Готові списки джерел за темами / Inflammatory component

Добірка наукової літератури з теми "Inflammatory component"

Автор: Grafiati

Опубліковано: 7 липня 2024

Оновлено: 7 липня 2024

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Статті в журналах з теми "Inflammatory component":

Heymann, Warren R. "The inflammatory component of androgenetic alopecia." Journal of the American Academy of Dermatology 86, no. 2 (February 2022): 301–2. http://dx.doi.org/10.1016/j.jaad.2021.11.013.

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Pantanowitz, Liron, Ashlee V. Moses, and Bruce J. Dezube. "The inflammatory component of Kaposi sarcoma." Experimental and Molecular Pathology 87, no. 2 (October 2009): 163–65. http://dx.doi.org/10.1016/j.yexmp.2009.07.001.

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JAYSON, M. I. V. "THE INFLAMMATORY COMPONENT OF MECHANICAL BACK PROBLEMS." Rheumatology 25, no. 2 (1986): 210–13. http://dx.doi.org/10.1093/rheumatology/25.2.210.

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Abell, E., and A. M. Kligman. "The Inflammatory Component of Male Pattern Alopecia." American Journal of Dermatopathology 11, no. 3 (June 1989): 287. http://dx.doi.org/10.1097/00000372-198906000-00023.

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Nakamura, M., and S. H. Ferreira. "A peripheral sympathetic component in inflammatory hyperalgesia." European Journal of Pharmacology 135, no. 2 (March 1987): 145–53. http://dx.doi.org/10.1016/0014-2999(87)90606-6.

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Prokop, Laurel Derks. "Isotretinoin: Possible Component Cause of Inflammatory Bowel Disease." American Journal of Gastroenterology 94, no. 9 (September 1999): 2568. http://dx.doi.org/10.1111/j.1572-0241.1999.02568.x.

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Prokop, L. "Isotretinoin: Possible component cause of inflammatory bowel disease." American Journal of Gastroenterology 94, no. 9 (September 1999): 2568. http://dx.doi.org/10.1016/s0002-9270(99)00459-1.

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AL-JANABI, M. A., K. SOLANKI, M. CRITCHLEY, M. L. SMITH, K. E. BRITTON, and E. C. HUSKISSON. "Radioleucoscintigraphy in osteoarthritis. Is there an inflammatory component?" Nuclear Medicine Communications 13, no. 10 (October 1992): 706–12. http://dx.doi.org/10.1097/00006231-199210000-00002.

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Szilagyi, Andrew. "Use of Prebiotics for Inflammatory Bowel Disease." Canadian Journal of Gastroenterology 19, no. 8 (2005): 505–10. http://dx.doi.org/10.1155/2005/415698.

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The relevance of diet in both the pathogenesis and the therapy of inflammatory bowel disease is an evolving science. Disturbance of intestinal microflora (dysbiosis) is putatively a key element in the environmental component causing inflammatory bowel disease. Prebiotics are among the dietary components used in an attempt to counteract dysbiosis. Such predominantly carbohydrate dietary components exert effects on the luminal environment by physicochemical changes through pH alteration, by production of short chain fatty acids and by selectively promoting putatively 'health-beneficial' bacteria. The present review elaborates on some of the background rationale and mechanisms on the use of prebiotics. Additionally, published animal and human trials are discussed.

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Дисертації з теми "Inflammatory component":

Coltman, Clare. "Oncastatin M is a key component of the inflammatory environment in multiple sclerosis." Thesis, University of the West of England, Bristol, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.431302.

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McElhanon, Kevin Edward. "Autoantibodies Targeting a Critical Component of Sarcolemma Resealing Contribute to Idiopathic Inflammatory Myopathy Pathophysiology." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1585998781690227.

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Cotena, A. "The long pentraxin 3 : a key component of innate immunity, modulates the inflammatory response to non self and self ligands." Doctoral thesis, Università degli Studi di Milano, 2009. http://hdl.handle.net/2434/64593.

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Goshovska, A. V. "Features of the vascular component at the stage of the placental complex formation against a background of inflammatory diseases of the female genital organs." Thesis, БДМУ, 2021. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18715.

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Pokrzywa, Malgorzata. "A Drosophila Disease-Model for Transthyretin-associated Amyloidosis." Doctoral thesis, Umeå : Umeå University, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1677.

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Martineau, Sabrina. "Etude des mécanismes moléculaires de l'épidermolyse bulleuse simple à partir de cellules souches humaines induites à la pluripotence." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASQ020.

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L'Epidermolyse bulleuse simplex (EBS) est une maladie cutanée principalement causée par des mutations dominantes dans les gènes codant les kératines 5 (KRT5) ou 14 (KRT14). Elle se caractérise notamment par la présence de cloques causées par un décollement de l'épiderme et une inflammation cutanée. D'un point de vue génétique, les mutations vont altérer l'assemblage du réseau de filaments intermédiaires de kératines dans les kératinocytes basaux de l'épiderme et entrainer une cytolyse cellulaire d'où la formation de cloques intra épidermiques. Il n'existe actuellement aucune approche thérapeutique efficace. La compréhension de la maladie et le développement de thérapies, ont été entravées par le manque de modèles cellulaires humains et murins relevant.Ainsi, l'objectif général de ma thèse a consisté à exploiter les propriétés des cellules souches induites à la pluripotence (hiPSc) pour modéliser l'EBS. Dans ce but, nous avons généré des kératinocytes à partir d'hiPSc provenant de patients EBS porteurs de mutations dans le gène KRT5 (Ker-EBS), et de patients sains (Ker-WT). La comparaison des Ker-EBS et Ker-WT nous a permis de montrer que les Ker-EBS récapitulent les principaux phénotypes associés à l'EBS à savoir une diminution de la prolifération cellulaire, une augmentation de la migration cellulaire, une altération des voies de signalisation (ERK et JNK), ainsi que des agrégats de filaments intermédiaires de kératines dans le cytoplasme, tel qu'observé dans kératinocytes primaires de l'EBS. Ces résultats démontrent que notre modèle cellulaire dérivés d'hiPSc est relevant pour l'étude de l'EBS.Afin d'identifier de nouveaux mécanismes moléculaires, une analyse trancriptomique comparant les Ker-EBS aux Ker-WT, a mis en évidence 138 gènes dérégulés, révélant un enrichissement dans les processus liés à la matrice extracellulaire, au packaging de l'ADN et à la réponse inflammatoire. La composante inflammatoire dans l'EBS n'ayant été que peu décrite, la suite de mes travaux a consisté à étudier le phénotype cytokinique pro-inflammatoire. Ainsi, nous avons pu démontrer, une augmentation de l'expression de l'IL-1α, IL-1β, IL-6, IL-8 (CXCL8), CXCL5, CXCL10, CXCL11, CCL5 dans les Ker-EBS, au niveau ARN en condition basale ou stimulée à l'IFNγ pour mimer un contexte pro- inflammatoire. Seules les chemokines CXCL10 et CXCL11 sont secrétées à forte concentration dans le surnagent de culture des Ker-EBS stimulés ou non, démontrant l'implication de ces cytokines dans l'EBS. En parallèle, afin de s'affranchir des biais notamment dus au fond génétique, au sexe, à l'âge des patients et à l'épigénétique, nous avons généré une lignée de Ker-EBS isogénique (Ker-EBS corrigée) par la technique CRISPR-Cas9. Nous avons ainsi pu démontrer que la lignée de Ker-EBS corrigée montrait une restauration du niveau d'expression des cytokines pro-inflammatoires citées précédemment, à un niveau proche des Ker-WT, confirmant un lien direct entre les mutations du gène KRT5 et la signature pro-inflammatoire. Pour conclure, notre nouveau modèle cellulaire nous a permis de reproduire les phénotypes pathologiques connus dans la littérature et de mettre en évidence une dérégulation de l'expression des cytokines pro-inflammatoire dans l'EBS, notamment CXCL10 et CXCL11. Enfin, l'ensemble de ces résultats font de ce modèle un outil pertinent pour permettre une meilleure compréhension des mécanismes moléculaires associés à la pathologie, notamment la composante inflammatoire, ce qui ouvre la voie à de nouvelles approches thérapeutiques
Epidermolysis bullosa simplex (EBS) is a skin disorder caused mainly by dominant mutations in genes coding for keratin 5 (KRT5) or 14 (KRT14) genes. It is characterized by the presence of blisters caused by epidermal detachment, and by other complications such as cutaneous inflammation. From a genetic point of view, the mutations will alter the assembly of the keratin intermediate filament network in basal keratinocytes of the epidermis, leading to cell cytolysis and the formation of intra-epidermal blisters. Currently no effective therapeutic approach it is available. Understanding of the disease and the development of therapies have been hampered by the lack and limitations of relevant human cell and mouse models.So, the general aim of my thesis was to exploit the properties of human induced pluripotent stem cells (hiPSc) to modelling EBS. For this purpose, we generate hiPSc-derived keratinocytes from EBS patients carrying KRT5 mutations (Ker-EBS), and from healthy patients (Ker-WT). Comparison of Ker-EBS and Ker-WT enabled to show that Ker-EBS recapitulates the main phenotypes associated with EBS, namely decreased cell proliferation, increased cell migration, altered signalling pathways (ERK and JNK), as well as aggregates of intermediate keratin filaments in the cytoplasm, as observed in primary EBS keratinocytes. These results demonstrate that our hiPSc-derived cell model is relevant for study EBS.In order to identify new molecular mechanisms, a trancriptomic analysis comparing Ker-EBS with Ker-WT revealed 138 deregulated genes, revealing an enrichment in processes linked to the extracellular matrix, DNA packaging and the inflammatory response. As the inflammatory component in EBS has been poorly described, my next step was to study the pro-inflammatory cytokine phenotype. Thus, we were able to demonstrate increased expression of IL-1α, IL-1β, IL-6, IL-8 (CXCL8), CXCL5, CXCL10, CXCL11, CCL5 in Ker-EBS, at RNA level under basal or IFNy-stimulated conditions to mimic a pro-inflammatory context. Only the chemokines CXCL10 and CXCL11 are secreted at high concentrations in the culture supernatants of stimulated and unstimulated Ker-EBS, demonstrating the involvement of these cytokines in EBS.In parallel, in order to avoid biases due to genetic background, gender, patient age and epigenetics, we generated an isogenic Ker-EBS line (corrected Ker-EBS) using the CRISPR-Cas9 technique. We were thus able to demonstrate that the corrected Ker-EBS line showed a restoration of the expression level of the pro-inflammatory cytokines mentioned above, to a level close to that of Ker-WT, confirming a direct link between mutations in the KRT5 gene and the pro-inflammatory signature.In conclusion, our new cellular model enabled us to reproduce the pathological phenotypes known in the literature, and to demonstrate deregulation of pro-inflammatory cytokine expression in EBS, notably CXCL10 and CXCL11. Taken together, these results make this model a relevant tool to allow a better understanding of the molecular mechanisms associated with the pathology, particularly the inflammatory component, paving the way for new therapeutic approaches

Wilson, Martin Robert. "Pulmonary inflammatory effects of environmental and surrogate environmental particulates and their components." Thesis, Edinburgh Napier University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270524.

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Chowdhury, Pratiti Home. "PM2.5 components and respiratory allergy： a series of in vitro studies focusing Asian cities." Kyoto University, 2017. http://hdl.handle.net/2433/227613.

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Yamamoto, Takayuki. "Studies on the safety of food and feed, and on the effects of plant derivedanti-inflammatory components." Kyoto University, 2016. http://hdl.handle.net/2433/215596.

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Анотація:

Kyoto University (京都大学)
0048
新制・課程博士
博士(農学)
甲第19770号
農博第2166号
新制||農||1040(附属図書館)
学位論文||H28||N4986(農学部図書室)
32806
京都大学大学院農学研究科食品生物科学専攻
(主査)教授河田照雄, 教授保川清, 教授橋本渉
学位規則第4条第1項該当

MILIA, CHIARA. "Evaluation of pain components in an animal model of chronic inflammatory pain: a study towards new therapeutics." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2018. http://hdl.handle.net/10281/199051.

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Il dolore cronico è una patologia cronica invalidante attualmente trattata con farmaci prevalentemente oppioidi, che comportano gravi effetti collaterali come stitichezza, depressione respiratoria, dipendenza e tolleranza. I ligandi I2 possiedono proprietà analgesiche e contrastano lo sviluppo della tolleranza se co-somministrati con oppioidi. CR4056, un nuovo farmaco I2-agonista, possiede efficacia analgesica dimostrata in diversi modelli animali di dolore cronico, in cui, inoltre, è stato osservato un forte effetto sinergico con la morfina. Lo scopo del mio studio era quindi quello di esaminare l'interazione tra morfina e CR4056 per quanto riguarda la tolleranza agli oppioidi, per chiarire la loro interazione farmacologica. A questo scopo, ho valutato gli effetti comportamentali della sinergia tra CR4056 e morfina sullo sviluppo e l'espressione della tolleranza nel modello CFA di dolore cronico. E’ stata anche valutata l'azione putativa di CR4056 sugli effetti collaterali indotti da oppioidi e sulla microgliosi spinale. È noto, infatti, che la microglia spinale ha un ruolo importante nel dolore cronico e nella tolleranza indotta da oppioidi, poiché in queste condizioni è stata osservata un'attivazione prolungata della microglia, legata al rilascio di fattori proinfiammatori. Infine, abbiamo mirato a comprendere meglio la sinergia della morfina CR4056 a livello molecolare. Infatti, è stato dimostrato che i neuroni DRG di modelli animali di dolore cronico mostrano una maggiore attivazione del recettore TRPV1, dipendente della fosforilazione di PKCε e dalla sua traslocazione sulla membrana cellulare. Inoltre, molti analgesici sono in grado di inibire la fosforilazione di PKCε in neuroni sensoriali in coltura. In dati preliminari non pubblicati, abbiamo osservato che morfina e CR4056 contrastano la traslocazione di PKCε indotta da fattori infiammatori in colture primarie di DRG di ratto. Pertanto, in questo lavoro abbiamo mirato a chiarire gli effetti delle somministrazioni acute di morfina o CR4056 in DRG ex vivo da ratti trattati con CFA, mediante quantificazione della fosforilazione di PKCε e dell'espressione di TRPV1, e nel midollo spinale, mediante valutazione della microgliosi. I miei risultati hanno dimostrato che l'infiammazione indotta da CFA ha innescato l'iperalgesia meccanica, contrastata dalla morfina o dal CR4056 in acuto. La somministrazione combinata di morfina e CR4056 ha causato una prevenzione dose-dipendente della tolleranza alla morfina, rispetto al gruppo trattato con sola morfina, in un paradigma breve (4 giorni) e lungo (14 giorni). Inoltre, quando CR4056 è stato co-somministrato con la morfina in ratti già tolleranti, è stato in grado di migliorarne l'attività analgesica. Negli stessi animali, l'attivazione della microglia spinale era maggiore nei ratti CFA, trattati con veicolo o morfina, ma non nel gruppo con somministrazione combinata di CR4056-morfina. Inoltre, la sinergia non era accompagnata da una modulazione additiva della costipazione da oppioidi. Nei DRG L4-L5 di ratti CFA abbiamo riscontrato un aumento significativo della fosforilazione di PKC-ε e della colocalizzazione tra PKC-ε e VR1, rispetto ai controlli e agli animali trattati in acuto (con CR4056 o morfina). Negli stessi animali, la microglia spinale è risultata significativamente attivata negli animali trattati con CFA rispetto ai controlli e agli animali trattati con CR4056, ma non ai ratti trattati con morfina. In conclusione, questi dati suggeriscono CR4056 come farmaco valido per prevenire e revertire la tolleranza agli oppioidi senza esacerbarne gli effetti collaterali. Inoltre, i dati in vitro su CR4056 e il meccanismo sinergico con morfina su PKCε sono stati validati in DRG ex vivo da ratti trattati con CFA. Ulteriori studi chiariranno gli effetti del trattamento combinato su DRG e midollo spinale al fine di comprendere il meccanismo della sinergia tra CR4056 e oppioidi.
Chronic pain is a disabling and long-lasting cross-pathology condition, currently treated with mostly opioid drugs, which are leading to severe side-effects such as constipation, respiratory depression, addiction and tolerance. I2 ligands showed analgesic properties and to contrast tolerance development in co-administration with opioids. CR4056, a novel I2-agonist drug, has proved to have analgesic efficacy in several animal models of chronic pain, in which, moreover, a strong synergistic effect with morphine has been observed. The aim of my study was therefore to examine the interaction between morphine and CR4056 regarding opioid tolerance, and to elucidate their pharmacological interaction. To this scope, I assessed behavioral effects of the synergy between CR4056 and morphine on tolerance development and expression in the CFA model of chronic pain. Putative CR4056 action on opioid-induced side effects and spinal microgliosis were also assessed. It is known, in fact, that spinal microglia have an important role in chronic pain and opioid-induced tolerance, since, in these conditions, a sustained microglia activation has been observed, linked to the release of pro-inflammatory factors. Lastly, we aimed to better understand CR4056-morphine synergy at molecular level. In fact, it has been shown that DRG neurons of animal models of chronic pain display higher activation of TRPV1 receptor, depending on PKCε phosphorylation and translocation to cell membrane. Moreover, there is evidence that several analgesics are able to inhibit PKCε phosphorylation in cultured sensory neurons. Interestingly, in preliminary unpublished data, we observed that morphine and CR4056 can contrast PKCε translocation induced by inflammatory factors in primary rat DRG cultures. Therefore, in this work we aimed to elucidate the effects of acute administrations of morphine or CR4056 in ex vivo DRG from CFA-treated rats, by quantification of PKCε phosphorylation and TRPV1 expression, and in the spinal cord, by evaluation of microgliosis. My results demonstrated that CFA-induced inflammation triggered mechanical hyperalgesia, acutely counteracted by morphine or CR4056. Combined administration of morphine with CR4056 caused a dose-dependent prevention of morphine tolerance, which was established in the morphine alone treated group, in a short (4 days) and in a long paradigm (14 days). Moreover, when CR4056 was co-administered with morphine in already tolerant rats, it was able to improve morphine analgesic activity. In the same animals, spinal microglia activation was augmented in CFA-injected rats, either vehicle- or morphine-treated, but not in the group with CR4056-morphine combined administration. Besides, the synergy was not accompanied by an additive modulation of opioid-induced constipation. In L4-L5 DRG of CFA-injected rats we found a significant increase in the phosphorylation of PKC-ε, as well as in the colocalization between PKC-ε and VR1, compared to sham animals and to acutely treated animals (with CR4056 or morphine). In the same animals, activated microglial cells were significantly increased in CFA vehicle-treated animals compared to control and CR4056-treated animals, but not to morphine-treated rats. In conclusion, these data suggest that CR4056 seems to be a valid drug to prevent and rescue opioid tolerance without exacerbate side-effects. Moreover, in vitro data on CR4056 and morphine synergistic mechanism on PKCε were validated in ex vivo DRG from CFA-treated rats. Further studies will be needed to elucidate effects of combined treatment on DRG and spinal cord in order to understand the mechanism of CR4056 and opioids synergy.

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Книги з теми "Inflammatory component":

Zhou, Jiaju. Zhong yao kang yan huo xing cheng fen: Anti-inflammatory active components in TCM. 8th ed. Beijing: Ke xue chu ban she, 2012.

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Klingenberg, Roland, and Ulf Müller-Ladner. Mechanisms of inflammation. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0270.

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This chapter provides a brief summary of the immune pathogenesis of atherosclerosis, highlighting shared features with inflammatory pathways in rheumatoid arthritis (RA) described in detail in Chapter 25.4. RA constitutes a prototype autoimmune disease primarily affecting the joints but also the heart and vessels associated with increased cardiovascular mortality. Recent years have produced a wealth of novel insights into the diversity of immune cell types which either propagate or dampen inflammation in atherogenesis. Expansion of this inherent anti-inflammatory component carried by regulatory T cells may constitute a new therapeutic target to harness the progression of atherosclerotic cardiovascular disease. Among the various inflammatory mediators involved in RA pathology, cytokines (tumour necrosis factor-α‎ and interleukin-6) have gained major interest as therapeutic targets with approved therapies available. In light of the many common features in the pathogenesis of RA and atherosclerosis, these biologics are currently being evaluated in cardiovascular patients. The recently published CANTOS trial showed that IL-1 inhibition reduced adverse cardiovascular events in patients with coronary artery disease demonstrating that inflammation is a genuine therapeutic target. The near future will provide more information whether inflammation is a bona fide cardiovascular risk factor based on completion of several clinical trials using anti-inflammatory approaches in patients with both cardiovascular disease and rheumatoid arthritis.

Freer, Phoebe E. Skin Lesions. Edited by Christoph I. Lee, Constance D. Lehman, and Lawrence W. Bassett. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190270261.003.0050.

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Skin lesions are commonly seen on breast imaging. Often, a raised skin lesion is encountered incidentally during screening mammography and can be mistaken for a mass within the breast parenchyma. In most cases, lesions confined within the dermis are benign. Occasionally, focal skin involvement may be the presenting sign of a breast cancer that is either locally extensive to the skin or has an inflammatory component. This chapter reviews the key imaging and clinical features of skin lesions that may be encountered either incidentally on breast imaging or on diagnostic imaging as an area of patient concern. Imaging features of skin lesions, the differential diagnoses, and further management will be reviewed. Topics discussed include benign epithelial cysts (i.e., sebaceous cyst and epidermal inclusion cysts), seborrheic keratosis, keloid and dermal nevi, cellulitis, and inflammatory and locally advanced breast cancers.

Machado, Pedro M. Inclusion body myositis. Edited by Hector Chinoy and Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0011.

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Sporadic inclusion body myositis (IBM) is an acquired muscle disorder associated with ageing, for which there is no effective treatment. It is characterized by a typical early clinical phenotype with (often asymmetric) weakness of the knee extensors and finger flexors, potential involvement of pharyngeal and upper-oesophageal muscles (which may contribute to malnutrition and aspiration), and progressive and slow deterioration, which may lead to severe disability and loss of quality of life. Muscle biopsy shows chronic myopathic features, lymphocytic infiltration with invasion of non-necrotic fibres, rimmed vacuoles, mitochondrial changes, and pathological accumulation of proteins in the muscle tissue. It remains uncertain whether IBM is primarily an immune-mediated inflammatory myopathy or a degenerative myopathy with an associated inflammatory component. This chapter will describe the clinical features, natural history, investigations, current pathogenic concepts, outcome measures, and therapeutic approaches in IBM. Despite recent clues, in many respects IBM remains an unsolved mystery.

Laffey, John G., and Brian P. Kavanagh. Hypercapnia in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0086.

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Hypercapnia is a central component of current ‘protective’ ventilator management. Hypercapnia, and the associated acidosis, has potentially important biologic effects on immune responses, injury and repair. Arterial carbon dioxide tension PaCO2 is tightly governed under physiological conditions and small elevations rapidly increase spontaneous minute ventilation. In the mechanically-ventilated patient, elevated PaCO2 usually reflects reduced elimination. This can be because tidal volume or respiratory rate delivered by the ventilator are reduced, or because of the diseased lung per se. Hypercapnia has many effects that are clinically obvious, but research over the last decade reveals important consequences on inflammatory and cellular mechanisms that are not apparent at the bedside.

Hahn, Robert G. Intravenous fluids in anaesthetic practice. Edited by Michel M. R. F. Struys. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0020.

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Infusion fluids may be regarded as drugs in the perioperative setting. The therapeutic effects of crystalloid solutions are strongly related to the administered volume, while fluids of the colloid type may also improve microcirculation and have anti-inflammatory properties. The anaesthetist should be able to handle all available infusion fluids and be aware of their benefits, limitations, and risks. Fluid administration programmes for surgery are traditionally based on a balance method in which perceived and measured losses are continuously replaced. Two outcome-guided approaches—restrictive and goal-directed fluid therapy—have been added in recent years. The latter places all patients on the top of the Frank–Starling curve by titrating repeated bolus infusions of colloid fluid while observing the stroke volume response. Areas where special consideration should be given to fluid therapy include burn injury, children, day surgery, endoscopic surgery, neurosurgery, induction of spinal and epidural anaesthesia, and in septic and trauma-related shock. As volume is the key component of infusion fluids, kinetic analysis of their disposition is based on their dilution effect on components already present in the blood, usually haemoglobin.

Lalvani, Ajit, and Katrina Pollock. Defences against infection. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0303.

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The immune system is classified into a series of component parts, each specialized to defend the host against infection. Cells of the innate immune system are distributed throughout the body, in the tissues, and in the circulation, to defend against the first signs of danger, combining the acute inflammatory response with the ability to kill and remove invading pathogens. Monocytes, macrophages, and neutrophils phagocytose and kill exogenous and endogenous targets, using both oxygen-dependent and oxygen-independent mechanisms. The adaptive immune system creates a structurally specific and prolonged response, mediated by lymphocytes to clear infection and generate immunological memory. In this chapter, the functions of the innate and adaptive immune system are reviewed, together with the clinical features and investigation of acquired and inherited immune deficiencies.

Eisen, Andrew. Motor neurone disease. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0009.

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In this chapter, the following ten key events in motor neurone disease, also known as amyotrophic lateral sclerosis (ALS), are considered: the first description of ALS by Cruveilhier; discovery of the first SOD1 mutation; use of the ALSFRS (functional rating scale) for determining therapeutic trial outcomes; the contentious issue of establishing the site of onset of ALS; clinical, pathological, and molecular evidence indicating that frontotemporal dementia and ALS are closely related; demonstration that ALS bears some resemblance to the transmissible spongiform encephalopathies; use of Riluzole as the approved therapy for ALS; the major inflammatory component of ALS; a Guamanian disorder that is biochemically and ultrastructurally similar to that of Alzheimer’s disease; and awareness that the true onset of ALS is unknown but certainly precedes clinical onset by years or decades.

Patel, Mayur B., and Pratik P. Pandharipande. Analgesics in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0043.

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Analgesia is a critical component of intensive care unit (ICU) care. Accordingly, understanding the mechanism, physiological consequences, and assessment of pain is important when caring for the ICU patient. Non-pharmacological approaches should be attempted before supplementing analgesia with pharmacological agents. Pharmacologically-based therapies are divided into regional and systemic therapies. Regional analgesic therapies target specific areas of the body while limiting the systemic effects of intravenous analgesics, but at the risk of invasiveness, local anaesthetic toxicity, and infection of in-dwelling catheters. Systemic analgesic therapy is comprised of two main categories—non-opioids and opioids. Typically, non-opioid analgesics are used as adjunctive therapies and consist of agents such as non-steroidal anti-inflammatory drugs, gabapentinoids, ketamine, or α‎2 agonists. Opioid analgesia in the ICU is commonly infusion-based using fentanyl, hydromorphone, morphine, or recently, remifentanil.

Takeshita, Junko, and Joel M. Gelfand. Epidemiology of psoriasis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0002.

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Psoriasis is a common chronic inflammatory disorder of the skin that is associated with multisystem effects. Approximately 125 million people worldwide are affected by psoriasis, nearly one quarter of whom have moderate to severe disease. The majority of patients with psoriasis have a waxing and waning course with variable periods of spontaneous disease improvement or clearance. A rapidly expanding body of epidemiologic literature suggests psoriasis to be associated with a greater comorbid disease burden than patients without psoriasis. In addition to psoriatic arthritis, cardiometabolic diseases, including metabolic syndrome and its component disorders, as well as major adverse cardiovascular events are the most common comorbidities of psoriasis; together they are the primary cause of premature mortality among moderate to severe psoriasis patients. Continued efforts to better understand currently known and identify other emerging comorbidities of psoriasis are critical.

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Частини книг з теми "Inflammatory component":

Ferrari, C. C., and F. J. Pitossi. "The Inflammatory Component of Neurodegenerative Diseases." In Handbook of Neurochemistry and Molecular Neurobiology, 395–406. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-30398-7_18.

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Olofsson, Peter, Malin Hultqvist, Lars I. Hellgren, and Rikard Holmdahl. "Phytol: A Chlorophyll Component with Anti-inflammatory and Metabolic Properties." In Recent Advances in Redox Active Plant and Microbial Products, 345–59. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-8953-0_13.

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Wilson, David J., and Marcelo de Abreu. "Spine Degeneration and Inflammation." In IDKD Springer Series, 197–213. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-71281-5_14.

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AbstractConventional radiographs and CT are primary investigations in spinal trauma. However MRI is the primary technique in the assessment of degenerative and inflammatory disorders. There are occasions when conventional radiographs, CT and bone scintigraphy assist in the diagnosis of degenerative and inflammatory disorders.A detailed understanding of anatomy and spine dynamic function is essential in the interpretation of imaging.Degenerative disorders including disc disease sometimes result in neural compression, facet joint and costovertebral arthropathy which is also potentially associated with spinal stenosis and neural compression. Scheuermann described a disorder with template irregularity that mimics degenerative disorders but is a genetic condition. Pars interarticularis stress fractures were once thought to be congenital in origin but are now regarded as stress injuries occurring in adolescence potentially leading to lifelong spondylolisthesis.Inflammatory joint disease is not just ankylosing spondylitis. There are a range of disorders, and the reporting practitioner must understand and appreciate the symptoms and signs on images. The early diagnosis of inflammatory arthropathy especially ankylosing spondylitis is essential in the effective management of the disease. Imaging is a major component of an accurate and effective diagnosis.

Knop, Nadja, and Erich Knop. "Regulation of the Inflammatory Component in Chronic Dry Eye Disease by the Eye-Associated Lymphoid Tissue (EALT)." In Research Projects in Dry Eye Syndrome, 23–39. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000315017.

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Grangette, Corinne. "Probiotics and Inflammatory Immune Responses." In Dietary Components and Immune Function, 591–610. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-061-8_32.

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Dziarski, R., A. J. Ulmer, and D. Gupta. "Interactions of CD14 with Components of Gram-Positive Bacteria." In CD14 in the Inflammatory Response, 83–107. Basel: KARGER, 1999. http://dx.doi.org/10.1159/000058761.

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Schwartz, Colin J., Eugene A. Sprague, Anthony J. Valente, Jim L. Kelley, Ellen H. Edwards, and C. Alan Suenram. "Inflammatory Components of the Human Atherosclerotic Plaque." In Pathobiology of the Human Atherosclerotic Plaque, 107–20. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3326-8_7.

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Foligné, Benoit, Joëlle Dewulf, Bruno Pot, Catherine Daniel, Michel Simonet, Sabine Poiret, Michaël Marceau, and Rodrigue Dessein. "Therapeutic Potential of Yersinia Anti-Inflammatory Components." In Advances In Experimental Medicine And Biology, 361–66. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-72124-8_33.

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Cao, Heping. "Cinnamon and Immune Actions: Potential Role in Tristetraprolin-Mediated Inflammatory Diseases." In Dietary Components and Immune Function, 553–65. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-061-8_30.

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Panchal, Sunil K., and Lindsay Brown. "Anti-inflammatory Components from Functional Foods for Obesity." In Pathophysiology of Obesity-Induced Health Complications, 285–303. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-35358-2_17.

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Тези доповідей конференцій з теми "Inflammatory component":

Piqué-Borràs, M.-R., M. Jaklin, J. Röhrl, A. Ammendola, and G. Künstle. "Mechanisms of action of a multi-component herbal preparation in inflammatory bowel disease: anti-inflammatory activity." In GA – 70th Annual Meeting 2022. Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1759299.

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Coimbra, Robson Carlos, Cristiane Carla Muniz, Juliana Silva de Oliveira, and Alexandre dos Santos Gomes. "Thermography as an aid in preventing injuries in football: Presentation of a possible curricular component in imaging courses." In V Seven International Multidisciplinary Congress. Seven Congress, 2024. http://dx.doi.org/10.56238/sevenvmulti2024-160.

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Thermography is a non-invasive method that records body thermal gradients and patterns, measuring the thermal radiation emitted by the body. It can be used to diagnose sports injuries, as it captures the infrared radiation emitted by the individual himself, without emission of external radiation. The injuries trigger inflammatory processes that generate heat, detectable by thermography before clinical signs appear, allowing preventive intervention. This technique allows you to measure temperatures and form thermal images, accurately locating injury points. Thus, it is possible to monitor the evolution of the inflammatory condition and prevent worsening, even when the injury is not yet clinically noticeable.

Monahan, R. C., L. Beaart- van de Voorde, C. Magro-Checa, T. Huizinga, H. Middelkoop, M. van Buchem, I. Ronen, A. Kaptein, and G. Steup-Beekman. "FRI0383 Changes in white matter microstructure correlate with sf-36 mental component subscore in inflammatory npsle." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.6249.

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Cheng, WanYun, Jenna Currier, Philip A. Bromberg, Robert Silbajoris, and James M. Samet. "Exposure To An Organic PM Component Induces Inflammatory And Adaptive Gene Expression Through Mitochondrial Oxidative Stress." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3232.

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Lussier, A. L., E. Yu, and P. Lindholm. "Is There an Inflammatory Component Present in Immersion Pulmonary Edema? Evidence From Increased Fractional Exhaled Nitric Oxide (FeNO)." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a5505.

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V.S., Ponamarev, and Atikov A.S. "he use of the complex drug "Penbex" in the treatment of idiopathic pathology of the upper respiratory tract of horses." In SPbVetScience. FSBEI HE St. Petersburg SUVM, 2023. http://dx.doi.org/10.52419/3006-2022-7-61-69.

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This article discusses the main problem of the use of drugs in the treatment of the inflammatory process of the upper respiratory tract. In most cases, medicines have only one component in their composition (the antibiotic), but modern science gives access to the use of drugs that are more complex in their composition.

Pidaparti, Ramana M., and Kevin R. Ward. "Airway Inflammation Induced by Mechanical Ventilation Through Multiscale Modeling." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80174.

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Inflammation has been recognized as a major integral component for most of the acute and chronic diseases. Inflammation can be initiated within the body as an innate process or by external factors such as infections and trauma. Inflammation is a complex and dynamic process, and involves nonlinearity and stochasticity. Without the inflammation, the harmful stimuli cannot be removed and the healing process cannot occur. However, an over-expression or under-expression of inflammatory responses can lead to severe consequences, such as Multiple Organ Dysfunction Syndrome (MODS), which is characterized by sequential organ failure. Acute lung injury (ALI) is typically one of the first manifestation of MODS. It can be triggered by external stimuli such as pathogens or from inflammatory mediators produced from various other processes ranging from other damaged organs or to blood transfusions to even the biomechanical forces of mechanical ventilation itself.

Schaub, R. G., C. J. Dunn, D. E. Tracey, W. E. Fleming, and M. D. Burdick. "THROMBOTIC AND INFLAMMATORY CHANGES IN ENDOTHELIAL CELLS INCUBATED WITH LEUKOCYTES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642860.

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Adhesion of leukocytes (WBC's) to vascular endothelial cells (EC's) is a component of inflammation, thrombosis and atherosclerosis. The purpose of this study was to assess the effect of WBC adhesion on the EC contribution to these pathologic events. Human WBC's were isolated and co-incubated with cultured human umbilical cord EC's. Supernatants and cell lysates (4 wells × 2) were obtained at 0.5,1,2, and 4 hours of incubation. EC's and WBC's (5 × 105) were-incubated alone or in combination. Supernatants and cell lysates were assayed for leukotriene B4 (LTB4), the thromboxane metabolite thromboxane B2 (TXB2) and the prostacyclin metabolite 6-keto prostaglandin FT alpha (6 keto) by RIA. Cell lysates were analyzed for cell associated procoagulant activity (PCA) by an APTT procedure, for plasminogen activator inhibitor (PAI) by an amidolytic assay and for IL-1 by a T-cell co-stimulator assay. Cellular and supernatant LTB4 was unmeasurable for both WBC's and WBC/EC cultures. WBC TXB2 showed a time dependent elevation which was unaffected by EC's. IL-1 activity was measurable at 2 hours and reach 14 U/ml in WBC's and 6 U/ml in EC/WBC cultures. Co-incubation of WBC's with EC's induced a 200% increase in both supernatant and cell associated 6 keto concentrations compared to EC's incubated alone. EC's and WBC's produced no PCA when incubated alone. PCA activity of the EC/WBC co-cultures was measurable at 2 hours and was 300-1500 U/ml after 4 hours. Coincubated EC's had a 50% decrease in cell PAI, suggesting an increased release of inhibitor from the cells. The prostacyclin and PAI release -along with the delayed expression of PCA activity are responses similar to those expected after EC exposure to cytokines. A source of these cytokines appears to be the WBC's which secreted measurable amounts of IL-1. WBC released IL-1 was sufficient to induce biochemical changes in EC's which can stimulate coagulation (PCA synthesis), inhibit fibrinolysis (PAI release), and enhance inflammation (prostacyclin synthesis). These results suggest that the release of WBC IL-1 can be sufficient to produce pro-thrombotic and inflammatory changes in EC's which are similar to those observed with the addition of exogenous IL-1 to EC cultures.

Pirogov, Aleksey, Anna Prikhodko, Evgeniya Afanas'eva, and Yuliy Perelman. "COMPARATIVE ASSESSMENT OF AIRWAY CELLULAR INFLAMMATION IN PATIENTS WITH BRONCHIAL ASTHMA IN RESPONSE TO HYPOSMOLAR AND COLD STIMULES." In XIV International Scientific Conference "System Analysis in Medicine". Far Eastern Scientific Center of Physiology and Pathology of Respiration, 2020. http://dx.doi.org/10.12737/conferencearticle_5fe01d9c45b256.10926397.

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An approach is presented to the study of cellular inflammation using cytological analysis of sputum in patients with bronchial asthma with different types of airway reaction to bronchoprovocation with cold air and distilled water. When the airways are hyperresponsive to hypoosmolar and cold stimuli, it has been established the activation of the neutrophilic component of bronchial granulocytes. Cold airway hyperresponsiveness is associated with an increase in neutrophil content and a concomitant decrease in the number of macrophages in the inflammatory pattern of the bronchi. An increase in sputum cytosis is inherent in a positive airway response to a hypoosmolar test with an unexpressed dynamics of the level of bronchial eosinophils.

Tayyem, Reema. "Dietary Patterns and Risk of Inflammatory Bowel Disease: Findings from a Case-Control Study." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0082.

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Scientific evidence shows that dietary patterns are associated with the risk of IBD, particularly among unhealthy and Western dietary patterns. However, Western dietary patterns are not exclusive to Western countries, as Jordanians are steadily moving towards a Western lifestyle, which includes an increased consumption of processed foods. This study aims to investigate the association between dietary patterns and the risk factors for IBD cases among Jordanian adults. This case-control study was conducted between November 2018 and December 2019 in the largest three hospitals in Jordan. Three hundred and thirty-five Jordanian adults aged between 18–68 years were enrolled in this study: one hundred and eighty-five IBD patients who were recently diagnosed with IBD (n = 100 for ulcerative colitis (UC) and n = 85 for Crohn’s disease (CD)) and 150 IBD-free controls. Participants were matched based on age and marital status. In addition, dietary data was collected from all participants using a validated food frequency questionnaire. Factor analysis and principal component analysis were used to determine the dietary patterns. Odds ratios (OR) and their 95% confidence interval (CI) were calculated using a multinomial logistic regression model. Two dietary patterns were identified among the study participants: high-vegetable and high-protein dietary patterns. There was a significantly higher risk of IBD with high-protein intake at the third and fourth quartiles in the non-adjusted model as well as the other two adjusted models. In contrast, the high-vegetable dietary pattern shows a significantly protective effect on IBD in the third and fourth quartiles in all the models. Thus, a high-vegetable dietary pattern may be protective against the risk of IBD, while a high-protein dietary pattern is associated with an increased risk of IBD among a group of the Jordanian population.

Звіти організацій з теми "Inflammatory component":

Casebere, Kelsey R., Michael G. Kaiser, and Susan J. Lamont. Bacterial Component Induced Inflammatory Response in Roosters from Diverse Genetic Lines. Ames (Iowa): Iowa State University, January 2015. http://dx.doi.org/10.31274/ans_air-180814-1319.

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Neodo, Anna, Fiona Augsburger, Jan Waskowski, Joerg C. Schefold, and Thibaud Spinetti. Monocytic HLA-DR expression and clinical outcomes in adult ICU patients with sepsis – a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0119.

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Review question / Objective: The scope of this review was defined using PICOTS framework where 1) population: adult critically ill patients with sepsis or septic shock; 2) index prognostic factor: cell surface protein expression of mHLA-DR in blood; 3) comparative factor: none; 4) outcomes to be predicted: mortality, secondary infections, length of stay, and organ dysfunction score (sequential organ failure assessment [SOFA], multiple organ dysfunction score [MODS], logistic organ dysfunction score [LODS]), composite outcomes where component endpoints consist of at least one of the outcomes stated above (e.g., “adverse outcome” defined as death or secondary infection), 5) timing (of the prediction horizon and the moment of prognosis): any; and 6) setting: ICU. Condition being studied: Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to severe infections. It can further progress to septic shock, which includes hemodynamic failure and increased mortality rates. A recent worldwide epidemiological study estimated 48.9 million sepsis cases and 11 million of sepsis-related deaths (~20% of global deaths in 2017). Although its management has advanced considerably, sepsis remains deadly and challenging to treat. The 28/30-day mortality averages around 25% for sepsis and 38% for septic shock in high-income countries. Current models describe the underlying pathophysiologic mechanisms of sepsis as an interplay between concurrent dysfunctional pro- and anti-inflammatory immune response.

Shpigel, Nahum Y., Ynte Schukken, and Ilan Rosenshine. Identification of genes involved in virulence of Escherichia coli mastitis by signature tagged mutagenesis. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7699853.bard.

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Mastitis, an inflammatory response of the mammary tissue to invading pathogenic bacteria, is the largest health problem in the dairy industry and is responsible for multibillion dollar economic losses. E. coli are a leading cause of acute mastitis in dairy animals worldwide and certainly in Israel and North America. The species E. coli comprises a highly heterogeneous group of pathogens, some of which are commensal residents of the gut, infecting the mammary gland after contamination of the teat skin from the environment. As compared to other gut microflora, mammary pathogenic E. coli (MPEC) may have undergone evolutionary adaptations that improve their fitness for colonization of the unique and varied environmental niches found within the mammary gland. These niches include competing microbes already present or accompanying the new colonizer, soluble and cellular antimicrobials in milk, and the innate immune response elicited by mammary cells and recruited immune cells. However, to date, no specific virulence factors have been identified in E. coli isolates associated with mastitis. The original overall research objective of this application was to develop a genome-wide, transposon-tagged mutant collection of MPEC strain P4 and to use this technology to identify E. coli genes that are specifically involved in mammary virulence and pathogenicity. In the course of the project we decided to take an alternative genome-wide approach and to use whole genomes bioinformatics analysis. Using genome sequencing and analysis of six MPEC strains, our studies have shown that type VI secretion system (T6SS) gene clusters were present in all these strains. Furthermore, using unbiased screening of MPEC strains for reduced colonization, fitness and virulence in the murine mastitis model, we have identified in MPEC P4-NR a new pathogenicity island (PAI-1) encoding the core components of T6SS and its hallmark effectors Hcp, VgrG and Rhs. Next, we have shown that specific deletions of T6SS genes reduced colonization, fitness and virulence in lactating mouse mammary glands. Our long-term goal is to understand the molecular mechanisms of host-pathogen interactions in the mammary gland and to relate these mechanisms to disease processes and pathogenesis. We have been able to achieve our research objectives to identify E. coli genes that are specifically involved in mammary virulence and pathogenicity. The project elucidated a new basic concept in host pathogen interaction of MPEC, which for the best of our knowledge was never described or investigated before. This research will help us to shed new light on principles behind the infection strategy of MPEC. The new targets now enable prevalence and epidemiology studies of T6SS in field strains of MPEC which might unveil new geographic, management and ecological risk factors. These will contribute to development of new approaches to treat and prevent mastitis by MPEC and perhaps other mammary pathogens. The use of antibiotics in farm animals and specifically to treat mastitis is gradually precluded and thus new treatment and prevention strategies are needed. Effective mastitis vaccines are currently not available, structural components and effectors of T6SS might be new targets for the development of novel vaccines and therapeutics.