[Surprising diagnosis after suspected appendicitis].

A 12-year-old boy presented at the emergency department because of right-sided abdominal pain. Laboratory findings and ultrasound examination were suggestive of acute appendicitis. During laparoscopy, an indurated omental mass was seen.

Experimental Conditions That Influence the Utility of 2'7'-Dichlorodihydrofluorescein Diacetate (DCFH-DA) as a Fluorogenic Biosensor for Mitochondrial Redox Status.

Oxidative stress has been causally linked to various diseases. Electron transport chain (ETC) inhibitors such as rotenone and antimycin A are frequently used in model systems to study oxidative stress. Oxidative stress that is provoked by ETC inhibitors can be visualized using the fluorogenic probe 2',7'-dichlorodihydrofluorescein-diacetate (DCFH-DA).

Optimal Use of 2',7'-Dichlorofluorescein Diacetate in Cultured Hepatocytes.

Oxidative stress is a state that arises when the production of reactive transients overwhelms the cell's capacity to neutralize the oxidants and radicals. This state often coincides with the pathogenesis and perpetuation of numerous chronic diseases. On the other hand, medical interventions such as radiation therapy and photodynamic therapy generate radicals to selectively damage and kill diseased tissue.

Analysis and Optimization of Conditions for the Use of 2',7'-Dichlorofluorescein Diacetate in Cultured Hepatocytes.

Numerous liver pathologies encompass oxidative stress as molecular basis of disease. The use of 2',7'-dichlorodihydrofluorescein-diacetate (DCFH-DA) as fluorogenic redox probe is problematic in liver cell lines because of membrane transport proteins that interfere with probe kinetics, among other reasons. The properties of DCFH-DA were analyzed in hepatocytes (HepG2, HepaRG) to characterize methodological issues that could hamper data interpretation and falsely skew conclusions.

The damage-associated molecular pattern HMGB1 is released early after clinical hepatic ischemia/reperfusion.

Objective And Background: Activation of sterile inflammation after hepatic ischemia/reperfusion (I/R) culminates in liver injury. The route to liver damage starts with mitochondrial oxidative stress and cell death during early reperfusion. The link between mitochondrial oxidative stress, damage-associate molecular pattern (DAMP) release, and sterile immune signaling is incompletely understood and lacks clinical validation.