCC tissues and cell lines. In addition, we indicated that high GIHCG expression was positively associated with poor overall survival. Moreover, ectopic expression of GIHCG enhanced TSCC cell cycle, proliferation, and migration. Elevated expression of GIHCG inhibited the miR‐429 expression in TSCC cells. We demonstrated that the expression level of miR‐429 was lower in TSCC tissues and cell lines. Low miR‐429 expression was positively associated with poor overall survival. We then determined the correlation between miR‐429 and GIHCG expression levels. A statistically significantly inverse correlation was observed between miR‐429 and GIHCG expression levels in TSCC tissues. In addition, overexpression of miR‐429 suppressed the TSCC cell cycle, proliferation, and migration. Elevated expression of GIHCG promoted TSCC cell cycle, proliferation, and migration through regulating miR‐429 expression. These results suggested that GIHCG increased TSCC progression through negative modulation of miR‐429. Our results suggested that GIHCG/miR‐429 might play a vital role in TSCC progression.
Long noncoding RNA‐RNCR3 overexpression deleteriously affects the growth of glioblastoma cells through miR‐185‐5p/Krüppel‐like factor 16 axis
Authors: Zhang Liang , Cao Yidong , Wei Minghao , Jiang Xue , Jia Dong 
Published: June 2018

AbstractGlioblastoma (GBM) is a devastating and highly aggressive tumor, which is apoptosis resistant and difficult to cure. Recently, long noncoding RNAs have been shown to play a pivotal role in GBM progression. Evidence has suggested that retinal noncoding RNA3 (RNCR3) is a GBM‐associated noncoding RNA and is under‐expressed in GBM. However, the function and mechanism of RNCR3 on GBM cell growth and apoptosis are still uncertain. In the current study, we found that the level of RNCR3 is decreased in U87, U251, U373, and A172 GBM cell lines when compared with the normal human astrocytes. Elevating long noncoding RNA RNCR3 expression markedly inhibits U87 and U251 cell survival and proliferation. Further studies indicated that RNCR3 overexpression promotes U87 and U251 cell apoptosis and activity caspase‐3/7. Moreover, we found that RNCR3 overexpression promotes Krüppel‐like factor 16 (KLF16) expression through inhibiting the level of miR‐185‐5p. We demonstrated that KLF16 is a direct target of miR‐185‐5p. An increased miR‐185‐5p level by a miR‐185‐5p mimic or decreased KLF16 by KLF16 small interfering RNA both reversed the function of RNCR3 overexpression on GBM cell growth and apoptosis. In summary, this study focuses on investigating the key molecular mechanisms of RNCR3 involved in GBM cell growth and apoptosis. Our data indicated that RNCR3 overexpression inhibits cell growth and induces its apoptosis through the miR‐185‐5p/KLF16 axis.
Silencing forkhead box M1 promotes apoptosis and autophagy through SIRT7/mTOR/IGF2 pathway in gastric cancer cells
Authors: Yu Wei , Cui Xiaofeng , Wan Zhongyi , Yu Yanhui , Liu Xiumin , Jin Lifang 
Published: June 2018

AbstractForkhead box M1 (FOXM1) was initially identified as an oncogenic transcription factor, and multiple lines of evidence have demonstrated that FOXM1 is abundantly expressed and plays an irreplaceable role in several types of human cancers. Also, evidence has shown the association of FOXM1 with gastric carcinoma metastasis and patients prognosis; however, the potential role and molecular mechanism of FOXM1 in gastric cancer cell apoptosis are still obscure. The current study indicates that FOXM1 is highly expressed in a variety of gastric carcinoma cell lines, such as BGC823, MGC803, AGS, and SGC‐7901, compared with the normal gastric mucosal epithelial cell lines CES‐1. FOXM1 silence markedly inhibits AGS and SGC‐7901 cell survival and proliferation, increases their apoptosis, and modulates apoptosis‐related protein expression, including reduced Bcl‐2 level and increased Bax and caspase‐3 levels. Further study showed that FOXM1 depletion induced cell autophagy through increasing the level of beclin‐1 and decreasing the P62 expression. We next corroborated that FOXM1 silence abolished the expression of Sirtuin 7 (SIRT7) and increased the level of insulin‐like growth factor 2 (IGF2) and mammalian target of rapamycin (mTOR). Finally, our data documented that the SIRT7/mTOR/IGF2 pathway was involved in the function of FOXM1 in AGS cell growth and apoptosis. In conclusion, these results confirmed that FOXM1 is involved in gastric carcinoma progression via the SIRT7/mTOR/IGF2 pathway.
microRNA‐146a is involved in rSjP40‐inhibited activation of LX‐2 cells by targeting Smad4 expression
Authors: Zhu Dandan , Hu Bin , Zhou Yonghua , Sun Xiaolei , Chen Jinling , Chen Liuting , Ji Zhaodong , Zhu Jinhua , Duan Yinong 
Published: June 2018

AbstractPrevious studies have demonstrated that the recombinant Schistosoma japonicum protein P40 (rSjP40) could inhibit activation of hepatic stellate cells (HSCs) through the TGF‐β1/Smads signaling pathway. Since multiple microRNAs could play essential roles in HSC activation and in the process of hepatic fibrosis through targeting Smads, we attempted to seek the potential microRNAs that could be involved in rSjP40‐induced inhibition of HSC activation. Using the method of quantitative real‐time PCR, we found that rSjP40 could induce miR‐146a expression in LX‐2 cells. The down‐regulated expression levels of Smad4 and α‐SMA in LX‐2 cells induced by rSjP40 were partially restored by an miR‐146a inhibitor. miR‐146a can be involved in rSjP40‐induced inhibition of HSC activation through targeting Smad4. These findings provide us a new idea to explore the potential mechanisms by which rSjP40 could regulate the process of hepatic fibrosis.
Valproic acid inhibits the protective effects of stromal cells against chemotherapy in breast cancer: Insights from proteomics and systems biology
Authors: Barneh Farnaz , Salimi Mona , Goshadrou Fatemeh , Ashtiani Minoo , Mirzaie Mehdi , Zali Hakimeh , Jafari Mohieddin 
Published: June 2018

AbstractInteraction between tumor and stromal cells is beginning to be decoded as a contributor to chemotherapy resistance. Here, we aim to take a system‐level approach to explore a mechanism by which stromal cells induce chemoresistance in cancer cells and subsequently identify a drug that can inhibit such interaction. Using a proteomic dataset containing quantitative data on secretome of stromal cells, we performed multivariate analyses and found that bone‐marrow mesenchymal stem cells (BM‐MSCs) play the most protective role against chemotherapeutics. Pathway enrichment tests showed that secreted cytokines from BM‐MSCs activated 4 signaling pathways including Janus kinase‐signal transducer and activator of transcription, phosphatidylinositol 3‐kinase‐protein kinase B, and mitogen‐activated protein kinase, transforming growth factor‐β in cancer cells collectively leading to nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐kB) transcription factor activation. Based on the data from integrated Library of Integrated Network‐Based Cellular Signatures (iLINCs) program, we found that among different drugs, valproic acid (VA) affected the expression of 34 genes within the identified pathways that are activated by stromal cells. Our in vitro experiments confirmed that VA inhibits NF‐kB activation in cancer cells. In addition, analyzing gene expression data in patients taking oral VA showed that this drug decreased expression of antioxidant enzymes culminating in increased oxidative stress in tumor cells. These results suggest that VA confines the protective role of stromal cells by inhibiting the adaptation mechanisms toward oxidative stress which is potentiated by stromal cells. Since VA is an already prescribed drug manifesting anticancer effects, this study provides a mechanistic insight for combination of VA with chemotherapy in the clinical setting.
Structural variations in hyperbranched polymers prepared via thermal polycondensation of lysine and histidine and their effects on DNA delivery
Authors: Alazzo Ali , Lovato Tatiana , Collins Hilary , Taresco Vincenzo , Stolnik Snjezana , Soliman Mahmoud , Spriggs Keith , Alexander Cameron 
Published: June 2018

AbstractThe successful clinical translation of nonviral gene delivery systems has yet to be achieved owing to the biological and technical obstacles to preparing a safe, potent, and cost‐effective vector. Hyperbranched polymers, compared with other polymers, have emerged as promising candidates to address gene delivery barriers owing to their relatively simple synthesis and ease of modification, which makes them more feasible for scale‐up and manufacturing. Here, we compare hyperbranched poly(amino acids) synthesised by copolymerising histidine and lysine, with hyperbranched polylysine prepared using the well‐known “ultrafacile” thermal polycondensation route, to investigate the effects of histidine units on the structure and gene delivery applications of the resultant materials. The conditions of polymerisation were optimised to afford water‐soluble hyperbranched polylysine‐co‐histidine of three different molar ratios with molecular masses varying from 13 to 30 kDa. Spectroscopic, rheological, and thermal analyses indicated that the incorporation of histidine modulated the structure of hyperbranched polylysine to produce a more dendritic polymer with less flexible branches. Experiments to probe gene delivery to A549 cells indicated that all the new hyperbranched polymers were well tolerated, but, surprisingly, the copolymers containing histidine were not more effective in transfecting a luciferase gene than were hyperbranched polylysines synthesised as established literature comparators. We attribute the variations in gene delivery efficacy to the changes induced in polymer architecture by the branching points at histidine residues, and we obtain structure–function information relating histidine content with polymer stiffness, pKa, and ability to form stable polyplexes with DNA. The results are of significance to nanomedicine design as they indicate that addition of histidine as a co‐monomer in the synthetic route to hyperbranched polymers not only changes the buffering capacity of the polymer but has significant effects on the overall structure, architecture, and gene delivery efficacy.