Graphene nanoplatelets (GNPs) are novel nanofillers possessing attractive characteristics, including robust compatibility with most polymers, high absolute strength, and cost effectiveness. In this study, GNPs were used to reinforce epoxy composite and epoxy/carbon fiber composite laminates to enhance their mechanical properties. The mechanical properties of GNPs/epoxy nanocomposite, such as ultimate tensile strength and flexure properties, were investigated. The fatigue life of epoxy/carbon fiber composite laminate with GPs-added 0.25 wt% was increased over that of neat laminates at all levels of cyclic stress. Consequently, significant improvement in the mechanical properties of ultimate tensile strength, flexure, and fatigue life was attained for these epoxy resin composites and carbon fiber-reinforced epoxy composite laminates.

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In this paper, a single compensation formula of adaptive conditional-probability estimator (ACPE) applied to fixed-width Booth multiplier is proposed. Based on the conditional-probability theory, the ACPE can be easily applied to large length Booth multipliers (such as 32-bit or larger) for achieving a higher accuracy performance. To consider the trade-off between accuracy and area cost, the ACPE provides varying column information to adjust the accuracy with respect to system requirements. The 16-bit ACPE Booth multiplier with = 3 reduces 28.9% silicon area with only 0.39 dB signal-to-noise ratio (SNR) loss when compared with post-truncated (P-T) Booth multiplier. Furthermore, the ACPE Booth multipliers are applied to two-dimensional (2-D) discrete cosine transform (DCT) to evaluate the system performance. Implemented in a TSMC 0.18 m CMOS process, the DCT core with ACPE ( = 3) can save 14.3% area cost with only 0.48 dB peak-signal-to-noise-ratio (PSNR) penalty compared to P-T method.

TDP-43 inclusions are found in many Alzheimer’s disease (AD) patients presenting faster disease progression and greater brain atrophy. Previously, we showed full-length TDP-43 forms spherical oligomers and perturbs amyloid-β (Aβ) fibrillization. To elucidate the role of TDP-43 in AD, here, we examined the effect of TDP-43 in Aβ aggregation and the attributed toxicity in mouse models. We found TDP-43 inhibited Aβ fibrillization at initial and oligomeric stages. Aβ fibrillization was delayed specifically in the presence of N-terminal domain containing TDP-43 variants, while C-terminal TDP-43 was not essential for Aβ interaction. TDP-43 significantly enhanced Aβ’s ability to impair long-term potentiation and, upon intrahippocampal injection, caused spatial memory deficit. Following injection to AD transgenic mice, TDP-43 induced inflammation, interacted with Aβ, and exacerbated AD-like pathology. TDP-43 oligomers mostly colocalized with intracellular Aβ in the brain of AD patients. We conclude that TDP-43 inhibits Aβ fibrillization through its interaction with Aβ and exacerbates AD pathology.