We have shown that the poor PBTI reliability of IIIV/high-k gate stacks is universally related to process thermal budget limitations. Low temperature anneal optimization and high-k nitridation reduce ...oxide defect density. In contrast to a wide distribution of defect levels in Al 2 O 3 , HfO 2 on InGaAs shows a minimum defect density ~0.2eV below the channel E C . By introducing an interface dipole, a significant reliability boost was demonstrated. While low thermal budget high-k quality and IIIV interface thermal stability constitute challenges, our results show that a reliable IIIV/high-k gate stack can be fabricated.
Compound semiconductors will play a crucial role in reaching the high datarates of future wireless systems operating in the mmWave or sub-THz bands at a decent energy consumption. Their compatibility ...with a Si platform is desired to enable a high level of integration (i.e., complex functionality), as well as large-volume, low-cost production. We report here the possibilities offered by nanoridge engineering to meet these targets.
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 InsP(3)R-mediated Ca(2+) release in maintaining cellular bioenergetics. Macroautophagy provides eukaryotes with an adaptive response to nutrient deprivation that prolongs survival. Constitutive InsP(3)R Ca(2+) signaling is required for macroautophagy suppression in cells in nutrient-replete media. In its absence, cells become metabolically compromised due to diminished mitochondrial Ca(2+) uptake. Mitochondrial uptake of InsP(3)R-released Ca(2+) is fundamentally required to provide optimal bioenergetics by providing sufficient reducing equivalents to support oxidative phosphorylation. Absence of this Ca(2+) transfer results in enhanced phosphorylation of pyruvate dehydrogenase and activation of AMPK, which activates prosurvival macroautophagy. Thus, constitutive InsP(3)R Ca(2+) release to mitochondria is an essential cellular process that is required for efficient mitochondrial respiration and maintenance of normal cell bioenergetics.
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 InsP sub(3)R-mediated Ca super(2+) release in maintaining cellular bioenergetics. Macroautophagy provides eukaryotes with an adaptive response to nutrient deprivation that prolongs survival. Constitutive InsP sub(3)R Ca super(2+) signaling is required for macroautophagy suppression in cells in nutrient-replete media. In its absence, cells become metabolically compromised due to diminished mitochondrial Ca super(2+) uptake. Mitochondrial uptake of InsP sub(3)R-released Ca super(2+) is fundamentally required to provide optimal bioenergetics by providing sufficient reducing equivalents to support oxidative phosphorylation. Absence of this Ca super(2+) transfer results in enhanced phosphorylation of pyruvate dehydrogenase and activation of AMPK, which activates prosurvival macroautophagy. Thus, constitutive InsP sub(3)R Ca super(2+) release to mitochondria is an essential cellular process that is required for efficient mitochondrial respiration and maintenance of normal cell bioenergetics.
Microscale thermal transport is no longer diffusive as the feature size of the devices becomes comparable with the mean free paths of the heat carriers. We present a Monte Carlo modelling framework ...with partial experimental validation that captures those effects from first principles in complex 3D transistor geometries. Steady state and transient simulation case studies on GaN HEMTs and InP nanoridge HBTs reveal peak temperature rises that are up to threefold larger than conventional predictions based on bulk diffusion.
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
2+
homeostasis. Antiapoptotic Bcl-x
...L
binds to the inositol trisphosphate receptor (InsP
3
R) Ca
2+
release channel to enhance Ca
2+
- and InsP
3
-dependent regulation of channel gating, resulting in reduced ER Ca
2+
, increased oscillations of cytoplasmic Ca
2+
concentration (Ca
2+
i
), and apoptosis resistance. However, it is controversial which InsP
3
R isoforms mediate these effects and whether reduced ER Ca
2+
or enhanced Ca
2+
i
signaling is most relevant for apoptosis protection. DT40 cell lines engineered to express each of the three mammalian InsP
3
R isoforms individually displayed enhanced apoptosis sensitivity compared with cells lacking InsP
3
R. In contrast, coexpression of each isoform with Bcl-x
L
conferred enhanced apoptosis resistance. In single-channel recordings of channel gating in native ER membranes, Bcl-x
L
increased the apparent sensitivity of all three InsP
3
R isoforms to subsaturating levels of InsP
3
. Expression of Bcl-x
L
reduced ER Ca
2+
in type 3 but not type 1 or 2 InsP
3
R-expressing cells. In contrast, Bcl-x
L
enhanced spontaneous Ca
2+
i
signaling in all three InsP
3
R isoform-expressing cell lines. These results demonstrate a redundancy among InsP
3
R isoforms in their ability to sensitize cells to apoptotic insults and to interact with Bcl-x
L
to modulate their activities that result in enhanced apoptosis resistance. Furthermore, these data suggest that modulation of ER Ca
2+
is not a specific requirement for ER-dependent antiapoptotic effects of Bcl-x
L
. Rather, apoptosis protection is conferred by enhanced spontaneous Ca
2+
i
signaling by Bcl-x
L
interaction with all isoforms of the InsP
3
R.
Members of the Bcl-2 family of proteins regulate apoptosis, with some of their physiological effects mediated by their modulation of endoplasmic reticulum (ER) Ca²⁺ homeostasis. Antiapoptotic${\rm ...Bcl}\text{-}{\rm x}_{{\rm L}}$binds to the inositol trisphosphate receptor (InsP₃R) Ca²⁺ release channel to enhance Ca²⁺- and InsP₃-dependent regulation of channel gating, resulting in reduced ER Ca²⁺, increased oscillations of cytoplasmic Ca²⁺ concentration$({\rm Ca}^{2+}_{{\rm i}})$, and apoptosis resistance. However, it is controversial which InsP₃R isoforms mediate these effects and whether reduced ER Ca²⁺ or enhanced${\rm Ca}^{2+}_{{\rm i}}$signaling is most relevant for apoptosis protection. DT40 cell lines engineered to express each of the three mammalian InsP₃R isoforms individually displayed enhanced apoptosis sensitivity compared with cells lacking InsP₃R. In contrast, coexpression of each isoform with${\rm Bcl}\text{-}{\rm x}_{{\rm L}}$conferred enhanced apoptosis resistance. In single-channel recordings of channel gating in native ER membranes,${\rm Bcl}\text{-}{\rm x}_{{\rm L}}$increased the apparent sensitivity of all three InsP₃R isoforms to subsaturating levels of InsP₃. Expression of${\rm Bcl}\text{-}{\rm x}_{{\rm L}}$reduced ER Ca²⁺ in type 3 but not type 1 or 2 InsP₃R-expressing cells. In contrast,${\rm Bcl}\text{-}{\rm x}_{{\rm L}}$enhanced spontaneous${\rm Ca}^{2+}_{{\rm i}}$signaling in all three InsP₃R isoform-expressing cell lines. These results demonstrate a redundancy among InsP₃R isoforms in their ability to sensitize cells to apoptotic insults and to interact with${\rm Bcl}\text{-}{\rm x}_{{\rm L}}$to modulate their activities that result in enhanced apoptosis resistance. Furthermore, these data suggest that modulation of ER Ca²⁺ is not a specific requirement for ER-dependent antiapoptotic effects of${\rm Bcl}\text{-}{\rm x}_{{\rm L}}$. Rather, apoptosis protection is conferred by enhanced spontaneous${\rm Ca}^{2+}_{{\rm i}}$signaling by${\rm Bcl}\text{-}{\rm x}_{{\rm L}}$interaction with all isoforms of the InsP₃R.
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 super(2+) homeostasis. Antiapoptotic ...Bcl-x sub(L) binds to the inositol trisphosphate receptor (InsP sub(3)R) Ca super(2+) release channel to enhance Ca super(2+)- and InsP sub(3)-dependent regulation of channel gating, resulting in reduced ER Ca super(2+), increased oscillations of cytoplasmic Ca super(2+) concentration (Ca super(2+) sub(i)), and apoptosis resistance. However, it is controversial which InsP sub(3)R isoforms mediate these effects and whether reduced ER Ca super(2+) or enhanced Ca super(2+) sub(i) signaling is most relevant for apoptosis protection. DT40 cell lines engineered to express each of the three mammalian InsP sub(3)R isoforms individually displayed enhanced apoptosis sensitivity compared with cells lacking InsP sub(3)R. In contrast, coexpression of each isoform with Bcl-x sub(L) conferred enhanced apoptosis resistance. In single-channel recordings of channel gating in native ER membranes, Bcl-x sub(L) increased the apparent sensitivity of all three InsP sub(3)R isoforms to subsaturating levels of InsP sub(3). Expression of Bcl-x sub(L) reduced ER Ca super(2+) in type 3 but not type 1 or 2 InsP sub(3)R-expressing cells. In contrast, Bcl-x sub(L) enhanced spontaneous Ca super(2+) sub(i) signaling in all three InsP sub(3)R isoform-expressing cell lines. These results demonstrate a redundancy among InsP sub(3)R isoforms in their ability to sensitize cells to apoptotic insults and to interact with Bcl-x sub(L) to modulate their activities that result in enhanced apoptosis resistance. Furthermore, these data suggest that modulation of ER Ca super(2+) is not a specific requirement for ER-dependent antiapoptotic effects of Bcl-x sub(L). Rather, apoptosis protection is conferred by enhanced spontaneous Ca super(2+) sub(i) signaling by Bcl-x sub(L) interaction with all isoforms of the InsP sub(3)R.
We present a review of our recent studies of BTI in FET devices fabricated in different material systems, highlighting the reliability opportunities and challenges of each device family. We discuss ...first the intrinsic reliability improvement offered by SiGe and Ge pMOS technologies when a Si cap is used to passivate the channel and to fabricate a standard SiCh/HfCh gate stack. We ascribe this superior reliability to a reduced interaction of channel holes with oxide defects, thanks to a favorable energy alignment of the (Si)Ge Fermi level to the dielectric stack We discuss gate stack optimization (Ge fraction, quantum well and Si cap thicknesses, channel strain engineering) for maximum BTI reliability, and we propose a simple model able to reproduce all the experimental trends. We then invoke the model to understand the excessive BTI in other high-mobility channel gate stacks, as Ge/GeOx/high-k and InGaAs/high-k Finally we discuss how to pursue a reduction of charge trapping in alternative material systems in order to boost the device reliability.
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