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Although MBE technology is over a quarter-century old, and has been outstandingly successful in the growth of semiconductor heterostructures, it has a large reserve of as-yet unexplored capabilities left, many of which are likely to play a role in the future evolution of MBE. Developments that can be anticipated are the additions of OMVPE techniques to MBE, for example, for gas etching and surface cleanup. A central problem will be finding MBEcompatible ways to achieve lateral pattern controldoi:10.1016/s0022-0248(02)02199-1 fatcat:7i4hyuettzg7bgdrmxeu77i3ry
more »... wn to the nanometer scale. Nanoimprint techniques are a good candidate for that. Self-assembled quantum dots will probably give way to lithographically defined quantum dots with much better control over size and placement. Heterostructures of materials other than semiconductors will be increasingly explored, like magnetic and superconducting structures, and may be even organics. r
et al., 1980; Kroemer and Chien, 1981; Kroemer, 1985) . ... From Kroemer, 1957c. FIG. 5. ...doi:10.1103/revmodphys.73.783 fatcat:qdfuygsirbc75hsftozkxxuwam
., Vol. 72, No. 1, January 2004 Herbert Kroemer ...doi:10.1119/1.1615526 fatcat:fuvhihdwkvhdlppcgsv27x3lzy
Immunogenic cell death (ICD) is a type of cell death that is accompanied by the release of damageassociated molecular patterns (DAMPs) and results in a dead-cell antigen-specific immune response. Here, we report that spautin-1, an inhibitor of ubiquitin-specific peptidases, triggers immunogenic cancer cell death in vitro and in vivo. The anticancer activity of spautin-1 occurs independent of autophagy inhibition, but depends on the intrinsic mitochondrial apoptosis pathway. Spautin-1 causesdoi:10.1080/2162402x.2018.1431086 pmid:29872558 pmcid:PMC5980348 fatcat:m7odus3elfavfj5wuhhvt7yzva
more »... chondrial oxidative injury, which results in JUN transcription factor activation in a JNK-dependent manner. Mechanistically, activation of JUN by spautin-1 leads to apoptosis by upregulation of pro-apoptotic BAD expression. Importantly, the release of TFAM, a mitochondrial DAMP, by apoptotic cells may contribute to spautin-1induced ICD via its action on the receptor AGER. Indeed, cancer cells treated with spautin-1 in vitro were able to elicit an anticancer immune response when inoculated in vivo, in the absence of any adjuvant. This immunogenic effect of spautin-1-treated cancer cells was lost when TFAM or AGER were neutralized by specific antibodies. Altogether, our results suggest that spautin-1 may stimulate an apoptotic pathway that results in ICD, in TFAM-and AGER-dependent fashion.
The sine-term in (20) may be written as a Fourier-Bessel series (see Appendix B), * firstname.lastname@example.org 2 1 1 J ,(29)and the parameter η reduces to η = ( )J 1 z ,(30) ...arXiv:cond-mat/0007482v2 fatcat:mz6xtwv6kvfolheg6n5ayr67gm
Additional details of some of the material presented here can be found in a longer 1999 review by Kroemer and Hu  , but even there the coverage is by no means complete. ... Kroemer proposed that they are not ordinary point defects, but are Tamm states at the InAs-AlSb interface  , inherent to the band structure of that interface. Alternatively, Shen et al. ...doi:10.1016/j.physe.2003.08.003 fatcat:thclhvsnqndfrf7ctag6khjlum
Ferroptosis is a form of nonapoptotic regulated cell death driven by iron-dependent lipid peroxidation. Autophagy involves a lysosomal degradation pathway that can either promote or impede cell death. A high level of autophagy has been associated with ferroptosis, but the mechanisms underpinning this relationship are largely elusive. We characterize the contribution of autophagy to ferroptosis in human cancer cell lines and mouse tumor models. We show that "clockophagy," the selectivedoi:10.1126/sciadv.aaw2238 pmid:31355331 pmcid:PMC6656546 fatcat:h3gg34vrifcq3m74ii2ql3xmgu
more »... n of the core circadian clock protein ARNTL by autophagy, is critical for ferroptosis. We identify SQSTM1 as a cargo receptor responsible for autophagic ARNTL degradation. ARNTL inhibits ferroptosis by repressing the transcription of Egln2, thus activating the prosurvival transcription factor HIF1A. Genetic or pharmacological interventions blocking ARNTL degradation or inhibiting EGLN2 activation diminished, whereas destabilizing HIF1A facilitated, ferroptotic tumor cell death. Thus, our findings reveal a new pathway, initiated by the autophagic removal of ARNTL, that facilitates ferroptosis induction.
Autophagy (which includes macro-, micro-, and chaperone-mediated autophagy) is an important biological mechanism for the elimination of damaged or obsolete macromolecules and organelles (Kroemer (C) ATP ...doi:10.1016/j.cmet.2011.04.008 pmid:21641551 pmcid:PMC3293110 fatcat:t6qxoxazrfdqrmf6o3o426bjie
The ability of cytosolic lipopolysaccharide (LPS) to activate caspase-11–dependent nonclassical inflammasome is intricately controlled to avoid excessive inflammatory responses. However, very little is known about the regulatory role of various metabolic pathways in the control of caspase-11 activation. Here, we demonstrate that l-adrenaline can act on receptor ADRA2B to inhibit the activation of the caspase-11 inflammasome by cytosolic LPS or Escherichia coli infection in macrophages.doi:10.1126/sciadv.aav5562 pmid:31131320 pmcid:PMC6531004 fatcat:wtmk6hfbmjd47ljc6boc52w2aa
more »... ine–induced cAMP production via the enzyme ADCY4 promotes protein kinase A (PKA) activation, which then blocks the caspase-11–mediated proteolytic maturation of interleukin-1β, gasdermin D (GSDMD) cleavage, and consequent DAMP release. Inhibition of PDE8A-mediated cAMP hydrolysis limits caspase-11 inflammasome activation and pyroptosis in macrophages. Consequently, pharmacological modulation of the ADRA2B-ADCY4-PDE8A-PKA axis, knockout of caspase-11 (Casp11−/−), or Gsdmd inactivation (GsdmdI105N/I105N) similarly protects against LPS-induced lethality in poly(I:C)-primed mice. Our results provide previously unidentified mechanistic insight into immune regulation by cAMP and represent a proof of concept that immunometabolism constitutes a potential therapeutic target in sepsis.
The discovery of TMEM173/STING-dependent innate immunity has recently provided guidance for the prevention and management of inflammatory disorders. Here, we show that myeloid TMEM173 occupies an essential role in regulating coagulation in bacterial infections through a mechanism independent of type I interferon response. Mechanistically, TMEM173 binding to ITPR1 controls calcium release from the endoplasmic reticulum in macrophages and monocytes. The TMEM173-dependent increase in cytosolicdoi:10.1016/j.chom.2020.02.004 pmid:32142632 pmcid:PMC7153529 fatcat:rojpem44cvhffekjc4ua5bhsdy
more »... ium drives Gasdermin D (GSDMD) cleavage and activation, which triggers the release of F3, the key initiator of blood coagulation. Genetic or pharmacological inhibition of the TMEM173-GSDMD-F3 pathway blocks systemic coagulation and improves animal survival in three models of sepsis (cecal ligation and puncture or bacteremia with Escherichia coli or Streptococcus pneumoniae infection). The upregulation of the TMEM173 pathway correlates with the severity of disseminated intravascular coagulation and mortality in patients with sepsis. Thus, TMEM173 is a key regulator of blood clotting during lethal bacterial infections.
The mouse PDAC cell line KPC was derived from tumors from KPC mice (Pdx1-Cre;K-Ras G12D/+ ;p53 R172H/+ ) and was a gift obtained from Herbert J. ... Selleck Chemicals S7840 MAK025 S8615 S7023 IKE MIAPaCa2 Selleck Chemicals ATCC S8877 CRL-1420 Erastin PANC1 Selleck Chemicals ATCC S7242 CCL-1469 RSL3 KPC Selleck Chemicals Southwestern Medical Center) Herbert ...doi:10.1016/j.celrep.2021.108767 pmid:33626342 fatcat:vyqyfunzcrclnhswrnd7y5jwgy
. † E-mail: email@example.com 0749-6036/99/050877 + 13 $30.00/0 c 1999 Academic Press In DL, the authors investigated the Shapiro steps induced, by high-frequency irradiation, in the dc currentvoltage ...doi:10.1006/spmi.1999.0704 fatcat:23uyqgakjbbylcnpvphuutfdsm
., 2014; Green and Kroemer, 2009; Khoo et al., 2014) . Recent studies have suggested surprising roles for TP53 in tumor suppression independent of cell-cycle arrest and apoptosis (Li et al., 2012) . ...doi:10.1016/j.celrep.2017.07.055 pmid:28813679 fatcat:pwnn3qnoifavjlhyk2wqzy7q4e
We have studied the current-voltage characteristics of superconducting weak links in which the coupling medium is the 2-D electron gas in InAs-based semiconductor quantum wells, with relatively large (typically 0.5 micron) separations between niobium electrodes. The devices exhibit Josephson-like current-voltage characteristics; however, the falloff of the differential resistance with decreasing temperature is thermally activated, and is orders of magnitude slower than for more conventionaldoi:10.1103/physrevb.58.11676 fatcat:lcelyohdyreivnfwn2fcikv5ie
more »... links. Most unexpectedly, the thermal activation energies are found to be proportional to the width of the device, taken perpendicular to the current flow. This behavior falls outside the range of established theories; we propose that it is a fluctuation effect caused by giant shot noise associated with multiple Andreev reflections. The possibility of non-equilibrium effects is discussed.
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