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Id: biblio-1283167 Autor: Alsagaby, Suliman A; Brewis, Ian A; Vijayakumar, Rajendran; Alhumaydhi, Fahad A; Alwashmi, Ameen S; Alharbi, Naif K; Al Abdulmonem, Waleed; Premanathan, Mariappan; Pratti, Guy; Fegan, Christopher; Pepper, Christopher; Brennan, Paul. Título: Proteomics-based identification of cancer-associated proteins in chronic lymphocytic leukaemia Fonte: Electron. j. biotechnol;52:1-12, July. 2021. tab, ilus, graf. Idioma: en. Resumo: BACKGROUND: Chronic lymphocytic leukaemia (CLL) is a neoplasm of B-cells characterized by variable prognosis. Exploring the proteome of CLL cells may provide insights into the disease. Therefore, eleven proteomics experiments were conducted on eleven primary CLL samples. RESULTS: We reported a CLL proteome consisting of 919 proteins (false discovery rate (FDR) 1%) whose identification was based on the sequencing of two or more distinct peptides (FDR of peptide sequencing 1%). Mass spectrometry-based protein identification was validated for four different proteins using Western blotting and specific antibodies in different CLL samples. Small sizes of nucleolin (~57 kDa and ~68 kDa) showed a potential association with good prognosis CLL cells (n = 8, p < 0.01). Compared with normal B-cells, CLL cells over-expressed thyroid hormone receptor-associated protein 3 (THRAP3; n = 9; p = 0.00007), which is implicated in cell proliferation; and heterochromatin protein 1-binding protein 3 (HP1BP3; n = 10; p = 0.0002), which promotes cell survival and tumourogenesis. A smaller form of HP1BP3, which may correspond to HP1BP3 isoform-2, was specifically identified in normal B-cells (n = 10; p = 0.0001). HP1BP3 and THRAP3 predicted poor prognosis of CLL (p 0.05). Consistently, THRAP3 and HP1BP3 were found to be associated with cancer-related pathways (p 0.05). CONCLUSIONS: Our findings add to the known proteome of CLL and confirm the prognostic importance of two novel cancer-associated proteins in this disease. Descritores: Leucemia Linfocítica Crônica de Células B Biomarcadores Tumorais/análise -Espectrometria de Massas Fatores de Transcrição/análise Proteínas Nucleares/análise Western Blotting Cromatografia Líquida Proteômica Proteínas de Ligação a DNA/análise Responsável: CL1.1 - Biblioteca Central

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Id: biblio-892928 Autor: Yang, Zhi-Gang; Ma, Xu-Dong; He, Zhao-Hui; Guo, Ying-xin. Título: miR-483-5p promotes prostate cancer cell proliferation and invasion by targeting RBM5 Fonte: Int. braz. j. urol;43(6):1060-1067, Nov.-Dec. 2017. graf. Idioma: en. Resumo: ABSTRACT Objective: miR-483-5p has been identified as a miRNA oncogene in certain cancers. However, its role in prostate cancer has not been sufficiently investigated. In this study, we investigated the role of miR-483-5p in prostate cancer and examined RBM5 regulation by miR-483-5p. Material and methods: Expression levels of miR-483-5p were determined by quantitative real-time PCR. The effect of miR-483-5p on proliferation was evaluated by MTT assay, cell invasion was evaluated by trans-well invasion assays, and target protein expression was determined by western blotting in LNCaP, DU-145, and PC-3 cells. Luciferase reporter plasmids were constructed to confirm the action of miR-483-5p on downstream target gene RBM5 in HEK-293T cells. Results: we observed that miR-483-5p was upregulated in prostate cancer cell lines and tissues. A miR-483-5p inhibitor inhibited prostate cancer cell growth and invasion in DU-145 and PC-3 cells. miR-483-5p directly bound to the 3' untranslated region (3'UTR) of RBM5 in HEK-293T cells. RBM5 overexpression inhibited prostate cancer cell growth and invasion in LNCaP cells. Enforced RBM5 expression alleviated miR-483-5p promotion of prostate cancer cell growth and invasion in LNCaP cells. Conclusion: The present study describes a potential mechanism underlying a miR-483-5p/RBM5 link that contributes to prostate cancer development. Descritores: Neoplasias da Próstata/genética Neoplasias da Próstata/patologia Regulação Neoplásica da Expressão Gênica/genética Proteínas de Ciclo Celular/metabolismo Regiões não Traduzidas/genética Proteínas Supressoras de Tumor/metabolismo MicroRNAs/fisiologia Proliferação de Células/genética Proteínas de Ligação a DNA/metabolismo Reação em Cadeia da Polimerase em Tempo Real -Neoplasias da Próstata/mortalidade Regulação para Baixo Regulação para Cima Proteínas de Ligação a RNA/metabolismo MicroRNAs/antagonistas & inibidores Linhagem Celular Tumoral Invasividade Neoplásica Limites: Humanos Masculino Responsável: BR1.1 - BIREME

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Id: biblio-974907 Autor: Kong, Jiangying; Liu, Zhuo; Cai, Feng; Xu, Xiaocheng; LiuI, Jun. Título: Relationship between the Asp1104His polymorphism of the nucleotide excision repair gene ERCC5 and treatment sensitivity to oxaliplatin in patients with advanced colorectal cancer in China Fonte: Clinics;73:e455, 2018. tab, graf. Idioma: en. Projeto: Hangzhou Municipal Science and Technology Commission; . Xiaoshan Science and Technology Commission of Hangzhou City. Resumo: OBJECTIVES: To study the relationship between the Asp1104His polymorphism of the nucleotide excision repair gene ERCC5 and treatment sensitivity to oxaliplatin in patients with advanced colorectal cancer (CRC) in China. METHODS: A group of 226 patients in the Department of Gastrointestinal Oncology at Zhejiang Xiaoshan Hospital from July 2011∼December 2016 and a control group of 226 normal healthy individuals were involved in this study. All patients were first diagnosed with advanced CRC and were treated with oxaliplatin-based chemotherapy. The genotype of ERCC5 at the site of amino acid 1104 was determined by a TaqMan probe-based real-time PCR approach. RESULTS: There were no differences in age or gender between the groups, but the percentages of smokers and individuals with a family history of cancer were significantly higher in the patient group than in the control group. Analysis of the G/C polymorphism frequency among the patients and the healthy controls showed that the frequencies of the CC genotype and the CC+GC genotype were significantly related to CRC, but no significant difference in these frequencies was found between genders. The analysis of the relationship between the 5-year survival rate and different genotypes showed that in the total patient group, regardless of gender, the 5-year survival rate was significantly associated with the Asp1104His polymorphism of ERCC5. CONCLUSIONS: The Asp1104His polymorphism of ERCC5 was associated with the risk and 5-year survival rate of CRC as well as treatment sensitivity to oxaliplatin. Descritores: Proteínas Nucleares/genética Neoplasias Colorretais/genética Neoplasias Colorretais/tratamento farmacológico Proteínas de Ligação a DNA/genética Endonucleases/genética Antineoplásicos/uso terapêutico -Fatores de Transcrição/genética Neoplasias Colorretais/mortalidade Estudos de Casos e Controles Polimorfismo de Nucleotídeo Único/genética Estimativa de Kaplan-Meier Oxaliplatina/uso terapêutico Genótipo Estadiamento de Neoplasias Limites: Humanos Masculino Feminino Pessoa de Meia-Idade Responsável: BR1.1 - BIREME

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Id: biblio-1090612 Autor: Azambuja, Alan A; Engroff, Paula; Silva, Bruna T; Zorzetti, Roberta C. S; Morrone, Fernanda B. Título: Evaluation of nuclear NF-κB, transglutaminase2, and ERCC1 as predictors of platinum resistance in testicular tumors Fonte: Int. braz. j. urol;46(3):353-362, May-June 2020. tab, graf. Idioma: en. Resumo: ABSTRACT Purpose: Testicular germ cells tumor (TGCT) are associated with a high cure rate and are treated with platinum-based chemotherapy. However, a group of testicular cancer patients may have a very unfavorable evolution and insensitivity to the main therapeutic agent chemotherapy (CT) cisplatin. The aim of this study was to evaluate the risk of recurrence and overall survival related to the expression of nuclear factor kappa-B (NF-κB), transglutaminase 2 (TG2) and excision repair cross-complementation group 1 (ERCC1) in patients with TGCT treated with platinum combinations. Patients and Methods: A retrospective study was performed with TGCT patients treated with platinum-based chemotherapy. Immunohistochemical analysis was performed and the expression was correlated with clinical and laboratory data. Results: Fifty patients were included, the mean age was 28.4 years (18 to 45), and 76% were non-seminoma. All patients were treated with standard cisplatin, etoposide and bleomycin or cisplatin, and etoposide. Patient's analyzed immunodetection for NF-κB, TG2, and ERCC1 were positive in 76%, 54% and 42%, respectively. Multivariate analysis identified that positive expressions to ERCC1 and NF-κB are independent risk factors for higher recurrence TGCT after chemotherapy (RR 2.96 and 3.16, respectively). Patients with positive expression of ERCC1 presented a poor overall survival rate for 10-year follow (p=0.001). Conclusions: The expression of ERCC1 and NF-κB give a worse prognosis for relapse, and only ERCC1 had an influence on the overall survival of TGCT patients treated with platinum-based chemotherapy. These may represent markers that predict poor clinical outcome and response to cisplatin. Descritores: Neoplasias Testiculares Transglutaminases/metabolismo NF-kappa B/metabolismo Proteínas de Ligação ao GTP/metabolismo Neoplasias Pulmonares -Prognóstico Protocolos de Quimioterapia Combinada Antineoplásica Estudos Retrospectivos Cisplatino Resistencia a Medicamentos Antineoplásicos/fisiologia Proteínas de Ligação a DNA Reparo do DNA Endonucleases Limites: Humanos Masculino Adulto Responsável: BR1.1 - BIREME

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Id: biblio-1013789 Autor: Ulloa, María Teresa; Sanhueza, Camila; Henríquez, Tania; Aguayo, Benjamín; Hermosilla, Germán; Porte, Lorena; Dabanch, Jeannette; Braun, Stephanie; Fica, Alberto; Briceño, Isabel; Osorio, Carlos Gonzalo. Título: Cepas chilenas de origen clínico de Vibrio cholerae no-O1, no-O139 portan los genes vcsN2, vcsC2, vcsV2, vspD, toxR2 y vopF del sistema de secreción T3SS2 presentes en una isla de patogenicidad / Chilean strains of clinical origin of non-O1, non-O139 Vibrio cholerae carry the genes vcsN2, vcsC2, vcsV2, vspD, toxR2 y vopF from secretion system T3SS2 present in an island of pathogenicity Fonte: Rev. chil. infectol;36(3):312-317, jun. 2019. tab, graf. Idioma: es. Resumo: Resumen Introducción. Los factores de virulencia de las cepas de Vibrio cholerae no-O1, no-O139 no son claramente conocidos. La cepa de origen septicémico NN1 Vibrio cholerae no-O1, no-O139 fue secuenciada previamente mediante la plataforma Illumina, detectándose en su genoma un fragmento de la isla de patogenicidad VPaI-7 de V. parahaemolyticus. Objetivo: detectar los genes de virulencia vcsN2, vcsC2, vcsV2, vspD, toxR2 y vopF en cepas chilenas clínicas de V. cholerae no-O1, no-O139. Material y Métodos: Un total de 9 cepas chilenas de origen clínico de Vibrio cholerae no-O1, no-O139 aisladas entre 2006-2012 fueron analizadas mediante ensayos de reacción de polimerasa en cadena (RPC, en inglés PCR) convencional para los genes de secreción tipo III codificados en dicha isla: vcsN2, vcsC2, vcsV2, vspD, toxR2 y vopF. Adicionalmente se determinó la presencia de los genes de virulencia hylA y rtxA. Además, se realizaron ensayos de repetitive element palindromic PCR (REP-PCR) y Enterobacterial repetitive intergenic consensus PCR (ERIC-PCR). Resultados: la mayoría (6/9) de las cepas chilenas de V. cholerae no-O1, no-O139 contiene todos los genes de secreción tipo III vcsN2, vcsC2, vcsV2, vspD, toxR2 y vopF, codificados en una isla de patogenicidad. Además, el total de las cepas (9/9) contiene los genes de virulencia hylA y rtxA. Conclusión: Estos resultados sugieren fuertemente la posibilidad que dichas cepas posean un potencial de virulencia importante en seres humanos. Backgound: The virulence factors of the Vibrio cholerae non-O1, non-O139 strains are not clearly known. The strain of septicemic origin NN1 Vibrio cholerae non-O1, non-O139 was sequenced previously by the Illumina platform. A fragment of the pathogenicity island VPaI-7 of V. parahaemolyticus was detected in its genome. Aim: To detect the virulence genes vcsN2, vcsC2, vcsV2, vspD, toxR2 y vopF in Chilean strains of V. cholerae non-O1, non-O139. Methods: A total of 9 Chilean strains of clinical origin of Vibrio cholerae non-O1, non-O139 isolated between 2006-2012 were analyzed by conventional PCR assays for type III secretion genes encoded on that island: vcsN2, vcsC2, vcsV2, vspD, toxR2 and vopF. Additionally, the presence of the virulence genes hylA and rtxA was determined. In addition, REP-PCR and ERIC-PCR assays were performed. Results: most (6/9) Chilean V. cholerae non-O1, non-O139 strains contain the type III secretion genes vcsN2, vcsC2, vcsV2, vspD, toxR2 and vopF, encoded in an island of pathogenicity. In addition, all (9/9) the strains contain the virulence genes hylA and rtxA. Conclusion: These results strongly suggest the possibility that those strains possess an important virulence potential in humans. Descritores: Proteínas de Bactérias/genética Fatores de Transcrição/genética Vibrio cholerae/genética Fatores de Virulência/genética Vibrio cholerae não O1/genética Ilhas Genômicas/genética Proteínas de Ligação a DNA/genética Sistemas de Secreção Tipo III/genética -Toxinas Bacterianas/genética Vibrio cholerae/isolamento & purificação Vibrio cholerae/patogenicidade Chile Reação em Cadeia da Polimerase Análise de Sequência de DNA Vibrio cholerae não O1/isolamento & purificação Vibrio cholerae não O1/patogenicidade Proteínas Hemolisinas/genética Limites: Humanos Responsável: CL1.1 - Biblioteca Central

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Id: biblio-950899 Autor: Wu, Tingting; Lin, Yun; Xie, Zhongguo. Título: MicroRNA-1247 inhibits cell proliferation by directly targeting ZNF346 in childhood neuroblastoma Fonte: Biol. Res;51:13, 2018. graf. Idioma: en. Resumo: BACKGROUND: Neuroblastoma (NB) represents the most common extracranial solid tumor in children. Accumulating evidence shows that microRNAs (miRs) play an important role in the carcinogenesis of NB. Here, we investigated the biological function of miR-1247 in NB in vitro. METHODS/RESULTS: We found miR-1247 was downregulated in NB tissues and cells using quantitative PCR analysis. Gain- and loss-of-function studies demonstrated that miR-1247 significantly suppressed cell proliferation and induced cell cycle G0/G1 phase arrest and cell apoptosis of NB cells in vitro by using MTT, colony formation assay and Flow cytometry analysis. Luciferase assay suggested ZNF346 was the target of miR-1247 and its expression could be down-regulated by miR-1247 overexpression using Western blotting. Furthermore, downregulation of ZNF346 by siRNA performed similar effects with overexpression of miR-1247 in NB cells. CONCLUSIONS: Our findings suggested miR-1247 directly targeted to repress ZNF346 expression, thus suppressing the progression of NB, which might be a novel therapeutic target against NB. Descritores: Proteínas de Ligação a RNA/metabolismo MicroRNAs/metabolismo Proteínas de Ligação a DNA/metabolismo Neuroblastoma/metabolismo -Fenótipo Fatores de Tempo Células Tumorais Cultivadas Regulação para Baixo Regulação Neoplásica da Expressão Gênica Pré-Escolar Proteínas de Ligação a RNA/genética Ensaio de Unidades Formadoras de Colônias MicroRNAs/genética Proliferação de Células/genética Proteínas de Ligação a DNA/genética Reação em Cadeia da Polimerase em Tempo Real Citometria de Fluxo Neuroblastoma/genética Neuroblastoma/patologia Limites: Humanos Masculino Feminino Responsável: CL1.1 - Biblioteca Central

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Id: biblio-1011407 Autor: Yin, Hongtao; Yu, Yan. Título: Identification of the targets of hematoporphyrin derivative in lung adenocarcinoma using integrated network analysis Fonte: Biol. Res;52:4, 2019. tab, graf. Idioma: en. Resumo: BACKGROUND: Hematoporphyrin derivative (HPD) has a sensibilization effect in lung adenocarcinoma. This study was conducted to identify the target genes of HPD in lung adenocarcinoma. METHODS: RNA sequencing was performed using the lung adenocarcinoma cell line A549 after no treatment or treatment with X-ray or X-ray + HPD. The differentially expressed genes (DEGs) were screened using Mfuzz package by noise-robust soft clustering analysis. Enrichment analysis was carried out using "BioCloud" online tool. Protein-protein interaction (PPI) network and module analyses were performed using Cytoscape software. Using WebGestalt tool and integrated transcription factor platform (ITFP), microRNA target and transcription factor (TF) target pairs were separately predicted. An integrated regulatory network was visualized with Cytoscape software. RESULTS: A total of 815 DEGs in the gene set G1 (continuously dysregulated genes along with changes in processing conditions [untreated-treated with X-ray-X-ray + treated with HPD]) and 464 DEGs in the gene set G2 (significantly dysregulated between X-ray + HPD-treated group and untreated/X-ray-treated group) were screened. The significant module identified from the PPI network for gene set G1 showed that ribosomal protein L3 (RPL3) gene could interact with heat shock protein 90 kDa alpha, class A member 1 (HSP90AA1). TFs AAA domain containing 2 (ATAD2) and protein inhibitor of activated STAT 1 (PIAS1) were separately predicted for the genes in gene set G1 and G2, respectively. In the integrated network for gene set G2, ubiquitin-specific peptidase 25 (USP25) was targeted by miR-200b, miR-200c, and miR-429. CONCLUSION: RPL3, HSP90AA1, ATAD2, and PIAS1 as well as USP25, which is targeted by miR-200b, miR-200c, and miR-429, may be the potential targets of HPD in lung adenocarcinoma. Descritores: Derivado da Hematoporfirina/farmacologia Redes Reguladoras de Genes/genética Adenocarcinoma de Pulmão/genética Neoplasias Pulmonares/genética -Proteínas Ribossômicas/efeitos dos fármacos Proteínas Ribossômicas/genética Fatores de Transcrição Análise por Conglomerados Regulação Neoplásica da Expressão Gênica Análise de Sequência de RNA Proteínas de Choque Térmico HSP90/efeitos dos fármacos Proteínas de Choque Térmico HSP90/genética Proteínas Modificadoras Pequenas Relacionadas à Ubiquitina/efeitos dos fármacos Proteínas Modificadoras Pequenas Relacionadas à Ubiquitina/genética MicroRNAs/metabolismo Linhagem Celular Tumoral Proteínas de Ligação a DNA/efeitos dos fármacos Proteínas de Ligação a DNA/genética Proteínas Inibidoras de STAT Ativados/efeitos dos fármacos Proteínas Inibidoras de STAT Ativados/genética Citometria de Fluxo ATPases Associadas a Diversas Atividades Celulares/efeitos dos fármacos ATPases Associadas a Diversas Atividades Celulares/genética Adenocarcinoma de Pulmão/tratamento farmacológico Adenocarcinoma de Pulmão/radioterapia Neoplasias Pulmonares/tratamento farmacológico Neoplasias Pulmonares/radioterapia Limites: Humanos Responsável: CL1.1 - Biblioteca Central

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Id: biblio-1058180 Autor: Sánchez, N; Hernández, M; Cruz, JP; Mellado, C. Título: Espectro fenotípico de Síndrome de CHARGE neonatal / Phenotypic spectrum of neonatal CHARGE syndrome Fonte: Rev. chil. pediatr;90(5):533-538, oct. 2019. tab, graf. Idioma: es. Resumo: INTRODUCCIÓN: El Síndrome de CHARGE (SCH), es un síndrome genético de amplia variabilidad fenotípica, de he rencia autosómica dominante, causado por variantes patogénicas en el gen CHD7. OBJETIVO: Descri bir el amplio espectro fenotípico de un SCH neonatal, heterocigoto para el gen CDH7 y la utilidad de la secuenciación en la confirmación diagnóstica, considerando los diagnósticos diferenciales. CASO CLÍNICO: recién nacida prematura de 34 semanas, con antecedentes prenatales de polihidroamnios severo, translucencia nucal aumentada y foco hiperecogénico cardiaco, con estudio de TORCH antenatal, que descartó infección congénita. Al nacer se pesquisó parálisis facial periférica, atresia de coanas, dismorfias múltiples, cardiopatía congénita y coloboma retinocoroideo bilateral. Las neuroimágenes mostraron hipoplasia de cóclea y de canales semicirculares bilaterales e hipoplasia pontocerebelosa. Los potenciales evocados auditivos mostraron hipoacusia sensorioneural profunda derecha y anacusia izquierda. Evolucionó con hipocalcemia y alteraciones en la inmunidad, confirmándose un hipoparatiroidismo e hipoplasia de timo. El cariograma fue normal y la amplificación de sondas dependiente de ligandos múltiples (MLPA) excluyó microdeleción 22q11.2. La sospecha clínica de SCH se confirmó con la detección de una variante patogénica en el gen CHD7. CONCLUSIONES: La su perposición de características clínicas del SCH con otros síndromes genéticos requiere confirmación genética molecular considerando diferencias en evolución, terapias y riesgos de recurrencia. INTRODUCTION: CHARGE syndrome is a genetic disorder of wide phenotypic variability, of autosomal dominant in heritance, caused by pathogenic variants in the CHD7 gene. OBJECTIVE: To describe the broad pheno typic spectrum of neonatal CHARGE syndrome, heterozygous for the CHD7 gene, and the usefulness of genome sequencing in diagnostic confirmation, considering differential diagnoses. CLINICAL CASE: 34-week preterm newborn, with severe prenatal history of polyhydramnios, increased nuchal trans- lucency, and hyperechogenic cardiac focus, with a TORCH study that ruled out congenital infection. Peripheral facial paralysis, choanal atresia, multiple dysmorphisms, congenital heart disease, and bilateral retinochoroidal coloboma were observed at birth. The neuroimaging study showed hypo plasia of the cochlea and bilateral semicircular canals, and pontocerebellar hypoplasia. The auditory evoked potentials showed deep right-sided sensorineural hearing loss and left anacusis. The patient developed hypocalcemia and immunological alterations, confirming hypoparathyroidism and thy mus hypoplasia. The karyogram was normal and 22q11.2 microdeletion was excluded through mul tiplex ligation-dependent probe amplification (MPLA). A pathogenic variant in the CHD7 gene was detected that confirmed the clinical suspicion of CHARGE syndrome. CONCLUSIONS: The overlap of clinical characteristics of CHARGE syndrome requires molecular genetic confirmation, considering differences in evolution, therapies, and recurrence risks with other genetic syndromes. Descritores: DNA Helicases/genética Proteínas de Ligação a DNA/genética Síndrome CHARGE/fisiopatologia -Fenótipo Síndrome CHARGE/diagnóstico Síndrome CHARGE/genética Mutação Limites: Humanos Feminino Recém-Nascido Tipo de Publ: Relatos de Casos Responsável: CL1.1 - Biblioteca Central

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Id: biblio-1132588 Autor: Li, Xin; Zhu, Zhengping; Li, Wei; Wei, Li; Zhao, Baocheng; Hao, Zheng. Título: Polymorphism in GRHL2 gene may contribute to noise-induced hearing loss susceptibility: a meta-analysis / Polimorfismo no gene GRHL2 pode contribuir para a suscetibilidade à perda auditivainduzida por ruído: uma metanálise Fonte: Braz. j. otorhinolaryngol. (Impr.);86(3):370-375, May-June 2020. tab, graf. Idioma: en. Projeto: Humanities and Social Sciences of Ministry of Education Planning Fund of China. Resumo: Abstract Instruction: Noise-induced hearing loss is a leading occupational disease caused by gene-environment interaction. The Grainy Like 2, GRHL2, is a candidate gene. In this regard, many studies have evaluated the association between GRHL2 and noise-induced hearing loss, although the results are ambiguous and conflicting. Objective: The purpose of this study was to identify a precise estimation of the association between rs3735715 polymorphism in GRHL2 gene and susceptibility of noise-induced hearing loss. Methods: A comprehensive search was performed to collect data up to July 8, 2018. Finally, 4 eligible articles were included in this meta-analysis comprising 2410 subjects. The pooled odds ratios with 95% confidence intervals were used to evaluate the strength of the association. Results: Significant association was found in the overall population in the dominant model (GA/AA vs. GG, odds ratio = 0.707, 95% confidence interval = 0.594-0.841) and allele model (G allele vs. A allele, odds ratio = 1.189, 95% confidence interval = 1.062-1.333). When stratified by source of the subjects, we also found association between rs3735715 and noise-induced hearing loss risk in the dominant model (GA/AA vs. GG, odds ratio = 0.634, 95% confidence interval = 0.514-0.783) and allele model (G allele vs. A allele, odds ratio = 1.206, 95% confidence interval = 1.054-1.379). Conclusion: Rs3735715 polymorphism in GRHL2 gene may influence the susceptibility of noise-induced hearing loss. Additional large, well-designed and functional studies are needed to confirm this association in different populations. Resumo Introdução: Perda auditiva induzida por ruído é uma das principais doenças ocupacionais causadas pela interação gene-ambiente. O Grainy Like 2, ou GRHL2 é um gene que tem sido considerado como candidato. Nesse sentido, muitos estudos avaliaram a associação entre o GRHL2 e perda auditiva induzida por ruído, embora os resultados sejam ambíguos e conflitantes. Objetivo: Identificar uma estimativa precisa da associação entre o polimorfismo rs3735715 no gene GRHL2 e a suscetibilidade à perda auditiva induzida por ruído. Método: Uma pesquisa abrangente foi feita para coletar dados até 8 de julho de 2018. No fim, quatro artigos elegíveis foram incluídos nesta metanálise, abrangeram 2.410 indivíduos. As odds ratios agrupadas com intervalos de confiança de 95% foram usadas para avaliar a força da associação. Resultados: Uma associação significante foi encontrada na população geral no modelo de dominância (GA/AA vs. GG, odds ratio = 0,707, intervalo de confiança 95% = 0,594-0,841) e modelo de alelo (alelo G vs. alelo A; odds ratio = 1,189, intervalo de confiança 95% = 1,062 a 1,333). Quando estratificados pelo local de trabalho dos indivíduos, também encontramos associação entre rs3735715 e risco de perda auditiva induzida por ruído no modelo de dominância (GA/AA vs. GG, odds ratio = 0,634, intervalo de confiança 95% = 0,514 ± 0,783) e modelo de alelo (alelo G vs. alelo A; odds ratio = 1,206, intervalo de confiança 95% = 1,054- 1,379). Conclusão: O polimorfismo Rs3735715 no gene GRHL2 pode influenciar a suscetibilidade à perda auditiva induzida por ruído. Estudos adicionais, amplos, bem desenhados e funcionais são necessários para confirmar essa associação em diferentes populações. Descritores: Fatores de Transcrição/genética Predisposição Genética para Doença/genética Polimorfismo de Nucleotídeo Único/genética Proteínas de Ligação a DNA/genética Perda Auditiva Provocada por Ruído/genética -Genótipo Ruído Ocupacional/efeitos adversos Doenças Profissionais/genética Limites: Humanos Responsável: BR1.1 - BIREME

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Id: biblio-887598 Autor: Ademoglu, Esra Nur; Gorar, Suheyla; Keskin, Muge; Carlioglu, Ayse; Ucler, Rifki; Erdamar, Husamettin; Culha, Cavit; Aral, Yalcin. Título: Serum nesfatin-1 levels are decreased in pregnant women newly diagnosed with gestational diabetes Fonte: Arch. endocrinol. metab. (Online);61(5):455-459, Sept.-Oct. 2017. tab, graf. Idioma: en. Resumo: ABSTRACT Objective To investigate serum nesfatin-1 levels at 24-28 weeks of pregnancy in women newly diagnosed with gestational diabetes and determine the association of nesfatin-1 with several metabolic parameters. Subjects and methods Forty women newly diagnosed with gestational diabetes at 24-28 weeks of pregnancy and 30 healthy pregnant women matched in age and gestational week were included in this cross-sectional study. Serum nesfatin-1 levels were analyzed using ELISA, and the relationship between nesfatin-1 and several metabolic parameters were assessed. Results Serum nesfatin-1 levels were found to be lower in women with gestational diabetes compared to the pregnant women in the control sample (p = 0.020). Multiple linear regression analysis revealed that nesfatin-1 was lower in participants with gestational diabetes independently from gestational age, BMI, HOMA-IR, fasting plasma glucose, and age. In correlation analysis, the only variable that was found to have a statistically significant correlation with nesfatin-1 was gestational age (p = 0.015, r = 0.30). Conclusion Lower nesfatin-1 levels in women with gestational diabetes compared to the control group at 24-28 weeks of gestation draws attention to nesfatin-1 levels in gestational diabetes and motivates further research in this area. Descritores: Proteínas de Ligação ao Cálcio/sangue Diabetes Gestacional/sangue Proteínas de Ligação a DNA/sangue Proteínas do Tecido Nervoso/sangue -Ensaio de Imunoadsorção Enzimática Biomarcadores/sangue Índice de Massa Corporal Estudos de Casos e Controles Estudos Transversais Jejum/sangue Idade Gestacional Diabetes Gestacional/diagnóstico Nucleobindinas Teste de Tolerância a Glucose Limites: Humanos Feminino Gravidez Adulto Responsável: BR1.1 - BIREME

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