Resumen La información epidemiológica es una herramienta orientadora de gran importancia al momento de establecer un diagnóstico clínico. En nuestro país son escasos los trabajos que describen la epidemiología de las enfermedades neurológicas, por lo cual nuevos aportes en el tema son relevantes, en especial si, a través de los mismos, se logra establecer la existencia de factores de riesgo asociados a algunas patologías. El objetivo del presente trabajo fue determinar la casuística de las enfermedades que afectan el sistema nervioso central en caninos de raza que asistieron a la policlínica de neurología de la Facultad de Veterinaria en el período comprendido entre enero de 2009 y junio de 2013 y determinar el efecto de la raza, sexo y edad en la ocurrencia de dichas enfermedades. Para ello, se realizó un estudio retrospectivo de 211 casos y 461 controles seleccionados al azar. Los casos se agruparon según sexo, edad y raza. Se evaluaron las variables de forma individual mediante Test exacto de Fisher y luego, se realizó análisis de regresión logística, para determinar el odds ratio, empleando un nivel de significación p<0,05. El 37,9% de los animales presentaron mielopatías, 33,6% encefalopatías, 19,4% encefalomielopatías, 7,6% síndromes vestibulares y 1,4% síndromes cerebelosos. En las enfermedades medulares ser macho actuó como un factor de riesgo (OR 2,27), así como ser adulto, siendo los OR para >1,5 y < 7 y ≥ 7 años de 2,56 y 2,78 respectivamente. Ninguna raza actuó como factor predisponente. No existió predisposición de sexo, edad y raza para el resto de las enfermedades neurológicas.

Summary Epidemiological data is very important when establishing clinical diagnosis. In Uruguay there are few studies that describe the epidemiology of neurological diseases, which make new contributions in the topic relevant, especially if it helps to establish risk factors associated to some diseases. The aim of this study was to determine the incidence of central nervous system diseases in purebred dogs which attended to neurology clinic of Faculty of Veterinary between January 2009 and June 2013 and to determinate the effect of breed, sex and age on the occurrence of these diseases. A retrospective study of 211 cases and 461 controls randomized were performed. The cases were grouped according to sex, age and breed. Logistic regression analysis was performed with p<0.05. 37.9% of the animals, had myelopathies, 33.6% encephalopathies, 19.4% encephalomyeopathies, 7.6% vestibular syndrome and 1.4% had cerebellar diseases. Race was not acted a risk factor in either group of diseases. In spinal diseases, being male acted as a risk factor with an OR of 2.27. Also, being puppy acted as a protective factor, being OR for 1.5 to 7 and ≥ 7 years 2.56 and 2.78 respectively. None breed acted as risk factor. There was no sex, breed nor age predisposition for the other neurological diseases.

After myocardial infarction (MI), activation of the immune system and inflammatory mechanisms, among others, can lead to ventricular remodeling and heart failure (HF). The interaction between these systemic alterations and corresponding changes in the heart has not been extensively examined in the setting of chronic ischemia. The main purpose of this study was to investigate alterations in cardiac gene and systemic cytokine profile in mice with post-ischemic HF. Plasma was tested for IgM and IgG anti-heart reactive repertoire and inflammatory cytokines. Heart samples were assayed for gene expression by analyzing hybridization to AECOM 32k mouse microarrays. Ischemic HF significantly increased the levels of total serum IgM (by 5.2-fold) and total IgG (by 3.6-fold) associated with a relatively high content of anti-heart specificity. A comparable increase was observed in the levels of circulating pro-inflammatory cytokines such as IL-1β (3.8X) and TNF-α (6.0X). IFN-γ was also increased by 3.1-fold in the MI group. However, IL-4 and IL-10 were not significantly different between the MI and sham-operated groups. Chemokines such as MCP-1 and IL-8 were 1.4- and 13-fold increased, respectively, in the plasma of infarcted mice. We identified 2079 well annotated unigenes that were significantly regulated by post-ischemic HF. Complement activation and immune response were among the most up-regulated processes. Interestingly, 21 of the 101 quantified unigenes involved in the inflammatory response were significantly up-regulated and none were down-regulated. These data indicate that post-ischemic heart remodeling is accompanied by immune-mediated mechanisms that act both systemically and locally.