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Neurogenesis is a complex process which governs embryonic brain development and is important for brain plasticity throughout the whole life. Postnatal neurogenesis occurs in neurogenic niches that ...regulate the processes of proliferation and differentiation of stem and progenitor cells driven by stimuli triggering mechanisms of neuroplasticity. In the neurogenic niches cells of glial and endothelial origin are the key regulators of neurogenesis. It is known that physiological neurogeneses is crucial for memory formation, whereas reparative neurogenesis provides partial repair of injured brain structures and compensation of neurological deficits caused by the brain injury. Dysregulation of neurogenesis is a characteristics feature of various neurodevelopmental and neurodegenerative diseases, particularly, Alzheimer’s disease representing a very important medical and social problem. In the in vitro model of the neurogenic niche using hippocampal neurospheres as a source of stem/progenitor cells and astrocytes, we have studied effects of astrocyte activation on the expression of markers of different stages of cell proliferation and differentiation. We found that aberrant mechanisms of development of stem and progenitor cells, caused by the beta-amyloid peptide (Аβ
1–42
), can be partially restored by targeted activation of GFAP-expressing cells in the neurogenic niche.
We introduce a set of new characterization techniques for the direct defect analysis of the sidewall surfaces of Nano-ridge, Nanowire, and FinFET based devices, being used in current (and future) ...logic and RF technologies. We demonstrate the application of these techniques on GaAs mesa, Nano-ridge, and InGaAs nano-wire based PIN diodes where surface defect densities are difficult to extract currently. We show that a close match in extracted density, with both measured data and calibrated TCAD simulations of above device types, is achieved validating the applicability of the techniques.
Charge trapping in the gate-oxide can cause significant degradation and reduce the operating lifetime of the device. Here, we study the kinetics of charge trapping in the InGaAs/Al 2 O 3 /HfO 2 ...gate-stack using Capture and Emission Time (CET) maps. The existence of two oxide defect bands, respectively above and below the conduction band of InGaAs, is implied by sensing charge trapping at positive and negative oxide electric fields. Within each band, two distinct populations of defect states are observed. The first defect population with relatively higher capture and emission energy barriers is found to affect the long term reliability of the device since the charge trapping in these defect states is slow, while the second population with relatively smaller capture and emission energy barriers affects the device stability particularly under high frequency operation. We argue that it is essential to characterize and study both defect populations in order to accurately estimate device lifetime under different operating applications.
In this letter, we show that conventional III-V MOSFETs with moderate/high In content channels (In 0.53 Ga 0.47 As or In 0.70 Ga 0.30 As) at scaled nodes are incompatible with mobile SoC designs, ...which often operate at intermediate/high V dd (0.7 V to ≥1 V) to achieve high frequency including during burst-mode. The incompatibility is due to conventional III-V FETs having too small bandgap, and thus too high leakage when operated at the increased voltages. We show that FETs with a more optimal lower In content, In 0.35 Ga 0.65 As, have the necessary combination of larger bandgap (~Si) and sufficiently high injection velocity (~2.5 times Si) to enable both low leakage and high performance (versus Si), across the entire V dd range of mobile SoC operation. We report for the first time the growth and characterization of ultra-thin In 0.35 Ga 0.65 As FETs with a standard 1nm EOT gate dielectric. Calibrated models show that In 0.35 Ga 0.65 As enables the highest performance at very low leakages at intermediate/high V dd in short channel FETs.
Mechanisms that regulate cellular metabolism are a fundamental requirement of all cells. Most eukaryotic cells rely on aerobic mitochondrial metabolism to generate ATP. Nevertheless, regulation of ...mitochondrial activity is incompletely understood. Here we identified an unexpected and essential role for constitutive InsP3R-mediated Ca2+ release in maintaining cellular bioenergetics. Macroautophagy provides eukaryotes with an adaptive response to nutrient deprivation that prolongs survival. Constitutive InsP3R Ca2+ signaling is required for macroautophagy suppression in cells in nutrient-replete media. In its absence, cells become metabolically compromised due to diminished mitochondrial Ca2+ uptake. Mitochondrial uptake of InsP3R-released Ca2+ is fundamentally required to provide optimal bioenergetics by providing sufficient reducing equivalents to support oxidative phosphorylation. Absence of this Ca2+ transfer results in enhanced phosphorylation of pyruvate dehydrogenase and activation of AMPK, which activates prosurvival macroautophagy. Thus, constitutive InsP3R Ca2+ release to mitochondria is an essential cellular process that is required for efficient mitochondrial respiration and maintenance of normal cell bioenergetics.
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▸ Constitutive InsP3R Ca2+ release suppresses autophagy in nutrient-rich conditions ▸ Absence of constitutive InsP3R Ca2+ release reduces cell ATP and activates AMP kinase ▸ Mitochondrial uptake of released Ca2+ is required for sufficient ATP production ▸ Constitutive ER-to-mitochondria Ca2+ transfer is essential for normal bioenergetics
DDT inhibits Na channel inactivation and deactivation, promotes Na channel activation and reduces the resting potential of
Xenopus oocytes expressing the Drosophila
para Na channel. These changes are ...only marginally influenced by the single mutation M918T (
super-kdr) but are reduced ∼10-fold by either the single mutation L1014F (
kdr) or the double mutation L1014F
+
M918T, both of which confer resistance to the pyrethroids permethrin and deltamethrin. We conclude that DDT binds either to or in the region of L1014 on IIS6 but only weakly to M918 on the IIS4–S5 linker, which is part of a high-affinity binding site for permethrin and deltamethrin.
3D Sequential integration has been envisioned to stack transistors in the same front-end process. A crucial challenge is the management of the thermal budget. This work focuses on Si nMOS gate stack ...challenges, specifically: for a top tier device, by inserting a thin LaSiO x interlayer between SiO 2 and HfO 2 a sufficient PBTI reliability is demonstrated without resorting to unsuitable high temperature anneals. This gate stack also offers good thermal stability for a pMOS over nMOS scenario.
Members of the Bcl-2 family of proteins regulate apoptosis, with some of their physiological effects mediated by their modulation of endoplasmic reticulum (ER) Ca... homeostasis. Antiapoptotic ...Bcl-... binds to the inositol trisphosphate receptor (InsP...R) Ca... release channel to enhance Ca... and InsP...-dependent regulation of channel gating, resulting in reduced ER ..., increased oscillations of cytoplasmic Ca... concentration (......), and apoptosis resistance. However, it is controversial which InsP...R isoforms mediate these effects and whether reduced ER ... or enhanced Ca...... signaling is most relevant for apoptosis protection. DT4O cell lines engineered to express each of the three mammalian InsP...R isoforms individually displayed enhanced apoptosis sensitivity compared with cells lacking InsP...R. In contrast, coexpression of each isoform with Bcl-x... conferred enhanced apoptosis resistance. In single-channel recordings of channel gating in native ER membranes, Bcl-x... increased the apparent sensitivity of all three InsP...R isoforms to subsaturating levels of InsP... Expression of Bcl-x... reduced ER Ca... in type 3 but not type 1 or 2 InsP...R-expressing cells. In contrast, Bcl-x... enhanced spontaneous ...... signaling in all three InsP...R isoform-expressing cell lines. These results demonstrate a redundancy among InsP...R isoforms in their ability to sensitize cells to apoptotic insults and to interact with Bcl-x... to modulate their activities that result in enhanced apoptosis resistance. Furthermore, these data suggest that modulation of ER ... is not a specific requirement for ER-dependent antiapoptotic effects of Bcl-x... Rather, apoptosis protection is conferred by enhanced spontaneous ...... signaling by Bcl-x... interaction with all isoforms of the InsP...R. (ProQuest-CSA LLC: ... denotes formulae/symbols omitted.)
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