Química e investigação: cinética química e as velocidades de reações

Anais do II Seminário Seminário Estadual PIBID do Paraná: tecendo saberes / organizado por Dulcyene Maria Ribeiro e Catarina Costa Fernandes — Foz do Iguaçu: Unioeste; Unila, 2014O presente trabalho foi elaborado a partir de experimentos realizados com estudantes da segunda série do ensino médio do Colégio Estadual Jardim Gisele, tendo como objetivo articular os conhecimentos prévios sobre velocidade de reação que haviam sido trabalhados em sala de aula com o problema proposto, estimulando sua participação e despertando o senso crítico dos mesmos a respeito do tema “Cinética química- velocidade de uma reação”. Coube aos estudantes refletir, discutir e explicar os problemas que lhes foram apresentados. Após cada experimento observou-se que os estudantes resolveram as problemáticas propostas refletindo por meio de hipóteses a melhor maneira de resolvê-la

MORTE ENCEFÁLICA E O CÓDIGO DE ÉTICA MÉDICA: NOVAS TENDÊNCIAS

Segundo a Resolução n. 1.480/1997 do Conselho Federal de Medicina (1997), “[...] a parada total e irreversível das funções encefálicas equivale à morte” e a morte encefálica será caracterizada por meio da realização de exames clínicos e complementares durante intervalos de tempo variáveis, próprios para determinadas faixas etárias, segundo o artigo 1º. O objetivo com este trabalho foi descrever o papel do médico, do ponto de vista ético e legal, no diagnóstico de morte encefálica. O método utilizado para o trabalho foi a pesquisa bibliográfica on-line e resoluções do Conselho Federal de Medicina. A principal causa de morte encefálica, que equivale à morte clínica, é o traumatismo cranioencefálico (SALLUM; ROSSATO; SILVA, 2011). A partir da Resolução do CFM n. 1.826/2007 foi possível perceber que, do ponto de vista ético e legal, após seu diagnóstico, é dever do médico retirar os procedimentos de suporte que mantinham artificialmente o funcionamento dos órgãos vitais utilizados até o momento de sua determinação (CONSELHO FEDERAL DE MEDICINA, 2007). Ainda, o médico deverá informar aos familiares ou representante legal o falecimento do paciente, bem como preencher a Declaração de Óbito, caso este não tenha sido ocasionado por meio violento, para as devidas providências pertinentes ao sepultamento (Meneses et al., 2010). Inclusive, para comprovar a suspeita de morte encefálica, são necessários dois exames complementares, em horários variáveis (DANTAS FILHO et al., 1996). Por meio do respectivo exame complementar é confirmado o diagnóstico: ausência de atividade elétrica cerebral, ausência de atividade metabólica cerebral ou ausência de perfusão sanguínea cerebral (GOGLIANO, 2009). A partir de dados obtidos e normas éticas existentes, concluiu-se que a irreversibilidade da morte encefálica autoriza o médico a retirar o suporte terapêutico utilizado até o momento de sua determinação. Tal assunto ainda assusta a sociedade por esta não estar devidamente familiarizada com esse tema, o que gera ansiedade, dúvidas e receios, mas o momento deve ser enfrentado de modo compreensivo, humano e solidário pelo médico. Em suma, o papel do médico é obedecer rigorosamene aos critérios diagnósticos preconizados pelo Conselho Federal de Medicina, orientar e confortar a família do paciente afetado, deixando os familiares seguros quanto à garantia do respeito aos direitos dos pacientes.Palavras-chave: Morte encefálica. Ética médica. Óbito. Diagnóstico

Risk management for companies focused on innovation processes

Risk is inherent to the activities of technology and innovation companies and to manage them represent an opportunity to improve the company capability to achieve its goals. The use of ERM models has been studied since the Committee of Sponsoring Organizations of the Treadway Commission guides. This article adapted the MIGGRI model for the context of an innovation company from a TSP in Brazil. Using a case study and a review from previous ERM literature, the article show that is possible to measure the risks that an innovation company faces, and that they may be managed with a view to supporting a company’s strategy. Were applied an economic analysis based on a MCS and an indicator of CFaR were applied to measure innovation risks. A strategic performance model for innovation companies are proposed and the benefit to implement Risk Management practices in innovation organizations was validated

Estudos de caracterização de pó de aciaria elétrica visando sua incorporação em materiais cerâmicos

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Polymorphisms and resistance mutations of hepatitis C virus on sequences in the European hepatitis C virus database

AIM: To evaluate the occurrence of resistant mutations in treatment-naïve hepatitis C virus (HCV) sequences deposited in the European hepatitis C virus database (euHCVdb). METHODS: The sequences were downloaded from the euHCVdb (https://euhcvdb.ibcp.fr/euHCVdb/). The search was performed for full-length NS3 protease, NS5A and NS5B polymerase sequences of HCV, separated by genotypes 1a, 1b, 2a, 2b and 3a, and resulted in 798 NS3, 708 NS5A and 535 NS5B sequences from HCV genotypes 1a, 1b, 2a, 2b and 3a, after the exclusion of sequences containing errors and/or gaps or incomplete sequences, and sequences from patients previously treated with direct antiviral agents (DAA). The sequence alignment was performed with MEGA 6.06 MAC and the resulting protein sequences were then analyzed using the BioEdit 7.2.5. for mutations associated with resistance. Only positions that have been described as being associated with failure in treatment in in vivo studies, and/or as conferring a more than 2-fold change in replication in comparison to the wildtype reference strain in in vitro phenotypic assays were included in the analysis. RESULTS: The Q80K variant in the NS3 gene was the most prevalent mutation, being found in 44.66% of subtype 1a and 0.25% of subtype 1b. Other frequent mutations observed in more than 2% of the NS3 sequences were: I170V (3.21%) in genotype 1a, and Y56F (15.93%), V132I (23.28%) and I170V (65.20%) in genotype 1b. For the NS5A, 2.21% of the genotype 1a sequences have the P58S mutation, 5.95% of genotype 1b sequences have the R30Q mutation, 15.79% of subtypes 2a sequences have the Q30R mutation, 23.08% of subtype 2b sequences have a L31M mutation, and in subtype 3a sequences, 23.08% have the M31L resistant variants. For the NS5B, the V321L RAV was identified in 0.60% of genotype 1a and in 0.32% of genotype 1b sequences, and the N142T variant was observed in 0.32% of subtype 1b sequences. The C316Y, S556G, D559N RAV were identified in 0.33%, 7.82% and 0.32% of genotype 1b sequences, respectively, and were not observed in other genotypes. CONCLUSION: HCV mutants resistant to DAAs are found in low frequency, nevertheless they could be selected and therapy could fail due resistance substitutions in HCV genome

Polymorphisms and resistance mutations of hepatitis C virus on sequences in the European hepatitis C virus database

AIM: To evaluate the occurrence of resistant mutations in treatment-naïve hepatitis C virus (HCV) sequences deposited in the European hepatitis C virus database (euHCVdb). METHODS: The sequences were downloaded from the euHCVdb (https://euhcvdb.ibcp.fr/euHCVdb/). The search was performed for full-length NS3 protease, NS5A and NS5B polymerase sequences of HCV, separated by genotypes 1a, 1b, 2a, 2b and 3a, and resulted in 798 NS3, 708 NS5A and 535 NS5B sequences from HCV genotypes 1a, 1b, 2a, 2b and 3a, after the exclusion of sequences containing errors and/or gaps or incomplete sequences, and sequences from patients previously treated with direct antiviral agents (DAA). The sequence alignment was performed with MEGA 6.06 MAC and the resulting protein sequences were then analyzed using the BioEdit 7.2.5. for mutations associated with resistance. Only positions that have been described as being associated with failure in treatment in in vivo studies, and/or as conferring a more than 2-fold change in replication in comparison to the wildtype reference strain in in vitro phenotypic assays were included in the analysis. RESULTS: The Q80K variant in the NS3 gene was the most prevalent mutation, being found in 44.66% of subtype 1a and 0.25% of subtype 1b. Other frequent mutations observed in more than 2% of the NS3 sequences were: I170V (3.21%) in genotype 1a, and Y56F (15.93%), V132I (23.28%) and I170V (65.20%) in genotype 1b. For the NS5A, 2.21% of the genotype 1a sequences have the P58S mutation, 5.95% of genotype 1b sequences have the R30Q mutation, 15.79% of subtypes 2a sequences have the Q30R mutation, 23.08% of subtype 2b sequences have a L31M mutation, and in subtype 3a sequences, 23.08% have the M31L resistant variants. For the NS5B, the V321L RAV was identified in 0.60% of genotype 1a and in 0.32% of genotype 1b sequences, and the N142T variant was observed in 0.32% of subtype 1b sequences. The C316Y, S556G, D559N RAV were identified in 0.33%, 7.82% and 0.32% of genotype 1b sequences, respectively, and were not observed in other genotypes. CONCLUSION: HCV mutants resistant to DAAs are found in low frequency, nevertheless they could be selected and therapy could fail due resistance substitutions in HCV genome

Polymorphisms and resistance mutations of hepatitis C virus on sequences in the European hepatitis C virus database

AIM: To evaluate the occurrence of resistant mutations in treatment-naïve hepatitis C virus (HCV) sequences deposited in the European hepatitis C virus database (euHCVdb). METHODS: The sequences were downloaded from the euHCVdb (https://euhcvdb.ibcp.fr/euHCVdb/). The search was performed for full-length NS3 protease, NS5A and NS5B polymerase sequences of HCV, separated by genotypes 1a, 1b, 2a, 2b and 3a, and resulted in 798 NS3, 708 NS5A and 535 NS5B sequences from HCV genotypes 1a, 1b, 2a, 2b and 3a, after the exclusion of sequences containing errors and/or gaps or incomplete sequences, and sequences from patients previously treated with direct antiviral agents (DAA). The sequence alignment was performed with MEGA 6.06 MAC and the resulting protein sequences were then analyzed using the BioEdit 7.2.5. for mutations associated with resistance. Only positions that have been described as being associated with failure in treatment in in vivo studies, and/or as conferring a more than 2-fold change in replication in comparison to the wildtype reference strain in in vitro phenotypic assays were included in the analysis. RESULTS: The Q80K variant in the NS3 gene was the most prevalent mutation, being found in 44.66% of subtype 1a and 0.25% of subtype 1b. Other frequent mutations observed in more than 2% of the NS3 sequences were: I170V (3.21%) in genotype 1a, and Y56F (15.93%), V132I (23.28%) and I170V (65.20%) in genotype 1b. For the NS5A, 2.21% of the genotype 1a sequences have the P58S mutation, 5.95% of genotype 1b sequences have the R30Q mutation, 15.79% of subtypes 2a sequences have the Q30R mutation, 23.08% of subtype 2b sequences have a L31M mutation, and in subtype 3a sequences, 23.08% have the M31L resistant variants. For the NS5B, the V321L RAV was identified in 0.60% of genotype 1a and in 0.32% of genotype 1b sequences, and the N142T variant was observed in 0.32% of subtype 1b sequences. The C316Y, S556G, D559N RAV were identified in 0.33%, 7.82% and 0.32% of genotype 1b sequences, respectively, and were not observed in other genotypes. CONCLUSION: HCV mutants resistant to DAAs are found in low frequency, nevertheless they could be selected and therapy could fail due resistance substitutions in HCV genome

Genetic Barrier to Direct Acting Antivirals in HCV Sequences Deposited in the European Databank

Background & Aims: Development of resistance results from mutations in the viral genome, and the presence of selective drug pressure leads to the emergence of a resistant virus population. The aim of this study was to analyze the impact of genetic variability on the genetic barrier to drug resistance to DAAs. Methods: The genetic barrier was quantified based on the number and type of nucleotide mutations required to impart resistance, considering full-length HCV NS3, NS5A and NS5B regions segregated by genotype into subtypes 1a, 1b, 2a, 2b and 3a. This study analyzed 789 NS3 sequences, 708 sequences and 536 NS5B sequences deposited in the European Hepatitis C Virus Database, in the following resistance-associated positions: NS3: F43/I/L/ S/V, Q80K/R, R155K/G, A156G/S/T and D168A/C/E/G/H/N/T/V/Y; NS5A: L/M28A/T/V, Q30E/H/R, L31F/I/M/V, H58D or P58S and Y93C/F/H/N/S; NS5B: S282P/R/T, C316H/N/Y, S368T, Y448C/H, S556G/R, D559R. Results: Variants that require only one transversion in NS3 were found in 4 positions and include F43S, R80K, R155K/G and A156T. The genetic barrier to resistance shows subtypic differences at position 155 of the NS3 gene where a single transition is necessary in subtype 1a. In the NS5A gene, 5 positions where only one nucleotide change can confer resistance were found, such as L31M which requires one transversion in all subtypes, except in 0.28% of 1b sequences; and R30H, generated by a single transition, which was found in 10.25% of the sequences of genotype 1b. Other subtypic differences were observed at position 58, where resistance is less likely in genotype 1a because a transversion is required to create the variant 58S. For the NS5B inhibitors, the genetic barrier at positions conferring resistance was nearly identical in subtypes 1a and 1b, and single transitions or transversions were necessary in 5 positions to generate a drug-resistant variant of HCV. The positions C316Y and S556D required only one transition in all genotypes, Y448H and S556 G/N/R positions required only one transition for up to 98.8%of the sequences analyzed. A single variant in position 448 in genotype 1a is less likely to become the resistance variant 448H because it requires two transversions. Also, in the position 559D a transversion and a transition were necessary to generate the resistance mutant D559H. Conclusion: Results revealed that in 14 out of 16 positions, conversion to a drug-resistant variant of HCV required only one single nucleotide substitutions threatening direct acting antivirals from all three classes

Tratamento de cromoblastomicose severa com a associação itraconazole e 5-flucitosina

Cromoblastomicose é uma infecção fúngica crônica do tecido subcutâneo causada pela inoculação traumática de um grupo específico de fungos através da pele, encontrados eventualmente em trabalhadores do campo descalços em países de clima tropical e subtropical. Relatamos aqui o caso de um paciente do sexo masculino com uma lesão dermatológica de crescimento lento e pruriginosa nos membros inferiores por 20 anos, diagnosticada e tratada com sucesso para cromoblastomicose. Apesar da prevalência desta doença em nossa região, o tratamento ainda é um desafio.Chromoblastomycosis is a chronic human melanized fungi infection of the subcutaneous tissue caused by traumatic inoculation of a specific group of dematiaceous fungi through the skin, often found in barefooted agricultural workers, in tropical and subtropical climate countries. We report the case of a male patient presenting a slow-growing pruriginous lesion on the limbs for 20 years, mistreated over that time, which was diagnosed and successfully treated as chromoblastomycosis. Besides the prevalence of this disease, treatment is still a clinical challenge