Pervasive gaps in Amazonian ecological research

Biodiversity loss is one of the main challenges of our time,1,2 and attempts to address it require a clear understanding of how ecological communities respond to environmental change across time and space.3,4 While the increasing availability of global databases on ecological communities has advanced our knowledge of biodiversity sensitivity to environmental changes,5,6,7 vast areas of the tropics remain understudied.8,9,10,11 In the American tropics, Amazonia stands out as the world's most diverse rainforest and the primary source of Neotropical biodiversity,12 but it remains among the least known forests in America and is often underrepresented in biodiversity databases.13,14,15 To worsen this situation, human-induced modifications16,17 may eliminate pieces of the Amazon's biodiversity puzzle before we can use them to understand how ecological communities are responding. To increase generalization and applicability of biodiversity knowledge,18,19 it is thus crucial to reduce biases in ecological research, particularly in regions projected to face the most pronounced environmental changes. We integrate ecological community metadata of 7,694 sampling sites for multiple organism groups in a machine learning model framework to map the research probability across the Brazilian Amazonia, while identifying the region's vulnerability to environmental change. 15%–18% of the most neglected areas in ecological research are expected to experience severe climate or land use changes by 2050. This means that unless we take immediate action, we will not be able to establish their current status, much less monitor how it is changing and what is being lost

Single Nucleotide Polymorphisms at +191 and +292 of Galectin-3 Gene (LGALS3) Related to Lower GAL-3 Serum Levels Are Associated with Frequent Respiratory Tract Infection and Vaso-Occlusive Crisis in Children with Sickle Cell Anemia

Submitted by Adagilson Silva ([email protected]) on 2017-06-05T13:08:05Z No. of bitstreams: 1 27603703 2016 men-sin.oa.PDF: 1008770 bytes, checksum: 82f0081628ade062bc08ce6be5782a03 (MD5)Approved for entry into archive by Adagilson Silva ([email protected]) on 2017-06-05T13:08:29Z (GMT) No. of bitstreams: 1 27603703 2016 men-sin.oa.PDF: 1008770 bytes, checksum: 82f0081628ade062bc08ce6be5782a03 (MD5)Made available in DSpace on 2017-06-05T13:08:29Z (GMT). No. of bitstreams: 1 27603703 2016 men-sin.oa.PDF: 1008770 bytes, checksum: 82f0081628ade062bc08ce6be5782a03 (MD5) Previous issue date: 2016Programa de Doutorado da Rede Nordeste de Biotecnologia. Recife, PE, Brasil.Universidade de Pernambuco. Instituto de Ciências Biológicas e Faculdade de Ciências Médicas. Recife, PE, Brasil.Universidade de Pernambuco. Instituto de Ciências Biológicas e Faculdade de Ciências Médicas. Recife, PE, Brasil.Universidade Federal de Pernambuco. Laboratório de Imunomodulação e Novas Abordagens Terapêutica (LINAT). Recife, PE, Brasil.Universidade de Pernambuco. Instituto de Ciências Biológicas e Faculdade de Ciências Médicas. Recife, PE, Brasil.Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.Fundação Hematologia e Hemoterapia de Pernambuco (HEMOPE). Recife, PE, Brasil.Universidade Federal de Pernambuco. Departamento de Ciências Biológicas. Recife, PE, Brasil.Universidade Federal de Pernambuco. Laboratório de Imunomodulação e Novas Abordagens Terapêutica (LINAT). Recife, PE, Brasil.Universidade Federal de Pernambuco. Departamento de Ciências Biológicas. Recife, PE, Brasil.Fundação Hematologia e Hemoterapia de Pernambuco (HEMOPE). Recife, PE, Brasil.Universidade Federal de Pernambuco. Laboratório de Imunomodulação e Novas Abordagens Terapêutica (LINAT). Recife, PE, Brasil.Programa de Doutorado da Rede Nordeste de Biotecnologia. Recife, PE, Brasil / Universidade de Pernambuco. Instituto de Ciências Biológicas e Faculdade de Ciências Médicas. Recife, PE, Brasil.Programa de Doutorado da Rede Nordeste de Biotecnologia. Recife, PE, Brasil / Universidade de Pernambuco. Instituto de Ciências Biológicas e Faculdade de Ciências Médicas. Recife, PE, Brasil.Patients with sickle cell anemia (SCA) may present chronic hemolytic anemia, vaso-occlusion and respiratory tract infection (RTI) episodes. Galectin-3 (GAL-3) is a multifunctional protein involved in inflammation, apoptosis, adhesion and resistance to reactive oxygen species. Studies point to a dual role for GAL-3 as both a circulation damage-associated molecular pattern and a cell membrane associated pattern recognition receptor

Serum galectin-3 levels are associated with <i>LGALS3</i> +191 and +292 combined genotypes in children with SCA.

<p>Statistical analysis of <i>LGALS3</i> combined genotype related of galectin-3 levels (high, intermediate and low) in which the serum concentrations in ng/ml were compared using Kruskal-Wallis test. High vs. intermediate: <i>p =</i> 0.1687; high vs. low: <i>p =</i> 0.0002; high vs. intermediate+low: <i>p</i> = 0.0098.</p

Clinical data of children with sickle cell anemia attended in Hemope Foundation—Recife/Brazil.

<p>Clinical data of children with sickle cell anemia attended in Hemope Foundation—Recife/Brazil.</p

<i>LGALS3</i> +191 and +292 diplotype of serum levels with vaso-occlusive crisis and respiratory tract infection in children with sickle cell anemia attended in Hemope Foundation—Recife/Brazil.

<p><i>LGALS3</i> +191 and +292 diplotype of serum levels with vaso-occlusive crisis and respiratory tract infection in children with sickle cell anemia attended in Hemope Foundation—Recife/Brazil.</p

Single Nucleotide Polymorphisms at +191 and +292 of Galectin-3 Gene (<i>LGALS3</i>) Related to Lower GAL-3 Serum Levels Are Associated with Frequent Respiratory Tract Infection and Vaso-Occlusive Crisis in Children with Sickle Cell Anemia

<div><p>Introduction</p><p>Patients with sickle cell anemia (SCA) may present chronic hemolytic anemia, vaso-occlusion and respiratory tract infection (RTI) episodes. Galectin-3 (GAL-3) is a multifunctional protein involved in inflammation, apoptosis, adhesion and resistance to reactive oxygen species. Studies point to a dual role for GAL-3 as both a circulation damage-associated molecular pattern and a cell membrane associated pattern recognition receptor.</p><p>Objective</p><p>To investigate associations between the SNPs of GAL-3 gene (<i>LGALS3</i>) and serum levels with RTI and vaso-occlusive crisis (VOC) in children with SCA.</p><p>Materials and Methods</p><p>SNPs +191 and +292 in <i>LGALS3</i> were studied using the TaqMan real-time PCR system; GAL-3 serum levels were measured by ELISA. The study included 79 children with SCA ranging from 2 to 12 years old.</p><p>Results</p><p>GAL-3 serum levels were associated with <i>LGALS3</i> +191 and +292 genotypes (<i>p</i> <0.0001; <i>p</i> = 0.0169, respectively). <i>LGALS3</i> +191, AA genotype was associated with low and CC with higher levels of GAL-3. For <i>LGALS3</i> +292, the CC genotype was associated with lower GAL-3 and AA with higher levels. Patients with Frequency of RTI (FRTI) ≥1 presented higher frequency of +191AA (<i>p</i> = 0.0263) and +292AC/CC genotypes (<i>p</i> = 0.0320). SNP +292 was associated with Frequency of VOC (FVOC) (<i>p</i> = 0.0347), whereas no association was shown with SNP +191 and FVOC. However, CA/AC and AA/CC genotypes with lower GAL-3 levels showed a higher frequency in patients with FRTI ≥1 (<i>p</i> = 0.0170; <i>p</i> = 0.0138, respectively). Also, patients with FVOC ≥1 presented association with CA/AC (<i>p</i> = 0.0228). <i>LGALS3</i> +191 and +292 combined genotypes related to low (<i>p</i> = 0.0263) and intermediate expression (<i>p</i> = 0.0245) were associated with FRTI ≥1. Lower GAL-3 serum levels were associated with FRTI ≥1 (<i>p</i> = 0.0426) and FVOC ≥1 (<i>p</i> = 0.0012).</p><p>Conclusion</p><p>Variation of GAL-3 serum levels related to SNPs at +191 and +292 may constitute a susceptibility factor for RTI and VOC frequency.</p></div