Predictors of unprovoked seizure after febrile seizure: short-term outcomes
INTRODUCTION/BACKGROUND:We performed this study to confirm the known risk factors and to identify possible new risk factors for subsequent unprovoked seizure after febrile seizure (FS) on Jeju Island, South Korea. METHODS:A population-based retrospective study of 204 children with FS, whose first FS developed between March 2003 and August 2011, and who were seen in the Pediatric Department at the Jeju National University Hospital. RESULTS:Two hundred four children (136 boys and 68 girls) were enrolled in this study. Simple FS was found in 107 children, and complex FS was found in 97 children. The average age at the first FS was 18.9 months. The average total number of FSs was 4.3. A family history of FS or epilepsy was found in 29.4% and 7.8% of patients, respectively. Abnormal findings of EEG were observed in 35.8%. Complex features in the first FS were noted in 28.9%. Subsequent unprovoked seizures occurred in 23.0%. Univariate analysis showed that low parental educational level was one of several variables that were significantly related to unprovoked seizure. Parental educational level was not included in the multivariate model because of an insufficient sample size. Multivariate analysis identified the following factors as significant predictors of unprovoked seizure: late onset of FS at age>3 years, complex features in the first FS, family history of epilepsy, and abnormal findings on EEG, and FS developed at a body temperature of <39Â°C. CONCLUSIONS:We confirmed the known risk factors for subsequent unprovoked seizure and found that low parental educational status may be a new prognostic indicator. However, further investigation using larger populations and a prospective design is needed to confirm that this is a valid prognostic factor for FS.
hMTH1 depletion promotes oxidative-stress-induced apoptosis through a Noxa- and caspase-3/7-mediated signaling pathway
Although the accumulation of 8-oxo-dGTP in DNA is associated with apoptotic cell death and mutagenesis, little is known about the exact mechanism of hMTH1-mediated suppression of oxidative-stress-induced cell death. Therefore, we investigated the regulation of DNA-damage-related apoptosis induced by oxidative stress using control and hMTH1 knockdown cells. Small interfering RNA (siRNA) was used to suppress hMTH1 expression in p53-proficient GM00637 and H460 cells, resulting in a significant increase in apoptotic cell death after H(2)O(2) exposure; however, p53-null, hMTH1-deficient H1299 cells did not exhibit H(2)O(2)-induced apoptosis. In addition, hMTH1-deficient GM00637 and H460 cells showed increased caspase-3/7 activity, cleaved caspase-8, and Noxa expression, and gamma-H2AX formation in response to H(2)O(2). In contrast, the caspase inhibitors, p53-siRNA, and Noxa-siRNA suppressed H(2)O(2)-induced cell death. Moreover, in 8-week (long-term) cultured H460 and H1299 cells, hMTH1 suppression increased cell death, Noxa expression, and gamma-H2AX after H(2)O(2) exposure, compared to 3-week (short-term) cultured cells. These data indicate that hMTH1 plays an important role in protecting cells against H(2)O(2)-induced apoptosis via a Noxa- and caspase-3/7-mediated signaling pathway, thus conferring a survival advantage through the inhibition of oxidative-stress-induced DNA damage.
Immunohistochemical detection of StarD6 in the rat nervous system
Steroidogenic acute regulatory (StAR)-related lipid transfer (START) domain 6 (StarD6) is known to be exclusively expressed in germ cells of testis. As little is known about StarD6 expression in the nervous system, we investigated the distribution of StarD6 in rat neural tissues. Immunoreactivity of StarD6 was detected in the brain, spinal cord and dorsal root ganglia; particularly cerebral cortex (layer V and VI), hippocampus, substantia gelatinosa of the spinal cord. We provided compelling evidence that multiple neuronal and glial populations were immunolabelled with anti-StarD6 antibody throughout the nervous system. We postulate that StarD6 might play an important role in lipid sensing of the nervous system based on its immunolocalization in this study.
Do benzodiazepines extend the duration of follow-up treatment in patients with bipolar disorder?
INTRODUCTION/BACKGROUND:In patients with bipolar disorder, relapse and recurrence from the premature discontinuation of pharmacotherapy are serious clinical problems. Thus, clinicians must make every effort to ensure the sufficient duration of continual treatment even after the remission of acute episodes. Here, we examine whether there is any association between benzodiazepine (BZD) use and the duration of follow-up treatment in patients with bipolar disorder. METHODS:The medical records of 70 bipolar patients hospitalized in a university hospital psychiatry ward were reviewed. Selected demographic and clinical variables, such as extent of BZD use and the total duration of outpatient follow-up treatment, were compared. RESULTS:The duration of maintenance treatment at the outpatient department differed significantly between patients who were or were not given BZDs during admission (571 vs. 179 days) and after discharge (836 vs. 154 days). The variables that differed significantly between patients who received follow-up treatment for 6 or more months and those who did not was the number of days of BZD administration during admission (11 vs. 5 days) and after discharge (280 vs. 7 days), and years of education (11 vs. 13 years). CONCLUSION/CONCLUSIONS:In the present study, BZDs are suggested as a possible adjunctive therapy for extending follow-up and thus preventing recurrence in patients with bipolar disorder.