RESUMO
Introducción: La enfermedad de Alzheimer (EA) es la principal causa de demencia, caracterizada por pérdida progresiva de memoria. Principal fuente de morbimortalidad en mayores de 65 años. En los últimos 20 años las muertes por EA han aumentado un 145% en el mundo. En Chile no hay estudios actuales que describan mortalidad por EA. El objetivo del presente trabajo es analizar y comparar las tasas de mortalidad (TM) por EA según sexo y grupo etario en Chile entre 2017-2021. Materiales y métodos: Estudio descriptivo, ecológico, sobre defunciones por EA entre 2017-2021 en Chile según sexo y grupo etario (n=10.223). Información obtenida de la base de datos del Departamento de Estadísticas e Información de Salud. Se realizó estadística descriptiva y cálculo de TM. No se requiere comité de ética. Resultados: La máxima TM del periodo fue 11,74 por cada 100.000 habitantes en 2021. El sexo femenino logró la mayor TM en este periodo. El grupo etario con mayor cantidad de defunciones fue el de 81 o más años con 76.6% (7.829) de las defunciones totales. Discusión: Se evidenció mantención y luego ascenso de TM por EA, podría deberse al aumento en la esperanza de vida. La mayor frecuencia de defunciones según sexo y edad, podría explicarse por mayor vulnerabilidad femenina a desarrollar EA y a cambios fisiológicos del envejecimiento. En conclusión, la TM por EA en Chile ha aumentado, probablemente secundario al aumento en la esperanza de vida. Se hace un llamado a continuar el estudio de la patología.
Introduction: Alzheimer's disease (AD) is the most common cause of dementia, characterized by progressive memory loss. It is the main source of morbidity and mortality in individuals over 65 years of age, with age being its primary non-modifiable risk factor. In the last 20 years, deaths from AD have increased by 145% worldwide. However, there are no current studies in Chile that describe mortality from AD. The objective of this study is to analyze and compare mortality rates due to AD according to sex and age group in the Chilean population during the years 2017-2021. Material and Methods: Descriptive, ecological study on deaths from AD between 2017-2021 in Chile, categorized by sex and age group (n=10,223). The database was obtained from the Department of Health Statistics and Information. Descriptive statistics and mortality rate calculations were performed. No ethics committee approval was required. Results: The maximum mortality rate (MR) was observed in 2021 with a value of 11.74 per 100,000 inhabitants. Women had the highest MR in this period. The age group with the highest number of deaths was 81 years or older, accounting for 76.6% (7,829) of the total deaths. Discussion: A plateau and subsequent increase in MR due to AD were observed, possibly explained by the increase in life expectancy. The higher frequency of deaths in women and specific age groups may be attributed to the higher vulnerability of women to developing AD and physiological changes related to aging. In conclusion, the MR from AD has increased in Chile, likely due to the rise in life expectancy, emphasizing the importance of continued research on this pathology.
Assuntos
Humanos , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Idoso , Idoso de 80 Anos ou mais , Adulto Jovem , Doença de Alzheimer/mortalidade , Doença de Alzheimer/epidemiologia , Chile/epidemiologia , Epidemiologia Descritiva , Distribuição por Idade e SexoRESUMO
Perinatal asphyxia (PA) is one of the most frequent risk factors for several neurodevelopmental disorders (NDDs) of presumed multifactorial etiology. Dysfunction of neuronal connectivity is thought to play a central role in the pathophysiology of NDDs. Because underlying causes of some NDDs begin before/during birth, we asked whether this clinical condition might affect accurate establishment of neural circuits in the hippocampus as a consequence of disturbed brain plasticity. We used a murine model that mimics the pathophysiological processes of perinatal asphyxia. Histological analyses of neurons (NeuN), dendrites (MAP-2), neurofilaments (NF-M/Hp) and correlative electron microscopy studies of dendritic spines were performed in Stratum radiatum of the hippocampal CA1 area after postnatal ontogenesis. Protein and mRNA analyses were achieved by Western blot and RT-qPCR. Behavioral tests were also carried out. NeuN abnormal staining and spine density were increased. RT-qPCR assays revealed a ß-actin mRNA over-expression, while Western blot analysis showed higher ß-actin protein levels in synaptosomal fractions in experimental group. M6a expression, protein involved in filopodium formation and synaptogenesis, was also increased. Furthermore, we found that PI3K/Akt/GSK3 pathway signaling, which is involved in synaptogenesis, was activated. Moreover, asphyctic animals showed habituation memory changes in the open field test. Our results suggest that abnormal synaptogenesis induced by PA as a consequence of excessive brain plasticity during brain development may contribute to the etiology of the NDDs. Consequences of this altered synaptic maturation can underlie some of the later behavioral deficits observed in NDDs.
Assuntos
Asfixia/patologia , Hipocampo/fisiopatologia , Plasticidade Neuronal/fisiologia , Análise de Variância , Animais , Asfixia/fisiopatologia , Aprendizagem da Esquiva/fisiologia , Espinhas Dendríticas/metabolismo , Espinhas Dendríticas/patologia , Espinhas Dendríticas/ultraestrutura , Comportamento Exploratório/fisiologia , Feminino , Hipocampo/metabolismo , Hipocampo/patologia , Hipocampo/ultraestrutura , Microscopia Eletrônica , Proteínas do Tecido Nervoso/genética , Proteínas do Tecido Nervoso/metabolismo , Gravidez , Células Piramidais/metabolismo , Células Piramidais/patologia , RNA Mensageiro/metabolismo , Ratos , Ratos Sprague-Dawley , Transdução de Sinais/fisiologia , Frações Subcelulares/metabolismo , Frações Subcelulares/ultraestruturaRESUMO
Ozone (O3) is a secondary pollutant, often above the norm in some areas of Santiago in the spring-summer period. It is formed in the atmosphere by photochemical reactions, between nitrogen oxides (NOx) and volatile organic compounds (VOCs), which have an important biogenic contribution (BVOCs). In this research the interrelationship between urban trees, their contribution to atmospheric ozone formation and particulate matter, and respiratory diseases in 6 communes in the province of Santiago was analyzed. The choice of the communes considered the number of inhabitants, the existence of stations monitoring air quality, the percentage of green areas and the geographical distribution. The results showed correlation between the type of species of urban trees, ozone, particulate matter and respiratory diseases: asthma and pneumonia. Necessity for replacement of exotic trees species by native species is concluded.
El ozono (O3) es un contaminante secundario, frecuentemente sobre la norma en algunas áreas de Santiago en el período primavera-verano. Se forma en la atmósfera por reacciones fotoquímicas, a partir de óxidos de nitrógeno (NOx) y compuestos orgánicos volátiles (COVs), los cuales tienen un aporte biogénico (COVsB) importante. En esta investigación se analizó la interrelación entre el arbolado urbano, su contribución a la formación de ozono y material particulado atmosféricos, y las afecciones respiratorias en 6 comunas de la provincia de Santiago. La elección de las comunas consideró el número de habitantes, la existencia de estaciones de monitoreo de calidad del aire, el porcentaje de áreas verdes y la distribución geográfica. Los resultados muestran que existe relación entre el tipo de especies del arbolado urbano, el ozono, el material particulado y las enfermedades respiratorias: asma y neumonía. Se concluye la necesidad de considerar el remplazo de especies exóticas por especies nativas.
Assuntos
Humanos , Ozônio/efeitos adversos , Doenças Respiratórias/epidemiologia , Árvores , Material Particulado/efeitos adversos , Pneumonia/epidemiologia , Doenças Respiratórias/etiologia , Asma/epidemiologia , Estações do Ano , Chile , Características de Residência , Área Urbana , Atmosfera , Poluição do Ar , Hospitalização/estatística & dados numéricosRESUMO
It is widely known that ionizing radiation is a physical agent broadly used to kill tumor cells during human cancer therapy. Unfortunately, adjacent normal tissues can concurrently undergo undesirable cell injury. Previous data of our laboratory demonstrated that exposure of developing rats to ionizing radiations induced a variety of behavioral differences respect to controls, including changes in associative memory and in anxiety state. However, there is a lack of data concerning modifications in different related pharmacological intermediaries. Therefore, the aim of the present study was to investigate whether the behavioral differences observed in young animals irradiated at birth might be underlain by early changes in PKCß1 levels which, in turn, could lead to changes in hippocampal GABAergic neurotransmission. Male Wistar rats were irradiated with 5Gy of X rays between 24 and 48 h after birth. Different pharmacological markers related to the affected behavioral tasks were assessed in control and irradiated hippocampus at 15 and 30 days, namely GABAA receptor, GAD65-67, ROS and PKCß1. Results showed that all measured parameters were increased in the hippocampus of 30-days-old irradiated animals. In contrast, in the hippocampus of 15-days-old irradiated animals only the levels of PKCß1 were decreased. These data suggest that PKCß1 might constitute a primary target for neonatal radiation damage on the hippocampus. Therefore, it could be hypothesized that an initial decrease in the levels of this protein can trigger a subsequent compensatory increase that, in turn, could be responsible for the plethora of biochemical changes that might underlie the previously observed behavioral alterations.
Assuntos
Ansiedade/etiologia , Memória/efeitos da radiação , Animais , Feminino , Hipocampo/enzimologia , Hipocampo/metabolismo , Hipocampo/efeitos da radiação , Masculino , Proteína Quinase C beta/metabolismo , Ratos , Ratos Wistar , Espécies Reativas de Oxigênio/metabolismo , Receptores de GABA-A/metabolismoRESUMO
Introducción: Entre los factores de riesgo para cáncer laríngeo (CL) son relevantes el consumo de tabaco y alcohol. Estos xenobióticos son metabolizados por un grupo de enzimas, entre las cuales están CYP1A1 y GSTM1, cuyas variantes polimórficas se postulan como factores de riesgo para esta enfermedad. Objetivos: Describir la frecuencia de las variantes de los polimorfismos de CYP1A1 y GSTM1 en un grupo de pacientes diagnosticados con CL. Analizar la posible correlación entre las variantes genéticas de ambas enzimas y la presencia de CL. Evaluar la influencia del hábito tabáquico en el riesgo de aparición de cáncer escamoso de laringe en pacientes con genotipos de riesgo. Material y método: Se seleccionaron 35 pacientes con CL entre los años 2000 y 2010 en Servicio de Otorrinolaringología del HBLT y 124 controles reclutados en el Centro de Investigaciones Farmacológicas y Toxicológicas (IFT). A todos los individuos se les registraron datos demográficos y extrajo una muestra de sangre para analizar las variantes polimórficas de CYP1A1 y GSTM1, mediante PCR-RFLP. Resultados: De un total de 35pacientes 54,3% presentan el genotipo GSTM1 (-/-) y 17,1% el genotipo CYP1A1*2A C/C. En el grupo control (n =140) estas frecuencias fueron de 19,35°% y 10,48%o, respectivamente. Se observó una correlación entre GSTM1 y el CL, estratificado por el hábito tabáquico y alcohólico. No se encontraron relaciones estadísticamente significativas con el hábito alcohólico y/o tabáquico. No se observaron asociaciones entre la patología y la combinación de genotipos o entre genotipos y el hábito tabáquico o alcohólico. Conclusiones: Los resultados muestran una asociación estadísticamente significativa entre la deleción de GSTM1 (-/-) y el riesgo de presentar CL, lo que refleja el importante papel que juega esta enzima en la desintoxicación de compuestos cancerígenos. Sin embargo, se requiere incrementar el número de pacientes para establecer apropiadamente la relación genético-ambiental que permite adjudicar un papel relevante a estos biomarcadores.
Introduction: Tobacco and alcohol consumption are recognized risk factors for squamous cell carcinoma of the larynx. These xenobiotics are metabolized by numerous enzymes, among which, CYP1A1 and GSTM1 gene polymorphisms have been identified as risk factors for developing tobacco related cancers as lung and laryngeal carcinomas. Nevertheless, these polymorphisms have not been studied in Chilean patients with squamous cell carcinoma of the larynx. Aim: To describe, for the first time, the frequency of CYP1A1 and GSTM1 gene polymorphisms in Chilean patients with squamous cell carcinoma of the larynx. Material and method: We conducted a case-control study. The case group consisted of 35 Chilean patients with squamous cell carcinoma of the larynx; the control group was formed by 124 Chilean subjects without cancer diagnosis. Demographic data as age, sex and quantification of tobacco smoking and alcohol consumption were recorded in all individuals. CYP1A1 and GSTM1 gene polymorphisms were evaluated by polymerase chain reaction and restriction enzymes (PCR-RFLP). Results: The frequency of CYP1A1*2A C/C genotype was 54, 3°% among laryngeal cancerpatients and 17,1%% among control subjects. The frequency ofGSTM1 (-/-) genotype was 19,35 %% among laryngeal cancer patients and 10,48%% among control subjects. There were no statistically significant relationships between this gene polymorphisms and tobacco smoking or alcohol consumption. There were no associations between the presence of both gene polymorphisms in the same individual and the presence of laryngeal cancer. Interestingly we found an OR of 8.69 (CI 2.90 to 26.01) for GSTM1 (-/-) polymorphism and laryngeal cancer, stratified by tobacco smoking and alcohol consumption. Conclusions: Our work shows that the deletion of GSTM1 could be an important risk factor for squamous cell carcinoma of the larynx in Chilean patients. This finding reflects the important role that detoxification of carcinogenic compounds plays in Chilean population. However, it is necessary to increase the number of studied patients to properly establish the genetic-environmental relationship ascribed to these biomarkers.
Assuntos
Humanos , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Idoso , Carcinoma de Células Escamosas/genética , Neoplasias Laríngeas/genética , Fumar Tabaco/efeitos adversos , Polimorfismo Genético , Polimorfismo de Fragmento de Restrição , Carcinoma de Células Escamosas/enzimologia , Biomarcadores , Estudos de Casos e Controles , Chile/epidemiologia , Projetos Piloto , Neoplasias Laríngeas/enzimologia , Fatores de Risco , Citocromo P-450 CYP1A1/genética , Fumar Tabaco/genética , Glutationa Transferase/genéticaRESUMO
Noise exposure is known to affect auditory structures in living organisms. However, it should not be ignored that many of the effects of noise are extra-auditory. Previous findings of our laboratory demonstrated that noise was able to induce behavioral alterations that are mainly related to the cerebellum (CE) and the hippocampus (HC). Therefore, the aim of this work was to reveal new data about the vulnerability of developing rat HC to moderate noise levels through the assessment of potential histological changes and hippocampal-related behavioral alterations. Male Wistar rats were exposed to noise (95-97 dB SPL, 2h daily) either for 1 day (acute noise exposure, ANE) or between postnatal days 15 and 30 (sub-acute noise exposure, SANE). Hippocampal histological evaluation as well as short (ST) and long term (LT) habituation and recognition memory assessments were performed. Results showed a mild disruption in the different hippocampal regions after ANE and SANE schemes, along with significant behavioral abnormalities. These data suggest that exposure of developing rats to noise levels of moderate intensity is able to trigger changes in the HC, an extra-auditory structure of the Central Nervous System (CNS), that could underlie the observed behavioral effects.
Assuntos
Sintomas Comportamentais/etiologia , Sintomas Comportamentais/patologia , Hipocampo/patologia , Ruído/efeitos adversos , Fatores Etários , Análise de Variância , Animais , Animais Recém-Nascidos , Comportamento Animal/fisiologia , Contagem de Células , Comportamento Exploratório , Feminino , Hipocampo/crescimento & desenvolvimento , Masculino , Aprendizagem em Labirinto/fisiologia , Desempenho Psicomotor/fisiologia , Ratos , Ratos Wistar , Reconhecimento Psicológico , Fatores de TempoRESUMO
Living organisms are exposed to potentially hazardous noise levels coming from the environment. Besides the direct effect on hearing, extra-auditory noise-associated effects should be considered. Since loud noise has been suggested to induce central nervous system symptoms, the aim of the present work was to investigate the effect of acute (ANE) and chronic noise exposures (CNE) on different behavioral tasks. To understand the mechanisms involved, levels of oxidative status markers were determined in two areas related to memory processes, the hippocampus (Hip) and the cerebellum (CE). 15-day-old male Wistar rats were exposed to loud noise (95-97 dB, 2h/day), at ANE or CNE. At 30 days, rats were subjected to different CE and Hip-related behavioral tasks. Reactive oxygen species (ROS) levels and antioxidant enzyme activities (CAT and SOD) were also assessed. Results show impairments in spatial and associative memory in noise-exposed animals. Moreover, a decrease in anxiety levels and an increase in habituation memory were observed in CNE animals. While an increase in cerebellar ROS levels was found early after the first noise exposure, a decrease was found in the CE and the Hip at 30 days. The activity of hippocampal CAT was increased early and remained high in ANE rats, while it was unchanged in the CE. Finally, although SOD activity was decreased immediately after the first noise exposure, its levels were increased at 30 days in ANE rats. In summary, the present study shows that an imbalance in oxidative status induced by noise exposure could underlie behavioral changes, some of which would be long-lasting.
Assuntos
Comportamento Animal , Catalase/metabolismo , Cerebelo/metabolismo , Hipocampo/metabolismo , Ruído , Espécies Reativas de Oxigênio/metabolismo , Superóxido Dismutase/metabolismo , Animais , Ansiedade/metabolismo , Ansiedade/psicologia , Aprendizagem da Esquiva , Habituação Psicofisiológica , Locomoção , Masculino , Aprendizagem em Labirinto , Memória , Atividade Motora , Testes Neuropsicológicos , Ratos , Ratos Wistar , Comportamento Espacial , Fatores de TempoRESUMO
On 17 May 2009, the first two cases of 2009 pandemic influenza A(H1N1) were confirmed in the Metropolitan region (Santiago, Chile). On 6 June 2009, Chile reported 500 confirmed cases, seven severe and two fatal. Because six of the severe cases and the two deaths occurred in the region of Los Lagos in southern Chile, a retrospective study was conducted using data on emergency room visits as well as laboratory viral surveillance, during the period from 1 April to 31 May, in order to establish the date of the beginning of the outbreak. From 1 to 27 June, data were collected in real time, to establish the real magnitude of the outbreak, describe its transmission, clinical severity and secondary attack rates. Confirmed cases, their household contacts and healthcare workers were interviewed. This analysis showed that the outbreak in Los Lagos started on 28 April. By 27 June, a total of 14.559 clinical cases were identified, affecting mostly 5-19 year-olds. The effective reproduction number during the initial phase (20 days) was 1.8 (1.6-2.0). Of the 190 confirmed cases with severe acute respiratory infection, 71 (37.4%) presented a risk condition or underlying illness.
Assuntos
Surtos de Doenças , Vírus da Influenza A Subtipo H1N1 , Influenza Humana/epidemiologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Criança , Pré-Escolar , Chile/epidemiologia , Serviço Hospitalar de Emergência/estatística & dados numéricos , Feminino , Humanos , Lactente , Influenza Humana/transmissão , Masculino , Pessoa de Meia-Idade , Vigilância da População , Estudos Retrospectivos , Fatores de Risco , Adulto JovemRESUMO
Objetivo: Describir el perfil epidemiológico de una muestra de pacientes beneficiarios del Servicio de Salud Bío Bío con examen de antígeno prostático sobre 4 ng/mL. Método: Se realizó un estudio transversal descriptivo donde se revisaron 436 fichas clínicas de pacientes con niveles APE > 4,0 ng/ml determinado en el Laboratorio Clínico del Hospital Dr. Víctor Ríos Ruiz, entre enero y junio del año 2006. También se obtuvo información a partir de los certificados de defunción y de anatomía patológica. Resultados: El 42,4 por ciento pertenecía a la comuna de Los Ángeles y el 57,6 por ciento restante se distribuye homogéneamente dentro de la región de Bío Bío. El promedio de edad de los pacientes fue de 72 años (31 a 98 años). El 75,6 por ciento pertenece a los grupos A y B del Fondo Nacional de Atención de Salud (FONASA), habiendo 10 por ciento sin afiliación conocida. El 63,4 por ciento presentaba hipertensión arterial. El 24,8 por ciento tuvo como diagnóstico cáncer de próstata (CaP) y el 58,2 por ciento hiperplasia benigna prostática. El 58,26 por ciento de los pacientes tuvo un valor de APE entre 4,00 a 10,00 ng/ml, el 34,59 por ciento entre 10,01 a 50,00 ng/ml y el 7,57por ciento un valor de APE >50,00 ng/ml. Conclusiones: El mayor porcentaje de los pacientes se concentra en la ciudad de Los Ángeles, siendo la mayoría del segmento A y B del fondo nacional de salud. La edad promedio fue de 72 años. La hipertensión arterial, la diabetes mellitus y el cáncer de próstata fueron las patologías más prevalentes en estos pacientes.
Objective: To describe the epidemiologic profile of a sample of patient beneficiaries of the Bio Bio Health Service with prostate specific antigen (PSA) up 4 ng/mL. Method: A descriptive cross-sectional study was made between January and June of 2006, where436 clinical histories of patients with levels APE up 4.0 ng/ml were reviewed. Also information from certificates of death and pathological anatomy was obtained. Results: The 42.4 percent belonged of Los Angeles province and the rest were distributed homogenous within Bio Bio region. The average of age of the patients was of 72 years old (31 to 98 years). The 75.6 percent belong to the groups A and B of the National Found of Health Attention (FONASA), being a 10.0 percent without well-known affiliation. The 63.4 percent presented arterial hypertension. The 24.8 percent present prostate cancer diagnostic (CaP) and the 58.2 percent had benign prostatic hyperplasia. 58.26 percent of the patients had a value of PSA between 4.0 to.10.0 ng/ml, the 34.59 percent between 10.01 to 50.00 ng/ml and the 7.57 percent a value of APE>50.00 ng/ml. Conclusions: The larger percentages of the patients live in the urban area of Los Angeles city, belonging most of the segment A and B of the National Found of Health Attention (FONASA). The average age was of 72 years. The hypertension arterial, the diabetes mellitus and the prostate cancer were the most prevalent pathologies in these patients.
Assuntos
Humanos , Masculino , Adulto , Pessoa de Meia-Idade , Idoso de 80 Anos ou mais , Antígeno Prostático Específico , Hiperplasia Prostática/epidemiologia , Neoplasias da Próstata/epidemiologia , Perfil de Saúde , Chile/epidemiologiaRESUMO
Cytochrome P450 enzymes are very important to metabolize anti-carcinogenic agents. Therefore, understanding the role of these enzymes and their allele variants in the bioactivation or detoxification of drugs could greatiy benefit antineoplastic pharmacotherapy. The aim of thís manuscrípt is to give information about metabohzing enzymes for antineoplastic agents and to relate the current situation in antitumoral pharmacotherapy with recent knowledge about cytochrome P450 enzymes. This is crucial for the future perspectives towards personalized pharmacotherapy. We summarize the role of cytochrome P450 enzymes in the resistance and bioactivation of several antitumor agents, their induction and repression mechanisms and the effect of genetic polymorphisms on variability of drug metabolization. The understanding of genetic variability will help to develop new research Unes on innovative therapeutic possibilities.