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Journal articles on the topic "Inatas"
Teixeira, William. "DESCARTES PODERIA TER ESCRITO O PREFÁCIO AOS NOVOS ENSAIOS DE LEIBNIZ?" Kínesis - Revista de Estudos dos Pós-Graduandos em Filosofia 11, no. 30 (December 31, 2019): 169–82. http://dx.doi.org/10.36311/1984-8900.2019.v11.n30.12.p169.
Full textMarques, Ubirajara Ranean de Azevedo. "Kant e o problema da origem das representações elementares: apontamentos." Trans/Form/Ação 13 (January 1990): 41–72. http://dx.doi.org/10.1590/s0101-31731990000100004.
Full textChiavegatto Filho, Alexandre Dias Porto, and Ruy Laurenti. "O sexo masculino vulnerável: razão de masculinidade entre os óbitos fetais brasileiros." Cadernos de Saúde Pública 28, no. 4 (April 2012): 720–28. http://dx.doi.org/10.1590/s0102-311x2012000400011.
Full textZanitelli, Leandro Martins. "DISCRIMINAÇÃO PRIVADA E O SEGUNDO PRINCÍPIO DA JUSTIÇA DE RAWLS." Kriterion: Revista de Filosofia 56, no. 132 (December 2015): 393–411. http://dx.doi.org/10.1590/0100-512x2015n13205lmz.
Full textAndrade, Paulo Estêvão, Paulo Sérgio Teixeira Prado, and João dos Santos Carmo. "Das representações numéricas inatas à matemática culturalmente construída." Temas em Psicologia 23, no. 1 (2015): 225–42. http://dx.doi.org/10.9788/tp2015.1-15.
Full textRios, Marcelo De Azevedo, Paulo Sérgio Flores Campos, and Roberto José Meyer Nascimento. "Doença periodontal e aterosclerose: uma revisão de 5 anos da resposta do hospedeiro frente ao desafio microbiano da porphyromonas gingivalis via imunidade inata através do receptor Toll-like." Revista de Ciências Médicas e Biológicas 10, no. 3 (January 1, 2011): 297. http://dx.doi.org/10.9771/cmbio.v10i3.5893.
Full textPereira Júnior, Alfredo. "Estatuto biológico do processamento de informação mental." Trans/Form/Ação 14 (December 1991): 139–53. http://dx.doi.org/10.1590/s0101-31731991000100008.
Full textAlmeida, Manoel C. "Neurociência, História da Matemática e Música: Conexões Interdisciplinares." REMATEC 16 (February 2, 2021): 01–15. http://dx.doi.org/10.37084/rematec.1980-3141.2021.n.p01-15.id319.
Full textAraújo de Oliveira, Natália. "Migração, identidade e políticas de desenvolvimento: configurações da formação social em uma cidade da Amazônia Legal Brasileira." Ágora 20, no. 1 (January 6, 2018): 80. http://dx.doi.org/10.17058/agora.v20i1.11641.
Full textCastañeda, Luzia Aurelia. "Eugenia e casamento." História, Ciências, Saúde-Manguinhos 10, no. 3 (December 2003): 901–30. http://dx.doi.org/10.1590/s0104-59702003000300006.
Full textDissertations / Theses on the topic "Inatas"
Gerlach, Raquel Fernanda. "Estudo do promotor do gene da cadeia alfa 2 do colageno tipo I em portadores de fibromatoge gengival hereditaria." [s.n.], 1998. http://repositorio.unicamp.br/jspui/handle/REPOSIP/290026.
Full textDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba
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Resumo: Há grande variação interindividual de fibroblastos gengivais em relação à síntese de proteínas da matriz. Esta variabilidade está bem documentada em casos de reação fibrótica gengival induzida por drogas, mas o mesmo não acontece em relação à Fibromatose Gengival Hereditária (FGH), condição em que há aument9 da secreção de colágeno normal na matriz extracelular. Condições particulares individuais como polimorfismos genéticos ou mutações podem influir na resposta de fibroblastos a estímulos do ambiente. Assim, procuramos identificar polimorfismos na região do promotor da cadeia alfa 2 do colágeno tipo 1 (COLIA2) em um grupo de pacientes normais (n=12) e outro de portadores de FGH (n=13). Além disso, também testamos a hipótese de alteração no padrão de metilação destaseqüência estar relacionada ao aumento da expressão do colágeno do tipo I em portadores de FGR. Primeiramente foi feita a amplificação por PCR da região do promotor da cadeia alfa 2 do colágeno entre -340 e +2 pares de base(bp), porção do promotor que possui mais seqüências reconhecidas como determinantes na interação com fatores de transcrição. A ste passo se seguiu a análise de heteroduplexes para a identificação de polimorfismos. Esta análise foi feita do seguinte modo: aquecimento das amostras a 98°C por 5 minutos, resfi-iamento a O°C e manutenção a 20°C por uma hora. A detecção de heteroduplexes foi feita em gel de poliacrilamida a 6%/ Tampão TBE, corado pelo método da prata. A análise de metilação foi feita através do uso de enzimas de restrição (HAL In e HP A n, que não clivam as suas seqüências de reconhecimento de DNA quando estas seqüências estiverem metiladas). Previamente à reação de PCR, o DNA foi digerido com as enzimas citadas. A metilação permitiria a amplificação da seqüência de DNA que estivesse metilada entre as regiões dos primers utilizados. Após a amplificação, as amostras foram submetidas a eletroforese em gel de poliacrilamida a 6%/ Tampão TBE, corado pelo método da prata.Não houve diferença na migração dos fi-agmentos' de DNA após a reação de heteroduplexes, nem foi detectada alteração no padrão de metilação entre os dois grupos de indivíduos. Estes achados indicam que mutações ou alteração no padrão de metilação da região do promotor do COLIA2 compreendida entre -340 e +2 bp provavelmente não estejam relacionadas ao crescimento gengival de portadores de FGR
Abstract: There is a great interindividual variation in gingival fibroblasts capacity for synthesizing extracellular matrix proteins. This variability is well-documented in patients exhibiting drug-induced gingival overgrowth, but it is still poorly understood in patients with Hereditary Gingival Fibromatosis (HGF). There is an increase in the amount of normal collagen secreted into the extracellular matrix of the gingiva of patients with HGF. IndividuaIs may carry genetic polymorphisms or mutations, which could determine the partem of fibroblasts response to environmental stimuli.hus, we tried to identify genetic polymorphisms in the promoter of the collagen type I alfa 2 chain (COLIA2) in a group of normal subjects (n=12) and another group of patients with HGF (n=13). Besides, we also tested the hypothesis that undermethylation of this sequence could be related to the overexpression of type I collagen in these patients. lnicially we amplified the COLIA2 promoter region from -340 to +2 bp by PCR, since this is the promoter region were most cis-acting-factors have been identified until now. Thereafter, heteroduplex analysis was performed by heating the samples 5 rninutes to 98°C, chilling at O°C, and maintaining them one hour at 20°C. The samples were run in a 6% polyacrilarnidel TBE gel, which was stained with silver for heteroduplexes detection. Methylation analysis was carried out using restriction enzymes which do not cut DNA when their recognition sites are methylated (HAL 111 e HPA 11). DNA was digested by these enzymes prior to PCR. Successful amplification of a selected fragment of the promoter where restriction sites of these two enzymes are found would mean that the sequence was methylated. The samples were run in a 6% polyacrilarnidel TBE gel, which was stained with silver. There was no difference in the rnigration of DNA fragments after the heteroduplex reaction, neither methylation partem alteration was detected between the two groups analysed. This may indicate that mutations or methylation pattern alteration in the promoter region of the COLIA2 reaching from -340 to +2 bp are probably not involved in the gingival overgrowth affecting patients with HGF
Mestrado
Biologia e Patologia Buco-Dental
Mestre em Ciências
Machado, Maria Angela Naval. "Analise dos heredogramas e das correlações clinicas da fibromatose gengival hereditaria, numa familia de 219 pessoas." [s.n.], 1996. http://repositorio.unicamp.br/jspui/handle/REPOSIP/289553.
Full textDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba
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Resumo: A F.G.H. como entidade isolada e não associada a síndromes, foi diagnosticada em um grupo familial há aproximadamente 15 anos. Atualmente este grupo se apresenta constituído no total de 219 indivíduos, dos quais 159 descendentes diretos apresentam risco de herdar a alteração. A análise de cinco gerações em dez heredogramas neste grupo familial mostrou que 64 indivíduos foram afetados e que a transmissão da fibromatose gengival ocorreu através de um gene autossômico dominante, a partir de um único indivíduo afetado. Diferentes formas de expressão clínica da F.G.H. foram observadas em indivíduos com idades similares em um mesmo heredograma deste grupo familial, confirmando a hipótese de expressividade variável deste gen. Os achados clínicos se mostraram dependentes do grau de expressão da F.G.H., revelando que quanto maior a expressão fenotípica, maior o aumento gengival e maior a chance de encontrar maloclusão. Os achados clínicos secundários a fibromatose gengival, mais freqüentes no grupo familial estudado, foram, o mal posicionamento dentário, falta de vedamento labial, ,respiração bucal e diastemas generalizados no arco superior e inferior, em conseqüência do spessamento gengiva!. A F.G.H. não foi detectada em .alguns heredogramas nas cinco gerações e estes indivíduos não portadores, não transmitiram para seus descendentes a F.G., sugerindo que a penetrância deste gene autossômico" dominante é completa. Estas conclusões estão em consonância com observações de outros autores, já descritas na literatura
Abstract: The hereditary gingival fibromatosis, as an isolated entity, has been diagnosed in a family group for approximately fifteen years. Nowadays this is a 219 persons group, of whom 159 have a chance to inherit the disorder. The evaluation, in ten genetic pedigree, of five generations in this family group, showed 64 atfected persons and that the transmission of the gingival fibromatosis was due to an autosomal dominant gen, proceeding from a single atfected person. A wide variability in expression of the hereditary gingival fibromatosis has been reported in persons of similar ages in a common pedigree of this family group, attesting the hypothesis of variable expressivity of this gene. Clínical findings showed to be dependent of the expression leveI of the her~ditary gingival fibromatosis, showing that the larger is the fenotipic expression, the larger is the gingival enlargement, and the larger is the chances of maloclusion. The secundary clinicals findings to the hereditary gingival fibromatosis most common shówed in this family group were, crowding, lack of labial closure, bucal breathing and generalized spacing on upper and lower archs, due to the excessive gengival bulk. The hereditary gingival fibromatosis was not found in some pedigrees of the five generations and those non afIected persons did not transmit the hereditary gingival fibromatosis to their descendents, suggesting that penetrance of this autosomal dominant gene is complete. Those conclusions were in conformity whith others author' s observations, reported in the literature. In this family group, the hereditary gingival fibromatosis was the only disorder found, not being associated with any other genetic syndromes
Mestrado
Mestre em Ciências
Sena, Lucas Schenatto de. "Forças seletivas que atuam na dinâmica do alelo mutante do gene ATXN2." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2018. http://hdl.handle.net/10183/187219.
Full textSpinocerebellar ataxia type 2 (SCA2) is caused by an expansion in a repetitive sequence of CAG codons (CAGexp) in exon 1 of the ATXN2 gene. The expanded polyglutamine tract is associated with a gain in toxic function, expressed predominantly in neurons. SCA2 is an autosomal dominant neurodegenerative condition, with onset between 30 and 40 years of age, manifestations due to progressive neurological disorders that lead to those affected in the wheelchair and reduced survival. Despite being a community of companies, as an anticipation, a frequency of SCA2, which is a place for the communities where it was observed, suggesting the existence of simultaneous favorable selective mechanisms. To ascertain this hypothesis, the present study, fitness estimate, a segregation and role of anticipation in a cohort of families with molecular diagnosis of SCA2. Data from families with molecular diagnoses performed at the Medical Genetics Service of the Hospital de Clínicas and stored in databases of restricted access to the researchers served as a basis to identify the population under study. Between 2016 and 2017, adult subjects belonging to these families were invited to participate in this study. After presenting their informed consent, these subjects provided data on all their relatives related to the family branch where the SCA2 segregated, allowing the construction of complete heredograms. Data from at least two informants per family should be convergent to be studied. The study variables were obtained from all subjects: date of birth, gender, relationship, birth order, symptomatic status and number of children. The date of death and the age of onset of the first symptom were noted where appropriate. The genetic fitness (or reproductive success) of patients with SCA2 was considered equal to w = W affected / W unaffected, where W was the median number of children in the group. 12 As the genotype was not available for most members of the SCA2 families, the phenotype was used to classify the subjects as affected or unaffected. To reduce the effects of potential memory and bias biases, two inclusion criteria were used: (1) to be older than a standard deviation above the mean age of symptom onset of the total group; and (2) there is complete information on the reproductive history of both the subject and the transmitting parent. The segregation analysis compared the number of siblings affected with that of the unaffected; as inclusion criterion, again all siblings studied should be older than a standard deviation from the mean age of complete cohort start age. Twenty-one of the 31 families diagnosed with SCA2 were recovered: subjects from one family refused to participate in the study, while the remaining 9 families were lost from follow-up. The heredograms studied included 1,017 people, 164 of whom were symptomatic - and 84 of them were still alive. As the mean age at onset was 36.6 (14.9) years, affected and unaffected subjects over 52 years of age were used to estimate fitness and segregation patterns. Sixty-seven affected subjects and 97 unaffected subjects were included in the fitness analysis and had a median of 3 and 2 children respectively, which resulted in a genetic fitness equal to 1.5 (p <0.025). The vast majority of affected children were born before the onset of symptoms of these parents. Finally, the fitness varied according to the age of onset of subjects, becoming smaller than the fitness of the unaffected subjects when the age of onset of symptoms was less than or equal to 20 years of age. Among the subjects included in the segregation analysis, there were 137 unaffected (59.6%) and 93 affected (40.4%), and this proportion was significantly different from that expected in a random segregation of alleles (p = 0.04 ). The age of onset was inversely proportional to the size of CAGexp in 49 individuals where molecular information was available (rho = -0.708, p <0.0001, 13 Spearman); each additional CAG repeat was associated with a reduction of 1.57 years at the onset age (p <0.003). The mean difference between the age of onset of the subjects and that of their affected parents was -10.77 years: that is, the age at the beginning of the generations pointed to the anticipation as a frequent phenomenon. Therefore, our results indicated that three selective forces may affect the recurrence of SCA2. SCA2 had an increased genetic fitness in patients with median or late onset ages. In contrast, we observed a distortion in segregation or favoring gametes with normal alleles - more than 95% of the time, with alleles with 22 replicates (CAG) 22 - or disfavoring the gametes with expanded alleles. Our result even suggests that high frequency of the allele (CAG) 22 on human chromosomes is explained by this selective advantage. Finally, our data suggest that anticipation is the most frequent occurrence in transmissions between affected, in the comparison between the ages of onset in subsequent generations. This last observation proposes that the transmission of unstable CAGexp tends to expand it further; this needs to be confirmed by the observation of completely genotyped brotherhoods in future studies. If it is confirmed, the tendency to anticipate should be associated with a reduced fitness in this affected. In conclusion, although the fitness of the affected individuals with the mean onset ages is increased, the frequency of ACS2 is not increasing in the population because other selective forces act in the opposite direction (negative selection): distorted segregation and favors the transmission of the allele normal and the tendency to anticipate.
Moraes, Renan Stoll. "A influência da história familiar de hipertensão sobre a associação entre a excreção urinária noturna de sódio e a pressão arterial em uma amostra populacional de adultos jovens." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 1994. http://hdl.handle.net/10183/139237.
Full textBackground The pathogenesis of essential hypertension, one of the most important risk factor for atherotrombotic diseases, is multifactorial, depending on the interaction between genetic and environmental factors. Sodium chloride stands out among the environmental determinants. The association between sodium intake and blood pressure has been investigated through several models. In cross-sectional surveys, conducted among different countries, it has been demonstrated a positive association between sodium intake and prevalence of hypertension. Otherwise, the association is weaker when explored among individuais living in the same society. A variation on the salt sensitivity across their inhabitants is an explanation for the difference in the intensity of the association. It would depend, mainly, trom the salt-sensitive individuais, an inheritable attribute. Objective To investigate the influence of the familial predisposition to hypertension on the association between blood pressure and urinary output of sodium in a probabilistic population sample of young adults. Methods Study design: observational, analytical, cross-sectional. Sampling: multiple stage, population-based, randomized cluster sampling. Variables: they were collected at domicile. The questionnaire asked about demografic, and socioeconomic characteristics, familial predisposition to hypertension, exposition to alcohol and smoke, gyneco-obstetric hist~:>rY, and use of medicines. When possible, the familial predisposition to hypertension was checked with the relatives living in the house. Anthropometric variables were measured in a standardized way. Sitting blood pressure was detemined with aneroid sphygmomanometers, periodically calibrated against mercury manometers. The average of two determinations was used in the analysis. Overnight urine was collected at home with detailed written instructions. Sodium and potassium concentrations were determined through flame spectrophotometry. Calcium was measured by the O-cresoftalein method (Cobas Mira automatized device). Statistical analysis: comparisons across the groups were performed by Chi-square statistics (categorical variables) and Student t-test or ANOVA (continous variables). Pearson's correlation coefficient was used to test the association between sodium excretion and blood pressure acording to the family predisposition to hypertension. Covariance was used to control for potential biases of the associations of interest. Results From a total of 432 eligible individuais, 389 (92.1 %) were interwied. Of these, 40.9°1Ó were younger than 35 years old. Six were excluded because the amount of urine was less than 100 ml. A total of 157 persons constitute the final sampling. Twentyseven individuais (17.20/0), who had two first degree relatives with hypertension, were included in the strong familial predisposition group. The remaining constituted the group with not-stron9 familial predisposition to hypertension. The Pearson's correlation coefficient between sodium excretion and systolic and diastolic blood pressure were statistically significant only in the strong predisposition group. Conclusions It was demonstrated that the familial predisposition to hypertension influences the association between urinary sodium excretion and blood pressure leveis. This association is strong only in individuais predisposed to hypertension. This finding, previously demonstrated in experimental models, was detected in individuais living under usual conditions. The proximity between blood pressure determination and urinary sampling utilized in this investigation strengthens the ides that the association between sodium intake and blood pressure is instantaneous. This is an additional explanation to the influence of familial predisposition to hypertension for the weak correlation observed in within society studies.
Teixeira, Rosa Chelminsky. "Viabilidade e eficiencia de um programa de hemoglobinopatias hereditaria em uma comunidade brasileira (Araras, SP) abordada a partir das gestantes." [s.n.], 1993. http://repositorio.unicamp.br/jspui/handle/REPOSIP/316558.
Full textTese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
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Doutorado
Genetica
Doutor em Ciências Biológicas
Silva, Luciana Pugliese da. "Caracterização molecular da deficiencia de proteina S." [s.n.], 1998. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308117.
Full textDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: A proteína S humana é uma glicoproteína plasmática vitamina K-dependente que age como cofator não enzimático da proteína C ativada na Via Anticoagulante da Proteína C. Além disso, a proteína S desempenha um papel independente da proteína C ativada inativando os fatores V e X ativados. A concentração plasmática da Proteína S é regulada por uma proteína de ligação que atua na Via Clássica do Complemento, a C4b. A proteína C4b forma complexos inativos com aproximadamente 60% da proteína S total, e somente a proteína S na sua forma livre pode exercer sua atividade de cofator da proteína C ativada. A deficiência hereditária de proteína S é uma causa comum de trombose venosa recorrente, e ocorre pela diminuição da atividade anticoagulante da proteína S. É uma doença relativamente rara e tem padrão de herança autossômico dominante o gene que controla a produção- da proteína S (PROS1) está localizado no cromossomo 3, próximo à região do centrômero, na posição 3p11.1 - 3q11.2. É constituído por 15 exons e 14 introns, abrangendo uma região de mais de 80 kb, que origina um mRNA de 3,5 a 4,0 kb. Nesta mesma região do cromossomo 3 há um pseudogene (PROS2) que possui 97% de homologia com a região codificadora do gene ativo. De acordo com um "database" de mutações no gene da proteína S, publicado em 1997 por GANDRILLE et aI., foram descritas 71 diferentes mutações de ponto sendo 19,8% mutações missense, 65,3% mutações missense, 12,8% mutações em sítio de "splicing" e 2% aboliam o codon de terminação natural da proteína. Foram também descritas 16 diferentes inserções/deleções e duas grandes deleções. Um total de doze polimorfismos raros foram descritos, incluindo o polimorfismo Heerlen, além de um polimorfismo freqüente, o dismorfismo neutro CCA/CCG. Os métodos de SSCP e CSGE possibilitam o rastreamento rápido e eficaz de mutações. O seqüenciamento de DNA permite a determinação precisa da alteração molecular responsável pela doença. No presente trabalho, estes métodos foram empregados no estudo do gene da proteína S (PROS1) de 8 pacientes com deficiência de proteína S que apresentaram trombose espontânea. Outras deficiências que predispõem à trombose foram avaliadas e não detectadas nestes pacientes. Com o emprego dessa estratégia metodológica foi possível detectar e identificar sete mutações de ponto em quatro dos oito pacientes estudados, incluindo uma mutação silenciosa, além de um polimorfismos em outro paciente. Das mutações encontradas somente uma foi detectada pelo método de SSCP. Considerando-se o quadro clínico/laboratorial dos pacientes estudados e a análise familiar, os resultados deste estudo sugerem que as mutações identificadas seriam responsáveis pela deficiência hereditária de proteína S. A identificação das mutações e sua correlação com o quadro clínico dos pacientes estudados neste trabalho contribuem para a compreensão da relação estrutura-função desta proteína. Também foram determinadas as freqüências, em diferentes grupos da população brasileira (recém-nascidos, caucasóides, negróides, índios e pacientes com trombose) do polimorfismo Heerlen e do dismorfismo neutro CCA/CCG. Os resultados obtidos nos diferentes grupos estudados, para polimorfismo Heerlen, não diferiram significativamente dos descritos anteriormente na literatura por BERTINA et aI., 1990. Este polimorfismo não foi identificado em nenhum dos pacientes estudados. As freqüências alélicas do dismorfismo neutro CCA/CCG não diferiram significativamente dos descritos na literatura por DIEPSTRATEN, et aI., 1991 e GANDRILLE et aI., 1995. Nossos resultados revelaram que na população negróides pode ter ocorrido um grau de miscigenação, já que a freqüência de heterozigotos foi elevada. A população indígena, apesar de ser considerada um isolado genético, mostrou um predomínio do genótipo heterozigoto. O polimorfismo CCA/CCG também foi empregado para análise de segregação nas famílias com deficiência de proteína S, e mostrou-se informativo em três famílias analisadas
Abstract: Human protein S is a plasmatic vitamin-K dependent glicoprotein that acts as a non-enzimatic cofactor of activated protein C in the protein C anticoagulant pathway. In addition to this protein S has an independent role that activated protein C, which is to inactivate factors Va and Xa. The plasmatic concentration of protein S is regulated by a C4b binding protein that acts on the Complement Classical Pathway. C4b protein forms inactive complexes with approximately 60% of total protein S, and only the free form of protein S its can act as a cofactor of activated protein C. The hereditary deficiency of protein S is a common cause of recurrent venous thrombosis, and occurs due to the decrease of the anticoagulant activity of protein S. It is a relatively rare disease and it has a dominant autossomic hereditary patteFI1. The gene which controls the production of protein S (PROS1) is Ipcated in chromosome 3, near the centromer region at position 3p11.1 - 3q11.2. It is formed by 15 exons and 14 introns comprising a region of over 80kb, which originates a mRNA of 3,5 to 4,0 kb. In this same region of chromosome 3 there is a pseudogene (PROS2) which is 97% homologous to the codifying region of the active gene. According to the protein S gene mutation database published by GANDRILLE et aI., 71 different point mutations were described, 19.8% were nonsense mutations, 65,3% were missense mutations, 12,8% were splice site mutations, and 2% abolished the natural codon termination of the protein. Sixteen different insertions/deletions and two large deletions were also described. A total of twelve rare polymorphisms were described including the Heerlen polymorphism and a frequent polymorphism, the neutral dimorphism CCA/CCG. The SSCP and CSGE analysis permit the quick and efficient screening of the mutations. Direct DNA sequencing permit the precise determination of the molecular alteration responsible for the disease. In this study these methods were used in the study of protein S gene (PROS1) of eight patients with protein S deficiency which presented spontaneous thrombosis. Other deficiencies which predispose to thrombosis were evaluated but were not detected. With the use of this methodology it was possible to detect and identify seven point mutations in four of the eight patients studied, including a silent mutation in addition to a polymorphism in another patient. Of the mutation found only one was detected by the SSCP method. Considering the clinical and laboratory data of the patients studied, together with the analysis of the family, the results of this study suggest that the mutations identified are responsible for the hereditary protein S deficiency. The identification of the mutations and its correlation to the clinical data of the patients studied contribute to the comprehension of the structural-functional relation of this protein. The frequencies of the Heerlen polymorphism and the neutral dimorphism CCA/CCG, in different groups of the Brazilian population (newborns, caucasoides, Black population, Indians and patients with thrombosis) were also determined. The results obtained in the different groups studied, for Heerlen polymorphism, did not differ significantly from those described previously in the literature by BERTINA et al, 1990. This polymorphism was not identified in any of the patients studied. The allelic frequencies of the neutral dismorphism CCA/CCG do not differ significantly from those described in literature by DIEPSTRATEN, et aI., 1991 and GANDRILLE et aI., 1995. Our results revealed that the miscigenation may have occurred in the Black population, in spite of being considered as a genetic isolate, showed a predomination of the heterozygous genotype. The CCA/CCG polymorphism was also used to analyze the segregation in families with protein S deficiency and was informative in three families that were analyzed.
Mestrado
Farmacologia
Mestre em Ciências Médicas
Dufloth, Rozany Mucha. "Carcinoma de mama hereditario em mulheres brasileiras : mutações dos genes BRCA1 e BRCA2, polimorfismos dos genes de reparo do DNA e caracterização imunoistoquimica pela tecnica de Tissue Microarray." [s.n.], 2004. http://repositorio.unicamp.br/jspui/handle/REPOSIP/313286.
Full textTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: OBJETIVOS: Identificar mutações nos genes BRCA1 e BRCA2 em uma população brasileira com câncer de mama hereditário; analisar a freqüência de polimorfismos nos genes XRCC1, XPD, XRCC3 e RAD51 em um grupo de pacientes brasileiras e sua associação com a susceptibilidade ao câncer de mama; analisar expressão das proteínas p63, CK5 e P-caderina em cânceres de mama familiar e esporádico. MÉTODOS: Este estudo teve componentes do tipo transversal e do tipo caso-controle. Foram constituídos quatro grupos: pacientes com câncer hereditário de mama; pacientes com câncer de mama esporádico; mulheres sem câncer de mama e com história familiar positiva de câncer de mama e/ou ovário; mulheres sem câncer de mama e sem história familiar de câncer de mama e/ou ovário. Foram coletados 10ml de sangue periférico para a realização de técnicas moleculares, nomeadamente Single Strand Conformation Polymorphism (SSCP) e Seqüenciação Direta. Espécimes de câncer de mama, conservados em blocos de parafina, foram selecionados no Laboratório de Patologia do Hospital das Clínicas/Unicamp, Brasil e no Laboratório de Patologia do Hospital São João/Universidade do Porto, Portugal, totalizando 168 casos. Dos blocos doadores foram extraídos cilindros de 2mm de diâmetro e depositados nos blocos de parafina receptores, usando Tissue Microarrayer (Beecher Instrumensts, Silver Spring, Maryland). Nestes cortes foi feita a pesquisa dos marcadores de diferenciação do fenótipo basal/mioepitelial. RESULTADOS: Foram identificadas quatro mutações (13%), sendo uma mutação no gene BRCA1 e três no gene BRCA2. No BRCA1 foi encontrada uma mutação do tipo frameshift. Duas mutações do BRCA2 são tipo nonsense e a outra do tipo unclassified variant. Não houve associação estatisticamente significante entre os alelos e genótipos dos polimorfismos dos genes de reparo do DNA, XRCC1, XPD, XRCC3 e RAD51. O câncer de mama familiar mostrou diferenças estatisticamente significantes do fenótipo imunoistoquímico dos marcadores de células basais/mioepiteliais (P-caderina, p63 and CK5), em relação aos cânceres esporádicos. CONCLUSÃO: Foram identificadas uma mutação no gene BRCA1 e três mutações no gene BRCA2 em mulheres com câncer de mama e história familiar de câncer de mama, o que correspondeu a uma freqüência de 13% (4/31). Não foi observada associação da susceptibilidade ao câncer de mama com os polimorfismos dos genes XRCC1, XPD, XRCC3 e RAD51 em um grupo de pacientes brasileiras. Os marcadores p63, CK5 e P-caderina foram mais freqüentemente expressos no câncer de mama familiar. A melhor caracterização do câncer familiar como entidade biológica distinta do câncer esporádico pode ser uma ferramenta útil para selecionar mulheres que deveriam submeter-se ao rastreamento de mutações nos genes BRCA1 e BRCA2
Abstract: OBJECTIVE: To identify mutations in BRCA1 and BRCA2 genes in a Brazilian population of women with hereditary breast cancer; to analyze the frequency of polymorphism in genes XRCC1, XPD, XRCC3 e RAD51 in a group of Brazilian patients and its association with breast cancer susceptibility; to analyze the expression of p63, CK5 and P-cadherin proteins in familial and sporadic breast cancers. METHODS: This study was in part transversal and in part crosssectional. The population evaluated in this study comprised four groups of women: patients with sporadic and familial breast cancers, women without breast cancer but with family history, women without breast cancer and without family history. The last group was the control group of this study. From each subject, 10ml of peripheral blood were collected to perform molecular analysis, namely Single Strand Conformation Polymorphism (SSCP) and Direct Sequencing. Paraffin blocks from breast cancer specimens were selected from the Pathology Laboratories from the Hospital das Clínicas/UNICAMP, Brazil and Hospital São João/Universidade do Porto, Portugal, totalising 168 cases. Cylinders with 2mm diameter were extracted from the donnor blocks using the Tissue Microarrayer technique (Beecher Instruments, Silver Spring, Maryland), and were sampled together to construct the receptor paraffin blocks. The analysis of mioepithelial differentiation/histogenesis was performed in these sections. Results analysis was carried out through the Chi-square test. RESULTS: Four mutations were identified: one in BRCA1 and three in BRCA2. A frameshift BRCA1 mutation, two nonsense BRCA2 and one unclassified variant BRCA2 mutation were identified. No statistically significant association between the alleles and genotypes DNA, XRCC1, XPD, XRCC3 and RAD51 polymorphism. Familial breast cancer was statistically different from sporadic cancer in regards of immunohistochemical phenotypes for basal/mioepithelial cell markers (Pcadherin, p63 and CK5). CONCLUSIONS: Thirteen percent of women with breast cancer and family history of breast cancer had at least one BRCA1 gene mutation and three BRCA2 gene mutations. We do not observe any statistical significance difference in the frequency of alleles and genotype of the genes XRCC1, XRCC3, XPD e RAD51 in the group of patients studied. The markers, CK5 e P-cadherin was more frequently in familial breast cancers. The characterization of familial breast cancer as a biological entity distinct from sporadic cancer might be a useful tool to select women that should be screened to BRCA1 and BRCA2 genes mutation triaging
Doutorado
Ciencias Biomedicas
Doutor em Tocoginecologia
Compri, Mariane Bernadete. "Programa comunitario de saude publica em hemoglobinopatias hereditarias : abordagem populacional a partir dos estudantes de Bragança Paulista/SP." [s.n.], 1995. http://repositorio.unicamp.br/jspui/handle/REPOSIP/316555.
Full textDissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
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Mestrado
Genetica
Mestre em Ciências Biológicas
Amaral, Vanessa Cristiane de Santana [UNESP]. "Contribuição diferencial do hipocampo ventral e do complexo amidalóide na modulação de respostas defensivas inatas e condicionadas de camundongos." Universidade Estadual Paulista (UNESP), 2011. http://hdl.handle.net/11449/100953.
Full textConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Quando os animais são confrontados com estímulos ambientais ameaçadores como a exposição ao predador ou estímulos como altura, iluminação e estímulos nociceptivos, exibem reações de defesa coordenadas e específicas. Nas últimas décadas, observa-se um crescente interesse pela utilização de estímulos naturalísticos para o estudo das bases neurais de emoções como o medo e ansiedade. Nesse contexto, o teste de exposição ao rato (RET), um novo modelo etológico de interação presa-predador, utilizando camundongos (presa) e ratos (predador), foi desenvolvido para avaliar a expressão de diferentes comportamentos defensivos na presa. Entretanto, poucos estudos foram conduzidos com esse modelo no intuito de investigar as bases neurais das respostas defensivas de camundongos expostos ao rato. Adicionalmente, evidências da literatura destacam que o hipocampo ventral (HV) e o complexo amidalóide (CA) parecem contribuir diferencialmente na modulação de respostas defensivas frente a estímulos proximais (predador) ou potenciais. Assim, o presente estudo foi conduzido para investigar o papel do HV e do CA nas respostas defensivas de camundongos exibidas diante do predador (rato) e do contexto associado ao predador. Para tal, o presente estudo foi dividido em quatro etapas. Na primeira delas, investigamos se o estresse da exposição ao predador no RET altera a secreção de corticosterona em camundongos e determinamos a magnitude e a duração desta secreção. Na segunda etapa, avaliamos o papel do HV e do CA, através da injeção local do agonista de receptores GABAA muscimol (0,1 μg/0,1 μl), na mediação de respostas comportamentais defensivas de camundongos expostos ao RET (situação proximal) e comparamos com aquelas apresentadas durante a exposição ao labirinto em cruz elevado (LCE - situação potencial). Subsequentemente, investigamos se camundongos expostos...
When animals are confronted with environmental threatening situations such as exposure to a predator as well as to height, high illumination and nociceptive stimuli they exhibit defensive behaviors. Over the past decades there has been a growing interest by the neuroscientists in the use of naturalistic stimuli to the study of the neural systems of the emotions such as fear and anxiety. In this context, the Rat Exposure Test (RET) which is a new ethological model of prey-predator interaction using mice (prey) and rats (predator) was developed in order to evaluate the expression of different defensive behaviors in the prey. However few studies using this model have been carried out with the objective of investigating the neural systems of the defensive behaviors in mice exposed to rats. In addition, evidence in literature has shown that the ventral hippocampus (VH) and the amygdaloid complex (AC) contribute differentially in the modulation of defensive behaviors during exposure to either potential or immediate stimuli (predator). Thus, the present study was aimed at investigating the role of VH and AC in the modulation of defensive behaviors of mice when exposed to predators (rats) as well as the predatory context. The experiment comprised four parts: (i) to investigate both whether stress regarding the exposure to the predator alters the corticosterone secretion in mice and to determine the magnitude and the duration of this secretion; (ii) the role of VH and AC was evaluated through local microinjection of the GABAA receptor agonist muscimol (0,1 μg/0,1 μl) in the modulation of defensive behavioral responses of mice exposed to RET (proximal aversive situation). The responses then were compared to those presented during to the exposure to the elevated plus-maze (EPM - potential aversive situation); (iii) to investigate whether mice exposed to natural predator (rat) in RET exhibit... (Complete abstract click electronic access below)
Amaral, Vanessa Cristiane de Santana. "Contribuição diferencial do hipocampo ventral e do complexo amidalóide na modulação de respostas defensivas inatas e condicionadas de camundongos /." São Carlos, 2011. http://hdl.handle.net/11449/100953.
Full textBanca: Cleopatra da Silva Planeta
Banca: Hélio Zangrossi Junior
Banca: Marcus Lira Brandão
Banca: Francisco Silveira Guimarães
Resumo: Quando os animais são confrontados com estímulos ambientais ameaçadores como a exposição ao predador ou estímulos como altura, iluminação e estímulos nociceptivos, exibem reações de defesa coordenadas e específicas. Nas últimas décadas, observa-se um crescente interesse pela utilização de estímulos naturalísticos para o estudo das bases neurais de emoções como o medo e ansiedade. Nesse contexto, o teste de exposição ao rato (RET), um novo modelo etológico de interação presa-predador, utilizando camundongos (presa) e ratos (predador), foi desenvolvido para avaliar a expressão de diferentes comportamentos defensivos na presa. Entretanto, poucos estudos foram conduzidos com esse modelo no intuito de investigar as bases neurais das respostas defensivas de camundongos expostos ao rato. Adicionalmente, evidências da literatura destacam que o hipocampo ventral (HV) e o complexo amidalóide (CA) parecem contribuir diferencialmente na modulação de respostas defensivas frente a estímulos proximais (predador) ou potenciais. Assim, o presente estudo foi conduzido para investigar o papel do HV e do CA nas respostas defensivas de camundongos exibidas diante do predador (rato) e do contexto associado ao predador. Para tal, o presente estudo foi dividido em quatro etapas. Na primeira delas, investigamos se o estresse da exposição ao predador no RET altera a secreção de corticosterona em camundongos e determinamos a magnitude e a duração desta secreção. Na segunda etapa, avaliamos o papel do HV e do CA, através da injeção local do agonista de receptores GABAA muscimol (0,1 μg/0,1 μl), na mediação de respostas comportamentais defensivas de camundongos expostos ao RET (situação proximal) e comparamos com aquelas apresentadas durante a exposição ao labirinto em cruz elevado (LCE - situação potencial). Subsequentemente, investigamos se camundongos expostos... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: When animals are confronted with environmental threatening situations such as exposure to a predator as well as to height, high illumination and nociceptive stimuli they exhibit defensive behaviors. Over the past decades there has been a growing interest by the neuroscientists in the use of naturalistic stimuli to the study of the neural systems of the emotions such as fear and anxiety. In this context, the Rat Exposure Test (RET) which is a new ethological model of prey-predator interaction using mice (prey) and rats (predator) was developed in order to evaluate the expression of different defensive behaviors in the prey. However few studies using this model have been carried out with the objective of investigating the neural systems of the defensive behaviors in mice exposed to rats. In addition, evidence in literature has shown that the ventral hippocampus (VH) and the amygdaloid complex (AC) contribute differentially in the modulation of defensive behaviors during exposure to either potential or immediate stimuli (predator). Thus, the present study was aimed at investigating the role of VH and AC in the modulation of defensive behaviors of mice when exposed to predators (rats) as well as the predatory context. The experiment comprised four parts: (i) to investigate both whether stress regarding the exposure to the predator alters the corticosterone secretion in mice and to determine the magnitude and the duration of this secretion; (ii) the role of VH and AC was evaluated through local microinjection of the GABAA receptor agonist muscimol (0,1 μg/0,1 μl) in the modulation of defensive behavioral responses of mice exposed to RET (proximal aversive situation). The responses then were compared to those presented during to the exposure to the elevated plus-maze (EPM - potential aversive situation); (iii) to investigate whether mice exposed to natural predator (rat) in RET exhibit... (Complete abstract click electronic access below)
Doutor
Books on the topic "Inatas"
Śeṭha, Ramaṇa Nārāyaṇa. Khopā inalā inalā. Sātārā: Śabdasevā Prakāśana, 1999.
Find full textde, Pina-Cabral J. M., ed. Motivação: Conceito, aspectos fundamentalmente inatos. Porto: Contraponto, 1985.
Find full textTeitelbaum, Michael. 3D-inator. White Plains, New York: Reader's Digest Children's Books, 2012.
Find full textTeitelbaum, Michael. Skate-inator. White Plains, New York: Reader's Digest Children's Books, 2012.
Find full textHadipranoto, Inanta. The exploration of Inanta: Inanta Hadipranoto keluar dari bingkai. [Semarang]: Inanta, 2004.
Find full textPaṃvāra, Vīrendra. Inamā kanakve āṇa basanta. [Dehradun]: Dhāda Prakāśana, 2004.
Find full textBook chapters on the topic "Inatas"
Casco, M. F., J. V. Misa, M. Defensor, Alipio Garcia, and A. Salvador. "Surface Structure Dependent Growth of InAs/InAlAs Quantum Wires on InP(100)." In Semiconductor Photonics: Nano-Structured Materials and Devices, 86–88. Stafa: Trans Tech Publications Ltd., 2007. http://dx.doi.org/10.4028/0-87849-471-5.86.
Full textSmith, Nigel. "Syagrus inajai." In Geobotany Studies, 465–67. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-05509-1_56.
Full textCarneiro, Maria João, Celeste Eusébio, Elisabeth Kastenholz, and Helena Alvelos. "Benefits of social tourism programmes for seniors: the case of the INATEL Foundation in Portugal." In Social tourism: global challenges and approaches, 41–55. Wallingford: CABI, 2021. http://dx.doi.org/10.1079/9781789241211.0041.
Full textCarneiro, Maria João, Celeste Eusébio, Elisabeth Kastenholz, and Helena Alvelos. "Benefits of social tourism programmes for seniors: the case of the INATEL Foundation in Portugal." In Social tourism: global challenges and approaches, 41–55. Wallingford: CABI, 2021. http://dx.doi.org/10.1079/9781789241211.0005a.
Full textMihlar, Mohamed. "Hazrat Inayat Khan." In Islam, Judaism, and Zoroastrianism, 278–81. Dordrecht: Springer Netherlands, 2018. http://dx.doi.org/10.1007/978-94-024-1267-3_2060.
Full textInaba, Masumi, and Yoshikata Inaba. "Sebaceous Gland Hypothesis of Androgenetic Alopecia (Inaba 1985; Inaba and Inaba 1992a)." In Androgenetic Alopecia, 175–78. Tokyo: Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-67038-4_19.
Full textPéronne, E., T. Polack, J. F. Lampin, A. Alexandrou, F. Fossard, F. H. Julien, J. Brault, and M. Gendry. "Femtosecond Mid-Infrared study of electron dynamics in self-organized InAs quantum wires on InAIAs/InP (001)." In Ultrafast Phenomena XII, 372–74. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-56546-5_108.
Full textInaba, Masumi, and Yoshikata Inaba. "The Inaba Method." In Human Body Odor, 171–234. Tokyo: Springer Japan, 1992. http://dx.doi.org/10.1007/978-4-431-66908-1_15.
Full textRyholt, Kim. "Inaros in Iceland and Elsewhere." In New Approaches in Demotic Studies, edited by Franziska Naether, 271–80. Berlin, Boston: De Gruyter, 2019. http://dx.doi.org/10.1515/9783110664874-013.
Full textShi, G. X., B. Xu, P. Jin, X. L. Ye, C. X. Cui, C. L. Zhang, J. Wu, and Z. G. Wang. "The Structural and Photoluminescence Character of InAs Quantum Dots Grown on a Combined InAlAs and GaAs Strained Buffer Layer." In Materials Science Forum, 1791–94. Stafa: Trans Tech Publications Ltd., 2005. http://dx.doi.org/10.4028/0-87849-960-1.1791.
Full textConference papers on the topic "Inatas"
COSTA, KATHARINE DYZIRRE DE MELO, IRINEU CLEMENTINO VIEIRA NETO, and THALITA OLIVEIRA DA SILVA BORBA. "ABORDAGEM DAS RESPOSTAS IMUNOLÓGICAS DA DOENÇA PERIODONTAL: UMA REVISÃO DE LITERATURA." In I Congresso Brasileiro de Imunologia On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1014.
Full textSilva, Laila Taniellen Rodrigues Da, Lucas Lopes Barbosa, Milane Da Silva Viana, Jorge Luis De Oliveira Borges, and Athauany Nogueira Dos Santos. "RELAÇÃO DA RESPOSTA IMUNE INATA E ADAPTATIVA À INFECÇÃO DE PARASITOS HELMÍNTICOS." In I Congresso Brasileiro de Parasitologia Humana On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1960.
Full textTonelli, Gabriel Bessa Tibery, Neslayne Louise Campiol, Manoel Henrique Carvalho, Bruno Pereira Garcia, and Janne Marques Silveira. "O PAPEL IMUNOMODULATÓRIO DOS HORMÔNIOS SEXUAIS NA COVID 19." In I Congresso Brasileiro de Imunologia On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/991.
Full textHsieh, I. J., C. C. Liao, C. Tsai, and Albert Chin. "From Strain-Compensated In0.80Ga0.20As/InAlAs to InAs/InAlAs HEMT's." In 1998 International Conference on Solid State Devices and Materials. The Japan Society of Applied Physics, 1998. http://dx.doi.org/10.7567/ssdm.1998.d-7-6.
Full textMATULIONIS, A., L. ARDARAVICIUS, J. LIBERIS, V. ANINKEVICIUS, and D. GASQUET. "HIGH-FREQUENCY NOISE IN InAIAs/InGaAs/InAlAs QUANTUM-WELL CHANNELS." In Proceedings of the 16th International Conference. WORLD SCIENTIFIC, 2001. http://dx.doi.org/10.1142/9789812811165_0116.
Full textNITTA, JUNSAKU, YIPING LIN, TATSUSHI AKAZAKI, and TAKAAKI KOGA. "G-FACTOR CONTROL IN AN InAs-INSERTED InGaAs/InAlAs HETEROSTRUCTURE." In Proceedings of the International Symposium on Mesoscopic Superconductivity and Spintronics — In the Light of Quantum Computation. WORLD SCIENTIFIC, 2005. http://dx.doi.org/10.1142/9789812701619_0057.
Full textLi, Xinxin, Kailing Zhang, Fatima Toor, Julian Treu, Lukas Stampfer, Gregor Koblmueller, and John P. Prineas. "Radiative and Nonradiative Recombination Coefficients of InAs/InAlAs Core-shell Nanowires." In CLEO: Applications and Technology. Washington, D.C.: OSA, 2018. http://dx.doi.org/10.1364/cleo_at.2018.jw2a.125.
Full textZhang, B., W. G. Ning, and F. M. Guo. "Resonant tunneling effect of InAs quantum dots grown on InAlAs/InP." In 2015 International Conference on Numerical Simulation of Optoelectronic Devices (NUSOD). IEEE, 2015. http://dx.doi.org/10.1109/nusod.2015.7292834.
Full textCoutinho, Luis Costa, Francilayra Adelina Da Silva Roseno, Laiane Oliveira Lima Soares, and Alexander Fernando Ribeiro Da Silva. "PATOGENICIDADE DA SALMONELLA SPP. E OS MECANISMOS DE ESCAPE IMUNOLÓGICO À LUZ DAS EVIDÊNCIAS DA LITERATURA EMERGENTE." In I Congresso Brasileiro de Imunologia On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/2017.
Full textHe, Wei-Zhi, Heng-Kuang Lin, Pei-Chin Chiu, Jen-Inn Chyi, Chih-Hsin Ko, Ta-Ming Kuan, Meng-Kuei Hsieh, Wen-Chin Lee, and Clement H. Wann. "N+-InGaAs/InAlAs recessed gates for InAs/AlSb HFET development." In 2010 22nd International Conference on Indium Phosphide and Related Materials (IPRM). IEEE, 2010. http://dx.doi.org/10.1109/iciprm.2010.5516406.
Full textReports on the topic "Inatas"
Twesten, R. D., J. M. Millunchick, S. R. Lee, D. M. Follstaedt, E. D. Jones, S. P. Ahrenkiel, Y. Zhang, and A. Mascarenhas. Microstructure of compositionally modulated InAlAs. Office of Scientific and Technical Information (OSTI), December 1996. http://dx.doi.org/10.2172/453541.
Full textBriggs, R. D., A. J. Howard, A. G. Baca, M. J. Hafich, and G. A. Vawter. A study of p-type ohmic contacts to InAlAs/InGaAs heterostructures. Office of Scientific and Technical Information (OSTI), December 1995. http://dx.doi.org/10.2172/212554.
Full textJones, E. D., J. L. Reno, Nobuo Kotera, and Y. Wang. Conduction band mass determinations for n-type InGaAs/InAlAs single quantum wells. Office of Scientific and Technical Information (OSTI), May 1998. http://dx.doi.org/10.2172/658197.
Full textLittle, J. W., S. W. Kennedy, R. P. Leavitt, M. L. Lucas, and K. A. Olver. A New Two-Color Infrared Photodetector Design Using INGAAS/INALAS Coupled Quantum Wells. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada393876.
Full textJones, E. D., C. P. Tigges, N. Kotera, T. Mishima, H. Nakamura, and N. Miura. Magnetoluminescence characterization of lattice matched n-type InGaAs/InAlAs MQW`s on InP. Office of Scientific and Technical Information (OSTI), December 1996. http://dx.doi.org/10.2172/453516.
Full textBhattacharya, P., and R. Gibala. Investigation on the MBE growth and properties of AlGaInAs/InP and InGaAs-InAlAs superlattices. Office of Scientific and Technical Information (OSTI), December 1989. http://dx.doi.org/10.2172/7122247.
Full textNosho, B. Z., B. R. Bennett, L. J. Whitman, and M. Goldenberg. Spontaneous Growth of an InAs Nanowire Lattice in an InAs/GaSb Superlattice. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada447719.
Full textKotera, N., K. Tanaka, H. Arimoto, N. Miura, E. D. Jones, T. Mishima, and M. Washima. Characterization of heavy masses of two-dimensional conduction subband in InGaAs/InAlAs MQW structures by pulsed cyclotron resonance technology. Office of Scientific and Technical Information (OSTI), May 1998. http://dx.doi.org/10.2172/658404.
Full textSchultz, Peter Andrew. Simple intrinsic defects in InAs :. Office of Scientific and Technical Information (OSTI), March 2013. http://dx.doi.org/10.2172/1095951.
Full textIkossi, Kiki. InAs Device Process Development and Characterization. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada413747.
Full text