Histology and histopathology Vol.17, nº 1 (2002)

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  • Publication
    Open Access
    Effects of chronic administration of either ethanol or pentanol on rat duodenum morphology
    (Murcia : F. Hernández, 2002) Vaquera, J.; Vaquera, A.; Girbes, T.
    The morphology of the rat duodenum after chronic treatment with 15% (v/v) ethanol and 4% (v/v) pentanol was studied. Male Wistar rats of experimental groups were given ethanol and pentanol for 15 weeks with food and fluid freely available. Ethanol-15% and 4% pentanol-fed rats showed a significantly reduced fluid and food intake as compared with control rats. The study of the mucosa indicated that the number of chronic inflammatory infiltrating (mononuclear cells) and goblet cells was higher in the groups of the ethanol- and pentanol-fed rats than in the control group. There was an increase in the thickness of the brush border in pentanolfed rats. Intervillus adhesion was concurrently observed in the pentanol-fed rats but not in the control or ethanolfed rats. After ethanol feeding many of the villi developed blebs at the apex of the villus or laterally on its upper half. These blebs generally remained intact. In contrast, after pentanol feeding no bleb formation was appreciated. The intake of ethanol and other short chain alcohols present in alcoholic beverages leads to mainfold disturbances on the rat duodenum. These findings suggest that the chronic ingestion of pentanol seems to promote cellular changes but less important than those observed after chronic ethanol ingestion.
  • Publication
    Open Access
    Expression of E-cadherin-catenin complex in human benign schwannomas
    (Murcia : F. Hernández, 2002) Hasegawa, M.; Muramatsu, N.; Tohma, Y.; Fukaya, K.; Fujisawa, H.; Hayashi, Yoshihiro; Tachibana, Osamu; Kida, S.; Yamashita, J.; Saito, K.
    The Ca2+-dependent cell adhesion molecule E-cadherin has been known to express in normal and reactive Schwann cells in rodents, and to play an important role in Schwann cell-Schwann cell adhesion and maintenance of peripheral nervous tissue architecture. However, little is known about expression of E-cadherin in schwannomas. The aim of the present study was to investigate the cellular expression and localization of E-cadherin, and its associated protein, alpha E-, alpha N- and beta-catenins in human schwannomas, which are supposed to derive from Schwann cells. We tested the hypothesis that these proteins might show an altered expression/distribution in schwannoma cells which correlates with their neoplastic behavior, including sparse cell-cell contact, as seen those in meningiomas and various carcinomas. In human schwannomas, however, E-cadherin, alpha E-catenin, and beta-catenin were detected by western blotting and i m m u n o h i s t o c h e m i s t r y, whereas alpha N-catenin was not. Immunoprecipitation using anti-E-cadherin antibody resulted in alpha E-catenin forming a complex with Ecadherin. SSCP analysis revealed no mutations in the transmembrane domain or in intracellular cateninbinding site of E-cadherin. These data suggest that the Ecadherin- alpha E-catenin complex is well preserved in human schwannoma cells, which is compatible with its benign behavior, and these molecules might be used as additional cell markers of Schwann cell-derived tumors.
  • Publication
    Open Access
    Alzheimer ß-amyloid peptides normal and abnormal localization
    (Murcia : F. Hernández, 2002) Takahashi, R.H.; Nam, E.E.; Edgar, M.; Gouras, G.K.
    Alzheimer's disease (AD) neuropathology is characterized by accumulation of “senile” plaques (SPs) and neurofibrillary tangles (NFTs) in vulnerable brain regions. SPs are principally composed of aggregates of up to 42/43 amino acid ß-amyloid (Aß) peptides. The discovery of familial AD (FAD) mutations in the genes for the amyloid precursor protein (APP) and presenilins (PSs), all of which increase Aß42 production, support the view that Aß is centrally involved in the pathogenesis of AD. Aß42 aggregates readily, and is thought to seed the formation of fibrils, which then act as templates for plaque formation. Aß is generated by the sequential intracellular cleavage of APP by ßsecretase to generate the N-terminal end of Aß, and intramembranous cleavage by g-secretase to generate the C-terminal end. Cell biological studies have demonstrated that Aß is generated in the ER, Golgi, and endosomal/lysosomal system. A central question involving the role of Aß in AD concerns how Aß causes disease and whether it is extracellular Aß deposition and/or intracellular Aß accumulation that initiates the disease process. The most prevalent view is that SPs are composed of extracellular deposits of secreted Aß and that Aß causes toxicity to surrounding neurons as extracellular SP. The recent emphasis on the intracellular biology of APP and Aß has led some investigators to consider the possibility that intraneuronal Aß may directly cause toxicity. In this review we will outline current knowledge of the localization of both intracellular and extracellular Aß.
  • Publication
    Open Access
    Influence of light-dark, seasonal and lunar cycles on the nuclear size of the pinealocytes of the rat
    (Murcia : F. Hernández, 2002) Martínez Soriano, F.; Armañanzas, E.; Ruíz Torner, A.; Valverde-Navarro, A.A.
    Morphological and physiological studies suggest a possible division of the pineal parenchyma into an external or “cortical” and another central or “medullar” layer. We have studied the possible influence of the light/dark, seasonal and lunar cycles on the nuclear size of the pinealocytes of the rat in both the hypothetical “cortical” and “medullar” layers. Forty male Wistar rats were used. Experiment was carried out in two seasons, winter and spring, two lunar phases, full moon and new moon, and the two circadian phases, photophase and scotophase. The nuclear volume of the pinealocytes, calculated from the Jacobj’s formula, was the karyometric parameter used as measurement of the nuclear size. Main results showed that nuclear volume of the cortical pinealocytes was greater than that of the medullar pinealocytes only during the photophases of winter new-moon days and spring full moon days, whereas in all the remaining situations, the greater nuclear sizes were found in the pinealocytes of the medullar layer. These results support the existence of independent morphological variations of the pinealocyte in the central and peripheral zones of the pineal gland.
  • Publication
    Open Access
    Expression of parathyroid hormone-related protein (PTHrP) in parathyroid tissue under normal and pathological conditions
    (Murcia : F. Hernández, 2002) Kitazawa, R.; Kitazawa, S.; Maeda, S.; Kobayashi, A.
    Parathyroid hormone-related protein (PTHrP), a factor responsible for malignancy associated hypercalcemia, plays a physiological roles such as bone development and placental calcium transport. The expression of PTHrP in adult human parathyroid tissues under normal and pathological conditions was analyzed. By immunohistochemistry, PTHrP expression was detected in 86% of normal parathyroid (12/14 cases), 74% of adenomas (14/19) and 89% of hyperplasia secondary to chronic renal failure (16/18). PTHrP protein was observed mainly in the cytoplasm of oxyphil cells, consistent with the localization of its mRNA demonstrated by in situ hybridization. The rate of PTHrP-positive cells was higher in areas consisting of oxyphil cells than in those of non-oxyphil cells, regardless of whether the parathyroid was normal or pathological. In the normal parathyroid, an age-related increase in PTHrP expression was observed with a relative increase in oxyphil cells, reflecting aging and deterioration of parathyroid tissue. In adenoma, cases with a predominance of oxyphil cells expressed PTHrP, whereas clear cell adenoma did not. In secondary hyperplasia, the rate of PTHrP-expressing cells was higher than in normal parathyroid or adenoma, with varying levels of expression among nodules. We speculate that PTHrP could act through the paracrine/ autocrine mechanism to regulate proliferation and d i fferentiation of normal and neoplastic parathyroid cells.