Keys to capturing the returning patient.
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Cynthia Hughes
Publications and source records attributed to Cynthia Hughes.
Oligomeric Bax is a component of the putative cytochrome c release channel MAC, mitochondrial apoptosis-induced channel.
Bcl-2 family proteins regulate apoptosis, in part, by controlling formation of the mitochondrial apoptosis-induced channel (MAC), which is a putative cytochrome c release channel induced early in the intrinsic apoptotic pathway. This channel activity was never observed in Bcl-2-overexpressing cells. Furthermore, MAC appears when Bax translocates to mitochondria and cytochrome c is released in cells dying by intrinsic apoptosis. Bax is a component of MAC of staurosporine-treated HeLa cells because MAC activity is immunodepleted by Bax antibodies. MAC is preferentially associated with oligomeric, not monomeric, Bax. The single channel behavior of recombinant oligomeric Bax and MAC is similar. Both channel activities are modified by cytochrome c, consistent with entrance of this protein into the pore. The mean conductance of patches of mitochondria isolated after green fluorescent protein-Bax translocation is significantly higher than those from untreated cells, consistent with onset of MAC activity. In contrast, the mean conductance of patches of mitochondria indicates MAC activity is present in apoptotic cells deficient in Bax but absent in apoptotic cells deficient in both Bax and Bak. These findings indicate Bax is a component of MAC in staurosporine-treated HeLa cells and suggest Bax and Bak are functionally redundant as components of MAC.
Apoptosis↗
Quality of life in psychogenic nonepileptic seizures.
PURPOSE: Psychogenic nonepileptic seizures (PNESs) are events that alter or seem to alter the neurologic function and, in their appearance, resemble epileptic seizures (ESs). In patients with ESs the psychological and medical aspects of epilepsy greatly influence the health-related quality of life (HRQOL). The relation between these factors and PNESs is not well established. In this study, we compared HRQOL in patients with PNESs with that of patients with ESs. METHODS: We evaluated 105 patients admitted to the Epilepsy Monitoring Unit of University Hospital between January 20, 2001, and January 20, 2002. Only patients with the definite diagnosis of ESs or PNESs were analyzed (n = 85). Patients completed an epilepsy-specific quality-of-life instrument (QOLIE-89), the Profile of Mood States (POMS), and Adverse Events Profile (AEP). We used t tests and regression analyses to contrast HRQOL in PNESs and ESs and to elucidate the main factors associated with HRQOL in patients with PNESs. RESULTS: In our sample, 45 patients had PNESs, and 40 had ESs. The overall HRQOL and scores on 13 of 19 QOLIE-89 subscales were significantly lower (i.e., worse) in PNES than in ES patients. AEP and scores on five of six POMS subscales also were worse in PNES patients than in ES patients. PNES versus ES diagnosis, POMS depression/dejection, and AEP were significant predictors of HRQOL, jointly explaining 65% variation in HRQOL. The lower HRQOL in PNESs versus ESs was in part explained by depression and AEP. CONCLUSIONS: Patients with PNESs have a lower HRQOL and worse mood problems than do patients with ESs. This disadvantage is primarily due to depression and medication side effects, although these factors influence QOL in much the same way in PNES and ES patients. These baseline HRQOL data on patients with PNESs can be used to evaluate the effects of treatment in this patient population.
Adult↗