RESUMO
The Bispectral Index (BIS) has been widely utilized to monitor patients' levels of consciousness during anesthesia. Despite its practicality and prevalence, BIS monitors have been reported to show erroneous readings due to various factors that interfere with the proper reading of the brain's electrical activity. We present a case where the BIS monitor misinterpreted the patient's cardiac activity as her neural activity and resulted in a falsely elevated BIS number despite proper placement and lack of underlying patient medical condition, including neurological injury. It is crucial to remain vigilant about monitoring and understanding BIS readings to assess patients' awareness and effectiveness of anesthesia properly.
RESUMO
Mitochondrial dysfunction can increase oxidative stress and extend lifespan in Caenorhabditis elegans. Homeostatic mechanisms exist to cope with disruptions to mitochondrial function that promote cellular health and organismal longevity. Previously, we determined that decreased expression of the cytosolic pentose phosphate pathway (PPP) enzyme transaldolase activates the mitochondrial unfolded protein response (UPRmt) and extends lifespan. Here we report that transaldolase (tald-1) deficiency impairs mitochondrial function in vivo, as evidenced by altered mitochondrial morphology, decreased respiration, and increased cellular H2O2 levels. Lifespan extension from knockdown of tald-1 is associated with an oxidative stress response involving p38 and c-Jun N-terminal kinase (JNK) MAPKs and a starvation-like response regulated by the transcription factor EB (TFEB) homolog HLH-30. The latter response promotes autophagy and increases expression of the flavin-containing monooxygenase 2 (fmo-2). We conclude that cytosolic redox established through the PPP is a key regulator of mitochondrial function and defines a new mechanism for mitochondrial regulation of longevity.
