bluuebunny/crossref_metadata_2025_split huggingface dataset:
Tectonic and Anthropogenic Microseismic Activity While Drilling Toward Supercritical Conditions in the Larderello‐Travale Geothermal Field, Italy
Authors: Minetto Riccardo , Montanari Domenico , Planès Thomas , Bonini Marco , Del Ventisette Chiara , Antunes Verónica , Lupi Matteo 
Published: January 2020

AbstractThis study investigates the seismic activity occurring at the Larderello‐Travale geothermal field, central Italy, from June 2017 to January 2018. We deployed a network composed of nine broadband stations around the Venelle 2 well drilling for supercritical fluids. During the experiment, we recognize two types of seismic events (type 1 and type 2). Type‐1 events have clear
and
wave arrivals and occur in clusters both above and below the K‐horizon, which is a seismic reflector marking a debated transition zone at depth. The distribution and evolution of the seismic sequences suggest that the K‐horizon could be interpreted as a fluid‐rich region at near‐lithostatic pressures. Type‐2 events usually occur in swarms and show a periodic pattern, a narrow frequency band, and almost identical waveforms. Their source is estimated to be located near the well, and their occurrence ceases after about 3 weeks from the conclusion of the drilling. We propose a causal link with the drilling operations where pressure fronts inside the well may promote phase changes and fluid flow across the drilled formations. Our study sheds light on the fluid‐driven tectonic and anthropogenic seismic activity at the Larderello‐Travale geothermal field. More generally, we show that microseismic activity occurring during drilling in high‐pressure and high‐temperature conditions can remain at low magnitudes and that geothermal wells targeting geothermal fluids in such systems may be handled safely despite the critical conditions encountered at depth. The drilling of the Venelle 2 well is an encouraging example for the development of geothermal energy in critical conditions.
The Atlantic Meridional Overturning Circulation in High‐Resolution Models
Authors: Hirschi Joël J.‐M. , Barnier Bernard , Böning Claus , Biastoch Arne , Blaker Adam T. , Coward Andrew , Danilov Sergey , Drijfhout Sybren , Getzlaff Klaus , Griffies Stephen M. , Hasumi Hiroyasu , Hewitt Helene , Iovino Doroteaciro , Kawasaki Takao , Kiss Andrew E. , Koldunov Nikolay , Marzocchi Alice , Mecking Jennifer V. , Moat Ben , Molines Jean‐Marc , Myers Paul G. , Penduff Thierry , Roberts Malcolm , Treguier Anne‐Marie , Sein Dmitry V. , Sidorenko Dmitry , Small Justin , Spence Paul , Thompson LuAnne , Weijer Wilbert , Xu Xiaobiao 
Published: January 2020

AbstractThe Atlantic meridional overturning circulation (AMOC) represents the zonally integrated stream function of meridional volume transport in the Atlantic Basin. The AMOC plays an important role in transporting heat meridionally in the climate system. Observations suggest a heat transport by the AMOC of 1.3 PW at 26°N—a latitude which is close to where the Atlantic northward heat transport is thought to reach its maximum. This shapes the climate of the North Atlantic region as we know it today. In recent years there has been significant progress both in our ability to observe the AMOC in nature and to simulate it in numerical models. Most previous modeling investigations of the AMOC and its impact on climate have relied on models with horizontal resolution that does not resolve ocean mesoscale eddies and the dynamics of the Gulf Stream/North Atlantic Current system. As a result of recent increases in computing power, models are now being run that are able to represent mesoscale ocean dynamics and the circulation features that rely on them. The aim of this review is to describe new insights into the AMOC provided by high‐resolution models. Furthermore, we will describe how high‐resolution model simulations can help resolve outstanding challenges in our understanding of the AMOC.
On the Transition From Initial Leader to Stepped Leader in Negative Cloud‐to‐Ground Lightning
Authors: Stolzenburg Maribeth , Marshall Thomas C. , Karunarathne Sumedhe 
Published: January 2020

AbstractHigh‐speed video and electric field change data are used to describe the first 5 ms of a negative cloud‐to‐ground flash. These observations reveal an evolution in character of the luminosity and electric field change pulses as two branches of the leader separately transition from initial leader to propagating as a negative stepped leader (SL). For the first time reported, there is evidence of weak luminosity coincident with the initiating event, a weak bipolar pulse 60 μs prior to the first initial breakdown (IB) pulse. During the IB stage, the initial leader advances intermittently at intervals of 100–280 μs, in separate light bursts that are bright for a few 20‐μs frames and are time coincident with IB pulses. In the intervals between IB pulses, the initial leader is dim or invisible during the earliest 1.8 ms. Within 2 ms, the leader propagation begins transitioning to an early SL phase, in which the leader tip advances at more regular intervals of 40–80 μs during relatively dim and brief steps which are coincident with SL pulses having short duration, small amplitude, and typically unipolar waveform. These data indicate that when the entire initial leader length behind the lower end begins to remain illuminated between bursts, the propagation mode changes from IB bursts to SL steps, and the IB stage ends. The results support a hypothesis that the early initial leader development occurs in the absence of a continuously hot channel, thus the initial leader propagation is physically unlike the self‐propagating SL advance.
Wildfire‐Smoke Aerosols Lead to Increased Light Use Efficiency Among Agricultural and Restored Wetland Land Uses in California's Central Valley
Authors: Hemes Kyle S. , Verfaillie Joseph , Baldocchi Dennis D. 
Published: January 2020

AbstractThere are few observational studies measuring the ecosystem‐scale productivity effects of changes in incident diffuse photosynthetically active radiation (PARdiffuse), especially related to wildfire smoke. Climate change‐induced increases to the duration and intensity of fire conditions have made smoke a common occurrence across western North America, with largely unquantified ecosystem feedbacks. Under equivalent amounts of radiation, increased atmospheric particulate matter could lead to a boost in productivity as scattering redistributes photons throughout multilayer canopies. In this work, we leverage a meso‐network of eddy covariance measurement sites across a unique array of managed and restored C3 and C4 canopy types to understand how recent wildfire smoke affected ecosystem productivity during the summer of 2018, an especially smoky year in the agriculturally productive Central Valley. We find that diffuse PARdiffuse increased by more than a third compared to the previous growing season, while total PAR was only slightly diminished. These conditions caused nearly a doubling of light use efficiency over the range of diffuse fraction observed, with the highest sensitivity to diffuse fraction exhibited by corn and alfalfa crops. We utilized an empirical model to assess the trade‐off between enhanced diffuse fraction and reduced total PAR. Under mean radiation conditions, daily integrated gross ecosystem productivity increased by 1.2–4.2% compared to the previous growing season. Finally, we explore the potential negative effect of heightened ozone, a copollutant often associated with wildfire. In addition to the effects of wildfire smoke, the results of this natural experiment can help validate future predictions of aerosol‐productivity feedbacks.
Utilization and Emergency Department Diversion as a Result of Pediatric Psychology Trainees Integrated in Pediatric Primary and Specialty Clinics
Authors: Pereira Lila M. , Wallace Jenna , Brown Whitney , Stancin Terry 
Published: January 2020

Purpose: Integrating behavioral health into primary care (PC) is known to be an effective approach to caring for children with complex health care needs. The purpose of this study was to describe the impact of embedding predoctoral psychology interns (PSY residents) in a continuity care clinic on behavioral health care utilization with additional attention paid to diverting emergency department (ED) visits. Method: Doctoral psychology PSY residents participated as team members in pediatric resident continuity care clinics and also were available to consult with specialty and urgent care clinic providers within the ambulatory center. During a 6-month period, services provided by PSY residents were tracked (numbers of warm-handoffs, behavioral consults [including covisits with pediatric residents], psychotherapy appointments, and crisis evaluations). Results: PSY residents completed 184 warm-handoffs, 250 same-day consults, and 223 follow-up appointments. Sixty-five patients attended group therapy sessions offered in the pediatric clinic. Of 23 patients evaluated for suicidal/homicidal ideation (who previously would have been referred immediately to the ED), 21 were stabilized in PC and only 2 required ED services. Conclusion: Integration of PSY trainees resulted in more than 700 rapid behavioral health services in 6 months, and diverted 91% of mental health crises from ED and other possible psychiatric hospitalization. Prior to integration, none of these services were provided on site. In addition to providing interprofessional team training, integrated continuity care clinics can improve access to behavioral health services and offer significant cost-saving opportunities to health care systems. Ways to promote interdisciplinary training will be identified. Implications for Impact Statement Embedding predoctoral psychology interns in a pediatric continuity care clinic can result in increased access to behavioral health clinicians and division of emergency department visits for high-risk patients. This model also increases opportunities for interdisciplinary training.
Degradation and modification of cochlear gap junction proteins in the early development of age-related hearing loss
Authors: Tajima Shori , Danzaki Keiko , Ikeda Katsuhisa , Kamiya Kazusaku 
Published: January 2020

AbstractAge-related hearing loss (ARHL) is the progressive, bilateral loss of high-frequency hearing in elderly people. Mutations in GJB2, encoding the cochlear gap junction protein connexin26 (Cx26), are the most frequent cause of hereditary deafness; however, a common molecular pathology between ARHL and GJB2-related hearing loss has not been reported. Here, we investigated the quantitative change in expression and molecular pathology of Cx26 in ARHL. We used C57BL/6J mice as a model of ARHL. Hearing levels that were evaluated by auditory brainstem response thresholds increased gradually between 4 and 32 weeks of age and increased sharply at 36 weeks. Gap junctions in the cochleae of 4-week-old mice had linear plaques along cell–cell junction sites. In contrast, the cochleae from 32-week-old mice had significantly shorter gap junctions. Severe hair cell loss was not observed during this period. Based on western blotting, Cx26 and connexin30 (Cx30) levels were significantly decreased at 32 weeks compared with 4 weeks.Moreover, Cx26 was more significantly enriched in the hydrophilic fraction at 4 weeks but was more significantly enriched in the hydrophobic fraction at 32 weeks, indicating an age-related conversion of this biochemical property. Thus, the hydrophobic conversion of Cx26 and disruption of gap junction proteins and plaques may be involved in the pathogenesis of ARHL and may occur before severe hair cell degeneration.
Polycomb-mediated repression of EphrinA5 promotes growth and invasion of glioblastoma
Authors: Ricci Barbara , Millner Thomas O. , Pomella Nicola , Zhang Xinyu , Guglielmi Loredana , Badodi Sara , Ceric Dario , Gemma Carolina , Cognolato Erica , Zhang Ying , Brandner Sebastian , Barnes Michael R. , Marino Silvia 
Published: January 2020

AbstractGlioblastoma (GBM) is the most common and most aggressive intrinsic brain tumour in adults. Integrated transcriptomic and epigenomic analyses of glioblastoma initiating cells (GIC) in a mouse model uncovered a novel epigenetic regulation of EfnA5. In this model, Bmi1 enhances H3K27me3 at theEfnA5locus and reinforces repression of selected target genes in a cellular context-dependent fashion. EfnA5 mediates Bmi1-dependent proliferation and invasion in vitro and tumour formation in an allograft model. Importantly, we show that this novel Polycomb feed-forward loop is also active in human GIC and we provide pre-clinical evidence of druggability of the EFNA5 signalling pathway in GBM xenografts overexpressing Bmi1.
Diversity and metabolism of Woeseiales bacteria, global members of marine sediment communities
Authors: Hoffmann Katy , Bienhold Christina , Buttigieg Pier Luigi , Knittel Katrin , Laso-Pérez Rafael , Rapp Josephine Z , Boetius Antje , Offre Pierre 
Published: January 2020

Abstract
Surveys of 16S rRNA gene sequences derived from marine sediments have indicated that a widely distributed group of Gammaproteobacteria, named “JTB255-Marine Benthic Group” (now the candidate order Woeseiales), accounts for 1–22% of the retrieved sequences. Despite their ubiquity in seafloor communities, little is known about their distribution and specific ecological niches in the deep sea, which constitutes the largest biome globally. Here, we characterized the phylogeny, environmental distribution patterns, abundance, and metabolic potential of Woeseiales bacteria with a focus on representatives from the deep sea. From a phylogenetic analysis of publicly available 16S rRNA gene sequences (≥1400 bp, n = 994), we identified lineages of Woeseiales with greater prevalence in the deep sea than in coastal environments, a pattern corroborated by the distribution of 16S oligotypes recovered from 28 globally distributed sediment samples. Cell counts revealed that Woeseiales bacteria accounted for 5 ± 2% of all microbial cells in deep-sea surface sediments at 23 globally distributed sites. Comparative analyses of a genome, metagenome bins, and single-cell genomes suggested that members of the corresponding clades are likely to grow on proteinaceous matter, potentially derived from detrital cell membranes, cell walls, and other organic remnants in marine sediments.
LncRNA AC093818.1 accelerates gastric cancer metastasis by epigenetically promoting PDK1 expression
Authors: Ba Ming-chen , Ba Zheng , Long Hui , Cui Shu-zhong , Gong Yuan-feng , Yan Zhao-fei , Lin Kun-peng , Wu Yin-bing , Tu Yi-nuo 
Published: January 2020

AbstractGastric cancer (GC) is a highly prevalent type of metastatic tumor. The mechanisms underlying GC metastasis are poorly understood. Some long noncoding RNAs (lncRNAs) reportedly play key roles in regulating metastasis of GC. However, the biological roles of five natural antisense lncRNAs (AC093818.1, CTD-2541M15.1, BC047644, RP11-597M12.1, and RP11-40A13.1) in GC metastasis remain unclear. In this study, the expression of these lncRNAs was measured by quantitative reverse transcription-polymerase chain reaction. Migration and invasion were evaluated by wound-healing and the Transwell assay, respectively. Stable cells were injected into the tail veins of nude mice. Sections of collected lung and liver tissues were stained using hematoxylin and eosin. Protein expression was analyzed by western blot. RNA immunoprecipitation (RIP) assay was used to verify whether the STAT3 and SP1 transcription factors bound to AC093818.1 in GC cells. Expression levels of the five lncRNAs, especially AC093818.1, were significantly upregulated in metastatic GC tissues relative to those in nonmetastatic GC tissues. AC093818.1 expression was correlated with invasion, lymphatic metastasis, distal metastasis, and tumor-node-metastasis stage. AC093818.1 expression was highly sensitive and specific in the diagnosis of metastatic or nonmetastatic GC. AC093818.1 overexpression promoted GC migration and invasion in vitro and in vivo. AC093818.1 overexpression increased PDK1, p-AKT1, and p-mTOR expression levels. AC093818.1 silencing decreased these expressions. AC093818.1 bound to transcription factors STAT3 and SP1, and SP1 or STAT3 silencing could alleviated the effect of AC093818.1 overexpression. The data demonstrate that lncRNA AC093818.1 accelerates gastric cancer metastasis by epigenetically promoting PDK1 expression. LncRNA AC093818.1 may be a potential therapeutic target for metastatic GC.
Lipid desaturation-associated endoplasmic reticulum stress regulates MYCN gene expression in hepatocellular carcinoma cells
Authors: Qin Xian-Yang , Su Ting , Yu Wenkui , Kojima Soichi 
Published: January 2020

AbstractHepatocellular carcinoma (HCC) is the second leading cause of cancer-related deaths worldwide due to its high rate of recurrence, in part because of cancer stem cell (CSC)-dependent “field cancerization”. Recently, we identified that the oncogene v-myc avian myelocytomatosis viral oncogene neuroblastoma derived homolog (MYCN) marked CSC-like subpopulations in heterogeneous HCC and served as a therapeutic target and prognostic marker for HCC. In this study, we explored the molecular basis of upregulated MYCN gene expression in HCC cells. Liquid chromatograph time-of-flight mass spectrometry-based metabolome analysis demonstrated that the content of unsaturated fatty acids was increased in MYCN high expression (MYCNhigh) CSC-like HCC cells. Inhibition of lipid desaturation using either the chemical inhibitor or siRNA/shRNA against stearoyl-CoA desaturase-1 (SCD1) suppressed cell proliferation as well as MYCN gene expression in MYCNhigh HCC cells, grown as both monolayer and spheres. Further mechanistic study using RNA-seq based transcriptome analysis revealed that endoplasmic reticulum (ER) stress related signaling networks such as endocannabinoid cancer inhibition pathway were under the control of SCD1 in MYCNhigh HCC cells. Furthermore, the expression of ER stress-inducible transcription suppressor cyclic AMP-dependent transcription factor (ATF3) was downregulated in MYCNhigh CSC-like HCC cells and CSC-rich spheroids, which was upregulated by inhibition of lipid desaturation or treatment with acyclic retinoid (ACR). Lipid profiling using NMR spectroscopy revealed that the ACR dramatically reduced the content of unsaturated fatty acids in HCC cells. The chemical inducer of ER stress inhibited MYCN gene expression, while the chemical inhibitor of ER stress or knockdown of ATF3 gene expression partially rescued the suppression of MYCN gene expression by ACR in MYCNhigh HCC cells. These data suggested that lipid desaturation-mediated ER stress signaling regulates MYCN gene expression in HCC cells and serves as a promising therapeutic target for the treatment and prevention of HCC.
Human BCL-G regulates secretion of inflammatory chemokines but is dispensable for induction of apoptosis by IFN-γ and TNF-α in intestinal epithelial cells
Authors: Woznicki Jerzy A. , Flood Peter , Bustamante-Garrido Milan , Stamou Panagiota , Moloney Gerry , Fanning Aine , Zulquernain Syed Akbar , McCarthy Jane , Shanahan Fergus , Melgar Silvia , Nally Ken 
Published: January 2020

AbstractProteins of the BCL-2 family are evolutionarily conserved modulators of apoptosis that function as sensors of cellular integrity. Over the past three decades multiple BCL-2 family members have been identified, many of which are now fully incorporated into regulatory networks governing the mitochondrial apoptotic pathway. For some, however, an exact role in cell death signalling remains unclear. One such ‘orphan’ BCL-2 family member is BCL-G (or BCL2L14). In this study we analysed gastrointestinal expression of humanBCL-Gin health and disease states, and investigated its contribution to inflammation-induced tissue damage by exposing intestinal epithelial cells (IEC) to IFN-γ and TNF-α, two pro-inflammatory mediators associated with gut immunopathology. We found that both BCL-G splice variants — BCL-GS(short) and BCL-GL(long) — were highly expressed in healthy gut tissue, and that their mRNA levels decreased in active inflammatory bowel diseases (for BCL-GS) and colorectal cancer (for BCL-GS/L). In vitro studies revealed that IFN-γ and TNF-α synergised to upregulate BCL-GS/Land to trigger apoptosis in colonic epithelial cell lines and primary human colonic organoids. Using RNAi, we showed that synergistic induction of IEC death was STAT1-dependent while optimal expression of BCL-GS/Lrequired STAT1, NF-κB/p65 and SWI/SNF-associated chromatin remodellers BRM and BRG1. To test the direct contribution of BCL-G to the effects of IFN-γ and TNF-α on epithelial cells, we used RNAi- and CRISPR/Cas9-based perturbations in parallel with isoform-specific overexpression of BCL-G, and found that BCL-G was dispensable for Th1 cytokine-induced apoptosis of human IEC. Instead, we discovered that depletion of BCL-G differentially affected secretion of inflammatory chemokines CCL5 and CCL20, thus uncovering a non-apoptotic immunoregulatory function of this BCL-2 family member. Taken together, our data indicate that BCL-G may be involved in shaping immune responses in the human gut in health and disease states through regulation of chemokine secretion rather than intestinal apoptosis.
SETD2 mutation in renal clear cell carcinoma suppress autophagy via regulation of ATG12
Authors: González-Rodríguez Patricia , Engskog-Vlachos Pinelopi , Zhang Hanzhao , Murgoci Adriana-Natalia , Zerdes Ioannis , Joseph Bertrand 
Published: January 2020

AbstractInactivating mutations in the SETD2 gene, encoding for a nonredundant histone H3 methyltransferase and regulator of transcription, is a frequent molecular feature in clear cell renal cell carcinomas (ccRCC). SETD2 deficiency is associated with recurrence of ccRCC and bears low prognostic values. Targeting autophagy, a conserved catabolic process with critical functions in maintenance of cellular homeostasis and cell conservation under stress condition, is emerging as a potential therapeutic strategy to combat ccRCC. Epigenetics-based pathways are now appreciated as key components in the regulation of autophagy. However, whether loss of function in the SETD2 histone modifying enzyme occurring in ccRCC cells may impact on their ability to undergo autophagy remained to be explored. Here, we report that SETD2 deficiency in RCC cells is associated with the aberrant accumulation of both free ATG12 and of an additional ATG12-containing complex, distinct from the ATG5–ATG12 complex. Rescue of SETD2 functions in the SETD2 deficiency in RCC cells, or reduction of SETD2 expression level in RCC cells wild type for this enzyme, demonstrates that SETD2 deficiency in RCC is directly involved in the acquisition of these alterations in the autophagic process. Furthermore, we revealed that deficiency in SETD2, known regulator of alternative splicing, is associated with increased expression of a short ATG12 spliced isoform at the depend of the canonical long ATG12 isoform in RCC cells. The defect in the ATG12-dependent conjugation system was found to be associated with a decrease autophagic flux, in accord with the role for this ubiquitin-like protein conjugation system in autophagosome formation and expansion. Finally, we report that SETD2 and ATG12 gene expression levels are associated with favorable respective unfavorable prognosis in ccRCC patients. Collectively, our findings bring further argument for considering the SETD2 gene status of ccRCC tumors, when therapeutic interventions, such as targeting the autophagic process, are considered to combat these kidney cancers.