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Готові списки джерел за темами / Inflammation

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Добірка наукової літератури з теми "Inflammation"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 16 листопада 2024

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Статті в журналах з теми "Inflammation"

1

Vijayendranath, Nayak S., Gunasheela S, Karthik M, and Hegde Aparna. "Healing by Inflammation - Prolotherapy." Case Reports in Dental Science 1, no. 1 (June 30, 2020): 9–14. http://dx.doi.org/10.46619/crds.2020.1-1003.

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Temporomandibular disorder (TMD) is a collective term used to describe a group of disorders related to temporomandibular region. It’s considered to be the common cause for orofacial pain. With the advancement of research, prolotherapy is considered to be the one of the treatment modalities to treat TMD, when the conservative management fails.

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2

J, Mancini-Filho. "Natural Antioxidants and Tissue Inflammation." Bioequivalence & Bioavailability International Journal 7, no. 2 (July 4, 2023): 1–3. http://dx.doi.org/10.23880/beba-16000203.

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The phenolic compounds present in food cover a wide range of structures that have different biological properties. Highlighting its antioxidant properties and the presence mainly of spices, herbs and other foods. Some compounds present in spices can be listed for their antioxidant activity, such as: cloves have eugenol, pinene in their composition, cinnamon also has eugenol, limonene, pinene, catechins and other phenolic compounds in their composition, anise has pinene, rutin, apigenin, oregano has apigenin, quercecin, rosmarinic, caffeic, p-coumaric acids, and others. Rosemary presents the carnosic, rosmarinic, caffeic and hydroxycinnamic. The tissue inflammatory process normally starts with the presence of free radicals that are associated with the oxidative process activated by reactive oxygen species represented by peroxides, superoxide ion, presence of hydroxyl radical, singlet oxygen, among others. The highlighted phenolic compounds have in their structure one or more hydroxyls that have the property of donating a hydrogen atom to free radical structures, which can block the triggering of the oxidative process and thus inflammation.

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3

Djaldetti, Meir. "Piperine – An Immunomodulator and Inflammation Mitigator." Journal of Clinical and Laboratory Research 2, no. 5 (June 3, 2021): 01–04. http://dx.doi.org/10.31579/2768-0487/027.

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Black pepper, one of the most widespread spices, gained the entitlement “King of spices” founded on its peculiar pungent test and therapeutic properties, both owed to its active alkaloid - piperine. Mounting evidence indicates that piperine possesses immunomodulatory and therapeutic activities. The aim of this mini review was to summarize the role of piperine in abolishing inflammation, its part in the immune activity of peripheral blood mononuclear- and a number of other cells, its capacity to elicit production of inflammatory cytokines and its function as a synergist endorsing the beneficial therapeutic effect of conventional anti-inflammatory drugs.

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4

H, Khazaei. "Overview of Orbital Inflammation/Unmet Needs." Open Access Journal of Ophthalmology 7, no. 2 (July 1, 2022): 1–6. http://dx.doi.org/10.23880/oajo-16000245.

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Diseases of the orbit and periorbital eye tissues manifest in a wide variety of clinical presentations. Space occupying lesions in the orbit include infections, inflammations, vascular malformations, and malignancies. The significant variation in presentations is due to the complex anatomy of the orbit and the heterogeneous nature of the multiple disease processes that present themselves as orbital inflammatory processes. Additionally, although specific disease entities often show similar patterns of orbital tissue involvement, there is still a spectrum of clinical presentations within disease processes, which furthermore overlap with other inflammatory etiologies. This heterogeneity creates a significant challenge in determining specific diagnoses and subsequently instituting timely medical and surgical management of patients with orbital inflammation. Despite advances in imaging, physical examination, and laboratory tests, a biopsy is often needed for diagnosis and to guide treatment. Unfortunately, the biopsy is too often read as non-specific or idiopathic inflammation, a term that gives minimal guidance to the patient or to the clinician. There is clearly a need for developing more specific and sensitive clinical diagnostic testing.

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5

Narula, Jagat, and Eloisa Arbustini. "Inflammation, Superadded Inflammation, and Out-of-Proportion Inflammation in Atherosclerosis." JAMA Cardiology 3, no. 10 (October 1, 2018): 912. http://dx.doi.org/10.1001/jamacardio.2018.2760.

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6

Ado, A. A. "Allergic inflammation." Kazan medical journal 29, no. 11-12 (January 12, 2022): 966–83. http://dx.doi.org/10.17816/kazmj90287.

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Relatively not so long ago, the doctrine of the inflammatory response was enriched by the concept of "allergic inflammation" (von Pirquet 1907-08). However, the subsequent experimental and clinical study of these inflammatory forms has deepened our understanding of the pathogenesis of each inflammatory reaction so much that it can rightfully be called a stage in the new history of inflammation. From time immemorial, the doctor knew the variety of forms of development and course of inflammation. The construction of these numerous modifications of inflammation in most cases remained unclear. In his practice, each doctor encounters forms of extremely rapidly developing inflammation. Notae verae inflammationis is especially prominent in these cases. Tissue lesions end in necrosis. This one symptom already indicates the rapid development of this form of inflammation. But the rate of its formation can also be registered when studying other inflammatory signs preceding necrosis. A characteristic feature of the development of a normal skin test in an allergic person is the appearance within the first half an hour, literally "before the eyes" of the observer, hyperemia, edema on the periphery of the injection and even infiltration at the injection site.

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7

Alderton, Gemma, and Seth Thomas Scanlon. "Inflammation." Science 374, no. 6571 (November 26, 2021): 1068–69. http://dx.doi.org/10.1126/science.abn1721.

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8

Miyamoto, Terumasa. "Inflammation." Ensho 13, no. 2 (1993): 99–100. http://dx.doi.org/10.2492/jsir1981.13.99.

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Miyamoto, Terumasa. "Inflammation." Ensho 9, no. 5 (1989): 357. http://dx.doi.org/10.2492/jsir1981.9.357.

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10

Lederer, Katy. "Inflammation." Colorado Review 43, no. 3 (2016): 128–30. http://dx.doi.org/10.1353/col.2016.0094.

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Дисертації з теми "Inflammation"

1

Lawrence, Clifford M. "Anthralin inflammation." Thesis, University of Newcastle Upon Tyne, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390318.

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2

Warke, T. J. "Childhood airways inflammation." Thesis, Queen's University Belfast, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268984.

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3

Jatta, Ken. "Inflammation in Atherosclerosis." Doctoral thesis, Örebro : Universitetsbiblioteket, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-478.

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4

Gilroy, Derek William. "Cyclooxygenase 2 inflammation." Thesis, Queen Mary, University of London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265077.

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5

Limb, G. A. "Lymphokines in inflammation." Thesis, Brunel University, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.373086.

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6

Peters, Caren Lorraine. "Hypoxia in inflammation." Thesis, University of Bath, 2003. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426151.

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7

Sanchez, Moral Lidia. "Role of ZEB1 in adenoma formation, inflammation and inflammation-driven carcinoma." Doctoral thesis, Universitat de Barcelona, 2019. http://hdl.handle.net/10803/667993.

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Multiple studies have highlighted the role of ZEB1 as critical regulator of tumor progression through the regulation of different hallmarks of cancer beyond the induction of EMT. The general aim of this dissertation is to characterize new potential mechanisms that regulate oncogenic transformation in colorectal carcinoma. The specific objectives of this dissertation are: 1. To identify new roles and targets of the transcription factor ZEB1 as a mediator of Wnt-induced intestinal adenoma formation. 2. To characterize ZEB1’s mechanism of action as a transcriptional regulator in inflammation and inflammation-induced carcinomas. To address these goals, a wide number of reagents and techniques have been used, namely, human samples of adenomas and CRC, CRC cell lines whose expression for different genes has been manipulated by overexpression or RNA interference, high throughput techniques (RNA and microbiota sequencing) and transgenic mouse models (ApcMin/+, Zeb1+/- and Mpg-/-). We found that ZEB1 expression in epithelial cells from intestinal adenomas increases adenoma formation and decreases life span in the ApcMin/+ mouse model, which is supported by decreased senescence and apoptosis in ApcMin/+/Zeb1+/+ mice when compared to ApcMin/+/Zeb1+/- counterparts. ZEB1 is both a target and a mediator of the Wnt signaling pathway. Here we provide two new mechanisms by which ZEB1 modulates the Wnt pathway through the regulation of AXIN2 and DACT2 expression. In addition, we found that ZEB1 promotes lipid accumulation in adenomas and colorectal cancer cell lines through the repression of the ATGL/PPARα/PGC-1α axis, which is critical for the degradation of lipid droplets. Besides, we show that ZEB1 is upregulated in the epithelial cells of ulcerative colitis patients and of mouse models of colitis, where its expression promotes intestinal inflammation and inflammatory tumorigenesis. ZEB1 exerts these functions, at least in part, through the increase of DNA damage and the inhibition of the MPG glycosylase, which is involved in DNA damage repair. Moreover, ZEB1 expression in CRC cells stimulates the production of ROS and IL1-β by macrophages which, in turn, reduce MPG expression in CRC cells. Altogether, from the results presented in this dissertation, it can be concluded that: 1. ZEB1 represses senescence and apoptosis during Wnt-induced intestinal adenoma formation. 2. ZEB1 potentiates Wnt signaling in intestinal adenomas through the activation of AXIN2 and the repression of DACT2. 3. ZEB1 induces accumulation of lipids in intestinal cells through Wnt-dependent repression of ATGL, PPARα and PGC-1α. 4. ZEB1 is upregulated in the epithelial cells of UC patients and of mouse models of colitis, where its expression promotes intestinal inflammation and inflammation-driven tumorigenesis. 5. ZEB1 promotes colitis and inflammation-driven CRC through the induction of DNA damage and the inhibition of the DNA repair glycosylase MPG. 6. ZEB1 expression in epithelial cells stimulates the production of ROS and IL1-β by macrophages that, in turn, reduce MPG expression in CRC cells. These results establish ZEB1 as an important regulator of intestinal adenoma formation, and describe ZEB1 as a mediator of inflammation and inflammation-driven carcinogenesis, setting ZEB1 as a potential therapeutic target in colorectal carcinoma.
Múltiples estudis han destacat el paper de ZEB1 com a regulador essencial de la progressió tumoral a través de la regulació de varis dels trets distintius del càncer més enllà de la inducció de la transició epiteli-mesènquima (EMT). Els resultats presentats en aquesta tesi indiquen que ZEB1 regula la formació de tumors intestinals des de les fases més inicials, i descriuen ZEB1 com un important inductor de colitis i de càncer de colon induït per inflamació. Hem trobat que l’expressió de ZEB1 en cèl·lules epitelials d’adenomes intestinals augmenta la formació d’adenomes i redueix la supervivència en el model de ratolí ApcMin/+. A més, en comparació amb els ratolins ApcMin/+/Zeb1+/+, els ratolins ApcMin/+/Zeb1+/- presenten més senescència i apoptosi. ZEB1 és tant una diana com un mediador de la via de senyalització Wnt. Els nostres resultats proporcionen dos nous mecanismes pels quals ZEB1 interacciona amb la via Wnt a través de la regulació de l’expressió d’AXIN2 i DACT2. Addicionalment, hem observat que ZEB1 promou l’acumulació de lípids a través de la repressió de l’eix ATGL/PPARα/PGC-1α, el qual té un paper crític en la degradació de les vesícules lipídiques. En paral·lel, hem demostrat que ZEB1 es troba sobreexpressat en cèl·lules epitelials de pacients de colitis ulcerativa i en models murins de colitis, on la seva expressió promou la inflamació intestinal i la tumorogènesi derivada de la inflamació. ZEB1 exerceix aquestes funcions, al menys en part, a través de l’augment de les lesions en l’ADN i la inhibició de MPG, una glicosilasa implicada en la reparació de les lesions en l’ADN. A més, l’expressió de ZEB1 en les cèl·lules de càncer de colon estimula la producció d’espècies reactives d’oxigen (ROS) i IL-1β per part dels macròfags que, a la vegada, redueix els nivells de MPG en les cèl·lules de càncer de colon. En conjunt, aquests resultats estableixen ZEB1 com un element regulador de la formació d’adenomes intestinals, així com un mediador de la inflamació i la carcinogènesi derivada de la inflamació, confirmant ZEB1 com a potencial diana terapèutica en càncer colorectal.

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8

Levick, Scott P. "Inflammation and cardiovascular remodelling /." [St. Lucia, Qld.], 2005. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19090.pdf.

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9

Blomgran, Parmis. "Inflammation and tendon healing." Doctoral thesis, Linköpings universitet, Avdelningen för Kirurgi, Ortopedi och Onkologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-142349.

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Tendons heal through three different overlapping phases; the inflammatory, proliferative and remodeling phase. Many studies have investigated what factors influence healing of tendons. However, little was known about inflammation and the immune cells present during Achilles tendon healing by the time this thesis started. We developed a flow cytometry method for our rat model of tendon healing, which enabled us to study different leukocyte subpopulations during Achilles tendon healing. The general aim of this thesis was to understand more about inflammation and the immune cell populations present during tendon healing and how the immune cell composition changes during normal tendon healing. Moreover, we investigated how different factors that are known to influence tendon healing affected the composition of the immune cell population. First, we described the immune cells during the time course of tendon healing focusing on different subpopulations of macrophages and T cells. Then, we studied how these cells were influenced by reduced mechanical loading. Mechanical loading prolonged the presence of M1 macrophages and delayed the switch to regulatory T cells and M2 macrophages compared to reduced mechanical loading. Next, the effect of nonsteroidal anti-inflammatory drugs (NSAIDs) on the leukocyte composition revealed that, even though NSAIDs influence the mechanical properties of healing tendon, this effect was not mediated via changes in the leukocyte sub-populations during early and mid-time tendon healing. Further, the effect of corticosteroids during the inflammatory and remodeling phases of tendon healing was an improved healing of tendons and a reduction of CD8a T cells when corticosteroid was administered after the inflammatory phase. Lastly, we investigated if impairment of tendon healing by NSAIDs was related to mechanotransduction or microdamage during mechanical loading and showed that NSAIDs impair tendon healing by reducing the response to microdamage. In conclusion, these studies show that inflammation plays an important role during Achilles tendon healing, and factors that influence healing can also alter the presence or polarization of immune cell populations.

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10

Eustace, Andrew David. "Syndecan 3 and inflammation." Thesis, University of Bristol, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.720843.

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Книги з теми "Inflammation"

1

Clausen, Björn E., and Jon D. Laman, eds. Inflammation. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6786-5.

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2

Górski, Andrzej, Hubert Krotkiewski, and Michał Zimecki, eds. Inflammation. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-015-9702-9.

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3

Pierangelo, Geppetti, and Holzer, Peter, Mag. rer. nat. Dr. phil., eds. Neurogenic inflammation. Boca Raton: CRC Press, 1996.

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4

Winyard, Paul G., and Derek A. Willoughby. Inflammation Protocols. New Jersey: Humana Press, 2003. http://dx.doi.org/10.1385/1592593747.

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5

Miyasaka, Masayuki, and Kiyoshi Takatsu, eds. Chronic Inflammation. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56068-5.

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6

Zierhut, Manfred, Carlos Pavesio, Shigeaki Ohno, Fernando Orefice, and Narsing A. Rao, eds. Intraocular Inflammation. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-540-75387-2.

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7

Man, Francis, and Simon J. Cleary, eds. Imaging Inflammation. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-23661-7.

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8

Challem, Jack. The Inflammation Syndrome. New York: John Wiley & Sons, Ltd., 2003.

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9

Rogers, Duncan F., and Louise E. Donnelly. Human Airway Inflammation. New Jersey: Humana Press, 2001. http://dx.doi.org/10.1385/1592591515.

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10

Seltzer, Samuel. Inflammation: An update. Chicago, Ill. (211 E. Chicago Ave., Suite 1501, Chicago 60611): Research and Education Foundation of the American Association of Endodontists, 1990.

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Частини книг з теми "Inflammation"

1

Bährle-Rapp, Marina. "Inflammation, auch: Inflammatio." In Springer Lexikon Kosmetik und Körperpflege, 279. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-71095-0_5191.

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Citerio, G., C. Giussani, Hugo Sax, Didier Pittet, Xiaoyan Wen, John A. Kellum, Angela M. Mills, et al. "Inflammation." In Encyclopedia of Intensive Care Medicine, 1230. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_3166.

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3

Hayashi, Nariyuki, and Dalton W. Dietrich. "Inflammation." In Brain Hypothermia Treatment, 28–29. Tokyo: Springer Japan, 2004. http://dx.doi.org/10.1007/978-4-431-53953-7_18.

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4

Elgazzar, Abdelhamid H., and Ismet Sarikaya. "Inflammation." In Nuclear Medicine Companion, 243–56. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-76156-5_9.

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Elgazzar, Abdelhamid H. "Inflammation." In Synopsis of Pathophysiology in Nuclear Medicine, 41–57. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-03458-4_4.

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6

Collins, Caitlin, Ellie Tzima, and Cam Patterson. "Inflammation." In Atherosclerosis, 43–52. Hoboken, NJ: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118828533.ch4.

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7

Neumann, Harald. "Inflammation." In Neuroprotection, 173–90. Weinheim, FRG: Wiley-VCH Verlag GmbH & Co. KGaA, 2005. http://dx.doi.org/10.1002/3527603867.ch9.

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Johnson, Susan K. "Inflammation." In Encyclopedia of Clinical Neuropsychology, 1803–4. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_561.

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9

Santiago, Jonas Francisco Y. "Inflammation." In Positron Emission Tomography with Computed Tomography (PET/CT), 35–48. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-05518-3_5.

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Rohleder, Nicolas, and Jutta M. Wolf. "Inflammation." In Encyclopedia of Behavioral Medicine, 1187–89. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_25.

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Тези доповідей конференцій з теми "Inflammation"

1

"Chronic Inflammation." In INTERNATIONAL CONFERENCE ON BIOLOGICAL RESEARCH AND APPLIED SCIENCE. Jinnah University for Women, 2024. http://dx.doi.org/10.37962/ibras/2024/105.

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Wang, Dingzhi, Lixia Guo, Wei Ning та Raymond N. DuBois. "Abstract A43: PPARδ promotes colonic inflammation and inflammation-associated tumorigenesis". У Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Oct 22-25, 2011; Boston, MA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1940-6207.prev-11-a43.

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Kwon, Byungsuk, and Hong Rae Cho. "CD137 reverse signaling in sterile inflammation: CD137L in sterile tissue inflammation." In 2012 7th International Forum on Strategic Technology (IFOST). IEEE, 2012. http://dx.doi.org/10.1109/ifost.2012.6357821.

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Kramer, Violet, Fan Chen, Daisuke Nonaka, and Angeliki Kazeros. "Paraneoplastic Pulmonary Eosinophilic Inflammation." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3995.

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Yousuf, Ahmed Javid, Gita Parekh, Sarah Parker, Sara Glover, Jo Finch, Liesl Carr, Vijay Mistry, et al. "EXACT-PRO correlates with FEV1 and systemic inflammation but not airway inflammation." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa2692.

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Visser, Tjaakje, Mirrin Dorresteijn, Anky Koenderman, Luke Leenen, Peter Pickkers, and Leo Koenderman. "Inhibition Of Acute Inflammation By C1-esteraseinhibitor In A Human Inflammation Model." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6034.

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Ford, M. L., B. W. Lewis, K. Heyob, T. Harshman, M. Guerau-De-Arellano, and R. D. Britt. "CD38 Promotes Th17 Inflammation in Aged Mice With Severe Allergic Airway Inflammation." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a2810.

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Machado, Luiza, Camila Santos, Bianca Leonardi, Andréia Rocha, Igor Fontana, Bruna Bellaver, Gianina Venturin, et al. "ACUTE PERIPHERAL INFLAMMATION IMPACT ON CEREBRAL GLUCOSE METABOLISM." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda072.

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Background: Neuroinflammation is a phenomenon already described in Alzheimer’s disease (AD). However, the effect of peripheral inflammation in AD is less understood. We recently demonstrated that severe sepsis causes acute brain metabolic disturbances. Nevertheless, whether mild acute peripheral inflammation affects brain metabolism remains unclear. Objective: We aimed at investigating the impact of mild acute peritonitis on glucose brain metabolism. Methods: Adult male wistar rats (n=6, per group) received a single intraperitoneal injection of 500 ml of carrageenan (CG, 500 µg of carrageenan i.p.) or saline (CO). Brain glucose metabolism was assessed using (18F) FDG-PET 4h after i.p. injections, which represents the first peak of inflammation. The peripheral inflammatory process was evaluated by analyzing the peritoneal lavage in a flow cytometer 48h after the injections, during the second peak of inflammation. Results: The CG animals presented a 5-fold increase in macrophages numbers (p0,05). However, carrageenan-induced inflammation did not cause acute changes in brain glucose metabolism (p>0,05). Conclusion: Mild acute peripheral inflammation does not change brain glucose metabolism. Further evaluations aiming to investigate long-term consequences of sustained mild inflammation are needed.

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Wang, Dingzhi, Lixia Guo, Wei Ning, Hong Wu, Rupesh Chaturved, Keith Wilson, and Raymond N. DuBois. "Abstract 1519: Peroxisome proliferator-activated receptor ≤ promotes colonic inflammation and inflammation-associated tumorigenesis." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1519.

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Latorre, Manuela, Chiara Baldini, Federica Novelli, Federico Dente, S. Grosso, P. Della Rossa, Silvana Cianchetti, Stefano Bombardieri, and Pierluigi Paggiaro. "Airway Inflammation And Systemic Inflammation In Churg-Strauss Syndrome: Two Faces Of Disease." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4207.

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Звіти організацій з теми "Inflammation"

1

Krueger, Lucas A., Donald C. Beitz, Robert L. Stuart, and Judith R. Stabel. Early Inflammation Disorder in Neonatal Calves. Ames (Iowa): Iowa State University, January 2015. http://dx.doi.org/10.31274/ans_air-180814-1290.

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Bach, Ronald R. Gulf War Illness Inflammation Reduction Trial. Fort Belvoir, VA: Defense Technical Information Center, October 2015. http://dx.doi.org/10.21236/ada626080.

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Alwagdani, Abdullah. Review Of mPGES-1 Inhibitors Based On The Benzoxazole And Its Isostere Scaffold For The Treatment Of Inflammatory Diseases. University of Tennessee Health Science Center, June 2024. http://dx.doi.org/10.21007/com.lsp.2024.0021.

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The vital role of the prostanoid pathway in inflammation, pain, cancer, Alzheimer’s and many other diseases has attracted the drug discovery community to discover targets for therapeutic development. Although existing non-steroidal anti-inflammatory drugs (NSAIDs) inhibiting cyclooxygenases (COX) are widely used, the side effects of these NSAIDs limit the ling time medication. Microsomal prostaglandin E synthase-1 (mPGES-1) is an attractive target that is overexpressed during inflammations, and it could be a safe alternative to NSAIDs for treating inflammatory diseases.Since the discovery of mPGES-1 in 1997, many inhibitors have been developed since 2001. Only a few compounds were able to make it to clinical trials, and only two molecules are in phase II clinical trials. Among the mPGES-1 inhibitors, benzoxazole, indole, and benzimidazole are the most explored chemical scaffolds, especially benzimidazole. One of the two inhibitors in the clinical trials is based on this scaffold. Here, we provide a review of mPGES-1's role in inflammation and inhibitors based on these scaffolds that are reported in the literature.

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Beal, M. F. Bioenergetic Approaches and Inflammation in MPTP Toxicity. Fort Belvoir, VA: Defense Technical Information Center, September 2005. http://dx.doi.org/10.21236/ada439263.

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Jerde, Travis J. Phosphoinositide-Driven Epithelial Proliferation in Prostatic Inflammation. Fort Belvoir, VA: Defense Technical Information Center, January 2008. http://dx.doi.org/10.21236/ada485294.

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Beal, M. F. Bioenergetic Approaches and inflammation of MPTP Toxicity. Fort Belvoir, VA: Defense Technical Information Center, September 2008. http://dx.doi.org/10.21236/ada488708.

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Beal, M. F. Bioenergetic Approaches and Inflammation of MPTP Toxicity. Fort Belvoir, VA: Defense Technical Information Center, September 2009. http://dx.doi.org/10.21236/ada508622.

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8

Jerde, Travis J., and Wade Bushman. Phosphoinositide-Driven Epithelial Proliferation in Prostatic Inflammation. Fort Belvoir, VA: Defense Technical Information Center, April 2009. http://dx.doi.org/10.21236/ada510023.

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Durbin, Megan C. The Effects of Exercise on Brain Inflammation. Fort Belvoir, VA: Defense Technical Information Center, June 2010. http://dx.doi.org/10.21236/ada524163.

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Broaddus, V. C. Role of Macrophage-induced Inflammation in Mesothelioma. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada582550.

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