bluuebunny/crossref_metadata_2025_split huggingface dataset:
What are they talking about? Pupil talk while translating Latin stories: a case study of a Year 7 class, using the Cambridge Latin Course
Authors: Wright Rebecca 
Published: May 2017

The objective of this case study is to consider the role of pupil talk in the translation of Latin. I consider that ‘talk’ within the Latin classroom is an important pedagogical tool to support the development of pupil knowledge and understanding and to promote independent learning. Firstly, I am particularly interested in pupils’ early acquisition of the Latin language through ‘talk’. In this study, I wanted to explore how they use talk to support each other and the issues they encounter, the use of available and additional support resources and the extent of grammatical terminology within their talk. With the latter, I was curious to investigate how much terminology infiltrated pupils’ speech, or indeed if it was absent, and the subsequent effect both of these might have. The oral translation of Latin is an accepted and traditional part of learning for pupils. Throughout my PGCE teacher training course, I have observed that the majority of pupils frequently and independently consult or choose to work with another pupil when translating. I considered it was both a valid and valuable learning strategy to explore and analyse in some depth. Such research would provide a constructive insight into this accepted but sometimes overlooked learning tool, and therefore could realistically inform and improve my future teaching practice. Lastly, research into pupil talk has its own intrinsic worth, as transcripts provide both thought-provoking and informative evidence of their own. Thus, I was keen, within my placement school, to discover and consider how the pupils responded and talked about the language together in pairs.
Drosophila caspase activity is required independently of apoptosis to produce active TNF/Eiger during nociceptive sensitization
Authors: Jo Juyeon , Im Seol Hee , Babcock Daniel T , Iyer Srividya C , Gunawan Felona , Cox Daniel N , Galko Michael J 
Published: May 2017

AbstractTumor necrosis factor (TNF) signaling is required for inflammatory nociceptive (pain) sensitization in Drosophila and vertebrates. Nociceptive sensitization in Drosophila larvae following UV-induced tissue damage is accompanied by epidermal apoptosis and requires epidermal-derived TNF/Eiger and the initiator caspase, Dronc. Major gaps remain regarding TNF function in sensitization, including the relationship between apoptosis/tissue damage and TNF production, the downstream signaling in this context, and the target genes that modulate nociceptive behaviors. Here, apoptotic cell death and thermal nociceptive sensitization are genetically and procedurally separable in a Drosophila model of UV-induced nociceptive sensitization. Activation of epidermal Dronc induces TNF-dependent but effector caspase-independent nociceptive sensitization in the absence of UV. In addition, knockdown of Dronc attenuated nociceptive sensitization induced by full-length TNF/Eiger but not by a constitutively soluble form. UV irradiation induced TNF production in both in vitro and in vivo, but TNF secretion into hemolymph was not sufficient to induce thermal nociceptive sensitization. Downstream mediators of TNF-induced sensitization included two TNF receptor-associated factors, a p38 kinase, and the transcription factor nuclear factor kappa B. Finally, sensory neuron-specific microarray analysis revealed downstream TNF target genes induced during thermal nociceptive sensitization. One of these, enhancer of zeste (E(z)), functions downstream of TNF during thermal nociceptive sensitization. Our findings suggest that an initiator caspase is involved in TNF processing/secretion during nociceptive sensitization, and that TNF activation leads to a specific downstream signaling cascade and gene transcription required for sensitization. These findings have implications for both the evolution of inflammatory caspase function following tissue damage signals and the action of TNF during sensitization in vertebrates.
Cryptotanshinone inhibits human glioma cell proliferation in vitro and in vivo through SHP-2-dependent inhibition of STAT3 activation
Authors: Lu Liang , Zhang Sulin , Li Cuixian , Zhou Chun , Li Dong , Liu Peiqing , Huang Min , Shen Xiaoyan 
Published: May 2017

AbstractMalignant gliomas (MGs) are one of the most common primary brain cancers in adults with a high mortality rate and relapse rate. Thus, finding better effective approaches to treat MGs has become very urgent. Here, we studied the effects of cryptotanshinone (CTS) on MGs in vitro and in vivo, and explored the underlying mechanisms. Effects of CTS in vitro on cell proliferation, cycle, migration and invasion were evaluated. The activation of JAK/STATs signaling was detected by western blot and immunofluorescenc staining. SHP-2 inhibitor or SiRNA were used to determine the involvement of SHP-2. The in vivo anti-MGs activity of CTS was studied with nude mice bearing intracerebral U87 xenografts. Our results revealed that CTS significantly inhibited the proliferation of MGs in vitro via inhibiting STAT3 signal pathway. The cell cycle was arrested at G0/G1 phase. Although CTS did not change the expression of total SHP-2 protein, the tyrosine phosphatase activity of SHP-2 protein was increased by CTS treatment in a dose-dependent manner in vivo and in vitro. SHP-2 inhibitor or SiRNA could reverse the inhibitory effect of CTS on phosphorylation of STAT3 Tyr705. In vivo study also showed that CTS inhibited the intracranial tumor growth and extended survival of nude mice bearing intracerebral U87 xenografts, confirming an inhibitory effect of CTS on MGs. Our results indicated CTS may be a potential therapeutic agent for MGs. The inhibitory action of CTS is largely attributed to the inhibition of STAT3 Tyr705 phosphorylation with a novel mechanism of upregulating the tyrosine phosphatase activity of SHP-2 protein.
miR-218-5p restores sensitivity to gemcitabine through PRKCE/MDR1 axis in gallbladder cancer
Authors: Wang Hui , Zhan Ming , Xu Sun-Wang , Chen Wei , Long Man-Mei , Shi Yong-Heng , Liu Qiang , Mohan Man , Wang Jian 
Published: May 2017

AbstractGallbladder cancer (GBC) is one of the most common malignancy of the biliary tract characterized by its high chemoresistant tendency. Although great progresses have been made in recent decades for treating many cancers with anticancer drugs, effective therapeutics methods for anti-GBC are still lacking. Therefore, investigations into identifying the mechanisms underlying the drug resistance of GBC are greatly needed. In this study, we show that miR-218-5p plays a critical role in gemcitabine resistance of GBC. miR-218-5p levels were significantly lower in GBC than adjacent non-cancer tissues, and which were also associated with patient prognosis. While miR-218-5p overexpression abrogated gemcitabine resistance of GBC cells, silencing of which exhibited the opposite effects. Via six microRNA targets prediction algorithms, we found that PRKCE is a potential target of miR-218-5p. Moreover, miR-218-5p overexpression repressed the luciferase activity of reporter constructs containing 3′-UTR of PRKCE and also reduced PRKCE expression. Further studies revealed that miR-218-5p promotes sensitivity of gemcitabine by abolishing PRKCE-induced upregulation of MDR1/P-gp. Taken together, our results imply that an intimate correlation between miR-218-5p and PRKCE/MDR1 axis abnormal expression is a key determinant of gemcitabine tolerance, and suggest a novel miR-218-5p-based clinical intervention target for GBC patients.
BASP1 interacts with oestrogen receptor α and modifies the tamoxifen response
Authors: Marsh Lindsey A , Carrera Samantha , Shandilya Jayasha , Heesom Kate J , Davidson Andrew D , Medler Kathryn F , Roberts Stefan GE 
Published: May 2017

AbstractTamoxifen binds to oestrogen receptor α (ERα) to elicit distinct responses that vary by cell/tissue type and status, but the factors that determine these differential effects are unknown. Here we report that the transcriptional corepressor BASP1 interacts with ERα and in breast cancer cells, this interaction is enhanced by tamoxifen. We find that BASP1 acts as a major selectivity factor in the transcriptional response of breast cancer cells to tamoxifen. In all, 40% of the genes that are regulated by tamoxifen in breast cancer cells are BASP1 dependent, including several genes that are associated with tamoxifen resistance. BASP1 elicits tumour-suppressor activity in breast cancer cells and enhances the antitumourigenic effects of tamoxifen treatment. Moreover, BASP1 is expressed in breast cancer tissue and is associated with increased patient survival. Our data have identified BASP1 as an ERα cofactor that has a central role in the transcriptional and antitumourigenic effects of tamoxifen.
Autophagy is essential for hearing in mice
Authors: Fujimoto Chisato , Iwasaki Shinichi , Urata Shinji , Morishita Hideaki , Sakamaki Yuriko , Fujioka Masato , Kondo Kenji , Mizushima Noboru , Yamasoba Tatsuya 
Published: May 2017

AbstractHearing loss is the most frequent sensory disorder in humans. Auditory hair cells (HCs) are postmitotic at late-embryonic differentiation and postnatal stages, and their damage is the major cause of hearing loss. There is no measurable HC regeneration in the mammalian cochlea, and the maintenance of cell function is crucial for preservation of hearing. Here we generated mice deficient in autophagy-related 5 (Atg5), a gene essential for autophagy, in the HCs to investigate the effect of basal autophagy on hearing acuity. Deletion of Atg5 resulted in HC degeneration and profound congenital hearing loss. In autophagy-deficient HCs, polyubiquitinated proteins and p62/SQSTM1, an autophagy substrate, accumulated as inclusion bodies during the first postnatal week, and these aggregates increased in number. These findings revealed that basal autophagy has an important role in maintenance of HC morphology and hearing acuity.
Structure and interstitial iodide migration in hybrid perovskite methylammonium lead iodide
Authors: Minns J. L. , Zajdel P. , Chernyshov D. , van Beek W. , Green M. A. 
Published: May 2017

AbstractHybrid perovskites form an emerging family of exceptional light harvesting compounds. However, the mechanism underpinning their photovoltaic effect is still far from understood, which is impeded by a lack of clarity on their structures. Here we show that iodide ions in the methylammonium lead iodide migrate via interstitial sites at temperatures above 280 K. This coincides with temperature dependent static distortions resulting in pseudocubic local symmetry. Based on bond distance analysis, the migrating and distorted iodines are at lengths consistent with the formation of I2 molecules, suggesting a 2I−→I2+2e− redox couple. The actual formula of this compound is thus (CH3NH3)PbI3−2x(I2)x where x∼0.007 at room temperature. A crucial feature of the tetragonal structure is that the methylammonium ions do not sit centrally in the A-site cavity, but disordered around two off-centre orientations that facilitate the interstitial ion migration via a gate opening mechanism.
Super-diffusion of excited carriers in semiconductors
Authors: Najafi Ebrahim , Ivanov Vsevolod , Zewail Ahmed , Bernardi Marco 
Published: May 2017

AbstractThe ultrafast spatial and temporal dynamics of excited carriers are important to understanding the response of materials to laser pulses. Here we use scanning ultrafast electron microscopy to image the dynamics of electrons and holes in silicon after excitation with a short laser pulse. We find that the carriers exhibit a diffusive dynamics at times shorter than 200 ps, with a transient diffusivity up to 1,000 times higher than the room temperature value,D0≈30 cm2s−1. The diffusivity then decreases rapidly, reaching a value ofD0roughly 500 ps after the excitation pulse. We attribute the transient super-diffusive behaviour to the rapid expansion of the excited carrier gas, which equilibrates with the environment in 100−150 ps. Numerical solution of the diffusion equation, as well asab initiocalculations, support our interpretation. Our findings provide new insight into the ultrafast spatial dynamics of excited carriers in materials.
Prolonged intracellular accumulation of light-inducible nanoparticles in leukemia cells allows their remote activation
Authors: Boto Carlos , Quartin Emanuel , Cai Yijun , Martín-Lorenzo Alberto , Cenador María Begoña García , Pinto Sandra , Gupta Rajeev , Enver Tariq , Sánchez-García Isidro , Hong Dengli , Pires das Neves Ricardo , Ferreira Lino 
Published: May 2017

AbstractLeukaemia cells that are resistant to conventional therapies are thought to reside in protective niches. Here, we describe light-inducible polymeric retinoic acid (RA)-containing nanoparticles (NPs) with the capacity to accumulate in the cytoplasm of leukaemia cells for several days and release their RA payloads within a few minutes upon exposure to blue/UV light. Compared to NPs that are not activated by light exposure, these NPs more efficiently reduce the clonogenicity of bone marrow cancer cells from patients with acute myeloid leukaemia (AML) and induce the differentiation of RA-low sensitive leukaemia cells. Importantly, we show that leukaemia cells transfected with light-inducible NPs containing RA can engraft into bone marrow in vivo in the proximity of other leukaemic cells, differentiate upon exposure to blue light and release paracrine factors that modulate nearby cells. The NPs described here offer a promising strategy for controlling distant cell populations and remotely modulating leukaemic niches.
Molecular basis for blue light-dependent phosphorylation of Arabidopsis cryptochrome 2
Authors: Liu Qing , Wang Qin , Deng Weixian , Wang Xu , Piao Mingxin , Cai Dawei , Li Yaxing , Barshop William D. , Yu Xiaolan , Zhou Tingting , Liu Bin , Oka Yoshito , Wohlschlegel James , Zuo Zecheng , Lin Chentao 
Published: May 2017

AbstractPlant cryptochromes undergo blue light-dependent phosphorylation to regulate their activity and abundance, but the protein kinases that phosphorylate plant cryptochromes have remained unclear. Here we show that photoexcited Arabidopsis cryptochrome 2 (CRY2) is phosphorylated in vivo on as many as 24 different residues, including 7 major phosphoserines. We demonstrate that four closely related Photoregulatory Protein Kinases (previously referred to as MUT9-like kinases) interact with and phosphorylate photoexcited CRY2. Analyses of the ppk123 and ppk124 triple mutants and amiR4k artificial microRNA-expressing lines demonstrate that PPKs catalyse blue light-dependent CRY2 phosphorylation to both activate and destabilize the photoreceptor. Phenotypic analyses of these mutant lines indicate that PPKs may have additional substrates, including those involved in the phytochrome signal transduction pathway. These results reveal a mechanism underlying the co-action of cryptochromes and phytochromes to coordinate plant growth and development in response to different wavelengths of solar radiation in nature.
Self-Selecting Resistive Switching Scheme Using TiO2 Nanorod Arrays
Authors: Huang Chi-Hsin , Chou Ta-Shun , Huang Jian-Shiou , Lin Shih-Ming , Chueh Yu-Lun 
Published: May 2017

AbstractIn this study, the resistive switching scheme using TiO2 nanorod arrays synthesized by a large-scale and low-cost hydrothermal process was reported. Especially, the nonlinear I–V characteristics of TiO2 nanorod arrays with a nonlinearity of up to ~10, which suppress the leakage current less than 10−4 Acm−2, were demonstrated, exhibiting a self-selecting resistive switching behavior. It provides a simple pathway for integration of RRAM crossbar arrays without additional stacking of active devices. The mechanisms of the nonlinear resistive switching behaviors were discussed in detail. In addition, the maximum array numbers of 79 for self-selecting RRAM cells were estimated. The results demonstrate an opportunity of using the concept of self-selecting resistive switching characteristics in a single material, which offers a new strategy to tackle the sneak path issue of RRAM in the crossbar arrays structure.
High-salt intake negatively regulates fat deposition in mouse
Authors: Cui Huanxian , Yang Shuyan , Zheng Maiqing , Liu Ranran , Zhao Guiping , Wen Jie 
Published: May 2017

AbstractHigh-salt (HS) intake contributes to hypertension and cardiopathy, but the effect of HS on fat deposition is controversial. Feed intake, fat mass, the percentage of abdominal fat, heat production, rate of oxygen consumption and the respiratory exchange ratio of mice on a HS diet were significantly decreased (P < 0.01 or 0.05) compared with mice on a normal-salt (NS) diet. An in vitro experiment with differentiating pre-adipocytes showed reduced fat deposition in the presence of high concentrations of NaCl (>0.05 M). Abdominal fat mRNA profiles and protein measurements showed that 5 known genes involved in lipolysis were up-regulated significantly and 9 genes related to lipogenesis were down-regulated in HS mice. Abundant genes and some proteins (ATP2a1, AGT, and ANGPTL4) related to calcium ion metabolism or the renin-angiotensin system (RAS) were differentially expressed between HS and NS mice. Of special interest, CREB1 phosphorylation (S133 and S142), a key factor involved in calcium signaling and other pathways, was up-regulated in HS mice. By IPA analysis, a network mediated by calcium was established providing the molecular mechanisms underlying the negative effect of HS on fat deposition.
Mitochondrial retrograde signaling connects respiratory capacity to thermogenic gene expression
Authors: Nam Minwoo , Akie Thomas E. , Sanosaka Masato , Craige Siobhan M. , Kant Shashi , Keaney Jr John F. , Cooper Marcus P. 
Published: May 2017

AbstractMitochondrial respiration plays a crucial role in determining the metabolic state of brown adipose tissue (BAT), due to its direct roles in thermogenesis, as well as through additional mechanisms. Here, we show that respiration-dependent retrograde signaling from mitochondria to nucleus contributes to genetic and metabolic reprogramming of BAT. In mouse BAT, ablation of LRPPRC (LRP130), a potent regulator of mitochondrial transcription and respiratory capacity, triggers down-regulation of thermogenic genes, promoting a storage phenotype in BAT. This retrograde regulation functions by inhibiting the recruitment of PPARγ to the regulatory elements of thermogenic genes. Reducing cytosolic Ca2+ reverses the attenuation of thermogenic genes in brown adipocytes with impaired respiratory capacity, while induction of cytosolic Ca2+ is sufficient to attenuate thermogenic gene expression, indicating that cytosolic Ca2+ mediates mitochondria-nucleus crosstalk. Our findings suggest respiratory capacity governs thermogenic gene expression and BAT function via mitochondria-nucleus communication, which in turn leads to either a thermogenic or storage mode.
Involvement Of Vascular Aldosterone Synthase In Phosphate-Induced Osteogenic Transformation Of Vascular Smooth Muscle Cells
Authors: Alesutan Ioana , Voelkl Jakob , Feger Martina , Kratschmar Denise V. , Castor Tatsiana , Mia Sobuj , Sacherer Michael , Viereck Robert , Borst Oliver , Leibrock Christina , Gawaz Meinrad , Kuro-o Makoto , Pilz Stefan , Tomaschitz Andreas , Odermatt Alex , Pieske Burkert , Wagner Carsten A. , Lang Florian 
Published: May 2017

AbstractVascular calcification resulting from hyperphosphatemia is a major determinant of mortality in chronic kidney disease (CKD). Vascular calcification is driven by aldosterone-sensitive osteogenic transformation of vascular smooth muscle cells (VSMCs). We show that even in absence of exogenous aldosterone, silencing and pharmacological inhibition (spironolactone, eplerenone) of the mineralocorticoid receptor (MR) ameliorated phosphate-induced osteo-/chondrogenic transformation of primary human aortic smooth muscle cells (HAoSMCs). High phosphate concentrations up-regulated aldosterone synthase (CYP11B2) expression in HAoSMCs. Silencing and deficiency of CYP11B2 in VSMCs ameliorated phosphate-induced osteogenic reprogramming and calcification. Phosphate treatment was followed by nuclear export of APEX1, a CYP11B2 transcriptional repressor. APEX1 silencing up-regulated CYP11B2 expression and stimulated osteo-/chondrogenic transformation. APEX1 overexpression blunted the phosphate-induced osteo-/chondrogenic transformation and calcification of HAoSMCs. Cyp11b2 expression was higher in aortic tissue of hyperphosphatemic klotho-hypomorphic (kl/kl) mice than in wild-type mice. In adrenalectomized kl/kl mice, spironolactone treatment still significantly ameliorated aortic osteoinductive reprogramming. Our findings suggest that VSMCs express aldosterone synthase, which is up-regulated by phosphate-induced disruption of APEX1-dependent gene suppression. Vascular CYP11B2 may contribute to stimulation of VSMCs osteo-/chondrogenic transformation during hyperphosphatemia.
Nimbolide upregulates RECK by targeting miR-21 and HIF-1α in cell lines and in a hamster oral carcinogenesis model
Authors: Kowshik Jaganathan , Mishra Rajakishore , Sophia Josephraj , Rautray Satabdi , Anbarasu Kumaraswamy , Reddy G. Deepak , Dixit Madhulika , Mahalingam Sundarasamy , Nagini Siddavaram 
Published: May 2017

AbstractReversion-inducing cysteine-rich protein with Kazal motifs (RECK), a potent inhibitor of matrix metalloproteinases (MMPs) is a common negative target of oncogenic signals and a potential therapeutic target for novel drug development. Here, we show that sequential RECKlessness stimulates angiogenesis and Notch signalling in the 7,12-dimethylbenz[a]anthracene (DMBA)-induced hamster buccal pouch (HBP) carcinogenesis model, a paradigm for oral oncogenesis and chemointervention. We also report the chemotherapeutic effect of nimbolide, a limonoid from the neem tree (Azadirachta indica) based on the upregulation of RECK as well as modulation of the expression of key molecules involved in invasion and angiogenesis. We demonstrate that nimbolide upregulates RECK by targeting miR-21, and HIF-1α resulting in reduced MMP activity and blockade of VEGF and Notch signalling. Nimbolide reduced microvascular density, confirming its anti-angiogenic potential. Molecular docking analysis revealed interaction of nimbolide with HIF-1α. Additionally, we demonstrate that nimbolide upregulates RECK expression via downregulation of HIF-1α and miR-21 by overexpression and knockdown experiments in SCC4 and EAhy926 cell lines. Taken together, these findings provide compelling evidence that targeting RECK, a keystone protein that regulates mediators of invasion and angiogenesis with phytochemicals such as nimbolide may be a robust therapeutic approach to prevent oral cancer progression.
CoCO3 from one-step micro-emulsion method as electrode materials for Faradaic capacitors
Authors: Wang Yanfang , Chang Zheng , Zhang Yi , Chen Bingwei , Fu Lijun , Zhu Yusong , Zhang Lixin , Wu Yuping 
Published: May 2017

AbstractFaradaic capacitor (FC) has been widely investigated during the past few decades, and dozens of prototypes have been proposed. However, it has not reached its full potential. In this work, we demonstrate a kind of FC comprising of a CoCO3 electrode. Synthesized through a micro-emulsion route, such CoCO3 shows low crystallinity and porous wool-ball structures stacked by needle-like individuals. It shows desirable electrochemical properties in terms of excellent high-rate performance and high reversibility. Also, it could deliver a capacitance of 440 F·g−1 at 1 A·g−1, and shows no capacitance decay after 1000 cycles. Since metal carbonate is capable of delivering good electrochemical performances and its preparation is easier and more cost-efficient, it should be a feasible candidate for electrode material of FC.