bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Rechargeable Li-Air Fuel Cell Battery Based on Garnet Solid Electrolytes
Authors: Sun Jiyang , Zhao Ning , Li Yiqiu , Guo Xiangxin , Feng Xuefei , Liu Xiaosong , Liu Zhi , Cui Guanglei , Zheng Hao , Gu Lin , Li Hong 
Published: January 2017

AbstractNon-aqueous Li-air batteries have been intensively studied in the past few years for their theoretically super-high energy density. However, they cannot operate properly in real air because they contain highly unstable and volatile electrolytes. Here, we report the fabrication of solid-state Li-air batteries using garnet (i.e., Li6.4La3Zr1.4Ta0.6O12, LLZTO) ceramic disks with high density and ionic conductivity as the electrolytes and composite cathodes consisting of garnet powder, Li salts (LiTFSI) and active carbon. These batteries run in real air based on the formation and decomposition at least partially of Li2CO3. Batteries with LiTFSI mixed with polyimide (PI:LiTFSI) as a binder show rechargeability at 200 °C with a specific capacity of 2184 mAh g−1carbon at 20 μA cm−2. Replacement of PI:LiTFSI with LiTFSI dissolved in polypropylene carbonate (PPC:LiTFSI) reduces interfacial resistance, and the resulting batteries show a greatly increased discharge capacity of approximately 20300 mAh g−1carbon and cycle 50 times while maintaining a cutoff capacity of 1000 mAh g−1carbon at 20 μA cm−2 and 80 °C. These results demonstrate that the use of LLZTO ceramic electrolytes enables operation of the Li-air battery in real air at medium temperatures, leading to a novel type of Li-air fuel cell battery for energy storage.
Time-of-Day Dictates Transcriptional Inflammatory Responses to Cytotoxic Chemotherapy
Authors: Borniger Jeremy C. , Walker II William H. , Gaudier-Diaz Monica M. , Stegman Curtis J. , Zhang Ning , Hollyfield Jennifer L. , Nelson Randy J. , DeVries A. Courtney 
Published: January 2017

AbstractMany cytotoxic chemotherapeutics elicit a proinflammatory response which is often associated with chemotherapy-induced behavioral alterations. The immune system is under circadian influence; time-of-day may alter inflammatory responses to chemotherapeutics. We tested this hypothesis by administering cyclophosphamide and doxorubicin (Cyclo/Dox), a common treatment for breast cancer, to female BALB/c mice near the beginning of the light or dark phase. Mice were injected intravenously with Cyclo/Dox or the vehicle two hours after lights on (zeitgeber time (ZT2), or two hours after lights off (ZT14). Tissue was collected 1, 3, 9, and 24 hours later. Mice injected with Cyclo/Dox at ZT2 lost more body mass than mice injected at ZT14. Cyclo/Dox injected at ZT2 increased the expression of several pro-inflammatory genes within the spleen; this was not evident among mice treated at ZT14. Transcription of enzymes within the liver responsible for converting Cyclo/Dox into their toxic metabolites increased among mice injected at ZT2; furthermore, transcription of these enzymes correlated with splenic pro-inflammatory gene expression when treatment occurred at ZT2 but not ZT14. The pattern was reversed in the brain; pro-inflammatory gene expression increased among mice injected at ZT14. These data suggest that inflammatory responses to chemotherapy depend on time-of-day and are tissue specific.
Dopaminergic modulation of performance monitoring in Parkinson’s disease: An event-related potential study
Authors: Seer Caroline , Lange Florian , Loens Sebastian , Wegner Florian , Schrader Christoph , Dressler Dirk , Dengler Reinhard , Kopp Bruno 
Published: January 2017

AbstractMonitoring one’s actions is essential for goal-directed performance. In the event-related potential (ERP), errors are followed by fronto-centrally distributed negativities. These error(-related) negativity (Ne/ERN) amplitudes are often found to be attenuated in patients with Parkinson’s disease (PD) compared to healthy controls (HC). Although Ne/ERN has been proposed to be related to dopaminergic neuronal activity, previous research did not find evidence for effects of dopaminergic medication on Ne/ERN amplitudes in PD. We examined 13 PD patients “on” and “off” dopaminergic medication. Their response-locked ERP amplitudes (obtained on correct [Nc/CRN] and error [Ne/ERN] trials of a flanker task) were compared to those of 13 HC who were tested twice as well, without receiving dopaminergic medication. While PD patients committed more errors than HC, error rates were not significantly modulated by dopaminergic medication. PD patients showed reduced Ne/ERN amplitudes relative to HC; however, this attenuation of response-locked ERP amplitudes was not specific to errors in this study. PD-related attenuation of response-locked ERP amplitudes was most pronounced when PD patients were on medication. These results suggest overdosing of dopaminergic pathways that are relatively spared in PD, but that are related to the generation of the Ne/ERN, notably pathways targeted on the medial prefrontal cortex.
Using the MitoB method to assess levels of reactive oxygen species in ecological studies of oxidative stress
Authors: Salin Karine , Auer Sonya K. , Villasevil Eugenia M. , Anderson Graeme J. , Cairns Andrew G. , Mullen William , Hartley Richard C. , Metcalfe Neil B. 
Published: January 2017

AbstractIn recent years evolutionary ecologists have become increasingly interested in the effects of reactive oxygen species (ROS) on the life-histories of animals. ROS levels have mostly been inferred indirectly due to the limitations of estimating ROS from in vitro methods. However, measuring ROS (hydrogen peroxide, H2O2) content in vivo is now possible using the MitoB probe. Here, we extend and refine the MitoB method to make it suitable for ecological studies of oxidative stress using the brown trout Salmo trutta as model. The MitoB method allows an evaluation of H2O2 levels in living organisms over a timescale from hours to days. The method is flexible with regard to the duration of exposure and initial concentration of the MitoB probe, and there is no transfer of the MitoB probe between fish. H2O2 levels were consistent across subsamples of the same liver but differed between muscle subsamples and between tissues of the same animal. The MitoB method provides a convenient method for measuring ROS levels in living animals over a significant period of time. Given its wide range of possible applications, it opens the opportunity to study the role of ROS in mediating life history trade-offs in ecological settings.
The relationship between vacuolation and initiation of PCD in rice (Oryza sativa) aleurone cells
Authors: Zheng Yan , Zhang Heting , Deng Xiaojiang , Liu Jing , Chen Huiping 
Published: January 2017

AbstractVacuole fusion is a necessary process for the establishment of a large central vacuole, which is the central location of various hydrolytic enzymes and other factors involved in death at the beginning of plant programmed cell death (PCD). In our report, the fusion of vacuoles has been presented in two ways: i) small vacuoles coalesce to form larger vacuoles through membrane fusion, and ii) larger vacuoles combine with small vacuoles when small vacuoles embed into larger vacuoles. Regardless of how fusion occurs, a large central vacuole is formed in rice (Oryza sativa) aleurone cells. Along with the development of vacuolation, the rupture of the large central vacuole leads to the loss of the intact plasma membrane and the degradation of the nucleus, resulting in cell death. Stabilizing or disrupting the structure of actin filaments (AFs) inhibits or promotes the fusion of vacuoles, which delays or induces PCD. In addition, the inhibitors of the vacuolar processing enzyme (VPE) and cathepsin B (CathB) block the occurrence of the large central vacuole and delay the progression of PCD in rice aleurone layers. Overall, our findings provide further evidence for the rupture of the large central vacuole triggering the PCD in aleruone layers.
Calcium-independent disruption of microtubule dynamics by nanosecond pulsed electric fields in U87 human glioblastoma cells
Authors: Carr Lynn , Bardet Sylvia M. , Burke Ryan C. , Arnaud-Cormos Delia , Leveque Philippe , O’Connor Rodney P. 
Published: January 2017

AbstractHigh powered, nanosecond duration, pulsed electric fields (nsPEF) cause cell death by a mechanism that is not fully understood and have been proposed as a targeted cancer therapy. Numerous chemotherapeutics work by disrupting microtubules. As microtubules are affected by electrical fields, this study looks at the possibility of disrupting them electrically with nsPEF. Human glioblastoma cells (U87-MG) treated with 100, 10 ns, 44 kV/cm pulses at a frequency of 10 Hz showed a breakdown of their interphase microtubule network that was accompanied by a reduction in the number of growing microtubules. This effect is temporally linked to loss of mitochondrial membrane potential and independent of cellular swelling and calcium influx, two factors that disrupt microtubule growth dynamics. Super-resolution microscopy revealed microtubule buckling and breaking as a result of nsPEF application, suggesting that nsPEF may act directly on microtubules.
Production of functional human nerve growth factor from the saliva of transgenic mice by using salivary glands as bioreactors
Authors: Zeng Fang , Li Zicong , Zhu Qingchun , Dong Rui , Zhao Chengcheng , Li Guoling , Li Guo , Gao Wenchao , Jiang Gelong , Zheng Enqin , Cai Gengyuan , Moisyadi Stefan , Urschitz Johann , Yang Huaqiang , Liu Dewu , Wu Zhenfang 
Published: January 2017

AbstractThe salivary glands of animals have great potential to act as powerful bioreactors to produce human therapeutic proteins. Human nerve growth factor (hNGF) is an important pharmaceutical protein that is clinically effective in the treatment of many human neuronal and non-neuronal diseases. In this study, we generated 18 transgenic (TG) founder mice each carrying a salivary gland specific promoter-driven hNGF transgene. A TG mouse line secreting high levels of hNGF protein in its saliva (1.36 μg/mL) was selected. hNGF protein was successfully purified from the saliva of these TG mice and its identity was verified. The purified hNGF was highly functional as it displayed the ability to induce neuronal differentiation of PC12 cells. Furthermore, it strongly promoted proliferation of TF1 cells, above the levels observed with mouse NGF. Additionally, saliva collected from TG mice and containing unpurified hNGF was able to significantly enhance the growth of TF1 cells. This study not only provides a new and efficient approach for the synthesis of therapeutic hNGF but also supports the concept that salivary gland from TG animals is an efficient system for production of valuable foreign proteins.
Tryptophan-2,3-Dioxygenase (TDO) deficiency is associated with subclinical neuroprotection in a mouse model of multiple sclerosis
Authors: Lanz Tobias V. , Williams Sarah K. , Stojic Aleksandar , Iwantscheff Simeon , Sonner Jana K. , Grabitz Carl , Becker Simon , Böhler Laura-Inés , Mohapatra Soumya R. , Sahm Felix , Küblbeck Günter , Nakamura Toshikazu , Funakoshi Hiroshi , Opitz Christiane A. , Wick Wolfgang , Diem Ricarda , Platten Michael 
Published: January 2017

AbstractThe catabolism of tryptophan to immunosuppressive and neuroactive kynurenines is a key metabolic pathway regulating immune responses and neurotoxicity. The rate-limiting step is controlled by indoleamine-2,3-dioxygenase (IDO) and tryptophan-2,3-dioxygenase (TDO). IDO is expressed in antigen presenting cells during immune reactions, hepatic TDO regulates blood homeostasis of tryptophan and neuronal TDO influences neurogenesis. While the role of IDO has been described in multiple immunological settings, little is known about TDO’s effects on the immune system. TDO-deficiency is neuroprotective in C. elegans and Drosophila by increasing tryptophan and specific kynurenines. Here we have determined the role of TDO in autoimmunity and neurodegeneration in experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis. We created reporter-TDO mice for in vivo imaging to show that hepatic but not CNS TDO expression is activated during EAE. TDO deficiency did not influence myelin-specific T cells, leukocyte infiltration into the CNS, demyelination and disease activity. TDO-deficiency protected from neuronal loss in the spinal cord but not in the optic nerves. While this protection did not translate to an improved overt clinical outcome, our data suggest that spatially distinct neuroprotection is conserved in mammals and support TDO as a potential target for treatment of diseases associated with neurodegeneration.
Quantification of spatiotemporal patterns of Ras isoform expression during development
Authors: Newlaczyl Anna U. , Coulson Judy M. , Prior Ian A. 
Published: January 2017

AbstractRas proteins are important signalling hubs frequently dysregulated in cancer and in a group of developmental disorders called Rasopathies. Three Ras genes encode four proteins that differentially contribute to these phenotypes. Using quantitative real-time PCR (qRT-PCR) we have measured the gene expression profiles of each of the Ras isoforms in a panel of mouse tissues derived from a full developmental time course spanning embryogenesis through to adulthood. In most tissues and developmental stages we observe a relative contribution of KRas4B > > NRas ≥ KRas4A > HRas to total Ras expression with KRas4B typically representing 60–99% of all Ras transcripts. KRas4A is the most dynamically regulated Ras isoform with significant up-regulation of expression observed pre-term in stomach, intestine, kidney and heart. The expression patterns assist interpretation of the essential role of KRas in development and the preponderance of KRas mutations in cancer.
Impairment of blood-brain barrier is an early event in R6/2 mouse model of Huntington Disease
Authors: Di Pardo Alba , Amico Enrico , Scalabrì Francesco , Pepe Giuseppe , Castaldo Salvatore , Elifani Francesca , Capocci Luca , De Sanctis Claudia , Comerci Laura , Pompeo Francesco , D’Esposito Maurizio , Filosa Stefania , Crispi Stefania , Maglione Vittorio 
Published: January 2017

AbstractBlood-brain barrier (BBB) breakdown, due to the concomitant disruption of the tight junctions (TJs), normally required for the maintenance of BBB function, and to the altered transport of molecules between blood and brain and vice-versa, has been suggested to significantly contribute to the development and progression of different brain disorders including Huntington’s disease (HD). Although the detrimental consequence the BBB breakdown may have in the clinical settings, the timing of its alteration remains elusive for many neurodegenerative diseases. In this study we demonstrate for the first time that BBB disruption in HD is not confined to established symptoms, but occurs early in the disease progression. Despite the obvious signs of impaired BBB permeability were only detectable in concomitance with the onset of the disease, signs of deranged TJs integrity occur precociously in the disease and precede the onset of overt symptoms. To our perspective this finding may add a new dimension to the horizons of pathological mechanisms underlying this devastating disease, however much remains to be elucidated for understanding how specific BBB drug targets can be approached in the future.
Giant Flexoelectro-optic Effect with Liquid Crystal Dimer CB7CB
Authors: Varanytsia Andrii , Chien Liang-Chy 
Published: January 2017

AbstractWe demonstrate a giant flexoelectro-optic behavior of liquid crystal dimer CB7CB. Flexoelectric properties of CB7CB experimentally characterized by measured angle of an in-plane rotation of helical axis (HA) in polymer stabilized uniform lying helix cholesteric liquid crystal. The 45° rotation of HA providing full intensity modulation of transmitted through a pair of crossed polarizers light, is achieved with 4.5 V/μm with a sub-millisecond electro-optic switching time. Reported properties enable application of CB7CB in applications of the flexoelectric effect in fast switching photonic and electro-optic devices.
The genetic overlap between mood disorders and cardiometabolic diseases: a systematic review of genome wide and candidate gene studies
Authors: Amare A T , Schubert K O , Klingler-Hoffmann M , Cohen-Woods S , Baune B T 
Published: January 2017

AbstractMeta-analyses of genome-wide association studies (meta-GWASs) and candidate gene studies have identified genetic variants associated with cardiovascular diseases, metabolic diseases and mood disorders. Although previous efforts were successful for individual disease conditions (single disease), limited information exists on shared genetic risk between these disorders. This article presents a detailed review and analysis of cardiometabolic diseases risk (CMD-R) genes that are also associated with mood disorders. First, we reviewed meta-GWASs published until January 2016, for the diseases ‘type 2 diabetes, coronary artery disease, hypertension’ and/or for the risk factors ‘blood pressure, obesity, plasma lipid levels, insulin and glucose related traits’. We then searched the literature for published associations of these CMD-R genes with mood disorders. We considered studies that reported a significant association of at least one of the CMD-R genes and ‘depression’ or ‘depressive disorder’ or ‘depressive symptoms’ or ‘bipolar disorder’ or ‘lithium treatment response in bipolar disorder’, or ‘serotonin reuptake inhibitors treatment response in major depression’. Our review revealed 24 potential pleiotropic genes that are likely to be shared between mood disorders and CMD-Rs. These genes includeMTHFR,CACNA1D,CACNB2,GNAS,ADRB1,NCAN,REST,FTO,POMC,BDNF,CREB,ITIH4,LEP,GSK3B,SLC18A1,TLR4,PPP1R1B,APOE,CRY2,HTR1A,ADRA2A,TCF7L2,MTNR1BandIGF1. A pathway analysis of these genes revealed significant pathways:corticotrophin-releasing hormone signaling,AMPK signaling,cAMP-mediated or G-protein coupled receptor signaling,axonal guidance signaling,serotonin or dopamine receptors signaling, dopamine-DARPP32 feedback in cAMP signaling,circadian rhythm signalingandleptin signaling. Our review provides insights into the shared biological mechanisms of mood disorders and cardiometabolic diseases.
Early onset of inflammation during ontogeny of bipolar disorder: the NLRP2 inflammasome gene distinctly differentiates between patients and healthy controls in the transition between iPS cell and neural stem cell stages
Authors: Vizlin-Hodzic D , Zhai Q , Illes S , Södersten K , Truvé K , Parris T Z , Sobhan P K , Salmela S , Kosalai S T , Kanduri C , Strandberg J , Seth H , Bontell T O , Hanse E , Ågren H , Funa K 
Published: January 2017

AbstractNeuro-inflammation and neuronal communication are considered as mis-regulated processes in the aetiology and pathology of bipolar disorder (BD). Which and when specific signal pathways become abnormal during the ontogeny of bipolar disorder patients is unknown. To address this question, we applied induced pluripotent stem cell (iPSC) technology followed by cortical neural differentiation on adipocyte-derived cells from BD type I patients (with psychotic episodes in psychiatric history) and healthy volunteers (controls). RNA sequencing in iPSC and cortical neural stem cell (NSC) lines were used to examine alterations between the transcriptomes from BD I and control samples during transition from the pluripotent stage towards the neural developmental stage. At the iPSC stage, the most highly significant differentially expressed gene (DEG) was the NLRP2 inflammasome (P=2.66 × 10−10). Also among 42 DEGs at the NSC stage, NLRP2 showed the strongest statistical significance (P=3.07 × 10−19). In addition, we have also identified several cytoskeleton-associated genes as DEGs from the NSC stage, such as TMP2, TAGLN and ACTA2; the former two genes are recognised for the first time to be associated with BD. Our results also suggest that iPSC-derived BD-cortical NSCs carry several abnormalities in dopamine and GABA receptor canonical pathways, underlining that our in vitro BD model reflects pathology in the central nervous system. This would indicate that mis-regulated gene expression of inflammatory, neurotransmitter and cytoskeletal signalling occurs during early fetal brain development of BD I patients.
MiR-137-derived polygenic risk: effects on cognitive performance in patients with schizophrenia and controls
Authors: Cosgrove D , Harold D , Mothersill O , Anney R , Hill M J , Bray N J , Blokland G , Petryshen T ,   The Wellcome Trust Case Control Consortium, Donnelly Peter , Bates Lesley , Barroso Ines , Blackwell Jenefer M , Bramon Elvira , Brown Matthew A , Casas Juan P , Corvin Aiden , Deloukas Panos , Duncanson Audrey , Jankowski Janusz , Markus Hugh S , Mathew Christopher G , Palmer Colin N A , Plomin Robert , Rautanen Anna , Sawcer Stephen J , Trembath Richard C , Viswanathan Ananth C , Wood Nicholas W , Spencer Chris C A , Band Gavin , Bellenguez Céline , Freeman Colin , Hellenthal Garrett , Giannoulatou Eleni , Hopkins Lucinda , Pirinen Matti , Pearson Richard , Strange Amy , Su Zhan , Vukcevic Damjan , Langford Cordelia , Hunt Sarah E , Edkins Sarah , Gwilliam Rhian , Blackburn Hannah , Bumpstead Suzannah J , Dronov Serge , Gillman Matthew , Gray Emma , Hammond Naomi , Jayakumar Alagurevathi , McCann Owen T , Liddle Jennifer , Potter Simon C , Ravindrarajah Radhi , Ricketts Michelle , Waller Matthew , Weston PaulWeston , Widaa SaraWidaa , Whittaker Pamela , Richards A , Mantripragada K , Owen M , O'Donovan M C , Gill M , Corvin A , Morris D W , Donohoe G 
Published: January 2017

AbstractVariants at microRNA-137 (MIR137), one of the most strongly associated schizophrenia risk loci identified to date, have been associated with poorer cognitive performance. As microRNA-137 is known to regulate the expression of ~1900 other genes, including several that are independently associated with schizophrenia, we tested whether this gene set was also associated with variation in cognitive performance. Our analysis was based on an empirically derived list of genes whose expression was altered by manipulation of MIR137 expression. This list was cross-referenced with genome-wide schizophrenia association data to construct individual polygenic scores. We then tested, in a sample of 808 patients and 192 controls, whether these risk scores were associated with altered performance on cognitive functions known to be affected in schizophrenia. A subgroup of healthy participants also underwent functional imaging during memory (n=108) and face processing tasks (n=83). Increased polygenic risk within the empirically derived miR-137 regulated gene score was associated with significantly lower performance on intelligence quotient, working memory and episodic memory. These effects were observed most clearly at a polygenic threshold of P=0.05, although significant results were observed at all three thresholds analyzed. This association was found independently for the gene set as a whole, excluding the schizophrenia-associated MIR137 SNP itself. Analysis of the spatial working memory fMRI task further suggested that increased risk score (thresholded at P=10−5) was significantly associated with increased activation of the right inferior occipital gyrus. In conclusion, these data are consistent with emerging evidence that MIR137 associated risk for schizophrenia may relate to its broader downstream genetic effects.