Total nutritional therapy : a nutrition education program for physicians

Objetivo: Casi la mitad de todos los pacientes hospitalizados se encuentran desnutridos y los médicos tienen muy poco conocimiento o apenas utilizan el soporte nutricional1. Para corregir este problema, la Federación Latinoamericana de Nutrición Parenteral y Enteral (FELANPE) ideó un curso introductorio de nutrición clínica para médicos de dos días, con el apoyo de los Laboratorios Abbott. El objetivo del tratamiento nutricional total (TNT) es ayudar al médico a aprovechar sus conocimientos de nutrición para incrementar la conciencia sobre malnutrición y aplicación del tratamiento nutricional. Desde 1997, más de 8.000 médicos han completado el curso TNT en 16 países latinoamericanos. Métodos y procedimientos experimentales: Durante 1999 y 2000, 675 participantes respondieron, seis meses después de haber terminado el curso TNT, a una encuesta en la que se pretendía averiguar la repercusión que había tenido el curso en el uso de la evaluación nutricional, los equipos de apoyo nutricional o las consultas sobre nutrición en la práctica clínica y si habían participado en alguna asociación o conferencia de nutrición. Resultados: La mayoría de los médicos que rellenaron la encuesta había aumentado el uso de las herramientas de evaluación nutricional y el tiempo dedicado a este tratamiento; asimismo, había aumentado el número de pacientes que recibieron tratamiento nutricional. Conclusiones: El curso TNT ha resultado un modelo eficiente para la educación de los médicos generales en nutrición clínica. Este curso debería integrarse en la formación de los médicos residentes.Q4Q3Objective: Almost half of all hospitalized patients are malnourished with low physician awareness or implementation of nutrition support1. To address this problem, a 2-day immersion course in clinical nutrition for physicians was developed by the Latin American Federation of Parenteral and Enteral Nutrition (FELANPE) with support from Abbott Laboratories. The goal of Total Nutritional Therapy (TNT) is to help physicians utilize this nutrition knowledge to increase their awareness of malnutrition and implementation of nutritional therapy. Since 1997, over 8,000 physicians have completed the TNT course in 16 Latin American countries. Research Methods & Procedures: During 1999 and 2000, 675 participants responded to a survey 6 months after having completed the TNT course to determine what impact the course had on the use of nutrition assessment, nutrition support teams, or nutrition consultations in their clinical practice, and if they had participated in any nutrition association or conferences. Results: The majority of physicians who completed the survey increased their use of nutrition assessment and time dedicated to nutrition therapy, and increased the number of their patients placed on nutrition therapy. Conclusions: The TNT course has been shown to be an efficient model of clinical nutrition education for general physicians. The course should be considered as part of the training of medical residents.https://orcid.org/0000-0003-0401-0743N/

SAP Regulates TH2 Differentiation and PKC-θ-Mediated Activation of NF-κB1

AbstractXLP is caused by mutations affecting SAP, an adaptor that recruits Fyn to SLAM family receptors. SAP-deficient mice recapitulate features of XLP, including increased T cell activation and decreased humoral responses post-infection. SAP-deficient T cells also show increased TCR-induced IFN-γ and decreased TH2 cytokine production. We demonstrate that the defect in IL-4 secretion in SAP-deficient T cells is independent of increased IFN-γ production. SAP-deficient cells respond normally to polarizing cytokines, yet show impaired TCR-mediated induction of GATA-3 and IL-4. Examination of TCR signaling revealed normal Ca2+ mobilization and ERK activation in SAP-deficient cells, but decreased PKC-θ recruitment, Bcl-10 phosphorylation, IκB-α degradation, and nuclear NF-κB1/p50 levels. Similar defects were observed in Fyn-deficient cells. SLAM engagement amplified PKC-θ recruitment in wt but not SAP- or Fyn-deficient cells, arguing that a SAP/Fyn-mediated pathway enhances PKC-θ/NF-κB1 activation and suggesting a role for this pathway in TH2 regulation

Expert range maps of global mammal distributions harmonised to three taxonomic authorities

Aim Comprehensive, global information on species' occurrences is an essential biodiversity variable and central to a range of applications in ecology, evolution, biogeography and conservation. Expert range maps often represent a species' only available distributional information and play an increasing role in conservation assessments and macroecology. We provide global range maps for the native ranges of all extant mammal species harmonised to the taxonomy of the Mammal Diversity Database (MDD) mobilised from two sources, the Handbook of the Mammals of the World (HMW) and the Illustrated Checklist of the Mammals of the World (CMW). Location Global. Taxon All extant mammal species. Methods Range maps were digitally interpreted, georeferenced, error-checked and subsequently taxonomically aligned between the HMW (6253 species), the CMW (6431 species) and the MDD taxonomies (6362 species). Results Range maps can be evaluated and visualised in an online map browser at Map of Life (mol.org) and accessed for individual or batch download for non-commercial use. Main conclusion Expert maps of species' global distributions are limited in their spatial detail and temporal specificity, but form a useful basis for broad-scale characterizations and model-based integration with other data. We provide georeferenced range maps for the native ranges of all extant mammal species as shapefiles, with species-level metadata and source information packaged together in geodatabase format. Across the three taxonomic sources our maps entail, there are 1784 taxonomic name differences compared to the maps currently available on the IUCN Red List website. The expert maps provided here are harmonised to the MDD taxonomic authority and linked to a community of online tools that will enable transparent future updates and version control.Output Status: Forthcoming/Available Online Output Type: Data Article Additional co-authors: Kira McCall, Ajay Ranipeta, Anna Schuerkmann, Michael A. Torselli, Thomas Lacher Jr, Russell A. Mittermeier, Anthony B. Rylands, Wes Sechrest, Don E. Wilson, Agustín M. Abba, Luis F. Aguirre, Joaquín Arroyo-Cabrales, Diego Astúa, Andrew M. Baker, Gill Braulik, Janet K. Braun, Jorge Brito, Peter E. Busher, Santiago F. Burneo, M. Alejandra Camacho, Paolo Cavallini, Elisandra de Almeida Chiquito, Joseph A. Cook, Tamás Cserkész, Gábor Csorba, Erika Cuéllar Soto, Valeria da Cunha Tavares, Tim R. B. Davenport, Thomas Deméré, Christiane Denys, Christopher R. Dickman, Mark D. B. Eldridge, Eduardo Fernandez-Duque, Charles M. Francis, Greta Frankham, William L. Franklin, Thales Freitas, J. Anthony Friend, Elizabeth L. Gadsby, Guilherme S. T. Garbino, Philippe Gaubert, Norberto Giannini, Thomas Giarla, Jason S. Gilchrist, Jaime Gongora, Steven M. Goodman, Sharon Gursky-Doyen, Klaus Hackländer, Mark S. Hafner, Melissa Hawkins, Kristofer M. Helgen, Steven Heritage, Arlo Hinckley, Stefan Hintsche, Mary Holden, Kay E. Holekamp, Rodney L. Honeycutt, Brent A. Huffman, Tatyana Humle, Rainer Hutterer, Carlos Ibáñez Ulargui, Stephen M. Jackson, Jan Janecka, Mary Janecka, Paula Jenkins, Rimvydas Juškaitis, Javier Juste, Roland Kays, C. William Kilpatrick, Tigga Kingston, John L. Koprowski, Boris Kryštufek, Tyrone Lavery, Thomas E. Lee Jr, Yuri L. R. Leite, Roberto Leonan M. Novaes, Burton K. Lim, Andrey Lissovsky, Raquel López-Antoñanzas, Adrià López-Baucells, Colin D. MacLeod, Michael A. Mares, Helene Marsh, Stefano Mattioli, Erik Meijaard, Ara Monadjem, F. Blake Morton, Grace Musser, Tilo Nadler, Ryan W. Norris, Agustina Ojeda, Nicté Ordóñez-Garza, Ulyses F. J. Pardiñas, Bruce D. Patterson, Ana Pavan, Michael Pennay, Calebe Pereira, Joyce Prado, Helder L. Queiroz, Matthew Richardson, Erin P. Riley, Stephen J. Rossiter, Daniel I. Rubenstein, Dennisse Ruelas, Jorge Salazar-Bravo, Stéphanie Schai-Braun, Cody J. Schank, Christoph Schwitzer, Lori K. Sheeran, Myron Shekelle, Georgy Shenbrot, Pipat Soisook, Sergio Solari, Richard Southgate, Mariella Superina, Andrew B. Taber, Maurício Talebi, Peter Taylor, Thong Vu Dinh, Nelson Ting, Diego G. Tirira, Susan Tsang, Samuel T. Turvey, Raul Valdez, Victor Van Cakenberghe, Geraldine Veron, Janette Wallis, Rod Wells, Danielle Whittaker, George Wittemyer, John Woinarski, Dietmar Zinner, Nathan S. Upham, Walter Jet

Follow-up study on lead exposure in children living in a smelter community in northern Mexico

<p>Abstract</p> <p>Background</p> <p>To study the changes of children lead exposure in the city of Torreon during the last five years, after environmental and public health interventions, using the timeline of lead in blood concentration as the biomarker of exposure and its relation to lead in soil concentrations.</p> <p>Methods</p> <p>This follow-up study started in 2001 and consisted of 232 children living in nine neighborhoods in Torreon. Children were tested at 0, 6, 12 and 60 months. Lead in blood concentrations, Hemoglobin, Zinc-Protoporphyrin, anthropometric measures and socioeconomic status questionnaire was supplied to the parents.</p> <p>Results</p> <p>Median and range of lead in blood concentrations obtained at 0, 6, 12, 60 months were: 10.12 μg/dl (1.9 - 43.8), 8.75 μg/dl (1.85 - 41.45), 8.4 μg/dl (1.7 - 35.8) and 4.4 μg/dl (1.3 - 30.3), respectively. The decrease of lead in blood levels was significantly related to ages 0, 6, 12 and 60 months of the follow-up study. The timeline of B-Pb was associated with the timeline of lead in soil concentrations.</p> <p>Conclusions</p> <p>B-Pb levels have significantly decreased in the group of children studied. This could be explained by a) environmental interventions by authorities and the smelter companies, b) normal changes in hygienic habits as children age and c) lead redistribution from blood to hard tissues.</p

HLA-DRB1 association with Henoch-Schonlein purpura

Objective: Henoch-Schönlein purpura (HSP) is the most common vasculitis in children but it is not exceptional in adults. Increased familial occurrence supports a genetic predisposition for HSP. In this context, an association with the human leukocyte antigen-HLA-DRB1*01 phenotype has been suggested in Caucasian individuals with HSP. However, data on the potential association of HSP with HLA-DRB1*01 were based on small case series. To further investigate this issue, we performed HLA-DRB1 genotyping of the largest series of HSP patients ever assessed for genetic studies in Caucasians. Methods: 342 Spanish patients diagnosed with HSP fulfilling the American College of Rheumatology and the Michel et al classification criteria, and 303 sex and ethnically matched controls were assessed. HLA-DRB1 alleles were determined using a PCR-Sequence-Specific-Oligonucleotide Probe (PCR-SSOP) method. Results: A statistically significant increase of HLA-DRB1*01 in HSP patients when compared with controls was found (43% vs 7%, respectively; p<0.001; odds ratio-OR=2.03 [1.43-2.87]). It was due to the increased frequency of HLA-DRB1*0103 phenotype in HSP (14% vs 2%; p<0.001; OR=8.27 [3.46-23.9]). These results remained statistically significant after adjusting for Bonferroni correction. In contrast, a statistically significant decreased frequency of the HLA-DRB1*0301 phenotype was observed in patients compared to controls (5.6% vs 18.1%, respectively; p<0.001, OR=0.26 [0.14-0.47]), even after adjustment for Bonferroni correction. No HLA-DRB1 association with specific features of the disease was found. Conclusion: Our study confirms an association of HSP with HLA-DRB1*01 in Caucasians. Also, a protective effect against the development of HSP appears to exist in Caucasians carrying the HLA-DRB1*03 phenotype

Protective Role of the Interleukin 33 rs3939286 Gene Polymorphism in the Development of Subclinical Atherosclerosis in Rheumatoid Arthritis Patients

OBJECTIVES: To determine whether the interleukin-33 (IL-33)-interleukin-1 receptor like 1 (IL-1RL1) signaling pathway is implicated in the risk of subclinical atherosclerosis in patients with rheumatoid arthritis (RA). METHODS: A total of 576 Spanish RA patients from Northern Spain were genotyped for 6 well-known IL33-IL1RL1 polymorphisms (IL33 rs3939286, IL33 rs7025417, IL33 rs7044343, IL1RL1 rs2058660, IL1RL1 rs2310173 and IL1RL1 rs13015714) by TaqMan genotyping assay. The presence of subclinical atherosclerosis was determined by the assessment of carotid intima-media thickness (cIMT) by carotid ultrasound (US). RESULTS: RA patients carrying the TT genotype of the IL33 rs3939286 polymorphism had lower cIMT values than those homozygous for the CC genotype (mean ± standard deviation (SD): 0.71 ± 0.14 mm versus 0.76 ± 0.16 mm, respectively) while patients carrying the CT genotype had intermediate cIMT values (mean ± SD: 0.73 ± 0.17 mm). Moreover, RA patients carrying the mutant allele T of the IL33 rs3939286 polymorphism exhibited significantly lower cIMT values than those carrying the wild allele C (mean ± SD: 0.72 ± 0.16 mm versus 0.75 ± 0.18 mm respectively; p = 0.04). The association of both genotype and allele frequencies of IL33 rs3939286 and cIMT levels remained statistically significant after adjustment for sex, age at the time of US study, follow-up and center (p = 0.006 and p = 0.0023, respectively), evidencing that the potential effect conferred by IL33 rs3939286 may be independent of confounder factors. No association with other IL33-IL1RL1 genetic variants was observed. CONCLUSIONS: In conclusion, our results may suggest a potential protective effect of the IL33 rs3939286 allele T in the risk of subclinical atherosclerosis in patients with RA

Role of PTPN22 and CSK gene polymorphisms as predictors of susceptibility and clinical heterogeneity in patients with Henoch-Schönlein purpura (IgA vasculitis)

INTRODUCTION: To determine whether the PTPN22 (protein tyrosine phosphatase nonreceptor 22)/CSK (c-src tyrosine kinase) pathway is implicated in the susceptibility and clinical heterogeneity of Henoch-Schönlein purpura (HSP) in the largest series of Caucasian HSP patients ever assessed for genetic studies. METHODS: A set of 329 Spanish patients diagnosed with HSP fulfilling the American College of Rheumatology and the Michel et al. classification criteria and 515 sex and ethnically matched controls were recruited in this study. Two well-known CSK (CSK rs34933034 and CSK rs1378942) and two functional PTPN22 (PTPN22 rs2476601 (R620W) and PTPN22 rs33996649 (R263Q)) polymorphisms, previously associated with autoimmunity, were genotyped with TaqMan single nucleotide polymorphism (SNP) genotyping assays. RESULTS: No significant differences in the genotype and allele frequencies between HSP patients and controls were observed when the CSK rs34933034, CSK rs1378942, PTPN22 rs2476601 (R620W) and PTPN22 rs33996649 (R263Q) polymorphisms were analyzed independently. In keeping with this observation, no significant differences were found when we assessed these polymorphisms combined conforming haplotypes. In addition, there were no differences in the allele or genotype frequencies when HSP patients were stratified according the age at disease onset, sex, presence of arthralgia/arthritis, nephritis or gastrointestinal manifestations. CONCLUSIONS: Our results do not support association between PTPN22/CSK and HSP