Coarse particles and hospital admissions due to respiratory diseases in children. An ecological time series study

Made available in DSpace on 2019-09-11T20:51:37Z (GMT). No. of bitstreams: 0 Previous issue date: 2018ABSTRACT BACKGROUND: Exposure to particulate matter (PM) is associated with hospitalizations due to respiratory diseases among children. DESIGN AND SETTING: An ecological time series study was carried out to identify the role of coarse fractions of particulate matter (PM10-2.5) in hospitalizations among children up to 10 years of age, in Piracicaba (SP) in the year 2015. METHODS: A generalized additive model of Poisson regression was used to estimate the risk of hospitalization due to acute laryngitis and tracheitis, pneumonia, bronchitis, bronchiolitis and asthma. Lags of 0 to 7 days were considered, and the model was adjusted for the temperature and relative humidity of the air and controlled for short and long-term exposure. Proportional attributable ratios, population-attributable fractions and hospital costs were calculated with increasing concentrations of these pollutants. RESULTS: 638 hospitalizations were evaluated during this period, with a mean of 1.75 cases per day (standard deviation, SD = 1.86). The daily averages were 22.45 µg/m3 (SD = 13.25) for the coarse fraction (PM10-2.5) and 13.32 µg/m3 (SD = 6.38) for the fine fraction. Significant risks of PM10-2.5 exposure were only observed at lag 0, with relative risk (RR) = 1.012, and at lag 6, with RR = 1.011. An increase of 5 µg/m3 in the coarse fraction concentration implied an increase in the relative risk of hospitalizations of up to 4.8%, with an excess of 72 hospitalizations and excess expenditure of US$ 17,000 per year. CONCLUSIONS: This study showed the impact of coarse-fraction exposure on hospital admissions among children due to respiratory diseases.[César, Ana Cristina Gobbo] Instituto Federal de Educação, Ciência e Tecnologia de São Paulo, BrazilNascimento, Luiz Fernando] Universidade de Taubaté, Brazi

Fatores genéticos e ambientais envolvidos na carciogênese gástrica

RACIONAL: O câncer de estômago é o segundo tipo mais comum de neoplasia no mundo. A carcinogênese de estômago é processo de múltiplos passos, podendo manifestar-se em várias etapas como gastrite superficial, gastrite atrófica crônica, metaplasia intestinal, displasia e, finalmente, como um carcinoma. Essas condições costumam ser seqüenciais e ocorrer num período de muitos anos como resultado da exposição a uma variedade de fatores endógenos e exógenos, que causam alterações genéticas. Os recentes avanços da genética molecular têm mostrado que o acúmulo dessas várias anormalidades, incluindo a ativação de oncogenes e a inativação de genes supressores de tumores, resultam no desenvolvimento do câncer. Alterações genéticas descritas em carcinomas gástricos incluem amplificações e mutações dos genes c-ERBB2, K-RAS, c-MET e TP53. O ganho de cromossomos também foi encontrado em várias combinações com perda de outros cromossomos e pode estar associado com a expressão elevada de oncogenes, que contribuem com a progressão tumoral. CONCLUSÃO: Essas mudanças genéticas em carcinomas evidenciam o processo de múltiplas etapas da carcinogênese gástrica, por meio do acúmulo de uma série de alterações

Fine particulate matter estimated by mathematical model and hospitalizations for pneumonia and asthma in children

Abstract Objective: To estimate the association between exposure to fine particulate matter with an aerodynamic diameter <2.5 microns (PM2.5) and hospitalizations for pneumonia and asthma in children. Methods: An ecological study of time series was performed, with daily indicators of hospitalization for pneumonia and asthma in children up to 10 years of age, living in Taubaté (SP) and estimated concentrations of PM2.5, between August 2011 and July 2012. A generalized additive model of Poisson regression was used to estimate the relative risk, with lag zero up to five days after exposure; the single pollutant model was adjusted by the apparent temperature, as defined from the temperature and relative air humidity, seasonality and weekday. Results: The values of the relative risks for hospitalization for pneumonia and asthma were significant for lag 0 (RR=1.051, 95%CI; 1.016 to 1.088); lag 2 (RR=1.066, 95%CI: 1.023 to 1.113); lag 3 (RR=1.053, 95%CI: 1.015 to 1.092); lag 4 (RR=1.043, 95%CI: 1.004 to 1.088) and lag 5 (RR=1.061, 95%CI: 1.018 to 1.106). The increase of 5mcg/m3 in PM2.5 contributes to increase the relative risk for hospitalization from 20.3 to 38.4 percentage points; however, the reduction of 5µg/m3 in PM2.5 concentration results in 38 fewer hospital admissions. Conclusions: Exposure to PM2.5 was associated with hospitalizations for pneumonia and asthma in children younger than 10 years of age, showing the role of fine particulate matter in child health and providing subsidies for the implementation of preventive measures to decrease these outcomes

Comparison of histological and molecular diagnosis of Helicobacter pylori in benign lesions and gastric adenocarcinoma

A colonização do Helicobacter pylori está associada com gastrite crônica, úlcera péptica, metaplasia intestinal, adenocarcinoma e linfoma gástrico. O objetivo desse estudo foi comparar os resultados do diagnóstico histológico usado de rotina na detecção do H. pylori com o diagnóstico molecular. Foram utilizadas amostras de 80 lesões gástricas (gastrite crônica, gastrite atrófica, úlcera gástrica e metaplasia intestinal), 18 amostras de adenocarcinoma gástrico e 10 amostras de mucosa gástrica normal H. pylori negativas (controle). Todas as amostras foram avaliadas histologicamente (coloração com hematoxilina-eosina e Giemsa) e pela PCR com a amplificação dos genes antígeno espécie-específico (H3H4) e urease A (H5H6) do H. pylori e pelo gene humano CYP1A1, como controle da qualidade do DNA. Nas amostras de lesão benigna e adenocarcinoma gástrico, a infecção foi detectada em 43% (42/98) e 71% (70/98), respectivamente, para os diagnósticos histológico e molecular (p = 0,0001). O teste de PCR detectou o H. pylori em 27,5% (22/80) das lesões gástricas benignas e em 50% (9/18) dos adenocarcinomas gástricos, com diagnóstico histológico negativo para essa bactéria. Cerca de 2,5% das amostras, exclusivamente de lesões benignas, com diagnóstico histológico positivo apresentaram resultado molecular negativo, para ambos os primers. Diferenças estatisticamente significantes foram encontradas entre os métodos histológico e molecular, em metaplasia intestinal (p = 0,0461) e adenocarcinoma gástrico (p = 0,0011), devido à subdetecção do H. pylori pelo método histológico, e provavelmente pela baixa densidade da bactéria conseqüente à atrofia severa da mucosa gástrica, nesses dois tipos de lesões. Nossos achados demonstram que o método de PCR é mais eficaz para diagnosticar a infecção por H. pylori, principalmente, em metaplasia intestinal e adenocarcinoma gástrico.Helicobacter pylori colonization is associated with chronic gastritis, peptic ulcers, intestinal metaplasia, adenocarcinoma and lymphoma of the stomach. The objective of this study was to compare the results of the routinely used histology with molecular diagnosis for the detection of H. pylori. Eighty samples from gastric lesions (chronic gastritis, atrophic gastritis, gastric ulcer, and intestinal metaplasia), 18 gastric adenocarcinoma and 10 normal mucosa H. pylori-negative (control) samples were obtained. All samples were examined histologically (hematoxylin-eosin and Giemsa staining), and PCR amplifications of the species-specific antigen gene (H3H4) and urease A gene segment (H5H6) of H. pylori were made, using the human gene CYP1A1 for DNA quality control. In the benign lesion and adenocarcinoma the infection was detected in 43% (42/98) and 71% (70/98) by histological and molecular diagnosis (p = 0.0001), respectively. The PCR test detected H. pylori in 27.5% (22/80) of the benign gastric lesions and in 50% (9/18) of the gastric adenocarcinoma cases, the histological diagnosis being negative for this bacterium. About 2.5% of the samples, exclusively from benign lesions and with a positive histological diagnosis, showed negative molecular results for both primers. Statistically significant differences were found between the histological and the molecular method in intestinal metaplasia (p = 0.0461) and gastric adenocarcinoma (p = 0.0011), due to underdetection of H. pylori by the histological method, which is probably due to the low density of the bacterium as a consequence of the severe atrophy of the gastric mucosa. Our findings suggest that PCR is the more efficient method for the assessment of H. pylori infection, especially in metaplasia and gastric adenocarcinoma.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP

Genetic alterations in benign lesions: Chronic gastritis and gastric ulcer

Aim: To investigate the occurrence of chromosome 3, 7, 8, 9, and 17 aneuploidies, TP53 gene deletion and p53 protein expression in chronic gastritis, atrophic gastritis and gastric ulcer, and their association with H pylori infection. Methods: Gastric biopsies from normal mucosa (NM, n = 10), chronic gastritis (CG, n = 38), atrophic gastritis (CAG, n = 13) and gastric ulcer (GU, n = 21) were studied using fluorescence in situ hybridization (FISH) and immunohistochemical assay. A modified Giemsa staining technique and PCR were used to detect H pylori. An association of the gastric pathologies and aneuploidies with H pylori infection was assessed. Results: Aneuploidies were increasingly found from CG (21%) to CAG (31%) and to GU (62%), involving mainly monosomy and trisomy 7, trisomies 7 and 8, and trisomies 7, 8 and 17, respectively. A significant association was found between H pylori infection and aneuploidies in CAG (P = 0.0143) and GU (P = 0.0498). No TP53 deletion was found in these gastric lesions, but p53-positive immunoreactivity was detected in 45% (5/11) and 12% (2/17) of CG and GU cases, respectively. However, there was no significant association between p53 expression and H pylori infection. Conclusion: The occurrence of aneuploidies in benign lesions evidences chromosomal instability in early stages of gastric carcinogenesis associated with H pylori infection, which may confer proliferative advantage. The increase of p53 protein expression in CG and GU may be due to overproduction of the wild-type protein related to an inflammatory response in mucosa. © 2006 The WJG Press. All rights reserved

Triagem neonatal para anemia falciforme, em um hospital geral de Taubaté, SP

Sickle cell disease occurs due to genetic alterations resulting in the production of hemoglobin S. Neonatal screening is essential for the diagnosis of this disease. An observational study in 8911 newborns in a general hospital of Taubaté who did the newborn screening test between 2005 and 2008. We analyzed test results from the database of the Pediatric Clinic and the medical records of newborns and their mothers, which are arranged by year, sex and ethnicity of those involved and the diagnostic test considered: normal hemoglobin profile (HbFA), anemia cell (HBFS), sickle cell trait (HbFAS), hemoglobin C trait (HbFAC) and hemoglobin D (HbFAD). The assessed 51.34% were male, 48.27% female and 0.39% were of indeterminate sex. Only one boy had sickle cell anemia (0.01%), 168 newborns (1.88%) were diagnosed with sickle cell trait. For the other variant hemoglobin, the representation was little significant. Correlating the ethnic group and the hemoglobin profiles showed that the majority of children with sickle cell trait is present and white mothers with the same skin color. Probably the majority of black and mulatto mothers were related to white men, contributing to the low frequency of children with sickle cell anemia.A doença falciforme se dá por alteração genética que resulta na produção da hemoglobina S. A triagem neonatal é fundamental para o diagnóstico dessa doença. Foi realizado um estudo observacional em 8911 recém-nascidos em um hospital geral de Taubaté, que fizeram o teste do pezinho, entre 2005 e 2008. Foram analisados os resultados de exames do banco de dados do Ambulatório de Pediatria e os prontuários dos recém-nascidos e suas mães, organizados por ano, sexo e etnias dos envolvidos. O diagnóstico do teste considerou: perfil hemoglobínico normal (HbFA), anemia falciforme (HbFS), traço falciforme (HbFAS), traço da hemoglobina C (HbFAC) e da hemoglobina D (HbFAD). Dos avaliados, 51,34% eram do sexo masculino, 48,27% do feminino e 0,39% de sexo não-determinado. Apenas um menino apresentou anemia falciforme (0,01%), e 168 recém-nascidos (1,88%) foram diagnosticados com traço falciforme. Para as demais variantes hemoglobínicas, a representatividade foi pouco significante. Correlacionando o grupo étnico e os perfis hemoglobínicos, observou-se que a maioria das crianças com traço falciforme é branca e apresenta mães com a mesma cor de pele. Provavelmente, a maioria das mães negras e pardas relacionou-se com homens brancos, contribuindo para a baixa frequência de crianças com anemia falciforme

Triagem neonatal para anemia falciforme, em um hospital geral de Taubaté, SP

Sickle cell disease occurs due to genetic alterations resulting in the production of hemoglobin S. Neonatal screening is essential for the diagnosis of this disease. An observational study in 8911 newborns in a general hospital of Taubaté who did the newborn screening test between 2005 and 2008. We analyzed test results from the database of the Pediatric Clinic and the medical records of newborns and their mothers, which are arranged by year, sex and ethnicity of those involved and the diagnostic test considered: normal hemoglobin profile (HbFA), anemia cell (HBFS), sickle cell trait (HbFAS), hemoglobin C trait (HbFAC) and hemoglobin D (HbFAD). The assessed 51.34% were male, 48.27% female and 0.39% were of indeterminate sex. Only one boy had sickle cell anemia (0.01%), 168 newborns (1.88%) were diagnosed with sickle cell trait. For the other variant hemoglobin, the representation was little significant. Correlating the ethnic group and the hemoglobin profiles showed that the majority of children with sickle cell trait is present and white mothers with the same skin color. Probably the majority of black and mulatto mothers were related to white men, contributing to the low frequency of children with sickle cell anemia.A doença falciforme se dá por alteração genética que resulta na produção da hemoglobina S. A triagem neonatal é fundamental para o diagnóstico dessa doença. Foi realizado um estudo observacional em 8911 recém-nascidos em um hospital geral de Taubaté, que fizeram o teste do pezinho, entre 2005 e 2008. Foram analisados os resultados de exames do banco de dados do Ambulatório de Pediatria e os prontuários dos recém-nascidos e suas mães, organizados por ano, sexo e etnias dos envolvidos. O diagnóstico do teste considerou: perfil hemoglobínico normal (HbFA), anemia falciforme (HbFS), traço falciforme (HbFAS), traço da hemoglobina C (HbFAC) e da hemoglobina D (HbFAD). Dos avaliados, 51,34% eram do sexo masculino, 48,27% do feminino e 0,39% de sexo não-determinado. Apenas um menino apresentou anemia falciforme (0,01%), e 168 recém-nascidos (1,88%) foram diagnosticados com traço falciforme. Para as demais variantes hemoglobínicas, a representatividade foi pouco significante. Correlacionando o grupo étnico e os perfis hemoglobínicos, observou-se que a maioria das crianças com traço falciforme é branca e apresenta mães com a mesma cor de pele. Provavelmente, a maioria das mães negras e pardas relacionou-se com homens brancos, contribuindo para a baixa frequência de crianças com anemia falciforme