Biomedical subjects

Trinidad Marchal

Publications and source records attributed to Trinidad Marchal.

4 recordsLinked to original sources

PubMed2006

[Diffuse cutaneous reticulohistiocytosis].

The reticulohistiocytoses make up a heterogeneous group of diseases whose origin lies in an accumulation of cells of histiocytic lineage in different tissues and primarily in the skin. Three main clinical forms have been described (multicentric, solitary, diffuse cutaneous), which present with identical histological, ultrastructural and immunohistochemical characteristics. We present a case of diffuse cutaneous reticulohistiocytosis, which is the least common clinical pattern in the spectrum of this disease.

Biopsy↗

PubMed2005

Melatonin prevents experimental liver cirrhosis induced by thioacetamide in rats.

Liver cirrhosis is a critical stage of chronic liver diseases that can produce liver failure, portal hypertension and hepatocarcinoma. Sustained oxidative stress plays a key role in cell damage and fibrosis induced during liver cirrhosis. We evaluated the effect of oxidative stress regulation by melatonin on the development of parenchymal destruction and stellate cell activation in experimental liver cirrhosis. Melatonin was administered to rats with liver cirrhosis induced by thioacetamide (TAA) for 1 or 3 months. Liver injury was assessed by serological analysis, as well as hematoxylin-eosin staining and the in situ apoptosis detection assay in liver sections. Oxidative stress was evaluated by lipoperoxide and reduced glutathione levels, and by the measurement of catalase and superoxide dismutase activities in liver and serum respectively. The activation of stellate cells was evaluated by alpha-smooth muscle actin expression in liver sections. Our results showed that TAA induced oxidative stress with extensive tissue damage and enhanced alpha-smooth muscle actin expression in liver. Melatonin prevented the oxidative stress-related changes associated with TAA toxicity. In conclusion, the study showed that melatonin prevents the tissue damage and fibrosis associated with TAA-induced liver cirrhosis in rats.

Animals↗

PubMed2004

Melatonin prevents oxidative stress and hepatocyte cell death induced by experimental cholestasis.

The induction of oxidative stress precedes liver injury during experimental obstructive jaundice (OJ). In this sense, different evidences suggest that melatonin (MEL), as antioxidant, may be useful in the protection against apoptosis and necrosis during experimental cholestasis. In addition, we will also assess if MEL-dependent protection is related to a recovery of antioxidant status disturbances induced by OJ. Cholestasis was achieved by double ligature and sectioning of the principal bile duct. MEL was injected intraperitoneally (500 microg/kg/day). Lipid peroxidation was evaluated by the measurement of malondialdehyde (MDA) content in liver. Different parameters related to antioxidant status, such as reduced glutathione (GSH), glutathione peroxidase (GPx), catalase and superoxide dismutase (SOD) were determined in liver. Liver injury was assessed by alanine amino-transferase (ALT) in serum, histological examination, DNA fragmentation and TUNEL assay. The activation of perisinusoidal stellate cells was evaluated by immunohistochemical measurement of alpha-smooth muscle actin in liver sections. The induction of OJ increased all the parameters related to apoptosis and necrosis in liver. The induction of liver injury was associated with stellate cell activation, as well as an increase in MDA (p < 0.0001) and a reduction in GSH, GPx, catalase and SOD content (p < 0.0001) in liver. MEL reduced hepatic apoptosis and necrosis (p < 0.004) with a significant improvement in all oxidative stress markers. In conclusion, our results showed that MEL recovered the antioxidant status and reduced apoptosis and necrosis induced by experimental cholestasis.

Animals↗

PubMed2002

Influence of marginal donors on liver preservation injury.

PURPOSE: The purpose of this study was to assess the accumulated effects of marginal donor quality factors on liver preservation injury (LPI). METHODS: The most recent 400 consecutive liver transplantations at our institution were reviewed. Marginal liver donor criteria included the following: older than 60 years, an intensive care unit stay under ventilatory support for more than 4 days, a cold ischemia time more than 14 hr, high inotropic drug use, prolonged hypotensive episodes for more than 1 hr and less than 60 mm Hg, a peak serum sodium more than 155 mEq/L, and high levels of bilirubin, alanine transferase, or amino transferase. The type of steatosis (macrovesicular or microvesicular) was quantified in four categories: no steatosis, mild (<30%), moderate (30-60%), and severe (> 60%). LPI was stratified histologically in four levels: no damage, mild, moderate, and severe injury. These variables were included in a logistic regression analysis for prediction of the probability of the appearance of LPI. RESULTS: Five variables showed an independent influence on LPI: high inotropic drug use (odds ratio [OR]=1.56), donor age (OR=1.017 per year), moderate to severe macrovesicular steatosis (OR=3.63), cold ischemia time (OR=1,109 per hour), and prolonged stay in an intensive care unit (OR=1.79). Severe LPI was present in 32.7% of the grafts from donors without any factor of the model; in 46.8% from donors with one factor (P =0.09); in 66.2% from donors with two factors (P =0.006); and in 78.3% from donors with at last three factors (P =0.002) (global P=0.0001; chi2 =21.8). CONCLUSIONS: LPI can be potentially predicted based on donor and graft conditions. Accumulation of factors is correlated with an increased effect on LPI.

Adult↗