bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sustainable coffee‐based CO2 adsorbents: toward a greener production via hydrothermal carbonization
Authors: Querejeta Nausika , Gil M. Victoria , Rubiera Fernando , Pevida Covadonga 
Published: November 2017

AbstractActivated carbons for adsorption of CO2 under flue gas conditions were prepared by means of hydrothermal carbonization (HTC) and subsequent CO2 activation of spent coffee grounds. The HTC of the samples consisted of their heating at moderate temperature with a high water content in autoclave. A preliminary screening concluded that 1:2 biomass/water ratio (spent coffee grounds as received) and no chemicals added during HTC with further activation in CO2 at 800°C for 1 h are suitable conditions to produce the CO2 adsorbents. In addition, the response surface methodology (RSM) successfully evaluated the combined effect of HTC temperature and dwell time, to maximize the CO2 capture capacity within the experimental region. Both the lowest temperature and dwell time (120°C, 3 h) resulted in the maximum CO2 capture capacity (2.95 wt.%). Two activated carbons (ACs) were then produced: one via hydrothermal carbonization optimized by means of response surface methodology (RSM) followed by CO2 activation (HC‐Co) and the other one by single‐step CO2 activation as described in the Group's patent ES2526259 (AC‐Co). Analysis of the features and performances of the two ACs revealed superior chemical and textural characteristics on HC‐Co for CO2 adsorption under post‐combustion capture conditions; HTC process is the sole responsible of this enhancement. Moreover, the proposed methodology to produce CO2 adsorbents from spent coffee grounds represents a more energy‐efficient approach. © 2017 Society of Chemical Industry and John Wiley & Sons, Ltd.
Motion artifact in studies of functional connectivity: Characteristics and mitigation strategies
Authors: Satterthwaite Theodore D. , Ciric Rastko , Roalf David R. , Davatzikos Christos , Bassett Danielle S. , Wolf Daniel H. 
Published: November 2017

AbstractMotion artifacts are now recognized as a major methodological challenge for studies of functional connectivity. As in‐scanner motion is frequently correlated with variables of interest such as age, clinical status, cognitive ability, and symptom severity, in‐scanner motion has the potential to introduce systematic bias. In this article, we describe how motion‐related artifacts influence measures of functional connectivity and discuss the relative strengths and weaknesses of commonly used denoising strategies. Furthermore, we illustrate how motion can bias inference, using a study of brain development as an example. Finally, we highlight directions of ongoing and future research, and provide recommendations for investigators in the field. Hum Brain Mapp, 40:2033–2051, 2019. © 2017 Wiley Periodicals, Inc.
Four in vivo g‐ratio‐weighted imaging methods: Comparability and repeatability at the group level
Authors: Ellerbrock Isabel , Mohammadi Siawoosh 
Published: November 2017

AbstractA recent method, denoted in vivo g‐ratio‐weighted imaging, has related the microscopic g‐ratio, only accessible by ex vivo histology, to noninvasive MRI markers for the fiber volume fraction (FVF) and myelin volume fraction (MVF). Different MRI markers have been proposed for g‐ratio weighted imaging, leaving open the question which combination of imaging markers is optimal. To address this question, the repeatability and comparability of four g‐ratio methods based on different combinations of, respectively, two imaging markers for FVF (tract‐fiber density, TFD, and neurite orientation dispersion and density imaging, NODDI) and two imaging markers for MVF (magnetization transfer saturation rate, MT, and, from proton density maps, macromolecular tissue volume, MTV) were tested in a scan–rescan experiment in two groups. Moreover, it was tested how the repeatability and comparability were affected by two key processing steps, namely the masking of unreliable voxels (e.g., due to partial volume effects) at the group level and the calibration value used to link MRI markers to MVF (and FVF). Our data showed that repeatability and comparability depend largely on the marker for the FVF (NODDI outperformed TFD), and that they were improved by masking. Overall, the g‐ratio method based on NODDI and MT showed the highest repeatability (90%) and lowest variability between groups (3.5%). Finally, our results indicate that the calibration procedure is crucial, for example, calibration to a lower g‐ratio value (g = 0.6) than the commonly used one (g = 0.7) can change not only repeatability and comparability but also the reported dependency on the FVF imaging marker. Hum Brain Mapp 39:24–41, 2018. © 2017 Wiley Periodicals, Inc.
Osteoblast-Derived Extracellular Vesicles Are Biological Tools for the Delivery of Active Molecules to Bone
Authors: Cappariello Alfredo , Loftus Alexander , Muraca Maurizio , Maurizi Antonio , Rucci Nadia , Teti Anna 
Published: November 2017

ABSTRACT

Extracellular vesicles (EVs) are newly appreciated regulators of tissue homeostasis and a means of intercellular communication. Reports have investigated the role of EVs and their cargoes in cellular regulation and have tried to fine-tune their biotechnological use, but to date very little is known on their function in bone biology. To investigate the relevance of EV-mediated communication between bone cells, we isolated EVs from primary mouse osteoblasts and assessed membrane integrity, size, and structure by transmission electron microscopy (TEM) and fluorescence-activated cell sorting (FACS). EVs actively shuttled loaded fluorochromes to osteoblasts, monocytes, and endothelial cells. Moreover, osteoblast EVs contained mRNAs shared with donor cells. Osteoblasts are known to regulate osteoclastogenesis, osteoclast survival, and osteoclast function by the pro-osteoclastic cytokine, receptor activator of nuclear factor κ-B ligand (Rankl). Osteoblast EVs were enriched in Rankl, which increased after PTH treatment. These EVs were biologically active, supporting osteoclast survival. EVs isolated from rankl–/– osteoblasts lost this pro-osteoclastic function, indicating its Rankl-dependence. They integrated ex vivo into murine calvariae, and EV-shuttled fluorochromes were quickly taken up by the bone upon in vivo EV systemic administration. Rankl–/– mice lack the osteoclast lineage and are negative for its specific marker tartrate-resistant acid phosphatase (TRAcP). Treatment of rankl–/– mice with wild-type osteoblast EVs induced the appearance of TRAcP-positive cells in an EV density-dependent manner. Finally, osteoblast EVs internalized and shuttled anti-osteoclast drugs (zoledronate and dasatinib), inhibiting osteoclast activity in vitro and in vivo. We conclude that osteoblast EVs are involved in intercellular communication between bone cells, contribute to the Rankl pro-osteoclastic effect, and shuttle anti-osteoclast drugs, representing a potential means of targeted therapeutic delivery. © 2017 The Authors. Journal of Bone and Mineral Research Published by Wiley Periodicals Inc.
Retracted: Effect of microRNA‐128 on cisplatin resistance of glioma SHG‐44 cells by targeting JAG1
Authors: Yi Dong‐Ye , Su Qing , Zhang Fang‐Cheng , Fu Peng , Zhang Qing , Cen Yong‐Cun , Zhao Hong‐Yang , Xiang Wei 
Published: November 2017

AbstractThis current study intends to investigate the effect of microRNA‐128 (miR‐128) on cisplatin (DDP) resistance in glioma SHG‐44 cells. SHG‐44/DDP cells were transfected with miR‐128 antisense oligonucleotide (ASO) and assigned into blank, resistance, NC, anti‐miR‐128, miR‐128 mimic, si‐JAG1, and anti‐miR‐128 + si‐JAG1 groups. qRT‐PCR and Western blotting were employed for determining expression of miR‐128, JAG1, Bax and Bcl‐2. MTT assay, Giemsa staining, and flow cytometry were applied to detect DDP resistance, cellular morphology, and cell cycle, respectively. JAG1 is targeted and negatively regulated by miR‐128. In in vitro experiments, compared with the blank group, the rest groups exhibited declined miR‐28 and Bax expression, lowered cell inhibition rate and apoptosis rate, but elevated JAG1 and Bcl‐2 expression with cells arrested in the S phase. Compared with the resistance group, the anti‐miR‐128 group showed decreasedBax expression along with a lowered cell inhibition rate and apoptosis rate, but increased JAG1 and Bcl‐2 expression with reduced cells arrested in the S phase; while the miR‐128 mimic group showed an opposite trend; the si‐JAG1 group showed decreased Bcl‐2 expression and reduced cells in the S phase. In in vivo experiments, compared with the resistance group, the tumor growth rate, tumor volume, and weight as well as JAG1 expression accelerated in the anti‐miR‐128 group; whereas the miR‐128 mimic and si‐JAG1 groups exhibited an opposite trend. Our findings demonstrated that miR‐128 ASO transfection might down‐regulate the expression of miR‐128 in SHG‐44/DDP and up‐regulate the DDP resistance in SHG‐44/DDP cells, providing a potential treatment target for glioma.
Expanding the CRISPR/Cas9 toolkit for Pichia pastoris with efficient donor integration and alternative resistance markers
Authors: Weninger Astrid , Fischer Jasmin E. , Raschmanová Hana , Kniely Claudia , Vogl Thomas , Glieder Anton 
Published: November 2017

AbstractKomagataella phaffii (syn. Pichia pastoris) is one of the most commonly used host systems for recombinant protein expression. Achieving targeted genetic modifications had been hindered by low frequencies of homologous recombination (HR). Recently, a CRISPR/Cas9 genome editing system has been implemented for P. pastoris enabling gene knockouts based on indels (insertion, deletions) via non‐homologous end joining (NHEJ) at near 100% efficiency. However, specifically integrating homologous donor cassettes via HR for replacement studies had proven difficult resulting at most in ∼20% correct integration using CRISPR/Cas9. Here, we demonstrate the CRISPR/Cas9 mediated integration of markerless donor cassettes at efficiencies approaching 100% using a ku70 deletion strain. The Ku70p is involved in NHEJ repair and lack of the protein appears to favor repair via HR near exclusively. While the absolute number of transformants in the Δku70 strain is reduced, virtually all surviving transformants showed correct integration. In the wildtype strain, markerless donor cassette integration was also improved up to 25‐fold by placing an autonomously replicating sequence (ARS) on the donor cassette. Alternative strategies for improving donor cassette integration using a Cas9 nickase variant or reducing off targeting associated toxicity using a high fidelity Cas9 variant were so far not successful in our hands in P. pastoris. Furthermore we provide Cas9/gRNA expression plasmids with a Geneticin resistance marker which proved to be versatile tools for marker recycling. The reported CRSIPR‐Cas9 tools can be applied for modifying existing production strains and also pave the way for markerless whole genome modification studies in P. pastoris.
Retracted: MicroRNA‐29b‐3p prevents Schistosoma japonicum‐induced liver fibrosis by targeting COL1A1 and COL3A1
Authors: Tao Ran , Fan Xiang‐Xue , Yu Hai‐Jing , Ai Guo , Zhang Hong‐Yue , Kong Hong‐Yan , Song Qi‐Qin , Huang Yu , Huang Jia‐Quan , Ning Qin 
Published: November 2017

AbstractSchistosomiasis is one of the world's major public health problems in terms of morbidity and mortality, causing granulomatous inflammation and cumulative fibrosis. This study explored in vivo and vitro effects of miR‐29b‐3p in granulomatous liver fibrosis by targeting COL1A1 and COL3A1 in Schistosoma japonicum infection. Thirty male Balb/c mice were assigned to normal control and model (percutaneous infection of cercariae of S. japonicum) groups. NIH‐3T3 mouse embryonic fibroblasts were designated into blank, NC, miR‐29b‐3p mimic, TGF‐β1, TGF‐β1 + NC, and TGF‐β1 + miR‐29b‐3p mimic groups. HE and Masson staining were employed to observe the pathological changes and collagenous fibrosis. The expression of α‐SMA, COL1A1, COL3A1, TIMP‐1 was determined by immunohistochemistry. The RT‐qPCR, Western blotting and immunofluorescence staining were conducted to determine expression of miR‐29b‐3p, COL1A1, and COL3A1. CCK‐8 assay and flow cytometry were performed to evaluate viability and apoptosis. The relative expression of miR‐29b‐3p decreased in the model group. The model group showed marked fibrosis in liver tissues. The expression of α‐SMA, COL1A1, COL3A1, TIMP‐1 was higher in the model group than that in the normal control group. Dual luciferase reporter gene assay revealed that miR‐29b‐3p directly targeted COL1A1 and COL3A1. Compared with the blank, NC, TGF‐β1 and TGF‐β1 + NC groups, the miR‐29b‐3p mimic group exhibited up‐regulated expression of miR‐29b‐3p and MMP‐9 but down‐regulated expression of TIMP‐1, HSP47, α‐SMA, COL1A1, and COL3A1; while lower cell viability but higher apoptosis rate showed. It indicated that miR‐29b‐3p prevents S. japonicum‐induced liver fibrosis by inhibiting COL1A1 and COL3A1.
The mechanism and potential targets of class II HDACs in angiogenesis
Authors: Hou Fei , Li Dandan , Yu Honglian , Kong Qingsheng 
Published: November 2017

AbstractAngiogenesis refers to the new blood vessels deriving from the existing blood vessels, and it is a complex regulatory process. Angiogenesis is associated with the normal development of the body and tumor growth and migration. The imbalance of histone deacetylase, as an epigenetic modification, could induce the production of diseases, such as cancer, metabolic diseases, etc., and it also plays an important role in angiogenesis. Many researches indicate that class II HDACs nuclear shuttle and its phosphorylation are necessary for the diseases and the protection of the collective itself. This paper will make a review for the relationship between II HDACs and angiogenesis under physiological and pathologic categories, looking forward to the disease treatment in the future.
Retracted: In vivo and in vitro effects of PTH1‐34 on osteogenic and adipogenic differentiation of human bone marrow‐derived mesenchymal stem cells through regulating microRNA‐155
Authors: Han Huan‐Sheng , Ju Fang , Geng Shuo 
Published: November 2017

AbstractThis study aimed to investigate the effect of parathyroid hormone (PTH1‐34) on osteogenic and adipogenic differentiation of hBMSCs by the regulation of miR‐155. A total of 36 adult volunteers were selected in this study. Effects of PTH1‐34 on the proliferation of hBMSCs and miR‐155 expression were investigated using a MTT assay. The hBMSCs were divided into blank, PTH1‐34, miR‐155 mimic, miR‐155 mimic negative control (NC), miR‐155 inhibitor, miR‐155 inhibitor NC, PTH1‐34 + miR‐155 mimic, PTH1‐34 + miR‐155 inhibitor, and NPS R‐568 groups. Postmenopausal osteoporosis (PMOP) mouse models were established by ovariectomy (OVX) and divided into ten groups. The RT‐qPCR and Western blotting assay were carried out to detect the expression of osteogenesis/adipogenic‐related genes and miR‐155, and osteogenesis/adipogenic‐related proteins. PTH1‐34 could promote hBMSCs proliferation and inhibit miR‐155 expression in a dose‐dependent manner. Compared with the blank control group, expressions of Runx2, and BSP was up‐regulated in the PTH1‐34 and miR‐155 inhibitor groups, while expressions of miR‐155, PPAR‐γ, lipoprotein lipase (LPL), fatty acid binding protein 4 (Fabp4), adiponectin, and CCAAT/enhancer binding protein α (C/EBPα) were down‐regulated. In the in vivo experiment, compared with the OVX group, the BMD and expressions of Runx2 and BSP was up‐regulated in the PTH1‐34, miR‐155 inhibitor, and PTH1‐34 + miR‐155 inhibitor groups, while expressions of PPAR‐γ, LPL, Fabp4, adiponectin, and C/EBPα were down‐regulated. The miR‐155 mimic and NPS R‐568 groups followed opposite trends. PTH1‐34 could promote the osteogenic differentiation and inhibits adipogenic differentiation of hBMSCs through down‐regulating miR‐155 in PMOP mice.
LncRNA CASC2 inhibited the viability and induced the apoptosis of hepatocellular carcinoma cells through regulating miR‐24‐3p
Authors: Fan Ji‐Chang , Zeng Fei , Le Yi‐Guan , Xin Lin 
Published: November 2017

AbstractCancer susceptibility candidate 2 (CASC2), a recently discovered long non‐coding RNA (lncRNA), was confirmed to play numerous roles in several human cancers. However, the involvement and concrete mechanism of CASC2 in hepatocellular carcinoma (HCC) still need to be further elucidated. The relative expressions of CASC2 and miR‐24‐3p in HCC tissue and cell lines were determined by quantitative real‐time PCR (qRT‐PCR). The effects of CASC2 and miR‐24‐3p on HCC cells were further assessed via cell viability and apoptosis. In vivo tumorigenesis assay was performed to verify the inhibition effect of CASC2 on the tumor growth and further clarify the important role of miR‐24‐3p in this mechanism. Compared with the paired normal tissues, the relative expression of CASC2 significantly reduced in the HCC tissues, while miR‐24‐3p as determined by qRT‐PCR obviously increased in the HCC tissues. This observation was also found in HCC cell lines. Meanwhile, the expression of CASC2 was negatively related to miR‐24‐3p expression in the HCC tissues (r = −0.804, P < 0.001). CASC2 could negatively regulate the expression of miR‐24‐3p in vitro. Moreover, CASC2 overexpression resulted in the growth inhibitory and apoptosis‐inducing effects on HCC cells, but the up‐regulation of miR‐24‐3p greatly eliminated the CASC2‐induced effects. The tumorigenesis of HCC cells was restrained significantly by CASC2 overexpression as shown by decreased tumor volume and growth rate. However, miR‐24‐3p up‐regulation rescued the inhibition of CASC2 on the tumor growth in tumor‐bearing mice. LncRNA CASC2 inhibited the viability and induced the apoptosis of HCC cells through regulating miR‐24‐3p.
Design of inhibitory peptide targeting Toxoplasma gondii RON4‐human β‐tubulin interactions by implementing structural bioinformatics methods
Authors: Vetrivel Umashankar , Nagarajan Hemavathy , Thirumudi Indhuja 
Published: November 2017

AbstractToxoplasma gondii an obligate intracellular parasite causes toxoplasmosis in homeothermic animals. Host invasion of this parasite is mediated by the formation of Moving Junction (MJ) complex which encompasses a network of microneme and Rhoptry Neck proteins (RONs) 2/4/5/8. Among these proteins, RON4 is the only cytosolic secretory protein that is considered as a crucial member, as it directly facilitates the motility of MJ complex by interacting with host tubulin. It is also prominently localized at the host‐pathogen interface during the invasion, thus projecting it as a potential drug target. The structure of RON4 is yet to be crystallized. Hence, in this study, fold recognition and Free Energy Landscape sampling was performed to predict the plausible 3D structure of RON4. Further, its interacting pattern with the reported crystal structure of human tubulin was analyzed using molecular docking. Subsequently, a β‐tubulin based inhibitory peptides were derived based on its interacting interface observed in RON4‐β‐tubulin docked complex. Following which, a stepwise validation of these peptides for various physico‐chemical properties and its homology with antimicrobial peptides were also screened. The peptide (RT_pep) surpassing all these validation filters was modeled and its stability was analysed by Molecular Dynamics simulation. To validate further, the stable conformation of the RT_pep was docked to RON4. Finally, essential molecular dynamics simulation was conducted to determine the stability and atomic motions of native RON4 and also to decipher its association with β‐tubulin and RT_pep. All these analyses cumulatively suggest the therapeutic potential of RT_pep in targeting toxoplasmosis.
HIF‐2α activated lncRNA NEAT1 promotes hepatocellular carcinoma cell invasion and metastasis by affecting the epithelial‐mesenchymal transition
Authors: Zheng Xiaowei , Zhang Yiwen , Liu Yujia , Fang Luo , Li Li , Sun Jiao , Pan Zongfu , Xin Wenxiu , Huang Ping 
Published: November 2017

AbstractThe aim of this study was to investigate the role of NEAT1 in hepatocellular carcinoma (HCC), and probe whether NEAT1 participate in the epithelial‐mesenchymal transition (EMT) and metastasis regulated by HIF‐2α. Expression of lncRNA NEAT1 was initially assessed in HCC tissues and in a series of HCC cell lines. The correlations between NEAT1 levels and HIF‐2α were analyzed through plasmid vector construction. The potential underlying mechanisms of NEAT1 in HCC were performed through in vitro and in vivo functional assays. Expression of NEAT1, HIF‐2α were significantly increased in HCC tissues and cell lines. Then, in vitro assays revealed that NEAT1 promotes EMT and metastasis by stimulating the inactivation of HIF‐2α in HCC. An in vivo animal model also demonstrated the cancer promotion mechanism of NEAT1. In this study, we found that the NEAT1 was high expression in HCC. NEAT1 promotes tumor cell EMT, migration and invasion capacities by stimulating the activation of HIF‐2α in HCC.
Epiregulin (EREG) is upregulated through an IL‐1β autocrine loop in Caco‐2 epithelial cells with reduced CFTR function
Authors: Massip‐Copiz Macarena , Clauzure Mariángeles , Valdivieso Ángel G. , Santa‐Coloma Tomás A. 
Published: November 2017

AbstractCFTR is a cAMP‐regulated chloride channel, whose mutations produce cystic fibrosis. The impairment of CFTR activity increases the intracellular Cl− concentration, which in turn produces an increased interleukin‐1β (IL‐1β) secretion. The secreted IL‐1β then induces an autocrine positive feedback loop, further stimulating IL‐1β priming and secretion. Since IL‐1β can transactivate the epidermal growth factor receptor (EGFR), we study here the levels of expression for different EGFR ligands in Caco‐2/pRS26 cells (expressing shRNA against CFTR resulting in a reduced CFTR expression and activity). The epiregulin (EREG), amphiregulin (AREG), and heparin binding EGF like growth factor (HBEGF) mRNAs, were found overexpressed in Caco‐2/pRS26 cells. The EREG mRNA had the highest differential expression and was further characterized. In agreement with its mRNA levels, Western blots (WB) showed increased EREG levels in CFTR‐impaired cells. In addition, EREG mRNA and protein levels were stimulated by incubation with exogenous IL‐1β and inhibited by the Interleukin 1 receptor type I (IL1R1) antagonist IL1RN, suggesting that the overexpression of EREG is a consequence of the autocrine IL‐1β loop previously described for these cells. In addition, the JNK inhibitor SP600125, and the EGFR inhibitors AG1478 and PD168393, also had an inhibitory effect on EREG expression, suggesting that EGFR, activated in Caco‐2/pRS26 cells, is involved in the observed EREG upregulation. In conclusion, in Caco‐2 CFTR‐shRNA cells, the EGFR ligand EREG is overexpressed due to an active IL‐1β autocrine loop that indirectly activates EGFR, constituting new signaling effectors for the CFTR signaling pathway, downstream of CFTR, Cl−, and IL‐1β.
Complete graph immersions and minimum degree
Authors: Dvořák Zdeněk , Yepremyan Liana 
Published: November 2017

AbstractAn immersion of a graph H in another graph G is a one‐to‐one mapping and a collection of edge‐disjoint paths in G, one for each edge of H, such that the path corresponding to the edge has endpoints and . The immersion is strong if the paths are internally disjoint from . We prove that every simple graph of minimum degree at least contains a strong immersion of the complete graph . This improves on previously known bound of minimum degree at least 200t obtained by DeVos et al. Our result supports a conjecture of Lescure and Meyniel (also independently proposed by Abu‐Khzam and Langston), which is the analogue of famous Hadwiger’s conjecture for immersions and says that every graph without a ‐immersion is ‐colorable.