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Driven-dissipative spin chain model based on exciton-polariton condensates
Sigurdsson, H.,Ramsay, A. J.,Ohadi, H.,Rubo, Y. G.,Liew, T. C. H.,Baumberg, J. J.,Shelykh, I. A. American Physical Society 2017 Physical Review B Vol.96 No.15
<P>An infinite chain of driven-dissipative condensate spins with uniform nearest-neighbor coherent coupling is solved analytically and investigated numerically. Above a critical occupation threshold the condensates undergo spontaneous spin bifurcation (becoming magnetized) forming a binary chain of spin-up or spin-down states. Minimization of the bifurcation threshold determines the magnetic order as a function of the coupling strength. This allows control of multiple magnetic orders via adiabatic (slow ramping of) pumping. In addition to ferromagnetic and antiferromagnetic ordered states we show the formation of a paired-spin ordered state vertical bar ... up arrow up arrow down arrow down arrow ... > as a consequence of the phase degree of freedom between condensates.</P>
Conformation as a Therapeutic Target in the Prionoses and other Neurodegenerative Conditions
Wisniewski, Thomas,Sigurdsson, Einar M.,Aucouturier, Pierre,Frangione, B. 한림대학교 환경·생명과학연구소 2000 국제학술회의 Vol.2000 No.-
Abnormal protein conformation is increasingly being recognized as part of the pathogenesis of numerous neurodegenerative conditions. The common theme in all these diseases is the conversion of a normal cellular and/or circulating protein into an insoluble, aggregated, β-sheet rich form which is deposited in the brain. The aggregated proteins can accumulate extracellularly, often in the form of amyloid, or intracellularly producing inclusion bodies. These deposits are toxic and produce neuronal dysfunction and death. A unique category of the conformational conditions are prion related diseases(or prionoses), where the etiology is thought to be related to conversion of the normal prion protein, PrP□ ,into an infectious and pathogenic form, PrP□. However, the most common of these disorders is Alzheimer's disease(AD) where the central events is thought to be the conversion of normal soluble amyloid(sAβ) into fibrillar Aβin the form of neuritic plaques and congophilic angiopathy. Our growing understanding of the mechanisms involved in this category of disease, raises the possibility of therapeutic approaches based directly on the prevention and reversal of pathologic protein conformations. Possible approaches include synthetic β-sheet breaker peptides, which our preliminary data suggest may be useful for both AD and the prionoses, as well as immunological approaches where an antibody and/or cell mediated response is triggered against the aggregating abnormal protein.
Conformation as a Therapeutic Target in the Prionoses and other Neurodegenerative Conditions
Wisniewski, Thomas,Sigurdsson, Einar M.,Aucouturier, Pierre,Frangione, B. 한림대학교 환경·생명과학연구소 2000 [일송 국제심포지엄] 노화와 만성퇴행성 신경질환 Vol.- No.3
Abnormal protein conformation is increasingly being recognized as part of the pathogenesis of numerous neurodegenerative conditions. The common theme in all these diseases is the conversion of a normal cellular and/or circulation protein into an insoluble, aggregated, β-sheet rich form which is deposited in the brain. The aggregated proteins can accumulate extracellularly, often in the form of amyloid, or intracellularly producing inclusion bodies. These deposits are toxic and produce neuronal dysfunction and death. A unique category of the conformational conditions are prion related diseases (or prionoses), where the etiology is thought to be related to conversion of the normal prion protein, PrP^c, into an infectious and pathogenic form, PrP^Sc. However, the most common of these disorders is Alzheimer's disease (AD) where the central event is thought to be the conversion of normal soluble amyloid (sAβ) into fibrillar Aβ in the form of neuritic plaques and congophilic angiopathy. Our growing understanding of the mechanisms involved in this category of disease, raises the pathologic protein conformations. Possible approaches include synthetic β-sheet breaker peptides, which our preliminary data suggest may be useful for both AD and the prionoses, as well as immunological approaches where an antibody and/or cell mediated response is triggered against the aggregation abnormal protein.
Ha, J.H.,Kwak, S.W.,Sigurdsson, A.,Chang, S.W.,Kim, S.K.,Kim, H.C. American Association of Endodontists] 2017 JOURNAL OF ENDODONTICS - Vol.43 No.10
Introduction: The aim of this study was to evaluate the effect of different pecking depth on the stress generated by the screw-in forces of a rotating endodontic file in simulated canals. Methods: Twenty simulated resin blocks with a J-shaped curvature were used. Twenty OneG files (MicroMega, Besancon, France) were assigned for a screw-in test depending on the pecking depth in 2 groups (n = 10). The files were operated at 300 rpm, and the up and down speed was controlled at 1 mm/s stroke velocity and a 10-millisecond dwell time using a customized device. The distances (pecking depth) for the pecking motion were 2 mm or 4 mm for each group; ''6 mm forward and 4 mm backward'' and ''6 mm forward and 2 mm backward'' movements were applied, respectively, for the 2 pecking groups. During the operation, the positive and negative apical loads were recorded at a rate of 50 Hz using customized software attached to the device. The maximum negative apical load (screw-in force [SF]) was recorded, and the total energy during pecking motion until the file reached the working length (cumulative screw-in forces [CSFs]) was computed. The data were analyzed using an independent t test at a significance level of 95%. Results: No significant difference in SF was found between the 2 groups of pecking depths. However, the longer pecking depth (4-mm group) showed a significantly larger CSF compared with the shorter pecking depth group (P < .05). Conclusions: The shorter pecking depth may generate lower overall stresses for the root dentin as well as the instrument.
Jon Petur Joelsson,Arni Asbjarnarson,Snaevar Sigurdsson,Jennifer Kricker,Bryndis Valdimarsdottir,Holmfridur Thorarinsdottir,Eir Starradottir,Thorarinn Gudjonsson,Saevar Ingthorsson,Sigurbergur Karason 한국실험동물학회 2022 Laboratory Animal Research Vol.38 No.3
Background: Mechanical ventilation is a life-saving therapy for critically ill patients, providing rest to the respiratory muscles and facilitating gas exchange in the lungs. Ventilator-induced lung injury (VILI) is an unfortunate side effect of mechanical ventilation that may lead to serious consequences for the patient and increase mortality. The four main injury mechanisms associated with VILI are: baro/volutrauma caused by overstretching the lung tissues; atelectrauma, caused by repeated opening and closing of the alveoli resulting in shear stress; oxygen toxicity due to use of high ratio of oxygen in inspired air, causing formation of free radicals; and biotrauma, the resulting biological response to tissue injury, that leads to a cascade of events due to excessive inflammatory reactions and may cause multi-organ failure. An often-overlooked part of the inflammatory reaction is oxidative stress. In this research, a mouse model of VILI was set up with three tidal volume settings (10, 20 and 30 mL/kg) at atmospheric oxygen level. Airway pressures and heart rate were monitored and bronchoalveolar lavage fluid (BALF) and lung tissue samples were taken. Results: We show a correlation between increased inflammation and barrier failure, and higher tidal volumes, evidenced by increased IL-6 expression, high concentration of proteins in BALF along with changes in expression of adhesion molecules. Furthermore, swelling of mitochondria in alveolar type II cells was seen indicating their dysfunction and senescence-like state. RNA sequencing data present clear increases in inflammation, mitochondrial biogenesis and oxidative stress as tidal volume is increased, supported by degradation of Keap1, a redox-regulated substrate adaptor protein. Conclusions: Oxidative stress seems to be a more prominent mechanism of VILI than previously considered, indicating that possible treatment methods against VILI might be identified by impeding oxidative pathways.
Spin Order and Phase Transitions in Chains of Polariton Condensates
Ohadi, H.,Ramsay, A. J.,Sigurdsson, H.,del Valle-Inclan Redondo, Y.,Tsintzos, S. I.,Hatzopoulos, Z.,Liew, T. C. H.,Shelykh, I. A.,Rubo, Y. G.,Savvidis, P. G.,Baumberg, J. J. American Physical Society 2017 Physical Review Letters Vol.119 No.6