Packages of Care for Epilepsy in Low- and Middle-Income Countries

In the second in a series of six articles on packages of care for mental health disorders in low- and middle-income countries, Caroline Mbuba and Charles Newton discuss treatment for epilepsy

The Eleventh and Twelfth Data Releases of the Sloan Digital Sky Survey: Final Data from SDSS-III

The third generation of the Sloan Digital Sky Survey (SDSS-III) took data from 2008 to 2014 using the original SDSS wide-field imager, the original and an upgraded multi-object fiber-fed optical spectrograph, a new near-infrared high-resolution spectrograph, and a novel optical interferometer. All of the data from SDSS-III are now made public. In particular, this paper describes Data Release 11 (DR11) including all data acquired through 2013 July, and Data Release 12 (DR12) adding data acquired through 2014 July (including all data included in previous data releases), marking the end of SDSS-III observing. Relative to our previous public release (DR10), DR12 adds one million new spectra of galaxies and quasars from the Baryon Oscillation Spectroscopic Survey (BOSS) over an additional 3000 deg2 of sky, more than triples the number of H-band spectra of stars as part of the Apache Point Observatory (APO) Galactic Evolution Experiment (APOGEE), and includes repeated accurate radial velocity measurements of 5500 stars from the Multi-object APO Radial Velocity Exoplanet Large-area Survey (MARVELS). The APOGEE outputs now include the measured abundances of 15 different elements for each star. In total, SDSS-III added 5200 deg2 of ugriz imaging; 155,520 spectra of 138,099 stars as part of the Sloan Exploration of Galactic Understanding and Evolution 2 (SEGUE-2) survey; 2,497,484 BOSS spectra of 1,372,737 galaxies, 294,512 quasars, and 247,216 stars over 9376 deg2; 618,080 APOGEE spectra of 156,593 stars; and 197,040 MARVELS spectra of 5513 stars. Since its first light in 1998, SDSS has imaged over 1/3 of the Celestial sphere in five bands and obtained over five million astronomical spectra. \ua9 2015. The American Astronomical Society

Inhibition of protein ubiquitination by paraquat and 1-methyl-4-phenylpyridinium impairs ubiquitin-dependent protein degradation pathways

Intracytoplasmic inclusions of protein aggregates in dopaminergic cells (Lewy bodies) are the pathological hallmark of Parkinson’s disease (PD). Ubiquitin (Ub), alpha [α]-synuclein, p62/sequestosome 1 and oxidized proteins are major components of Lewy bodies. However, the mechanisms involved in the impairment of misfolded/oxidized protein degradation pathways in PD are still unclear. PD is linked to mitochondrial dysfunction and environmental pesticide exposure. In this work, we evaluated the effect of the pesticide paraquat (PQ) and the mitochondrial toxin 1-methyl-4-phenylpyridinium (MPP+) on Ub-dependent protein degradation pathways. No increase in the accumulation of Ub-bound proteins or aggregates was observed in dopaminergic cells (SK-N-SH) treated with PQ or MPP+, or in mice chronically exposed to PQ. PQ decreased Ub protein content, but not its mRNA transcription. Protein synthesis inhibition with cycloheximide depleted Ub levels and potentiated PQ–induced cell death. Inhibition of proteasomal activity by PQ was found to be a late event in cell death progression, and had no effect on either the toxicity of MPP+ or PQ, or the accumulation of oxidized sulfenylated, sulfonylated (DJ-1/PARK7 and peroxiredoxins) and carbonylated proteins induced by PQ. PQ- and MPP+-induced Ub protein depletion prompted the dimerization/inactivation of the Ub-binding protein p62 that regulates the clearance of ubiquitinated proteins by autophagic. We confirmed that PQ and MPP+ impaired autophagy flux, and that the blockage of autophagy by the overexpression of a dominant-negative form of the autophagy protein 5 (dnAtg5) stimulated their toxicity, but there was no additional effect upon inhibition of the proteasome. PQ induced an increase in the accumulation of α-synuclein in dopaminergic cells and membrane associated foci in yeast cells. Our results demonstrate that inhibition of protein ubiquitination by PQ and MPP+ is involved in the dysfunction of Ub-dependent protein degradation pathways

Incidence rate of Aneurysmal SAH in Gwangju City and Jeollanamdo Province in 2007

Objective : The incidence of subarachnoid hemorrhage (SAH) worldwide varies considerably. In spite of many reports about the incidence of SAH, there has been no report about the incidence of SAH on the basis of the Korean population. The purpose of this hospital-based study was to assess the actual incidence rates of aneurysmal SAH in Gwangju city and Jeollanamdo province. Methods : All cases of SAH confirmed by computerized tomography (CT) between January 2007 and December 2007 were selected for analysis. For the data collection, three major training hospital and ten general hospitals working the CT in Gwangju city and four major general hospitals in Jeollanamdo province participate in this study. Results : According to the official census of Korea, the population was 1,413,444 in Gwangju city and 1,929,836 in Jeollanamdo province in 2007. There were 163 patients in Gwangju city and 266 patients in Jeollanamdo province confirmed SAH by CT in 2007. The crude and the age- and sex-adjusted annual incidence rates per 100,000 population for all ages in Gwangju city were 11.5 and 12.4 for aneurysmal SAH and in Jeollanamdo province were 13.8 and 10.8. The incidence was higher in women and increased with age. The gender distribution varied with age. At young ages, the incidence was higher in men while after the age of 40 years, the incidence was higher in women. Conclusion : In the present study, the age- and sex-adjusted annual incidence rates is 11.8 in Gwangju city and Jeollanamdo province. The incidence was higher in women and increased with age.de Rooij NK, 2007, J NEUROL NEUROSUR PS, V78, P1365, DOI 10.1136/jnnp.2007.117655Rothwell PM, 2004, LANCET, V363, P1925Corbin DOC, 2004, STROKE, V35, P1254, DOI 10.1161/01.STR.0000127371.24658.dfHamada J, 2004, NEUROSURGERY, V54, P31HAMADA J, 2004, NEUROSURGERY, V54, P37Broderick JP, 2003, STROKE, V34, P1375, DOI 10.1161/01.STR.0000074572.91827.F4Feigin VL, 2003, LANCET NEUROL, V2, P43Ohkuma H, 2002, STROKE, V33, P195Weir B, 2002, J NEUROSURG, V96, P3Ruigrok YM, 2001, STROKE, V32, P1173Inagawa T, 2000, J NEUROSURG, V93, P9582000, STROKE, V31, P1843Inagawa T, 1997, SURG NEUROL, V47, P47INAGAWA T, 1997, SURG NEUROL, V47, P52Numminen H, 1996, STROKE, V27, P1487INAGAWA T, 1995, STROKE, V26, P761