bluuebunny/crossref_metadata_2025_split huggingface dataset:
Impact of reduced rates of 2,4-D and glyphosate on sweetpotato growth and yield
Authors: Batts Thomas M. , Miller Donnie K. , Griffin James L. , Villordon Arthur O. , Stephenson Daniel O. , Jennings Kathrine M. , Chaudhari Sushila , Blouin David C. , Copes Josh T. , Smith Tara P. 
Published: June 2020

AbstractCommercialization of 2,4-D–tolerant crops is a major concern for sweetpotato producers because of potential 2,4-D drift that can cause severe crop injury and yield reduction. A field study was initiated in 2014 and repeated in 2015 to assess impacts of reduced rates of 2,4-D, glyphosate, or a combination of 2,4-D with glyphosate on sweetpotato. In one study, 2,4-D and glyphosate were applied alone and in combination at 1/10, 1/100, 1/250, 1/500, 1/750, and 1/1,000 of anticipated field use rates (1.05 kg ha−1 for 2,4-D and 1.12 kg ha−1 for glyphosate) to ‘Beauregard’ sweetpotato at storage root formation (10 days after transplanting [DAP]). In a separate study, all these treatments were applied to ‘Beauregard’ sweetpotato at storage root development (30 DAP). Injury with 2,4-D alone or in combination with glyphosate was generally equal or greater than with glyphosate applied alone at equivalent herbicide rates, indicating that injury is attributable mostly to 2,4-D in the combination. There was a quadratic increase in crop injury and quadratic decrease in crop yield (with respect to most yield grades) with increased rate of 2,4-D applied alone or in combination with glyphosate applied at storage root development. However, neither the results of this relationship nor of the significance of herbicide rate were observed on crop injury or sweetpotato yield when herbicide application occurred at storage root formation, with a few exceptions. In general, crop injury and yield reduction were greatest at the highest rate (1/10×) of 2,4-D applied alone or in combination with glyphosate, although injury observed at lower rates was also a concern after initial observation by sweetpotato producers. However, in some cases, yield reduction of U.S. no.1 and marketable grades was also observed after application of 1/250×, 1/100×, or 1/10× rates of 2,4-D alone or with glyphosate when applied at storage root development.
Detection of grassy weeds in bermudagrass with deep convolutional neural networks
Authors: Yu Jialin , Schumann Arnold W. , Sharpe Shaun M. , Li Xuehan , Boyd Nathan S. 
Published: June 2020

AbstractSpot spraying POST herbicides is an effective approach to reduce herbicide input and weed control cost. Machine vision detection of grass or grass-like weeds in turfgrass systems is a challenging task due to the similarity in plant morphology. In this work, we explored the feasibility of using image classification with deep convolutional neural networks (DCNN), including AlexNet, GoogLeNet, and VGGNet, for detection of crabgrass species (Digitaria spp.), doveweed [Murdannia nudiflora (L.) Brenan], dallisgrass (Paspalum dilatatum Poir.), and tropical signalgrass [Urochloa distachya (L.) T.Q. Nguyen] in bermudagrass [Cynodon dactylon (L.) Pers.]. VGGNet generally outperformed AlexNet and GoogLeNet in detecting selected grassy weeds. For detection of P. dilatatum, VGGNet achieved high F1 scores (≥0.97) and recall values (≥0.99). A single VGGNet model exhibited high F1 scores (≥0.93) and recall values (1.00) that reliably detected Digitaria spp., M. nudiflora, P. dilatatum, and U. distachya. Low weed density reduced the recall values of AlexNet at detecting all weed species and GoogLeNet at detecting Digitaria spp. In comparison, VGGNet achieved excellent performances (overall accuracy = 1.00) at detecting all weed species in both high and low weed-density scenarios. These results demonstrate the feasibility of using DCNN for detection of grass or grass-like weeds in turfgrass systems.
Potential Predictability of Net Primary Production in the Ocean
Authors: Krumhardt K. M. , Lovenduski N. S. , Long M. C. , Luo J. Y. , Lindsay K. , Yeager S. , Harrison C. 
Published: June 2020

Interannual variations in marine net primary production (NPP) contribute to the variability of available living marine resources, as well as influence critical carbon cycle processes. Here we provide a global overview of near‐term (1 to 10 years) potential predictability of marine NPP using a novel set of initialized retrospective decadal forecasts from an Earth System Model. Interannual variations in marine NPP are potentially predictable in many areas of the ocean 1 to 3 years in advance, from temperate waters to the tropics, showing a substantial improvement over a simple persistence forecast. However, some regions, such as the subpolar Southern Ocean, show low potential predictability. We analyze how bottom‐up drivers of marine NPP (nutrients, light, and temperature) contribute to its predictability. Regions where NPP is primarily driven by the physical supply of nutrients (e.g., subtropics) retain higher potential predictability than high‐latitude regions where NPP is controlled by light and/or temperature (e.g., the Southern Ocean). We further examine NPP predictability in the world's Large Marine Ecosystems. With a few exceptions, we show that initialized forecasts improve potential predictability of NPP in Large Marine Ecosystems over a persistence forecast and may aid to manage living marine resources.
Deoxycholic acid modulates the progression of gallbladder cancer through N6-methyladenosine-dependent microRNA maturation
Authors: Lin Ruirong , Zhan Ming , Yang Linhua , Wang Hui , Shen Hui , Huang Shuai , Huang Xince , Xu Sunwang , Zhang Zijie , Li Weijian , Liu Qiang , Shi Yongsheng , Chen Wei , Yu Jianxiu , Wang Jian 
Published: June 2020

AbstractBile acids (BAs), well-defined signaling molecules with diverse metabolic functions, play important roles in cellular processes associated with many cancers. As one of the most common BAs, deoxycholic acid (DCA) is originally synthesized in the liver, stored in the gallbladder, and processed in the gut. DCA plays crucial roles in various tumors; however, functions and molecular mechanisms of DCA in gallbladder cancer (GBC) still remain poorly characterized. Here, we analyzed human GBC samples and found that DCA was significantly downregulated in GBC, and reduced levels of DCA was associated with poor clinical outcome in patients with GBC. DCA treatment impeded tumor progression by halting cell proliferation. DCA decreased miR-92b-3p expression in an m6A-dependent posttranscriptional modification manner by facilitating dissociation of METTL3 from METTL3–METTL14–WTAP complex, which increased the protein level of the phosphatase and tensin homolog, a newly identified target of miR-92b-3p, and subsequently inactivated the PI3K/AKT signaling pathway. Our findings revealed that DCA might function as a tumor suppressive factor in GBC at least by interfering with miR-92b-3p maturation, and suggested that DCA treatment could provide a new therapeutic strategy for GBC.
Coexistence of genetically different Rhizophagus irregularis isolates induces genes involved in a putative fungal mating response
Authors: Mateus Ivan D , Rojas Edward C , Savary Romain , Dupuis Cindy , Masclaux Frédéric G , Aletti Consolée , Sanders Ian R 
Published: June 2020

Abstract
Arbuscular mycorrhizal fungi (AMF) are of great ecological importance because of their effects on plant growth. Closely related genotypes of the same AMF species coexist in plant roots. However, almost nothing is known about the molecular interactions occurring during such coexistence. We compared in planta AMF gene transcription in single and coinoculation treatments with two genetically different isolates of Rhizophagus irregularis in symbiosis independently on three genetically different cassava genotypes. Remarkably few genes were specifically upregulated when the two fungi coexisted. Strikingly, almost all of the genes with an identifiable putative function were known to be involved in mating in other fungal species. Several genes were consistent across host plant genotypes but more upregulated genes involved in putative mating were observed in host genotype (COL2215) compared with the two other host genotypes. The AMF genes that we observed to be specifically upregulated during coexistence were either involved in the mating pheromone response, in meiosis, sexual sporulation or were homologs of MAT-locus genes known in other fungal species. We did not observe the upregulation of the expected homeodomain genes contained in a putative AMF MAT-locus, but observed upregulation of HMG-box genes similar to those known to be involved in mating in Mucoromycotina species. Finally, we demonstrated that coexistence between the two fungal genotypes in the coinoculation treatments explained the number of putative mating response genes activated in the different plant host genotypes. This study demonstrates experimentally the activation of genes involved in a putative mating response and represents an important step towards the understanding of coexistence and sexual reproduction in these important plant symbionts.
Division of functional roles for termite gut protists revealed by single-cell transcriptomes
Authors: Nishimura Yuki , Otagiri Masato , Yuki Masahiro , Shimizu Michiru , Inoue Jun-ichi , Moriya Shigeharu , Ohkuma Moriya 
Published: June 2020

Abstract
The microbiome in the hindgut of wood-feeding termites comprises various species of bacteria, archaea, and protists. This gut community is indispensable for the termite, which thrives solely on recalcitrant and nitrogen-poor wood. However, the difficulty in culturing these microorganisms has hindered our understanding of the function of each species in the gut. Although protists predominate in the termite gut microbiome and play a major role in wood digestion, very few culture-independent studies have explored the contribution of each species to digestion. Here, we report single-cell transcriptomes of four protists species comprising the protist population in worldwide pest Coptotermes formosanus. Comparative transcriptomic analysis revealed that the expression patterns of the genes involved in wood digestion were different among species, reinforcing their division of roles in wood degradation. Transcriptomes, together with enzyme assays, also suggested that one of the protists, Cononympha leidyi, actively degrades chitin and assimilates it into amino acids. We propose that C. leidyi contributes to nitrogen recycling and inhibiting infection from entomopathogenic fungi through chitin degradation. Two of the genes for chitin degradation were further revealed to be acquired via lateral gene transfer (LGT) implying the importance of LGT in the evolution of symbiosis. Our single-cell-based approach successfully characterized the function of each protist in termite hindgut and explained why the gut community includes multiple species.
Expansion of myeloid-derived suppressor cells in patients with severe coronavirus disease (COVID-19)
Authors: Agrati Chiara , Sacchi Alessandra , Bordoni Veronica , Cimini Eleonora , Notari Stefania , Grassi Germana , Casetti Rita , Tartaglia Eleonora , Lalle Eleonora , D’Abramo Alessandra , Castilletti Concetta , Marchioni Luisa , Shi Yufang , Mariano Andrea , Song Jin-Wen , Zhang Ji-Yuan , Wang Fu-Sheng , Zhang Chao , Fimia Gian Maria , Capobianchi Maria R. , Piacentini Mauro , Antinori Andrea , Nicastri Emanuele , Maeurer Markus , Zumla Alimuddin , Ippolito Giuseppe 
Published: June 2020

AbstractSARS-CoV-2 is associated with a 3.4% mortality rate in patients with severe disease. The pathogenesis of severe cases remains unknown. We performed an in-depth prospective analysis of immune and inflammation markers in two patients with severe COVID-19 disease from presentation to convalescence. Peripheral blood from 18 SARS-CoV-2-infected patients, 9 with severe and 9 with mild COVID-19 disease, was obtained at admission and analyzed for T-cell activation profile, myeloid-derived suppressor cells (MDSCs) and cytokine profiles. MDSC functionality was tested in vitro. In four severe and in four mild patients, a longitudinal analysis was performed daily from the day of admission to the early convalescent phase. Early after admission severe patients showed neutrophilia, lymphopenia, increase in effector T cells, a persisting higher expression of CD95 on T cells, higher serum concentration of IL-6 and TGF-β, and a cytotoxic profile of NK and T cells compared with mild patients, suggesting a highly engaged immune response. Massive expansion of MDSCs was observed, up to 90% of total circulating mononuclear cells in patients with severe disease, and up to 25% in the patients with mild disease; the frequency decreasing with recovery. MDSCs suppressed T-cell functions, dampening excessive immune response. MDSCs decline at convalescent phase was associated to a reduction in TGF-β and to an increase of inflammatory cytokines in plasma samples. Substantial expansion of suppressor cells is seen in patients with severe COVID-19. Further studies are required to define their roles in reducing the excessive activation/inflammation, protection, influencing disease progression, potential to serve as biomarkers of disease severity, and new targets for immune and host-directed therapeutic approaches.
Glucocorticoids can induce BIM to trigger apoptosis in the absence of BAX and BAK1
Authors: Dong Li , Vaux David L. 
Published: June 2020

AbstractCells from two murine lymphoid lines died 24–48 h after treatment with the glucocorticoid dexamethasone. Deletion ofBaxandBak1prevented rapid apoptosis, but treatment with dexamethasone for greater 6 days still led to cell death that was characterized by release of cytochrome c into the cytosol, activation of caspases, and loss of cell membrane integrity. In WEHI7 thymoma cells, this did not occur whenBcl2l11(Bim)was deleted in addition toBaxandBak1. When these triple mutant lines were exposed to dexamethasone for 10 days, they arrested, but after dexamethasone was removed, they had 10-fold higher clone forming efficiency thanBax/Bak1double knock-out cells. Although induced over-expression of BIMs alone was not sufficient to induce the death ofBax−/−Bak1−/−Bim−/−cells, they did die when BIMs was induced in the presence of dexamethasone. These results suggest that dexamethasone induces production of BIM together with other, as yet unidentified proteins, that cause release of cytochrome c and apoptosis in the absence of BAX and BAK1.
Circ-MMP2 (circ-0039411) induced by FOXM1 promotes the proliferation and migration of lung adenocarcinoma cells in vitro and in vivo
Authors: Lv Xin , Huang Hongping , Feng Hui , Wei Zhonghua 
Published: June 2020

AbstractNumerous reports have stated the significance of cellular events such as proliferation, migration and EMT (epithelial-mesenchymal transition) for cancer development, but the related molecular mechanism remains elusive. FOXM1 (forkhead box transcription M1) is a nuclear co-activator participating in lung adenocarcinoma (LUAD). Thus, this study tried to explain the function of FOXM1 and its downstream molecular mechanism in LUAD. We uncovered FOXM1 upregulation in LUAD and demonstrated that FOXM1 facilitated β-catenin nuclear translocation to activate the transcription of downstream genes. Moreover, we discovered that FOXM1 transcriptionally activated circ0039411 which derived from matrix metallopeptidase 2 (MMP2) (also named as circ-MMP2), while MMP2 is a known downstream target of β-catenin. As for functional investigation, knockdown of circ-0039411 suppressed the proliferation, migration and EMT in LUAD cells and also hindered in vivo growth and metastasis of LUAD tumor. Mechanistically, circ-0039411 enhanced the stability of FOXM1 mRNA by recruiting IGF2BP3 (insulin like growth factor 2 mRNA binding protein 3), thus forming a positive feedback loop. In conclusion, this study revealed that FOXM1-induced circ-MMP2 (circ-0039411) contributes to malignant behaviors of LUAD cells via relying on FOXM1, potentially infusing inspirations for the search of new molecular targets for LUAD treatment.
NMMHC IIA triggers neuronal autophagic cell death by promoting F-actin-dependent ATG9A trafficking in cerebral ischemia/reperfusion
Authors: Wang Guangyun , Wang Tiezheng , Hu Yang , Wang Jieman , Wang Yan , Zhang Yuanyuan , Li Fang , Liu Wentao , Sun Yang , Yu Boyang , Kou Junping 
Published: June 2020

AbstractPrevious findings have shown that non-muscle myosin heavy-chain IIA (NMMHC IIA) is involved in autophagy induction triggered by starvation in D. melanogaster; however, its functional contribution to neuronal autophagy remains unclear. The aim of this study is to explore the function of NMMHC IIA in cerebral ischemia-induced neuronal autophagy and the underlying mechanism related to autophagy-related gene 9A (ATG9A) trafficking. Functional assays and molecular mechanism studies were used to investigate the role of NMMHC IIA in cerebral ischemia-induced neuronal autophagy in vivo and in vitro. A middle cerebral artery occlusion (MCAO) model in mice was used to evaluate the therapeutic effect of blebbistatin, a myosin II ATPase inhibitor. Herein, either depletion or knockdown of NMMHC IIA led to increased cell viability in both primary cultured cortical neurons and pheochromocytoma (PC12) cells exposed to oxygen–glucose deprivation/reoxygenation (OGD/R). In addition, NMMHC IIA and autophagic marker LC3B were upregulated by OGD/R, and inhibition of NMMHC IIA significantly reduced OGD-induced neuronal autophagy. Furthermore, NMMHC IIA-induced autophagy is through its interactions with F-actin and ATG9A in response to OGD/R. The NMMHC IIA–actin interaction contributes to ATG9A trafficking and autophagosome formation. Inhibition of the NMMHC IIA–actin interaction using blebbistatin and the F-actin polymerization inhibitor cytochalasin D significantly suppressed ATG9A trafficking and autophagy induction. Furthermore, blebbistatin significantly improved neurological deficits and infarct volume after ischemic attack in mice, accompanied by ATG9A trafficking and autophagy inhibition. These findings demonstrate neuroprotective effects of NMMHC IIA inhibition on regulating ATG9A trafficking-dependent autophagy activation in the context of cerebral ischemia/reperfusion.
Phosphorylation of eukaryotic initiation factor-2α (eIF2α) in autophagy
Authors: Humeau Juliette , Leduc Marion , Cerrato Giulia , Loos Friedemann , Kepp Oliver , Kroemer Guido 
Published: June 2020

AbstractThe integrated stress response is characterized by the phosphorylation of eukaryotic initiation factor-2α (eIF2α) on serine 51 by one out of four specific kinases (EIF2AK1 to 4). Here we provide three series of evidence suggesting that macroautophagy (to which we refer to as autophagy) induced by a variety of distinct pharmacological agents generally requires this phosphorylation event. First, the induction of autophagic puncta by various distinct compounds was accompanied by eIF2α phosphorylation on serine 51. Second, the modulation of autophagy by >30 chemically unrelated agents was partially inhibited in cells expressing a non-phosphorylable (S51A) mutant of eIF2α or lacking all four eIF2α kinases, although distinct kinases were involved in the response to different autophagy inducers. Third, inhibition of eIF2α phosphatases was sufficient to stimulate autophagy. In synthesis, it appears that eIF2α phosphorylation is a central event for the stimulation of autophagy.
LncRNA ANRIL acts as a modular scaffold of WDR5 and HDAC3 complexes and promotes alteration of the vascular smooth muscle cell phenotype
Authors: Zhang Chengxin , Ge Shangqing , Gong Wenhui , Xu Jinguo , Guo Zhixiang , Liu Zhuang , Gao Xiaotian , Wei Xiaoyong , Ge Shenglin 
Published: June 2020

AbstractMany studies have shown that long-noncoding RNA (lncRNA) is associated with cardiovascular disease, but its molecular mechanism is still unclear. In this study, we explored the role of lncRNA ANRIL in ox-LDL-induced phenotypic transition of human aortic smooth muscle cells (HASMC). The results of quantitative fluorescence PCR showed that the expression of ANRIL in patients with coronary atherosclerotic heart disease (CAD) was significantly higher than that in normal subjects. RNA-FISH detection showed that the ANRIL expression increased in HASMC treated by ox-LDL. Ox-LDL could upregulate the expression of ANRIL and ROS and promote the phenotypic transition of HASMC. After downregulation of ANRIL by siRNA, ROS level decreased and HASMC phenotypic transition alleviated. ANRIL could act as a molecular scaffold to promote the binding of WDR5 and HDAC3 to form WDR5 and HDAC3 complexes, they regulated target genes such as NOX1 expression by histone modification, upregulated ROS level and promote HASMC phenotype transition. Therefore, we found a new epigenetic regulatory mechanism for phenotype transition of VSMC, ANRIL was a treatment target of occlusive vascular diseases.
MCL1 inhibitors S63845/MIK665 plus Navitoclax synergistically kill difficult-to-treat melanoma cells
Authors: Mukherjee Nabanita , Skees Jenette , Todd Kaleb J. , West Drake A. , Lambert Karoline A. , Robinson William A. , Amato Carol M. , Couts Kasey L. , Van Gulick Robert , MacBeth Morgan , Nassar Kelsey , Tan Aik-Choon , Zhai Zili , Fujita Mayumi , Bagby Stacey M. , Dart Chiara R. , Lambert James R. , Norris David A. , Shellman Yiqun G. 
Published: June 2020

AbstractCurrent treatment for patients with metastatic melanoma include molecular-targeted therapies and immune checkpoint inhibitors. However, a subset of melanomas are difficult-to-treat. These melanomas include those without the genetic markers for targeted therapy, non-responsive to immunotherapy, and those who have relapsed or exhausted their therapeutic options. Therefore, it is necessary to understand and explore other biological processes that may provide new therapeutic approaches. One of most appealing is targeting the apoptotic/anti-apoptotic system that is effective against leukemia. We used genetic knockdown and pharmacologic approaches of BH3 mimetics to target anti-apoptotic BCL2 family members and identified MCL1 and BCLXL as crucial pro-survival members in melanoma. We then examined the effects of combining BH3 mimetics to target MCL1 and BCLXL in vitro and in vivo. These include clinical-trial-ready compounds such as ABT-263 (Navitoclax) and S63845/S64315 (MIK655). We used cell lines derived from patients with difficult-to-treat melanomas. In vitro, the combined inhibition of MCL1 and BCLXL resulted in significantly effective cell killing compared to single-agent treatment (p < 0.05) in multiple assays, including sphere assays. The combination-induced cell death was independent of BIM, and NOXA. Recapitulated in our mouse xenograft model, the combination inhibited tumor growth, reduced sphere-forming capacity (p < 0.01 and 0.05, respectively), and had tolerable toxicity (p > 0.40). Taken together, this study suggests that dual targeting of MCL1 and BCLXL should be considered as a treatment option for difficult-to-treat melanoma patients.