Necrotic stomatitis in a dolphin.

Necrotic stomatitis of undetermined etiology was found in an Atlantic bottlenosed dolphin, Tursiops truncatus. The case history, treatment and hematologic findings are described. The animal remained anorectic throughout the course of the illness, and was force fed on a daily basis for approximately 5 weeks.     

Necrotic death pathway in Fas receptor signaling

A caspase 8-deficient subline (JB6) of human Jurkat cells can be killed by the oligomerization of Fas-associated protein with death domain (FADD). This cell death process is not accompanied by caspase activation, but by necrotic morphological changes. Here, we show that the death effector domain of FADD is responsible for the FADD-mediated necrotic pathway. This process was accompanied by a loss of mitochondrial transmembrane potential (DeltaPsim), but not by the release of cytochrome c from mitochondria. Pyrrolidine dithiocarbamate, a metal chelator and antioxidant, efficiently inhibited the FADD-induced reduction of DeltaPsim and necrotic cell death. When human Jurkat, or its transformants, expressing mouse Fas were treated with Fas ligand or anti-mouse Fas antibodies, the cells died, showing characteristics of apoptosis. A broad caspase inhibitor (z-VAD-fmk) blocked the apoptotic morphological changes and the release of cytochrome c. However, the cells still died, and this cell death process was accompanied by a strong reduction in DeltaPsim, as well as necrotic morphological changes. The presence of z-VAD-fmk and pyrrolidine dithiocarbamate together blocked cell death, suggesting that both apoptotic and necrotic pathways can be activated through the Fas death receptor.     

Necrotic tumor growth: an analytic approach

The present paper deals with a free boundary problem modeling the growth process of necrotic multi-layer tumors. We prove the existence of flat stationary solutions and determine the linearization of our model at such an equilibrium. Finally, we compute the solutions of the stationary linearized problem and comment on bifurcation.     

Studies on Apple Canker Disease. The Necrotic Toxins Produced by Valsa ceratosperma

Several metabolites responsible for the toxic manifestations of Valsa ceratosperma (Toda et Fries) Maire, a phytopathogenic fungus of the Japanese apple canker, have been isolated from its culture filtrate after growth on apple branch extract. Chemical and spectrometric studies revealed the products to be degradation products of phlorizin which is a dominant component distributed in leaves, stems, fruits and roots of apple. The toxic substances were identified as 3-(p-hydroxyphenyl) propionic acid, phloroglucinol, p-hydroxyacetophenone, p-hydroxybenzoic acid and protocatechuic acid. All of these compounds except p-hydroxyacetophenone were detected in the lesions of apple trees infected by V. ceratosperma. The fungus cultivated in a medium containing added phlorizin also produced the five toxic substances mentioned above. These results suggest that phlorizin is involved in the specific relationship between the host and the pathogen, indicating that the degradation products of phlorizin play important roles in the production of symptoms of infected apple trees.     

Necrotic patches affect Acropora palmata (Scleractinia: Acroporidae) in the Mexican Caribbean.

An outbreak of necrotic patches was observed affecting Acropora palmata in the Mexican Caribbean in the summer of 1999. This study documents the tissue loss produced by these patches. Following a marked initial increase in the number of patches, there was a decrease in the appearance of new patches but the size of the patches increased throughout the study. In some cases patches expanded but in most cases they enlarged due to fusion of 2 or more patches. Patches recovered but not sufficiently to overcome damage in most colonies surveyed. Percentage tissue loss does not appear to be directly related to temperature but may be related to a combination of factors associated with prolonged summer doldrum-like conditions. The necrotic patch syndrome can have a substantial impact in tissue loss in affected A. palmata colonies.     

Necrotic volume increase and the early physiology of necrosis

Whether a lethally injured mammalian cell undergoes necrosis or apoptosis may be determined by the early activation of specific ion channels at the cell surface. Apoptosis requires K+ and Cl- efflux, which leads to cell shrinking, an active phenomenon termed apoptotic volume decrease (AVD). In contrast, necrosis has been shown to require Na+ influx through membrane carriers and more recently through stress-activated non-selective cation channels (NSCCs). These ubiquitous channels are kept dormant in viable cells but become activated upon exposure to free-radicals. The ensuing Na+ influx leads to cell swelling, an active response that may be termed necrotic volume increase (NVI). This review focuses on how AVD and NVI become conflicting forces at the beginning of cell injury, on the events that determine irreversibility and in particular, on the ion fluxes that decide whether a cell is to die by necrosis or by apoptosis.     

Anthranilate Fluorescence Marks a Calcium-Propagated Necrotic Wave That Promotes Organismal Death in C. elegans

For cells the passage from life to death can involve a regulated, programmed transition. In contrast to cell death, the mechanisms of systemic collapse underlying organismal death remain poorly understood. Here we present evidence of a cascade of cell death involving the calpain-cathepsin necrosis pathway that can drive organismal death in Caenorhabditis elegans. We report that organismal death is accompanied by a burst of intense blue fluorescence, generated within intestinal cells by the necrotic cell death pathway. Such death fluorescence marks an anterior to posterior wave of intestinal cell death that is accompanied by cytosolic acidosis. This wave is propagated via the innexin INX-16, likely by calcium influx. Notably, inhibition of systemic necrosis can delay stress-induced death. We also identify the source of the blue fluorescence, initially present in intestinal lysosome-related organelles (gut granules), as anthranilic acid glucosyl esters—not, as previously surmised, the damage product lipofuscin. Anthranilic acid is derived from tryptophan by action of the kynurenine pathway. These findings reveal a central mechanism of organismal death in C. elegans that is related to necrotic propagation in mammals—e.g., in excitotoxicity and ischemia-induced neurodegeneration. Endogenous anthranilate fluorescence renders visible the spatio-temporal dynamics of C. elegans organismal death.