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ABSTRACT Objective: To know the influence of the environment (family functionality, social support and neighbourhood and school environment) on the development of adolescent resilience. Methods: Descriptive, correlational design. A total of 184 adolescents from six schools in the Aranjuez district of Medellín participated. Probabilistic, two-stage sampling. Five scales were used to collect data: 1) The child and youth resilience measurement scale; 2) The neighbourhood environment questionnaire; 3) The family cohesion and adaptability assessment scale; 4) The multidimensional scale of perceived social support; and 5) The school environment questionnaire. Data were analysed though SPSS 24v software. Results: a relationship was found between resilience and neighbourhood environment (rs= .324, p = .000), family functionality (rs= .380, p = .000), social support (rs= .456, p = .000) and school environment (rs= .353, p = .000). In addition, resilience was explained in 35.8 % by the neighbourhood environment (β= .20; p = .012), family functionality (β = .13; p = .090), social support (β= .30; p = .000) and school environment (β = .15; p = .064). Conclusion: Adolescent resilient behaviour is influenced by social support, family functioning, and school and neighbourhood environment, all external factors fostering self-regulation, as mentioned by Roy's Nursing model.
RESUMEN Objetivo: conocer la influencia del ambiente (funcionalidad familiar, apoyo social y ambiente barrial y escolar) en el desarrollo de la resiliencia de los adolescentes. Métodos: diseño descriptivo, correlacional. Participaron 184 adolescentes de seis colegios de la comuna Aranjuez de Medellín. Muestreo probabilístico, bietápico. Para recolectar los datos, se aplicaron cinco escalas: 1) la escala child and youth resilience measure; 2) el cuestionario de ambiente barrial; 3) la escala de evaluación de cohesión y adaptabilidad familiar; 4) la escala multidimensional de apoyo social percibido; y 5) el cuestionario de ambiente escolar. Los datos se procesaron con el software SPSS 24v. Resultados: se encontró una relación entre la resiliencia y el ambiente barrial (rs = .324, p = .000), funcionalidad familiar (rs = .380, p = .000), apoyo social (rs = .456, p = .000) y ambiente escolar (rs = .353, p = .000). Además, la resiliencia fue explicada en un 35,8 % por el ambiente barrial (β=.20; p =.012), la funcionalidad familiar (β=.13; p =.090), el apoyo social (β=.30; p =.000) y el ambiente escolar (β=.15; p = .064). Conclusión: la conducta resiliente de los adolescentes es influenciada por el apoyo social, la funcionalidad familiar y el ambiente escolar y barrial, factores externos que favorecen la autorregulación, como lo menciona Roy en su modelo de enfermería.
RESUMO Objetivo: availar a influência do ambiente (funcionalidade familiar, apoio social e ambiente de bairro e escolar) no desenvolvimento da resiliência dos adolescentes. Métodos: desenho descritivo, correlacional. Participaram 184 adolescentes de seis colégios da comunidade Aranjuez, Medellín, Colômbia. Amostragem probabilística, bietápica. Para coletar os dados, foram aplicados cinco instrumentos: 1) a escala child and youth resilience measure; 2) o questionário de ambiente de bairro; 3) a escala de avaliação de coesão e adaptabilidade familiar; 4) a escala multidimensional de apoio social percebido; 5) o questionário de ambiente escolar. Os dados foram processados com o software SPSS 24v. Resultados: verificou-se relação entre a resiliência e o ambiente de bairro (rs = .324, p = .000), funcionalidade familiar (rs = .380, p = .000), apoio social (rs = .456, p = .000) e ambiente escolar (rs = .353, p = .000). Além disso, a resiliência foi explicada em 35,8 % pelo contexto de bairro (β =.20; p =.012), pela funcionalidade familiar (β =.13; p =.090), pelo apoio social (β =.30; p =.000) e pelo ambiente escolar (β =.15; p = .064). Conclusões: o comportamento resiliente dos adolescentes é influenciado pelo apoio social, pela funcionalidade familiar e pelo ambiente escolar e de bairro, fatores externos que favorecem a autorregulação, como mencionado por Roy no seu modelo de enfermagem.
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Humanos , Masculino , Feminino , Adolescente , Meio Social , Resiliência Psicológica , Adaptação Psicológica , AdolescenteRESUMO
INTRODUCTION: Drug toxicology is central to drug development. Despite improvements in our understanding of molecular and cell biology, high attrition rates in drug development continue, speaking to the difficulties of developing unequivocal methods to predict the efficacy and safety of drugs. AREAS COVERED: In this review, the authors provide a short overview of the 'omics' technologies that have been applied to drug toxicology, with an emphasis on a whole-genome DNA methylation analysis. Preliminary results from DNA methylation analysis technologies that may help in predicting response and efficacy of a drug are discussed. EXPERT OPINION: Currently, we cannot fully contextualize the application of epigenetics to the field of drug toxicology, as there are still many challenges to overcome before DNA methylation-based biomarkers can be effectively used in drug development. Comprehensive whole-genome DNA methylation methods for a unbiased analysis based on either microarray or next-generation sequencing need to be evaluated in drug toxicology in an intensive and systematic manner. Additionally, robust analysis systems need to be developed to decode the large amounts of data generated by whole-genome DNA methylation analyses as well as protocol standardization for reproducibility to develop meaningful databases that can be applied to drug toxicology.
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Metilação de DNA/efeitos dos fármacos , Avaliação Pré-Clínica de Medicamentos/métodos , Drogas em Investigação/efeitos adversos , Epigênese Genética/efeitos dos fármacos , Regulação da Expressão Gênica/efeitos dos fármacos , Animais , Biomarcadores/metabolismo , Avaliação Pré-Clínica de Medicamentos/tendências , Epigenômica/métodos , Epigenômica/tendências , Humanos , Metabolômica/métodos , Metabolômica/tendências , Farmacologia Clínica/métodos , Farmacologia Clínica/tendências , Proteômica/métodos , Proteômica/tendênciasRESUMO
The role of human papillomavirus (HPV) infection in penile carcinoma (PeC) is currently reported and about half of the PeC is associated with HPV16 and 18. We used a PCR-based strategy by using HPV general primers to analyze 86 penile carcinomas paraffin-embedded tissues. Some clinical data, the histological subtype, growth pattern, and differentiation degree were also collected. The amplified fragments were then sequenced to confirm the HPV type and for HPV16/18 variants. DNA samples were also subjected to relative real time PCR for hTERC gene copy number. Some clinical data were also collected. Global HPV frequency was 77.9%. Relative contributions was for HPV16 (85%), 31 (4.4%), 11 (4.4%), 58, 33, 18, and 59 (1.4% each one). Sequence analysis of HPV16 identified European variants and Asian-American (AAb-c) variants in 92% and in 8% of the samples, respectively. Furthermore hTERC gene amplification was observed in only 17% of the cases. Our results suggest that some members of HPV A9 group (represented by HPV16, 58, and 31) are the most frequent among PeC patients studied with an important contribution from HPV16 European variant. The hTERC gene amplification could be poorly related to penile epithelial tissue.
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Carcinoma/virologia , Papillomavirus Humano 16/isolamento & purificação , Infecções por Papillomavirus/virologia , Neoplasias Penianas/virologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Biomarcadores Tumorais/genética , Biópsia , Carcinoma/epidemiologia , Carcinoma/genética , Carcinoma/patologia , Distribuição de Qui-Quadrado , DNA Viral/isolamento & purificação , Amplificação de Genes , Genótipo , Testes de DNA para Papilomavírus Humano , Papillomavirus Humano 16/genética , Humanos , Masculino , México/epidemiologia , Pessoa de Meia-Idade , Infecções por Papillomavirus/epidemiologia , Inclusão em Parafina , Neoplasias Penianas/epidemiologia , Neoplasias Penianas/genética , Neoplasias Penianas/patologia , Fenótipo , Valor Preditivo dos Testes , RNA/genética , Reação em Cadeia da Polimerase em Tempo Real , Fatores de Risco , Telomerase/genética , Adulto JovemRESUMO
BACKGROUND: One of the most frequent malignancies in women worldwide is carcinoma of the uterine cervix. High-risk human papillomavirus (HPV) infection is considered the most important etiological factor of uterine cervical cancer. Our aim was to identify novel cellular genes that could potentially act as predictive molecular markers for human cervical cancer by means of cDNA arrays. METHODS: We used cDNA arrays to examine the expression profiles of six cell lines derived from human cervical cancer, three HPV+ tumor samples and three normal (HPV-) epithelium tissues. Data normalization was performed and the top overexpressed genes were obtained. Hierarchical cluster was performed and, to validate some of the differentially expressed genes between normal and carcinogenic samples, semi-quantitative RT-PCR, in situ hybridization and immunohistochemistry were performed in tissue samples. RESULTS: Four genes were demonstrated to be consistently overexpressed in invasive cervical cancer biopsies; three novel genes not previously related to cervical cancer: MMP10, Lamc2 and Claudin 1. Moreover, overexpression of IL6 and VEGF was corroborated. CONCLUSIONS: The identification of characteristic molecular changes in cervical cells by carcinogenesis and HPV infection can lead to a better understanding of cervical cancer. cDNA arrays are beginning to provide new possible molecular markers for prognosis and diagnosis. This technology could eventually help to elucidate the biological differences of the particular mechanisms associated with each different HPV-type infection and those with a poor prognosis.
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Análise de Sequência com Séries de Oligonucleotídeos , Papillomaviridae/genética , Neoplasias do Colo do Útero/genética , Neoplasias do Colo do Útero/virologia , Linhagem Celular Tumoral , Feminino , Perfilação da Expressão Gênica , Regulação Neoplásica da Expressão Gênica , Humanos , Imuno-Histoquímica , Hibridização In Situ , Infecções por Papillomavirus/complicações , Distribuição Aleatória , Neoplasias do Colo do Útero/etiologia , Neoplasias do Colo do Útero/patologiaRESUMO
BACKGROUND: Chromosomal Comparative Genomic Hybridization (CGH) has been applied to all stages of cervical carcinoma progression, defining a specific pattern of chromosomal imbalances in this tumor. However, given its limited spatial resolution, chromosomal CGH has offered only general information regarding the possible genetic targets of DNA copy number changes. METHODS: In order to further define specific DNA copy number changes in cervical cancer, we analyzed 20 cervical samples (3 pre-malignant lesions, 10 invasive tumors, and 7 cell lines), using the GenoSensor microarray CGH system to define particular genetic targets that suffer copy number changes. RESULTS: The most common DNA gains detected by array CGH in the invasive samples were located at the RBP1-RBP2 (3q21-q22) genes, the sub-telomeric clone C84C11/T3 (5ptel), D5S23 (5p15.2) and the DAB2 gene (5p13) in 58.8% of the samples. The most common losses were found at the FHIT gene (3p14.2) in 47% of the samples, followed by deletions at D8S504 (8p23.3), CTDP1-SHGC- 145820 (18qtel), KIT (4q11-q12), D1S427-FAF1 (1p32.3), D9S325 (9qtel), EIF4E (eukaryotic translation initiation factor 4E, 4q24), RB1 (13q14), and DXS7132 (Xq12) present in 5/17 (29.4%) of the samples. CONCLUSION: Our results confirm the presence of a specific pattern of chromosomal imbalances in cervical carcinoma and define specific targets that are suffering DNA copy number changes in this neoplasm.