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Varying concentrations of nano-Pr2O3 doped in “PVA + Sodium Citrate (90 : 10)” polyelectrolyte films are synthesized using solution cast technique and the films are characterized adopting FTIR, XRD, SEM, and DSC methods. The film with 3.0% of nano-Pr2O3 content is more homogenous and possesses more amorphous region that facilitate the deeper penetration of nanoparticles into the film causing more interactions between the functional groups of the polymeric film and nano-Pr2O3 particles and thereby turning the film more friendlily to the proton conductivity. The conductivity is maximum of 7 × 10−4 S/cm at room temperature for 3.0% nano-Pr2O3 film and at that composition, the activation energy and crystallinity are low. With increase in temperature, the conductivity is increasing and it is attributed to the hopping of interchain and intrachain ion movements and furthermore decrease in microscopic viscosity of the films. The major charge carriers are ions and not electrons. These films are incorporated successfully as polyelectrolytes in electrochemical cells which are evaluated for their discharge characteristics. It is found that the discharge time is maximum of 140 hrs with open circuit voltage of 1.78 V for film containing 3% of nano-Pr2O3 and this reflects its adoptability in the solid-state battery applications. [ABSTRACT FROM AUTHOR]

Information and Communication Technologies (ICT) are crucial in today's engineering applications in education, medicine and commercial systems. It devises accessibility for differently abled people as well. This is a survey-level study of the potential of ICT for the differently abled people. This paper presents the literature resources and the potential for the same in the field. Interestingly, it is noticed that a lot of accessibility features are within one's reach and are integrated in today's operating systems. These are rather unnoticed by many. This paper presents the results of the survey in the inception stage of the research work. Software applications such as screen readers (for e.g., JAWS) are available for visually challenged people. Cognitive systems development has the potential for devising solutions to differently abled people under Cognitive Impairment (CI). [ABSTRACT FROM AUTHOR]

The molecular mechanism and significance of endocytic processes involved in directional axon elongation are not well understood. The Unc-51 family of serine/threonine kinases was shown to be important for axon growth and was also linked to endocytosis, providing an entry point to study this problem. We found that mouse Unc-51-like kinase 1/2 (Ulk1/2) proteins are localized to vesicular structures in growth cones of mouse spinal sensory neurons. RNAi-mediated knockdown of Ulk1 and/or Ulk2 resulted in impaired endocytosis of nerve growth factor (NGF), excessive axon arborization, and severely stunted axon elongation. The evidence also indicates that Ulk1/2 mediates a non-clathrin-coated endocytosis in sensory growth cones. Interestingly, NGF can induce the interaction of Ulk1 with TrkA receptor complexes through promoting K63-polyubiquitination of Ulk1 and binding of Ulk1 to the scaffolding protein p62. These results and additional studies suggest that Ulk1/2 proteins regulate filopodia extension and neurite branching during sensory axon outgrowth, probably through regulating TrkA receptor trafficking and signaling. [ABSTRACT FROM AUTHOR]

Aggregated misfolded proteins are hallmarks of most neurodegenerative diseases. In a chronic disease state, including pathologic situations of oxidative stress, these proteins are sequestered into inclusions. Accumulation of aggregated proteins can be prevented by chaperones, or by targeting their degradation to the UPS. If the accumulation of these proteins exceeds their degradation, they may impair the function of the proteasome. Alternatively, the function of the proteasome may be preserved by directing aggregated proteins to the autophagy-lysosome pathway for degradation. Sequestosome 1/p62 has recently been shown to interact with polyubiquitinated proteins through its UBA domain and may direct proteins to either the UPS or autophagosome. P62 is present in neuronal inclusions of individuals with Alzheimer's disease and other neurodegenerative diseases. Herein, we review p62's role in signaling, aggregation, and inclusion formation, and specifically as a possible contributor to Alzheimer's disease. The use of p62 as a potential target for the development of therapeutics and as a disease biomarker is also discussed. [ABSTRACT FROM AUTHOR]