bluuebunny/crossref_metadata_2025_split huggingface dataset:
Validating the Integrated Multisatellite Retrievals for Global Precipitation Measurement in Terms of Diurnal Variability With Hourly Gauge Observations Collected at 50,000 Stations in China
Authors: Li Runze , Wang Kaicun , Qi Dan 
Published: September 2018

AbstractThe diurnal cycle of precipitation is a key feature in the Earth system and related to multiscale physical processes. The Integrated Multi‐satellitE Retrievals for Global Precipitation Measurement (IMERG) data are expected to improve its presentation of diurnal cycle, but how it really performs remains poorly known. This study compares the diurnal characteristics of the half‐hourly IMERG V05 Final Run product with the hourly rain gauge data collected at approximately 50,000 automatic weather stations in China during a 3‐year period (2014–2016). Our results show that IMERG performs well in terms of the diurnal cycle of precipitation amount but less well in terms of frequency and even worse in terms of intensity. Ground observations show that the frequency and intensity are rather stable for the diurnal cycle; however, IMERG shows strong fluctuations. Significant inverse correlation is found between the diurnal cycles of IMERG precipitation frequency and intensity; thus, the biases of these two variables offset and result in a better estimate of amount. A low probability of detection (POD≈50%) and a high false alarm ratio (FAR≈50%) are the major reasons for the inaccurate diurnal cycles of precipitation intensity and frequency. In particular, IMERG presents a false peak of frequency at approximately 23:00–01:00 (Beijing Time) because a large proportion of the data sources at this time contain the indirect estimates from thermal infrared observations. The significant underestimation of the frequency and overestimation of the intensity at approximately 09:00–11:00 and 20:00–22:00 is because the estimates primarily come from less accurate cross‐track microwave sensors.
Deltaproteobacteria (Pelobacter) and Methanococcoides are responsible for choline-dependent methanogenesis in a coastal saltmarsh sediment
Authors: Jameson Eleanor , Stephenson Jason , Jones Helen , Millard Andrew , Kaster Anne-Kristin , Purdy Kevin J , Airs Ruth , Murrell J Colin , Chen Yin 
Published: September 2018

Abstract
Coastal saltmarsh sediments represent an important source of natural methane emissions, much of which originates from quaternary and methylated amines, such as choline and trimethylamine. In this study, we combine DNA stable isotope probing with high throughput sequencing of 16S rRNA genes and 13C2-choline enriched metagenomes, followed by metagenome data assembly, to identify the key microbes responsible for methanogenesis from choline. Microcosm incubation with 13C2-choline leads to the formation of trimethylamine and subsequent methane production, suggesting that choline-dependent methanogenesis is a two-step process involving trimethylamine as the key intermediate. Amplicon sequencing analysis identifies Deltaproteobacteria of the genera Pelobacter as the major choline utilizers. Methanogenic Archaea of the genera Methanococcoides become enriched in choline-amended microcosms, indicating their role in methane formation from trimethylamine. The binning of metagenomic DNA results in the identification of bins classified as Pelobacter and Methanococcoides. Analyses of these bins reveal that Pelobacter have the genetic potential to degrade choline to trimethylamine using the choline-trimethylamine lyase pathway, whereas Methanococcoides are capable of methanogenesis using the pyrrolysine-containing trimethylamine methyltransferase pathway. Together, our data provide a new insight on the diversity of choline utilizing organisms in coastal sediments and support a syntrophic relationship between Bacteria and Archaea as the dominant route for methanogenesis from choline in this environment.
Ceramide synthase-6 confers resistance to chemotherapy by binding to CD95/Fas in T-cell acute lymphoblastic leukemia
Authors: Verlekar Dattesh , Wei Sung-Jen , Cho Hwangeui , Yang Shengping , Kang Min H. 
Published: September 2018

AbstractCeramide synthases (CERS) produce ceramides which are key intermediators in the biosynthesis of complex sphingolipids and play an important role in cell proliferation, differentiation, apoptosis and senescence. CERS6 is an isoform of ceramide synthases known to generate ceramides with C16 acyl chain (C16-Cer). CERS6 and C16-Cer levels were significantly higher in acute lymphoblastic leukemia (ALL) cells in comparison to peripheral blood mononuclear cells and T lymphocytes derived from healthy human volunteers. We investigated the role of CERS6 in chemo-resistance in T-ALL cell lines. Stable knockdown ofCERS6in CCRF-CEM and MOLT-4 cells resulted in increased sensitivity to ABT-737, a pan-BCL-2 inhibitor, while CCRF-CEM cells with exogenousCERS6expression showed resistance to ABT-737 relative to the vector control. The cytotoxic activity of ABT-737 inCERS6knockdown cells was significantly reduced by the addition of a caspase-8 inhibitor Z-IETD, suggesting that CERS6 alters the cytotoxicity via extrinsic pathway of apoptosis. By co-immunoprecipitation of CERS6 in CCRF-CEM cells, we identified CD95/Fas, a mediator of extrinsic apoptotic pathway, as a novel CERS6 binding partner. In Fas pull-down samples, FADD (Fas-associated protein with death domain) was detected at higher levels in cells withCERS6knockdown compared with control cells when treated with ABT-737, and this was reversed by the overexpression ofCERS6, demonstrating that CERS6 interferes with Fas–FADD DISC assembly. CERS6 may serve as a biomarker in determining the effectiveness of anticancer agents acting via the extrinsic pathway in T-ALL.
TNFR2 unlocks a RIPK1 kinase activity-dependent mode of proinflammatory TNFR1 signaling
Authors: Siegmund Daniela , Ehrenschwender Martin , Wajant Harald 
Published: September 2018

AbstractTNF is not only a major effector molecule of PAMP/DAMP-activated macrophages, but also regulates macrophage function and viability. We recently demonstrated that TNFR2 triggers necroptosis in macrophages with compromised caspase activity by two cooperating mechanisms: induction of endogenous TNF with subsequent stimulation of TNFR1 and depletion of cytosolic TRAF2-cIAP complexes. Here we show that TNFR2 activation in caspase-inhibited macrophages results in the production of endogenous TNF and TNFR1 stimulation followed by upregulation of A20, TRAF1, IL-6, and IL-1β. Surprisingly, TNFR1-mediated induction of IL-6 and IL-1β was clearly evident in response to TNFR2 stimulation but occurred not or only weakly in macrophages selectively and directly stimulated via TNFR1. Moreover, TNFR2-induced TNFR1-mediated gene induction was largely inhibited by necrostatin-1, whereas upregulation of A20 and TRAF1 by direct and exclusive stimulation of TNFR1 remained unaffected by this compound. Thus, treatment with TNFR2/ZVAD enables TNFR1 in macrophages to stimulate gene induction via a pathway requiring RIPK1 kinase activity. TNFR2/ZVAD-induced production of IL-6 and IL-1β was largely blocked in necroptosis-resistant MLKL- and RIPK3-deficient macrophages, whereas induction of A20 and TRAF1 remained unaffected. In sum, our results show that in caspase-inhibited macrophages TNFR2 not only triggers TNF/TNFR1-mediated necroptosis but also TNF/TNFR1-mediated RIPK3/MLKL-dependent and -independent gene induction.
ARHGAP9 suppresses the migration and invasion of hepatocellular carcinoma cells through up-regulating FOXJ2/E-cadherin
Authors: Zhang Hong , Tang Qing-Feng , Sun Meng-Yao , Zhang Chun-Yan , Zhu Jian-Yong , Shen Yu-Li , Zhao Bin , Shao Zhi-Yi , Zhang Li-Jun , Zhang Hong 
Published: September 2018

AbstractRho GTPase activating protein 9 (ARHGAP9), a member of RhoGAP family, has been identified as a RhoGAP for Cdc42 and Rac1. Here, we aimed to clarify the expression and functional role of ARHGAP9 in hepatocellular carcinoma (HCC). By analyzing TCGA (The Cancer Genome Atlas) LIHC (liver hepatocellular carcinoma) database, we found that ARHGAP9 expression was lower in HCC tissues than in normal liver tissues, and that patients with ARHGAP9 lower expression had a significant shorter overall survival time than those with ARHGAP9 higher expression. Cell counting kit-8 (CCK-8), transwell assays and in vivo experimental lung metastasis assay revealed that ARHGAP9 overexpression could inhibit HCC cell proliferation, migration and invasion, as well as HCC lung metastases. By next-generation RNA-sequencing, we identified that a transcription factor, Forkhead Box J2 (FOXJ2), was significantly induced by ARHGAP9 overexpression in HepG2 cells. Ectopic expression of FOXJ2 in HCC cell lines also exerted inhibitory effects on cell migration and invasion. Moreover, the inhibitory effects of ARHGAP9 on HCC cell migration and invasion was significantly attenuated by FOXJ2 knockdown. Luciferase reporter assay demonstrated that ARHGAP9 enhanced the transcription of E-cadherin (CDH1) via FOXJ2. Chromatin immunoprecipitation (ChIP) assay demonstrated that FOXJ2 modulated the transcription of E-cadherin (CDH1) by directly binding to its promoter. Furthermore, Pearson’s correlation analysis indicated that the mRNA levels of ARHGAP9 in HCC tissues were positively correlated with the mRNA levels of FOXJ2 and CDH1. These data clearly show that ARHGAP9/FOXJ2 inhibit cell migration and invasion during HCC development via inducing the transcription of CDH1.
RETRACTED ARTICLE: Identification of protein kinase inhibitors to reprogram breast cancer cells
Authors: Yuan Jie , Zhang Fan , You Meng , Yang Qin 
Published: September 2018

AbstractDirect reversion of cancers into normal-like tissues is an ideal strategy for cancer treatment. Recent reports have showed that defined transcription factors can induce reprogramming of cancer cells into pluripotent stem cells, supporting this notion. Here, we have developed a reprogramming method that uses a conceptually unique strategy for breast cancer cell treatment. We have screened a kinase inhibitor library and found that Rho-associated protein kinase (ROCK) and mammalian target of rapamycin (mTOR) kinase inhibitors can substitute for all transcription factors to be sufficient to reprogram breast cancer cells into progenitor cells. Furthermore, ROCK–mTOR inhibitors could reprogram breast cancer cells to another terminal lineage-adipogenic cells. Genome-wide transcriptional analysis shows that the induced fat-like cells have a profile different from breast cancer cells and similar to that of normal adipocytes. In vitro and in vivo tumorigenesis assays have shown that induced fat-like cells lose proliferation and tumorigenicity. Moreover, reprogramming treatment with ROCK–mTOR inhibitors prevents breast cancer local recurrence in mice. Currently, ROCK–mTOR inhibitors are already used as antitumor drugs in patients, thus, this reprogramming strategy has significant potential to move rapidly toward clinical trials for breast cancer treatment.
Recurrent WNT pathway alterations are frequent in relapsed small cell lung cancer
Authors: Wagner Alex H. , Devarakonda Siddhartha , Skidmore Zachary L. , Krysiak Kilannin , Ramu Avinash , Trani Lee , Kunisaki Jason , Masood Ashiq , Waqar Saiama N. , Spies Nicholas C. , Morgensztern Daniel , Waligorski Jason , Ponce Jennifer , Fulton Robert S. , Maggi Leonard B. , Weber Jason D. , Watson Mark A. , O’Conor Christopher J. , Ritter Jon H. , Olsen Rachelle R. , Cheng Haixia , Mukhopadhyay Anandaroop , Can Ismail , Cessna Melissa H. , Oliver Trudy G. , Mardis Elaine R. , Wilson Richard K. , Griffith Malachi , Griffith Obi L. , Govindan Ramaswamy 
Published: September 2018

AbstractNearly all patients with small cell lung cancer (SCLC) eventually relapse with chemoresistant disease. The molecular mechanisms driving chemoresistance in SCLC remain un-characterized. Here, we describe whole-exome sequencing of paired SCLC tumor samples procured at diagnosis and relapse from 12 patients, and unpaired relapse samples from 18 additional patients. Multiple somatic copy number alterations, including gains in ABCC1 and deletions in MYCL, MSH2, and MSH6, are identifiable in relapsed samples. Relapse samples also exhibit recurrent mutations and loss of heterozygosity in regulators of WNT signaling, including CHD8 and APC. Analysis of RNA-sequencing data shows enrichment for an ASCL1-low expression subtype and WNT activation in relapse samples. Activation of WNT signaling in chemosensitive human SCLC cell lines through APC knockdown induces chemoresistance. Additionally, in vitro-derived chemoresistant cell lines demonstrate increased WNT activity. Overall, our results suggest WNT signaling activation as a mechanism of chemoresistance in relapsed SCLC.
Differential regulation of chloride homeostasis and GABAergic transmission in the thalamus
Authors: Schmidt Tobias , Ghaffarian Nikoo , Philippot Camille , Seifert Gerald , Steinhäuser Christian , Pape Hans-Christian , Blaesse Peter 
Published: September 2018

AbstractThe thalamus is important for sensory integration with the ventrobasal thalamus (VB) as relay controlled by GABAergic projections from the nucleus reticularis thalami (NRT). Depending on the [Cl−]i primarily set by cation-chloride-cotransporters, GABA is inhibitory or excitatory. There is evidence that VB and NRT differ in terms of GABA action, with classical hyperpolarization in VB due to the expression of the Cl− extruder KCC2 and depolarizing/excitatory GABA action in the NRT, where KCC2 expression is low and Cl− accumulation by the Cl− inward transporter NKCC1 has been postulated. However, data on NKCC1 expression and functional analysis of both transporters are missing. We show that KCC2-mediated Cl− extrusion set the [Cl−]i in VB, while NKCC1 did not contribute substantially to Cl− accumulation and depolarizing GABA action in the NRT. The finding that NKCC1 did not play a major role in NRT neurons is of high relevance for ongoing studies on the therapeutic use of NKCC1 inhibitors trying to compensate for a disease-induced up-regulation of NKCC1 that has been described for various brain regions and disease states like epilepsy and chronic pain. These data suggest that NKCC1 inhibitors might have no major effect on healthy NRT neurons due to limited NKCC1 function.
Robust ferromagnetism in hydrogenated graphene mediated by spin-polarized pseudospin
Authors: Kim Hyunyoung , Bang Junhyeok , Kang Joongoo 
Published: September 2018

AbstractThe origin of the ferromagnetism in metal-free graphitic materials has been a decade-old puzzle. The possibility of long-range magnetic order in graphene has been recently questioned by the experimental findings that point defects in graphene, such as fluorine adatoms and vacancies, lead to defect-induced paramagnetism but no magnetic ordering down to 2 K. It remains controversial whether collective magnetic order in graphene can emerge from point defects at finite temperatures. This work provides a new framework for understanding the ferromagnetism in hydrogenated graphene, highlighting the key contribution of the spin-polarized pseudospin as a “mediator” of long-range magnetic interactions in graphene. Using first-principles calculations of hydrogenated graphene, we found that the unique ‘zero-energy’ position of H-induced quasilocalized states enables notable spin polarization of the graphene’s sublattice pseudospin. The pseudospin-mediated magnetic interactions between the H-induced magnetic moments stabilize the two-dimensional ferromagnetic ordering with Curie temperatures of Tc = nH × 34,000 K for the atom percentage nH of H adatoms. These findings show that atomic-scale control of hydrogen adsorption on graphene can give rise to a robust magnetic order.
Effect of inoculated and uninoculated aeration pretreatment on nutrients and phytotoxicity of anaerobic digestion effluent
Authors: Zhang Bangxi , Li Yun , Li Shuyan , Li Guoxue , Sun Qiaoping 
Published: September 2018

AbstractThis study investigates the influence of inoculated and uninoculated aeration pretreatment on nutrients and phytotoxicity of anaerobic digestion (AD) effluent. Swine manure AD effluent was inoculated with activated and anaerobic sludge, respectively. Our results show that aeration with the addition of activated sludge could reduce the phytotoxicity of AD effluent. Compared to the control treatment without any sludge addition, the addition of activated sludge resulted in a more significant reduction in the AD effluent salinity, NH4+ content, and organic matter (indicated by the chemical oxygen demand) when AD effluent was aerated for less than 8 hours. As a result, a much higher seed germination index (GI) was observed for the treatment with activated sludge addition, particularly when aerated for 4–5 hours, contributing the gas/water ratio of 20:1–30:1. On the other hand, no significant differences in the nutrient contents and GI value were observed for the control treatment and that with the addition of anaerobic sludge. Results from this study shed light on optimizing the management of AD effluent for agricultural application.
The E3 ubiquitin ligase Trim13 regulates Nur77 stability via casein kinase 2α
Authors: Huang Bin , Pei Han Zhong , Chang Hyeun-Wook , Baek Suk-Hwan 
Published: September 2018

AbstractNur77 is a member of the NR4A subfamily of nuclear receptors and has been shown to regulate various biological processes such as apoptosis and inflammation. Here, we show that Nur77 ubiquitination is mediated by the tripartite motif 13 (Trim13), a RING-type E3 ubiquitin ligase. The interaction between Nur77 and Trim13 was confirmed by co-immunoprecipitation. Moreover, we found that Lys539 in Nur77 ubiquitination is targeted for Trim13, which leads to Nur77 degradation. The Trim13-mediated ubiquitination of Nur77 was optimal in the presence of the E2 enzyme UbcH5. Importantly, in addition to Trim13-mediated ubiquitination, the stability of Nur77 was also regulated by casein kinase 2α (CK2α). Pharmacological inhibition of CK2 markedly increased Nur77 levels, whereas overexpression of CK2α, but not its inactive mutant, dramatically decreased Nur77 levels by promoting Nur77 ubiquitination. CK2α phosphorylated Ser154 in Nur77 and thereby regulated Nur77 protein levels by promoting its ubiquitin-mediated degradation. Importantly, we also show that degradation of Nur77 is involved in TNFα-mediated IL-6 production via CK2α and Trim13. Taken together, these results suggest that the sequential phosphorylation and ubiquitination of Nur77 controls its degradation, and provide a therapeutic approach for regulating Nur77 activity through the CK2α-Trim13 axis as a mechanism to control the inflammatory response.
Silencing of quinolinic acid phosphoribosyl transferase (QPT) gene for enhanced production of scopolamine in hairy root culture of Duboisia leichhardtii
Authors: Singh Pooja , Prasad Ratnum , Tewari Rashi , Jaidi Meraj , Kumar Susheel , Rout P. K. , Rahman Laiq ur 
Published: September 2018

AbstractScopolamine is a pharmaceutically important tropane alkaloid which is used therapeutically in the form of an anesthetic and antispasmodic drug. The present study demonstrates enhanced scopolamine production from transgenic hairy root clones of Duboisia leichhardtii wherein the expression of quinolinate phosphoribosyl transferase (QPT) gene was silenced using the QPT-RNAi construct under the control of CaMV 35 S promoter. The RNAi hairy roots clones viz. P4, P7, P8, and P12 showed the enhanced synthesis of scopolamine with significant inhibition of nicotine biosynthesis. Optimization of culture duration in combination with methyl jasmonate elicitor in different concentrations (50 µM-200 µM) was carried out. Maximum synthesis of scopolamine had obtained from HR clones P7 (8.84 ± 0.117 mg/gm) on the 30th day of cultivation. Conspicuously, elicitation with wound-associated hormone methyl jasmonate enhanced the yield of scopolamine 2.2 fold (19.344 ± 0.275 mg/gm) compared to the culture lacking the elicitor. The transgenic hairy roots cultures established with RNAi mediated silencing of quinolinate phosphoribosyl transferase gene provides an alternative approach to increase the yield of scopolamine in fulfilling the demand of this secondary metabolite.
Seafloor crustal deformation data along the subduction zones around Japan obtained by GNSS-A observations
Authors: Yokota Yusuke , Ishikawa Tadashi , Watanabe Shun-ichi 
Published: September 2018

AbstractCrustal deformation data obtained by geodetic observation networks are foundations in the fields of geodesy and seismology. These data are essential for understanding plate motion and earthquake sources and for simulating earthquake and tsunami scenarios. Although relatively scarce, seafloor geodetic data are particularly important for monitoring the behaviour of undersea interplate boundary regions. Since the mid-1990s, we have been developing the combined Global Navigation Satellite System-Acoustic ranging (GNSS-A) technique for realizing seafloor geodesy. This technique allows us to collect time series of seafloor crustal deformation. Our published data can be used to investigate several seismological phenomena along the subduction zones around Japan, namely the Nankai Trough, Sagami Trough and Japan Trench. These regions are globally important places in geodesy and seismology and are also suitable for comparison with other geophysical datasets. Our intention is for these data to promote further understanding of megathrust zones.
Traffic sign recognition using weighted multi‐convolutional neural network
Authors: Natarajan Sudha , Annamraju Abhishek Kumar , Baradkar Chaitree Sham 
Published: September 2018

Traffic signs play a crucial role in regulating traffic and facilitating cautious driving. Automatic traffic sign recognition is one of the key tasks in autonomous driving. Accuracy in the classification of traffic signs is therefore very important for the navigation of a vehicle. Here, a reliable and robust convolutional neural network (CNN) is presented for classifying these signs. The proposed classifier is a weighted multi‐CNN trained with a novel methodology. It achieves a near state‐of‐the‐art recognition rate of 99.59% when tested on the German traffic sign recognition benchmark dataset. Compared to the existing classifiers, the proposed one is a low‐complexity network that recognises a test image in 10 ms when running on an NVIDIA 980 Ti GPU system. The results demonstrate its suitability and reliability in high‐speed driving scenarios.