A model of traumatic brain injury in rats is influenced by neuroprotection of diurnal variation which improves motor behavior and histopathology in white matter myelin.

Traumatic brain injury (TBI) represents a significant public health concern and has been associated with high rates of morbidity and mortality. TBI generates two types of brain damage: primary and secondary. Secondary damage originates a series of pathophysiological processes, which include metabolic crisis, excitotoxicity, and neuroinflammation, which have deleterious consequences for neuronal function. However, neuroprotective mechanisms are also activated. The balance among these tissue responses, and its variations throughout the day determines the fate of the damage tissue. We have demonstrated less behavioral and morphological damage when a rat model of TBI was induced during the light hours of the day. Moreover, here we show that rats subjected to TBI in the dark lost less body weight than those subjected to TBI in the light, despite no change in food intake. Besides, the rats subjected to TBI in the dark had better performance in the beam walking test and presented less histological damage in the corpus callosum and the cingulum bundle, as shown by the Klüver-Barrera staining. Our results suggest that the time of day when the injury occurs is important. Thus, this data should be used to evaluate the pathophysiological processes of TBI events and develop better therapies.

[Right hematocolpos and hematometra with left renal agenesis. A rare association. Apropos a case]. / Hematocolpos y hematometra derechos con agenesia renal izquierda. Una rara asociación. A propósito de un caso.

Although this anomaly is seen more frequently, the present case is unique in that the genital anomaly (imperforate vagina with the subsequent hematocolpos and hematometra) was associated with contralateral renal agenesis, whereas the cases reported in the literature have all been ipsilateral. Like most of the cases, the presenting symptom was acute urinary retention arising from extrinsic compression of the genital mass on the lower urinary tract. The embryological aspects of the genitourinary system concerning the present case are discussed, as well as some of the hypotheses that have been put forward to explain the etiology of these anomalies, although these have been developed on the basis of the associated ipsilateral anomalies observed.