bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Reduction Properties of M–Doped (M=Zr, Gd) CeO2/YSZ Scaffolds Co–Infiltrated with Nickel
Authors: Maher R. C. , Kerherve G. , Payne D. J. , Yue X. , Connor P. A. , Irvine J. , Cohen L. F. 
Published: September 2018

AbstractIn recent years infiltration of materials into porous ceramic scaffolds has been shown to be an effective way of creating catalytically active components for solid oxide fuel cells (SOFCs). However, the redox properties of these novel structures are not well understood. Here, we use X‐ray photoelectron spectroscopy (XPS) and in‐situ Raman spectroscopy to investigate the oxidation properties of yttria‐stabilised zirconia (YSZ) scaffolds infiltrated with ceria (CeO2), gadolinium‐doped ceria (GDC) and zirconia‐doped ceria (ZDC), with and without Ni. XPS shows that doping ceria with zirconia increases the ratio of Ce3+ to Ce4+, while gadolinium doping results in a decrease of Ce3+. The presence of Ni increases the Ce3+/Ce4+ ratio for CeO2 and GDC, but had little effect on ZDC. We used the shift of the F2g Raman peak to monitor in‐situ, the oxidation state of ceria. In the as‐made compounds, we show that while the gadolinium and zirconium dopants significantly change the oxidation characteristics of ceria, the resulting materials are only significantly reduced above 500 °C when co‐infiltrated with Ni. In‐situ Raman monitoring during reduction as a function of temperature showed that while ZDC reduces much more readily than undoped ceria or GDC, the presence of Ni dominated the reduction dynamics.
The Impact of Aberrant Responses and Detection in Forced‐Choice Noncognitive Assessment
Authors: Kim Sooyeon , Moses Tim 
Published: September 2018

AbstractThe purpose of this study is to assess the impact of aberrant responses on the estimation accuracy in forced‐choice format assessments. To that end, a wide range of aberrant response behaviors (e.g., fake, random, or mechanical responses) affecting upward of 20%–30% of the responses was manipulated under the multi‐unidimensional pairwise preference (MUPP) model with forced‐choice format. Under each aberrance condition, we also computed the lz statistic (a common person‐fit index) to determine how well this index can accurately detect aberrant responses without erroneously misidentifying honest examinees. Some aberrant behaviors (e.g., limited responses) were more problematic than others (e.g., omitting) in terms of true trait level recovery. The lz statistic associated with each dimension of the MUPP form led to higher detection rates than did the overall lz statistic. When the dimensional lz approach was used, however, many honest examinees were misclassified as outliers. The detection rates of lz differed as a function of aberrant response types.
Crosscutting Literature on STEAM Ecosystems, Expectancy Value Theory, and Social Emotional Learning: A Metadata Synthesis
Authors: Rikoon Samuel , Finn Bridgid , Jackson Teresa , Inglese Patricia 
Published: September 2018

AbstractIn this report, we describe the initial stages of a crosscutting research effort to characterize literature reviewed across 8 different projects—each with objectives aligned toward improving student engagement in science, technology, engineering, arts, and mathematics (STEAM) fields. These projects sought to identify malleable factors (e.g., motivation, persistence) that could potentially be fostered to improve achievement motivation and build participation among historically underrepresented learners in STEAM pathways. Focusing on both the extent to which different broad and facet‐level constructs are both discussed and assessed in a diverse pool of literature, we developed a standardized reporting structure and catalogued detailed information on 236 unique references. We found that, as a proportion of the number of times constructs in the STEAM, expectancy value (EV) theory, and social emotional learning (SEL) spaces were discussed in the reviewed literature, they were assessed relatively infrequently. We also found high levels of overlap in the literature across the above 3 focal areas, highlighting both the need to document new assessments designed to support STEAM engagement and an opportunity to use them to evaluate expectancy value theory as a holistic model.
Disrupted interactions among the hippocampal, dorsal attention, and central‐executive networks in amnestic mild cognitive impairment
Authors: Chand Ganesh B. , Hajjar Ihab , Qiu Deqiang 
Published: September 2018

AbstractNeuroimaging investigations consistently demonstrate that the neural processes involve complex interactions between the large‐scale networks. Among those networks, the dorsal attention network (DAN) and the central‐executive network (CEN) have been previously shown to exhibit anti‐correlated activity with the default‐mode network (DMN) in cognitively normal people. In amnestic mild cognitive impairment (MCI) and Alzheimer's disease, the hippocampal network (HCN)—a key memory processing system—and its interactions with other networks have gathered central interest. The current study aims to evaluate the patterns of functional architectures of the HCN with the three networks—DAN, CEN, and DMN—in amnestic MCI and normal controls (NC) to test the hypothesis that the interactions of HCN with other networks alter in MCI. We recorded the resting state functional MRI, assessed patterns of functional architectures between the four networks using dynamical causal modeling, and compared between NC and MCI. Our analysis showed that the DAN modulates the activity between the HCN and the DMN in both MCI and NC. We further uncovered that the DAN modulates the activity between the HCN and the CEN in NC, but such modulation is impaired in MCI. We found an association between impaired modulation and Montreal cognitive assessment (R = 0.349). Overall, our findings provide important insight in understanding the neuroimaging signature of amnestic MCI and/or Alzheimer's disease.
Aberrant structural–functional coupling in adult cannabis users
Authors: Kim Dae‐Jin , Schnakenberg Martin Ashley M. , Shin Yong‐Wook , Jo Hang Joon , Cheng Hu , Newman Sharlene D. , Sporns Olaf , Hetrick William P. , Calkins Eli , O'Donnell Brian F. 
Published: September 2018

AbstractCellular studies indicate that endocannabinoid type‐1 retrograde signaling plays a major role in synaptic plasticity. Disruption of these processes by delta‐9‐tetrahydrocannabinol (THC) could produce alterations either in structural and functional brain connectivity or in their association in cannabis (CB) users. Graph theoretic structural and functional networks were generated with diffusion tensor imaging and resting‐state functional imaging in 37 current CB users and 31 healthy non‐users. The primary outcome measures were coupling between structural and functional connectivity, global network characteristics, association between the coupling and network properties, and measures of rich‐club organization. Structural–functional (SC–FC) coupling was globally preserved showing a positive association in current CB users. However, the users had disrupted associations between SC–FC coupling and network topological characteristics, most perturbed for shorter connections implying region‐specific disruption by CB use. Rich‐club analysis revealed impaired SC–FC coupling in the hippocampus and caudate of users. This study provides evidence of the abnormal SC–FC association in CB users. The effect was predominant in shorter connections of the brain network, suggesting that the impact of CB use or predispositional factors may be most apparent in local interconnections. Notably, the hippocampus and caudate specifically showed aberrant structural and functional coupling. These structures have high CB1 receptor density and may also be associated with changes in learning and habit formation that occur with chronic cannabis use.
Extracellular protease trypsin activates amiloride‐insensitive sodium channels in human leukemia cells
Authors: Sudarikova Anastasia V. , Vasileva Valeria Y. , Vassilieva Irina O. , Negulyaev Yuri A. , Morachevskaya Elena A. , Chubinskiy‐Nadezhdin Vladislav I. 
Published: September 2018

AbstractSodium influx is tightly regulated in the cells of blood origin. Amiloride‐insensitive sodium channels were identified as one of the main sodium‐transporting pathways in leukemia cells. To date, all known regulatory pathways of these channels are coupled with intracellular actin cytoskeleton dynamics. Here, to search for physiological mechanisms controlling epithelial Na+ channel (ENaC)‐like channels, we utilized leukemia K562 cells as a unique model to examine single channel behavior in a whole‐cell patch‐clamp experiments. We have shown for the first time that extracellular serine protease trypsin directly activates sodium channels in plasma membrane of K562 cells. The whole‐cell single current recordings clearly demonstrate no inhibition of trypsin‐activated channels by amiloride or benzamil. Involvement of proteolytic cleavage in channel opening was confirmed in experiments with soybean trypsin inhibitor. More importantly, stabilization of F‐actin with intracellular phalloidin did not prevent trypsin‐induced channel activation indicating no implication of cytoskeleton rearrangements in stimulatory effect of extracellular protease. Our data reveals a novel mechanism modulating amiloride‐insensitive ENaC‐like channel activity and integral sodium permeability in leukemia cells.
Perlecan/HSPG2: Signaling role of domain IV in chondrocyte clustering with implications for Schwartz‐Jampel Syndrome
Authors: Martinez Jerahme R. , Grindel Brian J. , Hubka Kelsea M. , Dodge George R. , Farach‐Carson Mary C. 
Published: September 2018

AbstractPerlecan/heparan sulfate proteoglycan 2 (HSPG2), a large HSPG, is indispensable for the development of musculoskeletal tissues, where it is deposited within the pericellular matrix (PCM) surrounding chondrocytes and disappears nearly completely at the chondro‐osseous junction (COJ) of developing long bones. Destruction of perlecan at the COJ converts an avascular cartilage compartment into one that permits blood vessel infiltration and osteogenesis. Mutations in perlecan are associated with chondrodysplasia with widespread musculoskeletal and joint defects. This study elucidated novel signaling roles of perlecan core protein in endochondral bone formation and chondrocyte behavior. Perlecan subdomains were tested for chondrogenic properties in ATDC5 cells, a model for early chondrogenesis. A region within domain IV of perlecan (HSPG2 IV‐3) was found to promote rapid prechondrocyte clustering. Introduction of the mutation (R3452Q) associated with the human skeletal disorder Schwartz‐Jampel syndrome limited HSPG2 IV‐3‐induced clustering. HSPG2 IV‐3 activity was enhanced when thermally unfolded, likely because of increased exposure of the active motif(s). HSPG2 IV‐3‐induced clustering was accompanied by the deactivation of key components of the focal adhesion complex, FAK and Src, with increased messenger RNA (mRNA) levels of precartilage condensation markers Sox9 and N‐cadherin (
Cdh2), and cartilage PCM components collagen II (
Col2a1) and aggrecan (
Acan). HSPG2 IV‐3 reduced signaling through the ERK pathway, where loss of ERK1/2 phosphorylation coincided with reduced FoxM1 protein levels and increased mRNA levels cyclin‐dependent kinase inhibitor 1C (Cdkn1c) and activating transcription factor 3 (
Atf3), reducing cell proliferation. These findings point to a critical role for perlecan domain IV in cartilage development through triggering chondrocyte condensation.
Catalpol inhibits TGF‐β1‐induced epithelial‐mesenchymal transition in human non–small‐cell lung cancer cells through the inactivation of Smad2/3 and NF‐κB signaling pathways
Authors: Wang Zuopei , Lu Yi , Sheng Bo , Ding Yi , Cheng Xiaoke 
Published: September 2018

AbstractCatalpol, one of the main active ingredients isolated from Rehmannia glutinosa, was reported to possess anticancer activity. However, the role of catalpol in transforming growth factor β1 (TGF‐β1)‐induced epithelial‐mesenchymal transition (EMT) in human non–small‐cell lung cancer (NSCLC) cells has not been elucidated. The objective of this study was to investigate the effect of catalpol on EMT in human NSCLC cells. Our results showed that catalpol significantly inhibited the TGF‐β1‐induced cell migration and invasion of A549 cells, as well as repressed matrix metalloproteinase (MMP)2 and MMP9 expression induced by TGF‐β1 in A549 cells. In addition, catalpol markedly repressed the EMT process in A549 cells in response to TGF‐β1. Furthermore, catalpol prevented the activation of Smad2/3 and nuclear factor κB (NF‐κB) signaling pathways induced by TGF‐β1 in A549 cells. In conclusion, these findings indicated that catalpol inhibits TGF‐β1‐induced EMT in human NSCLC cells through the inactivation of Smad2/3 and NF‐κB signaling pathways. Thus, catalpol may be a promising agent for the treatment of NSCLC.
NEAT1 contributes to ox‐LDL‐induced inflammation and oxidative stress in macrophages through inhibiting miR‐128
Authors: Chen Dou‐Dou , Hui Liang‐Liang , Zhang Xiang‐Cheng , Chang Qing 
Published: September 2018

AbstractLong noncoding RNAs (lncRNA) have been recognized as significant regulators in the progression of atherosclerosis (AS). Oxidized low‐density lipoprotein (ox‐LDL) can induce macrophage inflammation and oxidative stress, that serves important roles in AS. However, the exact function of lncRNA NEAT1 and its possible molecular mechanism in AS remain unclear. Here, we concentrated on the roles and molecular mechanisms of NEAT1 in AS development. In our current study, we observed that NEAT1 was elevated by ox‐LDL in a dose‐dependent and time‐dependent manner. RAW264.7 cell survival was greatly enhanced, and cell apoptosis was significantly inhibited by LV‐shNEAT1 transfection. In addition, knockdown of NEAT1 in RAW264.7 cells repressed CD36 expression and foam cell formation while NEAT1 overexpression shown an opposite process. Moreover, NEAT1 downregulation inhibited inflammation molecules including IL‐6, IL‐1β, and TNF‐α. Meanwhile, silencing of NEAT1 can also suppress reactive oxygen species (ROS) and malondialdehyde (MDA) levels with an enhancement of superoxide dismutase (SOD) activity in RAW264.7 cells. MicroRNAs are some short RNAs, and they can regulate multiple biological functions in many diseases including AS. Here, we found that miR‐128 expression was remarkably decreased in ox‐LDL‐incubated RAW264.7 cells. Interestingly, miR‐128 mimics was able to reverse AS‐correlated events induced by overexpression of NEAT1. By using bioinformatics analysis, miR‐128 was predicted as a target of NEAT1 and the correlation between them was validated in our study. Taken these together, it was implied that NEAT1 participated in ox‐LDL‐induced inflammation and oxidative stress in AS development through sponging miR‐128.
Polycistronic expression of the mitochondrial steroidogenic P450scc system in the HEK293T cell line
Authors: Efimova Vera S. , Isaeva Ludmila V. , Labudina Anastasia A. , Tashlitsky Vadim N. , Rubtsov Mikhail A. , Novikova Ludmila A. 
Published: September 2018

AbstractThe cholesterol hydroxylase/lyase (CHL) system, consisting of cytochrome P450scc, adrenodoxin (Adx) and adrenodoxin reductase (AdR), initiates mammalian steroidogenesis, converting cholesterol to pregnenolone. The foot‐and‐mouth disease virus 2A‐based method allows to express multiple proteins from a single transcript. We developed a 2A‐based multicistronic system for the coexpression of three bovine CHL system proteins as the self‐processing polyprotein pCoxIV‐P450scc‐2A‐Adx‐2A‐AdR‐GFP (pCoxIV‐CHL‐GFP), with a cleavable N‐terminal mitochondrial targeting presequence. HEK293T cells transfected with plasmid, containing complementary DNA (cDNA) for pCoxIV‐CHL‐GFP, efficiently performed the expression of P450scc‐2A, targeted to mitochondria, and Adx‐2A, AdR‐GFP and the fusion protein Adx‐2A‐AdR‐GFP, which were predominantly localized in the cytosol. Despite the spatial separation of expressed P450scc and redox partners, the transfected HEK293T cells were able to convert the steroid substrates of cytochrome P450scc to pregnenolone, whereas control HEK293T cells were not catalytically active. The presence of 2А peptide residue on the C‐terminus of P450scc did not preclude its enzymatic activity. HEK293T cells transfected with a vector directing the synthesis of only P450scc‐2A demonstrated cytochrome P450scc activity comparable to that of cells expressing all three CHL system components, and to that of nature steroidogenic cells. Thus, the P450scc activity detected in cells transfected with both constructed plasmids was the result of the effective functional coupling of the bovine cytochrome P450scc and endogenous mitochondrial electron transport proteins of HEK293T cells. The produced pregnenolone did not undergo further conversion to progesterone, which indicates the absence of catalytically active 3β‐hydroxysteroid dehydrogenase. Therefore, HEK293T cells may be suitable for the expression of steroidogenic enzymes and the study of their characteristics.
PlGF knockdown induced apoptosis through Wnt signaling pathway in gastric cancer stem cells
Authors: Akrami Hassan , Mehdizadeh Kiumars , Moradi Behrouz , Borzabadi Farahani Diba , Mansouri Kamran , Ghalib Ibraheem Alnajar Sajjad 
Published: September 2018

AbstractDespite the fact that much research has focused on gastric cancer, it is still a worldwide concern, because of the difficulties with factors such as signaling pathway crosstalk and gastric cancer stem cell (GCSC). Placental growth factor (PlGF) is one of these factors, and its tumorigenicity potential still remains a question. As a result, we have investigated the effect of PlGF knockdown on apoptosis and genes involved in the Wnt signaling pathway, and apoptosis in cancer stem cells derived from AGS an MKN‐45 gastric cancer cell lines. We isolated GCSCs from MKN‐45 and AGS cell lines on a nonadherent surface. Then the cell viability, the real‐time reverse transcription‐polymerase chain reaction data of the genes involved in the Wnt signaling pathway, and apoptosis were evaluated. Furthermore, DNA laddering was used to show the apoptotic effect and DNA fragmentation caused by the PlGF knockdown. Our investigation revealed that the PlGF knockdown with PlGF‐specific small interfering RNA at 40 pmol for GCSCs derived from MKN‐45 and AGS at 24 hours can significantly affect the cell viability, the Wnt signaling pathway, and the apoptosis‐related genes expression. In conclusion, we showed the PlGF knockdown may induce apoptosis via the Wnt signaling pathway in GCSCs.
Disruption of the redox balance with either oxidative or anti‐oxidative overloading as a promising target for cancer therapy
Authors: Farhood Bagher , Najafi Masoud , Salehi Eniseh , Hashemi Goradel Nasser , Nashtaei Maryam Shabani , Khanlarkhani Neda , Mortezaee Keywan 
Published: September 2018

AbstractOxidative stress acts as a double‐edged sword by being both a promoter and a suppressor of cancer. Moderate oxidative stress is beneficial for cancer cell proliferative and invasiveness features, while overexposure of the cells to oxidative insults could induce cancer cell apoptosis and reduce hypoxia along with modulating the immune system for regression of tumor. Cancer cells and cancer stem cells have highly efficient redox systems that make them resistant to oxidative insults. The redox disruptive approach is an area of current research and key for oxidative targeted cancer therapies. This disruption is applicable by using either oxidative or anti‐oxidative overloading strategies, specifically on cancer cells without influencing normal cells or tissues around tumor. The activity of tumor suppressor cells within tumor microenvironment is needed to be maintained in patients receiving such approaches.
Particulate matter 2.5 induced bronchial epithelial cell injury via activation of 5′‐adenosine monophosphate‐activated protein kinase‐mediated autophagy
Authors: Long Fei , Jiang Hong , Yi Hongli , Su Lili , Sun Jian 
Published: September 2018

AbstractThe impact of particulate matter 2.5 (PM2.5) on the respiratory system is a worldwide concern. However, the mechanisms by which PM2.5 causes disease are still unclear. In this study, we investigated the effect of PM2.5 on autophagy and studied the effect of PM2.5‐induced autophagy and 5′‐adenosine monophosphate‐activated protein kinase (AMPK) on cell proliferation, cell cycle, apoptosis, reactive oxygen species (ROS), and airway inflammation using human bronchial epithelial cells 16HBE140 cells. Results showed that exposure of cells to PM2.5 at a concentration of 100 μg/mL for 24 hours was most effective for inhibiting cell viability. PM2.5 induced cell arrest in the G0/G1 phase and increased mitochondrial membrane potential, ROS, and cell apoptosis with increasing concentration. PM2.5 downregulated cyclin D and matrix metallopeptidase‐9 (MMP‐9) expression but upregulated tissue inhibitor of metalloproteinases‐1 (TIMP‐1) expression, significantly promoted interleukin‐6 (IL‐6), and tumor necrosis factor‐α (TNF‐α) production, and enhanced the level and activation of AMPK. The levels of autophagy‐related protein 5 (ATG5), Beclin‐1, and LC3II/I were significantly increased by PM2.5. The activation of Unc‐51‐like autophagy activating kinase 1 was significantly inhibited by PM2.5. Moreover, ATG5 knockdown inhibited PM2.5‐induced autophagy, ROS, and cell apoptosis significantly. The expression of cyclin D, MMP‐9, and TIMP‐1 was reversed by ATG5 suppression. PM2.5‐induction of IL‐6 and TNF‐α was significantly inhibited by knockdown of ATG5. Thus, inhibition of autophagy protected the cells from PM2.5‐induced injury. PM2.5 induced injury in human bronchial epithelial cells via activation of AMPK‐mediated autophagy, suggesting possible therapeutic targets for the treatment of respiratory diseases.
Characterization of the vaginal microbiome during cytolytic vaginosis using high‐throughput sequencing
Authors: Xu Haihong , Zhang Xueying , Yao Wenwu , Sun Yi , Zhang Yanjun 
Published: September 2018

AbstractBackgroundCytolytic vaginosis (CV) is a common disease that results in pruritus, dyspareunia, and vulvar dysuria. However, the pathological mechanisms of the disease are still unclear. Compared to traditional methods, high‐throughput sequencing can obtain more accurate qualitative and quantitative information on the microbiome.MethodsWe collected 75 samples from 32 healthy women (average age 44 ± 8) and 43 patients with CV (average age 38 ± 8). We used high‐throughput sequencing of the 16S rRNA V3‐V4 region to characterize and compare the vaginal microbiota of patients with CV and healthy women and to identify potential biomarkers for CV.ResultsThe vaginal pH of patients with CV was ≤3.8, and the vaginal concentration of H2O2 was ≥2 μmol/L. Colony densities of Lactobacillus spp. in patients with CV ranged from +++ (5‐30) to ++++ (>30) and were significantly higher than those in healthy women. High‐throughput sequencing showed that Lactobacillus was the most prominent genus both in patients with CV and in healthy women, with abundances of 83.8% and 97.2%, respectively (P < 0.001). Lactobacillus crispatus was more abundant in patients with CV, whereas Lactobacillus sp. L‐YJ was more abundant in healthy women, with area under the curve (AUC) values of 0.9375 and 0.8379, respectively.ConclusionThe abundance of Lactobacillus spp. in CV patients was significantly different from that of healthy patients. Two suitable biomarkers, L. crispatus and Lactobacillus sp. L‐YJ, were identified. These results will be useful for the identification of women at risk of serious illness before they develop obvious symptoms.