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This random-effects model meta-analysis of double-blind, randomized placebo-controlled trials compared recurrence rates in bipolar disorder (BD) patients between antipsychotic/mood stabilizer discontinuation and maintenance groups.
We conducted systematic literature search of Embase, PubMed, and CENTRAL databases without language restriction from inception until 22 May 2020. Independent investigators assessed studies and extracted data. We calculated risk ratios (RRs) and numbers needed to benefit or harm (NNTB/NNTH). Primary outcome was the recurrence rate of any mood episode at 6 months. Secondary outcomes were recurrence rates of depressive episodes and manic/hypomanic/mixed episodes and all-cause discontinuation at 6 months. We also investigated these outcomes at 1, 3, 9, 12, 18, and 24 months.
We identified 22 studies (n = 5462) receiving aripiprazole, asenapine, divalproex, long-acting injectable (LAI)-aripiprazole, LAI-risperidone, lamotrigine, lithium, olanzapine, paliperidone, or quetiapine. Mean study duration was 64.50 ± 69.35 weeks. The maintenance group demonstrated lower recurrence rates of any mood episode, depressive episodes, and manic/hypomanic/mixed episodes as well as reduced all-cause discontinuation at every observational point. The RRs (95% confidence interval, NNTB/NNTH) of recurrence rate at 6 months were 0.61 (0.54–0.70, 5) for any mood episode, 0.72 (0.60–0.87, 13) for depressive episodes, and 0.45 (0.36–0.57, 6) for manic/hypomanic/mixed episodes. The RR for all-cause discontinuation at 6 months was 0.71 (0.61–0.82, 6).
Maintaining drug treatment during clinically stable BD prevented recurrence for up to 24 months. Discontinuation of medications for ⩾1 month significantly increased recurrence risk. However, 47.3% of patients who discontinued drugs for 6 months did not experience recurrence.
Quasi-periodic oscillations (QPOs) are believed to be indirect evidence for black holes. Several authors have reported detections of QPOs from Sgr A*, the nucleus of our Galaxy, in infrared and X-ray wavelength during flare-ups. Miyoshi et al. (2011) reported a tentative detection of QPOs in the 43 GHz light curve of Sgr A* obtained with the Very Long Baseline Array (VLBA). To confirm their detection, we reanalysed their VLBA data very conservatively. The 43 GHz flux was calculated for every 15 seconds by assuming a two-dimensional Gaussian-shape spatial structure. The Lomb-Scargle periodogram of the 43 GHz flux just after a millimeter wave flare of Sgr A*, shows three apparent peaks at 10.2, 14.6 and 32.1 min. Two of them are barely consistent with the previously reported QPOs. Using the resonant oscillation model, we estimated the spin parameter of the Sgr A* black hole to be 0.56 assuming the mass of 4.3 × 106M⊙.
In this paper, the effect of shock compression on the synthesis of a Bi-based oxide superconductor was investigated. Bi1.85-Pb0.35-Sr1.90-Ca2.05-Cu3.05-Ox calcined powder was shock-compacted around 20 GPa and 30 GPa, and divided specimens were annealed at 845 °C for 1, 6 and 48 hours. The specimens were evaluated by x-ray diffraction and scanning electron microscope.
The ultrastructure of Betz cells in the 5th layer of the primary motor cortex of 17 neurologically and psychiatrically normal control individuals was studied. Normal-appearing Betz cells showed a wide range of features including novel electron-dense inclusion bodies (Bunina-like bodies) resembling Bunina bodies characteristic of amyotrophic lateral sclerosis (ALS), accumulations of neurofilaments (10 nm in diameter), bundles of filaments (20–25 nm in diameter) thicker than neurofilaments, lamellar structures, lamellar bodies and structures similar to Hirano bodies. Among these ‘abnormal’ features, the presence of Bunina-like bodies may be an age-related nonspecific degenerative change, since they appeared more frequently in elderly individuals. The presence of these abnormal features—particularly the Bunina-like bodies—in the Betz cells of normal human brains must be considered in the assessment of the pathognomonic significance of such structures in ALS and other neurological diseases that affect the motor cortex.
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