subject:(Intercellular adhesion molecule ICAM 1)

1. 이, 광민. Effect of IBC isolated from Psoralea corylifolia on expression of adhesion molecule-1 in cerebrovascular endothelial cells.

Degree: 2014, Ajou University

URL: http://repository.ajou.ac.kr/handle/201003/10854 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000016127

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Brain inflammation has been implicated in various cerebral diseases. Leukocyte-infiltration into brain parenchyma is critically associated with in the development brain inflammation. Therefore, control of… (more)

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Brain inflammation has been implicated in various cerebral diseases. Leukocyte-infiltration into brain parenchyma is critically associated with in the development brain inflammation. Therefore, control of leukocyte infiltration is a very important therapeutic target for the treatment of neurodegenerative diseases accompanied with inflammation such as Alzheimer’s disease and stroke. Isobavachalcone (IBC), a flavonoid from Psoralea corylifolia, is known to possess a wide spectrum of biological activities, antibacterial, antifungal, anticancer, anti-reverse transcriptase, antitubercular and antioxidant. Recently, it was reported that IBC suppresses LPS-induced iNOS expression and is expected to be useful for preventing or treating neurodegenerative disease. However, the effect of IBC on leukocyte-endothelial adhesion and expression of intercellular adhesion molecule-1(ICAM-1) in brain endothelial cells remains unexplored. In this study, we examined the effect of IBC on ICAM expression and leukocyte adhesion in bEnd. 3 cells and explored the possible mechanisms therein involved. IBC significantly down-regulated LPS-induced ICAM-1 expression and leukocytes-endothelial adhesion. IBC suppressed LPS-induced sequential events for NF-kB activation, that is, IkB-α phosphorylation, p65 translocation into nucleus and NF-kB transcriptional activity. TLR4 conveys LPS-signal to intracellular compartment via MyD88- and TRIF-dependentpathways,whichculminateintheactivationofNF-kB. As well as, IBC attenuated MALP-2 (a TLR2, 6 specific ligand)-induced ICAM-1 expression, IkB-alpha phosphorylation and NF-kB transcriptional activation. suggesting inhibition of MyD88-dependentsignaling pathway. IBC also down-regulated poly[I:C] (a TLR3 specific ligand)-induced expression ofICAM-1 and IFN-β,which was mediated suppression of NF-kB or IFN-β transcriptional activity, respectively. These data indicate TRIF-dependent signaling pathway is also blocked by IBC. Taken together, our data suggest that IBC inhibits LPS-induced ICAM-1 expression and leukocyte adhesion in brain endothelialcells and these effects are mediated by blockade ofMyD88-dependentand TRIF-dependentsignaling pathways and in turn,inhibition ofNF-kB activity.

뇌의 염증반응은 다양한 뇌질환에서 공통적으로 나타나는 특징 중의 하나이다. 뇌의 염증반응에서의 백혈구의 침윤(infiltration)과 이동(migration)은 다양한 뇌 질환의 진행과정과 함께 중요한 관계성을 가지고 있다. 따라서 염증반응에서 leukocyte infiltration의 조절은 Alzheimer's disease와 stroke등을 포함하는 퇴행성 뇌질환의 치료를 위해 아주 중요한 치료적 target으로 여겨지고 있다. Leukocyte의 infiltration은 혈관 내벽에 존재하는 세포부착분자들에 의해 발생 되어지는 것으로 알려져 있으며 세포부착분자 중 ICAM-1의 발현에 의해 강한 부착을 유발하여 leukocyte의 infiltration과 migration에 주된 역할을 한다. ICAM-1은 염증인자에 의해 발현이 조절되며, 특히 뇌혈관 장벽을 구성하는 주된 세포인 뇌혈관 내피세포에서의 발현은 뇌질환 발병 과정에 있어 중요한 역할을 하는 것으로 알려져 있다.따라서 ICAM-1 분자의 작용을 조절함으로써 퇴행성 뇌질환 및 뇌 손상과정에서의 염증반응을 조절하려는 시도가 이루어져 왔다. 파고지(Psoralea corylifolia)는 중국과 동아시아에서 뇌 노화에 대한 보호와 치매치료에 사용되어져 왔다. 이 밖에도 관절염 개선효과, 항산화작용 및 항암작용 등이 보고되어 있다. 파고지에서 분리한 IBC는 NO의 생성과 iNOS의 발현을 억제함으로써 뇌 염증작용의 억제를 통해 퇴행성뇌질환에서 동반되어 나타나는 염증작용의 치료제로서의 적용가능성이 시사된바 있다. 본 연구에서는 파고지에서 유래된 flavonoid 성분인 IBC가 염증성 자극에 의한 뇌혈관…

Advisors/Committee Members: 대학원 의생명과학과, 201124156, 이, 광민.

Subjects/Keywords: Isobavachalcone (IBC); Lipopolysacchariode (LPS); intercellular adhesion molecule 1 (ICAM-1); NF-kB; cerebrovascular endothelial cells(bEnd.3); TLR4 signaling

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

이, �. (2014). Effect of IBC isolated from Psoralea corylifolia on expression of adhesion molecule-1 in cerebrovascular endothelial cells. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/10854 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000016127

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

이, 광민. “Effect of IBC isolated from Psoralea corylifolia on expression of adhesion molecule-1 in cerebrovascular endothelial cells.” 2014. Thesis, Ajou University. Accessed April 10, 2021. http://repository.ajou.ac.kr/handle/201003/10854 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000016127.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

이, 광민. “Effect of IBC isolated from Psoralea corylifolia on expression of adhesion molecule-1 in cerebrovascular endothelial cells.” 2014. Web. 10 Apr 2021.

Vancouver:

이 �. Effect of IBC isolated from Psoralea corylifolia on expression of adhesion molecule-1 in cerebrovascular endothelial cells. [Internet] [Thesis]. Ajou University; 2014. [cited 2021 Apr 10]. Available from: http://repository.ajou.ac.kr/handle/201003/10854 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000016127.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

이 �. Effect of IBC isolated from Psoralea corylifolia on expression of adhesion molecule-1 in cerebrovascular endothelial cells. [Thesis]. Ajou University; 2014. Available from: http://repository.ajou.ac.kr/handle/201003/10854 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000016127

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

2. 박, 태엽. Effect of Prostaglandin E2 on the Expression of Adhesion Molecules in Mouse Cerebrovascular Endothelial Cells.

Degree: 2013, Ajou University

URL: http://repository.ajou.ac.kr/handle/201003/8610 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000015076

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Prostaglandin E2 (PGE2) is known to be the principal pro-inflammatory prostanoid and play an important role in brain disease through binding to four G protein-coupled… (more)

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Prostaglandin E2 (PGE2) is known to be the principal pro-inflammatory prostanoid and play an important role in brain disease through binding to four G protein-coupled receptor (EP1-4). However, there have been contradictory reports on its actions in inflammation processes. For instance, PGE2 inhibits or stimulates ICAM-1 expression depending on the cell type and experimental conditions. Furthermore, the effect of PGE2 on ICAM-1 expression in cerebrovascular endothelial cells is mostly unknown. In this study, it was investigated the roles of PGE2 in the expression of ICAM-1 in primary cultured mouse brain endothelial cells and bEnd.3 cells and therein involved signaling pathways. PGE2 induced ICAM-1 expression at the levels of protein and mRNA levels in the time and dose dependent manner and the effects was mediated by EP1/4. In order to delineate the intracellular signaling pathway, cAMP dependent signaling events were investigated. Though dbcAMP and forskolin mimicked the effect of PGE2, PKA inhibitors did not show significant effect on PGE2-induced ICAM-1 expression. However, involvement of Epac was confirmed by experiments using specific stimulators and inhibitors, and siRNA technology. PGE2 and dbcAMP stimulated phosphorylation of Akt and GSK-3β, suggesting the role of PI3K/Akt in PGE2-induced ICAM-1 expression. This inference was supported by the separate experiment using a PI3K inhibitor, LY294002, constitutive active (CA) and dominant negative (DN) Akt constructs. PGE2 induced the activation of NF-κB, critical regulator of ICAM-1 expression and NF-κB inhibitors blocked PGE2 and dbcAMP-induced ICAM-1 expression. Interestingly, loss of Akt activity results in inhibition of NF-κB activation. Taken together, these data suggest that PGE2 induces ICAM-1 expression through activation of EP4/cAMP/Epac and PI3K/NF-κB axis.

Prostaglandin E2 (PGE2)는 대표적인 염증성 인자로서 4가지 형태의 수용체 (EP1-4)와 결합함으로써 뇌염증 질환을 조절하는 것으로 알려져 있다. 뇌혈관 내 피세포에서의 PGE2의 염증인자로서의 역할에 대해서는 서로 상반된 작용이 보고 되어 있음에도 불구하고 그 작용 기전에 대해서는 거의 알려진 바가 없다. 따라서 PGE2의 염증 조절 기전을 이해하는 것은 다양한 뇌혈관 질환을 치료하기 위해 필요한 중요한 쟁점중의 하나라 할 수 있다. 본 연구에서는 이러한 PGE2가 blood-brain barrier (BBB)의 주요한 구성요소 중 하나인 생쥐 뇌혈관 내피세포주 (bEnd.3) 및 일차배양 생쥐 뇌혈관 내피세포에서 세포간 부착분자의 발현에 미치는 영향과 그 조절기전에 대해 알아보았다. PGE2를 처리하여 세포부착분자의 발현 변화를 확인한 결과, PGE2는 농도 의존적으로 intercellular adhesion molecule-1 (ICAM-1)의 발현을 증가시켰을 뿐만 아니라 U937 monocyte-bEnd.3 endothelial cell adhesion 역시 증가시킴을 확인하였다. 이러한 PGE2의 효과는 EP subtype 특이적 효능제 및 길항제와 siRNA를 이용한 실험결과 EP1/4 receptor를 경유함이 확인되었고, cAMP 의존적 세포내 신호전달 기전이 관여함이 확인되었다. 이에 PKA와 Epac의 특이적 활성제 및 억제제를 처리한 결과, PKA는 ICAM-1의 발현에 영향을 주지 못한 반면, Epac의 경우 유의적으로 ICAM-1 발현을 증가시킴이 확인 되었다. 또한 PGE2와 cAMP는 Akt와 GSK-3β의 인산화를 증진시킴이 확인되었고 이는 PGE2에 의해 유도되는 ICAM-1 발현 과정과 PI3K/Akt 신호전달 기전이 상관관계가 있음을 보여주었다. 이러한 사실은 PI3K 억제제인 LY294002, constitutive active Akt, 그리고 dominant-negative Akt를 이용한 실험결과에 의해 재확인되었다. 또한 PGE2는 ICAM-1의 발현에 주요한 조절인자인 NF-κB의 활성화를 유도하였을 뿐만 아니라, NF-κB의 억제제에 의해 PGE2와 dbcAMP에 의해 유도된 ICAM-1의 발현 역시 억제됨이 확인 되었다. 끝으로 이러한 NF-κB 활성은 앞서 확인된 Akt의 활성 억제에 의해 저해됨이 확인되었다. 이러한 결과는 PGE2와 EP4의 결합을 통한 Epac…

Advisors/Committee Members: 대학원 의생명과학과, 200624067, 박, 태엽.

Subjects/Keywords: Prostaglandin E2 (PGE2); intercellular adhesion molecule 1 (ICAM-1); Exchange protein activated by cAMP (Epac); cAMP; NF-κB; bEnd.3 mouse cerebrovascular endothelial cells; 뇌혈관 내피세포

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

박, �. (2013). Effect of Prostaglandin E2 on the Expression of Adhesion Molecules in Mouse Cerebrovascular Endothelial Cells. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/8610 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000015076

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

박, 태엽. “Effect of Prostaglandin E2 on the Expression of Adhesion Molecules in Mouse Cerebrovascular Endothelial Cells.” 2013. Thesis, Ajou University. Accessed April 10, 2021. http://repository.ajou.ac.kr/handle/201003/8610 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000015076.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

박, 태엽. “Effect of Prostaglandin E2 on the Expression of Adhesion Molecules in Mouse Cerebrovascular Endothelial Cells.” 2013. Web. 10 Apr 2021.

Vancouver:

박 �. Effect of Prostaglandin E2 on the Expression of Adhesion Molecules in Mouse Cerebrovascular Endothelial Cells. [Internet] [Thesis]. Ajou University; 2013. [cited 2021 Apr 10]. Available from: http://repository.ajou.ac.kr/handle/201003/8610 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000015076.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

박 �. Effect of Prostaglandin E2 on the Expression of Adhesion Molecules in Mouse Cerebrovascular Endothelial Cells. [Thesis]. Ajou University; 2013. Available from: http://repository.ajou.ac.kr/handle/201003/8610 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000015076

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

3. Θανοπούλου, Ειρήνη. Μελέτη του πολυμορφισμού g.1548G>A ( K469E) στο γονίδιο του ενδοκυττάριου προσκολλητικού μορίου - 1 ( ICAM - 1) στο μη - μικροκυτταρικό καρκίνο του πνεύμονος.

Degree: 2012, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/29559

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Background ICAM-1, a cell adhesion molecule with a key role in inflammation andimmunosurveillance, has been implicated in carcinogenesis by facilitating instability oftumor environment. The K469E… (more)

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Background ICAM-1, a cell adhesion molecule with a key role in inflammation andimmunosurveillance, has been implicated in carcinogenesis by facilitating instability oftumor environment. The K469E single nucleotide polymorphism (SNP) (G>A), affectsICAM-1 mRNA splicing pattern; the alternatively spliced isoform (ICAM-1-S) lackstransmembrane and intracellular domain, which affects the structural and signaltransduction properties. Moreover, the expression of ICAM-1 is transcriptionallyregulated by p53 and this SNP has been shown to be related with apoptosis.Methods PCR-RFLP analysis was used to assess the K469E SNP status comparatively in204 NSCLC patients and 175 healthy sex-matched controls. This SNP was examined inrelation to tumor kinetic parameters [Ki-67 immunohistochemical evaluation andTUNEL assay], p53 IHC status and clinicopathological data in patients with operablestages.Results Both the genotype and allele frequency did not differ significantly betweenpatients and controls. The GG genotype was significantly higher in patients with positivelymph nodes (N1, p=0.038), while the patients with AG/AA genotypes had worsesurvival (39 vs 45 months, p=0.036) and tended to present in advanced stages (p=0.058).Moreover, the AG/AA genotypes exerted a synergistic effect with aberrant p53 on tumorprogression, while the GG genotype retained a better apoptotic index (p=0.031).Conclusions There seems to be a controversy regarding the involvement of ICAM-1K469E isoforms in NSCLC. This can be attributed collectively to the: 1) multiplepresence of ICAM-1 in diverse tissue components, 2) role of ICAM-1 in various stages ofmalignant development, and 3) differential structural and functional properties of theseisoforms.

Εισαγωγή Το ICAM-1, ένα προσκολλητικό μόριο με ρόλο κλειδί στη φλεγμονή και τηνανοσοεπιτήρηση, έχει θεωρηθεί ότι εμπλέκεται στην καρκινογένεση διευκολύνοντας τηναστάθεια του μικροπεριβάλλοντος του όγκου. Ο μονονουκλεοτιδικός πολυμορφισμόςg.1548G>A (K469E), επιδρά στη διαδικασία του εναλλακτικού ματίσματος του ICAM-1mRNA. Η ισομορφή ICAM-1-S δεν έχει διαμεμβρανική και ενδοκυττάρια περιοχή,γεγονός που επηρεάζει τις δομικές και σηματοδοτικές ιδιότητες. Επιπλέον, η έκφρασητου ICAM-1 ρυθμίζεται σε μεταγραφικό επίπεδο από την πρωτεΐνη p53 και αυτός οπολυμορφισμός έχει δειχθεί ότι σχετίζεται με την απόπτωση.Μέθοδοι Πραγματοποιήθηκε ανάλυση PCR-RFLP για την εκτίμηση της κατάστασης τουπολυμορφισμού σε 204 ασθενείς με ΜΜΚΠ και 175 υγιείς εθελοντές. Ο πολυμορφισμόςεξετάστηκε σε σχέση με τις κινητικές παραμέτρους του όγκου [Ki-67 ανοσοϊστοχημικήεκτίμηση και μέθοδος TUNEL], την ανοσοϊστοχημική έκφραση της πρωτεΐνης p53 καιτα κλινικοπαθολογικά δεδομένα των ασθενών με χειρουργήσιμα στάδια.Αποτελέσματα Οι συχνότητες των γονοτύπων και των αλληλίων δεν διέφερανσημαντικά μεταξύ ασθενών και υγιών εθελοντών. Ο γονότυπος GG σχετίστηκε μεσημαντική αύξηση της πιθανότητας εμφάνισης λεμφαδενικής νόσου (Ν1, p=0.038), ενώοι ασθενείς με AG/AA γονότυπους παρουσίαζαν χειρότερη επιβίωση (39 vs 45 μήνες,p=0.036) και προχωρημένα στάδια (p=0.058),…

Subjects/Keywords: Ενδοκυττάριο προσκολλητικό μόριο -1 (ICAM-1); Μη-μικροκυτταρικός καρκίνος του πνεύμονος; μονονουκλεοτιδικός πολυμορφισμός g.1548G>; A (K469E); Intercellular adhesion molecule -1 (ICAM- 1); Non-small cell lung cancer; g.1548A >; G polymorphism - K469E; p53

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Θανοπούλου, . �. (2012). Μελέτη του πολυμορφισμού g.1548G>A ( K469E) στο γονίδιο του ενδοκυττάριου προσκολλητικού μορίου - 1 ( ICAM - 1) στο μη - μικροκυτταρικό καρκίνο του πνεύμονος. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/29559

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Θανοπούλου, Ειρήνη. “Μελέτη του πολυμορφισμού g.1548G>A ( K469E) στο γονίδιο του ενδοκυττάριου προσκολλητικού μορίου - 1 ( ICAM - 1) στο μη - μικροκυτταρικό καρκίνο του πνεύμονος.” 2012. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed April 10, 2021. http://hdl.handle.net/10442/hedi/29559.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Θανοπούλου, Ειρήνη. “Μελέτη του πολυμορφισμού g.1548G>A ( K469E) στο γονίδιο του ενδοκυττάριου προσκολλητικού μορίου - 1 ( ICAM - 1) στο μη - μικροκυτταρικό καρκίνο του πνεύμονος.” 2012. Web. 10 Apr 2021.

Vancouver:

Θανοπούλου �. Μελέτη του πολυμορφισμού g.1548G>A ( K469E) στο γονίδιο του ενδοκυττάριου προσκολλητικού μορίου - 1 ( ICAM - 1) στο μη - μικροκυτταρικό καρκίνο του πνεύμονος. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2012. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/10442/hedi/29559.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Θανοπούλου �. Μελέτη του πολυμορφισμού g.1548G>A ( K469E) στο γονίδιο του ενδοκυττάριου προσκολλητικού μορίου - 1 ( ICAM - 1) στο μη - μικροκυτταρικό καρκίνο του πνεύμονος. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2012. Available from: http://hdl.handle.net/10442/hedi/29559

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Tasmania

4. Shukla, SD. Studies on microbial adhesion factors in smoking and chronic obstructive pulmonary disease (COPD).

Degree: 2016, University of Tasmania

URL: https://eprints.utas.edu.au/23493/1/Shukla_whole_thesis.pdf

► Background: Chronic obstructive pulmonary disease (COPD) is emerging as the third largest cause of human mortality worldwide, killing over more than 3 million people annually.… (more)

▼ Background: Chronic obstructive pulmonary disease (COPD) is emerging as the third largest cause of human mortality worldwide, killing over more than 3 million people annually. It is a defined as a chronic inflammatory lung disease characterized by airflow limitation that is not fully reversible. Tobacco smoking is the single most important causative factor for the development of COPD, especially in developed countries. Colonization/infection of the lower respiratory tract with microorganisms in COPD is likely to be one of the important factors driving inflammatory processes in the airways, possibly leading to long-term progression and exacerbations of the disease. Nontypeable Haemophilus influenzae (NTHi) and Streptococcus pneumonia (S. pneumoniae) are the most important pulmonary bacteria during both stable phase of disease and exacerbations of COPD, but the underlying mechanisms for their prominence in these conditions remain elusive. Exposure to cigarette smoke has been shown to significantly increase pulmonary tissue bacterial infections (with both NTHi and S. pneumoniae) in cell culture and animal models, as well as human lung samples. Bacterial adherence to lung epithelium and subsequent tissue invasion is known to be a crucial step in the pathogenesis of respiratory infections. Notably, platelet activating factor receptor (PAFr) has been established as the primary attachment molecule for both NTHi and S. pneumoniae. Moreover, intercellular adhesion molecule-1 (ICAM-1) serves as an entry receptor for not only the majority (~60%) of human rhinoviruses (HRVs), but also for NTHi. Although the expression of these microbial receptors have been investigated in smokers, the expression pattern of these adhesion molecules in COPD has not been reported till date. Aims: I have investigated the expression pattern of airway epithelial PAFr and ICAM-1 in both the large and small airways, as well as lung parenchyma in tissues from: smoker with normal spirometry, COPD subjects (smokers and ex-smokers), and a group with small dysfunction only. I have also investigated whether blocking PAFr reduces the bacterial adherence to bronchial cells pretreated with cigarette smoke. Methodology: I evaluated the expression of PAFr and ICAM-1 crosssectionally in both large (bronchial biopsies, EBB and resected lung tissue, RT) and small airways (RT) from: 16 EBB/8 RT smokers with normal lung function (NLFS); 10 with smoking-related small airway narrowing only; 15 EBB/8 RT COPD smokers; 12 EBB/10 RT COPD ex-smokers, and compared these with 15 EBB/9 RT control tissues (NC). Anti-PAFr/ICAM-1 immunostaining on paraffin-embedded tissue was quantified using computeraided image analysis. Moreover, human cultures bronchial epithelial BEAS-2B cells were exposed to cigarette smoke extract (CSE). PAFr and ICAM- 1 expression levels were determined using immunocytochemistry and qPCR. The epithelial cells were challenged with either NTHi or S. pneumoniae labeled with FITC, and bacterial adhesion was measured using immunofluorescence. The effect of a…

Subjects/Keywords: Airway epithelium; bacterial adhesion; COPD; Platelet activating factor receptor; Intercellular adhesion molecule-1; Respiratory infection

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APA (6^th Edition):

Shukla, S. (2016). Studies on microbial adhesion factors in smoking and chronic obstructive pulmonary disease (COPD). (Thesis). University of Tasmania. Retrieved from https://eprints.utas.edu.au/23493/1/Shukla_whole_thesis.pdf

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Shukla, SD. “Studies on microbial adhesion factors in smoking and chronic obstructive pulmonary disease (COPD).” 2016. Thesis, University of Tasmania. Accessed April 10, 2021. https://eprints.utas.edu.au/23493/1/Shukla_whole_thesis.pdf.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Shukla, SD. “Studies on microbial adhesion factors in smoking and chronic obstructive pulmonary disease (COPD).” 2016. Web. 10 Apr 2021.

Vancouver:

Shukla S. Studies on microbial adhesion factors in smoking and chronic obstructive pulmonary disease (COPD). [Internet] [Thesis]. University of Tasmania; 2016. [cited 2021 Apr 10]. Available from: https://eprints.utas.edu.au/23493/1/Shukla_whole_thesis.pdf.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Shukla S. Studies on microbial adhesion factors in smoking and chronic obstructive pulmonary disease (COPD). [Thesis]. University of Tasmania; 2016. Available from: https://eprints.utas.edu.au/23493/1/Shukla_whole_thesis.pdf

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Toledo

5. Torres-Palsa, Maria Jose. ICAM-1 in Skeletal Muscle Disease and Regeneration.

Degree: PhD, Exercise Science, 2016, University of Toledo

URL: http://rave.ohiolink.edu/etdc/view?acc_num=toledo1461860958

► Skeletal muscle tissue has the unique ability to restore its structure and function after sustaining trauma and disease. The primary purpose of this research dissertation… (more)

Subjects/Keywords: Physiology; Biology; Kinesiology; ICAM-1; skeletal muscle; regeneration; mdx; inflammatory response; adhesion molecule; muscle injury

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APA (6^th Edition):

Torres-Palsa, M. J. (2016). ICAM-1 in Skeletal Muscle Disease and Regeneration. (Doctoral Dissertation). University of Toledo. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=toledo1461860958

Chicago Manual of Style (16^th Edition):

Torres-Palsa, Maria Jose. “ICAM-1 in Skeletal Muscle Disease and Regeneration.” 2016. Doctoral Dissertation, University of Toledo. Accessed April 10, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1461860958.

MLA Handbook (7^th Edition):

Torres-Palsa, Maria Jose. “ICAM-1 in Skeletal Muscle Disease and Regeneration.” 2016. Web. 10 Apr 2021.

Vancouver:

Torres-Palsa MJ. ICAM-1 in Skeletal Muscle Disease and Regeneration. [Internet] [Doctoral dissertation]. University of Toledo; 2016. [cited 2021 Apr 10]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=toledo1461860958.

Council of Science Editors:

Torres-Palsa MJ. ICAM-1 in Skeletal Muscle Disease and Regeneration. [Doctoral Dissertation]. University of Toledo; 2016. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=toledo1461860958

6. 석, 선미. Cyclooxygenase-2 is Associated with Cadmium-induced ICAM-1 Expression in Brain Endothelial Cell.

Degree: 2005, Ajou University

URL: http://repository.ajou.ac.kr/handle/201003/1485 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000000192

►

Exposure to cadmium (Cd) was reported to be related with the increased incidence of neurodegenerative diseases including stroke, though underlying mechanism is not clearly understood.… (more)

▼

Exposure to cadmium (Cd) was reported to be related with the increased incidence of neurodegenerative diseases including stroke, though underlying mechanism is not clearly understood. In vivo studies showed that Cd accumulates out-side of blood brain barrier (BBB) and induces the leakage of BBB, suggesting brain endothelium as a putative target. Recently, we have reported that Cd stimulates ICAM-1 expression via NF-kB activation in bEnd.3 cerebrovascular endothelial cells. And also, we observed Cd induces cyclooxygenase-2 (COX-2) expression, and thereby prostaglandin E2 (PGE₂) production in bEnd.3. Based on the previous report that PGE₂ is one of the key regulators in the expression of cell adhesion molecule, in this study, we explored the possible role of COX-2 in Cd-induced ICAM-1 expression in bEnd.3. Cd upregulated ICAM-1 at the levels of mRNA and protein, but downregulated E-cadherin expression in bEnd.3. Other adhesion molecules such as VCAM-1 and VE-cadherin were not affected by Cd treatment. Cd-induced ICAM-1 expression was attenuated by COX-2 inhibitors, and effects of COX-2 inhibitors were blocked by exogenous PGE₂. COX-2 inhibitors recovered E-cadherin expression in bEnd.3 exposed to Cd. Cd increased leucocyte-adhesion to endothelial cells, which was mitigated by COX-2 inhibitors. These data strongly suggest that COX-2 is associated with Cd-induced ICAM-1 expression in bEnd.3. Pro-inflammatory cytokines such as TNFα and IL-1β increased ICAM-1 and COX-2 expression in bEnd.3, but COX-2 inhibitors minimally affected ICAM-1 expression, suggesting above results might be specific to Cd.

목적: 환경 독성 물질인 카드뮴이 뇌졸중을 포함한 각종 뇌질환의 발병율을 증가시킨다는 역학적인 조사는 이미 보고 된바 있으나 아직 그 작용기전에 대해서는 잘 알려져 있지 않다. 본 연구실에서는 이미 카드뮴이 뇌혈관 내피세포에서 염증인자 생성에 미치는 영향에 대한 관찰을 통해 cyclooxygenase (COX-2)의 발현과 prostaglandins (PGs)의 생성이 증가됨을 확인한 바 있다. 뇌졸중의 발병 요인 중 하나가 세포부착분자의 기능 장애이며, 이러한 세포부착분자 발현의 조절 인자 중 대표적인 것이 prostaglandin E₂ (PGE₂)이다. 본 연구에서는 카드뮴에 의해 유도되는 뇌 손상의 발현기전을 규명하기 위한 연구의 일환으로 카드뮴에 노출된 뇌혈관 내피세포의 intercellular adhesion molecule-1 (ICAM-1)발현에 있어 COX-2의 역할을 규명하고자 하였다. 재료 및 방법: American Type Culture Collection (USA)에서 구입한 생쥐 뇌혈관 내피세포주인 bEnd.3 세포에 카드뮴 처리 후 PGE₂ 생성을 확인하고자 enzyme-linked immunoassay (EIA)를 수행하였고, PGE₂ 생성과 세포부착분자 발현의 상관관계를 밝히고자 COX 저해제, PGE₂ 그리고 카드뮴을 함께 처리하여 RT-PCR과 형광면역조직화학검사법으로 ICAM-1, VCAM-1, E-cadherin 그리고 VE-cadherin의 발현 양상을 확인하였다. 그리고 카드뮴에 의해 유도되는 백혈구-내피세포 부착에서 대한 COX 저해제와 PGE₂의 영향을 알아보고자 monocyte adhesion assay를 수행하였다. 결과: bEnd.3에서 카드뮴 처리 후 증가된 PGE₂ 생성이 COX 저해제에 의해 억제됨을 확인할 수 있었다. 카드뮴은 ICAM-1 mRNA와 단백질 발현을 증가시켰다. 그리고 E-cadherin의 발현은 감소시켰으며 VCAM-1과 VE-cadherin은 발현 양상에 변화를 보이지 않았다. 또 카드뮴에 의해 유도된 ICAM-1의 발현은 COX 저해제에 의해 감소되었으며, 이러한 COX 저해제의 작용은 PGE₂에 의해 차단되어짐을 확인하였다. 한편 카드뮴에 노출된 bEnd.3에서 감소된 E-cadherin의 경우 COX 저해제에 의해 회복되었으며 이는 역시 PGE₂에 의해 다시 저해됨을 확인하였다. 또한 카드뮴 처리에 의해 증가된 백혈구-내피세포 부착은 COX 저해제에 의해 억제되었으며, PGE₂ 처리시 다시 증가됨을 확인하였다. 결론: 본 연구의 결과들은 카드뮴에 의한 세포부착분자 발현이 PGE₂ 생성을 매개로 하고 있을 가능성을 제시하고 있다.

"차례 국문요약 = ⅰ 차례 = ⅲ 그림차례 = ⅴ 표차례 = ⅵ Ⅰ. 서론 = 1 Ⅱ. 재료 및 방법 = 4 A. 시약 및 실험 기기 = 4 1. 시약 및 재료 = 4 2. 실험 기기 및 기구 = 4 B. 연구…

Advisors/Committee Members: 대학원 의학과, 200324269, 석, 선미.

Subjects/Keywords: Cadmium (Cd); Cyclooxygenase (COX-2); Prostaglandin; E₂(PGE₂); Intercellular adhesion molecule (ICAM-1); Brain microvascular endothelial cell(bEnd.3)

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

석, �. (2005). Cyclooxygenase-2 is Associated with Cadmium-induced ICAM-1 Expression in Brain Endothelial Cell. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/1485 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000000192

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

석, 선미. “Cyclooxygenase-2 is Associated with Cadmium-induced ICAM-1 Expression in Brain Endothelial Cell.” 2005. Thesis, Ajou University. Accessed April 10, 2021. http://repository.ajou.ac.kr/handle/201003/1485 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000000192.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

석, 선미. “Cyclooxygenase-2 is Associated with Cadmium-induced ICAM-1 Expression in Brain Endothelial Cell.” 2005. Web. 10 Apr 2021.

Vancouver:

석 �. Cyclooxygenase-2 is Associated with Cadmium-induced ICAM-1 Expression in Brain Endothelial Cell. [Internet] [Thesis]. Ajou University; 2005. [cited 2021 Apr 10]. Available from: http://repository.ajou.ac.kr/handle/201003/1485 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000000192.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

석 �. Cyclooxygenase-2 is Associated with Cadmium-induced ICAM-1 Expression in Brain Endothelial Cell. [Thesis]. Ajou University; 2005. Available from: http://repository.ajou.ac.kr/handle/201003/1485 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000000192

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Rochester

7. Ringo, Katherine; Dean, David A. Extracellular Matrix Protein CCN1 (Cyr61) Negatively Regulates Endothelial Cell Adhesion Molecules.

Degree: PhD, 2015, University of Rochester

URL: http://hdl.handle.net/1802/29780

► The extracellular matrix (ECM) is now recognized as an important cellular modulator, providing essential contextual cues for appropriate cellular behavior. CCN1 (Cysteine-rich 61 or Cyr61)… (more)

▼ The extracellular matrix (ECM) is now recognized as an important cellular modulator, providing essential contextual cues for appropriate cellular behavior. CCN1 (Cysteine-rich 61 or Cyr61) is an ECM-associated protein that binds to and signals through integrins and heparan sulfate proteoglycans, and has been shown to mediate a number of cellular responses including proliferation, differentiation, adhesion, migration, and apoptosis. Gene array studies have identified CCN1 as one of the most highly upregulated genes in a number of inflammatory lung disorders, including chronic obstructive pulmonary disease, hyperoxia-induced lung injury, ventilator-induced lung injury, and asthma. The role of CCN1 in lung inflammation, however, has only begun to be explored. The pathology of acute lung injury is driven by excessive inflammation, revolving around excessive neutrophil infiltration. Neutrophil infiltration is mediated by cell adhesion molecules, such as intercellular adhesion molecule 1 (ICAM1) expressed on vascular endothelial cells. Inflammatory cytokines such as tumor necrosis factor (TNF) play a central role in lung inflammation and induce expression of endothelial cell adhesion molecules. Our lab has previously shown that CCN1 can modulate TNF signaling in fibroblasts. Based on this, I hypothesized that CCN1 modulates expression of cell adhesion molecules in endothelial cells. In this thesis, I demonstrate that CCN1 negatively regulates the cell adhesion molecules ICAM1 and vascular cell adhesion molecule 1 (VCAM1) in response to multiple inflammatory stimuli. Further, I use inhibitor studies to identify the binding site on CCN1 that carries this functionality and demonstrate that integrins, but not heparan sulfate proteoglycans, are required for this regulation. Finally, I demonstrate that CCN1-mediated regulation of ICAM1 occurs at the mRNA level, is independent of canonical NF-B signaling, and involves Rac1 signaling. This novel role of CCN1 contributes to our understanding of the physiology of lung inflammation and provides a potential therapeutic target for treatment of acute lung injury.

Subjects/Keywords: CCN1 (Cyr61; Intercellular Adhesion Molecule 1 (ICAM1; Tumor Necrosis Factor (TNF); Endothelium

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ringo, Katherine; Dean, D. A. (2015). Extracellular Matrix Protein CCN1 (Cyr61) Negatively Regulates Endothelial Cell Adhesion Molecules. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/29780

Chicago Manual of Style (16^th Edition):

Ringo, Katherine; Dean, David A. “Extracellular Matrix Protein CCN1 (Cyr61) Negatively Regulates Endothelial Cell Adhesion Molecules.” 2015. Doctoral Dissertation, University of Rochester. Accessed April 10, 2021. http://hdl.handle.net/1802/29780.

MLA Handbook (7^th Edition):

Ringo, Katherine; Dean, David A. “Extracellular Matrix Protein CCN1 (Cyr61) Negatively Regulates Endothelial Cell Adhesion Molecules.” 2015. Web. 10 Apr 2021.

Vancouver:

Ringo, Katherine; Dean DA. Extracellular Matrix Protein CCN1 (Cyr61) Negatively Regulates Endothelial Cell Adhesion Molecules. [Internet] [Doctoral dissertation]. University of Rochester; 2015. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/1802/29780.

Council of Science Editors:

Ringo, Katherine; Dean DA. Extracellular Matrix Protein CCN1 (Cyr61) Negatively Regulates Endothelial Cell Adhesion Molecules. [Doctoral Dissertation]. University of Rochester; 2015. Available from: http://hdl.handle.net/1802/29780

University of Ghana

8. Ecklu-Mensah, G. The Role of an Intercellular Adhesion Molecule 1 Binding Motif in Plasmodium Falciparum Erythrocyte Membrane Protein 1 and Other Determinants Involved in Severe Malaria Pathogenesis .

Degree: 2017, University of Ghana

URL: http://ugspace.ug.edu.gh/handle/123456789/23576

► A central pathogenic feature in Plasmodium falciparum cerebral malaria (CM) is the sequestration of infected erythrocytes (IEs) which results in the obstruction of blood flow,… (more)

▼ A central pathogenic feature in Plasmodium falciparum cerebral malaria (CM) is the sequestration of infected erythrocytes (IEs) which results in the obstruction of blood flow, inflammation and damage to the endothelial cell barrier integrity. Adhesion is mediated by a family of approximately 60 highly variant parasite proteins called P. falciparum erythrocyte membrane protein 1 (PfEMP1), which are displayed on the surface of infected cells. All PfEMP1 contain multiple extracellular domains of Duffy binding like (DBL) and cysteine-rich interdomain region (CIDR) proteins that mediate adhesion to various host endothelial receptors such as intercellular adhesion molecule 1 (ICAM-1). An important unanswered question in malaria pathogenesis has always been whether a specific binding phenotype can be linked to any of the different severe malaria phenotypes. The broad objectives of this study were to investigate the involvement of an ICAM-1 binding motif in PfEMP1 in the development of CM, as well as to evaluate the contributions of the immune response and other determinants driving severe malaria complications. A highly conserved motif in DBLβ domain of group A PfEMP1 molecules was identified using sequence information. IEs expressing PfEMP1 containing the motif had a dual binding affinity for endothelial protein C receptor (EPCR) and ICAM-1 when tested under in vitro flow adhesion assays. Quantitative real time PCR (qPCR) showed higher transcription of this motif in parasites isolated from children with CM compared with non-cerebral severe malaria (p=0.020). The sequences defining the motif were exceptionally conserved and thus suggested its ability to induce cross-reactive responses. Broadly reactive cross-inhibitory antibodies against the motif were acquired following P. falciparum natural infections, in addition to being experimentally induced. Such cross-reactive antibodies interfered with ICAM-1 binding of recombinant motif-containing DBLβ domains and IEs from paediatric CM patients. These findings make the motif an attractive candidate to be included in a vaccine cocktail that seeks to prevent CM complications. Markers of endothelial activation (sICAM-1, sEPCR, Ang-2, HMGB1) in Ghanaian children with severe or uncomplicated malaria and their levels following resolution of infection were determined using ELISA. The levels were higher in malaria patients in comparison with healthy controls (p < 0.001). These levels declined significantly in convalescent patients except for high mobility group box 1 protein (HMGB1) which remained high to a similar degree as observed during infection (p > 0.05), an observation reported for the first time in malaria. Blood outgrowth endothelial cells (BOECs) from peripheral blood mononuclear cells of Ghanaian malaria patients were isolated and characterised as physiologically relevant cells to potentially study falciparum-infected erythrocyte adhesive interactions. Flow cytometry analysis showed that BOECs expressed several endothelial surface markers including malaria parasite…

Subjects/Keywords: Intercellular Adhesion Molecule 1 Binding Motif; Plasmodium Falciparum; Malaria Pathogenesis; Determinants; Ghana

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ecklu-Mensah, G. (2017). The Role of an Intercellular Adhesion Molecule 1 Binding Motif in Plasmodium Falciparum Erythrocyte Membrane Protein 1 and Other Determinants Involved in Severe Malaria Pathogenesis . (Doctoral Dissertation). University of Ghana. Retrieved from http://ugspace.ug.edu.gh/handle/123456789/23576

Chicago Manual of Style (16^th Edition):

Ecklu-Mensah, G. “The Role of an Intercellular Adhesion Molecule 1 Binding Motif in Plasmodium Falciparum Erythrocyte Membrane Protein 1 and Other Determinants Involved in Severe Malaria Pathogenesis .” 2017. Doctoral Dissertation, University of Ghana. Accessed April 10, 2021. http://ugspace.ug.edu.gh/handle/123456789/23576.

MLA Handbook (7^th Edition):

Ecklu-Mensah, G. “The Role of an Intercellular Adhesion Molecule 1 Binding Motif in Plasmodium Falciparum Erythrocyte Membrane Protein 1 and Other Determinants Involved in Severe Malaria Pathogenesis .” 2017. Web. 10 Apr 2021.

Vancouver:

Ecklu-Mensah G. The Role of an Intercellular Adhesion Molecule 1 Binding Motif in Plasmodium Falciparum Erythrocyte Membrane Protein 1 and Other Determinants Involved in Severe Malaria Pathogenesis . [Internet] [Doctoral dissertation]. University of Ghana; 2017. [cited 2021 Apr 10]. Available from: http://ugspace.ug.edu.gh/handle/123456789/23576.

Council of Science Editors:

Ecklu-Mensah G. The Role of an Intercellular Adhesion Molecule 1 Binding Motif in Plasmodium Falciparum Erythrocyte Membrane Protein 1 and Other Determinants Involved in Severe Malaria Pathogenesis . [Doctoral Dissertation]. University of Ghana; 2017. Available from: http://ugspace.ug.edu.gh/handle/123456789/23576

Florida Atlantic University

9. Merritt, Jordan. EFFECTS OF SPECIFIC PfEMP1 LIGATION INTERACTIONS WITH ICAM-1, INTEGRIN αVβ3, AND CD36 ON MONOCYTES IN AN IN VITRO MALARIANAÏVE HOST MODEL.

Degree: 2019, Florida Atlantic University

URL: http://fau.digital.flvc.org/islandora/object/fau:42196

►

Malaria is a severe global health problem that causes approximately 435,000 deaths per year. Any non-immune individual traveling to malaria endemic regions can be affected… (more)

Subjects/Keywords: Malaria; Plasmodium falciparum; Integrins; Monocytes; Intercellular Adhesion Molecule-1; CD36 Antigens; Adhesiveness

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Merritt, J. (2019). EFFECTS OF SPECIFIC PfEMP1 LIGATION INTERACTIONS WITH ICAM-1, INTEGRIN αVβ3, AND CD36 ON MONOCYTES IN AN IN VITRO MALARIANAÏVE HOST MODEL. (Thesis). Florida Atlantic University. Retrieved from http://fau.digital.flvc.org/islandora/object/fau:42196

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Merritt, Jordan. “EFFECTS OF SPECIFIC PfEMP1 LIGATION INTERACTIONS WITH ICAM-1, INTEGRIN αVβ3, AND CD36 ON MONOCYTES IN AN IN VITRO MALARIANAÏVE HOST MODEL.” 2019. Thesis, Florida Atlantic University. Accessed April 10, 2021. http://fau.digital.flvc.org/islandora/object/fau:42196.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Merritt, Jordan. “EFFECTS OF SPECIFIC PfEMP1 LIGATION INTERACTIONS WITH ICAM-1, INTEGRIN αVβ3, AND CD36 ON MONOCYTES IN AN IN VITRO MALARIANAÏVE HOST MODEL.” 2019. Web. 10 Apr 2021.

Vancouver:

Merritt J. EFFECTS OF SPECIFIC PfEMP1 LIGATION INTERACTIONS WITH ICAM-1, INTEGRIN αVβ3, AND CD36 ON MONOCYTES IN AN IN VITRO MALARIANAÏVE HOST MODEL. [Internet] [Thesis]. Florida Atlantic University; 2019. [cited 2021 Apr 10]. Available from: http://fau.digital.flvc.org/islandora/object/fau:42196.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Merritt J. EFFECTS OF SPECIFIC PfEMP1 LIGATION INTERACTIONS WITH ICAM-1, INTEGRIN αVβ3, AND CD36 ON MONOCYTES IN AN IN VITRO MALARIANAÏVE HOST MODEL. [Thesis]. Florida Atlantic University; 2019. Available from: http://fau.digital.flvc.org/islandora/object/fau:42196

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

10. Χαριτόπουλος, Κωνσταντίνος. Ανοσοϊστοχημική διερεύνηση προγνωστικών δεικτών στα κακοήθη μελανώματα του δέρματος.

Degree: 2000, Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); National and Kapodistrian University of Athens

URL: http://hdl.handle.net/10442/hedi/11952

Subjects/Keywords: Νευροπεπτίδια; Μελάνωμα; Ανοσοϊστοχημεία; Ιντεγκρίνη β3; Διακυτταριακό μόριο προσκόλλησης-1; Melanoma; Immunohistochemistry ( IHC); Integrin β3; Vasopressin; Intercellular adhesion molecule-1; ICAM-1; GRP; Gastrin releasing peptide

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Χαριτόπουλος, �. (2000). Ανοσοϊστοχημική διερεύνηση προγνωστικών δεικτών στα κακοήθη μελανώματα του δέρματος. (Thesis). Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); National and Kapodistrian University of Athens. Retrieved from http://hdl.handle.net/10442/hedi/11952

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Χαριτόπουλος, Κωνσταντίνος. “Ανοσοϊστοχημική διερεύνηση προγνωστικών δεικτών στα κακοήθη μελανώματα του δέρματος.” 2000. Thesis, Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); National and Kapodistrian University of Athens. Accessed April 10, 2021. http://hdl.handle.net/10442/hedi/11952.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Χαριτόπουλος, Κωνσταντίνος. “Ανοσοϊστοχημική διερεύνηση προγνωστικών δεικτών στα κακοήθη μελανώματα του δέρματος.” 2000. Web. 10 Apr 2021.

Vancouver:

Χαριτόπουλος �. Ανοσοϊστοχημική διερεύνηση προγνωστικών δεικτών στα κακοήθη μελανώματα του δέρματος. [Internet] [Thesis]. Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); National and Kapodistrian University of Athens; 2000. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/10442/hedi/11952.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Χαριτόπουλος �. Ανοσοϊστοχημική διερεύνηση προγνωστικών δεικτών στα κακοήθη μελανώματα του δέρματος. [Thesis]. Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); National and Kapodistrian University of Athens; 2000. Available from: http://hdl.handle.net/10442/hedi/11952

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

11. Καψογεώργου, Ευσταθία. Ρόλος των επιθηλιακών κυττάρων στην αυτοανοσία: έκφραση προσκολλητικών μορίων ICAM-1 και λειτουργικών συνενεργοποιητικών μορίων B7 από τα επιθηλιακά κύτταρα των σιελογόνων αδένων στο σύνδρομο Sjogren.

Degree: 2001, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/23809

Subjects/Keywords: Επιθηλιακά κύτταρα; Σιελογόνοι αδένες; Σύνδρομο Sjogren; Διακυτταρικό μόριο προσκόλλησης ICAM-1; Συνενεργοποιητικό μόριο B7.2; Καλλιέργεια; Epithelial cells; Salivary glands; Sjogren's syndrome; Intercellular adhesion molecule ICAM -1; Costimulatory molecule B7.2; Culture

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Καψογεώργου, . �. (2001). Ρόλος των επιθηλιακών κυττάρων στην αυτοανοσία: έκφραση προσκολλητικών μορίων ICAM-1 και λειτουργικών συνενεργοποιητικών μορίων B7 από τα επιθηλιακά κύτταρα των σιελογόνων αδένων στο σύνδρομο Sjogren. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/23809

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Καψογεώργου, Ευσταθία. “Ρόλος των επιθηλιακών κυττάρων στην αυτοανοσία: έκφραση προσκολλητικών μορίων ICAM-1 και λειτουργικών συνενεργοποιητικών μορίων B7 από τα επιθηλιακά κύτταρα των σιελογόνων αδένων στο σύνδρομο Sjogren.” 2001. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed April 10, 2021. http://hdl.handle.net/10442/hedi/23809.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Καψογεώργου, Ευσταθία. “Ρόλος των επιθηλιακών κυττάρων στην αυτοανοσία: έκφραση προσκολλητικών μορίων ICAM-1 και λειτουργικών συνενεργοποιητικών μορίων B7 από τα επιθηλιακά κύτταρα των σιελογόνων αδένων στο σύνδρομο Sjogren.” 2001. Web. 10 Apr 2021.

Vancouver:

Καψογεώργου �. Ρόλος των επιθηλιακών κυττάρων στην αυτοανοσία: έκφραση προσκολλητικών μορίων ICAM-1 και λειτουργικών συνενεργοποιητικών μορίων B7 από τα επιθηλιακά κύτταρα των σιελογόνων αδένων στο σύνδρομο Sjogren. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2001. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/10442/hedi/23809.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Καψογεώργου �. Ρόλος των επιθηλιακών κυττάρων στην αυτοανοσία: έκφραση προσκολλητικών μορίων ICAM-1 και λειτουργικών συνενεργοποιητικών μορίων B7 από τα επιθηλιακά κύτταρα των σιελογόνων αδένων στο σύνδρομο Sjogren. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2001. Available from: http://hdl.handle.net/10442/hedi/23809

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Universidade Estadual de Campinas

12. Egal, Erika Said Abu, 1980-. Expressão do ICAM-1 e da podoplanina (D2/40) na vilosite de etiologia desconhecida : Expression of ICAM-1 and podoplanin in villitis of unknown etiology.

Degree: Faculdade de Ciências Médicas; Programa de Pós-Graduação em Ciências Médicas, 2017, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/332166

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Orientadores: Albina Messias de Almeida Milani Altemani, Fernanda Viviane Mariano

Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas

Made available in DSpace… (more)

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Orientadores: Albina Messias de Almeida Milani Altemani, Fernanda Viviane Mariano

Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas

Made available in DSpace on 2018-09-05T16:55:33Z (GMT). No. of bitstreams: 1 Egal_ErikaSaidAbu_D.pdf: 3544306 bytes, checksum: 7fd06dceb80c438ee23e17debf45d54f (MD5) Previous issue date: 2017

Resumo: ICAM-1 (molécula de adesão intercelular-1) e podoplanina (PDPN)/ D2-40 são moléculas envolvidas na resposta inflamatória. ICAM-1 induz adesão célula-célula permitindo comunicação intercelular e participa no mecanismo de defesa mediado por células T. Na placenta, ICAM-1 está superexpressa no sinciciotrofoblasto das vilosidades inflamadas, possivelmente contribuindo para a migração de células imunes do espaço interviloso para o interior das vilosidades. PDPN/D2-40 é um reconhecido marcador de linfáticos e também está expresso em células imunes, tais como macrófagos associados à reação inflamatória e células Th17. Na placenta, D2-40 tem sido encontrado em células do estroma viloso ou formando arranjo plexiforme semelhante a sistema linfático. A patogênese da vilosite placentária ainda não está completamente elucidada e o estudo da expressão das proteínas ICAM-1 e D2-40/ PDPN nos possibilitará aumentar o conhecimento sobre o desenvolvimento da inflamação vilosa. Esta lesão placentária tem papel chave na transmissão vertical de agente infeccioso (da mãe para o feto) e na agressão imune materna a tecidos fetais. Material e métodos: Foram estudadas 22 placentas com vilosite sem agente etiológico identificável e 3 controles quanto a expressão imunoistoquímica de: a) ICAM-1 nas células imunes e trofoblasto e b) D2-40 no estroma viloso e células imunes. Além disso, foi examinada a co-expressão de: a) ICAM-1 com CD45, CD68 and CD3, b) D2-40 com CD45 e CD68 e comparada a expressão estromal de D2/40 com aquela de actina de músculo liso e vimentina. Resultados: Células imunes positivas para CD45, CD3 e CD68 e coexpressando ICAM-1 foram detectadas dentro das vilosidades inflamadas e formando agregados perivilosos aderidos a áreas de rotura trofoblástica. As vilosidades inflamadas com e sem rotura trofoblástica mostravam expressão de ICAM-1 no sinciciotrofoblasto. Naquelas com rotura trofoblástica, ICAM-1 foi detectado na maioria das células imunes perivilosas circundando estas áreas e em apenas pequena quantidade delas dentro do estroma viloso. Raras vilosidades inflamadas (< 5%) sem rotura trofoblástica e com expressão de ICAM-1 no sinciciotrofoblasto apresentavam aderência de células imunes. Em relação a D2-40, nas vilosidades normais, esta proteína estava expressa no estroma viloso delineando uma rede plexiforme, enquanto nas inflamadas, as células estromais D2-40 positivas formavam uma rede celular densa. Esta última mostrava aspecto correspondente àquela das células estromais vimentina positivas. Nas vilosidades inflamadas não foi observada expressão de actina músculo liso ou co-expressão significante de D2-40 com CD45 ou CD68. Conclusões: Em vilosidades…

Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS, Mariano, Fernanda Viviane, 1984-, Altemani, Albina Messias de Almeida Milani, 1953-, Soares, Andresa Borges, Cintra, Maria Letícia, Rogério, Fábio, Teixeira, Lucas Novaes.

Subjects/Keywords: Placenta; Molécula 1 de adesão intercelular; Inflamação; Proteína PDPN humana; Placenta; Intercellular adhesion molecule-1; Inflammation; PDPN protein, human; Villitis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Egal, Erika Said Abu, 1. (2017). Expressão do ICAM-1 e da podoplanina (D2/40) na vilosite de etiologia desconhecida : Expression of ICAM-1 and podoplanin in villitis of unknown etiology. (Doctoral Dissertation). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/332166

Chicago Manual of Style (16^th Edition):

Egal, Erika Said Abu, 1980-. “Expressão do ICAM-1 e da podoplanina (D2/40) na vilosite de etiologia desconhecida : Expression of ICAM-1 and podoplanin in villitis of unknown etiology.” 2017. Doctoral Dissertation, Universidade Estadual de Campinas. Accessed April 10, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/332166.

MLA Handbook (7^th Edition):

Egal, Erika Said Abu, 1980-. “Expressão do ICAM-1 e da podoplanina (D2/40) na vilosite de etiologia desconhecida : Expression of ICAM-1 and podoplanin in villitis of unknown etiology.” 2017. Web. 10 Apr 2021.

Vancouver:

Egal, Erika Said Abu 1. Expressão do ICAM-1 e da podoplanina (D2/40) na vilosite de etiologia desconhecida : Expression of ICAM-1 and podoplanin in villitis of unknown etiology. [Internet] [Doctoral dissertation]. Universidade Estadual de Campinas; 2017. [cited 2021 Apr 10]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/332166.

Council of Science Editors:

Egal, Erika Said Abu 1. Expressão do ICAM-1 e da podoplanina (D2/40) na vilosite de etiologia desconhecida : Expression of ICAM-1 and podoplanin in villitis of unknown etiology. [Doctoral Dissertation]. Universidade Estadual de Campinas; 2017. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/332166

University of Oulu

13. Juntti, H. (Hanna). Association of respiratory syncytial virus infection with asthma and atopic allergy.

Degree: 2008, University of Oulu

URL: http://urn.fi/urn:isbn:9789514287947

► Abstract Respiratory syncytial virus (RSV) infection may be associated with the development of asthma and atopy. The aim of the present study was to investigate… (more)

▼ Abstract Respiratory syncytial virus (RSV) infection may be associated with the development of asthma and atopy. The aim of the present study was to investigate this association and the related immunological mechanisms. Seventy-six children admitted to Oulu University Hospital in 1991–1994 for an RSV infection at an age of less than 12 months and healthy controls were called for a visit at the age of 6–10 years. Twenty subjects (26%) had asthma compared with 12 controls (16%) (difference 11%, 95% confidence interval (CI) –3% to 24%). Asthma had been diagnosed significantly earlier in the subjects. Eight per cent of the subjects had at least one positive skin prick test as compared with 43% of the controls (difference –35%, 95% CI –50% to –19%). Serum concentrations of interferon-γ and soluble intercellular adhesion molecule -1 were significantly higher among the subjects than among the controls and among the subjects with asthma or current wheezing than among the corresponding controls. All children born in Finland in 1986–1995 were arranged in birth cohorts by month and year of birth and grouped by exposure to an RSV epidemic at age 0–6 months, resulting in 97 exposed and 23 unexposed cohorts. The proportions of children taking asthma medication or receiving special reimbursement for asthma medication in 1995–2002 were similar in the unexposed and exposed cohorts. Altogether 47 children born between August and November 2001 with a cord blood sample taken were admitted to hospital (n = 26) or seen in an outpatient department (n = 21) for RSV infection before the age of six months. Twenty-eight children had some other respiratory viral infection and 84 children formed a group of healthy controls. High scores on a factor combining the cord blood interleukin-6 and interleukin-8 responses (as derived by factor analysis) were shown in logistic regression analysis to predict hospitalization for RSV infection by comparison with the healthy controls (odds ratio 2.29, 95% CI 1.21 to 4.33). We suggest that RSV does not induce asthma but inborn features of immunity affect the severity of RSV infection and the postinfectious development of asthma.

Subjects/Keywords: asthma; cord blood; cytokines; factor analysis; immediate hypersensitivity; intercellular adhesion molecule -1; respiratory syncytial virus infections

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Juntti, H. (. (2008). Association of respiratory syncytial virus infection with asthma and atopic allergy. (Doctoral Dissertation). University of Oulu. Retrieved from http://urn.fi/urn:isbn:9789514287947

Chicago Manual of Style (16^th Edition):

Juntti, H (Hanna). “Association of respiratory syncytial virus infection with asthma and atopic allergy.” 2008. Doctoral Dissertation, University of Oulu. Accessed April 10, 2021. http://urn.fi/urn:isbn:9789514287947.

MLA Handbook (7^th Edition):

Juntti, H (Hanna). “Association of respiratory syncytial virus infection with asthma and atopic allergy.” 2008. Web. 10 Apr 2021.

Vancouver:

Juntti H(. Association of respiratory syncytial virus infection with asthma and atopic allergy. [Internet] [Doctoral dissertation]. University of Oulu; 2008. [cited 2021 Apr 10]. Available from: http://urn.fi/urn:isbn:9789514287947.

Council of Science Editors:

Juntti H(. Association of respiratory syncytial virus infection with asthma and atopic allergy. [Doctoral Dissertation]. University of Oulu; 2008. Available from: http://urn.fi/urn:isbn:9789514287947

University of Southern California

14. Hsueh, Aaron Pang-Yu. Trafficking of targeted elastin‐like polypeptide nanoparticles in the lacrimal gland.

Degree: PhD, Pharmaceutical Sciences, 2017, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/602725/rec/7558

► Rapid clearance from the tears presents a formidable obstacle to the delivery of peptide drugs to the eye surface. This impedes therapies for ocular infections,… (more)

▼ Rapid clearance from the tears presents a formidable obstacle to the delivery of peptide drugs to the eye surface. This impedes therapies for ocular infections, wound healing, and dry‐eye disease that affect the vision of over four million Americans. To overcome this challenge, this thesis first explores a novel nanoparticle strategy to reach the ocular surface via receptor‐mediated transcytosis through the lacrimal gland (LG), responsible for the bulk of human tears. The LG abundantly expresses the coxsackievirus and adenovirus receptor (CAR); furthermore, we recently reported a peptide‐based ELP nanoparticle (KSI) that targets CAR on liver cells. This thesis reports the unexpected finding that KSI both targets and transcytoses into the LG acinar lumen, which drains to tear ducts. When followed using ex vivo live cell imaging KSI rapidly accumulates in the lumen formed by LG acinar cells. LG transduction with a Myosin Vb tail, which is a dominant negative inhibitor of transcytosis, inhibits lumenal accumulation. Transcytosis of KSI was confirmed in vivo by confocal and TEM imaging of LG tissue following administration of KSI nanoparticles. These findings suggest that it is possible to target nanomaterials to the tears by engaging receptors prevalent on the LG. This design strategy represents a new opportunity to overcome barriers to ocular delivery. ❧ Autoimmune diseases cause considerable morbidity, mortality, and healthcare cost each year in the United States. Although effective, current clinical treatment approaches which blunt all immune responses can depress beneficial immunity, increase rates of infections, cancer, and oxicity. Sjögren's syndrome is thought to be an autoimmune disease accompanying with the moderate‐to‐severe destruction of exocrine glands such as the lacrimal gland (LG) and salivary gland. Recent advances suggest that maintaining a balance of regulatory immune functions and effectors is critical for avoiding autoimmunity. ICAM-1 is considered a disease initiator for T‐cell activation and migration to inflamed tissues in autoimmunity. This thesis characterizes a bio‐polymeric nanoparticle assembled from a diblock copolymer ELP fused with a mouse intercellular adhesion molecule (ICAM)-1 targeting peptide. This material may form the basis of a new drug delivery platform for the targeting of therapeutic agents to intracellular compartments of diseased LG acinar cells (LGACs). Interestingly, this nanoparticle forms a multivalent and monodisperse nanoparticle with a radius of 21.9 nm, which was characterized by dynamic light scattering (DLS). This nanoparticle exhibits cross‐species activity, targeting human and mouse ICAM-1, internalizing into HeLa cells and mouse ICAM-1‐expressing HeLa cells. It is first trafficked to early endosomes before it accumulates in lysosomes. Similar targeting activity was observed in ex vivo and in vivo LGACs from male NOD mice, an established Sjögren’s Syndrome mouse model. This nanoparticle has a blood half‐life of 3.8 h compared with 7.2 h for its plain counterpart.… Advisors/Committee Members: Hamm-Alvarez, Sarah F. (Committee Chair), Mackay, John Andrew (Committee Member), Okamoto, Curtis Toshio (Committee Member), Shen, Wei-Chiang (Committee Member).

Subjects/Keywords: Coxsackievirus and adenovirus receptor; elastin‐like polypeptide; immune‐mediated inflammation; intercellular adhesion molecule-1; knob; multifunctional nanoparticle; transcytosis; lacrimal gland

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hsueh, A. P. (2017). Trafficking of targeted elastin‐like polypeptide nanoparticles in the lacrimal gland. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/602725/rec/7558

Chicago Manual of Style (16^th Edition):

Hsueh, Aaron Pang-Yu. “Trafficking of targeted elastin‐like polypeptide nanoparticles in the lacrimal gland.” 2017. Doctoral Dissertation, University of Southern California. Accessed April 10, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/602725/rec/7558.

MLA Handbook (7^th Edition):

Hsueh, Aaron Pang-Yu. “Trafficking of targeted elastin‐like polypeptide nanoparticles in the lacrimal gland.” 2017. Web. 10 Apr 2021.

Vancouver:

Hsueh AP. Trafficking of targeted elastin‐like polypeptide nanoparticles in the lacrimal gland. [Internet] [Doctoral dissertation]. University of Southern California; 2017. [cited 2021 Apr 10]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/602725/rec/7558.

Council of Science Editors:

Hsueh AP. Trafficking of targeted elastin‐like polypeptide nanoparticles in the lacrimal gland. [Doctoral Dissertation]. University of Southern California; 2017. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/602725/rec/7558

15. Letícia Barbosa Kawano Dourado. Ativação endotelial na granulomatose com poliangeíte (granulomatose de Wegener).

Degree: 2015, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5150/tde-11052015-141231/

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INTRODUÇÃO: Eventos vasculares e imunológicos são centrais na patogênese da granulomatose com poliangeíte (GPA). Moléculas de adesão celular tem papel fundamental no recrutamento de células… (more)

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INTRODUÇÃO: Eventos vasculares e imunológicos são centrais na patogênese da granulomatose com poliangeíte (GPA). Moléculas de adesão celular tem papel fundamental no recrutamento de células inflamatórias do sangue para os tecidos. Diferentes leitos vasculares apresentam particularidades na expressão de moléculas de adesão celular explicando talvez parte da especificidade da GPA por determinados órgãos. A elevação no nível sérico de moléculas de adesão celular e aumento da expressão destas em amostras de biópsia renal já foram demonstrados em pacientes com vasculite ANCA associada. No entanto, o fenômeno ainda não foi estudado in situ no pulmão. OBJETIVO: O objetivo deste estudo foi analisar o padrão de expressão endotelial pulmonar de três moléculas de adesão celular na GPA, in situ: molécula de adesão intercelular 1 (ICAM-1), molécula e adesão vascular 1 (VCAM-1) e E-selectina. MÉTODOS: Examinou-se a expressão endotelial de ICAM-1, VCAM-1, E-selectina usando marcação imuno-histoquímica em secções de pulmão fixadas e parafinadas de lesões de GPA (n = 8 casos, 90 secções transversais de vasos analisados). Foram também analisados controles positivos: amostras de pulmão de doença intersticial associada à esclerodermia (SScl) (n = 8 casos, 96 secções transversais de vasos analisados) e controles negativos (n = 9 casos, 90 secções transversais de vasos analisados). A quantificação imuno-histoquímica foi realizada no aumento de 400x usando a técnica de point-counting. RESULTADOS: ICAM-1: A expressão endotelial mediana de ICAM-1 esteve aumentada de forma semelhante na GPA e na SScl (81% and 73%, respectivamente; p = 0.97). A comparação com o grupo controle (26.3%) revelou diferença estatisticamente significativa entre controle e GPA (p <0.001) quanto entre controle e SScl (p = 0.017). VCAM-1: A expressão mediana de VCAM-1 esteve significativamente aumentada na GPA se comparada a SScl (79.5% vs 41.4%; p = 0.012), no entanto, a expressão endotelial de VCAM-1 nos controles também esteve moderadamente aumentada (49.8%) e não houve diferença estatística entre SScl e controles ( p = 0.549) ou entre GPA e controles (p = 0.242). E-selectina: A expressão endotelial mediana de E-selectina esteve aumentada de forma semelhante na GPA e SScl (100% e 88.2%, respectivamente; p = 0.272). A comparação com o grupo controle (13.8%) revelou diferença estatisticamente significativa entre controle e GPA (p < 0.001) e controle e SScl (p = 0.045). CONCLUSÃO: Esses achados evidenciam o fenômeno de ativação endotelial pulmonar in situ em lesões de GPA. O perfil de expressão de moléculas de adesão parece ter particularidades em diferentes doenças a exemplo da maior expressão de VCAM-1 na GPA em relação à SScl. Essas observações contribuem para o conhecimento fisiopatogênico na GPA.

INTRODUCTION: Vascular and immunologic processes are central to the pathogenesis of granulomatosis with polyangiitis (GPA). Endothelial cellular adhesion molecules have a central role in recruiting leukocytes to sites of inflammation. Moreover, different…

Advisors/Committee Members: Carmen Silvia Valente Barbas, Rimarcs Gomes Ferreira, Ronaldo Adib Kairalla, Mariana Silva Lima.

Subjects/Keywords: Endotélio vascular; Granulomatose com poliangeíte; Granulomatose de Wegener; Molécula 1 de adesão de célula vascular (VCAM-1); Molécula 1 de adesão intercelular (ICAM-1); Moléculas de adesão celular; Selectina-E; Cell adhesion molecules; Cell adhesion molecules intercellular ICAM-1; Cell adhesion molecules vascular VCAM-1; E-selectin; Endothelium; Granulomatosis with polyangiitis; Wegener granulomatosis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Dourado, L. B. K. (2015). Ativação endotelial na granulomatose com poliangeíte (granulomatose de Wegener). (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5150/tde-11052015-141231/

Chicago Manual of Style (16^th Edition):

Dourado, Letícia Barbosa Kawano. “Ativação endotelial na granulomatose com poliangeíte (granulomatose de Wegener).” 2015. Doctoral Dissertation, University of São Paulo. Accessed April 10, 2021. http://www.teses.usp.br/teses/disponiveis/5/5150/tde-11052015-141231/.

MLA Handbook (7^th Edition):

Dourado, Letícia Barbosa Kawano. “Ativação endotelial na granulomatose com poliangeíte (granulomatose de Wegener).” 2015. Web. 10 Apr 2021.

Vancouver:

Dourado LBK. Ativação endotelial na granulomatose com poliangeíte (granulomatose de Wegener). [Internet] [Doctoral dissertation]. University of São Paulo; 2015. [cited 2021 Apr 10]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5150/tde-11052015-141231/.

Council of Science Editors:

Dourado LBK. Ativação endotelial na granulomatose com poliangeíte (granulomatose de Wegener). [Doctoral Dissertation]. University of São Paulo; 2015. Available from: http://www.teses.usp.br/teses/disponiveis/5/5150/tde-11052015-141231/

Université de Montréal

16. Lapointe, Stéphanie. Rôle de la phospholipase A2 de type V dans le recrutement de leucocytes au foyer inflammatoire.

Degree: 2009, Université de Montréal

URL: http://hdl.handle.net/1866/2745

Subjects/Keywords: Leucocytes; sPLA2 -V; lipopolysaccharide; molécule d'adhérence intercellulaire 1(ICAM-1); molécule d'adhérence vasculaire 1 (VCAM-1); Inflammation; 12-épi-scalaradial; Leukocytes; vascular cell adhesion molecule-1; intercellular adhesion molecule-1; inflammation; Health Sciences - Pharmacology / Sciences de la santé - Pharmacologie (UMI : 0419)

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lapointe, S. (2009). Rôle de la phospholipase A2 de type V dans le recrutement de leucocytes au foyer inflammatoire. (Thesis). Université de Montréal. Retrieved from http://hdl.handle.net/1866/2745

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Lapointe, Stéphanie. “Rôle de la phospholipase A2 de type V dans le recrutement de leucocytes au foyer inflammatoire.” 2009. Thesis, Université de Montréal. Accessed April 10, 2021. http://hdl.handle.net/1866/2745.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Lapointe, Stéphanie. “Rôle de la phospholipase A2 de type V dans le recrutement de leucocytes au foyer inflammatoire.” 2009. Web. 10 Apr 2021.

Vancouver:

Lapointe S. Rôle de la phospholipase A2 de type V dans le recrutement de leucocytes au foyer inflammatoire. [Internet] [Thesis]. Université de Montréal; 2009. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/1866/2745.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Lapointe S. Rôle de la phospholipase A2 de type V dans le recrutement de leucocytes au foyer inflammatoire. [Thesis]. Université de Montréal; 2009. Available from: http://hdl.handle.net/1866/2745

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

17. Hsu, Janet. Targeting Intercellular Adhesion Molecule-1 to Enhance Delivery of Therapeutic Enzymes for Treatment of Lysosomal Storage Diseases.

Degree: Bioengineering, 2014, University of Maryland

URL: http://hdl.handle.net/1903/15932

► Lysosomal storage diseases (LSDs) are a group of more than 40 genetically inherited diseases that result from dysfunction of specific proteins, often an enzyme, located… (more)

▼ Lysosomal storage diseases (LSDs) are a group of more than 40 genetically inherited diseases that result from dysfunction of specific proteins, often an enzyme, located in lysosomes within cells which leads to abnormal lysosomal accumulation of specific macromolecules. As a result, cell malfunction occurs and escalates into multi-tissue and multi-organ failures, often resulting in premature death. For several early onset LSDs, the central nervous system (CNS) is also affected and manifests fatal neuropathic and/or neurodegenerative symptoms. Within the last two decades, treatment for selective LSDs has become clinically available. Specifically, enzyme replacement therapy (ERT) by intravenous injection of recombinant enzymes holds relevant promise. Yet current ERT results in suboptimal enzyme biodistribution to many target organs, including the peripheral organs and also the CNS. Delivery to the CNS is particularly impeded due to the tight blood-brain barrier (BBB) that strictly regulates passage between the circulation system and the brain tissue. We explored the use of targeted drug delivery systems to address this issue. Specifically, we focused on targeting intercellular adhesion molecule-1 (ICAM-1), a cell surface glycoprotein that is upregulated under pathological conditions, including LSDs. In this dissertation, using in vitro, cell culture, and in vivo techniques, we examined whether ICAM-1-targeted polymer nanocarriers: (1) enhance binding, uptake, and lysosomal delivery of different enzymes in cells, (2) provide targeting and transport across endothelial and subendthelial cells of the BBB, and (3) improve accumulation of lysosomal enzymes to peripheral organs and the brain. Results suggest that after intravenous injection of enzyme coupled to ICAM-1-targeted nanocarriers, ICAM-1 targeting shift these enzymes from the circulation to tissues, enhancing enzyme accumulation over non-targeted counterparts both in peripheral organs and the brain. This could be modulated by varying parameters such as the density of targeting antibodies on the carrier coat or the carrier bulk concentration. Also, ICAM-1-targeted nanocarriers were transported across BBB models followed by uptake and lysosomal transport to neuron-like cells. ICAM-1-targeted nanocarriers preferentially bound to diseased cells and were internalized and trafficked to lysosomes, resulting in degradation of the accumulated substrate. Therefore, overall, ICAM-1-targeting shows promise in improving ERT for LSD treatment. Advisors/Committee Members: Muro, Silvia (advisor).

Subjects/Keywords: Biomedical engineering; Blood-brain barrier; Enzyme replacement therapy; Intercellular adhesion molecule-1 (ICAM-1); Lysosomal storage diseases; Nanotechnology; Targeted drug delivery

…nanoparticles to intercellular adhesion molecule-1 (ICAM-1), a cell surface glycoprotein… …intercellular adhesion molecule-1 ASM .......................................... Acid sphingomyelinase… …umbilical vein endothelial cell ICAM-1 ..................................... Intercellular… …adhesion molecule-1 IgG ............................................ Immunoglobin G InsR… …22 2.7. ICAM-1-TARGETING STRATEGIES FOR LSD APPLICATIONS…

2 more images…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hsu, J. (2014). Targeting Intercellular Adhesion Molecule-1 to Enhance Delivery of Therapeutic Enzymes for Treatment of Lysosomal Storage Diseases. (Thesis). University of Maryland. Retrieved from http://hdl.handle.net/1903/15932

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Hsu, Janet. “Targeting Intercellular Adhesion Molecule-1 to Enhance Delivery of Therapeutic Enzymes for Treatment of Lysosomal Storage Diseases.” 2014. Thesis, University of Maryland. Accessed April 10, 2021. http://hdl.handle.net/1903/15932.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Hsu, Janet. “Targeting Intercellular Adhesion Molecule-1 to Enhance Delivery of Therapeutic Enzymes for Treatment of Lysosomal Storage Diseases.” 2014. Web. 10 Apr 2021.

Vancouver:

Hsu J. Targeting Intercellular Adhesion Molecule-1 to Enhance Delivery of Therapeutic Enzymes for Treatment of Lysosomal Storage Diseases. [Internet] [Thesis]. University of Maryland; 2014. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/1903/15932.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Hsu J. Targeting Intercellular Adhesion Molecule-1 to Enhance Delivery of Therapeutic Enzymes for Treatment of Lysosomal Storage Diseases. [Thesis]. University of Maryland; 2014. Available from: http://hdl.handle.net/1903/15932

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

18. Andressa Heimbecher Soares. Hipogonadismo associado à obesidade: efeitos do tratamento com citrato de clomifeno.

Degree: 2018, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5135/tde-13062018-074535/

► INTRODUÇÃO: A obesidade é uma das causas de hipogonadismo (HG) secundário no homem. A terapia de reposição padrão de testosterona (TRT) é associada à melhora… (more)

▼ INTRODUÇÃO: A obesidade é uma das causas de hipogonadismo (HG) secundário no homem. A terapia de reposição padrão de testosterona (TRT) é associada à melhora dos parâmetros metabólicos, mas pode levar à infertilidade. Apenas recentemente indicou-se que não há novas evidências nível 1 para apoiar uma conexão definitiva entre TRT e eventos cardiovasculares (CV). OBJETIVO: Avaliar os efeitos do Citrato de Clomifeno (CC) em homens jovens com hipogonadismo associado à obesidade diagnosticado por testosterona total (TT) <= 300 ng/dL em duas ocasiões, sintomas positivos no questionário ADAM, hormônio Luteinizante (LH) baixo ou inadequadamente normal (VR: 1,7 - 8,6 UI/L). MÉTODOS: Estudo randomizado, duplo cego, controlado por placebo (PLB), longitudinal em centro único. Setenta e oito pacientes com idade entre 36,5±7,8 anos, índice de massa corporal (IMC) 46,2±8,5 kg/m2 foram randomizados (1:1) para receber CC 50 mg ou PLB durante 12 semanas. Os pacientes foram avaliados através de: 1) Parâmetros clínicos: Questionário ADAM, número de intercursos sexuais, queixa de insatisfação com a vida sexual; 2) Parâmetros hormonais: dosagem sérica de TT, testosterona livre, Estradiol (E2), LH, hormônio folículo estimulante (FSH), SHBG, relação TT:E2; 3) Parâmetros de composição corporal: IMC, circunferência abdominal (CA) e análise de bioimpedanciometria; 4) Parâmetros metabólicos: pressão arterial sistólica e diastólica, glicemia em jejum (GJ), hemoglobina glicada (HbA1c), índice HOMA-IR, colesterol total e frações, triglicérides; 5) Parâmetros de resposta CV: dilatação fluxo mediada artéria braquial (FMDAB), níveis circulantes de sICAM-1, sVCAM-1, Selectina-sE e quantificação de células endoteliais progenitoras (CEPs) por citometria de fluxo; 6) Efeitos adversos: hematócrito, antígeno prostático específico sérico (PSA), questionário internacional de sintomas prostáticos (I-PSS), dosagem sérica de alanina aminotransferase (ALT), aspartato aminotransferase (AST), e efeitos adversos autorreferidos. RESULTADOS: Na randomização os dois grupos foram semelhantes em relação à idade (CC: 35,5±7,8 anos, PLB: 35,6±7,8; p= 0,951), IMC (CC: 45,5±11,3 kg/m2; PLB: 47,2±9,6; p= 0,470), CA (CC: 137,5±17,9 cm; PLB: 140,2±19,6; p= 0,526) e testosterona total (CC: 225,8±70,0 ng/dL; PLB: 216,0±72,1; p= 0,543). Não houve diferenças nos parâmetros de resposta clínica, exceto com relação à queixa de perda de vigor nas ereções (p < 0,001). Observou-se elevação significativa (p= < 0,001) de TT, Testosterona livre, E2, LH, FSH e SHBG no grupo CC em comparação com PLB. Houve um aumento significativo (p < 0,001) na massa magra e na massa muscular; e também na massa livre de gordura (p= 0,004). O CC reduziu HDL em comparação com PLB (p < 0,001) e não mostrou efeito em outros parâmetros metabólicos. Não houve significância estatística nos parâmetros CV, indicando efeito nulo do tratamento. CC reduziu ALT (p < 0,001) e aumentou o PSA (p= 0,023) dentro dos limites da normalidade. CONCLUSÕES: CC foi efetivo para melhorar os parâmetros de resposta hormonal e afetou… Advisors/Committee Members: Cintia Cercato, Daniela Calderaro, Edna Regina Nakandakare, Maria Elizabeth Rossi da Silva, Maria Teresa Zanella.

Subjects/Keywords: Células progenitoras endoteliais; Clomifeno; Hipogonadismo; Molécula 1 de adesão de célula vascular; Molécula 1 de adesão intercelular; Obesidade; Selectina E; Síndrome X metabólica; Testosterona; Vasodilatação; Eselectin, Endothelial progenitor cells; Hypogonadism; Intercellular adhesion molecule-1; Metabolic syndrome X, Clomiphene; Obesity; Testosterone; Vascular cell adhesion molecule-1; Vasodilation

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Soares, A. H. (2018). Hipogonadismo associado à obesidade: efeitos do tratamento com citrato de clomifeno. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5135/tde-13062018-074535/

Chicago Manual of Style (16^th Edition):

Soares, Andressa Heimbecher. “Hipogonadismo associado à obesidade: efeitos do tratamento com citrato de clomifeno.” 2018. Doctoral Dissertation, University of São Paulo. Accessed April 10, 2021. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-13062018-074535/.

MLA Handbook (7^th Edition):

Soares, Andressa Heimbecher. “Hipogonadismo associado à obesidade: efeitos do tratamento com citrato de clomifeno.” 2018. Web. 10 Apr 2021.

Vancouver:

Soares AH. Hipogonadismo associado à obesidade: efeitos do tratamento com citrato de clomifeno. [Internet] [Doctoral dissertation]. University of São Paulo; 2018. [cited 2021 Apr 10]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5135/tde-13062018-074535/.

Council of Science Editors:

Soares AH. Hipogonadismo associado à obesidade: efeitos do tratamento com citrato de clomifeno. [Doctoral Dissertation]. University of São Paulo; 2018. Available from: http://www.teses.usp.br/teses/disponiveis/5/5135/tde-13062018-074535/

Lehigh University

19. Bach, Steven. Integrin related cell interaction in primary T lymphocytes and cancer cells.

Degree: MS, Mechanical Engineering and Mechanics, 2013, Lehigh University

URL: https://preserve.lehigh.edu/etd/1416

► Integrins are a family of transmembrane adhesion proteins that mediatecell attachment to extracellular matrix or to another cell. The Tcell LFA-1 integrin and its interaction… (more)

▼ Integrins are a family of transmembrane adhesion proteins that mediatecell attachment to extracellular matrix or to another cell. The Tcell LFA-1 integrin and its interaction with its predominant ligand,ICAM-1, is known to regulate antigen-driven differentiation of naiveT cells into effector T cells, a process that is fundamental to adaptiveimmunity. The activation of LFA-1 on effector and naive T cells isstill unclear and requires further investigation for a more detailedunderstanding. In this work we quantitatively study primary T cells(both naive and effector) and their interaction with ICAM-1 usingatomic force microscopy (AFM). Measurements show that adhesion ofthe effector T cell is in general at least one order of magnitudehigher than that of the naive T cells. OKT3 treatment has a profoundimpact on T cell–ICAM-1 interaction, resulting in at least a 2-foldincrease in both detachment force and work. Our conclusions corroboratepast research that shows that there is a higher expression of LFA-1on effector T cells than naive T cells and that LFA-1 on effectorT cells is predominantly in the high affinity state. Our results alsopossibly indicate that a mixed population of high and low affinityLFA-1 is present on naive cells. Furthermore, given the response toOKT3 treatment, it is likely that it induces populations of LFA-1to change from low affinity to high affinity on both effector andnaive T cells. Taken together, our studies reveal in more detail theregulation and conformational states of high affinity LFA-1 on T cellswhich is critical to T cell activation. Additionally, we use AFM to look at the interaction between neuropilin-2 (NRP-2), a type I transmembrane glycoprotein, which is expressed on cancer cells and show that it interacts with α5 integrin on endothelial cells. Most importantly, our studies reveal that theinteraction mediates cancer cell vascular extravasation and promotesmetastasis. This research further supports the highly promising routeof preventing cancer metastasis by therapeutically blocking NRP-2and thereby greatly improving the prognoses of cancer patients. Advisors/Committee Members: Zhang, Xiaohui.

Subjects/Keywords: α5 integrin; atomic force microscopy; intercellular adhesion molecule-1; lymphocyte function-associated antigen-1; neuropilin-2; T cell; Biomedical Engineering and Bioengineering; Engineering

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Bach, S. (2013). Integrin related cell interaction in primary T lymphocytes and cancer cells. (Thesis). Lehigh University. Retrieved from https://preserve.lehigh.edu/etd/1416

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Bach, Steven. “Integrin related cell interaction in primary T lymphocytes and cancer cells.” 2013. Thesis, Lehigh University. Accessed April 10, 2021. https://preserve.lehigh.edu/etd/1416.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Bach, Steven. “Integrin related cell interaction in primary T lymphocytes and cancer cells.” 2013. Web. 10 Apr 2021.

Vancouver:

Bach S. Integrin related cell interaction in primary T lymphocytes and cancer cells. [Internet] [Thesis]. Lehigh University; 2013. [cited 2021 Apr 10]. Available from: https://preserve.lehigh.edu/etd/1416.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Bach S. Integrin related cell interaction in primary T lymphocytes and cancer cells. [Thesis]. Lehigh University; 2013. Available from: https://preserve.lehigh.edu/etd/1416

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

20. Ilinčić Branislava. Odnos inflamatornih biomarkera endotelne disfunkcije i ateroskleroze kod hiperalimentacione gojaznosti.

Degree: 2015, University of Novi Sad

URL: https://www.cris.uns.ac.rs/DownloadFileServlet/Disertacija143946221919893.pdf?controlNumber=(BISIS)95482&fileName=143946221919893.pdf&id=4170&source=OATD&language=en ; https://www.cris.uns.ac.rs/record.jsf?recordId=95482&source=OATD&language=en

► UVOD: Gojaznost je hronično, multifaktorijalno i kompleksno oboljenje povezano sa povećanim rizikom od aterosklerotskih kardiovaskularnih bolesti (KVB). Disfunkcija vaskularnog endotela predstavlja rani događaj u… (more)

▼ UVOD: Gojaznost je hronično, multifaktorijalno i kompleksno oboljenje povezano sa povećanim rizikom od aterosklerotskih kardiovaskularnih bolesti (KVB). Disfunkcija vaskularnog endotela predstavlja rani događaj u patofiziološkom kontinuumu aterosklerotskog procesa, a produženo izlaganje vaskularnog endotela faktorima rizika za aterosklerozu udruženim sa gojaznosti (insulinska rezistencija, dislipidemija, proinflamatorno/protrombozno stanje), može doprineti procesima aktivacije/disfunkcije endotela i progresiji ateroskleroze u supkliničku, odnosno kliničku formu bolesti. CILJ: Uporediti koncentracije solubilne forme adhezionih molekula – intracelularnog adhezivnog molekula –1 (sICAM–1) i E selektina (sE–selektin), između ispitanika sa hiperalimentacionim tipom gojaznosti i normalno uhranjenih zdravih ispitanika, kao i utvrditi eventualno postojanje razlika u koncentraciji sICAM–1 i sE–selektina između ispitanika kod kojih je merenjem debljine kompleksa intima medija karotidne arterije (IMK) uočen supklinički stadijum ateroskleroze i ispitanika koji imaju normalnu debljinu IMK. Ispitati povezanost parametara telesne kompozicije (ukupne masne mase tela i masne mase abdominalnih depoa), cirkulišućih koncentracija biomarkera disfunkcije vaskularnog endotela (sICAM–1 i sE–selektina) i IMK kod ispitanika sa hiperalimentacionim tipom gojaznosti. MATERIJAL I METODE: U istraživanje je uključeno 60 ispitanika sa hiperalimentacionim tipom gojaznosti bez pridruženih komorbiditeta i 30 zdravih normalno uhranjenih učesnika usklađenih sa ispitanicima po godinama života i polu koji su činili kontrolnu grupu. Svim ispitanicima su urađena antropometrijska merenja, analiza komponenata telesne kompozicije (bioelektrična impedansna analiza, Tanita Body Composition Analyzer BC – 418 MA III), laboratorijska analiza uzoraka krvi na automatizovanim analizatorskim sistemima sa određivanjem parametara metabolizma glukoze (bazalno i 2 h u toku oralnog glukoza tolerans testa), lipida i lipoproteina, inflamacije i homocisteina. Određivanje serumske koncentracije sICAM–1 i sE–selektina je vršeno ELISA tehnikom (R&D Systems, Inc. Minneapolis, USA). Vrednosti IMK–a su određivane pomoću karotidnog dupleks ultrazvuka (Aloka SSD–650 US system, Tokyo), a na osnovu izmerenih (IMK) i normalno očekivanih vrednosti IMK za svakog ispitanika je izračunavan IMK Z–skor. Supklinički stadijum ateroskleroze je definisan kao vrednost IMK Z–skora veća od 1 (što odgovara vrednosti IMK većoj od 95 percentila normalno očekivane vrednosti u odnosu na pol i godine života ispitanika). REZULTATI: Ispitanici sa hiperalimentacionim tipom gojaznosti su imali statistički značajno više vrednosti medijane serumske koncentracije sE–selektina u poređenju sa medijanom serumske koncetracije sE–selektina učesnika u kontrolnoj grupi (36,2 (33,21–43.7) vs. 25,14 (23,1–29,48) ng/mL, P=0,00). Gojazni ispitanici III stepena gojaznosti… Advisors/Committee Members: Stošić Zoran, Đerić Mirjana, Živančević Simonović Snežana, Ćurić Nikola, Stokić Edita, Žarkov Marija.

Subjects/Keywords: Gojaznost; Vaskularni endotel; E-selektin; Intracelularni adhezioni molekul 1; Ateroskleroza; Telesna kompozicija; Obesity; Endothelium, Vascular; E-Selectin; Intercellular Adhesion Molecule-1; Atherosclerosis; Body Composition

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Branislava, I. (2015). Odnos inflamatornih biomarkera endotelne disfunkcije i ateroskleroze kod hiperalimentacione gojaznosti. (Thesis). University of Novi Sad. Retrieved from https://www.cris.uns.ac.rs/DownloadFileServlet/Disertacija143946221919893.pdf?controlNumber=(BISIS)95482&fileName=143946221919893.pdf&id=4170&source=OATD&language=en ; https://www.cris.uns.ac.rs/record.jsf?recordId=95482&source=OATD&language=en

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Branislava, Ilinčić. “Odnos inflamatornih biomarkera endotelne disfunkcije i ateroskleroze kod hiperalimentacione gojaznosti.” 2015. Thesis, University of Novi Sad. Accessed April 10, 2021. https://www.cris.uns.ac.rs/DownloadFileServlet/Disertacija143946221919893.pdf?controlNumber=(BISIS)95482&fileName=143946221919893.pdf&id=4170&source=OATD&language=en ; https://www.cris.uns.ac.rs/record.jsf?recordId=95482&source=OATD&language=en.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Branislava, Ilinčić. “Odnos inflamatornih biomarkera endotelne disfunkcije i ateroskleroze kod hiperalimentacione gojaznosti.” 2015. Web. 10 Apr 2021.

Vancouver:

Branislava I. Odnos inflamatornih biomarkera endotelne disfunkcije i ateroskleroze kod hiperalimentacione gojaznosti. [Internet] [Thesis]. University of Novi Sad; 2015. [cited 2021 Apr 10]. Available from: https://www.cris.uns.ac.rs/DownloadFileServlet/Disertacija143946221919893.pdf?controlNumber=(BISIS)95482&fileName=143946221919893.pdf&id=4170&source=OATD&language=en ; https://www.cris.uns.ac.rs/record.jsf?recordId=95482&source=OATD&language=en.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Branislava I. Odnos inflamatornih biomarkera endotelne disfunkcije i ateroskleroze kod hiperalimentacione gojaznosti. [Thesis]. University of Novi Sad; 2015. Available from: https://www.cris.uns.ac.rs/DownloadFileServlet/Disertacija143946221919893.pdf?controlNumber=(BISIS)95482&fileName=143946221919893.pdf&id=4170&source=OATD&language=en ; https://www.cris.uns.ac.rs/record.jsf?recordId=95482&source=OATD&language=en

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

21. 関, 要. Demeanor of rivaroxaban in activated/inactivated FXa. : 凝固第X因子活性時 / 非活性時におけるRivaroxabanの振る舞い.

Degree: 博士（医学）, 2018, Saitama Medical University / 埼玉医科大学

URL: http://id.nii.ac.jp/1386/00000609/

►

Activated factor X (FXa) plays an important role in thrombin generation and inflammation. Factor X is not converted constitutively to FXa, but only after intrinsic… (more)

Subjects/Keywords: Cells, Cultured; Chemokine CCL2; Factor Xa; Factor Xa Inhibitors; Human Umbilical Vein Endothelial Cells; Humans; Intercellular Adhesion Molecule-1; Interleukin-8; Oligonucleotide Array Sequence Analysis; Receptors, Proteinase-Activated; Rivaroxaban

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❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

関, �. (2018). Demeanor of rivaroxaban in activated/inactivated FXa. : 凝固第X因子活性時 / 非活性時におけるRivaroxabanの振る舞い. (Thesis). Saitama Medical University / 埼玉医科大学. Retrieved from http://id.nii.ac.jp/1386/00000609/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

関, 要. “Demeanor of rivaroxaban in activated/inactivated FXa. : 凝固第X因子活性時 / 非活性時におけるRivaroxabanの振る舞い.” 2018. Thesis, Saitama Medical University / 埼玉医科大学. Accessed April 10, 2021. http://id.nii.ac.jp/1386/00000609/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

関, 要. “Demeanor of rivaroxaban in activated/inactivated FXa. : 凝固第X因子活性時 / 非活性時におけるRivaroxabanの振る舞い.” 2018. Web. 10 Apr 2021.

Vancouver:

関 �. Demeanor of rivaroxaban in activated/inactivated FXa. : 凝固第X因子活性時 / 非活性時におけるRivaroxabanの振る舞い. [Internet] [Thesis]. Saitama Medical University / 埼玉医科大学; 2018. [cited 2021 Apr 10]. Available from: http://id.nii.ac.jp/1386/00000609/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

関 �. Demeanor of rivaroxaban in activated/inactivated FXa. : 凝固第X因子活性時 / 非活性時におけるRivaroxabanの振る舞い. [Thesis]. Saitama Medical University / 埼玉医科大学; 2018. Available from: http://id.nii.ac.jp/1386/00000609/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

22. Vedvyas, Yogindra. SOMATOSTATIN RECEPTOR TYPE 2 (SSTR2) FOR ADOPTIVE T CELL IMAGING, STIMULATION, AND ELIMINATION.

Degree: PhD, Biomedical Engineering, 2018, Cornell University

URL: http://hdl.handle.net/1813/59687

► Harnessing the immune system to recognize and destroy tumor cells has been the central goal of anti-cancer immunotherapy. Adoptive cell therapy (ACT) is a treatment… (more)

▼ Harnessing the immune system to recognize and destroy tumor cells has been the central goal of anti-cancer immunotherapy. Adoptive cell therapy (ACT) is a treatment that uses a cancer patient's own T lymphocytes with anti-tumor activity, expanded in-vitro and re-infused into the patient. The ability to genetically engineer human lymphocytes and use them to mediate cancer regression in patients, which has recently been demonstrated, has opened possibilities for the extension of ACT immunotherapy to patients with a wide variety of cancer types and is a promising new approach to cancer treatment. Clinical monitoring of ACT utilizes serial blood analyses to discern T cell activity. While useful, these data are 1-dimensional and lack spatiotemporal information related to treatment efficacy or toxicity. In this dissertation, I have utilized a human genetic reporter, somatostatin receptor 2 (SSTR2), and PET, to quantitatively and longitudinally visualize whole-body T cell distribution and antitumor dynamics using a clinically approved radiotracer. Initial evaluations determined that SSTR2-expressing T cells were detectable at low densities with high sensitivity and specificity. While keeping a close eye on the status of immunotherapy is shown in the early part of this thesis, later topics address the ideal antigens to target tumors, more specifically targeting solid tumors. We turned to targeting inflammation, specifically intercellular adhesion molecule-1 (ICAM-1), as an ideal marker for solid tumors. ICAM-1, which has been implicated to play a critical role in tumor progression in various types of cancer, has also been linked to cancer metastases, where this molecule facilitates the spread of metastatic cancer cells to secondary sites. The unique expression profile of ICAM-1 throughout solid tumor microenvironment makes ICAM-1 an intriguing molecular target, as evidence suggests that approximately 25% of all human cancer worldwide is associated with chronic inflammation. Utilizing ICAM1 as a target, I share the success of using an ICAM1 specific chimeric antigen receptor (CAR) T cells to eliminate anaplastic thyroid cancer tumors, in a solid tumor mouse model. The first attempt was using the single-chain fragmentvariable of R6.5, an ICAM-1 specific antibody. Followed by the utilization of the active domain (I-domain) of the natural ligand to ICAM-1, lymphocyte function associated antigen-1 (LFA-1). For I-domain CAR, many engineered affinity variants were studies, to help determine the ideal antigen to affinity, to maintain CAR T cell persistence without any systemic toxicities sometimes observed with ACTs. Advisors/Committee Members: Jin, Moonsoo (chair), Nikitin, Alexander (committee member), Putnam, David A. (committee member).

Subjects/Keywords: Adoptive Cell Therapy (ACT); Chimeric Antigen Receptor (CAR) T cells; Inflammation and Cancer; Intercellular Adhesion Molecule-1 (ICAM-1); Positron emission tomography (PET); Somatostatin Receptor 2 (SSTR2); Biomedical engineering; Immunology; Chemical engineering

…the genes induced by the activation of NF-kB is intercellular adhesion molecule (ICAM… …adhesion molecule-1 (ICAM-1) targeting CAR-T for the treatment of aggressive thyroid… …adhesion molecules and is composed of five extracellular Immunoglobulin G-like domains. ICAM-1 is… …of ICAM-1 on tumors �� ...8 Difficulty with CAR T cell against solid cancer, and strategies… …21 References �� ….23 CHAPTER 2: CAR T THERAPY TARGETING ICAM-1…

10 more images…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Vedvyas, Y. (2018). SOMATOSTATIN RECEPTOR TYPE 2 (SSTR2) FOR ADOPTIVE T CELL IMAGING, STIMULATION, AND ELIMINATION. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/59687

Chicago Manual of Style (16^th Edition):

Vedvyas, Yogindra. “SOMATOSTATIN RECEPTOR TYPE 2 (SSTR2) FOR ADOPTIVE T CELL IMAGING, STIMULATION, AND ELIMINATION.” 2018. Doctoral Dissertation, Cornell University. Accessed April 10, 2021. http://hdl.handle.net/1813/59687.

MLA Handbook (7^th Edition):

Vedvyas, Yogindra. “SOMATOSTATIN RECEPTOR TYPE 2 (SSTR2) FOR ADOPTIVE T CELL IMAGING, STIMULATION, AND ELIMINATION.” 2018. Web. 10 Apr 2021.

Vancouver:

Vedvyas Y. SOMATOSTATIN RECEPTOR TYPE 2 (SSTR2) FOR ADOPTIVE T CELL IMAGING, STIMULATION, AND ELIMINATION. [Internet] [Doctoral dissertation]. Cornell University; 2018. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/1813/59687.

Council of Science Editors:

Vedvyas Y. SOMATOSTATIN RECEPTOR TYPE 2 (SSTR2) FOR ADOPTIVE T CELL IMAGING, STIMULATION, AND ELIMINATION. [Doctoral Dissertation]. Cornell University; 2018. Available from: http://hdl.handle.net/1813/59687

23. Cox, Maureen A. Adhesion molecule interactions influence the implementation of immune responses to infection.

Degree: PhD, 2012, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,1468

►

Interactions mediated by intercellular adhesion molecule-1 (ICAM-1) enhance both the antigenic and cytokine signals that CD8 T cells perceive, and these interactions have been suggested… (more)

▼

Interactions mediated by intercellular adhesion molecule-1 (ICAM-1) enhance both the antigenic and cytokine signals that CD8 T cells perceive, and these interactions have been suggested to be required for the formation of memory CD8 T cells. Following acute lymphocytic choriomeningitis virus (LCMV) infection of ICAM-1-/-mice, weobserve elevated numbers of �effector-phenotype� (CD127loKLRG-1hiIL-2-) virus-specific CD8 T cells well into the memory phase, while the development of memory-phenotype CD8 T cells (CD127hiKLRG-1loIL-2 producing) is not impaired. Theenhanced maintenance of effector-phenotype cells is due to ICAM-1 deficiency on non-T cell subsets, suggesting a role for ICAM-1 mediated interactions with the APC in programming efficient contraction of these cells. Although memory T cells do emerge and are maintained if ICAM-1 expression is abolished, the secondary proliferative capacity of these T cells is severely curtailed. During chronic infections the development of T cell memory is corrupted as the responding cells succumb to exhaustion and possible deletion. Following chronic LCMV clone-13 infection, greater numbers of functional virus-specific CD8 T cells are observed in the tissues and secondary lymphoid organs of ICAM-1-/-mice, suggesting a role for ICAM-1 in the exhaustion of these responses. We propose a model in which ICAM-1 acts to fine tune the immune response to both low and high doses of antigen, by operating to enhance weak but restrict strong responses. In the case of infections, we propose that ICAM-1 interactions serve to further drive activation of the CD8 T cells resulting in terminal differentiation or exhaustion of the CD8 T cells and programming the downsizing of the effector response.

PhD

1 online resource (xiii, 201 p.) :ill., digital, PDF file.

Microbiology

Joint Health Sciences

ICAM-1, CD8 T cell memory, viral infection

UNRESTRICTED

Advisors/Committee Members: Allan J. Zajac, William J. Britt<br>, David D. Chaplin<br>, Judith A. Kapp<br>, Casey T. Weaver..

Subjects/Keywords: CD8-Positive T-Lymphocytes – immunology.<; br>; CD8-Positive T-Lymphocytes – metabolism.<; br>; Cytokines – immunology<; br>; DNA Viruses – immunology<; br>; Immunologic Memory – physiology.<; br>; Infection – immunology<; br>; Intercellular Adhesion Molecule-1 – immunology.<; br>; Intercellular Adhesion Molecule-1 – metabolism.<; br>; RNA Viruses – immunology<; br>; Virus Diseases – immunology

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Cox, M. A. (2012). Adhesion molecule interactions influence the implementation of immune responses to infection. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1468

Chicago Manual of Style (16^th Edition):

Cox, Maureen A. “Adhesion molecule interactions influence the implementation of immune responses to infection.” 2012. Doctoral Dissertation, University of Alabama – Birmingham. Accessed April 10, 2021. http://contentdm.mhsl.uab.edu/u?/etd,1468.

MLA Handbook (7^th Edition):

Cox, Maureen A. “Adhesion molecule interactions influence the implementation of immune responses to infection.” 2012. Web. 10 Apr 2021.

Vancouver:

Cox MA. Adhesion molecule interactions influence the implementation of immune responses to infection. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2012. [cited 2021 Apr 10]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1468.

Council of Science Editors:

Cox MA. Adhesion molecule interactions influence the implementation of immune responses to infection. [Doctoral Dissertation]. University of Alabama – Birmingham; 2012. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1468

Vilnius University

24. Balčiūnas, Mindaugas. Kardiovaskulinių komplikacijų sąsajos su endotelio pažeidimo žymenimis po aortos vainikinių jungčių suformavimo operacijų.

Degree: Dissertation, Medicine, 2009, Vilnius University

URL: http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2009~D_20091109_151340-62166 ;

►

Endotelio funkcijos sutrikimas (disfunkcija) - būklė, apibūdinama padidėjusia adhezijos molekulių ekspresija, padidėjusia prouždegiminių veiksnių ir protrombotinių faktorių sinteze bei sutrikusia kraujagyslių tono reguliacija - yra… (more)

▼

Endotelio funkcijos sutrikimas (disfunkcija) - būklė, apibūdinama padidėjusia adhezijos molekulių ekspresija, padidėjusia prouždegiminių veiksnių ir protrombotinių faktorių sinteze bei sutrikusia kraujagyslių tono reguliacija - yra mirties dėl kardiovaskulinės patologijos, miokardo infarkto bei poreikio revaskuliarizacijos procedūroms išsivystymo rizikos veiksnys. Darbo tikslas buvo nustatyti endotelio pažeidimą atspindinčių žymenų, hs-CRP, sVCAM-1 ir sICAM-1 reikšmę, nuspėjant kardiovaskulines komplikacijas po aortos vainikinių jungčių suformavimo operacijos, atliktos dirbtinės kraujo apytakos sąlygomis. Nustatėme, kad didesnės priešoperacinės hs-CRP ir sVCAM-1 koncentracijos buvo nepriklausomi didesnės kardiovaskulinių komplikacijų po aortos vainikinių jungčių suformavimo operacijų rizikos žymenys. Po aortos vainikinių jungčių suformavimo operacijos nustatyta reikšmingai didesnė hs-CRP, sVCAM-1 ir sICAM-1 koncentracija, palyginus su priešoperaciniu koncentracijos lygiu. Patikimos žymenų koreliacijos su aortos užspaudimo, dirbtinės kraujo apytakos bei operacijos trukme neradome. Pacientams po aortos vainikinių jungčių suformavimo operacijos koreliacijos tarp pooperacinio sICAM-1, sVCAM-1 bei hs-CRP koncentracijos lygio ir kardiovaskulinių komplikacijų išsivystymo rizikos nebuvo nenustatyta.

The endothelial cell damage/dysfunction is associated with increased expression of adhesion molecules, synthesis of proinflammatory, prothrombotic factors and abnormal modulation of vascular tone. A growing body of evidence suggests that endothelial dysfunction is associated with future cardiovascular events including cardiac death, myocardial infarction and the need for revascularization procedures. The aim of the study was to evaluate the impact of markers of endothelial damage as predictors of cardiovascular events after on-pump coronary artery bypass grafting surgery. We found that higher concentrations preoperatively of hs-CRP and sVCAM-1 were independent markers for higher risk of cardiovascular events after coronary artery bypass grafting surgery. Concentration of hs-CRP, sVCAM-1 and sICAM-1 increased significantly after on-pump coronary artery bypass grafting surgery compared to preoperative level. However correlation between the duration of aortic cross-clamp, cardiopulmonary bypass or surgery and markers of endothelial damage was not found. Correlation between postoperative concentration of hs-CRP, sVCAM-1 and sICAM-1 and risk for cardiovascular events after coronary artery bypass grafting surgery was not found.

Advisors/Committee Members: Šipylaitė, Jūratė (Doctoral dissertation committee chair), Širvinskas, Edmundas (Doctoral dissertation committee member), Adukauskienė, Dalia (Doctoral dissertation committee member), Ručinskas, Kęstutis (Doctoral dissertation committee member), Gulbinovič, Jolanta (Doctoral dissertation committee member), Kinduris, Šarūnas (Doctoral dissertation opponent), Eidukaitė, Audronė (Doctoral dissertation opponent), Bagdonaitė, Loreta (Doctoral dissertation advisor).

Subjects/Keywords: Tirpi kraujagyslių ir tarpląstelinės sąveikos adhezijos molekulė-1; Didelio jautrumo C-reaktyvusis baltymas; Aortos vainikinių jungčių suformavimo operacija; Kardiovaskulinės komplikacijos; Endotelio pažeidimas; Soluble vascular cell and intercellular adhesion molecule-1; High sensitivity C-reactive protein; Coronary artery bypass grafting surgery; Cardiovascular events; Endothelial damage

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Balčiūnas, M. (2009). Kardiovaskulinių komplikacijų sąsajos su endotelio pažeidimo žymenimis po aortos vainikinių jungčių suformavimo operacijų. (Doctoral Dissertation). Vilnius University. Retrieved from http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2009~D_20091109_151340-62166 ;

Chicago Manual of Style (16^th Edition):

Balčiūnas, Mindaugas. “Kardiovaskulinių komplikacijų sąsajos su endotelio pažeidimo žymenimis po aortos vainikinių jungčių suformavimo operacijų.” 2009. Doctoral Dissertation, Vilnius University. Accessed April 10, 2021. http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2009~D_20091109_151340-62166 ;.

MLA Handbook (7^th Edition):

Balčiūnas, Mindaugas. “Kardiovaskulinių komplikacijų sąsajos su endotelio pažeidimo žymenimis po aortos vainikinių jungčių suformavimo operacijų.” 2009. Web. 10 Apr 2021.

Vancouver:

Balčiūnas M. Kardiovaskulinių komplikacijų sąsajos su endotelio pažeidimo žymenimis po aortos vainikinių jungčių suformavimo operacijų. [Internet] [Doctoral dissertation]. Vilnius University; 2009. [cited 2021 Apr 10]. Available from: http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2009~D_20091109_151340-62166 ;.

Council of Science Editors:

Balčiūnas M. Kardiovaskulinių komplikacijų sąsajos su endotelio pažeidimo žymenimis po aortos vainikinių jungčių suformavimo operacijų. [Doctoral Dissertation]. Vilnius University; 2009. Available from: http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2009~D_20091109_151340-62166 ;

Vilnius University

25. Balčiūnas, Mindaugas. Kardiovaskulinių komplikacijų sąsajos su endotelio pažeidimo žymenimis po aortos vainikinių jungčių suformavimo operacijų.

Degree: PhD, Medicine, 2009, Vilnius University

URL: http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2009~D_20091109_151352-50041 ;

►

Endotelio funkcijos sutrikimas (disfunkcija) - būklė, apibūdinama padidėjusia adhezijos molekulių ekspresija, padidėjusia prouždegiminių veiksnių ir protrombotinių faktorių sinteze bei sutrikusia kraujagyslių tono reguliacija - yra… (more)

▼

Endotelio funkcijos sutrikimas (disfunkcija) - būklė, apibūdinama padidėjusia adhezijos molekulių ekspresija, padidėjusia prouždegiminių veiksnių ir protrombotinių faktorių sinteze bei sutrikusia kraujagyslių tono reguliacija - yra mirties dėl kardiovaskulinės patologijos, miokardo infarkto bei poreikio revaskuliarizacijos procedūroms išsivystymo rizikos veiksnys. Darbo tikslas buvo nustatyti endotelio pažeidimą atspindinčių žymenų, hs-CRP, sVCAM-1 ir sICAM-1 reikšmę, nuspėjant kardiovaskulines komplikacijas po aortos vainikinių jungčių suformavimo operacijos, atliktos dirbtinės kraujo apytakos sąlygomis. Nustatėme, kad didesnės priešoperacinės hs-CRP ir sVCAM-1 koncentracijos buvo nepriklausomi didesnės kardiovaskulinių komplikacijų po aortos vainikinių jungčių suformavimo operacijų rizikos žymenys. Po aortos vainikinių jungčių suformavimo operacijos nustatyta reikšmingai didesnė hs-CRP, sVCAM-1 ir sICAM-1 koncentracija, palyginus su priešoperaciniu koncentracijos lygiu. Patikimos žymenų koreliacijos su aortos užspaudimo, dirbtinės kraujo apytakos bei operacijos trukme neradome. Pacientams po aortos vainikinių jungčių suformavimo operacijos koreliacijos tarp pooperacinio sICAM-1, sVCAM-1 bei hs-CRP koncentracijos lygio ir kardiovaskulinių komplikacijų išsivystymo rizikos nebuvo nenustatyta.

The endothelial cell damage/dysfunction is associated with increased expression of adhesion molecules, synthesis of proinflammatory, prothrombotic factors and abnormal modulation of vascular tone. A growing body of evidence suggests that endothelial dysfunction is associated with future cardiovascular events including cardiac death, myocardial infarction and the need for revascularization procedures. The aim of the study was to evaluate the impact of markers of endothelial damage as predictors of cardiovascular events after on-pump coronary artery bypass grafting surgery. We found that higher concentrations preoperatively of hs-CRP and sVCAM-1 were independent markers for higher risk of cardiovascular events after coronary artery bypass grafting surgery. Concentration of hs-CRP, sVCAM-1 and sICAM-1 increased significantly after on-pump coronary artery bypass grafting surgery compared to preoperative level. However correlation between the duration of aortic cross-clamp, cardiopulmonary bypass or surgery and markers of endothelial damage was not found. Correlation between postoperative concentration of hs-CRP, sVCAM-1 and sICAM-1 and risk for cardiovascular events after coronary artery bypass grafting surgery was not found.

Advisors/Committee Members: Šipylaitė, Jūratė (Doctoral dissertation committee chair), Širvinskas, Edmundas (Doctoral dissertation committee member), Adukauskienė, Dalia (Doctoral dissertation committee member), Ručinskas, Kęstutis (Doctoral dissertation committee member), Gulbinovič, Jolanta (Doctoral dissertation committee member), Kinduris, Šarūnas (Doctoral dissertation opponent), Eidukaitė, Audronė (Doctoral dissertation opponent), Griškevičius, Laimonas (Doctoral dissertation supervisor), Bagdonaitė, Loreta (Doctoral dissertation advisor).

Subjects/Keywords: Tirpi kraujagyslių ir tarpląstelinės sąveikos adhezijos molekulė-1; Didelio jautrumo C-reaktyvusis baltymas; Aortos vainikinių jungčių suformavimo operacija; Kardiovaskulinės komplikacijos; Endotelio pažeidimas; Soluble vascular cell and intercellular adhesion molecule-1; High sensitivity C-reactive protein; Coronary artery bypass grafting surgery; Cardiovascular events; Endothelial damage

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Balčiūnas, M. (2009). Kardiovaskulinių komplikacijų sąsajos su endotelio pažeidimo žymenimis po aortos vainikinių jungčių suformavimo operacijų. (Doctoral Dissertation). Vilnius University. Retrieved from http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2009~D_20091109_151352-50041 ;

Chicago Manual of Style (16^th Edition):

Balčiūnas, Mindaugas. “Kardiovaskulinių komplikacijų sąsajos su endotelio pažeidimo žymenimis po aortos vainikinių jungčių suformavimo operacijų.” 2009. Doctoral Dissertation, Vilnius University. Accessed April 10, 2021. http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2009~D_20091109_151352-50041 ;.

MLA Handbook (7^th Edition):

Balčiūnas, Mindaugas. “Kardiovaskulinių komplikacijų sąsajos su endotelio pažeidimo žymenimis po aortos vainikinių jungčių suformavimo operacijų.” 2009. Web. 10 Apr 2021.

Vancouver:

Balčiūnas M. Kardiovaskulinių komplikacijų sąsajos su endotelio pažeidimo žymenimis po aortos vainikinių jungčių suformavimo operacijų. [Internet] [Doctoral dissertation]. Vilnius University; 2009. [cited 2021 Apr 10]. Available from: http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2009~D_20091109_151352-50041 ;.

Council of Science Editors:

Balčiūnas M. Kardiovaskulinių komplikacijų sąsajos su endotelio pažeidimo žymenimis po aortos vainikinių jungčių suformavimo operacijų. [Doctoral Dissertation]. Vilnius University; 2009. Available from: http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2009~D_20091109_151352-50041 ;

26. Τσιντή, Μαρία. Μελέτη του ρόλου των φυλετικών ορμονών στην παθογένεια του συνδρόμου Sjogren: ανάλυση της έκφρασης οιστρογονικών υποδοχέων και της αποκρισιμότητας στα οιστρογόνα των επιθηλιακών κυττάρων των σιελογόνων αδένων.

Degree: 2012, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/31783

► Sjögren syndrome (SS) or autoimmune epithelitis is a chronic autoimmune disorder ofthe exocrine glands, mainly of the salivary and the lacrimal glands, that affects about1-3%… (more)

▼ Sjögren syndrome (SS) or autoimmune epithelitis is a chronic autoimmune disorder ofthe exocrine glands, mainly of the salivary and the lacrimal glands, that affects about1-3% of the general population and is characterized by strong female preponderance.Experimental evidence suggests that salivary gland epithelial cells (SGEC) are centralto the autoimmune lesion in SS, not only as target cells, but also as an activeparticipant in the induction and perpetuation of the autoimmune response. SGECappear to actively participate in immune responses and to possess immune function,whereas the perturbation of this function possibly contributes to the development ofthe autoimmune response in the context of the chronic activation of the epithelium.The strong female preponderance of the disease (women/men 9:1), as well as theusual occurrence of the disease around menopause led to the classic hypothesis thatestrogens are central to the pathophysiology of the disease, whereas experimentalanimal models have indicated the contribution of estrogens in disease pathogenesis.Experimental and epidemiological data indicate the paramount importance of bothSGEC and estrogens in SS pathogenesis, as well as that the salivary gland is normalysubjected to estrogenic influence. However, the expression and functional capacity ofestrogen receptor alpha and estrogen receptor beta (ERα and ERβ) in normal humansalivary epithelium as well as the estrogenic responsiveness and the expression ofERα and ERβ in the salivary epithelium of SS patients has not been assessed.In the present study, the expression and functional capacity of ERα and ERβ,the immunomodulatory potential of estrogens and the estrogenic effect in theproliferation and the induction of apoptosis in SGEC was initially assessed in normalsalivary epithelium. After the detection of the expression and of the functionalcapacity of ERα and ERβ proteins in normal salivary epithelium, the estrogenic responsiveness and the expression of ERα and ERβ proteins was comparativelyassessed in the salivary epithelium of SS patients and of healthy controls. Theexpression of ERα and ERβ proteins and their isoforms (ERαΔ3-isoform, ERβ1-long[currently regarded as the wild-type ERβ protein] and ERβ1-short forms and ERβ2-isoform) was analysed in tissue specimens (immunohistochemical experiments), aswell as in cultured non-neoplastic SGEC lines (immunohistochemical andimmunoblotting experiments), derived from minor salivary gland biopsies, frompatients that had undergone biopsy during their diagnostic evaluation for possible SS.Immunohistochemical experiments revealed strong expression of ERα, ERβ1 andERβ2 proteins, with similar staining pattern and intensity in both the nucleus andcytoplasm of SGEC. The epithelial expression of estrogen receptors was confirmedby immunoblotting experiments in cellular extracts from SGEC, where the full-lengthERα and the ERα-Δ3 isoform, ERβ1-long, ERβ1-short and ERβ2-long proteins weredetected. The application of a standard estrogenic inhibition assay of cytokine inducedadhesion…

Subjects/Keywords: Σύνδρομο Sjogren; Οιστρογονικοί υποδοχείς; Επιθηλιακά κύτταρα; Σιελογόνοι αδένες; Οιστρογονική αποκρισιμότητα; Ανοσορρυθμιστική επίδραση; Ιντερφερόνη-γ; Διακυτταρικό μόριο προσκόλλησης-1; Sjogren syndorme; Estrogen receptors; Epithelial cells; Salivary glands; Estrogenic responsiveness; Imunoregulatory role; Intercellular adhesion molecule-1

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Τσιντή, . �. (2012). Μελέτη του ρόλου των φυλετικών ορμονών στην παθογένεια του συνδρόμου Sjogren: ανάλυση της έκφρασης οιστρογονικών υποδοχέων και της αποκρισιμότητας στα οιστρογόνα των επιθηλιακών κυττάρων των σιελογόνων αδένων. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/31783

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Τσιντή, Μαρία. “Μελέτη του ρόλου των φυλετικών ορμονών στην παθογένεια του συνδρόμου Sjogren: ανάλυση της έκφρασης οιστρογονικών υποδοχέων και της αποκρισιμότητας στα οιστρογόνα των επιθηλιακών κυττάρων των σιελογόνων αδένων.” 2012. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed April 10, 2021. http://hdl.handle.net/10442/hedi/31783.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Τσιντή, Μαρία. “Μελέτη του ρόλου των φυλετικών ορμονών στην παθογένεια του συνδρόμου Sjogren: ανάλυση της έκφρασης οιστρογονικών υποδοχέων και της αποκρισιμότητας στα οιστρογόνα των επιθηλιακών κυττάρων των σιελογόνων αδένων.” 2012. Web. 10 Apr 2021.

Vancouver:

Τσιντή �. Μελέτη του ρόλου των φυλετικών ορμονών στην παθογένεια του συνδρόμου Sjogren: ανάλυση της έκφρασης οιστρογονικών υποδοχέων και της αποκρισιμότητας στα οιστρογόνα των επιθηλιακών κυττάρων των σιελογόνων αδένων. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2012. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/10442/hedi/31783.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Τσιντή �. Μελέτη του ρόλου των φυλετικών ορμονών στην παθογένεια του συνδρόμου Sjogren: ανάλυση της έκφρασης οιστρογονικών υποδοχέων και της αποκρισιμότητας στα οιστρογόνα των επιθηλιακών κυττάρων των σιελογόνων αδένων. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2012. Available from: http://hdl.handle.net/10442/hedi/31783

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

27. Φώτης, Λάμπρος. Μελέτη των μορίων προσκόλησης ICAM-1 και VCAM-1 στην αορτή επίμυων στην εξελικτική πορεία της πειραματικής αθηροσκλήρωσης.

Degree: 2011, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/27928

►

Introduction: Members of the immunoglobulin superfamily of endothelial adhesion molecules, vascular cell adhesion molecule (VCAM-1) and intercellular cell adhesion molecule (ICAM-1), strongly participate in leukocyte… (more)

▼

Introduction: Members of the immunoglobulin superfamily of endothelial adhesion molecules, vascular cell adhesion molecule (VCAM-1) and intercellular cell adhesion molecule (ICAM-1), strongly participate in leukocyte adhesion to the endothelium and play an important role in all stages of atherosclerosis. The aim of the study was to examine the expression of VCAM-1 and ICAM-1 in the aorta of rats at the early stages of atherosclerosis and the correlation with their concentration in the serum Materials and Methods: Forty four male rats, ten weeks of age, were divided in 4 groups. Groups A and C (n =12) were fed with rich cholesterol diet (enriched with 2% cholesterol) for 12 and 16 weeks respectively. Group B (regression group, n =12) was fed for the first 12 weeks with rich cholesterol diet and for another 4 weeks with normal diet. Group D (control group, n =8) was fed with normal diet for 12 weeks. After the euthanasia, we received the aorta of the animals. We measured the lipid profile, the concentration of soluble ICAM-1 and the immunohistochemical expression of ICAM-1 and VCAM-1 in the endothelium, media and vasa vasorum of the aorta Results: There were significant differences (p<0,05) in the expression of ICAM-1 between group C (maximum time of rich cholesterol diet) and all other groups in the three subjects of the aorta studied. There was regression of the expression of ICAM-1 in group B and significant differences (p<0,05) between group B and all the other groups, except group D in the expression of ICAM-1. There were no significant differences in the expression of VCAM-1 between any of the groups. The serum concentration of soluble ICAM-1 positively correlates with the expression of the molecule in the vasa vasorum (r=0,35, p <0,05) and the fibroblasts/smooth muscular cells (r=0,34, p<0,05) of the aorta. Conclusions: Rich cholesterol diet has an important role in the expression of ICAM-1 but not in the expression of VCAM-1 in the aorta of the rat, which is time dependent. The expression of ICAM-1 in the aorta regresses after the recess of rich cholesterol diet. Soluble ICAM-1 is a reliable mean of measuring the expression of ICAM-1 in the the aorta and mainly in the vasa vasorum and fibroblasts/smooth muscle cells.

Εισαγωγή: Τα μόρια προσκόλλησης ICAM-1(Intracellular Adhesion Molecule-1) και VCAM-1 (Vascular Cell Adhesion Molecule-1) συμμετέχουν στην προσκόλληση των λευκοκυττάρων στο ενδοθήλιο και διαδραματίζουν σημαντικό ρόλο σε όλα τα στάδια της αθηροσκλήρωσης. Σκοπός της μελέτης είναι η διερεύνηση της έκφρασης των μορίων προσκόλλησης ICAM-1 και VCAM-1 στην αορτή επίμυων στα πρώιμα στάδια της πειραματικής αθηροσκλήρωσης και η συσχέτισή τους με τα επίπεδα των μορίων στον ορό. Υλικά και Μέθοδοι: Χρησιμοποιήθηκαν 44 αρσενικοί επίμυες ηλικίας 10 εβδομάδων, οι οποίοι χωρίστηκαν σε 4 ομάδες. Οι ομάδες Α και Γ (n=12) έλαβαν αθηρογόνο δίαιτα (εμπλουτισμός με 2% χοληστερόλη) για 12 και 16 εβδομάδες αντιστοίχως. Η ομάδα Β (υποστροφής, n=12) έλαβε τις πρώτες 12 εβδομάδες αθηρογόνο δίαιτα και άλλες 4 κανονική…

Subjects/Keywords: Αθηροσκλήρωση; Μόρια προσκόλησης; Επίμυες; Αγγειακό κυτταρικό μόριο προσκόλησης; Διακυττάριο κυτταρικό μόριο προσκόλησης; Αορτή; Υπερχοληστερολαιμία; Atherosclerosis; Adhesion molecules; Rats; Vascular cell adhesion molecule; Intercellular cell adhesion molecule; Aorta; Hypercholesterolemia

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Φώτης, . �. (2011). Μελέτη των μορίων προσκόλησης ICAM-1 και VCAM-1 στην αορτή επίμυων στην εξελικτική πορεία της πειραματικής αθηροσκλήρωσης. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/27928

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Φώτης, Λάμπρος. “Μελέτη των μορίων προσκόλησης ICAM-1 και VCAM-1 στην αορτή επίμυων στην εξελικτική πορεία της πειραματικής αθηροσκλήρωσης.” 2011. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed April 10, 2021. http://hdl.handle.net/10442/hedi/27928.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Φώτης, Λάμπρος. “Μελέτη των μορίων προσκόλησης ICAM-1 και VCAM-1 στην αορτή επίμυων στην εξελικτική πορεία της πειραματικής αθηροσκλήρωσης.” 2011. Web. 10 Apr 2021.

Vancouver:

Φώτης �. Μελέτη των μορίων προσκόλησης ICAM-1 και VCAM-1 στην αορτή επίμυων στην εξελικτική πορεία της πειραματικής αθηροσκλήρωσης. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2011. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/10442/hedi/27928.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Φώτης �. Μελέτη των μορίων προσκόλησης ICAM-1 και VCAM-1 στην αορτή επίμυων στην εξελικτική πορεία της πειραματικής αθηροσκλήρωσης. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2011. Available from: http://hdl.handle.net/10442/hedi/27928

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ)

28. Γιονανλής, Λάζαρος. Συμβολή στην παθογένεια της ιδιοπαθούς ταχέως εξελισσόμενης σπειραματονεφρίτιδας.

Degree: 2003, Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ)

URL: http://hdl.handle.net/10442/hedi/13982

Subjects/Keywords: Ιδιοπαθής ταχέως εξελισσόμενη σπειραματονεφρίτιδα; Αντισώματα κατά κυτταροπλάσματος ουδετεροφίλων; Παθογενετικοί μηχανισμοί; Θεραπείας απάντηση; Ιντεγκρίνες; Διακυτταρικό μόριο προσκόλλησης ICAM-1; Αυξητικός παράγοντας μεταμόρφωσης TGF-B1; Τελικό σύμπλεγμα συμπληρώματος C5b-9; Idiopathic rapidly progressive glomerulonephritis; Antineutrophil cytoplasmic antibodies; Pathogenetic mechanisms; Response to treatment; Intercellular adhesion molecule ICAM -1; Transforming growth factor TGF-b1; Terminal complement component C5b-9

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Γιονανλής, . �. (2003). Συμβολή στην παθογένεια της ιδιοπαθούς ταχέως εξελισσόμενης σπειραματονεφρίτιδας. (Thesis). Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ). Retrieved from http://hdl.handle.net/10442/hedi/13982

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Γιονανλής, Λάζαρος. “Συμβολή στην παθογένεια της ιδιοπαθούς ταχέως εξελισσόμενης σπειραματονεφρίτιδας.” 2003. Thesis, Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ). Accessed April 10, 2021. http://hdl.handle.net/10442/hedi/13982.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Γιονανλής, Λάζαρος. “Συμβολή στην παθογένεια της ιδιοπαθούς ταχέως εξελισσόμενης σπειραματονεφρίτιδας.” 2003. Web. 10 Apr 2021.

Vancouver:

Γιονανλής �. Συμβολή στην παθογένεια της ιδιοπαθούς ταχέως εξελισσόμενης σπειραματονεφρίτιδας. [Internet] [Thesis]. Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ); 2003. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/10442/hedi/13982.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Γιονανλής �. Συμβολή στην παθογένεια της ιδιοπαθούς ταχέως εξελισσόμενης σπειραματονεφρίτιδας. [Thesis]. Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ); 2003. Available from: http://hdl.handle.net/10442/hedi/13982

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Boston University

29. Woolf, Nicholas Taylor. IGPR-1 is a novel adhesion molecule involved in colorectal tumor growth.

Degree: 2015, Boston University

URL: http://hdl.handle.net/2144/16006

► Colorectal cancer (CRC) is among the most prevalent and lethal cancers in the United States. The mechanisms by which tumor cells sense their microenvironment have… (more)

Subjects/Keywords: Molecular biology; IGPR-1; Adhesion molecule; Cancer; Colorectal; Metastasis; Tumor

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Woolf, N. T. (2015). IGPR-1 is a novel adhesion molecule involved in colorectal tumor growth. (Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/16006

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Woolf, Nicholas Taylor. “IGPR-1 is a novel adhesion molecule involved in colorectal tumor growth.” 2015. Thesis, Boston University. Accessed April 10, 2021. http://hdl.handle.net/2144/16006.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Woolf, Nicholas Taylor. “IGPR-1 is a novel adhesion molecule involved in colorectal tumor growth.” 2015. Web. 10 Apr 2021.

Vancouver:

Woolf NT. IGPR-1 is a novel adhesion molecule involved in colorectal tumor growth. [Internet] [Thesis]. Boston University; 2015. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/2144/16006.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Woolf NT. IGPR-1 is a novel adhesion molecule involved in colorectal tumor growth. [Thesis]. Boston University; 2015. Available from: http://hdl.handle.net/2144/16006

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Toronto

30. Mehrabian, Mohadeseh. The Prion Protein Controls Polysialylation of Neural Cell Adhesion Molecule 1 during Cellular Morphogenesis.

Degree: PhD, 2017, University of Toronto

URL: http://hdl.handle.net/1807/80732

► The cellular prion protein (PrPC) is one of the most studied mammalian proteins. Despite the ongoing efforts and the ubiquitous expression of PrPC in vertebrate… (more)

▼ The cellular prion protein (PrPC) is one of the most studied mammalian proteins. Despite the ongoing efforts and the ubiquitous expression of PrPC in vertebrate cells, the main function of this protein has remained enigmatic to date. Several lines of evidence pointed towards the involvement of PrPC in the morphogenetic reprogramming underlying the epithelial-tomesenchymal transition (EMT). To address this, we applied CRISPR-Cas9 genome engineering technique to establish multiple PrPC knockout cell models (Chapter 2). The follow-up studies uncovered a critical role of PrPC in EMT and showed that PrPC controls the polysialic acid (polySia) modification of neural cell adhesion molecule 1 (NCAM1). Surprisingly, this effect of PrPC on NCAM1 polysialylation relies on a novel signaling loop that modulates expression of ST8SIA2, one of the two polysialyltransferase enzymes responsible for adding polySia on NCAM1 (Chapter 3). Intriguingly, a comparative analysis revealed that PrPC levels correlate directly or inversely with ST8SIA2 levels in different cell models. Deep global proteome analyses of multiple PrP-deficient models not only uncovered surprising cell model-specific proteome shifts but also showed robust changes in the levels of MARCKS and BASP protein families at the plasma membrane. Further investigation of their involvement in a biology that controls NCAM1 polysialylation revealed that reduced levels of MARCKSL1 also led to a significant reduction of polySia-modified NCAM1 (Chapter 4). Data from this study emphasize a iii thus far underappreciated coordinated biology of PrP and NCAM1. A close comparison of knockout phenotypes in mice is consistent with a model, whereby several of the known phenotypes in PrP-deficient mice might be explained by the contribution of PrPC to NCAM1 polysialylation. Attempts to validate this model and to assert its significance for determining if perturbed PrPC signaling contributes to toxicity in prion diseases are ongoing and have not been included in this thesis at this time. Advisors/Committee Members: Schmitt-Ulms, Gerold, Laboratory Medicine and Pathobiology.

Subjects/Keywords: Neural cell adhesion molecule 1; polysialylation; Prion protein; ST8siaII; ZIP6; 0317

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mehrabian, M. (2017). The Prion Protein Controls Polysialylation of Neural Cell Adhesion Molecule 1 during Cellular Morphogenesis. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/80732

Chicago Manual of Style (16^th Edition):

Mehrabian, Mohadeseh. “The Prion Protein Controls Polysialylation of Neural Cell Adhesion Molecule 1 during Cellular Morphogenesis.” 2017. Doctoral Dissertation, University of Toronto. Accessed April 10, 2021. http://hdl.handle.net/1807/80732.

MLA Handbook (7^th Edition):

Mehrabian, Mohadeseh. “The Prion Protein Controls Polysialylation of Neural Cell Adhesion Molecule 1 during Cellular Morphogenesis.” 2017. Web. 10 Apr 2021.

Vancouver:

Mehrabian M. The Prion Protein Controls Polysialylation of Neural Cell Adhesion Molecule 1 during Cellular Morphogenesis. [Internet] [Doctoral dissertation]. University of Toronto; 2017. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/1807/80732.

Council of Science Editors:

Mehrabian M. The Prion Protein Controls Polysialylation of Neural Cell Adhesion Molecule 1 during Cellular Morphogenesis. [Doctoral Dissertation]. University of Toronto; 2017. Available from: http://hdl.handle.net/1807/80732

Open Access Theses and Dissertations