Publications by authors named "Maria E Biancardi"

Background: the shortage of donors of hepatocyte transplantation therapy led to the use of so-called marginal donors. Some donors may have a hepatic illnesses that is associated with hepatic preneoplasia with foci of altered hepatocytes (FAH).

Aims: to determine whether recipients developed FAH upon transplantation with hepatocytes from a preneoplastic liver and whether FAH progresses to a preneoplastic hepatocyte-derived tumor (PHDT), up to 60 days after transplantation.

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Background: One established model to induce hepatic preneoplasia (HP) (DEN 150) uses diethylnitrosamine (DEN) as initiator agent and 2-acetylaminofluorene (2-AAF) as a promoter drug. In addition, both chemicals cause liver cholestasis and fibrosis.

Aim: We compared DEN 150 model with another adapted by us, DEN 200 to simplify the first one and to evaluate the effectiveness of both treatments to induce HP in rats.

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Human cardiac valve allografts (HVAs) suffer injuries during the cryopreservation period. Here, we described structural, ultrastructural and functional damages suffered by HVAs after an increment of their cryostorage temperature (100 degree C). Two experimental groups of pulmonary and aortic HVAs were compared: cryopreserved (HVAcryo) and cryopreserved with temperature changes (HVAΔT).

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Cryopreserved human cardiac valve allografts could suffer lethal damages if the temperature is elevated during cryostorage. This work describes the functional and morphological alterations suffered by human cardiac valve allografts after a gradual increment of the cryostorage temperature from -147 degrees C to -47 degrees C due to a technical failure. Three experimental groups of human pulmonary and aortic allografts were compared: fresh, cryopreserved (-147 degrees C) and cryopreserved with temperature changes from -147 degrees C up to -47 degrees C and back to -147 degrees C.

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As vanadium was found to induce oxidative stress in the central nervous system, the morphological alterations of neurons and astroglial cells in adult rat central nervous system after vanadium exposure was studied, using histological markers of cellular injury. Animals were intraperitoneally injected with 3 mg/kg body weight of sodium metavanadate for 5 consecutive days. NADPH diaphorase histochemistry and heat shock protein (hsp) 70, glial fibrillary acidic protein (GFAP), and S-100 immunohistochemistry were performed in floating sections of several brain areas.

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In the present work we show morphological data of the in vivo susceptibility of CNS myelin to sodium metavanadate [V(+5)] in adult rats. The possible role of vanadium in behavioral alterations and in brain lipid peroxidation was also investigated. Animals were injected intraperitoneally (i.

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