Miracle-dz/UniFAR-FTUs huggingface dataset:
Range contraction enables harvesting to extinction

Significance Many threatened species including elephants, sturgeons, and bluefin tunas are harvested for high-value products. Species can be driven extinct if incentives to harvest do not diminish as populations decline; this occurs if harvest prices rise faster than costs with declining stock. Whereas recent conservation attention for these species has largely focused on market demand, we show—using a theoretical model and an empirical review—that contractions in species’ geographic ranges, which stabilize costs and may be especially common among terrestrial species, might often play a larger role in maintaining harvest incentives. Forces impacting ranges—such as patchy and declining habitats, schooling/herding behavior, and climate change—therefore merit greater attention in assessing overharvesting threats. Economic incentives to harvest a species usually diminish as its abundance declines, because harvest costs increase. This prevents harvesting to extinction. A known exception can occur if consumer demand causes a declining species’ harvest price to rise faster than costs. This threat may affect rare and valuable species, such as large land mammals, sturgeons, and bluefin tunas. We analyze a similar but underappreciated threat, which arises when the geographic area (range) occupied by a species contracts as its abundance declines. Range contractions maintain the local densities of declining populations, which facilitates harvesting to extinction by preventing abundance declines from causing harvest costs to rise. Factors causing such range contractions include schooling, herding, or flocking behaviors—which, ironically, can be predator-avoidance adaptations; patchy environments; habitat loss; and climate change. We use a simple model to identify combinations of range contractions and price increases capable of causing extinction from profitable overharvesting, and we compare these to an empirical review. We find that some aquatic species that school or forage in patchy environments experience sufficiently severe range contractions as they decline to allow profitable harvesting to extinction even with little or no price increase; and some high-value declining aquatic species experience severe price increases. For terrestrial species, the data needed to evaluate our theory are scarce, but available evidence suggests that extinction-enabling range contractions may be common among declining mammals and birds. Thus, factors causing range contraction as abundance declines may pose unexpectedly large extinction risks to harvested species.
Phosphorylation of Bovine Herpesvirus 1 VP8 Plays a Role in Viral DNA Encapsidation and Is Essential for Its Cytoplasmic Localization and Optimal Virion Incorporation

ABSTRACT VP8 is a major tegument protein of bovine herpesvirus 1 (BoHV-1) and is essential for viral replication in cattle. The protein undergoes phosphorylation after transcription through cellular casein kinase 2 (CK2) and a viral kinase, US3. In this study, a virus containing a mutated VP8 protein that is not phosphorylated by CK2 and US3 (BoHV-1-YmVP8) was constructed by homologous recombination in mammalian cells. When BoHV-1-YmVP8-infected cells were observed by transmission electron microscopy, blocking phosphorylation of VP8 was found to impair viral DNA encapsidation, resulting in release of incomplete viral particles to the extracellular environment. Consequently, less infectious virus was produced by the mutant virus than by wild-type (WT) virus. A comparison of mutant and WT VP8 by confocal microscopy revealed that mutant VP8 is nuclear throughout infection while WT VP8 is nuclear early during infection and is associated with the Golgi apparatus at later stages. This, together with the observation that mutant VP8 is present in virions, albeit in smaller amounts, suggests that the incorporation of VP8 may occur at two stages. The first takes place without the need for phosphorylation and before or during nuclear egress of capsids, whereas the second occurs in the Golgi apparatus and requires phosphorylation of VP8. The results indicate that phosphorylated VP8 plays a role in viral DNA encapsidation and in the secondary virion incorporation of VP8. To perform these functions, the cellular localization of VP8 is adjusted based on the phosphorylation status. IMPORTANCE In this study, phosphorylation of VP8 was shown to have a function in BoHV-1 replication. A virus containing a mutated VP8 protein that is not phosphorylated by CK2 and US3 (BoHV-1-YmVP8) produced smaller numbers of infectious virions than wild-type (WT) virus. The maturation and egress of WT and mutant BoHV-1 were studied, showing a process similar to that reported for other alphaherpesviruses. Interestingly, lack of phosphorylation of VP8 by CK2 and US3 resulted in reduced incorporation of viral DNA into capsids during mutant BoHV-1 infection, as well as lower numbers of extracellular virions. Furthermore, mutant VP8 remained nuclear throughout infection, in contrast to WT VP8, which is nuclear at early stages and Golgi apparatus associated late during infection. This correlates with smaller amounts of mutant VP8 in virions and suggests for the first time that VP8 may be assembled into the virions at two stages, with the latter dependent on phosphorylation.
Dual role of ALCAM in neuroinflammation and blood–brain barrier homeostasis

Significance Multiple sclerosis (MS) is an inflammatory disorder characterized by multifocal lesions in the central nervous system. These lesions are caused by infiltrating leukocytes that take advantage and/or actively participate in the disruption of the blood–brain barrier (BBB). In this study, the specific role of the adhesion molecule ALCAM (activated leukocyte cell adhesion molecule) present on BBB endothelial cells was assessed. We demonstrated that ALCAM knockout mice develop a more severe experimental autoimmune encephalomyelitis, the mouse model of MS, due to an increased permeability of the BBB. This phenotypic change is caused by a dysregulation of junctional molecules with which ALCAM indirectly binds, suggesting that in addition to its role in leukocyte transmigration, ALCAM regulates and maintains tight junction stability by acting as an adaptor molecule. Activated leukocyte cell adhesion molecule (ALCAM) is a cell adhesion molecule found on blood–brain barrier endothelial cells (BBB-ECs) that was previously shown to be involved in leukocyte transmigration across the endothelium. In the present study, we found that ALCAM knockout (KO) mice developed a more severe myelin oligodendrocyte glycoprotein (MOG)35–55–induced experimental autoimmune encephalomyelitis (EAE). The exacerbated disease was associated with a significant increase in the number of CNS-infiltrating proinflammatory leukocytes compared with WT controls. Passive EAE transfer experiments suggested that the pathophysiology observed in active EAE was linked to the absence of ALCAM on BBB-ECs. In addition, phenotypic characterization of unimmunized ALCAM KO mice revealed a reduced expression of BBB junctional proteins. Further in vivo, in vitro, and molecular analysis confirmed that ALCAM is associated with tight junction molecule assembly at the BBB, explaining the increased permeability of CNS blood vessels in ALCAM KO animals. Collectively, our data point to a biologically important function of ALCAM in maintaining BBB integrity.
Identification of Unknown Carboxydovore Bacteria Dominant in Deciduous Forest Soil via Succession of Bacterial Communities, coxL Genotypes, and Carbon Monoxide Oxidation Activity in Soil Microcosms

ABSTRACT Surveys of the coxL gene, encoding the large subunit of the CO dehydrogenase, are used as a standard approach in ecological studies of carboxydovore bacteria scavenging atmospheric CO. Recent soil surveys unveiled that the distribution of coxL sequences encompassing the atypical genotype coxL type I group x was correlated to the CO oxidation activity. Based on phylogenetic analysis including the available coxL reference genome sequences, this unusual genotype was assigned to an unknown member of the Deltaproteobacteria, with the coxL sequence from Haliangium ochraceum being the sole and closest reference sequence. Here we seek to challenge the proposed taxonomic assignation of the coxL group x genotype through the monitoring of CO consumption activity and microbial community successions during the colonization of sterile soil microcosms inoculated with indigenous microorganisms. In our study, we established that the estimated population density of Deltaproteobacteria was too small to account for the abundance of the coxL group x genotype detected in soil. Furthermore, we computed a correlation network to relate 16S rRNA gene profiles with the succession of coxL genotypes and CO uptake activity in soil. We found that most of the coxL genotypes for which the colonization profile displayed covariance with CO uptake activity were related to potential carboxydovore bacteria belonging to Actinobacteria and Alphaproteobacteria. Our analysis did not provide any evidence that coxL group x genotypes belonged to Deltaproteobacteria. Considering the colonization profile of CO-oxidizing bacteria and the theoretical energy yield of measured CO oxidation rates in soil microcosms, we propose that unknown carboxydovore bacteria harboring the atypical coxL group x genotype are mixotrophic K-strategists.
Assessment of an irritant gas plume model for epidemiologic study

Abstract Previously, we reported the development of a Hazard Prediction and Assessment Capability plume dispersion model of the 2005 Graniteville, South Carolina, USA accidental release of chlorine. Here, we assess this model by spatial and statistical comparison with post-incident observed environmental indicators of exposure and other types of observations. Spatial agreement was found when the model was compared to phytotoxic bleaching and corrosion events observed in 2 km radius around the release site. When spatially compared to locations of injured or killed animals, model predictions of the plume footprint were in relatively good agreement. Model-predicted human casualties differed from observed casualty counts primarily due to the shielding effect of buildings. A statistical comparison of observed dog health outcome-derived exposure vs. model predicted exposure showed relatively good agreement, particularly when a subcohort of indoor dogs was excluded. Evaluation and assessment of the building infiltration effect would further improve the model prior to application in epidemiologic study.
Handwritten Devanagari Character Recognition Using Layer-Wise Training of Deep Convolutional Neural Networks and Adaptive Gradient Methods

Handwritten character recognition is currently getting the attention of researchers because of possible applications in assisting technology for blind and visually impaired users, human–robot interaction, automatic data entry for business documents, etc. In this work, we propose a technique to recognize handwritten Devanagari characters using deep convolutional neural networks (DCNN) which are one of the recent techniques adopted from the deep learning community. We experimented the ISIDCHAR database provided by (Information Sharing Index) ISI, Kolkata and V2DMDCHAR database with six different architectures of DCNN to evaluate the performance and also investigate the use of six recently developed adaptive gradient methods. A layer-wise technique of DCNN has been employed that helped to achieve the highest recognition accuracy and also get a faster convergence rate. The results of layer-wise-trained DCNN are favorable in comparison with those achieved by a shallow technique of handcrafted features and standard DCNN.
Poultry Consumption and Arsenic Exposure in the U.S. Population

Background: Arsenicals (roxarsone and nitarsone) used in poultry production likely increase inorganic arsenic (iAs), monomethylarsonic acid (MMA), dimethylarsinic acid (DMA), and roxarsone or nitarsone concentrations in poultry meat. However, the association between poultry intake and exposure to these arsenic species, as reflected in elevated urinary arsenic concentrations, is unknown. Objectives: Our aim was to evaluate the association between 24-hr dietary recall of poultry consumption and arsenic exposure in the U.S. population. We hypothesized first, that poultry intake would be associated with higher urine arsenic concentrations and second, that the association between turkey intake and increased urine arsenic concentrations would be modified by season, reflecting seasonal use of nitarsone. Methods: We evaluated 3,329 participants ≥ 6 years old from the 2003–2010 National Health and Nutrition Examination Survey (NHANES) with urine arsenic available and undetectable urine arsenobetaine levels. Geometric mean ratios (GMR) of urine total arsenic and DMA were compared across increasing levels of poultry intake. Results: After adjustment, participants in the highest quartile of poultry consumption had urine total arsenic 1.12 (95% CI: 1.04, 1.22) and DMA 1.13 (95% CI: 1.06, 1.20) times higher than nonconsumers. During the fall/winter, participants in the highest quartile of turkey intake had urine total arsenic and DMA 1.17 (95% CI: 0.99, 1.39; p-trend = 0.02) and 1.13 (95% CI: 0.99, 1.30; p-trend = 0.03) times higher, respectively, than nonconsumers. Consumption of turkey during the past 24 hr was not associated with total arsenic or DMA during the spring/summer. Conclusions: Poultry intake was associated with increased urine total arsenic and DMA in NHANES 2003–2010, reflecting arsenic exposure. Seasonally stratified analyses by poultry type provide strong suggestive evidence that the historical use of arsenic-based poultry drugs contributed to arsenic exposure in the U.S. population. Citation: Nigra AE, Nachman KE, Love DC, Grau-Perez M, Navas-Acien A. 2017. Poultry consumption and arsenic exposure in the U.S. population. Environ Health Perspect 125:370–377; http://dx.doi. org/10.1289/EHP351
Whole-Genome Sequencing Accurately Identifies Resistance to Extended-Spectrum &bgr;-Lactams for Major Gram-Negative Bacterial Pathogens

Background There is marked interest in using DNA-based methods to detect antimicrobial resistance (AMR), with targeted polymerase chain reaction (PCR) approaches increasingly being incorporated into clinical care. Whole-genome sequencing (WGS) could offer significant advantages over targeted PCR for AMR detection, particularly for species where mutations are major drivers of AMR. Methods Illumina MiSeq WGS and broth microdilution (BMD) assays were performed on 90 bloodstream isolates of the 4 most common gram-negative bacteria causing bloodstream infections in neutropenic patients. The WGS data, including both gene presence/absence and detection of mutations in an array of AMR-relevant genes, were used to predict resistance to 4 β-lactams commonly used in the empiric treatment of neutropenic fever. The genotypic predictions were then compared to phenotypic resistance as determined by BMD and by commercial methods during routine patient care. Results Of 133 putative instances of resistance to the β-lactams of interest identified by WGS, only 87 (65%) would have been detected by a typical PCR-based approach. The sensitivity, specificity, and positive and negative predictive values for WGS in predicting AMR were 0.87, 0.98, 0.97, and 0.91, respectively. Using BMD as the gold standard, our genotypic resistance prediction approach had a significantly higher positive predictive value compared to minimum inhibitory concentrations generated by commercial methods (0.97 vs 0.92; P = .025). Conclusions These data demonstrate the potential feasibility of using WGS to guide antibiotic treatment decisions for patients with life-threatening infections for an array of medically important pathogens.
Mutations in the Schmallenberg Virus Gc Glycoprotein Facilitate Cellular Protein Synthesis Shutoff and Restore Pathogenicity of NSs Deletion Mutants in Mice

ABSTRACT Serial passage of viruses in cell culture has been traditionally used to attenuate virulence and identify determinants of viral pathogenesis. In a previous study, we found that a strain of Schmallenberg virus (SBV) serially passaged in tissue culture (termed SBVp32) unexpectedly displayed increased pathogenicity in suckling mice compared to wild-type SBV. In this study, we mapped the determinants of SBVp32 virulence to the viral genome M segment. SBVp32 virulence is associated with the capacity of this virus to reach high titers in the brains of experimentally infected suckling mice. We also found that the Gc glycoprotein, encoded by the M segment of SBVp32, facilitates host cell protein shutoff in vitro. Interestingly, while the M segment of SBVp32 is a virulence factor, we found that the S segment of the same virus confers by itself an attenuated phenotype to wild-type SBV, as it has lost the ability to block the innate immune system of the host. Single mutations present in the Gc glycoprotein of SBVp32 are sufficient to compensate for both the attenuated phenotype of the SBVp32 S segment and the attenuated phenotype of NSs deletion mutants. Our data also indicate that the SBVp32 M segment does not act as an interferon (IFN) antagonist. Therefore, SBV mutants can retain pathogenicity even when they are unable to fully control the production of IFN by infected cells. Overall, this study suggests that the viral glycoprotein of orthobunyaviruses can compensate, at least in part, for the function of NSs. In addition, we also provide evidence that the induction of total cellular protein shutoff by SBV is determined by multiple viral proteins, while the ability to control the production of IFN maps to the NSs protein. IMPORTANCE The identification of viral determinants of pathogenesis is key to the development of prophylactic and intervention measures. In this study, we found that the bunyavirus Gc glycoprotein is a virulence factor. Importantly, we show that mutations in the Gc glycoprotein can restore the pathogenicity of attenuated mutants resulting from deletions or mutations in the nonstructural protein NSs. Our findings highlight the fact that careful consideration should be taken when designing live attenuated vaccines based on deletions of nonstructural proteins since single mutations in the viral glycoproteins appear to revert attenuated mutants to virulent phenotypes.
Implantable cardioverter-defibrillators in adults with congenital heart disease: a systematic review and meta-analysis.

AIMS Sudden cardiac death is a major cause of mortality in adult congenital heart disease (ACHD) patients. The indications for implantable cardioverter-defibrillator (ICD) implantation in ACHD patients are still not well established. We aim to systematically review the literature on indications and outcome of ICD implantation in ACHD patients. METHODS AND RESULTS We performed a comprehensive search in EMBASE, MEDLINE, and Google Scholar to identify all studies on ICD implantation in ACHD patients. We used random effects models to calculate proportions and 95% confidence intervals. Of 1356 articles, 24 studies with 2162 patients were included, with a mean follow-up of 3.6 ± 0.9 years. Half of patients had tetralogy of Fallot. Mean age at implantation was 36.5 ± 5.5 years old and 66% was male. Implantable cardioverter-defibrillators were implanted for primary prevention in 53% (43.5-62.7). Overall, 24% (18.6-31.3) of patients received one or more appropriate ICD interventions (anti-tachycardia pacing or shocks) during 3.7 ± 0.9 years: 22% (16.9-28.8) of patients with primary prevention in 3.3 ± 0.3 years and 35% (26.6-45.2) of patients with secondary prevention in 4.3 ± 1.2 years. Inappropriate shocks occurred in 25% (20.1-31.0) in 3.7 ± 0.8 years and other, particularly lead-related complications in 26% (18.9-33.6) of patients in 3.8 ± 0.8 years. All-cause mortality was 10% during 3.7 ± 0.9 years. CONCLUSIONS In ACHD, remarkably high rates of appropriate ICD therapy were reported, both in primary and secondary prevention. Because of the young age and lower death rates, the cumulative beneficial effects are likely greater in ACHD patients than in acquired heart disease patients. However, considering the high rates of inappropriate shocks and complications, case-by-case weighing of costs and benefits, remains essential.
Photocatalytic degradation of phenazopyridine contaminant in soil with direct solar light

ABSTRACT Photocatalytic degradation of waste pharmaceutics, with solar radiation, is described here as a feasible method to purify pre-contaminated soils. Phenazopyridine has been used as a model soil contaminant. Two different nano-size powders have been first examined as catalysts, namely commercial TiO2 (anatase) and commercial ZnO. As the ZnO showed higher catalytic efficiency, the study was then focused on it. The commercial ZnO powder was then compared with lab-prepared ZnO powder, and the latter shows relatively higher efficiency. The ZnO was used in two different ways. In one way, dry ZnO catalyst powder was spread onto the soil, while in the other way the ZnO was sprayed onto the soil surface by a wet spray method. The spray technique shows slightly higher efficiency, in addition to being easier to apply at future large scale. Depending on conditions and type of photocatalyst used, up to 90% contaminant removal can be achieved in 30 min. In case of photocatalysis experiments, the reacted contaminant molecules undergo complete degradation with no detectable side reaction organic products. Possible evaporation or escape of organic contaminant, or other possibly resulting organics, is ruled out by a series of control experiments. Photodegradation process takes place only at the catalytic sites on the soil surface, where contaminant molecules that diffuse from the soil bulk are completely degraded. Other useful organisms inside the soil are not affected as they are kept away from catalyst sites. A plausible mechanism is proposed for the degradation process. GRAPHICAL ABSTRACT
Cued Reactivation of Motor Learning during Sleep Leads to Overnight Changes in Functional Brain Activity and Connectivity

Sleep plays a role in memory consolidation. This is demonstrated by improved performance and neural plasticity underlying that improvement after sleep. Targeted memory reactivation (TMR) allows the manipulation of sleep-dependent consolidation through intentionally biasing the replay of specific memories in sleep, but the underlying neural basis of these altered memories remains unclear. We use functional magnetic resonance imaging (fMRI) to show a change in the neural representation of a motor memory after targeted reactivation in slow-wave sleep (SWS). Participants learned two serial reaction time task (SRTT) sequences associated with different auditory tones (high or low pitch). During subsequent SWS, one sequence was reactivated by replaying the associated tones. Participants were retested on both sequences the following day during fMRI. As predicted, they showed faster reaction times for the cued sequence after targeted memory reactivation. Furthermore, increased activity in bilateral caudate nucleus and hippocampus for the cued relative to uncued sequence was associated with time in SWS, while increased cerebellar and cortical motor activity was related to time in rapid eye movement (REM) sleep. Functional connectivity between the caudate nucleus and hippocampus was also increased after targeted memory reactivation. These findings suggest that the offline performance gains associated with memory reactivation are supported by altered functional activity in key cognitive and motor networks, and that this consolidation is differentially mediated by both REM sleep and SWS.