Advanced search options

Advanced Search Options 🞨

Browse by author name (“Author name starts with…”).

Find ETDs with:

in
/  
in
/  
in
/  
in

Written in Published in Earliest date Latest date

Sorted by

Results per page:

Sorted by: relevance · author · university · dateNew search

You searched for subject:(inflammasome). Showing records 1 – 30 of 183 total matches.

[1] [2] [3] [4] [5] [6] [7]

Search Limiters

Last 2 Years | English Only

Degrees

Levels

Languages

Country

▼ Search Limiters

1. Riteau, Nicolas. Immunité innée et inflammasome : rôle des signaux de dangers endogènes : Innate immunity and inflammasome : role of endogenous danger signals.

Degree: Docteur es, Science du vivant. Immunologie, 2011, Université d'Orléans

La théorie du danger développée par Polly Matzinger stipule que l’attrait principal du système immunitaire ne réside pas dans la distinction entre le soi «… (more)

Subjects/Keywords: Inflammasome; Inflammasome

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Riteau, N. (2011). Immunité innée et inflammasome : rôle des signaux de dangers endogènes : Innate immunity and inflammasome : role of endogenous danger signals. (Doctoral Dissertation). Université d'Orléans. Retrieved from http://www.theses.fr/2011ORLE2038

Chicago Manual of Style (16th Edition):

Riteau, Nicolas. “Immunité innée et inflammasome : rôle des signaux de dangers endogènes : Innate immunity and inflammasome : role of endogenous danger signals.” 2011. Doctoral Dissertation, Université d'Orléans. Accessed October 20, 2019. http://www.theses.fr/2011ORLE2038.

MLA Handbook (7th Edition):

Riteau, Nicolas. “Immunité innée et inflammasome : rôle des signaux de dangers endogènes : Innate immunity and inflammasome : role of endogenous danger signals.” 2011. Web. 20 Oct 2019.

Vancouver:

Riteau N. Immunité innée et inflammasome : rôle des signaux de dangers endogènes : Innate immunity and inflammasome : role of endogenous danger signals. [Internet] [Doctoral dissertation]. Université d'Orléans; 2011. [cited 2019 Oct 20]. Available from: http://www.theses.fr/2011ORLE2038.

Council of Science Editors:

Riteau N. Immunité innée et inflammasome : rôle des signaux de dangers endogènes : Innate immunity and inflammasome : role of endogenous danger signals. [Doctoral Dissertation]. Université d'Orléans; 2011. Available from: http://www.theses.fr/2011ORLE2038


University of Oxford

2. Nordlander, Sofia. Innate sensing of bacterial flagellin in acute and chronic intestinal inflammation.

Degree: PhD, 2013, University of Oxford

 Flagellin is a highly immunogenic, bacterial protein considered to be abundant in the intestinal lumen. It has been reported to be an immunodominant antigen in… (more)

Subjects/Keywords: 616.07; Immunology; Mucosal immunology; inflammasome

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Nordlander, S. (2013). Innate sensing of bacterial flagellin in acute and chronic intestinal inflammation. (Doctoral Dissertation). University of Oxford. Retrieved from http://ora.ox.ac.uk/objects/uuid:775c4150-9b22-4008-9288-3a6053cbf4cc ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.647535

Chicago Manual of Style (16th Edition):

Nordlander, Sofia. “Innate sensing of bacterial flagellin in acute and chronic intestinal inflammation.” 2013. Doctoral Dissertation, University of Oxford. Accessed October 20, 2019. http://ora.ox.ac.uk/objects/uuid:775c4150-9b22-4008-9288-3a6053cbf4cc ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.647535.

MLA Handbook (7th Edition):

Nordlander, Sofia. “Innate sensing of bacterial flagellin in acute and chronic intestinal inflammation.” 2013. Web. 20 Oct 2019.

Vancouver:

Nordlander S. Innate sensing of bacterial flagellin in acute and chronic intestinal inflammation. [Internet] [Doctoral dissertation]. University of Oxford; 2013. [cited 2019 Oct 20]. Available from: http://ora.ox.ac.uk/objects/uuid:775c4150-9b22-4008-9288-3a6053cbf4cc ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.647535.

Council of Science Editors:

Nordlander S. Innate sensing of bacterial flagellin in acute and chronic intestinal inflammation. [Doctoral Dissertation]. University of Oxford; 2013. Available from: http://ora.ox.ac.uk/objects/uuid:775c4150-9b22-4008-9288-3a6053cbf4cc ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.647535


University of Texas Medical Branch – Galveston

3. [No author]. The Activation of the Inflammasome during Rickettsial Infection .

Degree: University of Texas Medical Branch – Galveston

 Rickettsiae are Gram-negative, obligately intracellular bacteria that infect endothelial cells and macrophages. The molecular mechanisms involved in interaction of rickettsiae with macrophages, however, remain poorly… (more)

Subjects/Keywords: Rickettsia; Inflammasome

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

author], [. (n.d.). The Activation of the Inflammasome during Rickettsial Infection . (Thesis). University of Texas Medical Branch – Galveston. Retrieved from http://hdl.handle.net/2152.3/11179

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

author], [No. “The Activation of the Inflammasome during Rickettsial Infection .” Thesis, University of Texas Medical Branch – Galveston. Accessed October 20, 2019. http://hdl.handle.net/2152.3/11179.

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

author], [No. “The Activation of the Inflammasome during Rickettsial Infection .” Web. 20 Oct 2019.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

author] [. The Activation of the Inflammasome during Rickettsial Infection . [Internet] [Thesis]. University of Texas Medical Branch – Galveston; [cited 2019 Oct 20]. Available from: http://hdl.handle.net/2152.3/11179.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Council of Science Editors:

author] [. The Activation of the Inflammasome during Rickettsial Infection . [Thesis]. University of Texas Medical Branch – Galveston; Available from: http://hdl.handle.net/2152.3/11179

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

4. Molyvdas, Adam. Το NLRP3 φλεγμονόσωμα στην χρόνια ιογενή ηπατική φλεγμονή.

Degree: 2017, University of Thessaly (UTH); Πανεπιστήμιο Θεσσαλίας

Background: Chronic viral hepatitis is a prevalent disease with major health implications. The mechanisms that are involved in the pathophysiology of chronic viral hepatitis are… (more)

Subjects/Keywords: Φλεγμονόσωμα; Ηπατίτιτδα; inflammasome; Hepatitis

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Molyvdas, A. (2017). Το NLRP3 φλεγμονόσωμα στην χρόνια ιογενή ηπατική φλεγμονή. (Thesis). University of Thessaly (UTH); Πανεπιστήμιο Θεσσαλίας. Retrieved from http://hdl.handle.net/10442/hedi/41928

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

Chicago Manual of Style (16th Edition):

Molyvdas, Adam. “Το NLRP3 φλεγμονόσωμα στην χρόνια ιογενή ηπατική φλεγμονή.” 2017. Thesis, University of Thessaly (UTH); Πανεπιστήμιο Θεσσαλίας. Accessed October 20, 2019. http://hdl.handle.net/10442/hedi/41928.

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

MLA Handbook (7th Edition):

Molyvdas, Adam. “Το NLRP3 φλεγμονόσωμα στην χρόνια ιογενή ηπατική φλεγμονή.” 2017. Web. 20 Oct 2019.

Vancouver:

Molyvdas A. Το NLRP3 φλεγμονόσωμα στην χρόνια ιογενή ηπατική φλεγμονή. [Internet] [Thesis]. University of Thessaly (UTH); Πανεπιστήμιο Θεσσαλίας; 2017. [cited 2019 Oct 20]. Available from: http://hdl.handle.net/10442/hedi/41928.

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

Council of Science Editors:

Molyvdas A. Το NLRP3 φλεγμονόσωμα στην χρόνια ιογενή ηπατική φλεγμονή. [Thesis]. University of Thessaly (UTH); Πανεπιστήμιο Θεσσαλίας; 2017. Available from: http://hdl.handle.net/10442/hedi/41928

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


University of Newcastle

5. Williams, Evan James. Strategies for reducing systemic inflammation in obesity.

Degree: PhD, 2019, University of Newcastle

Research Doctorate - Doctor of Philosophy (PhD)

The prevalence of overweight and obese individuals in Australia is currently 63% of adults according to current data… (more)

Subjects/Keywords: obesity; systemic inflammation; inflammasome; macrophages

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Williams, E. J. (2019). Strategies for reducing systemic inflammation in obesity. (Doctoral Dissertation). University of Newcastle. Retrieved from http://hdl.handle.net/1959.13/1401110

Chicago Manual of Style (16th Edition):

Williams, Evan James. “Strategies for reducing systemic inflammation in obesity.” 2019. Doctoral Dissertation, University of Newcastle. Accessed October 20, 2019. http://hdl.handle.net/1959.13/1401110.

MLA Handbook (7th Edition):

Williams, Evan James. “Strategies for reducing systemic inflammation in obesity.” 2019. Web. 20 Oct 2019.

Vancouver:

Williams EJ. Strategies for reducing systemic inflammation in obesity. [Internet] [Doctoral dissertation]. University of Newcastle; 2019. [cited 2019 Oct 20]. Available from: http://hdl.handle.net/1959.13/1401110.

Council of Science Editors:

Williams EJ. Strategies for reducing systemic inflammation in obesity. [Doctoral Dissertation]. University of Newcastle; 2019. Available from: http://hdl.handle.net/1959.13/1401110

6. Paoletti, Audrey. Étude des étapes précoces de l’infection par le VIH-1 : identification d’un nouveau point de contrôle immunitaire immunitaire impliquant le récepteur P2Y2 et la protéine NLRP3 : Study Of The Early Steps Of HIV-1 Infection : Identification Of A New Immune Checkpoint Involving P2Y2 And NLRP3.

Degree: Docteur es, Aspects moléculaires et cellulaires de la biologie, 2015, Paris Saclay

Plus de 34 millions de personnes dans le monde vivent avec le virus de l’immunodéficience humaine de type 1 (VIH-1). Cette pandémie est partiellement contrôlée… (more)

Subjects/Keywords: Vih-1; Récepteur purinergique; Inflammasome; Hiv-1; Purinergic receptor; Inflammasome

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Paoletti, A. (2015). Étude des étapes précoces de l’infection par le VIH-1 : identification d’un nouveau point de contrôle immunitaire immunitaire impliquant le récepteur P2Y2 et la protéine NLRP3 : Study Of The Early Steps Of HIV-1 Infection : Identification Of A New Immune Checkpoint Involving P2Y2 And NLRP3. (Doctoral Dissertation). Paris Saclay. Retrieved from http://www.theses.fr/2015SACLS240

Chicago Manual of Style (16th Edition):

Paoletti, Audrey. “Étude des étapes précoces de l’infection par le VIH-1 : identification d’un nouveau point de contrôle immunitaire immunitaire impliquant le récepteur P2Y2 et la protéine NLRP3 : Study Of The Early Steps Of HIV-1 Infection : Identification Of A New Immune Checkpoint Involving P2Y2 And NLRP3.” 2015. Doctoral Dissertation, Paris Saclay. Accessed October 20, 2019. http://www.theses.fr/2015SACLS240.

MLA Handbook (7th Edition):

Paoletti, Audrey. “Étude des étapes précoces de l’infection par le VIH-1 : identification d’un nouveau point de contrôle immunitaire immunitaire impliquant le récepteur P2Y2 et la protéine NLRP3 : Study Of The Early Steps Of HIV-1 Infection : Identification Of A New Immune Checkpoint Involving P2Y2 And NLRP3.” 2015. Web. 20 Oct 2019.

Vancouver:

Paoletti A. Étude des étapes précoces de l’infection par le VIH-1 : identification d’un nouveau point de contrôle immunitaire immunitaire impliquant le récepteur P2Y2 et la protéine NLRP3 : Study Of The Early Steps Of HIV-1 Infection : Identification Of A New Immune Checkpoint Involving P2Y2 And NLRP3. [Internet] [Doctoral dissertation]. Paris Saclay; 2015. [cited 2019 Oct 20]. Available from: http://www.theses.fr/2015SACLS240.

Council of Science Editors:

Paoletti A. Étude des étapes précoces de l’infection par le VIH-1 : identification d’un nouveau point de contrôle immunitaire immunitaire impliquant le récepteur P2Y2 et la protéine NLRP3 : Study Of The Early Steps Of HIV-1 Infection : Identification Of A New Immune Checkpoint Involving P2Y2 And NLRP3. [Doctoral Dissertation]. Paris Saclay; 2015. Available from: http://www.theses.fr/2015SACLS240


Georgia State University

7. Chesnokov, Anton P, Mr. Modulation of NALP3 Inflammasome Genes by Estrogen.

Degree: MS, Biology, 2011, Georgia State University

  Immunity is known to be sexually dimorphic. This dimorphism may be attributed to the action of different hormones. Aluminum is a component of several… (more)

Subjects/Keywords: Nalp3 inflammasome; Estrogen; IL-1beta; Aluminum hydroxide

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Chesnokov, Anton P, M. (2011). Modulation of NALP3 Inflammasome Genes by Estrogen. (Thesis). Georgia State University. Retrieved from https://scholarworks.gsu.edu/biology_theses/33

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

Chicago Manual of Style (16th Edition):

Chesnokov, Anton P, Mr. “Modulation of NALP3 Inflammasome Genes by Estrogen.” 2011. Thesis, Georgia State University. Accessed October 20, 2019. https://scholarworks.gsu.edu/biology_theses/33.

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

MLA Handbook (7th Edition):

Chesnokov, Anton P, Mr. “Modulation of NALP3 Inflammasome Genes by Estrogen.” 2011. Web. 20 Oct 2019.

Vancouver:

Chesnokov, Anton P M. Modulation of NALP3 Inflammasome Genes by Estrogen. [Internet] [Thesis]. Georgia State University; 2011. [cited 2019 Oct 20]. Available from: https://scholarworks.gsu.edu/biology_theses/33.

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

Council of Science Editors:

Chesnokov, Anton P M. Modulation of NALP3 Inflammasome Genes by Estrogen. [Thesis]. Georgia State University; 2011. Available from: https://scholarworks.gsu.edu/biology_theses/33

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


University of Oxford

8. Srinivasan, N. The role of inflammasomes in intestinal inflammation.

Degree: PhD, 2014, University of Oxford

 Single Nucleotide Polymorphisms (SNPs) in the intracellular pattern recognition receptor gene NLRP3 are associated with susceptibility to Crohn’s disease, a form of inflammatory bowel disease… (more)

Subjects/Keywords: 616.3; Immunology; Inflammasome; intestinal inflammation; mucosal immunity

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Srinivasan, N. (2014). The role of inflammasomes in intestinal inflammation. (Doctoral Dissertation). University of Oxford. Retrieved from http://ora.ox.ac.uk/objects/uuid:04ad577c-a8dd-46eb-811a-79a3980ff806 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596000

Chicago Manual of Style (16th Edition):

Srinivasan, N. “The role of inflammasomes in intestinal inflammation.” 2014. Doctoral Dissertation, University of Oxford. Accessed October 20, 2019. http://ora.ox.ac.uk/objects/uuid:04ad577c-a8dd-46eb-811a-79a3980ff806 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596000.

MLA Handbook (7th Edition):

Srinivasan, N. “The role of inflammasomes in intestinal inflammation.” 2014. Web. 20 Oct 2019.

Vancouver:

Srinivasan N. The role of inflammasomes in intestinal inflammation. [Internet] [Doctoral dissertation]. University of Oxford; 2014. [cited 2019 Oct 20]. Available from: http://ora.ox.ac.uk/objects/uuid:04ad577c-a8dd-46eb-811a-79a3980ff806 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596000.

Council of Science Editors:

Srinivasan N. The role of inflammasomes in intestinal inflammation. [Doctoral Dissertation]. University of Oxford; 2014. Available from: http://ora.ox.ac.uk/objects/uuid:04ad577c-a8dd-46eb-811a-79a3980ff806 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596000


University of Manchester

9. Edye, Michelle. Interleukin-1 signalling in disease.

Degree: 2015, University of Manchester

 The pro-inflammatory cytokine interleukin 1 (IL-1) is involved in numerous physiological and pathological processes. It contributes to thermoregulation, sleep, feeding behaviour and notably to the… (more)

Subjects/Keywords: Interleukin-1; Inflammation; Acidosis; Inflammasome; Seizure

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Edye, M. (2015). Interleukin-1 signalling in disease. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:293336

Chicago Manual of Style (16th Edition):

Edye, Michelle. “Interleukin-1 signalling in disease.” 2015. Doctoral Dissertation, University of Manchester. Accessed October 20, 2019. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:293336.

MLA Handbook (7th Edition):

Edye, Michelle. “Interleukin-1 signalling in disease.” 2015. Web. 20 Oct 2019.

Vancouver:

Edye M. Interleukin-1 signalling in disease. [Internet] [Doctoral dissertation]. University of Manchester; 2015. [cited 2019 Oct 20]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:293336.

Council of Science Editors:

Edye M. Interleukin-1 signalling in disease. [Doctoral Dissertation]. University of Manchester; 2015. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:293336

10. 김, 은형. Expression and function of the NLRP3 inflammasome in Behçet’s disease.

Degree: 2016, Ajou University

연구배경: 베체트병운 점막 및피부, 눈, 혈관, 신경 및 기타 여러 장기를 침범할 수 있는 임상적 특징을 가지는 만성, 재발성의 전신질환이다. 현재까지 베체트병에서 보이는 지속적인 염증… (more)

Subjects/Keywords: Behçet’s disease; inflammasome; NLRP3; interleukin-1β

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

김, . (2016). Expression and function of the NLRP3 inflammasome in Behçet’s disease. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/13061 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000021737

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

Chicago Manual of Style (16th Edition):

김, 은형. “Expression and function of the NLRP3 inflammasome in Behçet’s disease.” 2016. Thesis, Ajou University. Accessed October 20, 2019. http://repository.ajou.ac.kr/handle/201003/13061 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000021737.

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

MLA Handbook (7th Edition):

김, 은형. “Expression and function of the NLRP3 inflammasome in Behçet’s disease.” 2016. Web. 20 Oct 2019.

Vancouver:

김 . Expression and function of the NLRP3 inflammasome in Behçet’s disease. [Internet] [Thesis]. Ajou University; 2016. [cited 2019 Oct 20]. Available from: http://repository.ajou.ac.kr/handle/201003/13061 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000021737.

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

Council of Science Editors:

김 . Expression and function of the NLRP3 inflammasome in Behçet’s disease. [Thesis]. Ajou University; 2016. Available from: http://repository.ajou.ac.kr/handle/201003/13061 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000021737

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


McMaster University

11. Li, Yujin. Investigating the Role of the NLRP3 Inflammasome in Statin-Induced Myopathy.

Degree: MSc, 2016, McMaster University

As a front-line treatment for cardiovascular disease, statins are among some of the most widely prescribed drugs worldwide. Statins are effective at lowering cholesterol, but… (more)

Subjects/Keywords: Inflammasome; Statins; Myopathy; Prenylation; Caspase-1; Atrogenes

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Li, Y. (2016). Investigating the Role of the NLRP3 Inflammasome in Statin-Induced Myopathy. (Masters Thesis). McMaster University. Retrieved from http://hdl.handle.net/11375/20268

Chicago Manual of Style (16th Edition):

Li, Yujin. “Investigating the Role of the NLRP3 Inflammasome in Statin-Induced Myopathy.” 2016. Masters Thesis, McMaster University. Accessed October 20, 2019. http://hdl.handle.net/11375/20268.

MLA Handbook (7th Edition):

Li, Yujin. “Investigating the Role of the NLRP3 Inflammasome in Statin-Induced Myopathy.” 2016. Web. 20 Oct 2019.

Vancouver:

Li Y. Investigating the Role of the NLRP3 Inflammasome in Statin-Induced Myopathy. [Internet] [Masters thesis]. McMaster University; 2016. [cited 2019 Oct 20]. Available from: http://hdl.handle.net/11375/20268.

Council of Science Editors:

Li Y. Investigating the Role of the NLRP3 Inflammasome in Statin-Induced Myopathy. [Masters Thesis]. McMaster University; 2016. Available from: http://hdl.handle.net/11375/20268


Universitat de Valencia

12. Alegre Guerra, Fernando. Acute inflammatory and fibrogenic responses induced in liver cells by efavirenz .

Degree: 2017, Universitat de Valencia

 RESUMEN INTRODUCCIÓN Diversos agentes hepatotóxicos y enfermedades hepáticas pueden conducir al desarrollo de fibrosis hepática debido a la presencia de respuestas inflamatorias desreguladas (Kubes and… (more)

Subjects/Keywords: liver; hiv; efavirenz; inflammation; inflammasome; fibrogenesis

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Alegre Guerra, F. (2017). Acute inflammatory and fibrogenic responses induced in liver cells by efavirenz . (Doctoral Dissertation). Universitat de Valencia. Retrieved from http://hdl.handle.net/10550/58371

Chicago Manual of Style (16th Edition):

Alegre Guerra, Fernando. “Acute inflammatory and fibrogenic responses induced in liver cells by efavirenz .” 2017. Doctoral Dissertation, Universitat de Valencia. Accessed October 20, 2019. http://hdl.handle.net/10550/58371.

MLA Handbook (7th Edition):

Alegre Guerra, Fernando. “Acute inflammatory and fibrogenic responses induced in liver cells by efavirenz .” 2017. Web. 20 Oct 2019.

Vancouver:

Alegre Guerra F. Acute inflammatory and fibrogenic responses induced in liver cells by efavirenz . [Internet] [Doctoral dissertation]. Universitat de Valencia; 2017. [cited 2019 Oct 20]. Available from: http://hdl.handle.net/10550/58371.

Council of Science Editors:

Alegre Guerra F. Acute inflammatory and fibrogenic responses induced in liver cells by efavirenz . [Doctoral Dissertation]. Universitat de Valencia; 2017. Available from: http://hdl.handle.net/10550/58371

13. Bergin, Ronan. Analysis of the role of Pellino2 in the Activation of the NLRP3 Inflammasome.

Degree: 2015, RIAN

 The innate immune system is the first line of defence against invading pathogens and is responsible for both initial pathogen recognition and mounting an effective… (more)

Subjects/Keywords: Analysis; role; Pellino2; Activation; NLRP3 Inflammasome

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Bergin, R. (2015). Analysis of the role of Pellino2 in the Activation of the NLRP3 Inflammasome. (Thesis). RIAN. Retrieved from http://eprints.maynoothuniversity.ie/10393/

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

Chicago Manual of Style (16th Edition):

Bergin, Ronan. “Analysis of the role of Pellino2 in the Activation of the NLRP3 Inflammasome.” 2015. Thesis, RIAN. Accessed October 20, 2019. http://eprints.maynoothuniversity.ie/10393/.

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

MLA Handbook (7th Edition):

Bergin, Ronan. “Analysis of the role of Pellino2 in the Activation of the NLRP3 Inflammasome.” 2015. Web. 20 Oct 2019.

Vancouver:

Bergin R. Analysis of the role of Pellino2 in the Activation of the NLRP3 Inflammasome. [Internet] [Thesis]. RIAN; 2015. [cited 2019 Oct 20]. Available from: http://eprints.maynoothuniversity.ie/10393/.

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

Council of Science Editors:

Bergin R. Analysis of the role of Pellino2 in the Activation of the NLRP3 Inflammasome. [Thesis]. RIAN; 2015. Available from: http://eprints.maynoothuniversity.ie/10393/

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


UCLA

14. Maloy, Jeffrey Phillip. Characterization of an Intracellular Flagellar System in Pathogenic Burkholderia Species.

Degree: Microbiology, Immunology, & Molecular Genetics, 2017, UCLA

 Burkholderia pseudomallei and Burkholderia thailandensis are related facultative intracellular pathogens that infect a variety of cell types, escape into the cytoplasm of host cells, and… (more)

Subjects/Keywords: Microbiology; Immunology; Burkholderia; Flagella; Inflammasome; Melioidosis; NLRC4

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Maloy, J. P. (2017). Characterization of an Intracellular Flagellar System in Pathogenic Burkholderia Species. (Thesis). UCLA. Retrieved from http://www.escholarship.org/uc/item/11m9037f

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

Chicago Manual of Style (16th Edition):

Maloy, Jeffrey Phillip. “Characterization of an Intracellular Flagellar System in Pathogenic Burkholderia Species.” 2017. Thesis, UCLA. Accessed October 20, 2019. http://www.escholarship.org/uc/item/11m9037f.

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

MLA Handbook (7th Edition):

Maloy, Jeffrey Phillip. “Characterization of an Intracellular Flagellar System in Pathogenic Burkholderia Species.” 2017. Web. 20 Oct 2019.

Vancouver:

Maloy JP. Characterization of an Intracellular Flagellar System in Pathogenic Burkholderia Species. [Internet] [Thesis]. UCLA; 2017. [cited 2019 Oct 20]. Available from: http://www.escholarship.org/uc/item/11m9037f.

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

Council of Science Editors:

Maloy JP. Characterization of an Intracellular Flagellar System in Pathogenic Burkholderia Species. [Thesis]. UCLA; 2017. Available from: http://www.escholarship.org/uc/item/11m9037f

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


University of Vermont

15. Hoyt, Laura Rose. Inhibitory Effects of Ethanol on the NLRP3 Inflammasome.

Degree: Medicine, 2015, University of Vermont

  Immunosuppression is a major complication of alcoholism and contributes to increased rates of opportunistic infections and sepsis associated with the addiction. The NLRP3 inflammasome(more)

Subjects/Keywords: Ethanol; Alcohol; NLRP3; Inflammasome; Inflammation; Immunosuppression

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Hoyt, L. R. (2015). Inhibitory Effects of Ethanol on the NLRP3 Inflammasome. (Thesis). University of Vermont. Retrieved from https://scholarworks.uvm.edu/hcoltheses/194

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

Chicago Manual of Style (16th Edition):

Hoyt, Laura Rose. “Inhibitory Effects of Ethanol on the NLRP3 Inflammasome.” 2015. Thesis, University of Vermont. Accessed October 20, 2019. https://scholarworks.uvm.edu/hcoltheses/194.

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

MLA Handbook (7th Edition):

Hoyt, Laura Rose. “Inhibitory Effects of Ethanol on the NLRP3 Inflammasome.” 2015. Web. 20 Oct 2019.

Vancouver:

Hoyt LR. Inhibitory Effects of Ethanol on the NLRP3 Inflammasome. [Internet] [Thesis]. University of Vermont; 2015. [cited 2019 Oct 20]. Available from: https://scholarworks.uvm.edu/hcoltheses/194.

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

Council of Science Editors:

Hoyt LR. Inhibitory Effects of Ethanol on the NLRP3 Inflammasome. [Thesis]. University of Vermont; 2015. Available from: https://scholarworks.uvm.edu/hcoltheses/194

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


University of Iowa

16. Clay, Gwendolyn Mary. The role of NLR proteins in Leishmaniasis.

Degree: PhD, Molecular and Cell Biology, 2016, University of Iowa

  Leishmania species are vector-borne protozoan parasites that cause a spectrum of human diseases, with an estimated 12 million people infected in 88 countries. Inflammation… (more)

Subjects/Keywords: Inflammasome; Leishmania; Leishmaniasis; NLR; Cell Biology

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Clay, G. M. (2016). The role of NLR proteins in Leishmaniasis. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/5442

Chicago Manual of Style (16th Edition):

Clay, Gwendolyn Mary. “The role of NLR proteins in Leishmaniasis.” 2016. Doctoral Dissertation, University of Iowa. Accessed October 20, 2019. https://ir.uiowa.edu/etd/5442.

MLA Handbook (7th Edition):

Clay, Gwendolyn Mary. “The role of NLR proteins in Leishmaniasis.” 2016. Web. 20 Oct 2019.

Vancouver:

Clay GM. The role of NLR proteins in Leishmaniasis. [Internet] [Doctoral dissertation]. University of Iowa; 2016. [cited 2019 Oct 20]. Available from: https://ir.uiowa.edu/etd/5442.

Council of Science Editors:

Clay GM. The role of NLR proteins in Leishmaniasis. [Doctoral Dissertation]. University of Iowa; 2016. Available from: https://ir.uiowa.edu/etd/5442


Queens University

17. Wynick, Christopher. IL-27 Enhances LPS-Induced Proinflammatory Responses in Human Monocytes: Augmented Inflammasome Activity and IL-23 Expression .

Degree: Microbiology and Immunology, 2014, Queens University

 Inflammation plays an important role in responding to injury and combating infections. In this thesis, I examine how inflammation is regulated by cytokines responsible for… (more)

Subjects/Keywords: Inflammation; IL-27; Monocytes; Inflammasome; IL-23

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Wynick, C. (2014). IL-27 Enhances LPS-Induced Proinflammatory Responses in Human Monocytes: Augmented Inflammasome Activity and IL-23 Expression . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/12256

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

Chicago Manual of Style (16th Edition):

Wynick, Christopher. “IL-27 Enhances LPS-Induced Proinflammatory Responses in Human Monocytes: Augmented Inflammasome Activity and IL-23 Expression .” 2014. Thesis, Queens University. Accessed October 20, 2019. http://hdl.handle.net/1974/12256.

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

MLA Handbook (7th Edition):

Wynick, Christopher. “IL-27 Enhances LPS-Induced Proinflammatory Responses in Human Monocytes: Augmented Inflammasome Activity and IL-23 Expression .” 2014. Web. 20 Oct 2019.

Vancouver:

Wynick C. IL-27 Enhances LPS-Induced Proinflammatory Responses in Human Monocytes: Augmented Inflammasome Activity and IL-23 Expression . [Internet] [Thesis]. Queens University; 2014. [cited 2019 Oct 20]. Available from: http://hdl.handle.net/1974/12256.

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

Council of Science Editors:

Wynick C. IL-27 Enhances LPS-Induced Proinflammatory Responses in Human Monocytes: Augmented Inflammasome Activity and IL-23 Expression . [Thesis]. Queens University; 2014. Available from: http://hdl.handle.net/1974/12256

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


University of Tasmania

18. Ranson, NM. Inflammasome activity in the inflammatory bowel diseases.

Degree: 2018, University of Tasmania

 Ulcerative colitis (UC) and Crohn’s disease (CD) are characterised by chronic and recurrent inflammation of the gastrointestinal tract. The development of Inflammatory Bowel Diseases (IBD)… (more)

Subjects/Keywords: inflammation; inflammasome complexes; ulcerative colitis; Crohn's disease

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Ranson, N. (2018). Inflammasome activity in the inflammatory bowel diseases. (Thesis). University of Tasmania. Retrieved from https://eprints.utas.edu.au/29986/1/Ranson_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 (16th Edition):

Ranson, NM. “Inflammasome activity in the inflammatory bowel diseases.” 2018. Thesis, University of Tasmania. Accessed October 20, 2019. https://eprints.utas.edu.au/29986/1/Ranson_whole_thesis.pdf.

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

MLA Handbook (7th Edition):

Ranson, NM. “Inflammasome activity in the inflammatory bowel diseases.” 2018. Web. 20 Oct 2019.

Vancouver:

Ranson N. Inflammasome activity in the inflammatory bowel diseases. [Internet] [Thesis]. University of Tasmania; 2018. [cited 2019 Oct 20]. Available from: https://eprints.utas.edu.au/29986/1/Ranson_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:

Ranson N. Inflammasome activity in the inflammatory bowel diseases. [Thesis]. University of Tasmania; 2018. Available from: https://eprints.utas.edu.au/29986/1/Ranson_whole_thesis.pdf

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

19. Benaoudia, Sacha. Détection du LPS cytosolique : un crible CRISPR/Cas9 pangénomique identifie IRF2 comme régulateur de l’inflammasome non-canonique caspase-4 : Detection of cytosolic LPS : a genome-wide CRISPR/Cas9 screen identifies IRF2 as a regulator of the non-canonical inflammasome caspase-4.

Degree: Docteur es, Science de la vie, 2018, Lyon

Le lipopolysaccharide (LPS), un composant de la membrane des bactéries à Gram-négatif, active l’inflammasome non-canonique constitué chez l’homme des caspase-4/5 et chez la souris de… (more)

Subjects/Keywords: Caspase; Inflammasome; Mort cellulaire; LPS; Immunité innée; Caspase; Inflammasome; Cell death; LPS; Innate immunity; 570

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Benaoudia, S. (2018). Détection du LPS cytosolique : un crible CRISPR/Cas9 pangénomique identifie IRF2 comme régulateur de l’inflammasome non-canonique caspase-4 : Detection of cytosolic LPS : a genome-wide CRISPR/Cas9 screen identifies IRF2 as a regulator of the non-canonical inflammasome caspase-4. (Doctoral Dissertation). Lyon. Retrieved from http://www.theses.fr/2018LYSE1219

Chicago Manual of Style (16th Edition):

Benaoudia, Sacha. “Détection du LPS cytosolique : un crible CRISPR/Cas9 pangénomique identifie IRF2 comme régulateur de l’inflammasome non-canonique caspase-4 : Detection of cytosolic LPS : a genome-wide CRISPR/Cas9 screen identifies IRF2 as a regulator of the non-canonical inflammasome caspase-4.” 2018. Doctoral Dissertation, Lyon. Accessed October 20, 2019. http://www.theses.fr/2018LYSE1219.

MLA Handbook (7th Edition):

Benaoudia, Sacha. “Détection du LPS cytosolique : un crible CRISPR/Cas9 pangénomique identifie IRF2 comme régulateur de l’inflammasome non-canonique caspase-4 : Detection of cytosolic LPS : a genome-wide CRISPR/Cas9 screen identifies IRF2 as a regulator of the non-canonical inflammasome caspase-4.” 2018. Web. 20 Oct 2019.

Vancouver:

Benaoudia S. Détection du LPS cytosolique : un crible CRISPR/Cas9 pangénomique identifie IRF2 comme régulateur de l’inflammasome non-canonique caspase-4 : Detection of cytosolic LPS : a genome-wide CRISPR/Cas9 screen identifies IRF2 as a regulator of the non-canonical inflammasome caspase-4. [Internet] [Doctoral dissertation]. Lyon; 2018. [cited 2019 Oct 20]. Available from: http://www.theses.fr/2018LYSE1219.

Council of Science Editors:

Benaoudia S. Détection du LPS cytosolique : un crible CRISPR/Cas9 pangénomique identifie IRF2 comme régulateur de l’inflammasome non-canonique caspase-4 : Detection of cytosolic LPS : a genome-wide CRISPR/Cas9 screen identifies IRF2 as a regulator of the non-canonical inflammasome caspase-4. [Doctoral Dissertation]. Lyon; 2018. Available from: http://www.theses.fr/2018LYSE1219

20. Baron, Ludivine. Mécanismes d’activation de l’inflammasome NLRP3 par les micro- et les nano- particules dans un modèle d’inflammation pulmonaire chez la souris : Mechanisms of activation of the NLRP3 inflammasome by micro- and nano- particles in a murine model of lung inflammation.

Degree: Docteur es, Sciences du vivant. Immunologie, 2013, Université d'Orléans

Les mécanismes de défense de l’organisme contre des pathogènes ou des particules toxiques sont regroupés sous le terme d’Immunité. L’Immunité a développé plusieurs familles de… (more)

Subjects/Keywords: Adénosine; ATP; Inflammasome; Interleukines (IL); Cristaux; Nanoparticules; Adenosine; ATP; Inflammasome; Interleukines (IL); Crystals; Nanoparticles

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Baron, L. (2013). Mécanismes d’activation de l’inflammasome NLRP3 par les micro- et les nano- particules dans un modèle d’inflammation pulmonaire chez la souris : Mechanisms of activation of the NLRP3 inflammasome by micro- and nano- particles in a murine model of lung inflammation. (Doctoral Dissertation). Université d'Orléans. Retrieved from http://www.theses.fr/2013ORLE2037

Chicago Manual of Style (16th Edition):

Baron, Ludivine. “Mécanismes d’activation de l’inflammasome NLRP3 par les micro- et les nano- particules dans un modèle d’inflammation pulmonaire chez la souris : Mechanisms of activation of the NLRP3 inflammasome by micro- and nano- particles in a murine model of lung inflammation.” 2013. Doctoral Dissertation, Université d'Orléans. Accessed October 20, 2019. http://www.theses.fr/2013ORLE2037.

MLA Handbook (7th Edition):

Baron, Ludivine. “Mécanismes d’activation de l’inflammasome NLRP3 par les micro- et les nano- particules dans un modèle d’inflammation pulmonaire chez la souris : Mechanisms of activation of the NLRP3 inflammasome by micro- and nano- particles in a murine model of lung inflammation.” 2013. Web. 20 Oct 2019.

Vancouver:

Baron L. Mécanismes d’activation de l’inflammasome NLRP3 par les micro- et les nano- particules dans un modèle d’inflammation pulmonaire chez la souris : Mechanisms of activation of the NLRP3 inflammasome by micro- and nano- particles in a murine model of lung inflammation. [Internet] [Doctoral dissertation]. Université d'Orléans; 2013. [cited 2019 Oct 20]. Available from: http://www.theses.fr/2013ORLE2037.

Council of Science Editors:

Baron L. Mécanismes d’activation de l’inflammasome NLRP3 par les micro- et les nano- particules dans un modèle d’inflammation pulmonaire chez la souris : Mechanisms of activation of the NLRP3 inflammasome by micro- and nano- particles in a murine model of lung inflammation. [Doctoral Dissertation]. Université d'Orléans; 2013. Available from: http://www.theses.fr/2013ORLE2037

21. Awad, Fawaz. Pathophysiology of hereditary recurrent fever syndromes : cellular and molecular approaches : Pathophysiologie des fièvres récurrentes héréditaires : approches cellulaires et moléculaires.

Degree: Docteur es, Génétique humaine, 2014, Université Pierre et Marie Curie – Paris VI

Les fièvres récurrentes héréditaires (FRH) sont des maladies auto-inflammatoires transmises selon un mode mendélien. Elles se caractérisent par des accès fébriles récurrents spontanément résolutifs accompagnés… (more)

Subjects/Keywords: Fièvres récurrentes héréditaires; Fièvre méditerranéenne familiale; Inflammasome; Nlrp3; Pyrine; Macrophages; Hereditary recurrent fevers; Inflammasome; 570

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Awad, F. (2014). Pathophysiology of hereditary recurrent fever syndromes : cellular and molecular approaches : Pathophysiologie des fièvres récurrentes héréditaires : approches cellulaires et moléculaires. (Doctoral Dissertation). Université Pierre et Marie Curie – Paris VI. Retrieved from http://www.theses.fr/2014PA066394

Chicago Manual of Style (16th Edition):

Awad, Fawaz. “Pathophysiology of hereditary recurrent fever syndromes : cellular and molecular approaches : Pathophysiologie des fièvres récurrentes héréditaires : approches cellulaires et moléculaires.” 2014. Doctoral Dissertation, Université Pierre et Marie Curie – Paris VI. Accessed October 20, 2019. http://www.theses.fr/2014PA066394.

MLA Handbook (7th Edition):

Awad, Fawaz. “Pathophysiology of hereditary recurrent fever syndromes : cellular and molecular approaches : Pathophysiologie des fièvres récurrentes héréditaires : approches cellulaires et moléculaires.” 2014. Web. 20 Oct 2019.

Vancouver:

Awad F. Pathophysiology of hereditary recurrent fever syndromes : cellular and molecular approaches : Pathophysiologie des fièvres récurrentes héréditaires : approches cellulaires et moléculaires. [Internet] [Doctoral dissertation]. Université Pierre et Marie Curie – Paris VI; 2014. [cited 2019 Oct 20]. Available from: http://www.theses.fr/2014PA066394.

Council of Science Editors:

Awad F. Pathophysiology of hereditary recurrent fever syndromes : cellular and molecular approaches : Pathophysiologie des fièvres récurrentes héréditaires : approches cellulaires et moléculaires. [Doctoral Dissertation]. Université Pierre et Marie Curie – Paris VI; 2014. Available from: http://www.theses.fr/2014PA066394

22. Poli, Caroline. Il-26 : une cytokine pro-inflammatoire stimulant les cellules immunitaires innées myéloïdes : Il-26 : a pro-inflammatory cytokine that stimulates innate myeloid cells.

Degree: Docteur es, Immunologie, 2017, Angers

Physiologiquement, l’ADN, séquestré dans les noyaux, n’est pas détecté par les récepteurs de danger du système immunitaire. En revanche, au cours d’inflammations chroniques, une rupture… (more)

Subjects/Keywords: Inflammation; Mort cellulaire; Acides nucléiques; Sting; Inflammasome; Inflammation; Cell death; Nucleic acids; Sting; Inflammasome; 616.079

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Poli, C. (2017). Il-26 : une cytokine pro-inflammatoire stimulant les cellules immunitaires innées myéloïdes : Il-26 : a pro-inflammatory cytokine that stimulates innate myeloid cells. (Doctoral Dissertation). Angers. Retrieved from http://www.theses.fr/2017ANGE0068

Chicago Manual of Style (16th Edition):

Poli, Caroline. “Il-26 : une cytokine pro-inflammatoire stimulant les cellules immunitaires innées myéloïdes : Il-26 : a pro-inflammatory cytokine that stimulates innate myeloid cells.” 2017. Doctoral Dissertation, Angers. Accessed October 20, 2019. http://www.theses.fr/2017ANGE0068.

MLA Handbook (7th Edition):

Poli, Caroline. “Il-26 : une cytokine pro-inflammatoire stimulant les cellules immunitaires innées myéloïdes : Il-26 : a pro-inflammatory cytokine that stimulates innate myeloid cells.” 2017. Web. 20 Oct 2019.

Vancouver:

Poli C. Il-26 : une cytokine pro-inflammatoire stimulant les cellules immunitaires innées myéloïdes : Il-26 : a pro-inflammatory cytokine that stimulates innate myeloid cells. [Internet] [Doctoral dissertation]. Angers; 2017. [cited 2019 Oct 20]. Available from: http://www.theses.fr/2017ANGE0068.

Council of Science Editors:

Poli C. Il-26 : une cytokine pro-inflammatoire stimulant les cellules immunitaires innées myéloïdes : Il-26 : a pro-inflammatory cytokine that stimulates innate myeloid cells. [Doctoral Dissertation]. Angers; 2017. Available from: http://www.theses.fr/2017ANGE0068

23. Eichholz, Karsten. Influence de protéin[e]s de l'hôte sur la réponse immunitaire innée face aux adénovirus humains dans les phagocytes humains : Influence of host proteins on the innate immune response to human adenoviruses in human phagocytes.

Degree: Docteur es, Biologie Santé, 2015, Montpellier

Les adénovirus humains (HAdV) provoquent un large spectre de maladies cliniques chez les patients immunodéprimés et immunocompétents et sont également des outils polyvalents pour le… (more)

Subjects/Keywords: Cellule dendritique; Inflammasome; Adenoviridae; Innate sensors; Facteurs de coagulation; Dendritic cells; Inflammasome; Adenovirus; Innate sensors; Coagulation factors

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Eichholz, K. (2015). Influence de protéin[e]s de l'hôte sur la réponse immunitaire innée face aux adénovirus humains dans les phagocytes humains : Influence of host proteins on the innate immune response to human adenoviruses in human phagocytes. (Doctoral Dissertation). Montpellier. Retrieved from http://www.theses.fr/2015MONTS059

Chicago Manual of Style (16th Edition):

Eichholz, Karsten. “Influence de protéin[e]s de l'hôte sur la réponse immunitaire innée face aux adénovirus humains dans les phagocytes humains : Influence of host proteins on the innate immune response to human adenoviruses in human phagocytes.” 2015. Doctoral Dissertation, Montpellier. Accessed October 20, 2019. http://www.theses.fr/2015MONTS059.

MLA Handbook (7th Edition):

Eichholz, Karsten. “Influence de protéin[e]s de l'hôte sur la réponse immunitaire innée face aux adénovirus humains dans les phagocytes humains : Influence of host proteins on the innate immune response to human adenoviruses in human phagocytes.” 2015. Web. 20 Oct 2019.

Vancouver:

Eichholz K. Influence de protéin[e]s de l'hôte sur la réponse immunitaire innée face aux adénovirus humains dans les phagocytes humains : Influence of host proteins on the innate immune response to human adenoviruses in human phagocytes. [Internet] [Doctoral dissertation]. Montpellier; 2015. [cited 2019 Oct 20]. Available from: http://www.theses.fr/2015MONTS059.

Council of Science Editors:

Eichholz K. Influence de protéin[e]s de l'hôte sur la réponse immunitaire innée face aux adénovirus humains dans les phagocytes humains : Influence of host proteins on the innate immune response to human adenoviruses in human phagocytes. [Doctoral Dissertation]. Montpellier; 2015. Available from: http://www.theses.fr/2015MONTS059

24. Gicquel, Thomas. Implication des récepteurs purinergiques dans l'activation de l'inflammasome NLRP3 dans les macrophages : Involvement of purinergic receptors in NLRP3-inflammasome pathway from macrophages.

Degree: Docteur es, Biologie et sciences de la santé, 2014, Rennes 1

L’inflammasome NLRP3 est très impliqué dans de nombreuses pathologies inflammatoires comme la fibrose pulmonaire, la polyarthrite rhumatoïde, la goutte ou la maladie de Crohn. Cette… (more)

Subjects/Keywords: Inflammasome NLRP3; Récepteurs purinergiques; Atp; Macrophages; Interleukines; Inflammation; Immunité innée; NLRP3 inflammasome; Purinergic receptors; Atp; Macrophages; Interleukines; Inflammation; Innate immunity

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Gicquel, T. (2014). Implication des récepteurs purinergiques dans l'activation de l'inflammasome NLRP3 dans les macrophages : Involvement of purinergic receptors in NLRP3-inflammasome pathway from macrophages. (Doctoral Dissertation). Rennes 1. Retrieved from http://www.theses.fr/2014REN1B012

Chicago Manual of Style (16th Edition):

Gicquel, Thomas. “Implication des récepteurs purinergiques dans l'activation de l'inflammasome NLRP3 dans les macrophages : Involvement of purinergic receptors in NLRP3-inflammasome pathway from macrophages.” 2014. Doctoral Dissertation, Rennes 1. Accessed October 20, 2019. http://www.theses.fr/2014REN1B012.

MLA Handbook (7th Edition):

Gicquel, Thomas. “Implication des récepteurs purinergiques dans l'activation de l'inflammasome NLRP3 dans les macrophages : Involvement of purinergic receptors in NLRP3-inflammasome pathway from macrophages.” 2014. Web. 20 Oct 2019.

Vancouver:

Gicquel T. Implication des récepteurs purinergiques dans l'activation de l'inflammasome NLRP3 dans les macrophages : Involvement of purinergic receptors in NLRP3-inflammasome pathway from macrophages. [Internet] [Doctoral dissertation]. Rennes 1; 2014. [cited 2019 Oct 20]. Available from: http://www.theses.fr/2014REN1B012.

Council of Science Editors:

Gicquel T. Implication des récepteurs purinergiques dans l'activation de l'inflammasome NLRP3 dans les macrophages : Involvement of purinergic receptors in NLRP3-inflammasome pathway from macrophages. [Doctoral Dissertation]. Rennes 1; 2014. Available from: http://www.theses.fr/2014REN1B012

25. Robert, Sacha. Caractérisation des signaux de danger et de la signalisation cellulaire dans le développement de la fibrose hépatique : Characterisation of danger signals and cell signaling in the development of liver fibrosis.

Degree: Docteur es, Biologie, 2016, Rennes 1

La voie de signalisation de l’inflammasome est impliquée dans plusieurs pathologies inflammatoires dont la fibrose pulmonaire et plus récemment, elle a été mise en lumière… (more)

Subjects/Keywords: Inflammasome; Fibrose hépatique; Cytokine; Macrophage; Fibroblaste; Inflammation; Fibrolyse; Inflammasome; Liver fibrosis; Cytokine; Macrophage; Fibroblast; Inflammation; Fibrolysis

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Robert, S. (2016). Caractérisation des signaux de danger et de la signalisation cellulaire dans le développement de la fibrose hépatique : Characterisation of danger signals and cell signaling in the development of liver fibrosis. (Doctoral Dissertation). Rennes 1. Retrieved from http://www.theses.fr/2016REN1B016

Chicago Manual of Style (16th Edition):

Robert, Sacha. “Caractérisation des signaux de danger et de la signalisation cellulaire dans le développement de la fibrose hépatique : Characterisation of danger signals and cell signaling in the development of liver fibrosis.” 2016. Doctoral Dissertation, Rennes 1. Accessed October 20, 2019. http://www.theses.fr/2016REN1B016.

MLA Handbook (7th Edition):

Robert, Sacha. “Caractérisation des signaux de danger et de la signalisation cellulaire dans le développement de la fibrose hépatique : Characterisation of danger signals and cell signaling in the development of liver fibrosis.” 2016. Web. 20 Oct 2019.

Vancouver:

Robert S. Caractérisation des signaux de danger et de la signalisation cellulaire dans le développement de la fibrose hépatique : Characterisation of danger signals and cell signaling in the development of liver fibrosis. [Internet] [Doctoral dissertation]. Rennes 1; 2016. [cited 2019 Oct 20]. Available from: http://www.theses.fr/2016REN1B016.

Council of Science Editors:

Robert S. Caractérisation des signaux de danger et de la signalisation cellulaire dans le développement de la fibrose hépatique : Characterisation of danger signals and cell signaling in the development of liver fibrosis. [Doctoral Dissertation]. Rennes 1; 2016. Available from: http://www.theses.fr/2016REN1B016

26. Huck, Olivier. Infection et stimulation de cellules endothéliales par Porphyromonas gingivalis et son lipopolysaccharide : lien entre maladies parodontales et athérosclérose : Infection and stimulation of endothelial cells with porphyromonas gingivalis and its lipopolysaccharide : link between periodontal diseases and atherosclerosis.

Degree: Docteur es, Sciences de la vie et de la santé, 2013, Université de Strasbourg

Depuis plusieurs années, l’influence des pathologies parodontales sur certaines pathologies systémiques, notamment les maladies cardio-vasculaires et l’athérosclérose apparait de plus en plus évidente. Dans notre… (more)

Subjects/Keywords: Porphyromonas gingivalis; Maladies parodontales; Athérosclérose; Cathepsine B; Inflammasome; Porphyromonas gingivalis; Periodontal diseases; Atherosclerosis; Cathepsin B; Inflammasome; 616.13; 617.6

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Huck, O. (2013). Infection et stimulation de cellules endothéliales par Porphyromonas gingivalis et son lipopolysaccharide : lien entre maladies parodontales et athérosclérose : Infection and stimulation of endothelial cells with porphyromonas gingivalis and its lipopolysaccharide : link between periodontal diseases and atherosclerosis. (Doctoral Dissertation). Université de Strasbourg. Retrieved from http://www.theses.fr/2013STRAJ021

Chicago Manual of Style (16th Edition):

Huck, Olivier. “Infection et stimulation de cellules endothéliales par Porphyromonas gingivalis et son lipopolysaccharide : lien entre maladies parodontales et athérosclérose : Infection and stimulation of endothelial cells with porphyromonas gingivalis and its lipopolysaccharide : link between periodontal diseases and atherosclerosis.” 2013. Doctoral Dissertation, Université de Strasbourg. Accessed October 20, 2019. http://www.theses.fr/2013STRAJ021.

MLA Handbook (7th Edition):

Huck, Olivier. “Infection et stimulation de cellules endothéliales par Porphyromonas gingivalis et son lipopolysaccharide : lien entre maladies parodontales et athérosclérose : Infection and stimulation of endothelial cells with porphyromonas gingivalis and its lipopolysaccharide : link between periodontal diseases and atherosclerosis.” 2013. Web. 20 Oct 2019.

Vancouver:

Huck O. Infection et stimulation de cellules endothéliales par Porphyromonas gingivalis et son lipopolysaccharide : lien entre maladies parodontales et athérosclérose : Infection and stimulation of endothelial cells with porphyromonas gingivalis and its lipopolysaccharide : link between periodontal diseases and atherosclerosis. [Internet] [Doctoral dissertation]. Université de Strasbourg; 2013. [cited 2019 Oct 20]. Available from: http://www.theses.fr/2013STRAJ021.

Council of Science Editors:

Huck O. Infection et stimulation de cellules endothéliales par Porphyromonas gingivalis et son lipopolysaccharide : lien entre maladies parodontales et athérosclérose : Infection and stimulation of endothelial cells with porphyromonas gingivalis and its lipopolysaccharide : link between periodontal diseases and atherosclerosis. [Doctoral Dissertation]. Université de Strasbourg; 2013. Available from: http://www.theses.fr/2013STRAJ021

27. Besnard, Anne-Gaëlle. Etude des mécanismes immunitaires dans un modèle d'inflammation pulmonaire allergique chez la souris : rôles de l'interleukine-22 : Roles of interleukin-22 in a mouse model of allergic airways inflammation.

Degree: Docteur es, Biologie cellulaire et moléculaire, 2010, Université d'Orléans

L’asthme est une maladie inflammatoire chronique des voies aériennes. Chez les individus sensibles, l’inhalation d’allergènes entraine une inflammation pulmonaire se traduisant par des épisodes récurrents… (more)

Subjects/Keywords: Interleukine-22; Interleukine-17; Interleukine-33; Interleukine-1; NLRP3 inflammasome; Interleukin-22; Interleukin-17; Interleukin-33; Interleukin-1; NLRP3 inflammasome

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Besnard, A. (2010). Etude des mécanismes immunitaires dans un modèle d'inflammation pulmonaire allergique chez la souris : rôles de l'interleukine-22 : Roles of interleukin-22 in a mouse model of allergic airways inflammation. (Doctoral Dissertation). Université d'Orléans. Retrieved from http://www.theses.fr/2010ORLE2044

Chicago Manual of Style (16th Edition):

Besnard, Anne-Gaëlle. “Etude des mécanismes immunitaires dans un modèle d'inflammation pulmonaire allergique chez la souris : rôles de l'interleukine-22 : Roles of interleukin-22 in a mouse model of allergic airways inflammation.” 2010. Doctoral Dissertation, Université d'Orléans. Accessed October 20, 2019. http://www.theses.fr/2010ORLE2044.

MLA Handbook (7th Edition):

Besnard, Anne-Gaëlle. “Etude des mécanismes immunitaires dans un modèle d'inflammation pulmonaire allergique chez la souris : rôles de l'interleukine-22 : Roles of interleukin-22 in a mouse model of allergic airways inflammation.” 2010. Web. 20 Oct 2019.

Vancouver:

Besnard A. Etude des mécanismes immunitaires dans un modèle d'inflammation pulmonaire allergique chez la souris : rôles de l'interleukine-22 : Roles of interleukin-22 in a mouse model of allergic airways inflammation. [Internet] [Doctoral dissertation]. Université d'Orléans; 2010. [cited 2019 Oct 20]. Available from: http://www.theses.fr/2010ORLE2044.

Council of Science Editors:

Besnard A. Etude des mécanismes immunitaires dans un modèle d'inflammation pulmonaire allergique chez la souris : rôles de l'interleukine-22 : Roles of interleukin-22 in a mouse model of allergic airways inflammation. [Doctoral Dissertation]. Université d'Orléans; 2010. Available from: http://www.theses.fr/2010ORLE2044

28. Juruj, Carole. Étude de la régulation de l'inflammasome AIM2 dans des macrophages infectés par Francisella tularensis : Study of the regulation of AIM2 inflammasome in macrophages infected with Francisella Tularensis.

Degree: Docteur es, Infection et immunité, 2013, Université Claude Bernard – Lyon I

L'inflammasome est une voie de signalisation du système immunitaire inné impliquée dans la lutte contre les pathogènes et notamment dans la réponse aux infections bactérienne.… (more)

Subjects/Keywords: Inflammasome; AIM2; Francisella tularensis; Régulation; Caspase-1; Péroxynitrites; Inflammasome; AIM2; Francisella tularensis; Regulation; Caspase-1; Peroxynitrite; 616.079

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Juruj, C. (2013). Étude de la régulation de l'inflammasome AIM2 dans des macrophages infectés par Francisella tularensis : Study of the regulation of AIM2 inflammasome in macrophages infected with Francisella Tularensis. (Doctoral Dissertation). Université Claude Bernard – Lyon I. Retrieved from http://www.theses.fr/2013LYO10074

Chicago Manual of Style (16th Edition):

Juruj, Carole. “Étude de la régulation de l'inflammasome AIM2 dans des macrophages infectés par Francisella tularensis : Study of the regulation of AIM2 inflammasome in macrophages infected with Francisella Tularensis.” 2013. Doctoral Dissertation, Université Claude Bernard – Lyon I. Accessed October 20, 2019. http://www.theses.fr/2013LYO10074.

MLA Handbook (7th Edition):

Juruj, Carole. “Étude de la régulation de l'inflammasome AIM2 dans des macrophages infectés par Francisella tularensis : Study of the regulation of AIM2 inflammasome in macrophages infected with Francisella Tularensis.” 2013. Web. 20 Oct 2019.

Vancouver:

Juruj C. Étude de la régulation de l'inflammasome AIM2 dans des macrophages infectés par Francisella tularensis : Study of the regulation of AIM2 inflammasome in macrophages infected with Francisella Tularensis. [Internet] [Doctoral dissertation]. Université Claude Bernard – Lyon I; 2013. [cited 2019 Oct 20]. Available from: http://www.theses.fr/2013LYO10074.

Council of Science Editors:

Juruj C. Étude de la régulation de l'inflammasome AIM2 dans des macrophages infectés par Francisella tularensis : Study of the regulation of AIM2 inflammasome in macrophages infected with Francisella Tularensis. [Doctoral Dissertation]. Université Claude Bernard – Lyon I; 2013. Available from: http://www.theses.fr/2013LYO10074

29. Friard, Jonas. Les canaux anioniques sensibles au gonflement cellulaire : inhibiteurs, perméabilité, rôle dans la transition épithéliomésenchymateuse et l’inflammasome : Volume regulated anion channels : chloride channels, LRRC8/VRAC, glutathione, epithelial-mesenchymal transition, inflammasome, inhibitors.

Degree: Docteur es, Sciences de la vie et de la santé, 2018, Côte d'Azur

Les canaux anioniques ont toujours été sous-estimés par rapport aux canaux cationiques principalement en raison des difficultés à caractériser leurs identités moléculaires et par l'absence… (more)

Subjects/Keywords: Canaux chlorures; LRRC8/VRAC; Glutathion; Transition épithéliomésenchymateuse; Inflammasome; Inhibiteurs; Chloride channels; LRRC8/VRAC; Glutathione; Epithelial-mesenchymal transition; Inflammasome; Inhibitors

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Friard, J. (2018). Les canaux anioniques sensibles au gonflement cellulaire : inhibiteurs, perméabilité, rôle dans la transition épithéliomésenchymateuse et l’inflammasome : Volume regulated anion channels : chloride channels, LRRC8/VRAC, glutathione, epithelial-mesenchymal transition, inflammasome, inhibitors. (Doctoral Dissertation). Côte d'Azur. Retrieved from http://www.theses.fr/2018AZUR4093

Chicago Manual of Style (16th Edition):

Friard, Jonas. “Les canaux anioniques sensibles au gonflement cellulaire : inhibiteurs, perméabilité, rôle dans la transition épithéliomésenchymateuse et l’inflammasome : Volume regulated anion channels : chloride channels, LRRC8/VRAC, glutathione, epithelial-mesenchymal transition, inflammasome, inhibitors.” 2018. Doctoral Dissertation, Côte d'Azur. Accessed October 20, 2019. http://www.theses.fr/2018AZUR4093.

MLA Handbook (7th Edition):

Friard, Jonas. “Les canaux anioniques sensibles au gonflement cellulaire : inhibiteurs, perméabilité, rôle dans la transition épithéliomésenchymateuse et l’inflammasome : Volume regulated anion channels : chloride channels, LRRC8/VRAC, glutathione, epithelial-mesenchymal transition, inflammasome, inhibitors.” 2018. Web. 20 Oct 2019.

Vancouver:

Friard J. Les canaux anioniques sensibles au gonflement cellulaire : inhibiteurs, perméabilité, rôle dans la transition épithéliomésenchymateuse et l’inflammasome : Volume regulated anion channels : chloride channels, LRRC8/VRAC, glutathione, epithelial-mesenchymal transition, inflammasome, inhibitors. [Internet] [Doctoral dissertation]. Côte d'Azur; 2018. [cited 2019 Oct 20]. Available from: http://www.theses.fr/2018AZUR4093.

Council of Science Editors:

Friard J. Les canaux anioniques sensibles au gonflement cellulaire : inhibiteurs, perméabilité, rôle dans la transition épithéliomésenchymateuse et l’inflammasome : Volume regulated anion channels : chloride channels, LRRC8/VRAC, glutathione, epithelial-mesenchymal transition, inflammasome, inhibitors. [Doctoral Dissertation]. Côte d'Azur; 2018. Available from: http://www.theses.fr/2018AZUR4093

30. Bochaton, Thomas. Lésions d'ischémie-reperfusion myocardiques : régulation de la transition de perméabilité et rôle de l'activation de l'inflammation locale et systémique : Regulation of the mitochondrial permeability transition pore and myocardial reperfusion injuries.

Degree: Docteur es, Physiologie cardiaque et cardioprotection, 2016, Lyon

L'infarctus du myocarde est la première cause de mortalité dans le monde. La reperfusion précoce est le traitement central de la prise en charge thérapeutique.… (more)

Subjects/Keywords: Ischémie; Reperfusion; Sirtuine; Inflammation; Inflammasome; Post-condtionnement; Cyclosporine A; Ischémia; Reperfusion; Sirtuin; Inflammation; Inflammasome; Post-conditioning; Cyclosporine A; 571

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Bochaton, T. (2016). Lésions d'ischémie-reperfusion myocardiques : régulation de la transition de perméabilité et rôle de l'activation de l'inflammation locale et systémique : Regulation of the mitochondrial permeability transition pore and myocardial reperfusion injuries. (Doctoral Dissertation). Lyon. Retrieved from http://www.theses.fr/2016LYSE1289

Chicago Manual of Style (16th Edition):

Bochaton, Thomas. “Lésions d'ischémie-reperfusion myocardiques : régulation de la transition de perméabilité et rôle de l'activation de l'inflammation locale et systémique : Regulation of the mitochondrial permeability transition pore and myocardial reperfusion injuries.” 2016. Doctoral Dissertation, Lyon. Accessed October 20, 2019. http://www.theses.fr/2016LYSE1289.

MLA Handbook (7th Edition):

Bochaton, Thomas. “Lésions d'ischémie-reperfusion myocardiques : régulation de la transition de perméabilité et rôle de l'activation de l'inflammation locale et systémique : Regulation of the mitochondrial permeability transition pore and myocardial reperfusion injuries.” 2016. Web. 20 Oct 2019.

Vancouver:

Bochaton T. Lésions d'ischémie-reperfusion myocardiques : régulation de la transition de perméabilité et rôle de l'activation de l'inflammation locale et systémique : Regulation of the mitochondrial permeability transition pore and myocardial reperfusion injuries. [Internet] [Doctoral dissertation]. Lyon; 2016. [cited 2019 Oct 20]. Available from: http://www.theses.fr/2016LYSE1289.

Council of Science Editors:

Bochaton T. Lésions d'ischémie-reperfusion myocardiques : régulation de la transition de perméabilité et rôle de l'activation de l'inflammation locale et systémique : Regulation of the mitochondrial permeability transition pore and myocardial reperfusion injuries. [Doctoral Dissertation]. Lyon; 2016. Available from: http://www.theses.fr/2016LYSE1289

[1] [2] [3] [4] [5] [6] [7]

.