Scaling laws for the decay of multiqubit entanglement

We investigate the decay of entanglement of generalized N-particle Greenberger-Horne-Zeilinger (GHZ) states interacting with independent reservoirs. Scaling laws for the decay of entanglement and for its finite-time extinction (sudden death) are derived for different types of reservoirs. The latter is found to increase with the number of particles. However, entanglement becomes arbitrarily small, and therefore useless as a resource, much before it completely disappears, around a time which is inversely proportional to the number of particles. We also show that the decay of multi-particle GHZ states can generate bound entangled states.Comment: Minor mistakes correcte

Robustness of Entanglement as a Resource

The robustness of multipartite entanglement of systems undergoing decoherence is of central importance to the area of quantum information. Its characterization depends however on the measure used to quantify entanglement and on how one partitions the system. Here we show that the unambiguous assessment of the robustness of multipartite entanglement is obtained by considering the loss of functionality in terms of two communication tasks, namely the splitting of information between many parties and the teleportation of states.Comment: 11 pages, 5 figure

A influência das atividades mineradoras na alteração do pH e da alcalinidade em águas fluviais: o exemplo do rio Capivari, região do carste paranaense.

As atividades de mineração causam vários tipos de impactos ao meio ambiente. Este trabalho apresenta um estudo de impacto sobre recursos hídricos superficiais desenvolvidos numa bacia hidrográfica na região metropolitana de Curitiba (PR), onde se observaram modificações no pH e na alcalinidade nas águas do rio Capivari ocorridas num intervalo médio de doze anos. Foram avaliados 387 dias de amostragem da série 1986/1987 e 1.095 dias da série 1998/2000. Comparando-se as duas séries, observou-se que, ao longo deste período (1986-2000), a média do pH elevou-se, em média, 0,5 unidade, enquanto a alcalinidade aumentou em 15%. De 1980 a 2001, as áreas de mineração desta mesma bacia tiveram uma expansão de aproximadamente 47.000 m2/ano. Avaliações ao longo do rio revelaram, nos locais à jusante e mais próximos das pedreiras, que o pH apresenta valores mais altos, tornando-se alcalino, e a condutividade elétrica aumenta. Esses dados confirmam a hipótese de que a expansão das áreas de mineração provocaria alterações nos valores de pH e de alcalinidade das águas do rio Capivari

Decoupling the effect of mutant amyloid precursor protein (APP) from the effect of plaque on axonal transport dynamics in the living mouse brain: A correlation MRI-microscopy study

The parent protein for amyloid plaques, amyloid precursor protein (APP), mediates cargo‐motor attachments for intracellular transport. Axonal transport is decreased and the distal location of accumulation is altered in transgenic mice expressing human APP with the Swedish and Indiana mutations (APPSwInd) linked to Familial Alzheimer’s Disease, as detected by time‐lapse magnetic resonance imaging (MRI) of transport in living mouse brains (Bearer et al. 2017). Transport is also altered in brains of Down syndrome mice with 3 copies of APP gene. Questions now become whether expression of mutated APP effects transport dynamics independent of plaque, and do plaques alone contribute to transport defects? To address these we used the Tet‐Off system to decouple expression of APPSwInd from presence of plaques, and then studied transport using our MRI technique in three experimental groups of transgenic mice in which the timing and duration of APPSwInd expression, and thereby plaque formation, was altered with doxycycline: Group A (+ plaques, + APPSwInd); Group B (+ plaques, no APPSwInd), and group C (no plaques, + APPSwInd). Manganese‐enhanced MRI (MEMRI) allows us to perform cell biological experiments in live animals with T1‐weighted MRI in a Bruker 11.7T scanner (Medina et al 2016). Time‐lapse MR images were captured before and after stereotactic injection of Mn2+ (3‐5nL) into CA3 of the hippocampus at successive time‐points. Images of multiple individuals were aligned and processed with our automated computational pipeline (Medina et al. 2017) and statistical parametric mapping (SPM) performed. After MRI brains were harvested for histopathology or biochemistry. Results show that within group between time‐point have altered transport locations as well as diminished transport in all groups compared to wildtype (p<0.05 FDR n= 36). Preliminary ANOVA between‐group comparisons both by SPM and by region of interest measurements of images support the visual impression that APPSwInd expression alone may compromise transport. Groups A and B displayed plaques, but not C, and Western blots showed APPSwInd expressed 3.2‐fold over normal at sacrifice in Groups A and C but not B, with Aβ detected only in Groups A and B, where phospho‐tau was also present in dystrophic neurites surrounding plaques. Cholinergic neurons that project to hippocampus from the medial septal nucleus were decreased in Group C (p=0.0006 by ANOVA, n=15). Isolated hippocampal vesicles contained Mn2+, as well as Trk (NGF receptor), Rab 5 and 7 (associated with transport vesicles), suggesting a distinct vesicle population is affected by these APP mutations. These surprising results implicate mutated APPSwInd in transport defects, separable from the effect of plaque

Witnessing microtubule-based transport in the living brain: Impact of the cargomotor receptor, amyloid precursor protein, and Alzheimer’s plaques

Most amyloid precursor protein (APP)-based Alzheimer’s models overexpress mutant human APP resulting in Abeta plaques. Yet the relative contribution of this elevated APP and the presence of plaques to neurodegeneration remains a big question. APP’s role as a cargo-motor receptor for axonal transport suggests that overexpression might lead to increased transport. Indeed we showed that transport is increased in Down’s syndrome and decreased in APP knockout mice. Hence transport may be elevated in APP overexpressors and lead to either beneficial or deleterious consequences. Here we use high field microMRI with Mn2+, an MR contrast agent useful as a track-tracer, to pose this cell biological quest ion within the whole living brains of wildtype and Alzheimer’s model mice. Injection of Mn2+ into the CA3 region of the hippocampus results in measurable transport over time. Application of 3D unbiased whole brain image analysis detects all circuitry emanating from the hippocampus. By driving APP Swe/Ind transgene expression with a tetracycline-sensitive promoter, APPSwe/Ind expression can be decoupled from the presence of plaques with doxycycline (doxy). Three groups of mice were studied: group ‘A’ (no doxy, +plaques, +APP); group ‘B’ (doxy at 8 days before sacrifice, +plaques, no APP), and group ‘C’ (doxy prior to conception, and stopped 8 days before sacrifice, no plaques, +APP). Images were captured before and sequentionally after Mn2+ injection into CA 3 (1, 7, 25 hr). Images were aligned and analyzed by statistical parametric mapping to identify differential accumulation within the hippocampal projections. Histopathology revealed well-developed plaques in A and B, and Western blots showed human APP expressed five-fold over WT in in A and C. Our preliminary results show increased transport in A and C, with APP Swe/Ind expression when compared with B, where expression is suppressed. Cholinergic neurons in the medial septal nucleus were decreased as determined by anti-ChAT staining in Group C (p=0.0006 by one-way ANOVA, n=15). In conclusion, the effects of elevated APP expression are separable from consequences of plaque, and each may

Developing a Model for Slow Hypoxic Injury and Vascular Degeneration in Amyloid Burdened Brains

The breakdown of neurovascular systems may play a crucial role in the pathogenesis of Alzheimer’s disease. However whether this breakdown initiates a degenerative mechanism or is the consequence of some other deleterious process remains unknown. We examined hippocampal pathology in double transgenic mice overexpressing a human mutant gene encoding the amyloid precursor protein (APPSwe/Ind) using a combination of histochemistry and stereologic techniques. Expression of APPSwe/Ind in these mice is driven by a tetracycline-sensitive promoter. Tetracycline transcriptional activator (tTA), the second transgene, is driven in turn by a CAM KIIa promoter that is only active in neurons. Thus this double transgenic construct allows us to control expression of APPSwe/Ind with doxycycline. Utilizing this characteristic, we created three distinct experimental groups: A, display abeta plaque pathology and express APPSwe/Ind at time of sacrifice; B, display abeta plaque pathology but do not express APPSwe/Ind at time of sacrifice; and C, do not display abeta plaque pathology but do express APPSwe/Ind at time of sacrifice. Stereologic investigation revealed decreased hippocampal volume in groups A(n=5) and B(n=5) when compared to group C(n=5) and age-matched wildtype (n=9)

LPIN1 deficiency: A novel mutation associated with different phenotypes in the same family

Free PMC Article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5050266/Rhabdomyolysis (RM) is characterized by acute and often severe skeletal muscle damage resulting in myoglobinuria and, in severe cases, acute renal failure. In adults is typically due to trauma, intoxication or infection, whereas in children is frequently associated with inherited muscle disorders. LPIN1 mutations were identified as a cause of severe recurrent RM, which usually begin in childhood, and infections are the most frequent trigger.info:eu-repo/semantics/publishedVersio