Automobilismo: no calor da competição Automovilismo: en el calor de la competición Car racing: in the heat of competition

O presente artigo questiona o papel do calor como um fator de risco adicional para o acidente que vitimou Ayrton Senna. O automobilismo de competição constitui um desafio biológico, uma situação estressante do ponto de vista mental e físico. A manutenção da performance depende da disponibilidade de carboidratos e oxigênio, hidratação adequada e temperatura interna constante entre 37 e 38 graus centígrados. A dissipação do calor produzido pelo metabolismo ocorre através do aumento do fluxo de sangue para pele e produção de suor e manter a temperatura cerebral constante se constitui num problema permanente. Verificou-se experimentalmente que a energia necessária para dirigir um automóvel de corrida é comparável a um esporte como o voleibol. Durante uma corrida, o indivíduo está exposto a um microambiente quente na cabina, que pode atingir 50ºC, gerado por fontes de calor mecânicas e ambientais. O bloqueio da evaporação do suor pelo macacão resulta em umidade e desconforto pessoal, o que implica maior esforço mental para dirigir o carro. As medidas contra o calor começam antes da corrida, cuidando-se do estado nutricional, da hidratação e principalmente do condicionamento físico através de exercícios aeróbios regulares e adequados, que permitem aumentar a capacidade de trabalho e a tolerância ao calor, o que resulta em menor fadiga durante a corrida. Outro procedimento importante deveria ser a aclimatação prévia dos pilotos aos ambientes quentes e úmidos. Deve-se fazer o possível para reduzir o aquecimento do veículo e respeitar o sistema de bandeiras de advertência para os riscos de hipertermia. Em conclusão, embora Ayrton Senna fosse um indivíduo com maior risco de desenvolver hipertermia, independentemente de outras causas, não parece ter havido tempo de corrida suficiente para haver produção de calor metabólico capaz de aumentar excessivamente a temperatura interna do piloto nas condições ambientais do autódromo no dia de sua morte.<br>El presente artículo cuestiona el papel del calor como un factor de riesgo adicional para el accidente que sufrió Ayrton Senna. El automovilismo de competición constituye un desafío biológico, una situación estresante desde el punto de vista mental y físico. El mantenimiento de la performance depende de la disponibilidad de los carbohidratos y del oxígeno, hidratación adecuada y temperatura interna constante entre 37 y 38 grados centígrados. La disipación de calor producido por el metabolismo que ocurre a través del aumento del flujo de sangre para mantener la temperatura cerebral constante constituye un problema permanente. Se ha verificado experimentalmente que la energía requerida para conducir un auto de carrera es similar a la requerida para practicar un deporte como el voleibol. Durante una carrera, el individuo está expuesto a un microambiente caliente dentro de la cabina que puede llegar hasta los 50 grados centígrados generado por fuentes de calor como las mecánicas y las ambientales. El bloque del sudor por el mameluco resulta en humedad y disconfor personal, lo que implica un mayor esfuerzo personal para conducir el auto. Las medidas contra el calor comienzan antes de la carrera, cuidando el estado nutricional, la hidratación y principalmente el acondicionamiento físico a través de ejercicios aeróbicos regulares y adecuados, que permitan aumentar la capacidad de trabajo y la tolerancia al calor, lo que resulta en una menor fatiga durante la carrera. Otro procedimiento importante debería ser la aclimatación de los pilotos en ambientes calientes y húmedos. Se debe realizar lo posible en el acondicionamiento del vehículo para respetar el sistema de banderas de advertencia para los riesgos de hipertermia. En conclusión, si ahora Ayrton Senna fuera un individuo con mayor riesgo de desarrollar hipertermia, independientemente de otras causas, no parece haber habido tiempo suficiente en la carrera para la producción del calor metabólico capaz de aumentar excesivamente la temperatura interna del piloto en las condiciones ambientales del autódromo el día de su muerte.<br>The present study discusses the role of heat as an additional risk factor for the accident that killed the pilot Ayrton Senna. The competition car racing is a biological challenge, a stressing situation from the physical and mental point of view. The maintenance of performance depends on the oxygen and carbohydrates availability, adequate hydration and constant internal temperature, between 37 and 38ºC. The dissipation of heat produced by the metabolism occurs through the increase on the cutaneous blood flow and sweat and maintaining brain temperature constant becomes a permanent problem. It was experimentally verified that the energy required to the racecar driving is comparable to a sport such as volleyball. During a car race, the individual is exposed to a hot microenvironment in the cockpit, sometimes reaching 50ºC, generated by mechanical and environmental sources of heat. The obstruction of the sweat evaporation by the racesuit results in humidity and personal discomfort, what leads to higher mental effort to drive the car. The anti-heat measures are adopted before the race, considering the nutritional state, hydration and specially the physical conditioning through adequate and regular aerobic exercises that enable increasing the work capacity and the heat tolerance, resulting in lower fatigue during the car racing. Another important procedure should be the previous acclimation of pilots to hot and humid environments. All efforts should be done to reduce the vehicle heating and to respect the warning flag system for the risks of hyperthermia. Finally, although Ayrton Senna was an individual with higher risk of developing hyperthermia, regardless other causes, it seems not to have elapsed sufficient time of race in order to produce metabolic heat capable to increase excessively the pilot's internal temperature in the environmental conditions of the autodrome in the day of his death

International retrospective study of allogeneic hematopoietic cell transplantation for activated PI3K-delta syndrome.

BACKGROUND Activated phosphoinositide 3-kinase delta syndrome (APDS) is a combined immunodeficiency with a heterogeneous phenotype considered reversible by allogeneic hematopoietic cell transplantation (HCT). OBJECTIVES This study sought to characterize HCT outcomes in APDS. METHODS Retrospective data were collected on 57 patients with APDS1/2 (median age, 13 years; range, 2-66 years) who underwent HCT. RESULTS Pre-HCT comorbidities such as lung, gastrointestinal, and liver pathology were common, with hematologic malignancy in 26%. With median follow-up of 2.3 years, 2-year overall and graft failure-free survival probabilities were 86% and 68%, respectively, and did not differ significantly by APDS1 versus APDS2, donor type, or conditioning intensity. The 2-year cumulative incidence of graft failure following first HCT was 17% overall but 42% if mammalian target of rapamycin inhibitor(s) (mTORi) were used in the first year post-HCT, compared with 9% without mTORi. Similarly, 2-year cumulative incidence of unplanned donor cell infusion was overall 28%, but 65% in the context of mTORi receipt and 23% without. Phenotype reversal occurred in 96% of evaluable patients, of whom 17% had mixed chimerism. Vulnerability to renal complications continued post-HCT, adding new insights into potential nonimmunologic roles of phosphoinositide 3-kinase not correctable through HCT. CONCLUSIONS Graft failure, graft instability, and poor graft function requiring unplanned donor cell infusion were major barriers to successful HCT. Post-HCT mTORi use may confer an advantage to residual host cells, promoting graft instability. Longer-term post-HCT follow-up of more patients is needed to elucidate the kinetics of immune reconstitution and donor chimerism, establish approaches that reduce graft instability, and assess the completeness of phenotype reversal over time

International retrospective study of allogeneic hematopoietic cell transplantation for activated PI3K-delta syndrome.

BackgroundActivated phosphoinositide 3-kinase delta syndrome (APDS) is a combined immunodeficiency with a heterogeneous phenotype considered reversible by allogeneic hematopoietic cell transplantation (HCT).ObjectivesThis study sought to characterize HCT outcomes in APDS.MethodsRetrospective data were collected on 57 patients with APDS1/2 (median age, 13 years; range, 2-66 years) who underwent HCT.ResultsPre-HCT comorbidities such as lung, gastrointestinal, and liver pathology were common, with hematologic malignancy in 26%. With median follow-up of 2.3 years, 2-year overall and graft failure-free survival probabilities were 86% and 68%, respectively, and did not differ significantly by APDS1 versus APDS2, donor type, or conditioning intensity. The 2-year cumulative incidence of graft failure following first HCT was 17% overall but 42% if mammalian target of rapamycin inhibitor(s) (mTORi) were used in the first year post-HCT, compared with 9% without mTORi. Similarly, 2-year cumulative incidence of unplanned donor cell infusion was overall 28%, but 65% in the context of mTORi receipt and 23% without. Phenotype reversal occurred in 96% of evaluable patients, of whom 17% had mixed chimerism. Vulnerability to renal complications continued post-HCT, adding new insights into potential nonimmunologic roles of phosphoinositide 3-kinase not correctable through HCT.ConclusionsGraft failure, graft instability, and poor graft function requiring unplanned donor cell infusion were major barriers to successful HCT. Post-HCT mTORi use may confer an advantage to residual host cells, promoting graft instability. Longer-term post-HCT follow-up of more patients is needed to elucidate the kinetics of immune reconstitution and donor chimerism, establish approaches that reduce graft instability, and assess the completeness of phenotype reversal over time

Recent advancement in modern genomic tools for adaptation of Lablab purpureus L to biotic and abiotic stresses: present mechanisms and future adaptations

Not AvailableHyacinth bean is an important traditional plant with substantial medicinal value. Being imperative, it is still less explored crop on genomic and transcriptomic scale that has indexed it as an “orphan” crop for its genome revolution. Among different crop legumes such as pigeon pea, chickpea, cowpea, soybean and common bean, hyacinth bean also serves as a significant source of nutrition for both tropical and temperate regions and execute an imperative function in fixing biological nitrogen in agriculture. Nonetheless, the productivity of hyacinth bean is restrained due to environmental and biotic cues. Thus, understanding of the genomic functions and identification of probable genes/proteins for major agronomic traits through transcriptomic approaches has become imperative to improve stress tolerance in hyacinth bean. For understanding the plant stress tolerance mechanisms, the deployment of functional genomics approaches viz., proteomics and metabolomics have become imperious in breeding programs in developing countries. These approaches have been successfully used in other legume crops to create protein reference maps and their exploitation through comparative approaches can greatly enhance the research and understanding of hyacinth bean biological processes to changing environmental conditions. In this review, emerging epigenomics, proteomics, metabolomics and phenomics approaches and their achievements both in model/crop legumes are discussed. Additionally, the review also provides an overview of the applications of advanced proteomics, metabolomics and next-generation sequencing technologies in the discovery of candidate biomarkers for the development of agronomically refined hyacinth bean which may further ensure food and nutritional security under adverse climacteric conditions in developing countries.Not Availabl