Pervasive gaps in Amazonian ecological research

Biodiversity loss is one of the main challenges of our time, and attempts to address it require a clear understanding of how ecological communities respond to environmental change across time and space. While the increasing availability of global databases on ecological communities has advanced our knowledge of biodiversity sensitivity to environmental changes, vast areas of the tropics remain understudied. In the American tropics, Amazonia stands out as the world's most diverse rainforest and the primary source of Neotropical biodiversity, but it remains among the least known forests in America and is often underrepresented in biodiversity databases. To worsen this situation, human-induced modifications 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, 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

Identification Of Target Genes Using Gene Expression Profile Of Granulocytes From Patients With Chronic Myeloid Leukemia Treated With Tyrosine Kinase Inhibitors

Differential gene expression analysis by suppression subtractive hybridization with correlation to the metabolic pathways involved in chronic myeloid leukemia (CML) may provide a new insight into the pathogenesis of CML. Among the overexpressed genes found in CML at diagnosis are SEPT5, RUNX1, MIER1, KPNA6 and FLT3, while PAN3, TOB1 and ITCH were decreased when compared to healthy volunteers. Some genes were identified and involved in CML for the first time, including TOB1, which showed a low expression in patients with CML during tyrosine kinase inhibitor treatment with no complete cytogenetic response. In agreement, reduced expression of TOB1 was also observed in resistant patients with CML compared to responsive patients. This might be related to the deregulation of apoptosis and the signaling pathway leading to resistance. Most of the identified genes were related to the regulation of nuclear factor κB (NF-κB), AKT, interferon and interleukin-4 (IL-4) in healthy cells. The results of this study combined with literature data show specific gene pathways that might be explored as markers to assess the evolution and prognosis of CML as well as identify new therapeutic targets. © 2014 Informa UK, Ltd.55818611869Luatti, S., Additional chromosomal abnormalities in Philadelphia-positive clone: Adverse prognostic influence on frontline imatinib therapy: A GIMEMA Working Party on CML analysis (2012) Blood, 120, pp. 761-767Deininger, M.W., Goldman, J.M., Melo, J.V., The molecular biology of chronic myeloid leukemia (2000) Blood, 96, pp. 3343-3356Baran, Y., Saydam, G., Cumulative clinical experience from a decade of use: Imatinib as first-line treatment of chronic myeloid leukemia (2012) J Blood Med, 3, pp. 139-150Melo, J.V., Hughes, T.P., Apperley, J.F., Chronic myeloid leukemia (2003) Hematology Am Soc Hematol Educ Program, pp. 132-152Mascarenhas, C.C., New mutations detected by denaturing high performance liquid chromatography during screening of exon 6 bcr-abl mutations in patients with chronic myeloid leukemia treated with tyrosine kinase inhibitors (2009) Leuk Lymphoma, 50, pp. 1148-1154Wong, S., Sole BCR-ABL inhibition is insufficient to eliminate all myeloproliferative disorder cell populations (2004) Proc Natl Acad Sci USA, 101, pp. 17456-17461Inokuchi, K., Chronic myelogenous leukemia: From molecular biology to clinical aspects and novel targeted therapies (2006) J Nippon Med Sch, 73, pp. 178-192Park, S., Application of array comparative genomic hybridization in chronic myeloid leukemia (2013) Methods Mol Biol, 973, pp. 55-68Remsing Rix, L.L., Global target profile of the kinase inhibitor bosutinib in primary chronic myeloid leukemia cells (2009) Leukemia, 23, pp. 477-485Canalli, A.A., Granulocytic adhesive interactions and their role in sickle cell vaso-occlusion (2005) Hematology, 10, pp. 419-425Diatchenko, L., Suppression subtractive hybridization: A method for generating diff erentially regulated or tissue-specific cDNA probes and libraries (1996) Proc Natl Acad Sci USA, 93, pp. 6025-6030Diatchenko, L., Suppression subtractive hybridization: A versatile method for identifying diff erentially expressed genes (1999) Methods Enzymol, 303, pp. 349-380Hillmann, A., Dunne, E., Kenny, D., CDNA amplification by SMARTPCR and suppression subtractive hybridization (SSH)-PCR (2009) Methods Mol Biol, 496, pp. 223-243Ewing, B., Base-calling of automated sequencer traces using phred I. Accuracy assessment (1998) Genome Res, 8, pp. 175-185Ghosh, S., Global gene expression and Ingenuity biological functions analysis on PCBs 153 and 138 induced human PBMC in vitro reveals diff erential mode(s) of action in developing toxicities (2011) Environ Int, 37, pp. 838-857Gilmore, T.D., The Rel/NF-kappaB signal transduction pathway: Introduction (1999) Oncogene, 18, pp. 6842-6844Samy, R.P., Identification of a novel Calotropis procera protein that can suppress tumor growth in breast cancer through the suppression of NF-kappaB pathway (2012) PLoS One, 7, pp. e48514Albensi, B.C., Mattson, M.P., Evidence for the involvement of TNF and NF-kappaB in hippocampal synaptic plasticity (2000) Synapse, 35, pp. 151-159Li, F., Sethi, G., Targeting transcription factor NF-kappaB to overcome chemoresistance and radioresistance in cancer therapy (2010) Biochim Biophys Acta, 1805, pp. 167-180Pezzolesi, M.G., Comparative genomic and functional analyses reveal a novel cis-acting PTEN regulatory element as a highly conserved functional E-box motif deleted in Cowden syndrome (2007) Hum Mol Genet, 16, pp. 1058-1071Bidere, N., Casein kinase 1alpha governs antigen-receptorinduced NF-kappaB activation and human lymphoma cell survival (2009) Nature, 458, pp. 92-96Cerveira, N., Bizarro, S., Teixeira, M.R., MLL-SEPTIN gene fusions in hematological malignancies (2011) Biol Chem, 392, pp. 713-724Zhao, L.J., Functional features of RUNX1 mutants in acute transformation of chronic myeloid leukemia and their contribution to inducing murine full-blown leukemia (2012) Blood, 119, pp. 2873-2882Ichikawa, M., AML-1 is required for megakaryocytic maturation and lymphocytic diff erentiation, but not for maintenance of hematopoietic stem cells in adult hematopoiesis (2004) Nat Med, 10, pp. 299-304Blackmore, T.M., The transcriptional cofactor MIER1-beta negatively regulates histone acetyltransferase activity of the CREBbinding protein (2008) BMC Res Notes, 1, p. 68Kohler, M., Evidence for distinct substrate specificities of importin alpha family members in nuclear protein import (1999) Mol Cell Biol, 19, pp. 7782-7791Murati, A., Myeloid malignancies: Mutations, models and management (2012) BMC Cancer, 12, p. 304Daver, N., FLT3 mutations in myelodysplastic syndrome and chronic myelomonocytic leukemia (2013) Am J Hematol, 88, pp. 56-59Bai, Y., Itch E3 ligase-mediated regulation of TGF-beta signaling by modulating smad2 phosphorylation (2004) Mol Cell, 15, pp. 825-831Tzachanis, D., Tob is a negative regulator of activation that is expressed in anergic and quiescent T cells (2001) Nat Immunol, 2, pp. 1174-1182Naka, K., TGF-beta-FOXO signalling maintains leukaemiainitiating cells in chronic myeloid leukaemia (2010) Nature, 463, pp. 676-680Ezzeddine, N., Human TOB, an antiproliferative transcription factor, is a poly(A)-binding protein-dependent positive regulator of cytoplasmic mRNA deadenylation (2007) Mol Cell Biol, 27, pp. 7791-7801Kundu, J., Tob1 induces apoptosis and inhibits proliferation, migration and invasion of gastric cancer cells by activating Smad4 and inhibiting betacatenin signaling (2012) Int J Oncol, 41, pp. 839-84