• Animal cells and systems
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• v.4 no.4
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• pp.381-388
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• 2000

Using a murine T cell hybridoma, activation-induced cell death (AICD) was studied. As an in vitro model system for the AICD, 1 cell hybridoma expressing TCR/CD3 complex was incubated onto the immobilized purified anti-CD3 antibody. The immobilized anti-CD3 antibody induced AICD effectively up to 40%. At 1-100 $\mu$M range of SNP, an exogenous source of nitric oxide (NO), the cell proliferation was not affected, but at 1 mM SNP, cell proliferation was significantly reduced. The AICD of T cell hybridoma was inhibited by exogenous NO at non-cytotoxic concentration, In the cells undergoing AICD, the expressions of caspase-3 and FasL were detected, but not iNOS. Similar result was recognized in the apoptosis induced by dexamethasone, an apoptosis-inducing agent. However, the conversion from the inactive form of caspase-3 (32 kDa) to the active form (17 kDa) was significantly reduced in the cells in AICD induced by anti-CD3 antibody, With the result of increased PARP cleavage in the cells, we propose that another PARP cleavage pathway not involving caspase-3 may function in the anti-CD3 antibody induced AICD in the T cell hybridoma.

• BMB Reports
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• v.43 no.10
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• pp.656-663
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• 2010

Amyloid precursor protein (APP), which is critically involved in the pathogenesis of Alzheimer's disease (AD), is cleaved by gamma/epsilon-secretase activity and results in the generation of different lengths of the APP Intracellular C-terminal Domain (AICD). In spite of its small size and short half-life, AICD has become the focus of studies on AD pathogenesis. Recently, it was demonstrated that AICD binds to different intracellular binding partners ('adaptor protein'), which regulate its stability and cellular localization. In terms of choice of adaptor protein, phosphorylation seems to play an important role. AICD and its various adaptor proteins are thought to take part in various cellular events, including regulation of gene transcription, apoptosis, calcium signaling, growth factor, and $NF-{\kappa}B$ pathway activation, as well as the production, trafficking, and processing of APP, and the modulation of cytoskeletal dynamics. This review discusses the possible roles of AICD in the pathogenesis of neurodegenerative diseases including AD.

• Journal of Life Science
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• v.17 no.1 s.81
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• pp.18-23
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• 2007

Fe65, a neuron-specific adaptor protein, has two phosphotyrosine binding (PTB) domains. The second PTB (PTB2) domain interacts with intracellular domain fragment (AICD) of amyloid beta precursor protein (APP). Recent studies suggested that tile complex is composed of AICD and Fe65 transactivates genes that are responsible for neuronal cell death in Alzheimer's disease (AD). Therefore, a compound inhibiting the interaction between Fe65 and AICD can be a drug candidate to treat AD. However, it remains unclear how Fe65 recognizes AICD at a molecular level. Here, we report high-level production of the PTB2 domain of Fe65 in the baculovirus system. We found that the baculovirus system is an efficient method to obtain the Fe65 PTB2 domain, compared with the bacterial and mammalian expression systems. The purified recombinant protein was used for crystallization to determine its crystal structure helping to understand the molecular mechanism of Fe65-dependent signaling and to design its inhibitors.

• Journal of The Korean Dental Society of Anesthesiology
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• v.9 no.2
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• pp.116-118
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• 2009

The automatic implantable cardioverter defibrillator (AICD) has been widely used to treat recurrent malignant ventricular arrhythmia. Here, we case report 18 yr old patients implanted with Automatic implantable cardioverter defibrillator (AICD) who underwent surgical extraction under intravenous sedation and discuss the anesthetic implications for surgery.

• Proceedings of the IEEK Conference
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• 1999.06a
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• pp.1063-1066
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• 1999

The delay of cardiac depolarization wave detection in the conventional pacemakers or AICD (automatic implantable cardioverter/ defibrillator, or ICD) has been overlooked. However, it is known that the delay may cause hemodynamic problems and may prevent the proper operation of a new automatic feature, automatic capture verification, that is to be appeared in the near-future devices. In order to reduce the effects of the delay, a delay prevention algorithm was developed and tested by applying three human electrograms. The algorithm set the sensing threshold just above the measured noise level to reduce the detection delay. It is found that the low threshold was able to reduce the delay by 20msec(average) In most cases. The implementation results showed reliability and efficacy of the algorithm, and the algorithm could be applicable to the existing hardware and software of the conventional pacemakers and AICD without any significant modifications.

• Journal of Microbiology and Biotechnology
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• v.10 no.5
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• pp.573-579
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• 2000

Knowledge on the enzymes acting on p-amino-acid-containing peptides appears to be somewhat limited when compared with those acting on peptides composed on L-amino acids. Less than ten D-stereospecific enzymes are hitherto known. This review describes about several novel D-stereospecific peptidases and amidases of microbial origin, including D-aminopeptidase (E.C. 3.4.11.19), alkaline D-peptidase, and D-amino aicd amidase, which are applied to the synthesis of D-amino acid/or D-amino acid derivatives.

• IMMUNE NETWORK
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• v.11 no.6
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• pp.428-430
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• 2011

We previously demonstrated that in vivo engagement of CD137, a member of TNF receptor superfamily, can delete allorective $CD4^+$ T cells through the induction of activation-induced cell death (AICD) in chronic graft-versus-host disease (cGVHD) and subsequently reverse established cGVHD. In this study, we further showed that agonistic anti-CD137 mAb was highly effective in triggering AICD of donor $CD8^+$ T cells as well as donor $CD4^+$ T cells in the $C57BL/6{\rightarrow}unirradiated$ $(C57BL/6\;{\times}\;DBA/2)F1$ acute GVHD model. Our results suggest that strong allostimulation should facilitate AICD of both alloreactive $CD4^+$ and $CD8^+$ T cells induced by CD137 stimulation. Therefore, depletion of pathogenic T cells using agonistic anti-CD137 mAb combined with potent TCR stimulation may be used to block autoimmune or inflammatory diseases mediated by T cells.

• Korean Journal of Food Science and Technology
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• v.16 no.3
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• pp.285-290
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• 1984

Growth characteristics of six lactic acid bacteria in whey-soy milk mixtures were investigated to obtain basic informations for processing cheese-like product by coprecipitation of whey and soy proteins. Streptococcus cremoris and Lactobacillus acidophilus produced more aicd than other lactic acid bacteria both in whey-soy milk mixture and in soy milk. Lactic acid fermentation was accelerated in whey-soy milk mixture than in soy milk with all the lactic aicd bacteria, and specially with S. lactis and S. cremoris in great extent. The number of viable cell of 1:1 mixed culture of S. lactis and S. cremoris in whey soy milk mixture was about 10 times than in soymilk. It was mainly the effect of lactose in the whey that increased the acid production by lactic aicd bacteria in whey-soy milk mixture although the degree of acceleration depended on the ability of microorganism to use carbohydrates. The optimum amount of lactose added to soy milk to accelerate the acid production was 0.8g/100ml soy milk.

• The Journal of Internal Korean Medicine
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• v.28 no.1
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• pp.25-33
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• 2007

Background and Purpose : This study was to survey complication according to the TOAST classification and Sasangconstitution in first-ever AICD (acute ischemic cerebrovascular disease) patients. Methods : From 1 Oct. 2005 to 31 Oct. 2006. 97 patients with a first-ever stroke were included in the study. patients were hospitalized within 14 days after the onset of stroke at Kyungwon University Incheon Oriental Hospital. We recorded patient's complications according to the standard operation procedure of 'A stroke study for standardization and science on Korean Medicine' Results : Complications were recorded in 23 cases (24%). The most common complication was upper respiration infection in 11 cases (11%). No statistical significance was shown between complications of AICD and Sasangconstitutions, but complications rate of LAA was higher than SVO in AICD patients (odds ratio 4.17 95% CI 1.127${\sim}$7.307). Conclusions : To acquire more concrete data on this theme. we need further and larger scale research.

• The Korean Journal of Physiology and Pharmacology
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• v.18 no.1
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• pp.73-78
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• 2014

Cell death and survival are tightly controlled through the highly coordinated activation/inhibition of diverse signal transduction pathways to insure normal development and physiology. Imbalance between cell death and survival often leads to autoimmune diseases and cancer. Death receptors sense extracellular signals to induce caspase-mediated apoptosis. Acting upstream of CED-3 family proteases, such as caspase-3, Bcl-2 prevents apoptosis. Using short hairpin RNAs (shRNAs), we suppressed Bcl-2 expression in Jurkat T cells, and this increased TCR-triggered AICD and enhanced TNFR gene expression. Also, knockdown of Bcl-2 in Jurkat T cells suppressed the gene expression of FLIP, TNF receptor-associated factors 3 (TRAF3) and TRAF4. Furthermore, suppressed Bcl-2 expression increased caspase-3 and diminished nuclear factor kappa B (NF-${\kappa}B$) translocation.