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You searched for subject:(TLR4). Showing records 1 – 30 of 140 total matches.

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NSYSU

1. Chen, Pei-hsuan. Lack of TNF-α Receptor 1 Decreases Pseudomonas aeruginosa-induced Mortality in Burned Mice through Negative Regulation of Toll-like Receptor 4.

Degree: Master, Biological Sciences, 2008, NSYSU

 Tumor necrosis factor-alpha (TNF-α) is a potent proinflammatory cytokine, inducing the acute-phase response that leads to physiological changes that serve to eliminate the infecting organisms.… (more)

Subjects/Keywords: iNOS; TLR4

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

APA (6th Edition):

Chen, P. (2008). Lack of TNF-α Receptor 1 Decreases Pseudomonas aeruginosa-induced Mortality in Burned Mice through Negative Regulation of Toll-like Receptor 4. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0902108-125407

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):

Chen, Pei-hsuan. “Lack of TNF-α Receptor 1 Decreases Pseudomonas aeruginosa-induced Mortality in Burned Mice through Negative Regulation of Toll-like Receptor 4.” 2008. Thesis, NSYSU. Accessed September 24, 2020. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0902108-125407.

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

MLA Handbook (7th Edition):

Chen, Pei-hsuan. “Lack of TNF-α Receptor 1 Decreases Pseudomonas aeruginosa-induced Mortality in Burned Mice through Negative Regulation of Toll-like Receptor 4.” 2008. Web. 24 Sep 2020.

Vancouver:

Chen P. Lack of TNF-α Receptor 1 Decreases Pseudomonas aeruginosa-induced Mortality in Burned Mice through Negative Regulation of Toll-like Receptor 4. [Internet] [Thesis]. NSYSU; 2008. [cited 2020 Sep 24]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0902108-125407.

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

Council of Science Editors:

Chen P. Lack of TNF-α Receptor 1 Decreases Pseudomonas aeruginosa-induced Mortality in Burned Mice through Negative Regulation of Toll-like Receptor 4. [Thesis]. NSYSU; 2008. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0902108-125407

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


Mississippi State University

2. Jan, Basit Latief. INNATE IMMUNITY AND INFLAMMATION IN SEPSIS IN A MOUSE MODEL FOR BINGE DRINKING.

Degree: MS, Veterinary Medicine, College of, 2010, Mississippi State University

  Alcohol consumption is a significant risk-factor for mortality in patients with sepsis. This study was carried to investigate the mechanisms by which acute ethanol… (more)

Subjects/Keywords: TLR4; Ethanol

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APA (6th Edition):

Jan, B. L. (2010). INNATE IMMUNITY AND INFLAMMATION IN SEPSIS IN A MOUSE MODEL FOR BINGE DRINKING. (Masters Thesis). Mississippi State University. Retrieved from http://sun.library.msstate.edu/ETD-db/theses/available/etd-11122010-170231/ ;

Chicago Manual of Style (16th Edition):

Jan, Basit Latief. “INNATE IMMUNITY AND INFLAMMATION IN SEPSIS IN A MOUSE MODEL FOR BINGE DRINKING.” 2010. Masters Thesis, Mississippi State University. Accessed September 24, 2020. http://sun.library.msstate.edu/ETD-db/theses/available/etd-11122010-170231/ ;.

MLA Handbook (7th Edition):

Jan, Basit Latief. “INNATE IMMUNITY AND INFLAMMATION IN SEPSIS IN A MOUSE MODEL FOR BINGE DRINKING.” 2010. Web. 24 Sep 2020.

Vancouver:

Jan BL. INNATE IMMUNITY AND INFLAMMATION IN SEPSIS IN A MOUSE MODEL FOR BINGE DRINKING. [Internet] [Masters thesis]. Mississippi State University; 2010. [cited 2020 Sep 24]. Available from: http://sun.library.msstate.edu/ETD-db/theses/available/etd-11122010-170231/ ;.

Council of Science Editors:

Jan BL. INNATE IMMUNITY AND INFLAMMATION IN SEPSIS IN A MOUSE MODEL FOR BINGE DRINKING. [Masters Thesis]. Mississippi State University; 2010. Available from: http://sun.library.msstate.edu/ETD-db/theses/available/etd-11122010-170231/ ;


Oklahoma State University

3. Aravind, Shruthishree. Novel Effects of Opioids on Toll-like Receptor 4.

Degree: Department of Biochemistry and Molecular Biology, 2011, Oklahoma State University

 Opioid analgesics are now known to activate both classic opioid receptors and TLR4 on glial cells. Ongoing research in this field shows the involvement of… (more)

Subjects/Keywords: opioids; tlr4

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APA (6th Edition):

Aravind, S. (2011). Novel Effects of Opioids on Toll-like Receptor 4. (Thesis). Oklahoma State University. Retrieved from http://hdl.handle.net/11244/8526

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):

Aravind, Shruthishree. “Novel Effects of Opioids on Toll-like Receptor 4.” 2011. Thesis, Oklahoma State University. Accessed September 24, 2020. http://hdl.handle.net/11244/8526.

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

MLA Handbook (7th Edition):

Aravind, Shruthishree. “Novel Effects of Opioids on Toll-like Receptor 4.” 2011. Web. 24 Sep 2020.

Vancouver:

Aravind S. Novel Effects of Opioids on Toll-like Receptor 4. [Internet] [Thesis]. Oklahoma State University; 2011. [cited 2020 Sep 24]. Available from: http://hdl.handle.net/11244/8526.

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

Council of Science Editors:

Aravind S. Novel Effects of Opioids on Toll-like Receptor 4. [Thesis]. Oklahoma State University; 2011. Available from: http://hdl.handle.net/11244/8526

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


University of Otago

4. Mallard, Beth. The role of Toll-like receptor 4 in Concanavalin A-induced immune-mediated hepatitis .

Degree: 2011, University of Otago

 Background: Con A administration leads to T cell-mediated hepatitis in mice, the mechanism of which involves the cytokines interferon (IFN)-γ and tumour necrosis factor (TNF)-α.… (more)

Subjects/Keywords: TLR4; hepatitis; Con A

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APA (6th Edition):

Mallard, B. (2011). The role of Toll-like receptor 4 in Concanavalin A-induced immune-mediated hepatitis . (Doctoral Dissertation). University of Otago. Retrieved from http://hdl.handle.net/10523/606

Chicago Manual of Style (16th Edition):

Mallard, Beth. “The role of Toll-like receptor 4 in Concanavalin A-induced immune-mediated hepatitis .” 2011. Doctoral Dissertation, University of Otago. Accessed September 24, 2020. http://hdl.handle.net/10523/606.

MLA Handbook (7th Edition):

Mallard, Beth. “The role of Toll-like receptor 4 in Concanavalin A-induced immune-mediated hepatitis .” 2011. Web. 24 Sep 2020.

Vancouver:

Mallard B. The role of Toll-like receptor 4 in Concanavalin A-induced immune-mediated hepatitis . [Internet] [Doctoral dissertation]. University of Otago; 2011. [cited 2020 Sep 24]. Available from: http://hdl.handle.net/10523/606.

Council of Science Editors:

Mallard B. The role of Toll-like receptor 4 in Concanavalin A-induced immune-mediated hepatitis . [Doctoral Dissertation]. University of Otago; 2011. Available from: http://hdl.handle.net/10523/606


University of Otago

5. Muhamad, Marlini. The role of lipopolysaccharide/Toll-like Receptor 4 signalling pathway during liver regeneration after partial hepatectomy in mice .

Degree: 2011, University of Otago

 The process of liver regeneration after partial hepatectomy is very complex and is associated with signalling cascades involving initiation signals, transcription factors, cytokines, growth factors,… (more)

Subjects/Keywords: TLR4; LPS; liver regeneration

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APA (6th Edition):

Muhamad, M. (2011). The role of lipopolysaccharide/Toll-like Receptor 4 signalling pathway during liver regeneration after partial hepatectomy in mice . (Doctoral Dissertation). University of Otago. Retrieved from http://hdl.handle.net/10523/1695

Chicago Manual of Style (16th Edition):

Muhamad, Marlini. “The role of lipopolysaccharide/Toll-like Receptor 4 signalling pathway during liver regeneration after partial hepatectomy in mice .” 2011. Doctoral Dissertation, University of Otago. Accessed September 24, 2020. http://hdl.handle.net/10523/1695.

MLA Handbook (7th Edition):

Muhamad, Marlini. “The role of lipopolysaccharide/Toll-like Receptor 4 signalling pathway during liver regeneration after partial hepatectomy in mice .” 2011. Web. 24 Sep 2020.

Vancouver:

Muhamad M. The role of lipopolysaccharide/Toll-like Receptor 4 signalling pathway during liver regeneration after partial hepatectomy in mice . [Internet] [Doctoral dissertation]. University of Otago; 2011. [cited 2020 Sep 24]. Available from: http://hdl.handle.net/10523/1695.

Council of Science Editors:

Muhamad M. The role of lipopolysaccharide/Toll-like Receptor 4 signalling pathway during liver regeneration after partial hepatectomy in mice . [Doctoral Dissertation]. University of Otago; 2011. Available from: http://hdl.handle.net/10523/1695


Virginia Tech

6. Denko, Laura Michelle. Cellular Reprogramming in Skeletal Muscle after Repeated Exposures to Endotoxin.

Degree: MS, Human Nutrition, Foods, and Exercise, 2012, Virginia Tech

 Obesity-related metabolic derangements have been linked to toll-like receptor 4 (TLR4), an innate immune system receptor, due to its role in proinflammatory pathways. Lipopolysaccharide (LPS),… (more)

Subjects/Keywords: TLR4; endotoxin; LPS; skeletal muscle

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APA (6th Edition):

Denko, L. M. (2012). Cellular Reprogramming in Skeletal Muscle after Repeated Exposures to Endotoxin. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/76808

Chicago Manual of Style (16th Edition):

Denko, Laura Michelle. “Cellular Reprogramming in Skeletal Muscle after Repeated Exposures to Endotoxin.” 2012. Masters Thesis, Virginia Tech. Accessed September 24, 2020. http://hdl.handle.net/10919/76808.

MLA Handbook (7th Edition):

Denko, Laura Michelle. “Cellular Reprogramming in Skeletal Muscle after Repeated Exposures to Endotoxin.” 2012. Web. 24 Sep 2020.

Vancouver:

Denko LM. Cellular Reprogramming in Skeletal Muscle after Repeated Exposures to Endotoxin. [Internet] [Masters thesis]. Virginia Tech; 2012. [cited 2020 Sep 24]. Available from: http://hdl.handle.net/10919/76808.

Council of Science Editors:

Denko LM. Cellular Reprogramming in Skeletal Muscle after Repeated Exposures to Endotoxin. [Masters Thesis]. Virginia Tech; 2012. Available from: http://hdl.handle.net/10919/76808


National University of Ireland – Galway

7. Henry, Rebecca Jane. Endocannabinoid regulation of neuroinflammatory responses following acute systemic viral (TLR3) and bacterial (TLR4) infection .

Degree: 2015, National University of Ireland – Galway

 Toll like receptors (TLRs) are key players in host defence, homeostasis and response to injury. However, uncontrolled and aberrant TLR activation has been proposed to… (more)

Subjects/Keywords: Endocannabinoid; Neuroinflammation; TLR3; TLR4; Physiology

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APA (6th Edition):

Henry, R. J. (2015). Endocannabinoid regulation of neuroinflammatory responses following acute systemic viral (TLR3) and bacterial (TLR4) infection . (Thesis). National University of Ireland – Galway. Retrieved from http://hdl.handle.net/10379/5312

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):

Henry, Rebecca Jane. “Endocannabinoid regulation of neuroinflammatory responses following acute systemic viral (TLR3) and bacterial (TLR4) infection .” 2015. Thesis, National University of Ireland – Galway. Accessed September 24, 2020. http://hdl.handle.net/10379/5312.

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

MLA Handbook (7th Edition):

Henry, Rebecca Jane. “Endocannabinoid regulation of neuroinflammatory responses following acute systemic viral (TLR3) and bacterial (TLR4) infection .” 2015. Web. 24 Sep 2020.

Vancouver:

Henry RJ. Endocannabinoid regulation of neuroinflammatory responses following acute systemic viral (TLR3) and bacterial (TLR4) infection . [Internet] [Thesis]. National University of Ireland – Galway; 2015. [cited 2020 Sep 24]. Available from: http://hdl.handle.net/10379/5312.

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

Council of Science Editors:

Henry RJ. Endocannabinoid regulation of neuroinflammatory responses following acute systemic viral (TLR3) and bacterial (TLR4) infection . [Thesis]. National University of Ireland – Galway; 2015. Available from: http://hdl.handle.net/10379/5312

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

8. Oldenburg, Reid. Immunomodulatory properties of mycobacterial phenolic glycolipids : Propriétés immunomodulatrices des phénol-glycolipides mycobactériens.

Degree: Docteur es, Sciences de la vie et de la santé. Immunologie, 2016, Sorbonne Paris Cité

La biosynthèse de phénol-glycolipides (PGL) par Mycobacterium tuberculosis et M. leprae favorise l’invasion des macrophages via l'interaction de la partie saccharidique des PGL avec le… (more)

Subjects/Keywords: Phénol-glycolipides mycobactériens; TLR4; TRIF; Mycobacterial phenolic glycolipids; TLR4; TRIF

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APA (6th Edition):

Oldenburg, R. (2016). Immunomodulatory properties of mycobacterial phenolic glycolipids : Propriétés immunomodulatrices des phénol-glycolipides mycobactériens. (Doctoral Dissertation). Sorbonne Paris Cité. Retrieved from http://www.theses.fr/2016USPCC234

Chicago Manual of Style (16th Edition):

Oldenburg, Reid. “Immunomodulatory properties of mycobacterial phenolic glycolipids : Propriétés immunomodulatrices des phénol-glycolipides mycobactériens.” 2016. Doctoral Dissertation, Sorbonne Paris Cité. Accessed September 24, 2020. http://www.theses.fr/2016USPCC234.

MLA Handbook (7th Edition):

Oldenburg, Reid. “Immunomodulatory properties of mycobacterial phenolic glycolipids : Propriétés immunomodulatrices des phénol-glycolipides mycobactériens.” 2016. Web. 24 Sep 2020.

Vancouver:

Oldenburg R. Immunomodulatory properties of mycobacterial phenolic glycolipids : Propriétés immunomodulatrices des phénol-glycolipides mycobactériens. [Internet] [Doctoral dissertation]. Sorbonne Paris Cité; 2016. [cited 2020 Sep 24]. Available from: http://www.theses.fr/2016USPCC234.

Council of Science Editors:

Oldenburg R. Immunomodulatory properties of mycobacterial phenolic glycolipids : Propriétés immunomodulatrices des phénol-glycolipides mycobactériens. [Doctoral Dissertation]. Sorbonne Paris Cité; 2016. Available from: http://www.theses.fr/2016USPCC234


Uniwersytet im. Adama Mickiewicza w Poznaniu

9. Sikorski, Krzysztof. STAT1 – główny czynnik regulatorowy w zapaleniu i dysfunkcji naczyniowej .

Degree: 2013, Uniwersytet im. Adama Mickiewicza w Poznaniu

 Cytokina pro-zapalna interferon-gamma (IFNγ) oraz receptor Toll-podobny 4 (TLR4) współdziałają w leukocytach powodując zwiększoną odpowiedź zapalną: znaczny wzrost ekspresji chemokin i cytokin. Stawiamy hipotezę, że… (more)

Subjects/Keywords: miażdżyca; atherosclerosis; IFN-gamma; Receptor TLR4; TLR4; JAK-STAT; śródbłonek; endothelium

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APA (6th Edition):

Sikorski, K. (2013). STAT1 – główny czynnik regulatorowy w zapaleniu i dysfunkcji naczyniowej . (Doctoral Dissertation). Uniwersytet im. Adama Mickiewicza w Poznaniu. Retrieved from http://hdl.handle.net/10593/6444

Chicago Manual of Style (16th Edition):

Sikorski, Krzysztof. “STAT1 – główny czynnik regulatorowy w zapaleniu i dysfunkcji naczyniowej .” 2013. Doctoral Dissertation, Uniwersytet im. Adama Mickiewicza w Poznaniu. Accessed September 24, 2020. http://hdl.handle.net/10593/6444.

MLA Handbook (7th Edition):

Sikorski, Krzysztof. “STAT1 – główny czynnik regulatorowy w zapaleniu i dysfunkcji naczyniowej .” 2013. Web. 24 Sep 2020.

Vancouver:

Sikorski K. STAT1 – główny czynnik regulatorowy w zapaleniu i dysfunkcji naczyniowej . [Internet] [Doctoral dissertation]. Uniwersytet im. Adama Mickiewicza w Poznaniu; 2013. [cited 2020 Sep 24]. Available from: http://hdl.handle.net/10593/6444.

Council of Science Editors:

Sikorski K. STAT1 – główny czynnik regulatorowy w zapaleniu i dysfunkcji naczyniowej . [Doctoral Dissertation]. Uniwersytet im. Adama Mickiewicza w Poznaniu; 2013. Available from: http://hdl.handle.net/10593/6444


University of Georgia

10. Foote, Matthew Ian. Structural modification of E. Coli lipid A and KDO-lipid IVA.

Degree: 2014, University of Georgia

 Lipopolysaccharides from gram negative bacteria are responsible for signal transduction for the proinflammatory response in cells by initiating formation of TLR4/MD-2 protein complexes. Excess LPS… (more)

Subjects/Keywords: LIPID; LIPOPOLYSACCHARIDE; ESCHERICHIA COLI; TLR4; MD-2

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APA (6th Edition):

Foote, M. I. (2014). Structural modification of E. Coli lipid A and KDO-lipid IVA. (Thesis). University of Georgia. Retrieved from http://hdl.handle.net/10724/26896

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):

Foote, Matthew Ian. “Structural modification of E. Coli lipid A and KDO-lipid IVA.” 2014. Thesis, University of Georgia. Accessed September 24, 2020. http://hdl.handle.net/10724/26896.

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

MLA Handbook (7th Edition):

Foote, Matthew Ian. “Structural modification of E. Coli lipid A and KDO-lipid IVA.” 2014. Web. 24 Sep 2020.

Vancouver:

Foote MI. Structural modification of E. Coli lipid A and KDO-lipid IVA. [Internet] [Thesis]. University of Georgia; 2014. [cited 2020 Sep 24]. Available from: http://hdl.handle.net/10724/26896.

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

Council of Science Editors:

Foote MI. Structural modification of E. Coli lipid A and KDO-lipid IVA. [Thesis]. University of Georgia; 2014. Available from: http://hdl.handle.net/10724/26896

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


University of Cincinnati

11. Allen, Jessica L. Inhibition by Proxy: Modulation of TLR4-driven B cell responses by RP105.

Degree: PhD, Medicine : Immunobiology, 2010, University of Cincinnati

 Consistent with their important roles in both adaptive and innate immune responses, B lymphocytes express both somatically-recombined, antigen-specific receptors of the adaptive immune system and… (more)

Subjects/Keywords: Immunology; TLR4; RP105; B cells; BAFF

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APA (6th Edition):

Allen, J. L. (2010). Inhibition by Proxy: Modulation of TLR4-driven B cell responses by RP105. (Doctoral Dissertation). University of Cincinnati. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ucin1275658195

Chicago Manual of Style (16th Edition):

Allen, Jessica L. “Inhibition by Proxy: Modulation of TLR4-driven B cell responses by RP105.” 2010. Doctoral Dissertation, University of Cincinnati. Accessed September 24, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1275658195.

MLA Handbook (7th Edition):

Allen, Jessica L. “Inhibition by Proxy: Modulation of TLR4-driven B cell responses by RP105.” 2010. Web. 24 Sep 2020.

Vancouver:

Allen JL. Inhibition by Proxy: Modulation of TLR4-driven B cell responses by RP105. [Internet] [Doctoral dissertation]. University of Cincinnati; 2010. [cited 2020 Sep 24]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1275658195.

Council of Science Editors:

Allen JL. Inhibition by Proxy: Modulation of TLR4-driven B cell responses by RP105. [Doctoral Dissertation]. University of Cincinnati; 2010. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1275658195


University of Arizona

12. Thompson, Austen Lowell. Morphine Induced Osteolysis and Hyperalgesia in Models of Traumatic and Pathologic Fracture: Potential for Cannabinoid-Based Therapeutics .

Degree: 2020, University of Arizona

 Pain is the most common reason patients seek out medical attention, although its etiology is different case by case. The over-prescription as well as misuse… (more)

Subjects/Keywords: bone cancer; cannabinoids; fracture; opioids; pain; TLR4

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APA (6th Edition):

Thompson, A. L. (2020). Morphine Induced Osteolysis and Hyperalgesia in Models of Traumatic and Pathologic Fracture: Potential for Cannabinoid-Based Therapeutics . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/641744

Chicago Manual of Style (16th Edition):

Thompson, Austen Lowell. “Morphine Induced Osteolysis and Hyperalgesia in Models of Traumatic and Pathologic Fracture: Potential for Cannabinoid-Based Therapeutics .” 2020. Doctoral Dissertation, University of Arizona. Accessed September 24, 2020. http://hdl.handle.net/10150/641744.

MLA Handbook (7th Edition):

Thompson, Austen Lowell. “Morphine Induced Osteolysis and Hyperalgesia in Models of Traumatic and Pathologic Fracture: Potential for Cannabinoid-Based Therapeutics .” 2020. Web. 24 Sep 2020.

Vancouver:

Thompson AL. Morphine Induced Osteolysis and Hyperalgesia in Models of Traumatic and Pathologic Fracture: Potential for Cannabinoid-Based Therapeutics . [Internet] [Doctoral dissertation]. University of Arizona; 2020. [cited 2020 Sep 24]. Available from: http://hdl.handle.net/10150/641744.

Council of Science Editors:

Thompson AL. Morphine Induced Osteolysis and Hyperalgesia in Models of Traumatic and Pathologic Fracture: Potential for Cannabinoid-Based Therapeutics . [Doctoral Dissertation]. University of Arizona; 2020. Available from: http://hdl.handle.net/10150/641744


Universidad de Chile

13. Rossel Salas, Eduardo David. Modelamiento de sitios de acoplamiento e interacciones proteína-proteína en receptores tipo toll.

Degree: 2012, Universidad de Chile

 Enfermedades como la sepsis, artritis reumatoide, tendinitis, entre otras, están ligadas a respuestas pro-inflamatorias anómalas. En ellas participan citoquinas pro-inflamatorias y factores de transcripción activados… (more)

Subjects/Keywords: Receptores tipo Toll; Proteínas adaptadoras; TLR4

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APA (6th Edition):

Rossel Salas, E. D. (2012). Modelamiento de sitios de acoplamiento e interacciones proteína-proteína en receptores tipo toll. (Thesis). Universidad de Chile. Retrieved from http://repositorio.uchile.cl/handle/2250/112353

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):

Rossel Salas, Eduardo David. “Modelamiento de sitios de acoplamiento e interacciones proteína-proteína en receptores tipo toll.” 2012. Thesis, Universidad de Chile. Accessed September 24, 2020. http://repositorio.uchile.cl/handle/2250/112353.

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

MLA Handbook (7th Edition):

Rossel Salas, Eduardo David. “Modelamiento de sitios de acoplamiento e interacciones proteína-proteína en receptores tipo toll.” 2012. Web. 24 Sep 2020.

Vancouver:

Rossel Salas ED. Modelamiento de sitios de acoplamiento e interacciones proteína-proteína en receptores tipo toll. [Internet] [Thesis]. Universidad de Chile; 2012. [cited 2020 Sep 24]. Available from: http://repositorio.uchile.cl/handle/2250/112353.

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

Council of Science Editors:

Rossel Salas ED. Modelamiento de sitios de acoplamiento e interacciones proteína-proteína en receptores tipo toll. [Thesis]. Universidad de Chile; 2012. Available from: http://repositorio.uchile.cl/handle/2250/112353

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


National University of Ireland – Galway

14. Faiyaz, Rahiman Sharief. Role of LPS/TLR4 and complement signaling in liver regeneration after partial hepatectomy .

Degree: 2018, National University of Ireland – Galway

 Liver regeneration after partial hepatectomy (PH) is a complex process involving an inflammatory response that is followed by the proliferation of both parenchymal and nonparenchymal… (more)

Subjects/Keywords: Regeneration; Liver; TLR4; Complement; Medicine; Physiology

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APA (6th Edition):

Faiyaz, R. S. (2018). Role of LPS/TLR4 and complement signaling in liver regeneration after partial hepatectomy . (Thesis). National University of Ireland – Galway. Retrieved from http://hdl.handle.net/10379/14621

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):

Faiyaz, Rahiman Sharief. “Role of LPS/TLR4 and complement signaling in liver regeneration after partial hepatectomy .” 2018. Thesis, National University of Ireland – Galway. Accessed September 24, 2020. http://hdl.handle.net/10379/14621.

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

MLA Handbook (7th Edition):

Faiyaz, Rahiman Sharief. “Role of LPS/TLR4 and complement signaling in liver regeneration after partial hepatectomy .” 2018. Web. 24 Sep 2020.

Vancouver:

Faiyaz RS. Role of LPS/TLR4 and complement signaling in liver regeneration after partial hepatectomy . [Internet] [Thesis]. National University of Ireland – Galway; 2018. [cited 2020 Sep 24]. Available from: http://hdl.handle.net/10379/14621.

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

Council of Science Editors:

Faiyaz RS. Role of LPS/TLR4 and complement signaling in liver regeneration after partial hepatectomy . [Thesis]. National University of Ireland – Galway; 2018. Available from: http://hdl.handle.net/10379/14621

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


Australian National University

15. Menon, Deepthi. The biological roles of glutathione transferase Omega 1 .

Degree: 2015, Australian National University

 Glutathionylation is the reversible redox modification of protein thiols by disulphide formation with glutathione. Glutathionylation can alter protein structure and activity in response to changes… (more)

Subjects/Keywords: GSTO1-1; TLR4; glutathionylation; LPS; inflammation

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APA (6th Edition):

Menon, D. (2015). The biological roles of glutathione transferase Omega 1 . (Thesis). Australian National University. Retrieved from http://hdl.handle.net/1885/14281

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):

Menon, Deepthi. “The biological roles of glutathione transferase Omega 1 .” 2015. Thesis, Australian National University. Accessed September 24, 2020. http://hdl.handle.net/1885/14281.

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

MLA Handbook (7th Edition):

Menon, Deepthi. “The biological roles of glutathione transferase Omega 1 .” 2015. Web. 24 Sep 2020.

Vancouver:

Menon D. The biological roles of glutathione transferase Omega 1 . [Internet] [Thesis]. Australian National University; 2015. [cited 2020 Sep 24]. Available from: http://hdl.handle.net/1885/14281.

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

Council of Science Editors:

Menon D. The biological roles of glutathione transferase Omega 1 . [Thesis]. Australian National University; 2015. Available from: http://hdl.handle.net/1885/14281

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


Uniwersytet im. Adama Mickiewicza w Poznaniu

16. Chmielewski, Stefan. Integracja szlaków sygnalizacyjnych interferonu gamma i receptora TLR4 w procesie zapalnym naczyń krwionośnych, warunkowana czynnikami transkrypcyjnymi STAT1 i IRF .

Degree: 2014, Uniwersytet im. Adama Mickiewicza w Poznaniu

 Hipoteza zakładała, że w komórkach nienależących do układu immunologicznego, takich jak komórki śródbłonka oraz mięśni gładkich, integracja szlaków sygnalizacyjnych JAK/STAT i TLR4 za pośrednictwem czynnika… (more)

Subjects/Keywords: STAT1; TLR4; IRF; miażdżyca; nadciśnienie; atherosclerosis; hypertension

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APA (6th Edition):

Chmielewski, S. (2014). Integracja szlaków sygnalizacyjnych interferonu gamma i receptora TLR4 w procesie zapalnym naczyń krwionośnych, warunkowana czynnikami transkrypcyjnymi STAT1 i IRF . (Doctoral Dissertation). Uniwersytet im. Adama Mickiewicza w Poznaniu. Retrieved from http://hdl.handle.net/10593/12307

Chicago Manual of Style (16th Edition):

Chmielewski, Stefan. “Integracja szlaków sygnalizacyjnych interferonu gamma i receptora TLR4 w procesie zapalnym naczyń krwionośnych, warunkowana czynnikami transkrypcyjnymi STAT1 i IRF .” 2014. Doctoral Dissertation, Uniwersytet im. Adama Mickiewicza w Poznaniu. Accessed September 24, 2020. http://hdl.handle.net/10593/12307.

MLA Handbook (7th Edition):

Chmielewski, Stefan. “Integracja szlaków sygnalizacyjnych interferonu gamma i receptora TLR4 w procesie zapalnym naczyń krwionośnych, warunkowana czynnikami transkrypcyjnymi STAT1 i IRF .” 2014. Web. 24 Sep 2020.

Vancouver:

Chmielewski S. Integracja szlaków sygnalizacyjnych interferonu gamma i receptora TLR4 w procesie zapalnym naczyń krwionośnych, warunkowana czynnikami transkrypcyjnymi STAT1 i IRF . [Internet] [Doctoral dissertation]. Uniwersytet im. Adama Mickiewicza w Poznaniu; 2014. [cited 2020 Sep 24]. Available from: http://hdl.handle.net/10593/12307.

Council of Science Editors:

Chmielewski S. Integracja szlaków sygnalizacyjnych interferonu gamma i receptora TLR4 w procesie zapalnym naczyń krwionośnych, warunkowana czynnikami transkrypcyjnymi STAT1 i IRF . [Doctoral Dissertation]. Uniwersytet im. Adama Mickiewicza w Poznaniu; 2014. Available from: http://hdl.handle.net/10593/12307


Universitat de Valencia

17. Alfonso Loeches, Silvia. Implicación de los receptores TLR4 en el daño cerebral causado por el consumo de alcohol .

Degree: 2012, Universitat de Valencia

 El abuso de alcohol puede causar daño cerebral y en ciertos casos cursa con neurodegeneración, aunque los mecanismos moleculares de estos efectos se desconocen. El… (more)

Subjects/Keywords: ALCOHOL; DAÑO CEREBRAL; RECEPTORES TLR4; INFLAMASOMA NLRP3

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

APA (6th Edition):

Alfonso Loeches, S. (2012). Implicación de los receptores TLR4 en el daño cerebral causado por el consumo de alcohol . (Doctoral Dissertation). Universitat de Valencia. Retrieved from http://hdl.handle.net/10550/24273

Chicago Manual of Style (16th Edition):

Alfonso Loeches, Silvia. “Implicación de los receptores TLR4 en el daño cerebral causado por el consumo de alcohol .” 2012. Doctoral Dissertation, Universitat de Valencia. Accessed September 24, 2020. http://hdl.handle.net/10550/24273.

MLA Handbook (7th Edition):

Alfonso Loeches, Silvia. “Implicación de los receptores TLR4 en el daño cerebral causado por el consumo de alcohol .” 2012. Web. 24 Sep 2020.

Vancouver:

Alfonso Loeches S. Implicación de los receptores TLR4 en el daño cerebral causado por el consumo de alcohol . [Internet] [Doctoral dissertation]. Universitat de Valencia; 2012. [cited 2020 Sep 24]. Available from: http://hdl.handle.net/10550/24273.

Council of Science Editors:

Alfonso Loeches S. Implicación de los receptores TLR4 en el daño cerebral causado por el consumo de alcohol . [Doctoral Dissertation]. Universitat de Valencia; 2012. Available from: http://hdl.handle.net/10550/24273

18. Machado, Sanseray da Silveira Cruz. Caracterização do eixo imune-pineal: glândula pineal como alvo para lipopolissacarídeo (LPS).

Degree: Mestrado, Fisiologia Geral, 2010, University of São Paulo

O fator de transcrição nuclear kappa B (NFKB), central na resposta inflamatória, é constitutivamente expresso em glândulas pineais de rato. A inibição da translocação nuclear… (more)

Subjects/Keywords: Glândula pineal; Lipopolissacarídeo; Lipopolysaccharide; Melatonin; Melatonina; NFKB; NFKB; Pineal gland; TLR4; TLR4

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APA (6th Edition):

Machado, S. d. S. C. (2010). Caracterização do eixo imune-pineal: glândula pineal como alvo para lipopolissacarídeo (LPS). (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/41/41135/tde-06122010-100938/ ;

Chicago Manual of Style (16th Edition):

Machado, Sanseray da Silveira Cruz. “Caracterização do eixo imune-pineal: glândula pineal como alvo para lipopolissacarídeo (LPS).” 2010. Masters Thesis, University of São Paulo. Accessed September 24, 2020. http://www.teses.usp.br/teses/disponiveis/41/41135/tde-06122010-100938/ ;.

MLA Handbook (7th Edition):

Machado, Sanseray da Silveira Cruz. “Caracterização do eixo imune-pineal: glândula pineal como alvo para lipopolissacarídeo (LPS).” 2010. Web. 24 Sep 2020.

Vancouver:

Machado SdSC. Caracterização do eixo imune-pineal: glândula pineal como alvo para lipopolissacarídeo (LPS). [Internet] [Masters thesis]. University of São Paulo; 2010. [cited 2020 Sep 24]. Available from: http://www.teses.usp.br/teses/disponiveis/41/41135/tde-06122010-100938/ ;.

Council of Science Editors:

Machado SdSC. Caracterização do eixo imune-pineal: glândula pineal como alvo para lipopolissacarídeo (LPS). [Masters Thesis]. University of São Paulo; 2010. Available from: http://www.teses.usp.br/teses/disponiveis/41/41135/tde-06122010-100938/ ;

19. Marinou, Eleni. Μελέτη πολυμορφισμών σε γονίδια που σχετίζονται με τη μη ειδική ανοσιακή απόκριση σε παθήσεις του ανώτερου πεπτικού.

Degree: 2013, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

[…] Ο σκοπός της παρούσας διδακτορικής διατριβής είναι η διερεύνηση πιθανής συμμετοχής των πολυμορφισμών του TLR4 Asp299Gly και Thr399Ile, καθώς και του NOD1 G796A, στη λοίμωξη από ελικοβακτηρίδιο του πυλωρού και στη φλεγμονώδη αντίδραση του γαστρικού βλεννογόνου. […]

Subjects/Keywords: Υποδοχέας TLR4; Υποδοχέας NOD1; Πολυμορφισμοί; Ελικοβακτηρίδιο του Πυλωρού; TLR4; NOD1; Polymorphisms; Helicobacter pylori

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APA (6th Edition):

Marinou, E. (2013). Μελέτη πολυμορφισμών σε γονίδια που σχετίζονται με τη μη ειδική ανοσιακή απόκριση σε παθήσεις του ανώτερου πεπτικού. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/41249

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):

Marinou, Eleni. “Μελέτη πολυμορφισμών σε γονίδια που σχετίζονται με τη μη ειδική ανοσιακή απόκριση σε παθήσεις του ανώτερου πεπτικού.” 2013. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed September 24, 2020. http://hdl.handle.net/10442/hedi/41249.

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

MLA Handbook (7th Edition):

Marinou, Eleni. “Μελέτη πολυμορφισμών σε γονίδια που σχετίζονται με τη μη ειδική ανοσιακή απόκριση σε παθήσεις του ανώτερου πεπτικού.” 2013. Web. 24 Sep 2020.

Vancouver:

Marinou E. Μελέτη πολυμορφισμών σε γονίδια που σχετίζονται με τη μη ειδική ανοσιακή απόκριση σε παθήσεις του ανώτερου πεπτικού. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2013. [cited 2020 Sep 24]. Available from: http://hdl.handle.net/10442/hedi/41249.

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

Council of Science Editors:

Marinou E. Μελέτη πολυμορφισμών σε γονίδια που σχετίζονται με τη μη ειδική ανοσιακή απόκριση σε παθήσεις του ανώτερου πεπτικού. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2013. Available from: http://hdl.handle.net/10442/hedi/41249

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

20. Dubois, Natasha. Caractérisation de la réponse immune induite par un adjuvant comprenant un agoniste du TLR4 dans des modèles murins : Characterization of the immune response to a TLR4-based adjuvant in murine models.

Degree: Docteur es, Immunologie, 2016, Université Paris-Saclay (ComUE)

En 2014 la Tuberculose (TB) à dépassé le VIH comme la principale cause de décès par maladie infectieuse dans le monde soulignant le besoin urgent… (more)

Subjects/Keywords: Adjuvant; Tlr4; Th1; Lymphocytes B; Innée; Adaptative; Adjuvant; Tlr4; Th1; B cells; Innate; Adaptative

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APA (6th Edition):

Dubois, N. (2016). Caractérisation de la réponse immune induite par un adjuvant comprenant un agoniste du TLR4 dans des modèles murins : Characterization of the immune response to a TLR4-based adjuvant in murine models. (Doctoral Dissertation). Université Paris-Saclay (ComUE). Retrieved from http://www.theses.fr/2016SACLS131

Chicago Manual of Style (16th Edition):

Dubois, Natasha. “Caractérisation de la réponse immune induite par un adjuvant comprenant un agoniste du TLR4 dans des modèles murins : Characterization of the immune response to a TLR4-based adjuvant in murine models.” 2016. Doctoral Dissertation, Université Paris-Saclay (ComUE). Accessed September 24, 2020. http://www.theses.fr/2016SACLS131.

MLA Handbook (7th Edition):

Dubois, Natasha. “Caractérisation de la réponse immune induite par un adjuvant comprenant un agoniste du TLR4 dans des modèles murins : Characterization of the immune response to a TLR4-based adjuvant in murine models.” 2016. Web. 24 Sep 2020.

Vancouver:

Dubois N. Caractérisation de la réponse immune induite par un adjuvant comprenant un agoniste du TLR4 dans des modèles murins : Characterization of the immune response to a TLR4-based adjuvant in murine models. [Internet] [Doctoral dissertation]. Université Paris-Saclay (ComUE); 2016. [cited 2020 Sep 24]. Available from: http://www.theses.fr/2016SACLS131.

Council of Science Editors:

Dubois N. Caractérisation de la réponse immune induite par un adjuvant comprenant un agoniste du TLR4 dans des modèles murins : Characterization of the immune response to a TLR4-based adjuvant in murine models. [Doctoral Dissertation]. Université Paris-Saclay (ComUE); 2016. Available from: http://www.theses.fr/2016SACLS131

21. Merle, Nicolas. Mechanisms of complement activation under hemolytic conditions : Mécanismes d’activation du système du complément dans des conditions hémolytiques.

Degree: Docteur es, Immunologie, 2017, Sorbonne Paris Cité

Le système du complément est une cascade de défense immunitaire complexe et étroitement régulée, conduisant à des dommages tissulaires lorsqu’il est suractivé. L’hème, un motif… (more)

Subjects/Keywords: Maladies hémolytiques; Hème; Système du complément; TLR4; Cellule endothéliale; Néphropathie; Hemolytic diseases; Heme; Complement system; TLR4; Endothelial cells; Nephropathy; 616.97

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APA (6th Edition):

Merle, N. (2017). Mechanisms of complement activation under hemolytic conditions : Mécanismes d’activation du système du complément dans des conditions hémolytiques. (Doctoral Dissertation). Sorbonne Paris Cité. Retrieved from http://www.theses.fr/2017USPCB076

Chicago Manual of Style (16th Edition):

Merle, Nicolas. “Mechanisms of complement activation under hemolytic conditions : Mécanismes d’activation du système du complément dans des conditions hémolytiques.” 2017. Doctoral Dissertation, Sorbonne Paris Cité. Accessed September 24, 2020. http://www.theses.fr/2017USPCB076.

MLA Handbook (7th Edition):

Merle, Nicolas. “Mechanisms of complement activation under hemolytic conditions : Mécanismes d’activation du système du complément dans des conditions hémolytiques.” 2017. Web. 24 Sep 2020.

Vancouver:

Merle N. Mechanisms of complement activation under hemolytic conditions : Mécanismes d’activation du système du complément dans des conditions hémolytiques. [Internet] [Doctoral dissertation]. Sorbonne Paris Cité; 2017. [cited 2020 Sep 24]. Available from: http://www.theses.fr/2017USPCB076.

Council of Science Editors:

Merle N. Mechanisms of complement activation under hemolytic conditions : Mécanismes d’activation du système du complément dans des conditions hémolytiques. [Doctoral Dissertation]. Sorbonne Paris Cité; 2017. Available from: http://www.theses.fr/2017USPCB076


University of Toledo Health Science Campus

22. Smith, Laura Ann. Effects of Bacterial Products on Human Blood Leukocytes.

Degree: MSBS, College of Graduate Studies, 2006, University of Toledo Health Science Campus

 Tumor necrosis factor alpha (TNF-alpha) is a protein that can be produced in large amounts by tissue macrophages and monocytes in response to bacterial products.… (more)

Subjects/Keywords: CMLP; TLR4; Sepsis; TNF-alpha

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APA (6th Edition):

Smith, L. A. (2006). Effects of Bacterial Products on Human Blood Leukocytes. (Masters Thesis). University of Toledo Health Science Campus. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=mco1164046331

Chicago Manual of Style (16th Edition):

Smith, Laura Ann. “Effects of Bacterial Products on Human Blood Leukocytes.” 2006. Masters Thesis, University of Toledo Health Science Campus. Accessed September 24, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=mco1164046331.

MLA Handbook (7th Edition):

Smith, Laura Ann. “Effects of Bacterial Products on Human Blood Leukocytes.” 2006. Web. 24 Sep 2020.

Vancouver:

Smith LA. Effects of Bacterial Products on Human Blood Leukocytes. [Internet] [Masters thesis]. University of Toledo Health Science Campus; 2006. [cited 2020 Sep 24]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=mco1164046331.

Council of Science Editors:

Smith LA. Effects of Bacterial Products on Human Blood Leukocytes. [Masters Thesis]. University of Toledo Health Science Campus; 2006. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=mco1164046331


University of Louisville

23. Sengupta, Shuvasree. Revisiting neutrophil responses to toll-like receptor 4 : influence of ligand structures and cellular environments.

Degree: PhD, 2017, University of Louisville

  Neutrophils respond to bacterial LPS through Toll-like receptor 4 (TLR4), which activates or potentiates immune defensive functions and prolongs cell survival. Activation of TLR4(more)

Subjects/Keywords: TLR4; neutrophils; MPLA; accessory cells; survival; CF; Medical Immunology; Medical Microbiology

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APA (6th Edition):

Sengupta, S. (2017). Revisiting neutrophil responses to toll-like receptor 4 : influence of ligand structures and cellular environments. (Doctoral Dissertation). University of Louisville. Retrieved from 10.18297/etd/2772 ; https://ir.library.louisville.edu/etd/2772

Chicago Manual of Style (16th Edition):

Sengupta, Shuvasree. “Revisiting neutrophil responses to toll-like receptor 4 : influence of ligand structures and cellular environments.” 2017. Doctoral Dissertation, University of Louisville. Accessed September 24, 2020. 10.18297/etd/2772 ; https://ir.library.louisville.edu/etd/2772.

MLA Handbook (7th Edition):

Sengupta, Shuvasree. “Revisiting neutrophil responses to toll-like receptor 4 : influence of ligand structures and cellular environments.” 2017. Web. 24 Sep 2020.

Vancouver:

Sengupta S. Revisiting neutrophil responses to toll-like receptor 4 : influence of ligand structures and cellular environments. [Internet] [Doctoral dissertation]. University of Louisville; 2017. [cited 2020 Sep 24]. Available from: 10.18297/etd/2772 ; https://ir.library.louisville.edu/etd/2772.

Council of Science Editors:

Sengupta S. Revisiting neutrophil responses to toll-like receptor 4 : influence of ligand structures and cellular environments. [Doctoral Dissertation]. University of Louisville; 2017. Available from: 10.18297/etd/2772 ; https://ir.library.louisville.edu/etd/2772

24. João Felipe Mota. Efeito da suplementação da vitamina E (a-tocoferol) ou D3 na expressão gênica de TLR4 e adipocinas. Estudos in vivo e in vitro.

Degree: 2011, Universidade Federal de São Paulo

A alta ingestão de dieta hiperlipídica induz obesidade e resistência à insulina, aspectos relacionados à inflamação crônica. A ativação do receptor toll like 4 (TLR4)… (more)

Subjects/Keywords: TLR4; Dieta hiperlipídica; Obesidade; Estresse oxidativo; NUTRICAO; Estresse inflamatório

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APA (6th Edition):

Mota, J. F. (2011). Efeito da suplementação da vitamina E (a-tocoferol) ou D3 na expressão gênica de TLR4 e adipocinas. Estudos in vivo e in vitro. (Thesis). Universidade Federal de São Paulo. Retrieved from http://www.bdtd.unifesp.br/tede//tde_busca/arquivo.php?codArquivo=2096

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):

Mota, João Felipe. “Efeito da suplementação da vitamina E (a-tocoferol) ou D3 na expressão gênica de TLR4 e adipocinas. Estudos in vivo e in vitro.” 2011. Thesis, Universidade Federal de São Paulo. Accessed September 24, 2020. http://www.bdtd.unifesp.br/tede//tde_busca/arquivo.php?codArquivo=2096.

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

MLA Handbook (7th Edition):

Mota, João Felipe. “Efeito da suplementação da vitamina E (a-tocoferol) ou D3 na expressão gênica de TLR4 e adipocinas. Estudos in vivo e in vitro.” 2011. Web. 24 Sep 2020.

Vancouver:

Mota JF. Efeito da suplementação da vitamina E (a-tocoferol) ou D3 na expressão gênica de TLR4 e adipocinas. Estudos in vivo e in vitro. [Internet] [Thesis]. Universidade Federal de São Paulo; 2011. [cited 2020 Sep 24]. Available from: http://www.bdtd.unifesp.br/tede//tde_busca/arquivo.php?codArquivo=2096.

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

Council of Science Editors:

Mota JF. Efeito da suplementação da vitamina E (a-tocoferol) ou D3 na expressão gênica de TLR4 e adipocinas. Estudos in vivo e in vitro. [Thesis]. Universidade Federal de São Paulo; 2011. Available from: http://www.bdtd.unifesp.br/tede//tde_busca/arquivo.php?codArquivo=2096

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

25. Tang, Alan Tien. The Molecular Pathogenesis Of Cerebral Cavernous Malformations.

Degree: 2018, University of Pennsylvania

 Cerebral cavernous malformation (CCM) is a human genetic, cerebrovascular disease that is caused by loss of function mutations in three non-homologous protein coding genes: KRIT1,… (more)

Subjects/Keywords: Cerebral cavernous malformation; Endothelium; Genetics; MEKK3; Microbiome; TLR4; Biology

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APA (6th Edition):

Tang, A. T. (2018). The Molecular Pathogenesis Of Cerebral Cavernous Malformations. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/2696

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):

Tang, Alan Tien. “The Molecular Pathogenesis Of Cerebral Cavernous Malformations.” 2018. Thesis, University of Pennsylvania. Accessed September 24, 2020. https://repository.upenn.edu/edissertations/2696.

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

MLA Handbook (7th Edition):

Tang, Alan Tien. “The Molecular Pathogenesis Of Cerebral Cavernous Malformations.” 2018. Web. 24 Sep 2020.

Vancouver:

Tang AT. The Molecular Pathogenesis Of Cerebral Cavernous Malformations. [Internet] [Thesis]. University of Pennsylvania; 2018. [cited 2020 Sep 24]. Available from: https://repository.upenn.edu/edissertations/2696.

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

Council of Science Editors:

Tang AT. The Molecular Pathogenesis Of Cerebral Cavernous Malformations. [Thesis]. University of Pennsylvania; 2018. Available from: https://repository.upenn.edu/edissertations/2696

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


University of Rochester

26. Croasdell, Amanda; Phipps, Richard P. Specialized Pro-resolving Mediators Act on the Innate Immune System to Attenuate Pulmonary Inflammation.

Degree: PhD, 2016, University of Rochester

 Toxic stimuli, such as cigarette smoke, air pollution, and infection, can disrupt the normal functions of immune cells, resulting in dysregulated and excessive inflammatory responses.… (more)

Subjects/Keywords: Macrophages; Specialized pro-solving mediators; Resolvins; TLR4; Cigarette smoke; Lung infection

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APA (6th Edition):

Croasdell, Amanda; Phipps, R. P. (2016). Specialized Pro-resolving Mediators Act on the Innate Immune System to Attenuate Pulmonary Inflammation. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/31502

Chicago Manual of Style (16th Edition):

Croasdell, Amanda; Phipps, Richard P. “Specialized Pro-resolving Mediators Act on the Innate Immune System to Attenuate Pulmonary Inflammation.” 2016. Doctoral Dissertation, University of Rochester. Accessed September 24, 2020. http://hdl.handle.net/1802/31502.

MLA Handbook (7th Edition):

Croasdell, Amanda; Phipps, Richard P. “Specialized Pro-resolving Mediators Act on the Innate Immune System to Attenuate Pulmonary Inflammation.” 2016. Web. 24 Sep 2020.

Vancouver:

Croasdell, Amanda; Phipps RP. Specialized Pro-resolving Mediators Act on the Innate Immune System to Attenuate Pulmonary Inflammation. [Internet] [Doctoral dissertation]. University of Rochester; 2016. [cited 2020 Sep 24]. Available from: http://hdl.handle.net/1802/31502.

Council of Science Editors:

Croasdell, Amanda; Phipps RP. Specialized Pro-resolving Mediators Act on the Innate Immune System to Attenuate Pulmonary Inflammation. [Doctoral Dissertation]. University of Rochester; 2016. Available from: http://hdl.handle.net/1802/31502


Boston University

27. LeBlanc III, Robert H. The role of microglia and Toll-like Receptor-4 in neuronal apoptosis in a subarachnoid hemorrhage model.

Degree: MS, Medical Sciences, 2014, Boston University

 BACKGROUND A subarachnoid hemorrhage (SAH) is a bleed into the subarachnoid space surrounding the brain. This disease affects roughly 30,000 Americans each year and approximately… (more)

Subjects/Keywords: Neurosciences; Microglia; Neuroinflammation; Toll-like Receptor-4 (TLR4); Subarachnoid hemorrhage

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APA (6th Edition):

LeBlanc III, R. H. (2014). The role of microglia and Toll-like Receptor-4 in neuronal apoptosis in a subarachnoid hemorrhage model. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/15357

Chicago Manual of Style (16th Edition):

LeBlanc III, Robert H. “The role of microglia and Toll-like Receptor-4 in neuronal apoptosis in a subarachnoid hemorrhage model.” 2014. Masters Thesis, Boston University. Accessed September 24, 2020. http://hdl.handle.net/2144/15357.

MLA Handbook (7th Edition):

LeBlanc III, Robert H. “The role of microglia and Toll-like Receptor-4 in neuronal apoptosis in a subarachnoid hemorrhage model.” 2014. Web. 24 Sep 2020.

Vancouver:

LeBlanc III RH. The role of microglia and Toll-like Receptor-4 in neuronal apoptosis in a subarachnoid hemorrhage model. [Internet] [Masters thesis]. Boston University; 2014. [cited 2020 Sep 24]. Available from: http://hdl.handle.net/2144/15357.

Council of Science Editors:

LeBlanc III RH. The role of microglia and Toll-like Receptor-4 in neuronal apoptosis in a subarachnoid hemorrhage model. [Masters Thesis]. Boston University; 2014. Available from: http://hdl.handle.net/2144/15357


University of South Carolina

28. Kimono, Diana Agnes. Microbiome Targeted Therapies in Gulf War Illness.

Degree: PhD, Environmental Health Sciences, 2020, University of South Carolina

  Gulf war illness (GWI) is a chronic multisymptomatic disorder affecting about 30% of veterans of the 1990-1991 Persian Gulf war. Affected veterans complain of… (more)

Subjects/Keywords: Environmental Health; Akkermasia muciniphila; BDNF; Butyrate; Gulf war illness; Microbiome; TLR4

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

APA (6th Edition):

Kimono, D. A. (2020). Microbiome Targeted Therapies in Gulf War Illness. (Doctoral Dissertation). University of South Carolina. Retrieved from https://scholarcommons.sc.edu/etd/5812

Chicago Manual of Style (16th Edition):

Kimono, Diana Agnes. “Microbiome Targeted Therapies in Gulf War Illness.” 2020. Doctoral Dissertation, University of South Carolina. Accessed September 24, 2020. https://scholarcommons.sc.edu/etd/5812.

MLA Handbook (7th Edition):

Kimono, Diana Agnes. “Microbiome Targeted Therapies in Gulf War Illness.” 2020. Web. 24 Sep 2020.

Vancouver:

Kimono DA. Microbiome Targeted Therapies in Gulf War Illness. [Internet] [Doctoral dissertation]. University of South Carolina; 2020. [cited 2020 Sep 24]. Available from: https://scholarcommons.sc.edu/etd/5812.

Council of Science Editors:

Kimono DA. Microbiome Targeted Therapies in Gulf War Illness. [Doctoral Dissertation]. University of South Carolina; 2020. Available from: https://scholarcommons.sc.edu/etd/5812


Universiteit Utrecht

29. van den Borne, P. Changing blood flow in peripheral artery disease.

Degree: 2014, Universiteit Utrecht

 Cardiovascular disease (CVD) is the leading cause of death globally and it is predicted this will remain to increase throughout 2030 to an estimated 23,3… (more)

Subjects/Keywords: Arteriogenesis; inflammation; CXCL10; CD200-CD200R; TLR4; exosomes; LTB4; atherosclerosis; AAA

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

APA (6th Edition):

van den Borne, P. (2014). Changing blood flow in peripheral artery disease. (Doctoral Dissertation). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/294660

Chicago Manual of Style (16th Edition):

van den Borne, P. “Changing blood flow in peripheral artery disease.” 2014. Doctoral Dissertation, Universiteit Utrecht. Accessed September 24, 2020. http://dspace.library.uu.nl:8080/handle/1874/294660.

MLA Handbook (7th Edition):

van den Borne, P. “Changing blood flow in peripheral artery disease.” 2014. Web. 24 Sep 2020.

Vancouver:

van den Borne P. Changing blood flow in peripheral artery disease. [Internet] [Doctoral dissertation]. Universiteit Utrecht; 2014. [cited 2020 Sep 24]. Available from: http://dspace.library.uu.nl:8080/handle/1874/294660.

Council of Science Editors:

van den Borne P. Changing blood flow in peripheral artery disease. [Doctoral Dissertation]. Universiteit Utrecht; 2014. Available from: http://dspace.library.uu.nl:8080/handle/1874/294660

30. 蔡, 君柔. A shorter variant of BTBD2 as a novel negative regulator of IRF-associated signalling : IRF-依存性シグナル伝達の抑制因子としてのBTBD2(新規)バリアント.

Degree: 博士(医学), 2013, Nagasaki University / 長崎大学

 IRF family members are important transcription factors involved in TLR and RLR signalling and type I IFN expression. Many cellular factors are reportedly associated with… (more)

Subjects/Keywords: BTBD2; Interferon regulatory factors(IRFs); Toll-like Receptor 4(TLR4)

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

APA (6th Edition):

蔡, . (2013). A shorter variant of BTBD2 as a novel negative regulator of IRF-associated signalling : IRF-依存性シグナル伝達の抑制因子としてのBTBD2(新規)バリアント. (Thesis). Nagasaki University / 長崎大学. Retrieved from http://hdl.handle.net/10069/35432

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):

蔡, 君柔. “A shorter variant of BTBD2 as a novel negative regulator of IRF-associated signalling : IRF-依存性シグナル伝達の抑制因子としてのBTBD2(新規)バリアント.” 2013. Thesis, Nagasaki University / 長崎大学. Accessed September 24, 2020. http://hdl.handle.net/10069/35432.

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

MLA Handbook (7th Edition):

蔡, 君柔. “A shorter variant of BTBD2 as a novel negative regulator of IRF-associated signalling : IRF-依存性シグナル伝達の抑制因子としてのBTBD2(新規)バリアント.” 2013. Web. 24 Sep 2020.

Vancouver:

蔡 . A shorter variant of BTBD2 as a novel negative regulator of IRF-associated signalling : IRF-依存性シグナル伝達の抑制因子としてのBTBD2(新規)バリアント. [Internet] [Thesis]. Nagasaki University / 長崎大学; 2013. [cited 2020 Sep 24]. Available from: http://hdl.handle.net/10069/35432.

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

Council of Science Editors:

蔡 . A shorter variant of BTBD2 as a novel negative regulator of IRF-associated signalling : IRF-依存性シグナル伝達の抑制因子としてのBTBD2(新規)バリアント. [Thesis]. Nagasaki University / 長崎大学; 2013. Available from: http://hdl.handle.net/10069/35432

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

[1] [2] [3] [4] [5]

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