First-principles study of the inversion thermodynamics and electronic structure of FeM2X4 (thio)spinels (M = Cr, Mn, Co, Ni; X = O, S)

FeM2X4 spinels, where M is a transition metal and X is oxygen or sulfur, are candidate materials for spin filters, one of the key devices in spintronics. We present here a computational study of the inversion thermodynamics and the electronic structure of these (thio)spinels for M = Cr, Mn, Co, Ni, using calculations based on the density functional theory with on-site Hubbard corrections (DFT+U). The analysis of the configurational free energies shows that different behaviour is expected for the equilibrium cation distributions in these structures: FeCr2X4 and FeMn2S4 are fully normal, FeNi2X4 and FeCo2S4 are intermediate, and FeCo2O4 and FeMn2O4 are fully inverted. We have analyzed the role played by the size of the ions and by the crystal field stabilization effects in determining the equilibrium inversion degree. We also discuss how the electronic and magnetic structure of these spinels is modified by the degree of inversion, assuming that this could be varied from the equilibrium value. We have obtained electronic densities of states for the completely normal and completely inverse cation distribution of each compound. FeCr2X4, FeMn2X4, FeCo2O4 and FeNi2O4 are half-metals in the ferrimagnetic state when Fe is in tetrahedral positions. When M is filling the tetrahedral positions, the Cr-containing compounds and FeMn2O4 are half-metallic systems, while the Co and Ni spinels are insulators. The Co and Ni sulfide counterparts are metallic for any inversion degree together with the inverse FeMn2S4. Our calculations suggest that the spin filtering properties of the FeM2X4 (thio)spinels could be modified via the control of the cation distribution through variations in the synthesis conditions

Using the yes/no recognition response pattern to detect memory malingering

Schindler S, Kißler J, Kühl K-P, Hellweg R, Bengner T. Using the yes/no recognition response pattern to detect memory malingering. BMC Psychology. 2013;1(1): 12.Background Detection of feigned neurocognitive deficits is a challenge for neuropsychological assessment. We conducted two studies to examine whether memory malingering is characterized by an elevated proportion of false negatives during yes/no recognition testing and whether this could be a useful measure for assessment. Methods Study 1 examined 51 participants claiming compensation due to mental disorders, 51 patients with affective disorders not claiming compensation and 13 patients with established dementia. Claimants were sub-divided into suspected malingerers (n = 11) and non-malingerers (n = 40) according to the Test of Memory Malingering (TOMM). In study 2, non-clinical participants were instructed to either malinger memory deficits due to depression (n = 20), or to perform normally (n = 20). Results In study 1, suspected malingerers had more false negative responses on the recognition test than all other groups and false negative responding was correlated with Minnesota-Multiphasic Personality Inventory (MMPI) measures of deception. In study 2, using a cut-off score derived from the clinical study, the number of false negative responses on the yes/no recognition test predicted group membership with comparable accuracy as the TOMM, combining both measures yielded the best classification. Upon interview, participants suspected the TOMM more often as a malingering test than the yes/no recognition test. Conclusion Results indicate that many malingers adopt a strategy of exaggerated false negative responding on a yes/no recognition memory test. This differentiates them from both dementia and affective disorder, recommending false negative responses as an efficient and inconspicuous screening measure of memory malingering

The nucleotide prodrug CERC‐913 improves mtDNA content in primary hepatocytes from DGUOK‐deficient rats

Loss‐of‐function mutations in the deoxyguanosine kinase (DGUOK) gene result in a mitochondrial DNA (mtDNA) depletion syndrome. DGUOK plays an important role in converting deoxyribonucleosides to deoxyribonucleoside monophosphates via the salvage pathway for mtDNA synthesis. DGUOK deficiency manifests predominantly in the liver; the most common cause of death is liver failure within the first year of life and no therapeutic options are currently available. in vitro supplementation with deoxyguanosine or deoxyguanosine monophosphate (dGMP) were reported to rescue mtDNA depletion in DGUOK‐deficient, patient‐derived fibroblasts and myoblasts. CERC‐913, a novel ProTide prodrug of dGMP, was designed to bypass defective DGUOK while improving permeability and stability relative to nucleoside monophosphates. To evaluate CERC‐913 for its ability to rescue mtDNA depletion, we developed a primary hepatocyte culture model using liver tissue from DGUOK‐deficient rats. DGUOK knockout rat hepatocyte cultures exhibit severely reduced mtDNA copy number (~10%) relative to wild type by qPCR and mtDNA content remains stable for up to 8 days in culture. CERC‐913 increased mtDNA content in DGUOK‐deficient hepatocytes up to 2.4‐fold after 4 days of treatment in a dose‐dependent fashion, which was significantly more effective than dGMP at similar concentrations. These early results suggest primary hepatocyte culture is a useful model for the study of mtDNA depletion syndromes and that CERC‐913 treatment can improve mtDNA content in this model