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You searched for subject:(Animal arthritis). Showing records 1 – 20 of 20 total matches.

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University of Gothenburg / Göteborgs Universitet

1. Bian, Li. The role of S100A4 protein as a regulator of inflammation and bone metabolism in experimental arthritis.

Degree: 2011, University of Gothenburg / Göteborgs Universitet

 S100A4 belongs to the family of calcium-binding S100 proteins and modulates cell proliferation, cytoskeletal rearrangement, cell motility, and angiogenesis. Increased levels of S100A4 expression correlate… (more)

Subjects/Keywords: S100A4; arthritis; animal model; bone; inflammation

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APA (6th Edition):

Bian, L. (2011). The role of S100A4 protein as a regulator of inflammation and bone metabolism in experimental arthritis. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/26277

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):

Bian, Li. “The role of S100A4 protein as a regulator of inflammation and bone metabolism in experimental arthritis.” 2011. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed December 06, 2019. http://hdl.handle.net/2077/26277.

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

MLA Handbook (7th Edition):

Bian, Li. “The role of S100A4 protein as a regulator of inflammation and bone metabolism in experimental arthritis.” 2011. Web. 06 Dec 2019.

Vancouver:

Bian L. The role of S100A4 protein as a regulator of inflammation and bone metabolism in experimental arthritis. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2011. [cited 2019 Dec 06]. Available from: http://hdl.handle.net/2077/26277.

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

Council of Science Editors:

Bian L. The role of S100A4 protein as a regulator of inflammation and bone metabolism in experimental arthritis. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2011. Available from: http://hdl.handle.net/2077/26277

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

2. Risi, Natalia. Uso da vocalização como indicador patológico em leitões na fase de maternidade.

Degree: Mestrado, Física do Ambiente Agrícola, 2010, University of São Paulo

O estudo da vocalização em animais de produção tem sido uma metodologia amplamente utilizada para avaliar as condições de bem-estar às quais os animais são… (more)

Subjects/Keywords: Animal health; Animal vocalization.; Arthritis; Artrite; Bioacoustics; Bioacústica; Saúde animal; Suínos; Swine; Vocalização animal.

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APA (6th Edition):

Risi, N. (2010). Uso da vocalização como indicador patológico em leitões na fase de maternidade. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/11/11131/tde-23062010-093056/ ;

Chicago Manual of Style (16th Edition):

Risi, Natalia. “Uso da vocalização como indicador patológico em leitões na fase de maternidade.” 2010. Masters Thesis, University of São Paulo. Accessed December 06, 2019. http://www.teses.usp.br/teses/disponiveis/11/11131/tde-23062010-093056/ ;.

MLA Handbook (7th Edition):

Risi, Natalia. “Uso da vocalização como indicador patológico em leitões na fase de maternidade.” 2010. Web. 06 Dec 2019.

Vancouver:

Risi N. Uso da vocalização como indicador patológico em leitões na fase de maternidade. [Internet] [Masters thesis]. University of São Paulo; 2010. [cited 2019 Dec 06]. Available from: http://www.teses.usp.br/teses/disponiveis/11/11131/tde-23062010-093056/ ;.

Council of Science Editors:

Risi N. Uso da vocalização como indicador patológico em leitões na fase de maternidade. [Masters Thesis]. University of São Paulo; 2010. Available from: http://www.teses.usp.br/teses/disponiveis/11/11131/tde-23062010-093056/ ;

3. Yamasaki, Simone Cristina. Efeitos do veneno de Apis mellifera e do metotrexato sobre peptidases do plasma, do líquido e membrana sinoviais e de leucócitos circulantes em ratos com artrite induzida por colágeno tipo II.

Degree: Mestrado, Biotecnologia, 2010, University of São Paulo

Atividades peptidásicas têm sido relacionadas à artrite reumatoide (AR). Os mecanismos de ação do tratamento usual, o metotrexato (MTX), e de terapias alternativos da AR,… (more)

Subjects/Keywords: Animal arthritis; Animal poisons; Artrite animal; Ativação enzimática; Colágeno; Collagen; Enzyme activation; Mice; Peptídeos; Peptides; Ratos; Venenos de origem animal

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APA (6th Edition):

Yamasaki, S. C. (2010). Efeitos do veneno de Apis mellifera e do metotrexato sobre peptidases do plasma, do líquido e membrana sinoviais e de leucócitos circulantes em ratos com artrite induzida por colágeno tipo II. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/87/87131/tde-03032011-104355/ ;

Chicago Manual of Style (16th Edition):

Yamasaki, Simone Cristina. “Efeitos do veneno de Apis mellifera e do metotrexato sobre peptidases do plasma, do líquido e membrana sinoviais e de leucócitos circulantes em ratos com artrite induzida por colágeno tipo II.” 2010. Masters Thesis, University of São Paulo. Accessed December 06, 2019. http://www.teses.usp.br/teses/disponiveis/87/87131/tde-03032011-104355/ ;.

MLA Handbook (7th Edition):

Yamasaki, Simone Cristina. “Efeitos do veneno de Apis mellifera e do metotrexato sobre peptidases do plasma, do líquido e membrana sinoviais e de leucócitos circulantes em ratos com artrite induzida por colágeno tipo II.” 2010. Web. 06 Dec 2019.

Vancouver:

Yamasaki SC. Efeitos do veneno de Apis mellifera e do metotrexato sobre peptidases do plasma, do líquido e membrana sinoviais e de leucócitos circulantes em ratos com artrite induzida por colágeno tipo II. [Internet] [Masters thesis]. University of São Paulo; 2010. [cited 2019 Dec 06]. Available from: http://www.teses.usp.br/teses/disponiveis/87/87131/tde-03032011-104355/ ;.

Council of Science Editors:

Yamasaki SC. Efeitos do veneno de Apis mellifera e do metotrexato sobre peptidases do plasma, do líquido e membrana sinoviais e de leucócitos circulantes em ratos com artrite induzida por colágeno tipo II. [Masters Thesis]. University of São Paulo; 2010. Available from: http://www.teses.usp.br/teses/disponiveis/87/87131/tde-03032011-104355/ ;


University of Sydney

4. Zaki, Sanaa. Why does my joint hurt: Understanding disease phenotype and pain relationships using mouse models of arthritis .

Degree: 2016, University of Sydney

 Osteoarthritis (OA), characterised by progressive joint-wide pathology, is a major health problem accounting for 48% of people living with chronic pain. There are no treatments… (more)

Subjects/Keywords: osteoarthritis; pain; DRG; animal models; knee joint; arthritis

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APA (6th Edition):

Zaki, S. (2016). Why does my joint hurt: Understanding disease phenotype and pain relationships using mouse models of arthritis . (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/16354

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):

Zaki, Sanaa. “Why does my joint hurt: Understanding disease phenotype and pain relationships using mouse models of arthritis .” 2016. Thesis, University of Sydney. Accessed December 06, 2019. http://hdl.handle.net/2123/16354.

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

MLA Handbook (7th Edition):

Zaki, Sanaa. “Why does my joint hurt: Understanding disease phenotype and pain relationships using mouse models of arthritis .” 2016. Web. 06 Dec 2019.

Vancouver:

Zaki S. Why does my joint hurt: Understanding disease phenotype and pain relationships using mouse models of arthritis . [Internet] [Thesis]. University of Sydney; 2016. [cited 2019 Dec 06]. Available from: http://hdl.handle.net/2123/16354.

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

Council of Science Editors:

Zaki S. Why does my joint hurt: Understanding disease phenotype and pain relationships using mouse models of arthritis . [Thesis]. University of Sydney; 2016. Available from: http://hdl.handle.net/2123/16354

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


Northeastern University

5. Jain, Shardool. Macrophage targeted tuftsin-modified alginate nanoparticles as non-viral delivery system for anti-inflammatory gene therapy in the treatment of rheumatoid arthritis.

Degree: PhD, School of Pharmacy, 2014, Northeastern University

 The goal of this project is to develop and characterize a macrophage targeted alginate polymer based gene delivery system for the treatment of rheumatoid arthritis(more)

Subjects/Keywords: targeted delivery; Polymeric drug delivery systems; Nanoparticles; Therapeutic use; Gene therapy; Rheumatoid arthritis; Treatment; Rheumatoid arthritis; Animal models; Alginates; Macrophages

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APA (6th Edition):

Jain, S. (2014). Macrophage targeted tuftsin-modified alginate nanoparticles as non-viral delivery system for anti-inflammatory gene therapy in the treatment of rheumatoid arthritis. (Doctoral Dissertation). Northeastern University. Retrieved from http://hdl.handle.net/2047/D20204485

Chicago Manual of Style (16th Edition):

Jain, Shardool. “Macrophage targeted tuftsin-modified alginate nanoparticles as non-viral delivery system for anti-inflammatory gene therapy in the treatment of rheumatoid arthritis.” 2014. Doctoral Dissertation, Northeastern University. Accessed December 06, 2019. http://hdl.handle.net/2047/D20204485.

MLA Handbook (7th Edition):

Jain, Shardool. “Macrophage targeted tuftsin-modified alginate nanoparticles as non-viral delivery system for anti-inflammatory gene therapy in the treatment of rheumatoid arthritis.” 2014. Web. 06 Dec 2019.

Vancouver:

Jain S. Macrophage targeted tuftsin-modified alginate nanoparticles as non-viral delivery system for anti-inflammatory gene therapy in the treatment of rheumatoid arthritis. [Internet] [Doctoral dissertation]. Northeastern University; 2014. [cited 2019 Dec 06]. Available from: http://hdl.handle.net/2047/D20204485.

Council of Science Editors:

Jain S. Macrophage targeted tuftsin-modified alginate nanoparticles as non-viral delivery system for anti-inflammatory gene therapy in the treatment of rheumatoid arthritis. [Doctoral Dissertation]. Northeastern University; 2014. Available from: http://hdl.handle.net/2047/D20204485

6. Mendes, Mariana Trivilin. Aminopeptidase básica e leucotrieno-A4-hidrolase em ratos sensíveis e insensíveis à indução de artrite por colágeno tipo II.

Degree: Mestrado, Fisiologia Geral, 2013, University of São Paulo

Atualmente, ainda é incerto se a hidrólise de L-arginil-β-naftilamida (ArgNA) e do leucotrieno (LT) A4 pela LT-A4-hidrolase (LT-A4-H) (EC 3.3.2.6) e pela aminopeptidase básica (APB)… (more)

Subjects/Keywords: Aminopeptidase; Aminopeptidase; Animal model; Arthritis; Artrite; Autoimmunity; Autoimunidade; Bifunctional enzymes; Enzimas bifuncionais; Leucotrieno; Leukotriene; Modelo animal

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APA (6th Edition):

Mendes, M. T. (2013). Aminopeptidase básica e leucotrieno-A4-hidrolase em ratos sensíveis e insensíveis à indução de artrite por colágeno tipo II. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/41/41135/tde-04062013-100941/ ;

Chicago Manual of Style (16th Edition):

Mendes, Mariana Trivilin. “Aminopeptidase básica e leucotrieno-A4-hidrolase em ratos sensíveis e insensíveis à indução de artrite por colágeno tipo II.” 2013. Masters Thesis, University of São Paulo. Accessed December 06, 2019. http://www.teses.usp.br/teses/disponiveis/41/41135/tde-04062013-100941/ ;.

MLA Handbook (7th Edition):

Mendes, Mariana Trivilin. “Aminopeptidase básica e leucotrieno-A4-hidrolase em ratos sensíveis e insensíveis à indução de artrite por colágeno tipo II.” 2013. Web. 06 Dec 2019.

Vancouver:

Mendes MT. Aminopeptidase básica e leucotrieno-A4-hidrolase em ratos sensíveis e insensíveis à indução de artrite por colágeno tipo II. [Internet] [Masters thesis]. University of São Paulo; 2013. [cited 2019 Dec 06]. Available from: http://www.teses.usp.br/teses/disponiveis/41/41135/tde-04062013-100941/ ;.

Council of Science Editors:

Mendes MT. Aminopeptidase básica e leucotrieno-A4-hidrolase em ratos sensíveis e insensíveis à indução de artrite por colágeno tipo II. [Masters Thesis]. University of São Paulo; 2013. Available from: http://www.teses.usp.br/teses/disponiveis/41/41135/tde-04062013-100941/ ;

7. Dias, Renata Gonçalves. Caracterização da inflamação articular induzida por fosfolipase A2 - grupo II A: determinação das alterações histopatológicas, comportamentais e mediação química.

Degree: PhD, Farmacologia, 2010, University of São Paulo

As fosfolipases A2 secretadas, particularmente do grupo II são abundantes nos venenos de serpentes, incluindo o gênero Bothrops e estão envolvidas em diversos processos fisiológicos… (more)

Subjects/Keywords: Bothrops asper; Bothrops asper; Animal arthritis; Articular Inflammation; Artrite animal; Dor; Fosfolipases; Inflamação articular; Miotoxina; Myotoxin; Pain; Phospholipases; Poison of animal origin; Serpentes; Snakes; Venenos de origem animal

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APA (6th Edition):

Dias, R. G. (2010). Caracterização da inflamação articular induzida por fosfolipase A2 - grupo II A: determinação das alterações histopatológicas, comportamentais e mediação química. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/42/42136/tde-14012011-125021/ ;

Chicago Manual of Style (16th Edition):

Dias, Renata Gonçalves. “Caracterização da inflamação articular induzida por fosfolipase A2 - grupo II A: determinação das alterações histopatológicas, comportamentais e mediação química.” 2010. Doctoral Dissertation, University of São Paulo. Accessed December 06, 2019. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-14012011-125021/ ;.

MLA Handbook (7th Edition):

Dias, Renata Gonçalves. “Caracterização da inflamação articular induzida por fosfolipase A2 - grupo II A: determinação das alterações histopatológicas, comportamentais e mediação química.” 2010. Web. 06 Dec 2019.

Vancouver:

Dias RG. Caracterização da inflamação articular induzida por fosfolipase A2 - grupo II A: determinação das alterações histopatológicas, comportamentais e mediação química. [Internet] [Doctoral dissertation]. University of São Paulo; 2010. [cited 2019 Dec 06]. Available from: http://www.teses.usp.br/teses/disponiveis/42/42136/tde-14012011-125021/ ;.

Council of Science Editors:

Dias RG. Caracterização da inflamação articular induzida por fosfolipase A2 - grupo II A: determinação das alterações histopatológicas, comportamentais e mediação química. [Doctoral Dissertation]. University of São Paulo; 2010. Available from: http://www.teses.usp.br/teses/disponiveis/42/42136/tde-14012011-125021/ ;


Universidade do Rio Grande do Sul

8. Oliveira, Patricia Gnieslaw de. Avaliação da eficácia de um antagonista do receptor do peptídeo liberador da gastrina em modelos experimentais de artrite.

Degree: 2011, Universidade do Rio Grande do Sul

O peptídeo liberador da gastrina (GRP) é o homologo mamífero da bombesina (BN). Ambos GRP e seus receptores têm sido encontrados na sinóvia de pacientes… (more)

Subjects/Keywords: Animal model; Artrite experimental; Artrite reumatóide; RC-3095; Receptores da bombesina; Rheumatoid arthritis; Colágeno tipo III; Neuropeptide; Soroalbumina bovina

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APA (6th Edition):

Oliveira, P. G. d. (2011). Avaliação da eficácia de um antagonista do receptor do peptídeo liberador da gastrina em modelos experimentais de artrite. (Thesis). Universidade do Rio Grande do Sul. Retrieved from http://hdl.handle.net/10183/35035

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):

Oliveira, Patricia Gnieslaw de. “Avaliação da eficácia de um antagonista do receptor do peptídeo liberador da gastrina em modelos experimentais de artrite.” 2011. Thesis, Universidade do Rio Grande do Sul. Accessed December 06, 2019. http://hdl.handle.net/10183/35035.

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

MLA Handbook (7th Edition):

Oliveira, Patricia Gnieslaw de. “Avaliação da eficácia de um antagonista do receptor do peptídeo liberador da gastrina em modelos experimentais de artrite.” 2011. Web. 06 Dec 2019.

Vancouver:

Oliveira PGd. Avaliação da eficácia de um antagonista do receptor do peptídeo liberador da gastrina em modelos experimentais de artrite. [Internet] [Thesis]. Universidade do Rio Grande do Sul; 2011. [cited 2019 Dec 06]. Available from: http://hdl.handle.net/10183/35035.

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

Council of Science Editors:

Oliveira PGd. Avaliação da eficácia de um antagonista do receptor do peptídeo liberador da gastrina em modelos experimentais de artrite. [Thesis]. Universidade do Rio Grande do Sul; 2011. Available from: http://hdl.handle.net/10183/35035

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

9. Πανδής, Ιωάννης. Ανάλυση του βιολογικού ρόλου των μικρών RNA σε ζωικά πειραματικά πρότυπα φλεγμονοδών ασθενειών του ανθρώπου.

Degree: 2012, University of Ioannina; Πανεπιστήμιο Ιωαννίνων

Objective:Rheumatoid arthritis (RA) is a chronic systemic inflammatory diseasecharacterised by synovial hyperplasia and consequent formation offibrous tissue termed pannus, cartilage degradation and bone erosionwith bone… (more)

Subjects/Keywords: Ρευματοειδής αρθρίτιδα; ΜικροRNA; Πειραματικά πρότυπα ασθενειών; Παράγοντας νέκρωσης όγκων; Βιοπληροφορική; Rheumatoid arthritis; MicroRNAs; Animal models; Tumour necrosis factor; Bioinformatics

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APA (6th Edition):

Πανδής, . . (2012). Ανάλυση του βιολογικού ρόλου των μικρών RNA σε ζωικά πειραματικά πρότυπα φλεγμονοδών ασθενειών του ανθρώπου. (Thesis). University of Ioannina; Πανεπιστήμιο Ιωαννίνων. Retrieved from http://hdl.handle.net/10442/hedi/29025

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):

Πανδής, Ιωάννης. “Ανάλυση του βιολογικού ρόλου των μικρών RNA σε ζωικά πειραματικά πρότυπα φλεγμονοδών ασθενειών του ανθρώπου.” 2012. Thesis, University of Ioannina; Πανεπιστήμιο Ιωαννίνων. Accessed December 06, 2019. http://hdl.handle.net/10442/hedi/29025.

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

MLA Handbook (7th Edition):

Πανδής, Ιωάννης. “Ανάλυση του βιολογικού ρόλου των μικρών RNA σε ζωικά πειραματικά πρότυπα φλεγμονοδών ασθενειών του ανθρώπου.” 2012. Web. 06 Dec 2019.

Vancouver:

Πανδής . Ανάλυση του βιολογικού ρόλου των μικρών RNA σε ζωικά πειραματικά πρότυπα φλεγμονοδών ασθενειών του ανθρώπου. [Internet] [Thesis]. University of Ioannina; Πανεπιστήμιο Ιωαννίνων; 2012. [cited 2019 Dec 06]. Available from: http://hdl.handle.net/10442/hedi/29025.

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

Council of Science Editors:

Πανδής . Ανάλυση του βιολογικού ρόλου των μικρών RNA σε ζωικά πειραματικά πρότυπα φλεγμονοδών ασθενειών του ανθρώπου. [Thesis]. University of Ioannina; Πανεπιστήμιο Ιωαννίνων; 2012. Available from: http://hdl.handle.net/10442/hedi/29025

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


Iowa State University

10. Cutlip, Randall Curry. Cytopathologic alterations induced by the agent of ovine chlamydial polyarthritis.

Degree: 1971, Iowa State University

Subjects/Keywords: Veterinary pathology; Arthritis; Sheep; Animal Sciences; Veterinary Medicine

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APA (6th Edition):

Cutlip, R. C. (1971). Cytopathologic alterations induced by the agent of ovine chlamydial polyarthritis. (Thesis). Iowa State University. Retrieved from https://lib.dr.iastate.edu/rtd/4391

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):

Cutlip, Randall Curry. “Cytopathologic alterations induced by the agent of ovine chlamydial polyarthritis.” 1971. Thesis, Iowa State University. Accessed December 06, 2019. https://lib.dr.iastate.edu/rtd/4391.

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

MLA Handbook (7th Edition):

Cutlip, Randall Curry. “Cytopathologic alterations induced by the agent of ovine chlamydial polyarthritis.” 1971. Web. 06 Dec 2019.

Vancouver:

Cutlip RC. Cytopathologic alterations induced by the agent of ovine chlamydial polyarthritis. [Internet] [Thesis]. Iowa State University; 1971. [cited 2019 Dec 06]. Available from: https://lib.dr.iastate.edu/rtd/4391.

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

Council of Science Editors:

Cutlip RC. Cytopathologic alterations induced by the agent of ovine chlamydial polyarthritis. [Thesis]. Iowa State University; 1971. Available from: https://lib.dr.iastate.edu/rtd/4391

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


Freie Universität Berlin

11. Präger, Thomas. Use of animal models in orthodontic research.

Degree: 2015, Freie Universität Berlin

 In this paper three animal models which are well established in orthodontic research were used. The rabbit model served to induce an arthritis of the… (more)

Subjects/Keywords: animal model; juvenile idiopathic arthritis; orthodontic tooth movement; skeletal anchorage; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit

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APA (6th Edition):

Präger, T. (2015). Use of animal models in orthodontic research. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-4522

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):

Präger, Thomas. “Use of animal models in orthodontic research.” 2015. Thesis, Freie Universität Berlin. Accessed December 06, 2019. http://dx.doi.org/10.17169/refubium-4522.

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

MLA Handbook (7th Edition):

Präger, Thomas. “Use of animal models in orthodontic research.” 2015. Web. 06 Dec 2019.

Vancouver:

Präger T. Use of animal models in orthodontic research. [Internet] [Thesis]. Freie Universität Berlin; 2015. [cited 2019 Dec 06]. Available from: http://dx.doi.org/10.17169/refubium-4522.

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

Council of Science Editors:

Präger T. Use of animal models in orthodontic research. [Thesis]. Freie Universität Berlin; 2015. Available from: http://dx.doi.org/10.17169/refubium-4522

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


University of Florida

12. Grimstein, Christian. Alpha-1 Antitrypsin Protein and Gene Therapies for the Prevention of Rheumatoid Arthritis in Mouse Models.

Degree: PhD, Pharmaceutical Sciences - Pharmacy, 2008, University of Florida

 Rheumatoid arthritis (RA) is an autoimmune disease characterized by immune cell infiltration, synovial hyperplasia, and progressive destruction of bone and cartilage, affecting about 1% of… (more)

Subjects/Keywords: Animal models; Antibodies; Arthritis; Autoantibodies; Control groups; Cytokines; Diseases; Gene therapy; Medical treatment; Rheumatoid arthritis; alpha1antitrypsin, arthritis, doxycycline, genetherapy

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APA (6th Edition):

Grimstein, C. (2008). Alpha-1 Antitrypsin Protein and Gene Therapies for the Prevention of Rheumatoid Arthritis in Mouse Models. (Doctoral Dissertation). University of Florida. Retrieved from http://ufdc.ufl.edu/UFE0023517

Chicago Manual of Style (16th Edition):

Grimstein, Christian. “Alpha-1 Antitrypsin Protein and Gene Therapies for the Prevention of Rheumatoid Arthritis in Mouse Models.” 2008. Doctoral Dissertation, University of Florida. Accessed December 06, 2019. http://ufdc.ufl.edu/UFE0023517.

MLA Handbook (7th Edition):

Grimstein, Christian. “Alpha-1 Antitrypsin Protein and Gene Therapies for the Prevention of Rheumatoid Arthritis in Mouse Models.” 2008. Web. 06 Dec 2019.

Vancouver:

Grimstein C. Alpha-1 Antitrypsin Protein and Gene Therapies for the Prevention of Rheumatoid Arthritis in Mouse Models. [Internet] [Doctoral dissertation]. University of Florida; 2008. [cited 2019 Dec 06]. Available from: http://ufdc.ufl.edu/UFE0023517.

Council of Science Editors:

Grimstein C. Alpha-1 Antitrypsin Protein and Gene Therapies for the Prevention of Rheumatoid Arthritis in Mouse Models. [Doctoral Dissertation]. University of Florida; 2008. Available from: http://ufdc.ufl.edu/UFE0023517

13. Totoson, Perle. Dysfonction endothéliale et polyarthrite rhumatoïde : cinétique, mécanismes et traitements. Etude chez le rat : Endothelial dysfunction and rheumatoïd arthritis : time-course, mechanisms and treatment. Study in adjuvant-induced arthritis rat model.

Degree: Docteur es, Sciences de la vie et de la santé, 2015, Besançon

La polyarthrite rhumatoïde (PR) représente le plus fréquent des rhumatismes inflammatoires chroniques. En plus d’une atteinte ostéo-articulaire responsable de l’invalidité fonctionnelle, la PR est associée… (more)

Subjects/Keywords: Polyarthrite rhumatoïde; Dysfonction endothéliale; Inflammation; Cardiovasculaire; Modèle animal; Etanercept; Thérapeutique; Diagnostic; Rheumatoid arthritis; Endothelial dysfunction; Inflammation; Cardiovascular; Animal model; Etanercept; Therapeutic; Diagnosis; 616.7; WE 346

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APA (6th Edition):

Totoson, P. (2015). Dysfonction endothéliale et polyarthrite rhumatoïde : cinétique, mécanismes et traitements. Etude chez le rat : Endothelial dysfunction and rheumatoïd arthritis : time-course, mechanisms and treatment. Study in adjuvant-induced arthritis rat model. (Doctoral Dissertation). Besançon. Retrieved from http://www.theses.fr/2015BESA3013

Chicago Manual of Style (16th Edition):

Totoson, Perle. “Dysfonction endothéliale et polyarthrite rhumatoïde : cinétique, mécanismes et traitements. Etude chez le rat : Endothelial dysfunction and rheumatoïd arthritis : time-course, mechanisms and treatment. Study in adjuvant-induced arthritis rat model.” 2015. Doctoral Dissertation, Besançon. Accessed December 06, 2019. http://www.theses.fr/2015BESA3013.

MLA Handbook (7th Edition):

Totoson, Perle. “Dysfonction endothéliale et polyarthrite rhumatoïde : cinétique, mécanismes et traitements. Etude chez le rat : Endothelial dysfunction and rheumatoïd arthritis : time-course, mechanisms and treatment. Study in adjuvant-induced arthritis rat model.” 2015. Web. 06 Dec 2019.

Vancouver:

Totoson P. Dysfonction endothéliale et polyarthrite rhumatoïde : cinétique, mécanismes et traitements. Etude chez le rat : Endothelial dysfunction and rheumatoïd arthritis : time-course, mechanisms and treatment. Study in adjuvant-induced arthritis rat model. [Internet] [Doctoral dissertation]. Besançon; 2015. [cited 2019 Dec 06]. Available from: http://www.theses.fr/2015BESA3013.

Council of Science Editors:

Totoson P. Dysfonction endothéliale et polyarthrite rhumatoïde : cinétique, mécanismes et traitements. Etude chez le rat : Endothelial dysfunction and rheumatoïd arthritis : time-course, mechanisms and treatment. Study in adjuvant-induced arthritis rat model. [Doctoral Dissertation]. Besançon; 2015. Available from: http://www.theses.fr/2015BESA3013

14. Mussard, Julie. Etude fonctionnelle du « Toll-like receptor 9 » et des neutrophiles au cours de l’inflammation : implication dans le développement de la polyarthrite rhumatoïde et d’un modèle expérimental : Functional study of toll-like receptor 9 and neutrophils in inflammation : involvement in the development of rheumatoid arthritis and experimental arthritis.

Degree: Docteur es, Biologie, 2015, Sorbonne Paris Cité

La polyarthrite rhumatoïde (PR) est le rhumatisme inflammatoire le plus fréquent dont l’étiologie reste inconnue. Le rôle de l’immunité adaptative est bien décrit dans cette… (more)

Subjects/Keywords: Immunité innée; Polyarthrite rhumatoïde; Modèle animal; Neutrophiles; Récepteur Toll-like 9 (TLR9); C1q; Innate immunity; Rheumatoid arthritis; Animal model; Neutrophils; Toll-like recptor 9

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APA (6th Edition):

Mussard, J. (2015). Etude fonctionnelle du « Toll-like receptor 9 » et des neutrophiles au cours de l’inflammation : implication dans le développement de la polyarthrite rhumatoïde et d’un modèle expérimental : Functional study of toll-like receptor 9 and neutrophils in inflammation : involvement in the development of rheumatoid arthritis and experimental arthritis. (Doctoral Dissertation). Sorbonne Paris Cité. Retrieved from http://www.theses.fr/2015USPCD015

Chicago Manual of Style (16th Edition):

Mussard, Julie. “Etude fonctionnelle du « Toll-like receptor 9 » et des neutrophiles au cours de l’inflammation : implication dans le développement de la polyarthrite rhumatoïde et d’un modèle expérimental : Functional study of toll-like receptor 9 and neutrophils in inflammation : involvement in the development of rheumatoid arthritis and experimental arthritis.” 2015. Doctoral Dissertation, Sorbonne Paris Cité. Accessed December 06, 2019. http://www.theses.fr/2015USPCD015.

MLA Handbook (7th Edition):

Mussard, Julie. “Etude fonctionnelle du « Toll-like receptor 9 » et des neutrophiles au cours de l’inflammation : implication dans le développement de la polyarthrite rhumatoïde et d’un modèle expérimental : Functional study of toll-like receptor 9 and neutrophils in inflammation : involvement in the development of rheumatoid arthritis and experimental arthritis.” 2015. Web. 06 Dec 2019.

Vancouver:

Mussard J. Etude fonctionnelle du « Toll-like receptor 9 » et des neutrophiles au cours de l’inflammation : implication dans le développement de la polyarthrite rhumatoïde et d’un modèle expérimental : Functional study of toll-like receptor 9 and neutrophils in inflammation : involvement in the development of rheumatoid arthritis and experimental arthritis. [Internet] [Doctoral dissertation]. Sorbonne Paris Cité; 2015. [cited 2019 Dec 06]. Available from: http://www.theses.fr/2015USPCD015.

Council of Science Editors:

Mussard J. Etude fonctionnelle du « Toll-like receptor 9 » et des neutrophiles au cours de l’inflammation : implication dans le développement de la polyarthrite rhumatoïde et d’un modèle expérimental : Functional study of toll-like receptor 9 and neutrophils in inflammation : involvement in the development of rheumatoid arthritis and experimental arthritis. [Doctoral Dissertation]. Sorbonne Paris Cité; 2015. Available from: http://www.theses.fr/2015USPCD015


Kyoto University

15. Okabe, Namiko. Suppressor of TCR signaling-2 (STS-2) suppresses arthritis development in mice .

Degree: 2018, Kyoto University

Subjects/Keywords: suppressor of TCR signaling-2; IL-2; animal model; collagen-induced arthritis; rheumatoid arthritis

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APA (6th Edition):

Okabe, N. (2018). Suppressor of TCR signaling-2 (STS-2) suppresses arthritis development in mice . (Thesis). Kyoto University. Retrieved from http://hdl.handle.net/2433/232089

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):

Okabe, Namiko. “Suppressor of TCR signaling-2 (STS-2) suppresses arthritis development in mice .” 2018. Thesis, Kyoto University. Accessed December 06, 2019. http://hdl.handle.net/2433/232089.

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

MLA Handbook (7th Edition):

Okabe, Namiko. “Suppressor of TCR signaling-2 (STS-2) suppresses arthritis development in mice .” 2018. Web. 06 Dec 2019.

Vancouver:

Okabe N. Suppressor of TCR signaling-2 (STS-2) suppresses arthritis development in mice . [Internet] [Thesis]. Kyoto University; 2018. [cited 2019 Dec 06]. Available from: http://hdl.handle.net/2433/232089.

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

Council of Science Editors:

Okabe N. Suppressor of TCR signaling-2 (STS-2) suppresses arthritis development in mice . [Thesis]. Kyoto University; 2018. Available from: http://hdl.handle.net/2433/232089

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

16. Tiniakou, Ioanna. The role of apolipoprotein A-I in the atheroprotective functions of high-density lipoprotein (HDL).

Degree: 2015, University of Crete (UOC); Πανεπιστήμιο Κρήτης

 Numerous epidemiological and clinical studies have demonstrated an inverse correlation between plasma high-density lipoprotein (HDL) cholesterol levels and the risk for coronary heart disease in… (more)

Subjects/Keywords: Λιποπρωτείνη υψηλής πυκνότητας; Απολιποπρωτείνη Α-Ι; Φλεγμονή; Ρευματοειδής αρθρίτιδα; Αθηροσκλήρωση; Φυσικές μεταλλάξεις; Αυτοανοσία; Δενδριτικά κύτταρα; Πειραματικά μοντέλα ποντικών; Διαγονιδιακά ποντίκια; Μυελοπεροξειδάση; GANLT2; High-density lipoprotein; Apolipoprotein A-I; Inflammation; Rheumatoid arthritis; Atherosclerosis; Natural mutations; Autoimmunity; Dendritic cells; Animal models; Transgenic mice; Myeloperoxidase; GALNT2

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APA (6th Edition):

Tiniakou, I. (2015). The role of apolipoprotein A-I in the atheroprotective functions of high-density lipoprotein (HDL). (Thesis). University of Crete (UOC); Πανεπιστήμιο Κρήτης. Retrieved from http://hdl.handle.net/10442/hedi/35985

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):

Tiniakou, Ioanna. “The role of apolipoprotein A-I in the atheroprotective functions of high-density lipoprotein (HDL).” 2015. Thesis, University of Crete (UOC); Πανεπιστήμιο Κρήτης. Accessed December 06, 2019. http://hdl.handle.net/10442/hedi/35985.

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

MLA Handbook (7th Edition):

Tiniakou, Ioanna. “The role of apolipoprotein A-I in the atheroprotective functions of high-density lipoprotein (HDL).” 2015. Web. 06 Dec 2019.

Vancouver:

Tiniakou I. The role of apolipoprotein A-I in the atheroprotective functions of high-density lipoprotein (HDL). [Internet] [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2015. [cited 2019 Dec 06]. Available from: http://hdl.handle.net/10442/hedi/35985.

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

Council of Science Editors:

Tiniakou I. The role of apolipoprotein A-I in the atheroprotective functions of high-density lipoprotein (HDL). [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2015. Available from: http://hdl.handle.net/10442/hedi/35985

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


Swedish University of Agricultural Sciences

17. Bremer, Hanna. Canine immune-mediated disease.

Degree: 2018, Swedish University of Agricultural Sciences

 Immune-mediated diseases in dogs constitute a large group of disorders with the common attribute that they are caused by dysfunctions in the immune system. Broadly… (more)

Subjects/Keywords: dogs; autoimmune diseases; autoimmunity; antibodies; immunological factors; arthritis; gene expression; animal diseases; Antinuclear antibodies; autoimmunity; dog; gene expression; ILF2; ILF3; immune-mediated rheumatic disease; Nova Scotia duck tolling retriever; steroid-responsive meningitis-arteritis; systemic lupus erythematosus

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APA (6th Edition):

Bremer, H. (2018). Canine immune-mediated disease. (Doctoral Dissertation). Swedish University of Agricultural Sciences. Retrieved from https://pub.epsilon.slu.se/15432/

Chicago Manual of Style (16th Edition):

Bremer, Hanna. “Canine immune-mediated disease.” 2018. Doctoral Dissertation, Swedish University of Agricultural Sciences. Accessed December 06, 2019. https://pub.epsilon.slu.se/15432/.

MLA Handbook (7th Edition):

Bremer, Hanna. “Canine immune-mediated disease.” 2018. Web. 06 Dec 2019.

Vancouver:

Bremer H. Canine immune-mediated disease. [Internet] [Doctoral dissertation]. Swedish University of Agricultural Sciences; 2018. [cited 2019 Dec 06]. Available from: https://pub.epsilon.slu.se/15432/.

Council of Science Editors:

Bremer H. Canine immune-mediated disease. [Doctoral Dissertation]. Swedish University of Agricultural Sciences; 2018. Available from: https://pub.epsilon.slu.se/15432/

18. Britschka, Zelia Maria Nogueira. "Efeito antiinflamatório da lama negra de Peruíbe em diferentes modelos experimentais de artrite".

Degree: PhD, Reumatologia, 2006, University of São Paulo

Investigar a eficácia da lama negra brasileira como tratamento para inflamação em modelos experimentais de artrite. O efeito antiinflamatório de aplicações de lama foi comparado… (more)

Subjects/Keywords: Arthritis rheumatoid/chemically induced; Arthritis rheumatoid/therapy; Artrite reumatóide/induzido quimicamente; Artrite reumatóide/terapia; Cartilage; Cartilagem; Modelos animais; Models animal; Mud therapy/methods; Osteoarthritis/therapy; Osteoartrite/terapia; Terapia por lama/métodos

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APA (6th Edition):

Britschka, Z. M. N. (2006). "Efeito antiinflamatório da lama negra de Peruíbe em diferentes modelos experimentais de artrite". (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5145/tde-17042006-111503/ ;

Chicago Manual of Style (16th Edition):

Britschka, Zelia Maria Nogueira. “"Efeito antiinflamatório da lama negra de Peruíbe em diferentes modelos experimentais de artrite".” 2006. Doctoral Dissertation, University of São Paulo. Accessed December 06, 2019. http://www.teses.usp.br/teses/disponiveis/5/5145/tde-17042006-111503/ ;.

MLA Handbook (7th Edition):

Britschka, Zelia Maria Nogueira. “"Efeito antiinflamatório da lama negra de Peruíbe em diferentes modelos experimentais de artrite".” 2006. Web. 06 Dec 2019.

Vancouver:

Britschka ZMN. "Efeito antiinflamatório da lama negra de Peruíbe em diferentes modelos experimentais de artrite". [Internet] [Doctoral dissertation]. University of São Paulo; 2006. [cited 2019 Dec 06]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5145/tde-17042006-111503/ ;.

Council of Science Editors:

Britschka ZMN. "Efeito antiinflamatório da lama negra de Peruíbe em diferentes modelos experimentais de artrite". [Doctoral Dissertation]. University of São Paulo; 2006. Available from: http://www.teses.usp.br/teses/disponiveis/5/5145/tde-17042006-111503/ ;


ETH Zürich

19. Stok, Kathryn. Biological quantification of murine osteoarticular joints following treatment using stem cell-based gene therapy.

Degree: 2008, ETH Zürich

Subjects/Keywords: ARTHRITIS (PATHOLOGIE); GENETISCHE THERAPIEN (MEDIZIN); STAMMZELLEN (CYTOLOGIE, HISTOLOGIE); GELENKE (TIERPHYSIOLOGIE, TIERMORPHOLOGIE); RASTERMIKROSKOPE + RASTERMIKROSKOPIE; LASERABTASTUNG + LASERREGISTRIERUNG (LASERTECHNIK); MURIDAE (ZOOLOGIE); ARTHRITIS (PATHOLOGY); GENETIC THERAPIES (MEDICINE); STEM CELLS (CYTOLOGY, HISTOLOGY); ARTICULATIONS (ANIMAL PHYSIOLOGY, ANIMAL MORPHOLOGY); SCANNING MICROSCOPES + SCANNING MICROSCOPY; LASER SCANNING + LASER RECORDING (LASER ENGINEERING); MURIDAE (ZOOLOGY); info:eu-repo/classification/ddc/610; Medical sciences, medicine

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APA (6th Edition):

Stok, K. (2008). Biological quantification of murine osteoarticular joints following treatment using stem cell-based gene therapy. (Doctoral Dissertation). ETH Zürich. Retrieved from http://hdl.handle.net/20.500.11850/150391

Chicago Manual of Style (16th Edition):

Stok, Kathryn. “Biological quantification of murine osteoarticular joints following treatment using stem cell-based gene therapy.” 2008. Doctoral Dissertation, ETH Zürich. Accessed December 06, 2019. http://hdl.handle.net/20.500.11850/150391.

MLA Handbook (7th Edition):

Stok, Kathryn. “Biological quantification of murine osteoarticular joints following treatment using stem cell-based gene therapy.” 2008. Web. 06 Dec 2019.

Vancouver:

Stok K. Biological quantification of murine osteoarticular joints following treatment using stem cell-based gene therapy. [Internet] [Doctoral dissertation]. ETH Zürich; 2008. [cited 2019 Dec 06]. Available from: http://hdl.handle.net/20.500.11850/150391.

Council of Science Editors:

Stok K. Biological quantification of murine osteoarticular joints following treatment using stem cell-based gene therapy. [Doctoral Dissertation]. ETH Zürich; 2008. Available from: http://hdl.handle.net/20.500.11850/150391


ETH Zürich

20. Doll, Fabia N. Development of therapeutic proteins for the treatment of rheumatoid arthritis and chronic cardiac rejection.

Degree: 2014, ETH Zürich

Subjects/Keywords: PROTEINE, POLYPEPTIDE, ENZYME, ENZYMINHIBITOREN, PEPTIDE (PHARMAZIE); HYBRIDPROTEINE + REKOMBINANTE PROTEINE; ANIMAL MODELS IN MEDICINE; CYTOKINES (IMMUNOLOGY); TARGETED DRUGS (PHARMACOLOGY); GELENKRHEUMATISMUS + RHEUMATOIDE ARTHRITIS + CHRONISCHE POLYARTHRITIS (PATHOLOGIE); DRUG DEVELOPMENT + DRUG DESIGN + DRUG DISCOVERY (PHARMACY); ANTIKÖRPERTECHNIKEN (IMMUNOLOGISCHE TECHNIKEN); ZIELGERICHTETE ARZNEIMITTEL (PHARMAKOLOGIE); ARZNEIMITTELENTWICKLUNG + ARZNEIMITTELDESIGN + ARZNEIMITTELENTDECKUNG; PROTEINS, POLYPEPTIDES, ENZYMES, ENZYME INHIBITORS, PEPTIDES (PHARMACY); TIERISCHE MODELLE IN DER MEDIZIN; JOINT RHEUMATISM + RHEUMATOID ARTHRITIS + CHRONIC POLYARTHRITIS (PATHOLOGY); HYBRID PROTEINS + RECOMBINANT PROTEINS; ANTIBODY TECHNIQUES (IMMUNOLOGICAL TECHNIQUES); ZYTOKINE (IMMUNOLOGIE); info:eu-repo/classification/ddc/610; Medical sciences, medicine

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APA (6th Edition):

Doll, F. N. (2014). Development of therapeutic proteins for the treatment of rheumatoid arthritis and chronic cardiac rejection. (Doctoral Dissertation). ETH Zürich. Retrieved from http://hdl.handle.net/20.500.11850/91687

Chicago Manual of Style (16th Edition):

Doll, Fabia N. “Development of therapeutic proteins for the treatment of rheumatoid arthritis and chronic cardiac rejection.” 2014. Doctoral Dissertation, ETH Zürich. Accessed December 06, 2019. http://hdl.handle.net/20.500.11850/91687.

MLA Handbook (7th Edition):

Doll, Fabia N. “Development of therapeutic proteins for the treatment of rheumatoid arthritis and chronic cardiac rejection.” 2014. Web. 06 Dec 2019.

Vancouver:

Doll FN. Development of therapeutic proteins for the treatment of rheumatoid arthritis and chronic cardiac rejection. [Internet] [Doctoral dissertation]. ETH Zürich; 2014. [cited 2019 Dec 06]. Available from: http://hdl.handle.net/20.500.11850/91687.

Council of Science Editors:

Doll FN. Development of therapeutic proteins for the treatment of rheumatoid arthritis and chronic cardiac rejection. [Doctoral Dissertation]. ETH Zürich; 2014. Available from: http://hdl.handle.net/20.500.11850/91687

.