Signal pathway responsible for hepatocyte preconditioning by nitric oxide.

Nitric oxide (NO) improves liver resistance to hypoxia/reperfusion injury acting as a mediator of hepatic preconditioning. However, the mechanisms involved are still poorly understood. In this study, we have investigated the mechanisms by which short-term exposure to the NO donor (Z)-1-(N-methyl-N-[6-(N-methylammoniohexyl)amino])-diazen-1-ium-1,2-diolate (NOC-9) increases hepatocyte tolerance to hypoxic injury.

Modified S-plasty: an alternative to the elliptical excision to reduce the length of suture.

Background: When the tension obtainable with an elliptical excision of a skin lesion would be excessive, instead of resorting to skin grafts or flaps, it is possible to apply an alternative plastic that reduces the length of the suture by approximately one third and assumes a curved lazy-S profile, also improving aesthetic result.

Methods: This is obtained with a modified shortened S-plasty, which distributes the vectors of tension in two different directions at the apices and in the central part. The traction on the suture line is reduced, facilitating wound healing.

Signal pathway involved in the development of hypoxic preconditioning in rat hepatocytes.

Ischemic preconditioning improves liver resistance to hypoxia and reduces reperfusion injury following transplantation. However, the intracellular signals that mediate the development of liver hypoxic preconditioning are largely unknown. We have investigated the signal pathway leading to preconditioning in freshly isolated rat hepatocytes.

Ethanol potentiates hypoxic liver injury: role of hepatocyte Na(+) overload.

Centrilobular hypoxia has been suggested to contribute to hepatic damage caused by alcohol intoxication. However, the mechanisms involved are still poorly understood. We have investigated whether alterations of Na(+) homeostasis might account for ethanol-mediated increase in hepatocyte sensitivity to hypoxia.

Hormonal modulation of GM-CSF receptor alpha-chain in in vitro models of endometrial cancer.

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a cytokine that stimulates the proliferation and differentiation of bone marrow progenitors. Moreover, the presence and activity of GM-CSF and its receptor (GM-CSF-r) has been documented on tissues and cell lines of a non-hemopoietic origin. In this paper we studied the expression and putative role of GM-CSF and GM-CSF-r in endometrial cancer.

Alterations of Na(+) homeostasis in hepatocyte reoxygenation injury.

Reperfusion injury represents an important cause of primary graft non-function during liver transplantation. However, the mechanism responsible for cellular damage during reoxygenation has not yet been completely understood. We have investigated whether changes in intracellular Na(+) distribution might contribute to cause hepatocyte damage during reoxygenation buffer after 24 h of cold storage.

CD44 signaling through p56lck involves lateral association with CD4 in human CD4+ T cells.

CD44 is a family of mucin-like membrane proteins generated by alternative splicing of several exons, and participate in T cell adhesion and activation. CD44-mediated signaling involves activation of p56(lck) and leads to ZAP-70 phosphorylation. The aim of the present study was to identify the signaling pathways that follow CD44-triggered ZAP-70 phosphorylation and the molecular mechanisms underlying the CD44 interaction with p56(lck).

Hydroxyethyl radicals in ethanol hepatotoxicity.

Alcoholic patients and experimental animals exposed to ethanol display biochemical signs of oxidative damage, suggesting a possible role of free radicals in causing some of the toxic effects of alcohol. The use of electron spin resonance (ESR) spectroscopy associated with spin trapping technique has demonstrated that hydroxyethyl radicals are generated during ethanol metabolism by the microsomal monoxygenase system, involving the alcohol-inducible cytochrome P450 2E1 (CYP2E1). Recent observations in rats fed intragastrically with a high fat diet containing ethanol indicate that the formation of hydroxyethyl radicals is associated with stimulation of lipid peroxidation and development of liver damage.