ABSTRACT
La resina poliéster (P-4) se ha utilizado en varias técnicas anatómicas, gracias a su bajo costo, fácil manejo y obtención. Entre ellas la inclusión, que se realiza en capas dejando muestras relativamente opacas y de un grosor que no permite ver claramente las estructuras. También encontramos la plastinación de cortes anatómicos, técnica más sofisticada, compleja y de un alto costo económico. El objetivo fue idear un método de inclusión para cortes anatómicos, que mejore la calidad de la técnica clásica. Se utilizaron cortes anatómicos de segmento distal de miembro inferior humano y de un grosor promedio de 0,5 cm fijados con acetona y cortes de encéfalo de vacuno de igual grosor, fijados con formalina acuosa al 10%. La totalidad de las muestras son deshidratadas en acetona a -17 °C. Posteriormente se impregnan e incluyen en resina poliéster (P-4) a temperatura ambiente. Se obtuvieron muestras con una buena transparencia y solidez que permite ver en detalle muchas estructuras, similar a la obtenida con la técnica de plastinación en resina. Mediante un método relativamente fácil de realizar es posible obtener piezas anatómicas de muy buena calidad.
The polyester resin (P-4) has been used in several anatomical techniques, due to its low cost, easy handling and elicit. Among them, the inclusion, which is performed on samples leaving relatively opaque layers and an important thickness which does not allow a clear vision of the structures. There is also the plastination of anatomical slices with this polymer which although, technically sophisticated and complex has a high economic cost. The objective is to develop a method for anatomical section inclusion, improving the quality of classic technique. Distal segment of human lower limb anatomical slices were used with an average thickness of 0.5 cm fixed with acetone and bovine brain slices equal thickness, fixed with 10% aqueous formalin. All the samples are dried in acetone at -17 °C. Subsequently, they are impregnated and included on polyester resin (P-4) at room temperature. Samples were obtained with good transparency and solidity that allows observation of details of many structures, similar to that obtained with the resin plastination technique. Using this relatively easy method we can get very good quality anatomical samples.
Subject(s)
Humans , Animals , Histological Techniques/methods , Polyesters , Resins, Synthetic , Tissue Preservation/methodsABSTRACT
Histiocytic necrotizing lymphadenitis (also known as Kikuchi-Fujimoto's disease) is an uncommon, benign and self-limiting lymph disease. We report three patients aged 14, 22 and 50 years, who presented with fever and cervical lymphadenopathy, accompanied by skin lesions and joint pain in two of the three cases. One of the patient's sister suffered from histiocytic necrotizing lymphadenitis. Laboratory abnormalities varied and findings included leucopenia, relative neutrophilia, elevated C reactive protein, erythrocyte sedimentation rate and ferritin. Basic laboratory screening tests were performed on all patients to rule out autoimmune and infectious diseases. Lymph node biopsy and subsequent pathological examination were essential to establish the diagnosis. All patients received antibiotics at some point of their hospital stay. Two patients required glucocorticoid treatment, while the remaining case experienced a spontaneous recovery. Its pathogenesis is still unknown, but clinical and histopathological studies suggest a connection with autoimmune diseases. There is no established treatment, but apparently the disease responds to the administration of glucocorticoids.
Subject(s)
Adolescent , Female , Humans , Male , Middle Aged , Young Adult , Histiocytic Necrotizing Lymphadenitis/diagnosisABSTRACT
INTRODUCCIÓN: La epilepsia del lóbulo temporal se desarrolla como consecuencia de insultos cerebrales como trauma, infartos, infección o convulsiones. Los circuitos neuronales del lóbulo temporal, incluyendo al hipocampo, se reorganizan generando redes hiperexcitables, el foco epiléptico, proceso denominado epileptogénesis; en cambio, la corteza cerebral es más resistente a la reorganización. La epileptogénesis en el hipocampo está mediada en parte por óxido nítrico, sintetizado por la óxido nítrico sintasa neuronal y por la neurotrofina BDNF, cuyo receptor es TrkB. Estas proteínas están localizadas en las sinapsis excitadoras y podrían estar implicadas en la sensibilidad diferencial entre el hipocampo y corteza cerebral a la epileptogénesis. OBJETIVO: Lograr un acercamiento a los mecanismos que participan en la sensibilidad diferencial a la epileptogénesis entre el hipocampo y la corteza, después de convulsiones. MATERIAL Y MÉTODO: Se indujeron convulsiones en ratas mediante inyección de kainato. Se obtuvieron membranas sinápticas reselladas (sinaptosomas) de corteza e hipocampo. En ellas, se cuantificó la co-localización de óxido nítrico sintasa neuronal, TrkB y un marcador de sinapsis excitadoras (Prosap2) mediante técnicas inmunohistoquímicas. Los resultados expresados como por ciento promedio +/- error estándar se sometieron a prueba de t-student. RESULTADOS: TrkB y óxido nítrico sintasa neuronal aumentaron de 20,6 +/- 3,5 por ciento a 35,7 +/- 2,6 por ciento (p = 0,0008) y de 32,4 +/- 3,8 por ciento a 51,5 +/- 3,5 por ciento (p = 0,0003), respectivamente, en sinaptosomas excitadores hipocampales después de convulsiones. En sinaptosomas excitadoras de cerebro corteza no se observaron cambios significativos. DISCUSIÓN: óxido nítrico sintasa neuronal y TrkB se asocian a sinapsis excitadoras hipocampales después de convulsiones, pudiendo contribuir así a la epileptogénesis. La cerebrocorteza es resistente a esta reorganización molecular.
INTRODUCTION: Temporal lobe epilepsy develops as a consequence of brain insults such as trauma, stroke, infection, or seizures. The temporal lobe circuit, including the hippocampus, reorganizes generating hyper-excitable networks and, therefore, the epileptic focus, process called epileptogenesis. Where as, the cerebral cortex is more resistant to the reorganization. Temporal lobe epileptogenesis is mediated partly by neuronal nitric oxide synthase and the neurotrophin BDNF with its receptor TrkB. These proteins are localized at excitatory synapses and might be involved in the differential sensitivity of the hippocampus and cerebral cortex to epileptogenesis. OBJECTIVE: Getting closer to mechanisms involved in epileptogenesis differential sensitivity between the hippocampus and cortex after seizures. MATERIAL AND METHOD: Seizures were induced in rats by injection of kainic acid. Resealed synaptic membranes (synaptosomes) were obtained from cortex and hippocampus. Then the co-localization of neuronal nitric oxide synthase, TrkB and a marker of excitatory synapses (Prosap2/Shank3) was quantified by immunohistochemistry. The results were expressed as mean +/- standard error and subjected to t-student test. RESULTS: TrkB and neuronal nitric oxide synthase increased from 20.6 +/- 3.5 percent to 35.7 +/- 2.6 percent (p = 0.0008) and from 32.4 +/- 3.8 percent to 51.5 +/- 3.5 percent (p = 0.0003), respectively in excitatory hippocampal synaptosomes after seizures. In excitatory cerebrocortical synaptosomes no significant changes were observed. DISCUSSION: neuronal nitric oxide synthase and TrkB associate to excitatory hippocampal synapses after seizures, thereby probably contributing to epileptogenesis. The cerebral cortex is resistant to this molecular reorganization.