Contributions of Microgravity Test Results to the Design of Spacecraft Fire Safety Systems

Experiments conducted in spacecraft and drop towers show that thin-sheet materials have reduced flammability ranges and flame-spread rates under quiescent low-gravity environments (microgravity) as compared to normal gravity. Furthermore, low-gravity flames may be suppressed more easily by atmospheric dilution or decreasing atmospheric total pressure than their normal-gravity counterparts. The addition of a ventilating air flow to the low-gravity flame zone, however, can greatly enhance the flammability range and flame spread. These results, along with observations of flame and smoke characteristics useful for microgravity fire-detection 'signatures', promise to be of considerable value to spacecraft fire-safety designs. The paper summarizes the fire detection and suppression techniques proposed for the Space Station Freedom and discusses both the application of low-gravity combustion knowledge to improve fire protection and the critical needs for further research

Viola sororia Willd.

https://thekeep.eiu.edu/herbarium_specimens_byname/20242/thumbnail.jp

The MOMENT to search for CP violation

Journal of High Energy Physics 2016.3 (2016): 197 reproduced by permission of Scuola Internazionale Superiore di Studi Avanzati (SISSA)In this letter, we analyze for the first time the physics reach in terms of sensitivity to leptonic CP violation of the proposed MuOn-decay MEdium baseline NeuTrino beam (MOMENT) experiment, a novel neutrino oscillation facility that would operate with neutrinos from muon decay. Apart from obtaining a sufficiently intense flux, the bottlenecks to the physics reach of this experiment will be achieving a high enough suppression of the atmospheric background and, particularly, attaining a sufficient level of charge identification. We thus present our results as a function of these two factors. As for the detector, we consider a very massive Gd-doped Water Cherenkov detector. We find that MOMENT will be competitive with other currently planned future oscillation experiments if a charge identification of at least 80 % can be achieved at the same time that the atmospheric background can be suppressed by at least a factor of ten. We also find a large synergy of MOMENT with the current generation of neutrino oscillation experiments, T2K and NOvA, which significantly enhances its final sensitivityThe work of MB was supported by the Göran Gustafsson Foundation. PC and EFM acknowledge financial support from the European Union through the ITN INVISIBLES (Marie Curie Actions, PITN-GA-2011-289442-INVISIBLES). EFM also acknowledges support from the EU through the FP7 Marie Curie Actions CIG NeuProbes (PCIG11- GA-2012-321582) and the Spanish MINECO through the “Ramon y Cajal” programme (RYC2011-07710) and the project FPA2009-09017. MB and EFM were also supported by the Spanish MINECO through the Centro de excelencia Severo Ochoa Program under grant SEV-2012-0249. MB would also like to thank the Instituto de Física Teórica, Madrid, for warm hospitality during the time when this work was initiated. PC would like to thank the Mainz Institute for Theoretical Physics for hospitality and partial support during completion of this work. Fermilab is operated by Fermi Research Alliance, LLC under Contract No. DE-AC02-07CH11359 with the United States Department of Energ

Urban forms, physical activity and body mass index: a cross-city examination using ISS Earth Observation photographs

Johnson Space Center has archived thousands of astronauts acquired Earth images. Some spectacular images have been widely used in news media and in k-12 class room, but their potential utilizations in health promotion and disease prevention have relatively untapped. The project uses daytime ISS photographs to define city forms and links them to city or metropolitan level health data in a multicity context. Road connectivity, landuse mix and Shannon's information indices were used in the classification of photographs. In contrast to previous remote-sensing studies, which tend to focus on a single city or a portion of a city, this project utilized photographs of 39 U.S. cities. And in contrast to previous health-promotion studies on the built environment, which tend to rely on survey respondents' responses to evaluate road connectivity or mixed land use for a single study site, the project examined the built environments of multiple cities based on ISS photos. It was found that road connectivity and landuse mix were not statistically significant by themselves, but the composite measure of the Shannon index was significantly associated with physical activity, but not BMI. Consequently, leisure-time physical activity seems to be positively associated with the urban complexity scale. It was also concluded that unless they are planned or designed in advance, photographs taken by astronauts generally are not appropriate for a study of a single-site built environment nor are they appropriate for a study of infectious diseases at a local scale. To link urban built environment with city-wide health indicators, both the traditional nadir view and oblique views should be emphasized in future astronauts' earth observation photographs

Mudas de regeneração natural da floresta com araucária: canela-sassafrás.

bitstream/item/86608/1/Folder-Canela-sassafras-2008.pd

Genome Evolution and the Emergence of Fruiting Body Development in Myxococcus xanthus

BACKGROUND: Lateral gene transfer (LGT) is thought to promote speciation in bacteria, though well-defined examples have not been put forward. METHODOLOGY/PRINCIPLE FINDINGS: We examined the evolutionary history of the genes essential for a trait that defines a phylogenetic order, namely fruiting body development of the Myxococcales. Seventy-eight genes that are essential for Myxococcus xanthus development were examined for LGT. About 73% of the genes exhibit a phylogeny similar to that of the 16S rDNA gene and a codon bias consistent with other M. xanthus genes suggesting vertical transmission. About 22% have an altered codon bias and/or phylogeny suggestive of LGT. The remaining 5% are unique. Genes encoding signal production and sensory transduction were more likely to be transmitted vertically with clear examples of duplication and divergence into multigene families. Genes encoding metabolic enzymes were frequently acquired by LGT. Myxobacteria exhibit aerobic respiration unlike most of the delta Proteobacteria. M. xanthus contains a unique electron transport pathway shaped by LGT of genes for succinate dehydrogenase and three cytochrome oxidase complexes. CONCLUSIONS/SIGNIFICANCE: Fruiting body development depends on genes acquired by LGT, particularly those involved in polysaccharide production. We suggest that aerobic growth fostered innovation necessary for development by allowing myxobacteria access to a different gene pool from anaerobic members of the delta Proteobacteria. Habitat destruction and loss of species diversity could restrict the evolution of new bacterial groups by limiting the size of the prospective gene pool

Etiological study of the sensorioneural deafness in high risk newborns

Orientador: Edi Lucia Sartorato, Marilia Fontenele e Silva CamaraDissertação (mestrado) - Universidade Estadual de Campinas, Instituto de BiologiaResumo: A perda auditiva em recém-nascidos de alto risco, varia de 20-40 em cada 1000 nascimentos. Em uma porcentagem variável de casos, a etiologia é ambiental, decorrente de fatores pré, peri ou pós-natais ou pode ainda ser de origem genética. O principal objetivo deste projeto foi determinar a etiologia da perda auditiva em crianças admitidas em unidades de terapia intensivas neonatais (UTIN) e avaliar a contribuição de outros fatores, principalmente medicamentos ototóxicos. Assim, foram selecionados 4 grupos: 25 crianças nascidas prematuras, de UTIN e com perda auditiva (grupo A), 25 crianças nascidas prematuras, de UTIN e sem perda auditiva (grupo B), 25 crianças nascidas a termo e com perda auditiva (grupo C) e 25 crianças nascidas a termo sem perda auditiva (grupo D), onde foram estudadas as principais mutações que levam à perda auditiva neurossensorial não-sindrômica: 35delG (no gene GJB2), mutações mitocondriais A7445G, G7444A (no gene CO1), A1555G, C1494T, A827G, T961G e 961delT/insC (no gene 12S rRNA e, em geral, moduladas pelo uso de antibióticos aminoglicosídeos), deleções ?(GJB6-D13S1830) e ?(GJB6-D13S1854), no gene GJB6. Em casos em que não se encontrou uma mutação que justificasse a perda, o gene GJB2 foi sequenciado. Foram encontrados no grupo A 1 indivíduo com a mutação V37I (gene GJB2) em heterozigose e 2 com a mutação A827G. No grupo B foram encontrados 3 indivíduos com a mutação A827G. No grupo C foram encontrados 5 indivíduos com a mutação A827G e 5 com a mutação 35delG em homozigose. No grupo D foi encontrado apenas 1 indivíduo com a mutação A827G. Estes resultados mostraram que a mutação A827G pode estar sendo modulada por mais de um fator, como aminoglicosídeos ou genes nucleares moduladores. A mutação 35delG parece estar diretamente relacionada a perdas congênitas profundas e pré-linguais. Na comparação dos grupos A e B o Teste de Mann-Whitney mostrou significância na média do período de internação entre eles (p-valor = 0,003), mostrando que esta diferença pode ser a principal causa da perda auditiva no grupo A. E na comparação dos grupos A e C, o Teste de Mood mostrou diferença altamente significativa de perda auditiva de ambas orelhas entre estes grupos (Orelha esquerda: p-valor = 0,002 e Orelha direita: p-valor = 0,000), sendo as perdas no grupo A severas e no grupo C profundas, mostrando que no grupo C esta perda é provavelmente causada por fatores genéticos, que levam a perdas profundas, bilaterais e pré-linguais como mostram estudos prévios feitos com o gene GJB2. No caso de indivíduos com perda auditiva, onde não foram encontradas mutações, há a possibilidade de que esta tenha sido causada por fatores ambientais ou ainda por mutações não pesquisadas neste trabalho. Deste modo, é de extrema importância o rastreamento genético para o diagnóstico precoce, otimizando, assim, as chances de desenvolvimento da fala e linguagem.Abstract: The frequency of sensorioneural hearing loss in high-risk newborns is 20-40 in 1000 births. In many cases, the cause is environmental, due to prenatal, perinatal and postnatal factors, or caused by genetic factors. The main objectives of this project were to determine the etiology of the hearing loss in children admitted into Neonatal Intensive Care Unit (NICU) and compare with other factors, mainly ototoxic medication. 4 different groups were selected: 25 pre-matures (from NICU) with sensorioneural nonsyndromic hearing loss (group A), 25 pre-matures (from NICU) without hearing loss (group B); 25 full term children with sensorioneural nonsyndromic hearing loss (group C) and 25 full term children without hearing loss (group D). The main mutations which cause hearing loss were studied: 35delG (GJB2 gene), A7445G, G7444A (CO1 mitochondrial gene), A1555G, C1494T, A827G, T961G and 961delT/insC (in the 12S rRNA mitochondrial gene and, in general, modulated by aminoglycosides), ?(GJB6-D13S1830) and ?(GJB6-D13S1854) (in the GJB6 gene). The complete GJB2 gene was sequenced in cases where the 35delG mutation wasn't found, or where it was found in heterozygosis. 1 child was found with V37I in heterozygosis (GJB2 gene) and 2 with the A827G mutation in group A. 3 children were found with the A827G mutation in group B. 5 children were found with the A827G mutation and 5 others with 35delG in homozygosis in group C. In group D only 1 child was found with the mutation A827G. These results show that A827G mutations might be modulated by more than one factor, like aminoglycosides or nuclear modifier genes. The 35delG mutation might be directly related to prelingual profound congenit losses. Comparing groups A and B, Mann- Whitney's Test showed significant results in the NICU period average (p-value = 0,003), indicating that this diference could be the major cause of hearing loss in group A. The Mood Test showed highly significant hearing loss diference in both ears between groups A and C (left ear p-value = 0,002 and right ear p-value = 0,000), showing severe loss in group A and profound loss in group C, indicating that in group C this loss is probably caused by genetic factors that induce prelingual bilateral profound loss, as related in previous GJB2 studies. In cases of hearing loss where mutations couldn't be found, it is possible that it has been caused by other mutations not studied or environmental causes. Therefore, the screening of mutations is important because it could provide better chances of developing speech and language.MestradoGenetica Animal e EvoluçãoMestre em Genética e Biologia Molecula

Molecular studies of sudden deaf

Orientador: Edi Lucia Sartorato, Norma de Oliveira PenidoDissertação (mestrado) - Universidade Estadual de Campinas, Instituto de BiologiaResumo: As causas da perda auditiva podem ser genéticas, ambientais ou causadas por comorbidades. As principais comorbidades incluem algumas doenças infecciosas, hematológicas, neurológicas e principalmente o schwannoma vestibular. Por sua vez, a Surdez Súbita caracterizase como uma surdez sensorioneural de 30dB em pelo menos 3 freqüências contínuas, de aparecimento abrupto e sem causa conhecida que pode manifestar-se em qualquer faixa etária, ocorrendo repentinamente ou de forma progressiva em um período de até 72 horas, podendo ser unilateral ou bilateral associado ou não a zumbidos e com menos freqüência a tonturas. Foram estudados 38 pacientes e indivíduos controles ouvintes onde 22 são provenientes da Universidade Federal de São Paulo formando o grupo A e 16 são provenientes da Fono Audio Clínica de Fortaleza (CE). O principal objetivo desse projeto foi determinar possíveis causas genéticas da Surdez Súbita nos indivíduos estudados. Para isso foi feito o rastreamento de mutações no gene da conexina 26 (GJB2), a detecção das deleções D(GJB6-D13S1830) e D(GJB6-D13S1854) no gene GJB6 e das mutações A1555G, C1494T, A827G, T961G e 961delT/insC presentes nos genes mitocondriais MTRNR1 (12S rRNA) e G7444A, A7445G presentes nos genes mitocondriais COI/MTTS1 (tRNAser(UCN)). Foi ainda rastreada a mutação G28T no gene TRMU, envolvido na modulação do fenótipo observado em algumas mutações mitocondriais. O sequenciamento automático das amostras foi realizado para detecção de outras mutações no gene GJB2. Dentre os indivíduos analisados, não foram encontrados nenhum com mutações genéticas nos genes GJB2 e GJB6. Três indivíduos apresentaram a mutação V27I um polimorfismo ainda sem correlação com a perda auditiva. A mutação G7444A foi encontrada em um indivíduo do grupo controle. Uma vez que esse indivíduo é ouvinte acredita-se que esta mutação isolada não possa causar perda auditiva mesmo associada com as mutações G28T do gene TRMU e A827G como foi observado nesse caso. A mutação A827G foi encontrada em 6 indivíduos 3 do grupo surdo e 3 do grupo controle, mas também não pôde ser correlacionada à perda auditiva nesses casos. A mutação G28T do gene TRMU foi encontrada em 14 indivíduos, sendo 9 pacientes surdos e 5 indivíduos do grupo controle, porém não foi possível associar essa mutação a perda auditiva. Pelos resultados obtidos nesse trabalho não foi possível a associação da Surdez Súbita com as mutações em nenhum dos genes estudados. Devido à grande heterogeneidade clínica e genética envolvida, ainda não é possível nem excluir ou afirmar a respeito dos aspectos genéticos da Surdez Súbita.Abstract: Several factors have been postulated to elicit the etiology of idiopathic sudden sensorineural hearing loss. Sudden deafness is characterized as a sensorioneural disturb, having an abrupt onset and an unknown cause that can be revealed in any age, occurring suddenly or in a progressive way in a 3 day period, of more than 30dB hearing loss at three consecutive frequencies. It can be unilateral or bilateral with tinnitus present and giddiness. In this work 38 patients were studied with their hearing control. Of all this patients, 22 were originating of Federal University of São Paulo São Paulo forming the group A and 16 were from Fono Audio Clinica in Fortaleza (CE) forming the group B. The main objective of this project was to determine possible genetics causes of sudden deafness in patients who lost suddenly their hearing. The main causes of genetic deafness were researched, initiating for the screening of 35delG mutation in the connexin 26 gene (GJB2), D(GJB6-D13S1830) and _(GJB6-D13S1854) deletions, A1555G, C1494T, A827G, T961G and 961delT/insC mutation present in mitochondrial gene MTRNR1 (12S rRNA) and G7444A, A7445G present in mitochondrial gene COI/MTTS1 (tRNAser(UCN)). Screening for the mutation G28T present in TRMU was also made. Then, complete GJB2 gene was screened for other mutations and polymorphisms. Of all patients analyzed, was not found mutation in genes GJB2 and GJB6. Three patients showed a mutation V27I that is a polymorphism still without relation with hearing loss. The mutation G7444A was found in one individual of the control group. Once that this patient has a normal hearing it is strongly suggestive that this mutation by itself can not cause a hearing loss, even if it is associated with two other mutations, the A827G mutation and G28T (TRMU) mutation. The mutation A827G was found in 6 individuals, 3 from deaf patients and 3 from control individuals, but it is no possible to relation this mutation with the hearing loss. The mutation of the gene TRMU was found in 14 individuals, being 9 deaf patients and 5 control individuals. Despite of this mutation being in a regulation gene, it is unknown the relation between this mutation and the hearing loss. With this results we can conclude that idiopathic sudden deafness can not be caused by a mutation in any of this genes studied. Shall the large clinical heterogeneity and genetic involved on those cases, is still impossible a certain conclusion. We can not exclude the fact that these mutations can be in regions not studied in this work and related with the hearing loss.MestradoGenetica Animal e EvoluçãoMestre em Genética e Biologia Molecula