bluuebunny/crossref_metadata_2025_split huggingface dataset:
Controlling water hyacinth infestation in Lake Tana using Fungal pathogen from Laboratory level upto pilot scale
Authors: Admas Adugnaw , Sahile Samuel , Agidie Aklilu , Menale Hailu , Gedefaw Tadelo , Teshome Menberu 
Published: January 2020

ABSTRACTWater hyacinth (Eichhornia crassipes) is one of the most dangerous aquatic weeds for Lake Tana and other water body in Ethiopia. To reduce its invasion biological, chemical and physical control methods can be used. Use of natural biological enemies of the weed to discourage its propagation is one of the best recommended options by scientfic society. Among them, there are more fungi naturally a pathogen for water hyacinth and other plants. To use those patogenes to manage water hyacinth infestation in Lake Tana infected plant material by fungi were collected from three weredas (Amba Gyorgese, Dabat and Debarke) around Gondar at 20 Peasant associations (PAs) since Novmber 2015. The collection was done from infected Faba bean leaves and roots. All isolated fungus was attempted to infect the collected healthy water hyacinth in laboratory and green house. Among isolated fungus species Rhizoctonia solani, Aspergillus flatus, Tricothcium roseum, Fusarium spp and Aspergillus niger fungi show high moderate disease severity on the healthy water hyacinth at temporarey green house and laboratory. Disease severity scale was recorded using modified NAHEMA et al. (200). By following those experiments to show its efficiency, the effective pathogens on laboratory and green house were released to 16 m2 open ponds since September 2016, in University of Gondar. In this study, we have recorded scientific data that shows the fungi were high potencial to attack healthy water hyacinth at above 26 oc and at less than 25 % humidity. From this research also we have observed the most infected water hyacinth by fungi have not produced flower and it can not re generate by seed in the next propagation sesaon.Finally, before directly release the fungi on Lake Tana its impacts were studied in the Goregora, at Kuame Michel kebela for a year in open ponds and in controlled wet land areas that not linked to the Lake by taking some common aquatic plants and fish from the Lake. Fortunatelly, those fungi have not impact on aquatic plant like Echinochloa and Cyperus papyrus grass, water quality and fish.
Dispersal limitation and fire feedbacks maintain mesic savannas in Madagascar
Authors: Goel Nikunj , Van Vleck Erik , Aleman Julie C. , Staver A. Carla 
Published: January 2020

AbstractMadagascar is regarded by some as one of the most degraded landscapes on Earth, with estimates suggesting that 90% of forests have been lost to indigenous Tavy farming. However, the extent of this degradation has been challenged: paleoecological data, phylogeographic analysis, and species diversity maps indicate that pyrogenic savannas in Central Madagascar pre-date human arrival, even though rainfall is sufficient to allow forest expansion into Central Madagascar. These observations raise a question—if savannas in Madagascar are not anthropogenic, how then are they maintained in regions where the climate can support forest? Observation reveals that the savanna-forest boundary coincides with a dispersal barrier—the escarpment of the Central Plateau. Using a stepping-stone model, we show that in a limited dispersal landscape, a stable savanna-forest boundary can form due to fire-vegetation feedbacks. This novel phenomenon, referred to as range pinning, could explain why eastern lowland forests have not expanded into the mesic savannas of the Central Highlands. This work challenges the view that highland savannas in Madagascar are derived by human-lit fires and, more importantly, suggests that partial dispersal barriers and strong non-linear feedbacks can pin biogeographical boundaries over a wide range of environmental conditions, providing a temporary buffer against climate change.
Chemical constituents involved in e-cigarette, or vaping product use-associated lung injury (EVALI)
Authors: Muthumalage Thivanka , Friedman Michelle R. , McGraw Matthew D. , Friedman Alan E. , Rahman Irfan 
Published: January 2020

AbstractBackgroundThe Centers for Disease Control (CDC) declared e-cigarette (e-cig), or vaping product use-associated lung injury (EVALI) a national outbreak due to the high incidence of emergency department admissions and deaths. Investigators have identified vitamin E acetate (VEA) as the plausible cause for EVALI, based on compounds found in bronchoalveolar lavage fluid.ObjectivesWe defined the chemical constituents present in e-cig cartridges associated with EVALI and compared constituents to medical-grade and cannabidiol (CBD) containing cartridges.MethodsWe measured chemicals and elemental metals in e-liquid and vapor phases of e-cig counterfeit cartridges by Gas Chromatography (GC) and Mass Spectrometry (MS), EPA method TO-15 by GCMS, and ICP-MS analysis.ResultsWe have identified chemical constituents in e-cig vaping tetrahydrocannabinol (THC)-containing counterfeit cartridges compared to medical-grade and cannabidiol (CBD) containing cartridges. Apart from VEA and THC, other potential toxicants correlated with EVALI included solvent-derived hydrocarbons, silicon conjugated compounds, various terpenes, pesticides/plasticizers/polycaprolactones, and metals. These chemicals are known to cause symptoms, such as cough, shortness of breath or chest pain, nausea, vomiting or diarrhea, fatigue, fever, or weight loss, all symptoms presenting in patients with EVALI.ConclusionThis study provides insights into understanding the chemical-induced disease mechanism of acute lung injury.
Should I shrink or should I flow? – body size adjustment to thermo-oxygenic niche
Authors: Walczyńska Aleksandra , Gudowska Agnieszka , Sobczyk Łukasz 
Published: January 2020

AbstractOrganisms adjust their size according to temperature and supposedly also respond to its negative covariate, oxygen. To what extent is size a response to temperature or oxygen? We analyzed the thermo-oxygenic niche for the community of 188 rotifer species. Evolution toward ranges of thermal tolerance occurred separately from evolution toward their optima. Body size was adjusted to both temperature and oxygen, but the cues for body size response differed; size was either driven by optimal temperatures or by the oxygen tolerance range. Animals are clearly separated into generalists or specialists, and their evolutionary body size adjustment is realized through differential responses to environmental factors. Oxygen is as important as temperature in the evolution of body size and ecological niche preference. An important conclusion from this study is that oxygen deprivation following global warming seems to be as problematic for the studied organisms as the temperature increase itself.
Quantifying Epithelial Plasticity as a Platform to Reverse Epithelial Injury
Authors: Nishida Kristine , Ghosh Baishakhi , Chandrala Lakshmana , Mahmud Saborny , Chen Si , Khosla Atulya Aman , Katz Joseph , Sidhaye Venkataramana K. 
Published: January 2020

AbstractEpithelial surfaces lining the lung serve as the primary environmental gaseous interface, and are subject to common life-limiting diseases, including COPD (Chronic Obstructive Pulmonary Disease). Despite the critical role of epithelial cells in pulmonary health and disease, quantitative models are lacking but are required given the large patient to patient variability to characterize the epithelial plasticity that follows injury. We have identified a series of assessments to quantitatively identify the changes that occur in the epithelium and to identify targets that reverse injury. The injured epithelium has decreased ciliary function and monolayer height, which in the case of cells derived from COPD patients results in an overall disorganization of structure. Injury causes the cells to shift to an unjammed state, with corresponding increases in the velocity correlation length implicating cell shape and stiffness as fundamental to the injury response. Specific inhibitors of actin polymerization (LatA), of MAPK/ERK kinase (U0126) and Nrf-2 pathway activation (CDDO-Me) push the epithelium back towards a jammed state with decreased cell movement and correlation length, as well as improve barrier function and CBF. These studies attest to cell intrinsic properties that allow for a transition to an unjammed state, and that quantitative phenotypic analysis can identify potential specific pharmacologic targets in a given patient and provide insight into basic mechanisms of cellular damage.One Sentence SummaryEnvironmental toxins undermine tissue integrity by manipulating transitions from jammed to unjammed states, thereby mimicking or inducing disease.
Distinct components of photoperiodic light are differentially encoded by the mammalian circadian clock
Authors: Tackenberg Michael C. , Hughey Jacob J. , McMahon Douglas G. 
Published: January 2020

ABSTRACTSeasonal light cycles influence multiple physiological functions and are mediated through photoperiodic encoding by the circadian system. Despite our knowledge of the strong connection between seasonal light input and downstream circadian changes, less is known about the specific components of seasonal light cycles that are encoded and induce persistent changes in the circadian system. Using combinations of three T cycles (23, 24, 26 hr.) and two photoperiods per T cycle (Long and Short, with duty cycles scaled to each T cycle), we investigate after-effects of entrainment to these six light cycles. We measure locomotor behavior duration (α), period (τ), and entrained phase angle (Ψ)in vivo, and SCN phase distribution (σϕ), τ, and Ψex vivoin order to refine our understanding of critical light components for influencing particular circadian properties. We find that photoperiod and T cycle length both drive determination ofin vivoΨ but differentially influence after-effects in α and τ, with photoperiod driving changes in α and photoperiod length and T cycle length combining to influence τ. Using skeleton photoperiods, we demonstrate thatin vivoΨ is determined by both parametric and non-parametric components, while changes in α are driven non-parametrically. Within theex vivoSCN, we find that Ψ and σϕof the PER2∷LUCIFERASE rhythm follow closely with their likely behavioral counterparts (Ψ and α of the locomotor activity rhythm), while also confirming previous reports of τ after-effects of gene expression rhythms showing negative correlations with behavioral τ after-effects in response to T cycles. We demonstrate that within-SCN σϕchanges, thought to underly α changesin vivo, are induced primarily non-parametrically. Taken together, our results demonstrate distinct components of seasonal light input differentially influence Ψ, α, and τ, and suggest the possibility of separate mechanisms driving the persistent changes in circadian behaviors mediated by seasonal light.
25-Hydroxycholesterol amplifies microglial IL-1β production in an apoE isoform-dependent manner
Authors: Wong Man Ying , Lewis Michael , Doherty James J. , Shi Yang , Sullivan Patrick M. , Qian Mingxing , Covey Douglas F. , Petsko Gregory A. , Holtzman David M. , Paul Steven M. , Luo Wenjie 
Published: January 2020

AbstractGenome-wide association studies associated with Alzheimer’s disease (AD) have implicated pathways related to both lipid homeostasis and innate immunity in the pathophysiology of AD. However, the exact cellular and chemical mediators of neuroinflammation in AD remain poorly understood. The oxysterol 25-hydroxycholesterol (25-HC) is an important immunomodulator produced by peripheral macrophages with wide-ranging effects on cell signaling and innate immunity. Genetic variants of the enzyme responsible for 25-HC production, cholesterol 25-hydroxylase (CH25H), have been found to be associated with AD. In the present study, we found that the CH25H expression is upregulated in human AD brain tissue and in transgenic mouse brain tissue bearing amyloid-β (Aβ) plaques or tau pathology. Treatment with the toll-like receptor 4 (TLR4) agonist lipopolysaccharide (LPS) markedly upregulates CH25H expression in the mouse brainin vivo. LPS also stimulates CH25H expression and 25-HC secretion in cultured mouse primary microglia. We also found that LPS-induced microglial production of the pro-inflammatory cytokine IL1β is markedly potentiated by 25-HC and attenuated by genetic deletion of CH25H. Microglia expressing apolipoprotein E4 (apoE4), a genetic risk factor for AD, produce greater amounts of 25-HC than apoE3-expressing microglia following treatment with LPS. Remarkably, treatment of microglia with 25-HC results in a much greater level of IL1β secretion in LPS-activated apoE4-expressing microglia than in apoE2- or apoE3-expressing microglia. Blocking potassium efflux or inhibiting caspase-1 prevents 25-HC-potentiated IL1β release in apoE4-expressing microglia, indicating the involvement of caspase-1/NLRP3 inflammasome activity. 25-HC may function as a microglial secreted inflammatory mediator in brain, promoting IL1β-mediated neuroinflammation in an apoE isoform-dependent manner (E4≫E2/E3) and thus may be an important mediator of neuroinflammation in AD.
Sex differences in cardiometabolic traits at four life stages: cohort study with repeated metabolomics
Authors: Bell Joshua A. , Santos Ferreira Diana L. , Fraser Abigail , Soares Ana Luiza G. , Howe Laura D. , Lawlor Deborah A. , Carslake David , Smith George Davey , O’Keeffe Linda M. 
Published: January 2020

AbstractBackgroundMales experience higher rates of coronary heart disease (CHD) than females, but the circulating traits underpinning this difference are poorly understood. We examined sex differences in detailed cardiometabolic traits measured at four life stages, spanning childhood to middle adulthood.Methods and ResultsData were from the Avon Longitudinal Study of Parents and Children cohort study. 229 traits quantified from targeted metabolomics (nuclear magnetic resonance spectroscopy) including lipoprotein subclass-specific cholesterol and triglycerides, amino acids, glucose, and inflammatory glycoprotein acetyls were measured repeatedly in offspring (Generation 1 (G1)) born in 1991-92 and once in their parents (Generation 0 (G0)). Measurements in G1 were once in childhood (mean age 8y), twice in adolescence (16y and 18y) and once in early adulthood (25y), and in G0 once in middle adulthood (50y). Linear regression models were used to examine differences in standardized traits for males compared with females on each occasion (serial cross-sectional associations). 7,727 G1s (49% male) and 6,500 G0s (29% male) contributed to analyses. At age 8y, total lipids in very-low-density lipoproteins (VLDL) were lower in males than females; levels were higher in males than females at age 16y and were higher still by age 18y and age 50y (in G0) for medium-or-larger subclasses. Larger sex differences at older ages were most pronounced for triglycerides in VLDL – e.g. male levels were 0.19 standard deviation (SD) units (95% CI=0.12, 0.26) higher at age 18y, 0.50 SD (95% CI=0.42, 0.57) higher at age 25y, and 0.62 SD (95% CI=0.55, 0.68) higher at age 50y. Cholesterol in VLDL and low-density lipoproteins (LDL) was generally lower in males, with inconsistent sex differences across ages. Apolipoprotein-B was generally lower in males than females. Branched chain amino acids were consistently higher in males after age 8y with the largest sex difference of all traits at all ages seen for leucine at age 50y (1.53 SD, 95% CI=1.47, 1.58 higher in males compared with females). Males had consistently lower glycoprotein acetyls across ages.ConclusionsOur results suggest that males begin to have higher VLDL triglycerides in adolescence, and that this sex difference is larger at older ages. Sex differences in other CHD-related traits, including LDL cholesterol, apolipoprotein-B, and inflammatory glycoproteins, show the opposite pattern with age, with higher levels among females. Higher triglyceride content may therefore be a key factor underpinning the higher age-adjusted rate of CHD among males; causal analyses of this and other traits are needed to understand whether they differentially affect CHD risk among males and females.
Immune-checkpoint engagement as predictive biomarkers in clear cell renal cell carcinoma and melanoma
Authors: Sánchez-Magraner Lissete , Miles James , Baker Claire , Applebee Christopher J , Lee Dae-Jin , Elsheikh Somaia , Lashin Shaimaa , Withers Katriona , Watts Andrew , Parry Richard , Edmead Christine , Lopez Jose Ignacio , Mehta Raj , Ward Stephen G , Parker Peter J. , Larijani Banafshé 
Published: January 2020

ABSTRACTMany cancers are termed immuno-evasive due to expression of immuno-modulatory ligands. Programmed death ligand-1 (PD-L1) and cluster of differentiation 80/86 (CD80/86) interact with their receptors, programmed death receptor-1 (PD-1) and cytotoxic T-lymphocyte associated protein-4 (CTLA-4), on tumour infiltrating leukocytes, thus eliciting immunosuppression. Immunotherapies aimed at blocking these interactions are revolutionising cancer treatments, albeit in an inadequately described patient subset.Our prognostic assay, utilising amplified two-site time-resolved Förster resonance energy transfer (iFRET), quantifies PD-1/ PD-L1 and CTLA-4/ CD80 cell-cell interactions in single cell assays and tumour biopsies. iFRET efficiencies demonstrate, in cell-cell engagement models, that receptor-ligand interactions are significantly lower with anti-PD-1 or anti-CTLA-4 blocking antibodies. In patient samples, iFRET detects immune-cell/tumour-cell interaction variance in different cancers. These results revealed inter-cancer, inter-patient and intra-tumoural heterogeneity of engaged immune-checkpoints, contradicting their ligand expression patterns. Exploiting spatio-temporal interactions of immune-checkpoint proteins defined biomarker functionality for determining whether checkpoint inhibitors are appropriate treatments.Statement of SignificanceQuantitative photophysics exploitation in determining immune-checkpoint engagement, as predictive biomarkers in cancers led to revealing inter-cancer, inter-patient and intra-tumoural heterogeneity of the engaged immune-checkpoints. This receptor-ligand interaction did not reflect simple expression patterns of these immuno-modulatory proteins. Our findings may affect immunotherapies aimed at blocking these intercellular interactions in patients.
Comparison of a second-generation trabecular bypass (iStentinject) to ab interno trabeculectomy (Trabectome) byexact matching
Authors: Yousef Yousef Al , Strzalkowska Alicja , Hillenkamp Jost , Rosentreter André , Loewen Nils A. 
Published: January 2020

AbstractPurposeTo achieve a highly balanced comparison of trabecular bypass stenting (IS2, iStent inject)with ab interno trabeculectomy (T, Trabectome) byexact matching. In a similar study, IS1 (1st generation iStent) had shown a loss of effect at 6 months.Methods53 IS2 eyes were matched to 3446 T eyes. Patients were matched using exact matching by baseline IOP, the number of glaucoma medications, and glaucoma type and using nearest neighbor matching by age. Individuals without a close match were excluded. All surgeries were combined with phacoemulsification.ResultsA total of 78 eyes (39 in each group) could be matched as exact pairs with a baseline IOP of 18.3±5.1 mmHg and glaucoma medications of 2.7±1.2 in each. IOP in IS2 was reduced to 14.6±4.2 mmHg at 3 months and in T to a minimum of 13.1±3.2 mmHg at 1 month. In IS2, IOP began to rise again at 6 months, eventually exceeding baseline. At 24 months, IOP in IS2 was 18.8±9.0 mmHg and in T 14.2±3.5 mmHg. IS2 had a higher average IOP than T at all postoperative visits (p<0.05 at 1, 12, 18 months). Glaucoma medications decreased to 2.0±1.5 in IS2 and to 1.5±1.4 in T.ConclusionT resulted in a larger and sustained IOP reduction compared to IS2 where a rebound occurred after six months to slightly above preoperative values. This time course fits bioreactivity data of the IS1.
IRESbase: a Comprehensive Database of Experimentally Validated Internal Ribosome Entry Sites
Authors: Zhao Jian , Li Yan , Wang Cong , Zhang Haotian , Zhang Hao , Jiang Bin , Guo Xuejiang , Song Xiaofeng 
Published: January 2020

AbstractInternal Ribosome Entry Sites (IRESs) are functional RNA elements that can directly recruit ribosomes to an internal position of the mRNA in a cap-independent manner to initiate translation. Recently, IRES elements have attracted much attention for their critical roles in various processes including translation initiation of a new type of RNA, circular RNA, with no 5′ cap to support classical cap-dependent translation. Thus, an integrative data resource of IRES elements with experimental evidences will be useful for further studies. In this study, we present a comprehensive database of IRESs (IRESbase) by curating the experimentally validated functional minimal IRES elements from literature and annotating their host linear and circular RNA information. The current version of IRESbase contains 1328 IRESs, including 774 eukaryotic IRESs and 554 viral IRESs from 11 eukaryotic organisms and 198 viruses. As our database collected only IRES of minimal length with functional evidences, the median length of IRESs in IRESbase is 174 nucleotides. By mapping IRESs to human circRNAs and lncRNAs, 2191 circRNAs and 168 lncRNAs were found to contain at least one entire or partial IRES sequences. The IRESbase is available athttp://reprod.njmu.edu.cn/cgi-bin/iresbase/index.php.
SREBP1 regulates mitochondrial metabolism in oncogenicKRASexpressing NSCLC
Authors: Ruiz Christian F. , Montal Emily D. , Haley John A. , Haley John D. 
Published: January 2020

AbstractCancer cells require extensive metabolic reprogramming in order to provide the bioenergetics and macromolecular precursors needed to sustain a malignant phenotype. MutantKRASis a driver oncogene that is well known for its ability to regulate the ERK and PI3K signaling pathways. However, it is now appreciated that KRAS can promote tumor growth via upregulation of anabolic metabolism. We recently showed that oncogenic KRAS promotes a gene expression program ofde novo lipogenesisin non-small cell lung cancer (NSCLC). To define the mechanism(s) responsible, we focused on the lipogenic transcription factor SREBP1. We observed that KRAS increases SREBP1 expression and genetic knockdown of SREBP1 significantly inhibited cell proliferation of mutantKRAS-expressing cells. Unexpectedly, lipogenesis was not significantly altered in cells subject to SREBP1 knockdown. Carbon tracing metabolic studies showed a significant decrease in oxidative phosphorylation and RNA-seq data revealed a significant decrease in mitochondrial encoded subunits of the electron transport chain (ETC). Taken together, these data support a novel role, distinct from lipogenesis, of SREBP1 on mitochondrial function in mutantKRASNSCLC.