RESUMO
Objetivo: identificar os fatores que interferem na comunicação entre as equipes de enfermagem durante o handover de troca de turno em clínicas cirúrgicas, e sua interface com a segurança do paciente. Método: estudo quantitativo, observacional, com análise descritiva, realizado de abril a julho de 2019, por meio de um roteiro de observação e um formulário, em nove clínicas cirúrgicas de um hospital universitário. Resultados: observou-se 54 handovers e participaram 123 profissionais de enfermagem. Dentre os fatores analisados, destaca-se, a ausência de instrumento padronizado de handover (85,19%) e presença de ruídos sonoros (77,78%). A maioria dos participantes (86,93%) apontaram a omissão de informações, na transferência de cuidados, como o fator mais prejudicial para assistência. Conclusão: os fatores que interferiram na comunicação durante o handover foram: ruídos sonoros, omissão de informações, ausência de instrumento padronizado e atrasos dos profissionais. Acredita-se que a identificação desses fatores contribua para o desenvolvimento de melhores estratégias.
Objective: to identify factors affecting communication between nursing teams during shift handover on surgical wards, and how it interfaces with patient safety. Method: this quantitative, observational study, with descriptive analysis, was conducted on nine surgical wards of a university hospital from April to July 2019, using an observation script and record form. Results: 54 nursing shift handovers were observed, and 123 nursing personnel participated. Of particular note among the factors analyzed were absence of a standardized handover instrument (85.19%) and the presence of noise (77.78%). Most of the participants (86.93%) pointed to missing information at handover as the factor most prejudicial to care. Conclusion: the factors that interfered with communication during handover were: noise, omission of information, absence of a standardized instrument, and staff lateness. It is believed that identifying these factors will help develop better strategies.
Objetivo: identificar los factores que afectan la comunicación entre los equipos de enfermería durante la transferencia de turno en las salas quirúrgicas y cómo interactúa con la seguridad del paciente. Método: este estudio cuantitativo, observacional, con análisis descriptivo, se realizó en nueve salas quirúrgicas de un hospital universitario de abril a julio de 2019, utilizando un guión de observación y formulario de registro. Resultados: se observaron 54 traspasos de turno de enfermería y participaron 123 personal de enfermería. Entre los factores analizados destacan la ausencia de un instrumento de traspaso estandarizado (85,19%) y la presencia de ruido (77,78%). La mayoría de los participantes (86,93%) señaló la falta de información en la entrega como el factor más perjudicial para la atención. Conclusión: los factores que interfirieron en la comunicación durante el traspaso fueron: ruido, omisión de información, ausencia de instrumento estandarizado y tardanza del personal. Se cree que identificar estos factores ayudará a desarrollar mejores estrategias.
Assuntos
Humanos , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Adulto Jovem , Comunicação , Segurança do Paciente , Transferência da Responsabilidade pelo Paciente/normas , Hospitais Universitários , Relações Interprofissionais , Equipe de Enfermagem , Equipe de Assistência ao Paciente/normas , Brasil , Troca de Informação em Saúde , Cuidados de Enfermagem/normasRESUMO
Estima-se que o Schistosoma mansoni esteja presente em 19 estados brasileiros e um dos fatores responsáveis pela expansão da esquistossomose é a migração de indivíduos de áreas endêmicas, principalmente do Nordeste do país. O presente estudo teve por objetivo avaliar a ocorrência da esquistossomose entre trabalhadores, migrantes da Região Nordeste do país, que atuavam em Conceição da Barra, norte do Espírito Santo, no corte da cana-de-açúcar para uma indústria de produção de álcool. Para a determinação dos parasitos intestinais, foram utilizadas as técnicas de sedimentação espontânea e Kato-Katz. Dos 287 indivíduos analisados, 45 (15,7 por cento), provenientes dos estados de Alagoas, Pernambuco e Bahia, estavam positivos para S. mansoni. Do total de positivos, 38 (84,4 por cento) eram provenientes do estado de Alagoas, 6 (13,3 por cento) do estado de Pernambuco e apenas 1 (2,2 por cento) do estado da Bahia. Os resultados indicam a possibilidade de expansão da esquistossomose na região norte do Espírito Santo.
It is estimated that Schistosoma mansoni is present in 19 Brazilian states and one of the factorsresponsible for the spread of schistosomiasis is the migration of individuals from endemic areas,particularly from northeastern Brazil. In the municipality of Conceição da Barra, northern stateof Espírito Santo, the present study aimed to evaluate the occurrence of schistosomiasis amongsugarcane cutting workers in the alcohol industry, who migrated from the northeastern region ofthe country. For the diagnosis of intestinal parasites, spontaneous sedimentation and Kato-Katztechniques were used. Of the 287 individuals analyzed, 45 (15.7 por cento), from the states of Alagoas,Pernambuco and Bahia, were positive for S. mansoni. Of the total positive individuals, 38 (84.4 por cento)were from the state of Alagoas, 6 (13.3 por cento) from Pernambuco and 1 (2.2 por cento) from Bahia. The resultsindicate the possibility of schistosomiasis expansion in the northern state of Espírito Santo.
Assuntos
Humanos , Emigrantes e Imigrantes , Doenças Negligenciadas , Schistosoma mansoni , EsquistossomoseRESUMO
A recent genome-wide association study (GWAS) suggested that polymorphisms in or around the genes HCP5, HLA-C and ZNRD1 confer restriction against HIV-1 viral replication or disease progression. Here, we also find that these alleles are associated with different aspects of HIV disease, albeit mainly in European Americans. Additionally, we offer that because the GWAS cohort was a subset of HIV-positive individuals, selected based in part on having a low viral load, the observed associations for viral load are magnified compared with those we detect in a large well-characterized prospective natural history cohort of HIV-1-infected persons. We also find that because of linkage disequilibrium (LD) patterns, the dominant viral load- and disease-influencing associations for the ZNRD1 or HLA-C and HCP5 alleles are apparent mainly when these alleles are present in HLA-A10- or HLA-B*57-containing haplotypes, respectively. ZNRD1 alleles lacking HLA-A10 did not confer disease protection whereas ZNRD1-A10 haplotypes did. When examined in isolation, the HCP5-G allele associates with a slow disease course and lower viral loads. However, in multivariate models, after partitioning out the protective effects of B*57, the HCP5-G allele associates with disease-acceleration and enhanced viral replication; these associations for HCP5-G are otherwise obscured because of the very strong LD between this allele and a subset of protective B*57 alleles. Furthermore, HCP5 and HLA-C alleles stratify B*57-containing genotypes into those that associate with either striking disease retardation or progressive disease, providing one explanation for the long-standing conundrum of why some HLA-B*57-carrying individuals are long-term non-progressors, whereas others exhibit progressive disease. Collectively, these data generally underscore the strong dependence of genotype-phenotype relationships upon cohort design, phenotype selection, LD patterns and populations studied. They specifically demonstrate that the influence of ZNRD1 alleles on disease progression rates are attributable to HLA-A10, help clarify the relationship between the HCP5, HLA-C and HLA-B*57 alleles, and reaffirm a critical role of HLA-B*57 alleles in HIV disease. Furthermore, as the protective B*57-containing genotypes convey striking salutary effects independent of their strong impact on viral control, it is conceivable that T cell-based therapeutic vaccine strategies aimed at reducing viral loads may be inadequate for limiting AIDS progression, raising the potential need for complementary strategies that target viral load-independent determinants of pathogenesis.
Assuntos
Proteínas de Ligação a DNA/genética , Infecções por HIV/genética , Antígenos HLA-A/genética , Antígenos HLA-B/genética , Antígenos HLA-C/genética , Complexo Principal de Histocompatibilidade/genética , Negro ou Afro-Americano , Alelos , Progressão da Doença , Genótipo , Infecções por HIV/fisiopatologia , Sobreviventes de Longo Prazo ao HIV , HIV-1/genética , HIV-1/imunologia , Humanos , Estimativa de Kaplan-Meier , Desequilíbrio de Ligação , Fenótipo , Polimorfismo Genético , RNA Longo não Codificante , RNA não Traduzido , Carga Viral , População Branca/genéticaRESUMO
BACKGROUND: The in vivo impact of mannose-binding lectin (MBL), a molecule involved in innate immunity, on the pathogenesis of human immunodeficiency virus (HIV)-1 infection and AIDS is unknown. METHODS: A total of 1102 HIV-positive and 2213 HIV-negative adult subjects were screened for polymorphisms in the coding and promoter regions of MBL2, the gene that encodes MBL. RESULTS: Variations in MBL2 did not influence the risk of acquiring HIV-1. Heterozygosity for coding mutations (O allele) and homozygosity for the -221 promoter polymorphism (X allele) in MBL2 were associated with a delay in and an accelerated rate of disease progression, respectively. MBL2 variations influenced the rate of progression to AIDS-defining illnesses. In a multivariate model, the effects of MBL2 variations were independent of several parameters known to influence disease progression, including steady-state viral load, baseline CD4(+) T cell counts, and delayed-type hypersensitivity skin test responses, an in vivo marker of cell-mediated immunity. The effects of MBL2 variations were most evident in those who possessed protective genotypes of CCR5 and a high copy number of CCL3L1, the most potent HIV-suppressive CCR5 ligand. CONCLUSIONS: MBL2 genotypes are independent determinants of HIV disease progression and heterozygosity for MBL2 coding mutations confer disease-retarding effects. MBL-dependent immune responses may play a role in the pathogenesis of HIV infection.
Assuntos
Predisposição Genética para Doença , Infecções por HIV/genética , Infecções por HIV/metabolismo , HIV-1 , Lectina de Ligação a Manose/genética , Adulto , Alelos , Estudos de Coortes , Genótipo , Infecções por HIV/imunologia , Haplótipos , Heterozigoto , Humanos , Lectina de Ligação a Manose/imunologia , Lectina de Ligação a Manose/metabolismo , Mutação , Polimorfismo Genético , Regiões Promotoras Genéticas/genética , Fatores de TempoRESUMO
Studies in humans and in experimental models of HIV-1 infection indicate an important role for monocyte chemoattractant protein-1 (MCP-1; also known as CC chemokine ligand 2), a potent chemoattractant and activator of mononuclear phagocytes (MP) in the pathogenesis of HIV-associated dementia (HAD). We determined the influence of genetic variation in MCP-1 on HIV-1 pathogenesis in large cohorts of HIV-1-infected adults and children. In adults, homozygosity for the MCP-1 -2578G allele was associated with a 50% reduction in the risk of acquiring HIV-1. However, once HIV-1 infection was established, this same MCP-1 genotype was associated with accelerated disease progression and a 4.5-fold increased risk of HAD. We examined the molecular and cellular basis for these genotype-phenotype associations and found that the mutant MCP-1 -2578G allele conferred greater transcriptional activity via differential DNA-protein interactions, enhanced protein production in vitro, increased serum MCP-1 levels, as well as MP infiltration into tissues. Thus, MCP-1 expression had a two-edged role in HIV-1 infection: it afforded partial protection from viral infection, but during infection, its proinflammatory properties and ability to up-regulate HIV-1 replication collectively may contribute to accelerated disease progression and increased risk of dementia. Our findings suggest that MCP-1 antagonists may be useful in HIV-1 infection, especially for HAD, and that HIV+ individuals possessing the MCP-1 -2578G allele may benefit from early initiation of antiretroviral drugs that effectively cross the blood-brain barrier. In a broader context, the MCP-1 -2578G allele may serve as a genetic determinant of outcome of other disease states in which MP-mediated tissue injury is central to disease pathogenesis.