SpectraNet–53: A deep residual learning architecture for predicting soluble solids content with VIS–NIR spectroscopy

This work presents a new deep learning architecture, SpectraNet-53, for quantitative analysis of fruit spectra, optimized for predicting Soluble Solids Content (SSC, in Brix). The novelty of this approach resides in being an architecture trainable on a very small dataset, while keeping a performance level on-par or above Partial Least Squares (PLS), a time-proven machine learning method in the field of spectroscopy. SpectraNet-53 performance is assessed by determining the SSC of 616 Citrus sinensi L. Osbeck 'Newhall' oranges, from two Algarve (Portugal) orchards, spanning two consecutive years, and under different edaphoclimatic conditions. This dataset consists of short-wave near-infrared spectroscopic (SW-NIRS) data, and was acquired with a portable spectrometer, in the visible to near infrared region, on-tree and without temperature equalization. SpectraNet-53 results are compared to a similar state-of-the-art architecture, DeepSpectra, as well as PLS, and thoroughly assessed on 15 internal validation sets (where the training and test data were sampled from the same orchard or year) and on 28 external validation sets (training/test data sampled from different orchards/years). SpectraNet-53 was able to achieve better performance than DeepSpectra and PLS in several metrics, and is especially robust to training overfit. For external validation results, on average, SpectraNet-53 was 3.1% better than PLS on RMSEP (1.16 vs. 1.20 Brix), 11.6% better in SDR (1.22 vs. 1.10), and 28.0% better in R2 (0.40 vs. 0.31).project NIBAP ALG-01-0247-FEDER-037303, project OtiCalFrut ALG-010247-FEDER-033652info:eu-repo/semantics/publishedVersio

Microlensing as a probe of the Galactic structure; 20 years of microlensing optical depth studies

Microlensing is now a very popular observational astronomical technique. The investigations accessible through this effect range from the dark matter problem to the search for extra-solar planets. In this review, the techniques to search for microlensing effects and to determine optical depths through the monitoring of large samples of stars will be described. The consequences of the published results on the knowledge of the Milky-Way structure and its dark matter component will be discussed. The difficulties and limitations of the ongoing programs and the perspectives of the microlensing optical depth technique as a probe of the Galaxy structure will also be detailed.Comment: Accepted for publication in General Relativity and Gravitation. General Relativity and Gravitation in press (2010) 0

The GLEAMing of the first supermassive black holes

Galaxie

Taxonomy of the order Mononegavirales: update 2016

In 2016, the order Mononegavirales was emended through the addition of two new families (Mymonaviridae and Sunviridae), the elevation of the paramyxoviral subfamily Pneumovirinae to family status (Pneumoviridae), the addition of five free-floating genera (Anphevirus, Arlivirus, Chengtivirus, Crustavirus, and Wastrivirus), and several other changes at the genus and species levels. This article presents the updated taxonomy of the order Mononegavirales as now accepted by the International Committee on Taxonomy of Viruses (ICTV)

Optical properties of self organized silver nanocolumns

9th International Conference on Laser Ablation, Tenerife, Spain, September 24-28, 2007N

BCR-ABL V280G mutation, potential role in imatinib resistance: First case report

Export Date: 28 December 2017 Correspondence Address: Azevedo, A.P.; Department of Clinical Pathology, Hospital São Francisco Xavier, Centro Hospitalar Lisboa Ocidental, Estrada do Forte do Alto do Duque, Portugal; email: [email protected] Chemicals/CAS: glycine, 56-40-6, 6000-43-7, 6000-44-8; hydroxyurea, 127-07-1; imatinib, 152459-95-5, 220127-57-1; nilotinib, 641571-10-0; valine, 7004-03-7, 72-18-4 References: Radich, J.P., Shah, N.P., Mauro, M.J., Integrating current treatment options for TKIresistant chronic myeloid leukemia (2014) Clin Adv Hematol Oncol, 12 (11), pp. 3-17; Savona, M.R., Molecular monitoring and minimal residual disease in the management of chronic myelogenous leukemia (2014) J Community Support Oncol, 12, pp. 171-178; Kantarjian, H.M., Cortes, J., La Rosée, P., Hochhaus, A., Optimizing therapy for patients with chronic myelogenous leukemia in chronic phase (2010) Cancer, 116, pp. 1419-1430; Weisberg, E., Manley, P.W., Cowan-Jacob, S.W., Hochhaus, A., Griffin, J.D., Second generation inhibitors of BCR-ABL for the treatment of imatinib-resistant chronic myeloid leukaemia (2007) Nat Rev Cancer, 7, pp. 345-356; Nicolini, F.E., Corm, S., Lê, Q.H., Mutation status and clinical outcome of 89 imatinib mesylate-resistant chronic myelogenous leukemia patients: A retrospective analysis from the French intergroup of CML (Fi(phi)-LMC GROUP) (2006) Leukemia, 20, pp. 1061-1066; Soverini, S., Colarossi, S., Gnani, A., Contribution of ABL kinase domain mutations to imatinib resistance in different subsets of Philadelphia-positive patients: By the GIMEMA Working Party on Chronic Myeloid Leukemia (2006) Clin Cancer Res, 12, pp. 7374-7379; Sokal, J.E., Cox, E.B., Baccarani, M., Prognostic discrimination in “good-risk” chronic granulocytic leukemia (1984) Blood, 63, pp. 789-799; Hasford, J., Pfirrmann, M., Hehlmann, R., A new prognostic score for survival of patients with chronic myeloid leukemia treated with interferon alfa. Writing Committee for the Collaborative CML Prognostic Factors Project Group (1998) J Natl Cancer Inst, 90, pp. 850-858; Hasford, J., Baccarani, M., Hoffmann, V., Predicting complete cytogenetic response and subsequent progression-free survival in 2060 patients with CML on imatinib treatment: The EUTOS score (2011) Blood, 118, pp. 686-692; Gromicho, M., Magalhães, M., Torres, F., Instability of mRNA expression signatures of drug transporters in chronic myeloid leukemia patients resistant to imatinib (2013) Oncol Rep, 29, pp. 741-750; Liu, L.L., Li, F., Pao, W., Michor, F., Dose-dependent mutation rates determine optimum erlotinib dosing strategies for EGFR mutant non-small cell lung cancer patients (2015) Plos ONE, 10; Tang, C., Schafranek, L., Watkins, D.B., Tyrosine kinase inhibitor resistance in chronic myeloid leukemia cell lines: Investigating resistance pathways (2011) Leuk Lymphoma, 52, pp. 2139-2147; Hayakawa, H., Ichihara, E., Ohashi, K., Lower gefitinib dose led to earlier resistance acquisition before emergence of T790M mutation in epidermal growth factor receptor-mutated lung cancer model (2013) Cancer Sci, 104, pp. 1440-1446; Santos, F.P., Kantarjian, H., Fava, C., Clinical impact of dose reductions and interruptions of second-generation tyrosine kinase inhibitors in patients with chronic myeloid leukaemia (2010) Br J Haematol, 150, pp. 303-312; Van Obbergh, F., Knoops, L., Devos, T., The clinical relevance of imatinib plasma trough concentrations in chronic myeloid leukemia. A Belgian study [published online ahead of print December 22, 2016] Clin Biochem; Vine, J., Cohen, S.B., Ruchlemer, R., Polymorphisms in the human organic cation transporter and the multidrug resistance gene: Correlation with imatinib levels and clinical course in patients with chronic myeloid leukemia (2014) Leuk Lymphoma, 55, pp. 2525-2531; Sundar, H., Radich, J., Optimizing patient care in chronic phase Chronic Myelogenous Leukemia: A multidisciplinary approach (2016) J Natl Compr Cancer Netw, 14, pp. s1-s6; McDougall, J., Ramsey, S.D., Radich, J., What happens when imatinib goes generic? (2016) J Natl Compr Canc Netw, 14, pp. 128-131; Hochhaus, A., Saglio, G., Hughes, T.P., Long-term benefits and risks of frontline nilotinib vs imatinib for chronic myeloid leukemia in chronic phase: 5-year update of the randomized ENESTnd trial (2016) Leukemia, 30, pp. 1044-1054; Cortes, J.E., Saglio, G., Kantarjian, H.M., Final 5-year study results of DASISION: The dasatinib versus imatinib study in treatment-naïve chronic myeloid leukemia patients trial (2016) J Clin Oncol, 34, pp. 2333-2340; Druker, B.J., Guilhot, F., O’Brien, S.G., Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia (2006) N Engl J Med, 355, pp. 2408-2417; Soverini, S., De Benedittis, C., Mancini, M., Martinelli, G., Mutations in the BCRABL1 kinase domain and elsewhere in chronic myeloid leukemia (2015) Clin Lymphoma Myeloma Leuk, 15, pp. S120-S128; O’Brien, S., Radich, J.P., Abboud, C.N., Chronic myelogenous leukemia, version 1.2015 (2014) J Natl Compr Canc Netw, 12, pp. 1590-1610; Baccarani, M., Deininger, M.W., Rosti, G., European LeukemiaNet recommendations for the management of chronic myeloid leukemia: 2013 (2013) Blood, 122, pp. 872-884; Deininger, M.W., Molecular monitoring in CML and the prospects for treatmentfree remissions (2015) Hematology am Soc Hematol Educ Program, 2015, pp. 257-263; Soverini, S., Hochhaus, A., Nicolini, F.E., BCR-ABL kinase domain mutation analysis in chronic myeloid leukemia patients treated with tyrosine kinase inhibitors: Recommendations from an expert panel on behalf of European LeukemiaNet (2011) Blood, 118, pp. 1208-1215; Soverini, S., Branford, S., Nicolini, F.E., Implications of BCR-ABL1 kinase domain- mediated resistance in chronic myeloid leukemia (2014) Leuk Res, 38, pp. 10-20; Machova Polakova, K., Kulvait, V., Benesova, A., Next-generation deep sequencing improves detection of BCR-ABL1 kinase domain mutations emerging under tyrosine kinase inhibitor treatment of chronic myeloid leukemia patients in chronic phase (2015) J Cancer Res Clin Oncol, 141, pp. 887-899; Jabbour, E., Saglio, G., Hughes, T.P., Kantarjian, H., Suboptimal responses in chronic myeloid leukemia: Implications and management strategies (2012) Cancer, 118, pp. 1181-1191; Gruber, T.A., Chang, M.S., Sposto, R., Müschen, M., Activation-induced cytidine deaminase accelerates clonal evolution in BCR-ABL1-driven B-cell lineage acute lymphoblastic leukemia (2010) Cancer Res, 70, pp. 7411-7420Introduction: The identification of BCR-ABL expression as the defining leukemogenic event in chronic myeloid leukemia (CML) and the introduction of BCR-ABL tyrosine kinase inhibitors in 2001 have revolutionized disease management, leading to a reduction in mortality rates and accordingly an increase in the estimated prevalence of CML. Case report: Based on medical records and clinical follow-up, the authors present the case of a Philadelphia chromosome–positive CML patient who developed resistance to imatinib. Quantitative reverse transcription-polymerase chain reaction testing revealed a V280G BCR-ABL mutation. Discussion and conclusions: This is the first report describing a new BCR-ABL kinase domain mutation—V280G—that might be associated with resistance to imatinib. Approximately 15% to 30% of patients treated with imatinib discontinue treatment due to resistance or intolerance. More than 90 BCR-ABL mutations were detected so far, conferring variable degrees of drug resistance, with consequent clinical, therapeutic, and prognostic impact. © The Author(s) 2017.publishersversionpublishe