Relevant bibliographies by topics / ICA512

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Academic literature on the topic 'ICA512'

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Published: 4 June 2021
Last updated: 13 February 2022

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Journal articles on the topic "ICA512"

1

Gianani, R., D. U. Rabin, C. F. Verge, L. Yu, S. R. Babu, M. Pietropaolo, and G. S. Eisenbarth. "ICA512 Autoantibody Radioassay." Diabetes 44, no. 11 (November 1, 1995): 1340–44. http://dx.doi.org/10.2337/diab.44.11.1340.

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2

Gianani, R., D. U. Rabin, C. F. Verge, L. Yu, S. R. Babu, M. Pietropaolo, and G. S. Eisenbarth. "ICA512 autoantibody radioassay." Diabetes 44, no. 11 (November 1, 1995): 1340–44. http://dx.doi.org/10.2337/diabetes.44.11.1340.

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3

Torkko, Juha M., M. Evangelina Primo, Ronald Dirkx, Anne Friedrich, Antje Viehrig, Elisa Vergari, Barbara Borgonovo, et al. "Stability of proICA512/IA-2 and Its Targeting to Insulin Secretory Granules Require β4-Sheet-Mediated Dimerization of Its Ectodomain in the Endoplasmic Reticulum." Molecular and Cellular Biology 35, no. 6 (January 5, 2015): 914–27. http://dx.doi.org/10.1128/mcb.00994-14.

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The type 1 diabetes autoantigen ICA512/IA-2/RPTPN is a receptor protein tyrosine phosphatase of the insulin secretory granules (SGs) which regulates the size of granule stores, possibly via cleavage/signaling of its cytosolic tail. The role of its extracellular region remains unknown. Structural studies indicated that β2- or β4-strands in the mature ectodomain (ME ICA512) form dimers in vitro . Here we show that ME ICA512 prompts proICA512 dimerization in the endoplasmic reticulum. Perturbation of ME ICA512 β2-strand N-glycosylation upon S508A replacement allows for proICA512 dimerization, O -glycosylation, targeting to granules, and conversion, which are instead precluded upon G553D replacement in the ME ICA512 β4-strand. S508A/G553D and N506A/G553D double mutants dimerize but remain in the endoplasmic reticulum. Removal of the N-terminal fragment (ICA512-NTF) preceding ME ICA512 allows an ICA512-ΔNTF G553D mutant to exit the endoplasmic reticulum, and ICA512-ΔNTF is constitutively delivered to the cell surface. The signal for SG sorting is located within the NTF RESP18 homology domain (RESP18-HD), whereas soluble NTF is retained in the endoplasmic reticulum. Hence, we propose that the ME ICA512 β2-strand fosters proICA512 dimerization until NTF prevents N506 glycosylation. Removal of this constraint allows for proICA512 β4-strand-induced dimerization, exit from the endoplasmic reticulum, O -glycosylation, and RESP18-HD-mediated targeting to granules.
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4

Trajkovski, Mirko, Hassan Mziaut, Anke Altkrüger, Joke Ouwendijk, Klaus-Peter Knoch, Stefan Müller, and Michele Solimena. "Nuclear translocation of an ICA512 cytosolic fragment couples granule exocytosis and insulin expression in β-cells." Journal of Cell Biology 167, no. 6 (December 13, 2004): 1063–74. http://dx.doi.org/10.1083/jcb.200408172.

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Islet cell autoantigen 512 (ICA512)/IA-2 is a receptor tyrosine phosphatase-like protein associated with the insulin secretory granules (SGs) of pancreatic β-cells. Here, we show that exocytosis of SGs and insertion of ICA512 in the plasma membrane promotes the Ca2+-dependent cleavage of ICA512 cytoplasmic domain by μ-calpain. This cleavage occurs at the plasma membrane and generates an ICA512 cytosolic fragment that is targeted to the nucleus, where it binds the E3-SUMO ligase protein inhibitor of activated signal transducer and activator of transcription-y (PIASy) and up-regulates insulin expression. Accordingly, this novel pathway directly links regulated exocytosis of SGs and control of gene expression in β-cells, whose impaired insulin production and secretion causes diabetes.
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Myers, M. A., M. R. Laks, S. J. Feeney, T. E. Mandel, M. Koulmanda, A. Bone, J. Barley, M. J. Rowley, and I. R. Mackay. "Antibodies to ICA512/IA-2 in Rodent Models of IDDM." Journal of Autoimmunity 11, no. 3 (June 1998): 265–72. http://dx.doi.org/10.1006/jaut.1998.0192.

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Sosa, Laura, Juha M. Torkko, María E. Primo, Ramiro E. Llovera, Pamela L. Toledo, Antonella S. Rios, F. Luis Gonzalez Flecha, et al. "Biochemical, biophysical, and functional properties of ICA512/IA-2 RESP18 homology domain." Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics 1864, no. 5 (May 2016): 511–22. http://dx.doi.org/10.1016/j.bbapap.2016.01.013.

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Mayrhofer, M., D. U. Rabin, L. Messenger, E. Standl, and A. G. Ziegler. "Value of ICA512 antibodies for prediction and diagnosis of type 1 diabetes." Early Human Development 47, no. 1 (January 1997): 106. http://dx.doi.org/10.1016/s0378-3782(97)81307-2.

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8

Sanda, Srinath. "Increasing ICA512 autoantibody titers predict development of abnormal oral glucose tolerance tests." Pediatric Diabetes 19, no. 2 (July 14, 2017): 271–76. http://dx.doi.org/10.1111/pedi.12542.

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9

Mayrhofer, M., D. U. Rabin, L. Messenger, E. Standl, and A. G. Ziegler. "Value of ICA512 antibodies for prediction and diagnosis of type 1 diabetes." Experimental and Clinical Endocrinology & Diabetes 104, no. 03 (July 15, 2009): 228–34. http://dx.doi.org/10.1055/s-0029-1211447.

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10

Mziaut, H., S. Kersting, K. P. Knoch, W. H. Fan, M. Trajkovski, K. Erdmann, H. Bergert, F. Ehehalt, H. D. Saeger, and M. Solimena. "ICA512 signaling enhances pancreatic -cell proliferation by regulating cyclins D through STATs." Proceedings of the National Academy of Sciences 105, no. 2 (January 4, 2008): 674–79. http://dx.doi.org/10.1073/pnas.0710931105.

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Dissertations / Theses on the topic "ICA512"

1

Schubert, Sandra. "The Role of [beta]2-Syntrophin Phosphorylation in Secretory Granule Exocytosis." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2006. http://nbn-resolving.de/urn:nbn:de:swb:14-1146851994562-42414.

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The trafficking of insulin secretory granules(SGs) of pancreatic b-cells is a tightly controlled complex network. Increasing evidence indicates that the cortical actin cytoskeleton modulates the mobility and exocytosis of SGs,yet the mechanisms anchoring SGs to the cytoskeleton is not completely understood.It has been shown by Ort et al.(2000,2001) that the cytoplasmic tail of an intrinsic membrane protein of the SGs named ICA512/IA-2 binds the PDZ domain of b2-syntrophin,which in turn binds to the F-actin-binding protein utrophin. These data also indicate that stimulation of SG exocytosis affects the phosphorylation of b2-syntrophin,hence altering its binding to ICA512.Therefore a model was proposed whereby SGs are anchored to the actin cytoskeleton through the ICA512/b2-syntrophin complex, whose dynamics are regulated by phosphorylation.To test this model GFP-b2-syntrophin stable INS-1 cell clones were generated.GFP-b2-syntrophin expression and localization pattern were similar to those of the endogenous protein. Electron microscopy showed that in GFP-b2-syntrophin INS-1 cells the number of SGs with a pear-like shape was increased relative to control cells. Insulin content and stimulated secretion were increased in three GFP-â2-syntrophin INS-1 cell clones,compared to non-transfected INS-1 cells and INS-1 cells expressing GFP. These increments correlated with the different expression levels of GFP-b2-syntrophin in the three GFP-b2-syntrophin INS-1 cell clones. These findings support the hypothesis that b2-syntrophin regulates the trafficking and exocytosis of SGs by modulating their tethering to the actin cytoskeleton.In order to confirm the proposed model, the phosphorylation of b2-syntrophin was investigated in more detail. Similar to endogenous b2-syntrophin,GFP-b2-syntrophin underwent Ca2+-dependent and okadaic acid-sensitive dephosphorylation upon stimulation of insulin secretion. Stimulation-dependent dephosphorylation was confirmed by immunoprecipitation of 32P-labeled GFP-b2-syntrophin.Mass spectrometry of immunoprecipitated GFP-b2-syntrophin allowed the identification of four serine-phosphorylation sites (S75,S90,S213,S373) that could affect the binding to ICA512.Mutants,in which all four phosphoserines, were replaced by either asp or ala to mimic(S/D) or prevent(S/A) phosphorylation were expressed in INS-1 cells. All S/D mutants retained a cortical localization,but by immunoblotting the pattern of the S75D allele differed from wild type and all other S/D alleles.Conversely, all S/A alleles were diffused cytosolically, except S213A,which was still restricted to the cortex. Finally, pull down assays showed increased binding of ICA512 to the S75A and S90D alleles compared to wild type b2-syntrophin,while the opposite was observed with the S75D and S90A mutants.Additionally,both the S75 and the S213 allele conform a consensus for phosphorylation by Cdk5,which is known to modulate insulin secretion. The phosphorylation of GFP-b2-syntrophin and particularly the S75 allele by Cdk5 was exhibited with pharmacological inhibitors,by in vitro phosphorylation and by RNAi. Taken together, these findings are consistent with the model by which phosphorylation of b2-syntrophin modulates the tethering of SGs to the cytoskeleton, and thereby their mobility and exocytosis. Specifically, the data of this thesis suggest that Cdk5-dependent phosphorylation of the S75 site of GFP-b2-syntrophin facilitates insulin secretion by reducing the interaction of b2-syntrophin with ICA512,thereby decreasing the actin cytoskeleton constrain on SG mobility. This process could occur in combination with the phosphatase-dependent dephosphorylation of b2-syntrophin at phosphosites other than S75
Der Transport Insulin-gefüllter sekretorische Granula(SG) ist ein streng kontrollierter komplexer Prozess.Es gibt vermehrt Beweise,dass das kortikale Actinzytoskelett die Ausschüttung der SGs beeinflusst.Bisher ist der Mechanismus der Verankerung von SGs am Zytoskelett noch nicht vollständig aufgeklärt.Ort et al.(2000,2001) haben gezeigt,daß der zytosoplasmatische Teil des trans-membranen SG-Proteins ICA512 mit der PDZ-Domäne von b2-Syntrophin interagiert.Dieses Protein bindet das F-Actin-Bindeprotein Utrophin.Die Ergebnisse zeigen außerdem,daß durch Stimulation der SG-Exozytose der Phosphorilierungsstatus von b2-Syntrophin beeinflusst wird,woraus ein verändertes Bindungsvermögen zu ICA512 resultiert.Es wurde ein Funktionsmodel vorgestellt,in dem sich SGs durch die Interaktion des ICA512/b2-Syntrophin Komplexes an das Actinzytoskelett binden.Dabei wird die Bindedynamik durch Phosphorilierung reguliert.Um dieses Model zu etablieren,wurden stabile GFP-b2-Syntrophin produzierende INS-1-Zellklone erzeugt.Die zelluläre Lokalisation und das Expressionsmuster von GFP-b2-Syntrophin stimmen mit dem des endogenen Proteins überein.Elektronenmikroskopie zeigte eine größe Anzahl oval-verformter SGs in GFP-b2-Syntrophin INS-1-Zellen im Vergleich zu Kontrollzellen.Verglichen mit nicht-transfizierten INS-1 Zellen waren in drei GFP-b2-Syntrophin INS-1-Zellklonen der Insulingehalt der Zellen und die stimulierte Insulinsekretion erhöht.Die Werte korrelierten mit den unterschiedlichen GFP-b2-Syntrophin Expressionsmengen der Klone.Diese Ergebnisse untermauern die Hypothese,daß b2-Syntrophin den Transport und die Sekretion der SGs durch Modulation ihres Bindevermögens an Actin reguliert.Um das postulierte Model genauer zu prüfen,wurde die Phosphorilierung von b2-Syntrophin detaillierter untersucht.Das GFP-Protein wurde,ähnlich dem endogenen b2-Syntrophin,durch Stimulation der Insulinausschüttung dephosphoriliert.Diese Dephosphorilierung ist Ca2+-abhängig und Okadeinsäuresensitiv.Die stimulationsabhängige Dephosphorilierung wurde durch Immunoprezipitation von 32P-markiertem GFP-b2-Syntrophin bestätigt.Massenspektrometrie des präzipitierten Proteins ermöglichte die Identifikation von vier Serin-Phosphorilierungsstellen(S75,S90,S213,S373),welche die Bindung zu ICA512 beeinflussen könnten.Mutanten,in denen die vier Phosphoserine durch Asp beziehungsweise Ala ersetzt wurden,um entweder eine Phosphorilierung(S/D) oder Dephosphorilierung(S/A) nachzuahmen,wurden in INS-1-Zellen exprimiert.Alle S/D Mutanten blieben kortikal lokalisiert.Das Expressionsmuster des S75D Allels unterschied sich jedoch von denen des Wild-Typs(wt).Im Gegensatz dazu waren alle S/A Allele zytosolisch verteilt.Eine Ausnahme bildete S213A,das an der Zellkortex lokalisiert blieb.Im Vergleich zu wt b2-Syntrophin zeigten PullDown-Assays eine erhöhte Bindung von ICA512 zu den S75A und S90D Allelen.Das Gegenteil konnte für die S75D und S90A Mutanten nachgewiesen werden.S75,S90 und S213 sind in einer Konsensussequenz für Cdk5-Phosphorilierung enthalten.Diese Kinase kann die Insulinsekretion regulieren.Die Phosphorilierung von b2-Syntrophin,insbesondere des S75 Allels durch Cdk5 wurde durch pharmakologische Inhibitoren,in vitro-Phosphorilierung und RNAi demonstriert.Zusammenfassend stimmen diese Erkenntnisse mit dem Model überein,daß die Phosphorilierung von b2-Syntrophin die Vernetzung von SGs mit Actin und dadurch deren Mobilität und Exozytose moduliert.Im Speziellen postulieren die Ergebnisse dieser Arbeit eine Cdk5-abhängige Phosphorilierung der S75 Stelle des b2-Syntrophins.Durch eine verminderte Interaktion von b2-Syntrophin und ICA512 erleichtert diese Mutante vermutlich die Insulinsekretion,da der Einfluss des Actinzytoskeletts auf die Granulamobilität vermindert ist.Dieser Prozess ereignet sich möglicherweise in Kombination mit einer Dephosphorilierung des b2-Syntrophins.in Kombination mit einer Dephosphorilierung des b2-Syntrophins
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2

Schubert, Sandra. "The Role of [beta]2-Syntrophin Phosphorylation in Secretory Granule Exocytosis." Doctoral thesis, Technische Universität Dresden, 2005. https://tud.qucosa.de/id/qucosa%3A23710.

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Abstract:
The trafficking of insulin secretory granules(SGs) of pancreatic b-cells is a tightly controlled complex network. Increasing evidence indicates that the cortical actin cytoskeleton modulates the mobility and exocytosis of SGs,yet the mechanisms anchoring SGs to the cytoskeleton is not completely understood.It has been shown by Ort et al.(2000,2001) that the cytoplasmic tail of an intrinsic membrane protein of the SGs named ICA512/IA-2 binds the PDZ domain of b2-syntrophin,which in turn binds to the F-actin-binding protein utrophin. These data also indicate that stimulation of SG exocytosis affects the phosphorylation of b2-syntrophin,hence altering its binding to ICA512.Therefore a model was proposed whereby SGs are anchored to the actin cytoskeleton through the ICA512/b2-syntrophin complex, whose dynamics are regulated by phosphorylation.To test this model GFP-b2-syntrophin stable INS-1 cell clones were generated.GFP-b2-syntrophin expression and localization pattern were similar to those of the endogenous protein. Electron microscopy showed that in GFP-b2-syntrophin INS-1 cells the number of SGs with a pear-like shape was increased relative to control cells. Insulin content and stimulated secretion were increased in three GFP-â2-syntrophin INS-1 cell clones,compared to non-transfected INS-1 cells and INS-1 cells expressing GFP. These increments correlated with the different expression levels of GFP-b2-syntrophin in the three GFP-b2-syntrophin INS-1 cell clones. These findings support the hypothesis that b2-syntrophin regulates the trafficking and exocytosis of SGs by modulating their tethering to the actin cytoskeleton.In order to confirm the proposed model, the phosphorylation of b2-syntrophin was investigated in more detail. Similar to endogenous b2-syntrophin,GFP-b2-syntrophin underwent Ca2+-dependent and okadaic acid-sensitive dephosphorylation upon stimulation of insulin secretion. Stimulation-dependent dephosphorylation was confirmed by immunoprecipitation of 32P-labeled GFP-b2-syntrophin.Mass spectrometry of immunoprecipitated GFP-b2-syntrophin allowed the identification of four serine-phosphorylation sites (S75,S90,S213,S373) that could affect the binding to ICA512.Mutants,in which all four phosphoserines, were replaced by either asp or ala to mimic(S/D) or prevent(S/A) phosphorylation were expressed in INS-1 cells. All S/D mutants retained a cortical localization,but by immunoblotting the pattern of the S75D allele differed from wild type and all other S/D alleles.Conversely, all S/A alleles were diffused cytosolically, except S213A,which was still restricted to the cortex. Finally, pull down assays showed increased binding of ICA512 to the S75A and S90D alleles compared to wild type b2-syntrophin,while the opposite was observed with the S75D and S90A mutants.Additionally,both the S75 and the S213 allele conform a consensus for phosphorylation by Cdk5,which is known to modulate insulin secretion. The phosphorylation of GFP-b2-syntrophin and particularly the S75 allele by Cdk5 was exhibited with pharmacological inhibitors,by in vitro phosphorylation and by RNAi. Taken together, these findings are consistent with the model by which phosphorylation of b2-syntrophin modulates the tethering of SGs to the cytoskeleton, and thereby their mobility and exocytosis. Specifically, the data of this thesis suggest that Cdk5-dependent phosphorylation of the S75 site of GFP-b2-syntrophin facilitates insulin secretion by reducing the interaction of b2-syntrophin with ICA512,thereby decreasing the actin cytoskeleton constrain on SG mobility. This process could occur in combination with the phosphatase-dependent dephosphorylation of b2-syntrophin at phosphosites other than S75.
Der Transport Insulin-gefüllter sekretorische Granula(SG) ist ein streng kontrollierter komplexer Prozess.Es gibt vermehrt Beweise,dass das kortikale Actinzytoskelett die Ausschüttung der SGs beeinflusst.Bisher ist der Mechanismus der Verankerung von SGs am Zytoskelett noch nicht vollständig aufgeklärt.Ort et al.(2000,2001) haben gezeigt,daß der zytosoplasmatische Teil des trans-membranen SG-Proteins ICA512 mit der PDZ-Domäne von b2-Syntrophin interagiert.Dieses Protein bindet das F-Actin-Bindeprotein Utrophin.Die Ergebnisse zeigen außerdem,daß durch Stimulation der SG-Exozytose der Phosphorilierungsstatus von b2-Syntrophin beeinflusst wird,woraus ein verändertes Bindungsvermögen zu ICA512 resultiert.Es wurde ein Funktionsmodel vorgestellt,in dem sich SGs durch die Interaktion des ICA512/b2-Syntrophin Komplexes an das Actinzytoskelett binden.Dabei wird die Bindedynamik durch Phosphorilierung reguliert.Um dieses Model zu etablieren,wurden stabile GFP-b2-Syntrophin produzierende INS-1-Zellklone erzeugt.Die zelluläre Lokalisation und das Expressionsmuster von GFP-b2-Syntrophin stimmen mit dem des endogenen Proteins überein.Elektronenmikroskopie zeigte eine größe Anzahl oval-verformter SGs in GFP-b2-Syntrophin INS-1-Zellen im Vergleich zu Kontrollzellen.Verglichen mit nicht-transfizierten INS-1 Zellen waren in drei GFP-b2-Syntrophin INS-1-Zellklonen der Insulingehalt der Zellen und die stimulierte Insulinsekretion erhöht.Die Werte korrelierten mit den unterschiedlichen GFP-b2-Syntrophin Expressionsmengen der Klone.Diese Ergebnisse untermauern die Hypothese,daß b2-Syntrophin den Transport und die Sekretion der SGs durch Modulation ihres Bindevermögens an Actin reguliert.Um das postulierte Model genauer zu prüfen,wurde die Phosphorilierung von b2-Syntrophin detaillierter untersucht.Das GFP-Protein wurde,ähnlich dem endogenen b2-Syntrophin,durch Stimulation der Insulinausschüttung dephosphoriliert.Diese Dephosphorilierung ist Ca2+-abhängig und Okadeinsäuresensitiv.Die stimulationsabhängige Dephosphorilierung wurde durch Immunoprezipitation von 32P-markiertem GFP-b2-Syntrophin bestätigt.Massenspektrometrie des präzipitierten Proteins ermöglichte die Identifikation von vier Serin-Phosphorilierungsstellen(S75,S90,S213,S373),welche die Bindung zu ICA512 beeinflussen könnten.Mutanten,in denen die vier Phosphoserine durch Asp beziehungsweise Ala ersetzt wurden,um entweder eine Phosphorilierung(S/D) oder Dephosphorilierung(S/A) nachzuahmen,wurden in INS-1-Zellen exprimiert.Alle S/D Mutanten blieben kortikal lokalisiert.Das Expressionsmuster des S75D Allels unterschied sich jedoch von denen des Wild-Typs(wt).Im Gegensatz dazu waren alle S/A Allele zytosolisch verteilt.Eine Ausnahme bildete S213A,das an der Zellkortex lokalisiert blieb.Im Vergleich zu wt b2-Syntrophin zeigten PullDown-Assays eine erhöhte Bindung von ICA512 zu den S75A und S90D Allelen.Das Gegenteil konnte für die S75D und S90A Mutanten nachgewiesen werden.S75,S90 und S213 sind in einer Konsensussequenz für Cdk5-Phosphorilierung enthalten.Diese Kinase kann die Insulinsekretion regulieren.Die Phosphorilierung von b2-Syntrophin,insbesondere des S75 Allels durch Cdk5 wurde durch pharmakologische Inhibitoren,in vitro-Phosphorilierung und RNAi demonstriert.Zusammenfassend stimmen diese Erkenntnisse mit dem Model überein,daß die Phosphorilierung von b2-Syntrophin die Vernetzung von SGs mit Actin und dadurch deren Mobilität und Exozytose moduliert.Im Speziellen postulieren die Ergebnisse dieser Arbeit eine Cdk5-abhängige Phosphorilierung der S75 Stelle des b2-Syntrophins.Durch eine verminderte Interaktion von b2-Syntrophin und ICA512 erleichtert diese Mutante vermutlich die Insulinsekretion,da der Einfluss des Actinzytoskeletts auf die Granulamobilität vermindert ist.Dieser Prozess ereignet sich möglicherweise in Kombination mit einer Dephosphorilierung des b2-Syntrophins.in Kombination mit einer Dephosphorilierung des b2-Syntrophins.
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Kelle, Nicole [Verfasser], and Leticia [Akademischer Betreuer] Oliveira-Ferrer. "Einfluss von ICAM1, ICAM2 und BCAM auf die Metastasierung und die Prognose des Ovarialkarzinoms / Nicole Kelle ; Betreuer: Leticia Oliveira-Ferrer." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2019. http://d-nb.info/1181328934/34.

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4

Kelle, Nicole [Verfasser], and Ferrer Leticia [Akademischer Betreuer] Oliveira. "Einfluss von ICAM1, ICAM2 und BCAM auf die Metastasierung und die Prognose des Ovarialkarzinoms / Nicole Kelle ; Betreuer: Leticia Oliveira-Ferrer." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2019. http://nbn-resolving.de/urn:nbn:de:gbv:18-96219.

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5

Allingham, Michael John Burridge Keith. "Novel roles for ICAM1 in leukocyte transendothelial migration." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2007. http://dc.lib.unc.edu/u?/etd,1208.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2007.
Title from electronic title page (viewed Mar. 26, 2008). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department Cell and Developmental Biology." Discipline: Cell and Developmental Biology; Department/School: Medicine.
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Bonan, Stéphanie. "Rôle d’ICAM-1 dans le remodelage de la matrice extracelllulaire par les fibroblastes tumoraux." Thesis, Nice, 2016. http://www.theses.fr/2016NICE4043/document.

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Les carcinomes évoluent dans un microenvironnement inflammatoire composé de cellules stromales (fibroblastes, cellules endothéliales et immunitaires) immergées dans une matrice extracellulaire (MEC). Les fibroblastes associés aux carcinomes (FACs) déposent et remodèlent la MEC dans le but de la rendre permissive à la croissance et l’invasion tumorale. Parmi les facteurs pro-inflammatoires responsables de l’activation des fibroblastes résidents, la cytokine Leukemia Inhibitory Factor (LIF) détient un rôle capital. En régulant l’activité de la chaîne légère de la myosine II (MLC-II), LIF induit la contractilité du cytosquelette d’actomyosine, générant des forces de tension et le remodelage de la MEC par les FACs. En revanche, les gènes régulés par LIF impliqués dans le phénotype pro-invasif des FACs ne sont pas connus. A l’aide d’un criblage phénotypique en trois dimensions, nous avons identifiés ICAM-1 comme régulateur majeur du remodelage de la MEC par les FACs. Nous démontrons qu’ICAM-1 est nécessaire et suffisant pour induire la réorganisation de la MEC indispensable à l’invasion collective des cellules de carcinome squameux. En effet, ICAM-1 est un régulateur de la contractilité cellulaire dépendante de la voie de signalisation RhoA-ROCK et de la kinase Src. De plus, la contractilité cellulaire régule l’expression d’ICAM-1, menant ainsi à une boucle de régulation positive. Nous proposons alors qu’ICAM-1 représente une cible thérapeutique afin de lutter contre l’invasion tumorale et la dissémination métastatique
Acto-myosin contractility in carcinoma-associated fibroblasts leads to the assembly of the tumor extracellular matrix. The pro-inflammatory cytokine LIF governs fibroblast activation in cancer by regulating the myosin light chain 2 activity. So far, however, how LIF mediates cytoskeleton contractility remains unknown. Using phenotypic screening assays based on knock down of LIF-dependent genes in fibroblasts, we identified ICAM1 as a crucial regulator of stroma fibroblast proinvasive matrix remodeling. We demonstrate that ICAM1 is necessary and sufficient to promote inflammation-dependent extracellular matrix organization, which leads to cancer cell invasion. Indeed, ICAM1 mediates generation of acto-myosin contractility downstream of the Src kinases in stromal fibroblasts. Moreover, acto-myosin contractility regulates ICAM1 expression, establishing a positive feedback signaling. Thus, targeting stromal ICAM1 might constitute a possible therapeutic mean to counteract tumor cell invasion and dissemination
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Costa, Raimundo Nonato Pereira da. "Polimorfismo dos genes PSGL-1, ICAM1, CD18, mieloperoxidade e manifestações clinicas na anemia falciforme." [s.n.], 2004. http://repositorio.unicamp.br/jspui/handle/REPOSIP/316739.

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Orientador: Fernando Ferreira Costa
Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: Anemia falciforme (AF) é uma doença monogênica, mas com uma apresentação clínica variável, devido a possível associação com outros genes. Especula-se que nesta doença genes envolvidos com a resposta inflamatória tenham efeito epistático. A mieloperoxidase (MPO) é uma enzima com atividade antimicrobicida, sendo encontrada nos grânulos azurofilicos dos neutrófilos. O polimorfismo A-463MPO diminui a expressão desta enzima, podendo este alelo ser possível marcador para eventos infecciosos em pacientes com defesa imune já comprometida. Neste estudo 97 pacientes com AF acompanhado pelo ambulatório de hematologia-Unicamp foram inicialmente divididos em dois grupos, conforme o número de internamentos hospitalares para antibioticoterapia: pacientes que não apresentaram infecção com necessidade de intemação (64 pacientes) e um segundo grupo onde ocorreu pelo menos 1 episódio de hospitalização devido a infecção (33 pacientes). O grupo controle foi composto por 48 indivíduos sadios negros da Babia-BrasiL Pacientes e controles foram genotipados para o polimorfismo G/A-463MPO, através da técnica de "Conformation Sensitive Gel Eletrophoresis" (CSGE) e sequenciamento automatizado. Observou-se que a presença do genótipo AA ou AG está associado a maior número de eventos infecciosos (P=O.005 OR=3.8). Esta correlação também foi observada na análise quanto à presença do alelo A-463MPO (P=0.004 OR=2.7). Este achado sugere que deficiência de MPO em pacientes com AF provavelmente favorece a ocorrência de eventos infecciosos. Vaso oclusão é o principal evento nas crises dolorosas dos pacientes com anemia falciforme (AF) e marcadores genéticos de risco para eventos vaso oclusivos ainda são desconhecidos. Polimorfismos em genes envolvidos na adesão celular PSGL-l (VNTR no exon 2), ICAM-1 G241R e K461E) e CD18 (V441V) foram genotipados em 103 pacientes com AF. Os pacientes foram inicialmente divididos em dois grupos: pacientes em que ocorre acidente vascular cerebral (AF+A VC,16 pacientes) e pacientes sem ocorrência de A VC (AF-A VC, 87 pacientes). Posteriormente, os pacientes foram divididos em outros dois grupos: pacientes em que foi detectado um dos seguintes eventos: A VC, síndrome torácica aguda (STA), necrose asséptica de cólo de fêmur (NACF) e priapismo (AF+FVO, 35 pacientes) e pacientes em que não ocorrem essas complicações (AF-FVO, 70 pacientes). PSGL-l é um receptor nas células mielóides e linfócitos T estimulados de alta afinidade para P-selectinas, tendo fundamental papel na adesão dos leucócitos às plaquetas e ao endotélio. O gene contém 3 variantes alélicas (A, B, C) de um número variável de repetição "in tandem" (VNTR). A análise das freqüências dos genótipos e alelos revelou associação da variante B com o grupo AF+FVO [p=O.04, IC 95% OR=2 (1-4)] e quase significante com os casos de A VC [p=0.09, IC 95% OR=2 (0.8-4.9)], enquanto que o alelo A revelou nível significativo de associação com o grupo AF+FVO [p=O.Ol IC 95% OR=O.5 (0.2 0.9)]. O gene da molécula de adesão leucócitário CD-I8 é a beta-2 subunidade das integrinas a_heterodímeros. O polimorfismo C1323T foi recentemente implicado como fator de risco para fenômenos vaso oc1usivos. O estudo deste polimorfismo em pacientes portadores de anemia falciforme não revelou associação significativa com FVO ou A VC. ICAM-l é uma molécula da superfamília das imunoglobulinas com importante papel na adesão das células endotelial-leucócitos durante a resposta inflamatória. No mínimo dois sítios polimórficos são conhecidos R241E e K469E. Ambos sítios estão envolvidos na ligação aos contrareceptores Mac-I e LF A-I. A análise destes polimorfismos através da técnica de CSGE e seqüenciamento, revelou uma associação significativa do heterozigoto K469E para risco a A VC [P=0.02 IC 95% OR=3.6 (1.1-12.3)]. No entanto, o estudo falhou em demonstrar associação alélica com os casos de A VC ou FVO. Como não se conhece bem a relação funcional deste polimorfismo, maiores estudos são necessários incluindo análise funcional, para se esclarecer o real papel deste polimorfismo ao risco a AVC
Abstract: Not informed
Mestrado
Genetica Medica
Mestre em Genética e Biologia Molecular
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Zhang, Lixiao. "HYPERHOMOCYSTEINEMIA ACCELERATES STROKE-INDUCED BRAIN INJURY VIA PROMOTING ENDOTHELIAL ACTIVATION AND INFLAMMATORY CELL INFILTRATION: THE ROLE OF ICAM1-MEDIATED NEUTROPHIL AND MONOCYTE INFILTRATION." Diss., Temple University Libraries, 2017. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/450002.

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Pharmacology
Ph.D.
Background: Epidemiology, clinical trials and meta-analysis studies have established that Hyperhomocysteinemia (HHcy) is an independent risk factor for stroke. However, the exact molecular mechanism underlying the HHcy-induced risk of stroke is unclear. Our study aims to investigate the role of HHcy in stroke. Methods and results: We established a mice mode of focal ischemic stroke, termed transient Middle Cerebral Artery Occlusion (tMCAO) and conducted surgery on a mice model of HHcy (plasma homocysteine level ~150μM), in which a Zn2+ inducible human cystathionine β-synthase (CBS) transgene was introduced to circumvent the neonatal lethality of the CBS gene deficiency (Tg-hCBS Cbs-/- mice). Fourteen-week-old male mice were used in the experiment. A student’s t-test was used for the evaluation of the statistical significance between the two groups. For the comparison across multiple groups, one-way ANOVA was used. We found that HHcy 1) increased the infarction volume from 42.3 ± 4.9 mm
Temple University--Theses
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Cavichioli, Débora. "Poliformismos dos genes LIGHT, MMP9, LTα, LGALS2, VCAM1, ICAM1, E-SELECTINA e NFκB podem estar associados com doença arterial coronariana." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/9/9136/tde-10092012-140624/.

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INTRODUÇÃO: A síndrome coronariana aguda (SCA) constitui uma síndrome clínica geralmente causada por doença arterial coronariana (DAC) aterosclerótica e está associada ao infarto agudo do miocárdio (IAM) que pode muitas vezes levar a óbito. Aterosclerose é uma doença progressiva, sistêmica e de inicio precoce caracterizada pelo acúmulo de lipides e elementos fibrosos nas grandes artérias e recentemente foi considerada como uma afecção de origem inflamatória. OBJETIVO: Avaliar a frequência genotípica de E-SELECTINA, MMP9, LIGHT, LTα, VCAM1, ICAM1, LGALS2 e NFκB em pacientes com infarto agudo do miocárdio (IAM), angina instável (AI) e indivíduos que foram submetidos á angiocoronariografia e que apresentaram ausência de processo ateromatoso significativo. Assim como analisar a associação dos polimorfismos com a concentração sérica das formas solúveis das proteínas com a expressão gênica em leucócitos do sangue periférico, procurando estabelecer modelo de analise menos invasiva da aterosclerose. CASUÍSTICA E MÉTODOS: O estudo foi realizado em um grupo de pacientes recrutados no Instituto Dante Pazzanese de Cardiologia (IDPC) com infarto agudo do miocárdio, angina instável e indivíduos que foram submetidos á angiocoronariografia e que apresentaram ausência de processo ateromatoso significativo. Foram incluídos no estudo 93 indivíduos sendo 47 com IAM com e sem supra ST compondo o grupo IAM e 46 com AI ou que foram submetidos á angiocoronariografia e que apresentaram ausência de processo ateromatoso significativo compondo o grupo SIAM, de ambos os sexos com idades entre 45 e 90 anos. Foi realizado o estudo dos polimorfismos dos genes LIGHT (rs344560 e rs2291668), MMP9 (rs17576), LTα (rs909253 e rs1041981), LGALS2 (rs7291467), VCAM1 (rs3176878), ICAM1 (rs281432), E-SELECTINA (rs5368) e NFκB (rs17032705) por pirosequenciamento, a análise da expressão dos genes LIGHT, MMP9, LTα, VCAM1, ICAM1 e NFκB por PCR em tempo real e a dosagem das formas solúveis de VCAM1, ICAM1, E-SELECTINA e MMP9 utilizando o sistema LUMINEX. RESULTADOS: A frequência alélica e genotípica dos polimorfismos estudados (LIGHT [rs344560 e rs2291668], MMP9 [rs17576)] LTα [rs909253 e rs1041981], LGALS2 [rs7291467], VCAM1 [rs3176878], ICAM1 [rs281432], E-SELECTINA [rs5368] e NFκB [rs17032705]) não apresentou relação com doença arterial coronariana. Foi encontrada associação da expressão de LTα com síndrome coronariana aguda (p<0,05) e relação de alguns dos polimorfismos estudados (6+3279C>T de LGALS2, 8+10029G>A de NFκB, 332-3499C>G de ICAM1, Lys178Glu de LIGHT e Asp693Asp de VCAM1) com alterações na expressão gênica, formas solúveis e parâmetros bioquímicos. CONCLUSÕES: Não houve associação dos polimorfismos estudados com síndrome coronariana aguda assim como não houve associação das formas solúveis. Em relação á expressão gênica, foi encontrada associação da expressão de LTα com síndrome coronariana aguda (p<0,05) e alguns dos polimorfismos estudados (6+3279C>T de LGALS2, 8+10029G>A de NFκB, 332-3499C>G de ICAM1, Lys178Glu de LIGHT e Asp693Asp de VCAM1)ocasionaram alterações da expressão gênica, formas solúveis e parâmetros bioquímicos.
BACKGROUND: : Acute coronary syndrome (ACS) is a clinical syndrome usually caused by atherosclerotic coronary artery disease (CAD) and is associates with acute myocardial infarction (AMI) and sometimes can take to death. Atherosclerosis is a progressive disease characterized by the accumulation of lipides and fibrous elements in arteries and recently was considered a disease of inflammatory origin. OBJECTIVE: : Evaluated the genotypic frequency of E-SELECTIN, MMP9, LIGHT, LTα, VCAM1, ICAM1, LGALS2 e NFκB in patients with acute myocardial infarction, unstable angina and individuals who were submitted to coronary angiography and had absence of significant atheromathous process. As well as analyze the polymorphism association with serum concentration of protein soluble forms with gene expression in peripheral blood leukocytes trying to establish a model less invasive to analyze atherosclerosis MATERIALS AND METHODS: : Study in a group of patients recruited in Dante Pazzanese of Cardiology Institute with acute myocardial infarction, unstable angina and in individuals who showed no significant atheromatous process. The study included 93 patients (47 with acute myocardial infarction and 46 with unstable angina or individuals who showed no significant atheromatous process) of both sexes with ages between 45 and 90 years. The genes polymorphisms study was by pyrosequencing, the gene expression was by PCR real time and soluble forms was dosage by LUMINEX. RESULTS: : The allelic and genotypic polymorphisms frequency studied (LIGHT [rs344560 e rs2291668], MMP9 [rs17576)] LTα [rs909253 e rs1041981], LGALS2 [rs7291467], VCAM1 [rs3176878], ICAM1 [rs281432], E-SELECTINA [rs5368] e NFκB [rs17032705]) don\'t presented relation with coronary arterial disease. Was found association with LTα gene expression and coronary acute syndrome (p<0,05) and relation of some polymorphism studied (6+3279C>T de LGALS2, 8+10029G>A de NFκB, 332-3499C>G de ICAM1, Lys178Glu de LIGHT e Asp693Asp de VCAM1) with changes in gene expression, serum soluble forms and biochemical parameters. CONCLUSION: : Do not have association between polymorphisms studied and serum soluble forms with acute coronary syndrome. Was found association with LTα gene expression and coronary acute syndrome (p<0,05) and relation of some polymorphism studied (6+3279C>T de LGALS2, 8+10029G>A de NFκB, 332-3499C>G de ICAM1, Lys178Glu de LIGHT e Asp693Asp de VCAM1) with changes in gene expression, serum soluble forms and biochemical parameters.
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Albrecht, Letusa. "Análise do repertório de genes variantes de Plasmodium falciparum da amazônia e identificação de genes variantes relacionados ao fenótipo de citoaderência a ICAM1 de isolados de Rondônia." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/42/42135/tde-23092008-153317/.

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Nesta tese estudamos os repertórios das famílias multigênicas var (domínio DBLa), rif e stevor, importantes fatores de virulência, de Plasmodium falciparum em isolados brasileiros. Mostramos que estas famílias multigênicas podem ser conservadas entre diferentes isolados no Brasil, sugerindo que o repertório de genes variantes pode ser limitado em algumas localidades. Identificamos menos polimorfismos nos genes stevor que os genes var ou rif. Constatamos que genes var podem ser conservados ao longo do tempo em isolados brasileiros. Identificamos também os domínios DBLa e DBLb de genes var associados a citoaderência a CHOICAM1 em isolados de Rondônia. Mediante ensaios de ELISA, mostramos que domínios DBLbICAM foram reconhecidos de modo heterogêneo. Por citometria de fluxo, demonstramos que o parasita aderente em ICAM1 foi reconhecido majoritariamente pelo plasma de pacientes com infecção sintomática e menos de infecção assintomática. Além disso, identificamos por PCR em tempo real os genes var transcritos no clone 3D7 aderente em diferentes linhagens de células CHO.
Herein, we studied the repertoire of multigenic families of var (DBLa domain), rif and stevor from brazilian isolates of Plasmodium falciparum. We showed that these multigenic families could be conserved among different isolates from Brazil, suggesting that the repertoire of variant genes can be limited in certain areas. We identified less polymorphism in stevor genes than in var or rif genes. We also demonstrated that var genes can be conserved over time in Brazilian isolates and identified the DBLa and DBLb domains from var genes associated with cytoadherence to CHOICAM1 in Rondonian isolates. ELISA assays showed that these DBLbICAM domains were recognized in a heterogeneous fashion. By flow cytometry, we demonstrated that ICAM1-adherent parasites were stronger recognized by plasma from symptomatic infections than from non-symptomatic infections. Finally, we profiled the var gene transcripts in 3D7 parasites adherent to different CHO cells by real time PCR.
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Books on the topic "ICA512"

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Weiland, Hasso, Anthony D. Rollett, and William A. Cassada, eds. ICAA13 Pittsburgh. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-48761-8.

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Weiland, Hasso, Anthony D. Rollett, and William A. Cassada, eds. ICAA13: 13th International Conference on Aluminum Alloys. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9781118495292.

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Book chapters on the topic "ICA512"

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Kessler, Olaf, Davit Zohrabyan, Benjamin Milkereit, and Christoph Schick. "Monitoring Precipitation during Rapid Quenching of Aluminium Alloys by Calorimetric Reheating Experiments." In ICAA13 Pittsburgh, 43–48. Cham: Springer International Publishing, 2012. http://dx.doi.org/10.1007/978-3-319-48761-8_8.

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Tayon, Wesley A., Marcia S. Domack, and Stephen J. Hales. "Correlation of Fracture Behavior with Microstructure in Friction Stir Welded, and Spin-Formed Al-Li 2195 Domes." In ICAA13 Pittsburgh, 623–28. Cham: Springer International Publishing, 2012. http://dx.doi.org/10.1007/978-3-319-48761-8_90.

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Biradar, N. S., and R. Raman. "Tailored Welding Technique for High Strength Al-Cu Alloy for Higher Mechanical Properties." In ICAA13 Pittsburgh, 945–50. Cham: Springer International Publishing, 2012. http://dx.doi.org/10.1007/978-3-319-48761-8_142.

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Ashida, Maki, and Zenji Horita. "Microstructures and Mechanical properties of Al-Al2O3 Composites Processed by Disk-HPT and Ring-HPT." In ICAA13 Pittsburgh, 1011–16. Cham: Springer International Publishing, 2012. http://dx.doi.org/10.1007/978-3-319-48761-8_151.

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Murakami, Tomoatsu, Kenji Matsuda, Tokimasa Kawabata, and Susumu Ikeno. "Tem Observation of Precipitates in Al-Mg-Ge Alloys with Different Mg2Ge Contents." In ICAA13 Pittsburgh, 1279–81. Cham: Springer International Publishing, 2012. http://dx.doi.org/10.1007/978-3-319-48761-8_196.

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Sample, Vivek M., and William A. Cassada. "Purification using high pressure molten aluminum." In ICAA13 Pittsburgh, 1343–48. Cham: Springer International Publishing, 2012. http://dx.doi.org/10.1007/978-3-319-48761-8_206.

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Zhang, L., D. G. Eskin, A. Miroux, and L. Katgerman. "Role of Solute and Transition Metals in Grain Refinement of Aluminum Alloys under Ultrasonic Melt Treatment." In ICAA13 Pittsburgh, 1389–94. Cham: Springer International Publishing, 2012. http://dx.doi.org/10.1007/978-3-319-48761-8_212.

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Okada, Minemitsu, and Seiichi Hirano. "Effect of Annealing Condition on Earing and Texture Formation in Cold Rolled AA5182 Aluminum Alloy." In ICAA13 Pittsburgh, 1587–92. Cham: Springer International Publishing, 2012. http://dx.doi.org/10.1007/978-3-319-48761-8_238.

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Li, X., W. Tang, and A. P. Reynolds. "Visualization of Material Flow in Friction Extrusion." In ICAA13 Pittsburgh, 1659–64. Cham: Springer International Publishing, 2012. http://dx.doi.org/10.1007/978-3-319-48761-8_248.

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McQueen, H. J. "Examining the Mechanisms of Dynamic Recrystallization (DRX) in Two-Phase Al Alloys." In ICAA13 Pittsburgh, 1761–66. Cham: Springer International Publishing, 2012. http://dx.doi.org/10.1007/978-3-319-48761-8_263.

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Conference papers on the topic "ICA512"

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Torkko, J., P. Toledo, A. Müller, C. Wegbrod, A. Sönmez, M. Solimena, and M. Ermácora. "ICA512 RESP18 homology domain is protein condensing factor and insulin fibrillation inhibitor." In Diabetes Kongress 2019 – 54. Jahrestagung der DDG. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1688114.

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Fichot, Florian, R. Gonzalez, P. Chatelard, B. Lefevre, and N. Garnier. "ICARE2 LATE PHASE DEGRADATION MODELS APPLICATION TO TMI-2 ACCIDENT." In Heat and Mass Transfer in Severe Nuclear Reactor Accidents. Proceedings of the International Symposium. Connecticut: Begellhouse, 1995. http://dx.doi.org/10.1615/ichmt.1995.radtransfprocheatmasstransfsevnuclreactacc.130.

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de Luze, Olivier, Georges Repetto, Nathalie Seiler, and Christina Dominguez. "Preliminary Analysis of Phebus FPT3 Experiment with the Severe Accident ICARE2 Code." In 14th International Conference on Nuclear Engineering. ASMEDC, 2006. http://dx.doi.org/10.1115/icone14-89191.

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The last test of the international Phebus Fission Product (FP) program, named FPT-3, has been performed in November 2004 at Cadarache. It used boron carbide as absorber material, instead of Ag-In-Cd in the previous tests. Such absorber material is used in power plants like BWR, VVER, some western type PWR and EPR, and the importance of its effects on the main degradation phenomena is still to be assessed. This paper relates the main experimental events issued from the test together with the interpretation work coming out from code calculations. Several results were unexpected and some are of importance for safety analyses, particularly concerning cladding oxidation and fuel degradation. The test interpretation has been undertaken with the ICARE2 code, developed by IRSN “Institut de Radioprotection et de Suˆrete´ Nucle´aire”. ICARE2 is the stand alone part of the mechanistic ICARE/CATHARE code, built for safety analyses purposes. In the last code versions, models deal with the degradation and the oxidation of the B4C control rod. Already validated against QUENCH experiments, these models have been applied to the Phebus FPT-3 conditions. Calculations show that, although general trends of the test are very well reproduced, specific effects concerning the interaction of B4C with the neighbouring rods cannot be calculated. Better detailed physical analysis and prediction capabilities of calculation tools are expected to come out from the International Source Term Program, in particular from the results of the BECARRE separate-effect-tests performed at IRSN. Though the detailed modelling of such interactions has still to be improved, the Phe´bus FP series of integral experiments have proved the capability of the program to significantly improve our understanding of the source term issue and important aspects of core degradation.
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Chatelard, Patrick, Joe¨lle Fleurot, Olivier Marchand, and Patrick Drai. "Assessment of ICARE/CATHARE V1 Severe Accident Code." In 14th International Conference on Nuclear Engineering. ASMEDC, 2006. http://dx.doi.org/10.1115/icone14-89307.

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The ICARE/CATHARE code system has been developed by the French “Institut de Radioprotection et de Suˆrete´ Nucle´aire” (IRSN) in the last decade for the detailed evaluation of Severe Accident (SA) consequences in a primary system. It is composed of the coupling of the core degradation IRSN code ICARE2 and of the thermalhydraulics French code CATHARE2. It has been extensively used to support the level 2 Probabilistic Safety Assessment (PSA-2) of the 900 MWe PWR. This paper presents the synthesis of the ICARE/CATHARE V1 assessment which was conducted in the frame of the “International ICARE/CATHARE Users’ Club”, under the management of IRSN. The ICARE/CATHARE V1 validation matrix is composed of more than 60 experiments, distributed in few thermal-hydraulics non-regression tests (to handle the front end phase of a severe accident), numerous Separate-Effect Tests, about 30 Integral Tests covering both the early and the late degradation phases, as well as a “circuit” experiment including hydraulics loops. Finally, the simulation of the TMI-2 accident was also added to assess the code against real conditions. This validation task was aimed at assessing the ICARE/CATHARE V1 capabilities (including the standalone ICARE2 V3mod1 version) and also at proposing recommendations for an optimal use of this version (“Users’ Guidelines”). Thus, with a correct account for the recommended guidelines, it appeared that the last ICARE/CATHARE V1 version could be reasonably used to perform best-estimate reactor studies up to a large corium slumping into the lower head.
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Kisselev, A., A. Voltcheck, V. F. Strizhov, A. Derugin, A. Porracchia, R. Gonzalez, and F. Jacq. "VERIFICATION OF MODIFIED VERSION OF SFD INTEGRAL CODE ICARE2 AGAINST C0RA-W2 (ISP-36) EXPERIMENTAL DATA." In Heat and Mass Transfer in Severe Nuclear Reactor Accidents. Proceedings of the International Symposium. Connecticut: Begellhouse, 1995. http://dx.doi.org/10.1615/ichmt.1995.radtransfprocheatmasstransfsevnuclreactacc.110.

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Lin, C., P. Tseng, F. Sung, and Y. Li. "The Association between ICAM1 Polymorphism and Second-Hand Smoke Exposure in Childhood Asthma." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5424.

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Hirz, Taghreed, Justine Esmenjaud, Anne Evesque, Doriane Mathe-Poloni, and Charles Dumontet. "Abstract 5014: Neutrophils protect B-cell lymphomas against chemotherapy via cell-cell interactions mediated by CD44 and ICAM1 receptors." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5014.

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Duspiva, Jirˇi´. "Implications of Quench Bundle Test Simulations for Plant Applications With MELCOR Code." In 16th International Conference on Nuclear Engineering. ASMEDC, 2008. http://dx.doi.org/10.1115/icone16-48168.

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Reflooding of an uncovered and overheated core is one of the most expected measures during the early phase of a severe accident progression. The capability of analytical tools to model correctly processes during independent sub-phases of this accident progression is on different levels, and the most concentrated effort is focused on the study of fuel cladding quenching topic. The main objective of the Forschungszentrum Karlsruhe (Germany) Quench experimental program is to investigate the hydrogen generation during the reflooding of overheated core. The Nuclear Research Institute Rez (hereafter NRI) contributes to this program by the analytical simulation of the Quench bundle experiments with the MELCOR code mainly and ICARE2 code as well since 2000. The NRI analyses covered the Quench-01, Quench-03 and Quench-06 with version MELCOR 1.8.5 (including reflood model), and Quench-01 and Quench-11 tests with the latest version MELCOR 1.8.6. The tests Quench-01 and Quench-06 were characteristic of the lower reflooding onset temperature (1900–2050 K), and the tests Quench-03 and Quench-11 had high reflooding onset temperature (&gt; 2350 K) with the fast heat-up phase before reflooding. The integral code MELCOR is capable to sufficiently predict the heat up and reflooding phases for the tests with the lower onset temperature, but the Quench-03 test with high onset temperature was not predicted correctly starting in the heat-up phase and also the hydrogen generation during bundle reflooding was significantly underpredicted. The interpretation of the Quench-03 test with ICARE2 code confirmed the MELCOR results, but its more detail description enabled to identify a cause. The underestimation of the bundle temperatures is influenced by the shroud insulation behaviour, which could be interpreted as the reduction of heat losses through shroud and simultaneously more intensive heat-up of a bundle. The phenomenon, which causes this behaviour, is not yet known, and is not important for plant applications, although it is relevant for the test interpretation. Also the interpretation of the Quench-11 showed an importance of correct modeling of the bundle shroud, which is in the MELCOR 1.8.6 simulated by newly implemented independent component. The Quench-11 test analysis showed simplified failure criteria for the cases when the shroud is not supported by the former components, which are assumed in the basic MELCOR model fundamentals. Concerning the plant application of the MELCOR code for the scenario with the overheated core reflooding, the user has to give attention on the correct treatment of heat losses through shroud and its degradation modeling, mainly if the shroud supporting formers absent in the core periphery design. Hydrogen generation during reflooding is predicted well for lower onset temperatures (below 2100 K) and slightly underpredicted for higher onset temperatures. It is important to take these code capabilities into account because a reflooding of the reactor core will consist of varied reflooding onset temperatures.
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MAKIEVSKAYA, C. I., V. V. SIDLYARCHUK, L. A. ZINOVKINA, and R. A. ZINOVKIN. "THE MITOCHONDRIAL-TARGETED COMPOUNDS C12TPP AND DNP DECREASE ICAM1 EXPRESSION IN EA.HY926 CELLS AND CAUSE CPG HYPERMETHYLATION IN ITS PROMOTER REGION." In HOMO SAPIENS LIBERATUS. TORUS PRESS, 2020. http://dx.doi.org/10.30826/homosapiens-2020-32.

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Koizume, Shiro, Shin Ito, Yoshiyasu Nakamura, Mitsuyo Yoshihara, Yasuo Takano, and Yohei Miyagi. "Abstract 502: Sp1 and HIFs mediate synergistic activation of ICAM1 gene under serum starved hypoxia and promotes growth of ovarian cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-502.

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