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Se presentan los resultados de un estudio histológico de huesos con implante de hidroaxiapatita y titanio por Microscopía Electrónica de Barrido (MEB). A tal efecto se utilizaron huesos de fémur de conejos preparados de la misma manera que para la histología por MET (Microscopía Electrónica de Transmisión) pero sin descalcificar.

Renal ischemia-reperfusion is the cause of acute renal insufficiency, which exerts a high mortality index. Nowadays, the treatments used for the recovery of the kidney submitted to ischemia-reperfusion have a limited success. For this reason, it is necessary to look for effective therapeutic strategies that help to prevent renal damage. The most prominent histopathological feature of renal ischemia-reperfusion is the lesion of the cortical proximal tubules. The objective of this work was to evaluate the effect of ozone oxidative preconditioning on the morphology of renal cortex proximal tubules against ischemia-reperfusion damage. Renal cortex pieces from 16 rats were studied. Rats were divided into four groups: control, ischemia-reperfusion damaged (60 min of ischemia followed by 180 min of reperfusion), and two groups of rats preconditioned with ozone (0.5 and 1.1 mg/kg body weight respectively) and submitted to ischemia-reperfusion. Samples were processed following conventional Spurr resin embedding. Semithin sections were prepared and analyzed qualitative and quantitatively by Light Microscopy. Morphological markers of ischemia-reperfusion-induced renal damage on renal proximal tubules were identified as: loss of the brush border, tubular swelling, increase of tubular areas and perimeters, tubular necrosis and increase of epithelial cell nuclei in tubular lumen, related to the formation of casts. Ozone oxidative preconditioning led to the recovery of proximal tubules morphology. Since ozone therapy protects epithelial cells of renal proximal tubules, it could be considered as an efficient tool against renal ischemia-reperfusion damage. [ABSTRACT FROM AUTHOR]

Ototoxic therapeutic drugs are among the major causes of auditory damage. Hearing loss is produced as a result of irreversible injury of cochlear hair cells. These cells lack regenerative capacity in mammals, so their loss induces permanent deafness. In vitro and in vivo models of deafness are used to research therapeutic alternatives to treat hearing losses. Nowadays, one of the most widespread models is the aminoglycoside-induced damage in organotypical cultures of neonatal cochleae. In these studies, damage of the organ of Corti hair and supporting cells has been revealed. The aim of this work was to revise the morphological changes induced by aminoglycoside antibiotics on organotypical cultures of the organ of Corti with special emphasis on the methods employed. Neomycin and gentamicin are the most employed aminoglycosides in organotypical cultures. In this work kanamicin-induced generation of cochlear cells in vitro was showed at the first time. After the first hours of exposition, hair cells undergo degenerative changes such as pathological vesicle formation and disruption of their sterereocilia bundles. Severe damage due to prolonged exposure induces hair cell death and the neighbour supporting cells form a phalangeal scar. Provided the similarities between ototoxicity induced changes in vivo and in vitro, organotypical cultures of the organ of Corti might be employed to validate potentially otoprotective therapies. [ABSTRACT FROM AUTHOR]

Deafness is one of the most widespread disabilities in the world. Its incidence in Cuba is 2.1 per 1,000 inhabitants. The origin of deafness is mainly sensorineural. This kind of hearing loss is caused by death of cochlear hair cells (located in the organ of Corti), which induces degeneration of spiral ganglion neurons. In a previous light microscopy study using a rat model of ototoxicity, it was observed that the organ of Corti was damaged since the second week of deafness, whereas the loss of spiral ganglion neurons was not significant until the eighth week of deafness. In order to define the onset of degenerative changes, a study by Transmission Electron Microscopy of the organ of Corti and spiral ganglion neurons was carried out. Rat cochleae sampled after 2, 4, 8 and 16 weeks of deafness and healthy controls were analyzed. The supporting cells of the organ of Corti were damaged since the second week. Type I spiral ganglion neurons showed progressive degenerative changes since the fourth week. Myelin sheaths of the peripheral processes innervating the organ of Corti showed signs of degeneration since the fourth week of deafness. Most of the remaining neurons exhibited complete demyelination at sixteen weeks of deafness, resulting in the pathological type III spiral ganglion neurons. The above results indicate that the injury of the organ of Corti induces ultrastructural degenerative changes of the spiral ganglion neurons before the significant loss of these cells and their dendrites. [ABSTRACT FROM AUTHOR]