2 research outputs found
Highly Reliable Performance of Flexible Synaptic Devices Based on PVP–GO QD Nanocomposites Due to the Formation of Directional Filaments
The metallic conductive filament
(CF) model, which serves as an
important conduction mechanism for realizing synaptic functions in
electronic devices, has gained recognition and is the subject of extensive
research. However, the formation of CFs within the active layer is
plagued by issues such as uncontrolled and random growth, which severely
impacts the stability of the devices. Therefore, controlling the growth
of CFs and improving the performance of the devices have become the
focus of that research. Herein, a synaptic device based on polyvinylpyrrolidone
(PVP)/graphene oxide quantum dot (GO QD) nanocomposites is proposed.
Doping GO QDs in the PVP provides a large number of active centers
for the reduction of silver ions, which allows, to a certain extent,
the growth of CFs to be controlled. Because of this, the proposed
device can simulate a variety of synaptic functions, including the
transition from long-term potentiation to long-term depression, paired-pulse
facilitation, post-tetanic potentiation, transition from short-term
memory to long-term memory, and the behavior of the “learning
experience”. Furthermore, after being bent repeatedly, the
devices were still able to simulate multiple synaptic functions accurately.
Finally, the devices achieved a high recognition accuracy rate of
89.39% in the learning and inference tests, producing clear digit
classification results
PP2A regulates kinetochore-microtubule attachment during meiosis I in oocyte
<p>Studies using <i>in vitro</i> cultured oocytes have indicated that the protein phosphatase 2A (PP2A), a major serine/threonine protein phosphatase, participates in multiple steps of meiosis. Details of oocyte maturation regulation by PP2A remain unclear and an <i>in vivo</i> model can provide more convincing information. Here, we inactivated PP2A by mutating genes encoding for its catalytic subunits (PP2Acs) in mouse oocytes. We found that eliminating both PP2Acs caused female infertility. Oocytes lacking PP2Acs failed to complete 1<sup>st</sup> meiotic division due to chromosome misalignment and abnormal spindle assembly. In mitosis, PP2A counteracts Aurora kinase B/C (AurkB/C) to facilitate correct kinetochore-microtubule (KT-MT) attachment. In meiosis I in oocyte, we found that PP2Ac deficiency destabilized KT-MT attachments. Chemical inhibition of AurkB/C in PP2Ac-null oocytes partly restored the formation of lateral/merotelic KT-MT attachments but not correct KT-MT attachments. Taken together, our findings demonstrate that PP2Acs are essential for chromosome alignments and regulate the formation of correct KT-MT attachments in meiosis I in oocytes.</p