ARMC5 Primary Bilateral Macronodular Adrenal Hyperplasia Associated with a Meningioma: A Family Report.

Primary bilateral adrenal macronodular hyperplasia is characterized by functioning adrenal macronodules and variable cortisol secretion. Familial clustering suggests a genetic cause that has been confirmed with the identification of some genetic mutations, including inactivating germline mutations, in armadillo repeat containing 5 (ARMC5) gene. The identification of the pathogenic variant enables the physician to identify and treat these patients earlier and more effectively. It has also been noticed that patients with germline causative variants show a different clinical spectrum, presenting specific clinical characteristics, as the association with the presence of meningiomas.

Blood-derived phagocytes in the cerebellar cortex of the rat after chronic alcohol consumption.

Past work showed that chronic alcohol consumption induces massive degeneration in the rat cerebellar cortex. To study the subsequent process of nervous tissue repair, followed itself by a remodelling activity, groups of alcohol-treated rats for 3 and 6 months were used and the results compared with the respective age-matched controls. From the wide variety of cells which display phagocytic activity in the mammalian brain it was found, based on qualitative observations, that two types were clearly involved in the removal of the alcohol-induced degenerated debris: the resident microglial cells and the non-resident brain macrophages. This assumption was corroborated by the study of their origin, using carbon particles and latex beeds intravenously injected, which showed that brain macrophages were the sole population to be labelled. These observations fit with the multiple origin concept for neural phagocytosis which postulates that different cell types can be recruited for the removal of the damaged neural tissue depending on the severity of the lesions and on the extension of the blood vessels damage.

Cell loss in the cerebellum and hippocampal formation of adult rats after long-term low-protein diet.

Whereas quite a number of previous reports have shown that the developing brain is vulnerable to protein deprivation, the mature CNS is usually considered resistant to this condition. To explore this assumption the present experimental model was built on groups of 2-month-old rats fed with a low-protein diet (8% casein) for 6, 12, and 18 months and respective age-matched controls fed for the same periods with a standard laboratory chow (27% casein). The numerical density of cerebellar granule cells was estimated using three different stereological procedures (classical, unfolding, and disector). By all methods a significant cell loss was demonstrated. In the hippocampal region the numerical densities of dentate gyrus granule cells and the CA3 pyramidal cells were estimated using the unbiased disector method. A significative and progressive loss of neurons was likewise found. The occurrence of cell loss after lengthy periods of undernutrition in adulthood is thus an issue of paramount importance if extrapolation can be made to the human brain.