[Demyelination of the central nervous system associated with adrenocortical atrophy].
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Until a few years ago, radial glial cells were seen primarily as providing a supporting role to guide the migration of newborn neurons in the developing central nervous system. Recent studies, however, suggest that not only do radial glial cells give rise to new neurons during development, but that they also may become the neural stem cells that reside in the neurogenic regions of the adult central nervous system. So, should we rethink the role of radial glial cells? Do they play a part in providing new neurons in the adult brain, and could radial glial cells have the potential to repair degenerating neurons in the adult central nervous system?
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Prostatic atrophy is a benign lesion that may mimic adenocarcinoma histologically and on imaging. It is more frequent in the peripheral zone and has gained importance with the increasing use of needle biopsies. Diffuse atrophy occurs secondarily to radiotherapy and/or endocrine therapy. Inflammation and/or chronic local ischemia may cause focal atrophy with an increasing frequency in age. Atrophy may be classified morphologically into diffuse and focal. The latter may be partial, complete or combined. Partial focal atrophy is the most frequent mimicker of adenocarcinoma on needle biopsies. Complete focal atrophy may be subtyped into simple, sclerotic and hyperplastic (or postatrophic hyperplasia). Combined lesions are frequent and partial atrophy may precede complete atrophy. The several morphologic types of focal atrophy may represent a morphologic continuum and the hyperplastic (or postatrophic hyperplasia) subtype seems to be at the extreme end of this continuum. Chronic inflammation associated to focal atrophy (proliferative inflammatory atrophy) has been linked to high-grade prostatic intraepithelial neoplasia and/or carcinoma. This link, however, remains controversial in the literature. The question whether inflammation directly produces tissue damage and atrophy or some other insult induces atrophy directly, with inflammation occurring secondarily, is still unresolved. An intriguing finding that needs further studies is a possible association of extent of atrophy to serum PSA elevation.
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Both atrophic and dysplastic cervical squamous epithelia show lack of maturation, nuclear crowding, and increased nuclear/cytoplasmic ratio. Because of these similarities, distinguishing dysplasia from atrophy in cervical biopsies from elderly patients is often problematic. Because dysplasia shows increased proliferation and atrophy has decreased proliferation, the possible utility of MIB-1 in distinguishing dysplasia from atrophy was evaluated. One or more of the following criteria were present in all nine cases with dysplasia and in none of the 17 cases with atrophy: MIB-1 expression in > 20% of cells in the basal one-third of the epithelium, > 5% of cells in the middle one-third of the epithelium, and > 1% of cells in the upper one-third of the epithelium. MIB-1 immunostaining is useful in distinguishing dysplasia from atrophy.
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This study addresses two issues regarding prostatic atrophy: (1) the histologic features of atrophy as seen on needle biopsy results and how they affect the diagnosis of atrophy and (2) the cellular kinetics of atrophy and what it suggests about the mechanism of atrophy. We reviewed hematoxylin and eosin sections for 103 prostate needle biopsy specimens with atrophy. Each biopsy specimen was classified as either simple atrophy (large atrophic glands without crowding: 53 cases) or postatrophic hyperplasia (PAH) (crowded focus of small atrophic acini: 50 cases). Cell proliferation in both the atrophic and benign glands was evaluated in 103 cases by immunohistochemistry using antibodies against MIB-1. The TdT-mediated dUTP-biotin nick-end labeling technique was performed on 61 cases to quantitate apoptosis in atrophic and benign glands. Thirty-two percent of cases showed chronic inflammation, 21% showed acute inflammation, 14% showed nucleoli, and 1% showed mitoses. In comparison to simple atrophy, PAH contained more frequent prominent nucleoli (p < 0.0001) and acute inflammation (p < 0.0001), yet not chronic inflammation. In a multivariate analysis, acute inflammation and PAH pattern influenced the presence of prominent nucleoli. Staining for MIB-1 was greater in atrophic (27.5 cells/1000 cells) than in benign glands (3.5 cells/1000 cells), greater in PAH than in simple atrophy (p= 0.0015), and greater with acute (p = 0.05) but not chronic inflammation. In a multivariate analysis, only the pattern of atrophy and not acute inflammation was found to influence MIB-1. The rate of apoptosis was negligible in both the benign and atrophic glands, did not vary with pattern of atrophy, and did not correlate with MIB-1. Despite the atrophic appearance, atrophic glands in PAH show more proliferative activity than benign, nonatrophic glands and show no evidence of active involution, justifying the term "postatrophic hyperplasia" for this pattern of atrophy. Prominent nucleoli are seen more frequently in postatrophic hyperplasia, even in the absence of acute inflammation. To avoid a potential erroneous diagnosis of cancer, a constellation of features suggestive of malignancy should be considered, rather than relying on prominent nucleoli as the sole criteria for the diagnosis of prostate cancer.
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To describe the morphology of focal prostatic atrophy and propose a comprehensive histologic classification for a proper diagnostic recognition.A broad immunohistochemical study was performed as an adjunct to its recognition as well as a contribution to pathogenesis.A morphologic continuum was seen on needle biopsies. Chronic inflammation was present only in complete atrophy. Immunohistochemical findings in partial atrophy are similar to normal acini. Luminal compartment in complete atrophy shows aberrant expression of 34betaE12 favoring an intermediate phenotype. ERG negativity in all variants of atrophy may have value in the identification of the lesion.The morphologic findings favor a continuum probably partially preceding complete atrophy. Chronic inflammation may be a secondary phenomenon seen only in complete atrophy. Overexpression in complete atrophy of glutathione S-transferase pi relates to oxidative stress possibly related to chronic ischemia, of c-Met favors the concept that intermediate cells may be target for carcinogenesis, and of CD44 may be related to the recruitment of inflammatory cells.
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