[Paraneoplastic opsoclonus-myoclonus syndrome].

Opsoclonus-myoclonus syndrome (OMS) is a rare neurological disorder characterized by a combination of main symptoms: opsoclonus, myoclonus, ataxia, psychoemotional and behavioral disturbances. OMS can develop in children as a result of immunopathological processes against the background of infectious or oncological pathology and lead to persistent neurological deficit. A case of ten-year observation of paraneoplastic OMS associated with neuroblastoma in a child is presented.

The role of flavin-containing enzymes in mitochondrial membrane hyperpolarization and ROS production in respiring Saccharomyces cerevisiae cells under heat-shock conditions.

Heat shock is known to accelerate mitochondrial ROS production in Saccharomyces cerevisiae cells. But how yeast mitochondria produce ROS under heat-shock condition is not completely clear. Previously, it was shown that ROS production in heat-stressed fermenting yeast cells was accompanied by mitochondrial membrane potential (MMP) increase.

Relation between cell death progression, reactive oxygen species production and mitochondrial membrane potential in fermenting Saccharomyces cerevisiae cells under heat-shock conditions.

Moderate heat shock increased reactive oxygen species (ROS) production that led to cell death in glucose-grown Saccharomyces cerevisiae cells. Conditions that disturb mitochondrial functions such as treatment by uncouplers and petite mutation were shown to inhibit ROS production and protects cell from thermal death. Hence, mitochondria are responsible for ROS production and play an active role in cell death.

[Induction of Hsp104 synthesis in Saccharomyces cerevisiae is inhibited by the petite mutation in the stationary growth phase].

The elevation of Hsp104 (heat shock protein) content under heat shock plays a key role in yeast (Saccharomyces cerevisiae) cells. Hsp104 synthesis is increased under heat stress in the stationary growth phase. As shown, the loss of mitochondrial DNA (petite mutation) inhibited the induction of the Hsp104 synthesis under heat stress (39 degrees C) during the transition to the stationary growth phase.

Mechanism of Saccharomyces cerevisiae yeast cell death induced by heat shock. Effect of cycloheximide on thermotolerance.

The mechanism of yeast cell death induced by heat shock was found to be dependent on the intensity of heat exposure. Moderate (45°C) heat shock strongly increased the generation of reactive oxygen species (ROS) and cell death. Pretreatment with cycloheximide (at 30°C) suppressed cell death, but produced no effect on ROS production.