A vortex population viability analysis model for the Chacoan peccary (catagonus wagneri)

El quimilero o taguá (Catagonus wagneri) es una especie amenazada, endémica del Chaco Seco, para la cual disponemos de poca información. Para estimar cuantitativamente el riesgo de disminución y extinción de sus poblaciones silvestres generamos modelos de viabilidad poblacional. Con estos modelos matemáticos se pueden identificar factores naturales y antrópicos complejos que interactúan y que influyen en la persistencia y la salud de una población. Los modelos también se pueden utilizar para evaluar los efectos de diferentes estrategias de gestión, permitiendo identificar las acciones de conservación más efectivas para una población o especie. Además, estos modelos se pueden usar para identificar las necesidades de investigación debido a que ponen en evidencia los vacíos de información sobre la especie. Utilizando estos modelos, evaluamos la proyección poblacional en las condiciones actuales y en comparación con posibles variaciones existentes en el sistema. Para generar los parámetros ingresados en los modelos realizamos una reunión de especialistas y una revisión bibliográfica. Trabajó con valores de línea de base (base), mínimos (mín.) y máximos (máx.). Generamos diferentes modelos ante diferentes escenarios y testeamos la sensibilidad a la incertidumbre de cada modelo. Esto permitió establecer prioridades de investigación. Además, determinamos los tamaños mínimos de población viable considerando la incertidumbre y analizamos los posibles efectos de la caza en una población de esta especie.Fil: Leus, Kritin. International Union for Conservation of Nature. Species Survival Commission; DinamarcaFil: Altrichter, Mariana. International Union for Conservation of Nature. Species Survival Commission; Estados UnidosFil: Desbiez, Arnaud. International Union for Conservation of Nature. Species Survival Commission; BrasilFil: Camino, Micaela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Nordeste. Centro de Ecología Aplicada del Litoral. Universidad Nacional del Nordeste. Centro de Ecología Aplicada del Litoral; ArgentinaFil: Giordano, Anthony J.. S.P.E.C.I.E.S.; Estados UnidosFil: Campos Krauer, Juan Manuel. University of Florida. Department of Wildlife Ecology and Conservation; Estados Unidos. Centro Chaqueño para la Conservación y la Investigación; ParaguayFil: Brooks, Daniel M.. Houston Museum Of Natural Science; Estados UnidosFil: Thompson, Jeffrey. Consejo Nacional de Ciencia y Tecnología; ParaguayFil: Núñez Regueiro, Mauricio Manuel. University of Florida. Department of Wildlife Ecology and Conservation; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentin

Predicting the current distribution of the chacoan peccary (catagonus wagneri) in the gran Chaco

The Chacoan peccary (Catagonus wagneri), or Tagua, an endemic species living in the Chaco eco¬region, is endangered by highly increasing deforestation rates across the region, particularly in the last decade. This situation highlights the need to better understand the current distribution of the species, as well as how environmental conditions affect habitat suitability. This study predicts the distribution of the Chacoan peccary and evaluates the current environmental conditions in the Chaco for this species. Using six environmental variables and 177 confirmed occurrence records (from 2000 to 2015) provided by researchers, we developed a Species Distribution Model (SDM) applying the Maxent algorithm. The final model was highly accurate and significant (p < 0.001; AUC 0.860 ± 0.0268; omission error 1.82 %; post¬hoc validation of omission error using independent presence¬only records 1.33 %), predicting that 46.24 % of the Chaco is suitable habitat for the Chacoan peccary, with the most important areas concentrated in the middle of Paraguay and northern Argentina. Land cover, isothermality and elevation were the variables that better explained the habitat suitability for the Chacoan peccary. Despite some portions of suitable areas occurring inside protected areas, the borders and the central portions of suitable areas have recently suffered from intensive deforestation and development, and most of the highly suitable areas for the species are not under protection. The results provide fundamental insights for the establishment of priority Chacoan peccary conservation areas within its rangeFil: Paschoaletto Micchi, Katia Maria. Universidade Do Sao Paulo. Escola Superior de Agricultura Luiz de Queiroz Esalq; Brasil. Conservation Breeding Specialist Group Brazilian network; BrasilFil: Silva Angelieri, Cintia Camila. Universidade Do Sao Paulo. Escola Superior de Agricultura Luiz de Queiroz Esalq; BrasilFil: Altrichter, Mariana. Prescott College; Estados UnidosFil: Desbiez, Arnaud. Royal Zoological Society of Scotland. Edimburgo; Reino Unido. Conservation Breeding Specialist Group Brazilian network; BrasilFil: Yanosky, Alberto. Asociación Guyra Paraguay. Asunción; ParaguayFil: Campos Krauer, Juan Manuel. Centro Chaqueño para la Conservación y la Investigación; ParaguayFil: Torres, Ricardo Jose. Universidad Nacional de Córdoba. Facultad de Ciencias Exactas, Físicas y Naturales; ArgentinaFil: Camino, Micaela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Nordeste. Centro de Ecología Aplicada del Litoral. Universidad Nacional del Nordeste. Centro de Ecología Aplicada del Litoral; ArgentinaFil: Cabral, Hugo. Asociación Guyra Paraguay. Asunción; ParaguayFil: Cartés, José. Asociación Guyra Paraguay. Asunción; ParaguayFil: Cuellar, Rosa Leny. Fundación Kaa Iya; BoliviaFil: Gallegos, Marcelo. Secretaría de Ambiente de la Provincia de Salta. Programa Guardaparques; ArgentinaFil: Giordano, Anthony J.. No especifica;Fil: Decarre, Julieta. Instituto Nacional de Tecnología Agropecuaria. Centro de Investigación de Recursos Naturales. Instituto de Recursos Biológicos; ArgentinaFil: Maffei, Leonardo. Wildlife Conservation Society. Lima; PerúFil: Neris, Nora. Universidad Nacional de Asunción; ParaguayFil: Saldivar Bellassai, Silvia. Itaipu Binacional; ParaguayFil: Wallace, Robert. Wildlife Conservation Society. New York; Estados UnidosFil: Lizarraga, Leónidas. Delegación Regional Noroeste. Sistema de Información de Biodiversidad de la Administración de Parques Nacionales. Salta; ArgentinaFil: Thompson, Jeffrey. Universidad Nacional de Asunción; ParaguayFil: Velilla, Mariela. Universidad Nacional de Asunción; Paragua

A New High-Resolution Map of World Mountains and an Online Tool for Visualizing and Comparing

Answers to the seemingly straightforward questions “what is a mountain?” and “where are the mountains of the world?” are in fact quite complex, and there have been few attempts to map the mountains of the earth in a consistent and rigorous fashion. However, knowing exactly where mountain ecosystems are distributed on the planet is a precursor to conserving them, as called for in Sustainable Development Goals 6 and 15 of the United Nations 2030 Agenda for Sustainable Development. In this article we first compare 3 characterizations of global mountain distributions, including a new, high-resolution (250 m) map of global mountains derived from terrain characteristics. We show how differences in conceptual definition, methodology, and spatial resolution of source data can result in differences in the extent and location of lands classed as mountains. For example, the new 250-m resource documents a larger global mountain extent than previous characterizations, although it excludes plateaus, hilly forelands, and other landforms that are often considered part of mountain areas. We then introduce the Global Mountain Explorer, a new web-based application specifically developed for exploration, visualization, and comparison of these maps. This new open-access tool is an intuitive and versatile resource suitable for a broad range of users and applications

Sirolimus and kidney growth in autosomal dominant polycystic kidney disease

BACKGROUND: In autosomal dominant polycystic kidney disease (ADPKD), aberrant activation of the mammalian target of rapamycin (mTOR) pathway is associated with progressive kidney enlargement. The drug sirolimus suppresses mTOR signaling. METHODS: In this 18-month, open-label, randomized, controlled trial, we sought to determine whether sirolimus halts the growth in kidney volume among patients with ADPKD. We randomly assigned 100 patients between the ages of 18 and 40 years to receive either sirolimus (target dose, 2 mg daily) or standard care. All patients had an estimated creatinine clearance of at least 70 ml per minute. Serial magnetic resonance imaging was performed to measure the volume of polycystic kidneys. The primary outcome was total kidney volume at 18 months on blinded assessment. Secondary outcomes were the glomerular filtration rate and urinary albumin excretion rate at 18 months. RESULTS: At randomization, the median total kidney volume was 907 cm(3) (interquartile range, 577 to 1330) in the sirolimus group and 1003 cm(3) (interquartile range, 574 to 1422) in the control group. The median increase over the 18-month period was 99 cm(3) (interquartile range, 43 to 173) in the sirolimus group and 97 cm(3) (interquartile range, 37 to 181) in the control group. At 18 months, the median total kidney volume in the sirolimus group was 102% of that in the control group (95% confidence interval, 99 to 105; P=0.26). The glomerular filtration rate did not differ significantly between the two groups; however, the urinary albumin excretion rate was higher in the sirolimus group. CONCLUSIONS: In adults with ADPKD and early chronic kidney disease, 18 months of treatment with sirolimus did not halt polycystic kidney growth. (ClinicalTrials.gov number, NCT00346918.

Upregulation of the cell-cycle regulator RGC-32 in Epstein-Barr virus-immortalized cells

Epstein-Barr virus (EBV) is implicated in the pathogenesis of multiple human tumours of lymphoid and epithelial origin. The virus infects and immortalizes B cells establishing a persistent latent infection characterized by varying patterns of EBV latent gene expression (latency 0, I, II and III). The CDK1 activator, Response Gene to Complement-32 (RGC-32, C13ORF15), is overexpressed in colon, breast and ovarian cancer tissues and we have detected selective high-level RGC-32 protein expression in EBV-immortalized latency III cells. Significantly, we show that overexpression of RGC-32 in B cells is sufficient to disrupt G2 cell-cycle arrest consistent with activation of CDK1, implicating RGC-32 in the EBV transformation process. Surprisingly, RGC-32 mRNA is expressed at high levels in latency I Burkitt's lymphoma (BL) cells and in some EBV-negative BL cell-lines, although RGC-32 protein expression is not detectable. We show that RGC-32 mRNA expression is elevated in latency I cells due to transcriptional activation by high levels of the differentially expressed RUNX1c transcription factor. We found that proteosomal degradation or blocked cytoplasmic export of the RGC-32 message were not responsible for the lack of RGC-32 protein expression in latency I cells. Significantly, analysis of the ribosomal association of the RGC-32 mRNA in latency I and latency III cells revealed that RGC-32 transcripts were associated with multiple ribosomes in both cell-types implicating post-initiation translational repression mechanisms in the block to RGC-32 protein production in latency I cells. In summary, our results are the first to demonstrate RGC-32 protein upregulation in cells transformed by a human tumour virus and to identify post-initiation translational mechanisms as an expression control point for this key cell-cycle regulator

Hexokinase 3 enhances myeloid cell survival via non-glycolytic functions.

The family of hexokinases (HKs) catalyzes the first step of glycolysis, the ATP-dependent phosphorylation of glucose to glucose-6-phosphate. While HK1 and HK2 are ubiquitously expressed, the less well-studied HK3 is primarily expressed in hematopoietic cells and tissues and is highly upregulated during terminal differentiation of some acute myeloid leukemia (AML) cell line models. Here we show that expression of HK3 is predominantly originating from myeloid cells and that the upregulation of this glycolytic enzyme is not restricted to differentiation of leukemic cells but also occurs during ex vivo myeloid differentiation of healthy CD34+ hematopoietic stem and progenitor cells. Within the hematopoietic system, we show that HK3 is predominantly expressed in cells of myeloid origin. CRISPR/Cas9 mediated gene disruption revealed that loss of HK3 has no effect on glycolytic activity in AML cell lines while knocking out HK2 significantly reduced basal glycolysis and glycolytic capacity. Instead, loss of HK3 but not HK2 led to increased sensitivity to ATRA-induced cell death in AML cell lines. We found that HK3 knockout (HK3-null) AML cells showed an accumulation of reactive oxygen species (ROS) as well as DNA damage during ATRA-induced differentiation. RNA sequencing analysis confirmed pathway enrichment for programmed cell death, oxidative stress, and DNA damage response in HK3-null AML cells. These signatures were confirmed in ATAC sequencing, showing that loss of HK3 leads to changes in chromatin configuration and increases the accessibility of genes involved in apoptosis and stress response. Through isoform-specific pulldowns, we furthermore identified a direct interaction between HK3 and the proapoptotic BCL-2 family member BIM, which has previously been shown to shorten myeloid life span. Our findings provide evidence that HK3 is dispensable for glycolytic activity in AML cells while promoting cell survival, possibly through direct interaction with the BH3-only protein BIM during ATRA-induced neutrophil differentiation

Modulation of enhancer looping and differential gene targeting by Epstein-Barr virus transcription factors directs cellular reprogramming

Epstein-Barr virus (EBV) epigenetically reprogrammes B-lymphocytes to drive immortalization and facilitate viral persistence. Host-cell transcription is perturbed principally through the actions of EBV EBNA 2, 3A, 3B and 3C, with cellular genes deregulated by specific combinations of these EBNAs through unknown mechanisms. Comparing human genome binding by these viral transcription factors, we discovered that 25% of binding sites were shared by EBNA 2 and the EBNA 3s and were located predominantly in enhancers. Moreover, 80% of potential EBNA 3A, 3B or 3C target genes were also targeted by EBNA 2, implicating extensive interplay between EBNA 2 and 3 proteins in cellular reprogramming. Investigating shared enhancer sites neighbouring two new targets (WEE1 and CTBP2) we discovered that EBNA 3 proteins repress transcription by modulating enhancer-promoter loop formation to establish repressive chromatin hubs or prevent assembly of active hubs. Re-ChIP analysis revealed that EBNA 2 and 3 proteins do not bind simultaneously at shared sites but compete for binding thereby modulating enhancer-promoter interactions. At an EBNA 3-only intergenic enhancer site between ADAM28 and ADAMDEC1 EBNA 3C was also able to independently direct epigenetic repression of both genes through enhancer-promoter looping. Significantly, studying shared or unique EBNA 3 binding sites at WEE1, CTBP2, ITGAL (LFA-1 alpha chain), BCL2L11 (Bim) and the ADAMs, we also discovered that different sets of EBNA 3 proteins bind regulatory elements in a gene and cell-type specific manner. Binding profiles correlated with the effects of individual EBNA 3 proteins on the expression of these genes, providing a molecular basis for the targeting of different sets of cellular genes by the EBNA 3s. Our results therefore highlight the influence of the genomic and cellular context in determining the specificity of gene deregulation by EBV and provide a paradigm for host-cell reprogramming through modulation of enhancer-promoter interactions by viral transcription factors

Zika Virus Infection as a Cause of Congenital Brain Abnormalities and Guillain-Barré Syndrome: Systematic Review.

BACKGROUND The World Health Organization (WHO) stated in March 2016 that there was scientific consensus that the mosquito-borne Zika virus was a cause of the neurological disorder Guillain-Barré syndrome (GBS) and of microcephaly and other congenital brain abnormalities based on rapid evidence assessments. Decisions about causality require systematic assessment to guide public health actions. The objectives of this study were to update and reassess the evidence for causality through a rapid and systematic review about links between Zika virus infection and (a) congenital brain abnormalities, including microcephaly, in the foetuses and offspring of pregnant women and (b) GBS in any population, and to describe the process and outcomes of an expert assessment of the evidence about causality. METHODS AND FINDINGS The study had three linked components. First, in February 2016, we developed a causality framework that defined questions about the relationship between Zika virus infection and each of the two clinical outcomes in ten dimensions: temporality, biological plausibility, strength of association, alternative explanations, cessation, dose-response relationship, animal experiments, analogy, specificity, and consistency. Second, we did a systematic review (protocol number CRD42016036693). We searched multiple online sources up to May 30, 2016 to find studies that directly addressed either outcome and any causality dimension, used methods to expedite study selection, data extraction, and quality assessment, and summarised evidence descriptively. Third, WHO convened a multidisciplinary panel of experts who assessed the review findings and reached consensus statements to update the WHO position on causality. We found 1,091 unique items up to May 30, 2016. For congenital brain abnormalities, including microcephaly, we included 72 items; for eight of ten causality dimensions (all except dose-response relationship and specificity), we found that more than half the relevant studies supported a causal association with Zika virus infection. For GBS, we included 36 items, of which more than half the relevant studies supported a causal association in seven of ten dimensions (all except dose-response relationship, specificity, and animal experimental evidence). Articles identified nonsystematically from May 30 to July 29, 2016 strengthened the review findings. The expert panel concluded that (a) the most likely explanation of available evidence from outbreaks of Zika virus infection and clusters of microcephaly is that Zika virus infection during pregnancy is a cause of congenital brain abnormalities including microcephaly, and (b) the most likely explanation of available evidence from outbreaks of Zika virus infection and GBS is that Zika virus infection is a trigger of GBS. The expert panel recognised that Zika virus alone may not be sufficient to cause either congenital brain abnormalities or GBS but agreed that the evidence was sufficient to recommend increased public health measures. Weaknesses are the limited assessment of the role of dengue virus and other possible cofactors, the small number of comparative epidemiological studies, and the difficulty in keeping the review up to date with the pace of publication of new research. CONCLUSIONS Rapid and systematic reviews with frequent updating and open dissemination are now needed both for appraisal of the evidence about Zika virus infection and for the next public health threats that will emerge. This systematic review found sufficient evidence to say that Zika virus is a cause of congenital abnormalities and is a trigger of GBS

Establishing the teratogenicity of Zika and evaluating causal criteria

The teratogenicity of the Zika virus was considered established in 2016, and is an interesting case because three different sets of causal criteria were used to assess teratogenicity. This paper appeals to the thesis of Russo and Williamson (2007) to devise an epistemological framework that can be used to compare and evaluate sets of causal criteria. The framework can also be used to decide when enough criteria are satisfied to establish causality. Arguably, the three sets of causal criteria considered here offer only a rudimentary assessment of mechanistic studies, and some suggestions are made as to alternative ways to establish causality