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Статті в журналах з теми "Pulmonary acute inflammation"
Arndt, Patrick G., Brian Strahan, Yue Wang, Chunmei Long, Keisuke Horiuchi, and Bruce Walcheck. "Leukocyte ADAM17 Regulates Acute Pulmonary Inflammation." PLoS ONE 6, no. 5 (May 16, 2011): e19938. http://dx.doi.org/10.1371/journal.pone.0019938.
Повний текст джерелаSavin, Innokenty A., Marina A. Zenkova, and Aleksandra V. Sen’kova. "Pulmonary Fibrosis as a Result of Acute Lung Inflammation: Molecular Mechanisms, Relevant In Vivo Models, Prognostic and Therapeutic Approaches." International Journal of Molecular Sciences 23, no. 23 (November 29, 2022): 14959. http://dx.doi.org/10.3390/ijms232314959.
Повний текст джерелаEckle, Tobias, Michael Koeppen, and Holger K. Eltzschig. "Role of Extracellular Adenosine in Acute Lung Injury." Physiology 24, no. 5 (October 2009): 298–306. http://dx.doi.org/10.1152/physiol.00022.2009.
Повний текст джерелаSpond, J., N. Case, R. W. Chapman, Y. Crawley, R. W. Egan, J. Fine, J. A. Hey, et al. "Inhibition of experimental acute pulmonary inflammation by pirfenidone." Pulmonary Pharmacology & Therapeutics 16, no. 4 (August 2003): 207–14. http://dx.doi.org/10.1016/s1094-5539(03)00026-9.
Повний текст джерелаSingh, Baljit, Jacqueline W. Pearce, Lakshman N. Gamage, Kyathanahalli Janardhan, and Sarah Caldwell. "Depletion of pulmonary intravascular macrophages inhibits acute lung inflammation." American Journal of Physiology-Lung Cellular and Molecular Physiology 286, no. 2 (February 2004): L363—L372. http://dx.doi.org/10.1152/ajplung.00003.2003.
Повний текст джерелаSelby, C., and W. Macnee. "Factors Affecting Neutrophil Transit During Acute Pulmonary Inflammation: Minireview." Experimental Lung Research 19, no. 4 (January 1993): 407–28. http://dx.doi.org/10.3109/01902149309064355.
Повний текст джерелаMirakaj, Valbona, Cyril A. Thix, Stefanie Laucher, Carina Mielke, Julio C. Morote-Garcia, Marthe A. Schmit, Janek Henes, Klaus E. Unertl, David Köhler, and Peter Rosenberger. "Netrin-1 Dampens Pulmonary Inflammation during Acute Lung Injury." American Journal of Respiratory and Critical Care Medicine 181, no. 8 (April 15, 2010): 815–24. http://dx.doi.org/10.1164/rccm.200905-0717oc.
Повний текст джерелаMancuso, Peter. "Obesity and lung inflammation." Journal of Applied Physiology 108, no. 3 (March 2010): 722–28. http://dx.doi.org/10.1152/japplphysiol.00781.2009.
Повний текст джерелаJung, Ayoung, Sung-Hyun Kim, Jun-Young Yang, Jayoung Jeong, Jong Kwon Lee, Jae-Ho Oh, and Jin Hee Lee. "Effect of Pulmonary Inflammation by Surface Functionalization of Zinc Oxide Nanoparticles." Toxics 9, no. 12 (December 6, 2021): 336. http://dx.doi.org/10.3390/toxics9120336.
Повний текст джерелаZiablitsev, D. S., O. O. Dyadyk, and S. V. Ziablitsev. "ACTIVITY OF ANGIOTENSIN-CONVERSING ENZYME-2 IN ACUTE PULMONARY INFLAMMATION." Medical Science of Ukraine (MSU) 17, no. 3 (September 30, 2021): 3–14. http://dx.doi.org/10.32345/2664-4738.3.2021.01.
Повний текст джерелаДисертації з теми "Pulmonary acute inflammation"
Simpson, A. John. "The effects of elafin gene augmentation on acute pulmonary inflammation." Thesis, University of Edinburgh, 2002. http://hdl.handle.net/1842/25189.
Повний текст джерелаKurti, Stephanie P. "The impact of lifestyle, age, and sex on systemic and airway inflammation and oxidative stress." Diss., Kansas State University, 2017. http://hdl.handle.net/2097/35294.
Повний текст джерелаDepartment of Kinesiology
Craig A. Harms
The overall aim of this dissertation was to determine the impact of lifestyle (i.e. habitual and acute physical activity and diet), age, and sex on systemic and airway inflammation and oxidative stress. In study 1 (Chapter 2) we examined the impact of habitual physical activity level on the post-prandial airway inflammatory response following an acute bout of moderate intensity exercise. Results indicated that the mean exhaled nitric oxide (eNO; marker of airway inflammation) response increased for all groups at two hours post high-fat meal (HFM) (~6%) and returned to baseline by four hours post-HFM. However, there was a varying eNO response from baseline to four hours in the group that exercised in the post-prandial period compared to the group that remained sedentary. These findings suggest airway inflammation occurs after a HFM when exercise is performed in the post-prandial period, regardless of habitual physical activity level. In study 2 (Chapter 3) we investigated the post-prandial oxidative stress response to meals of varying calories and fat. Specifically, we assessed the post-prandial airway and systemic 8-isoprostane (a marker of oxidative stress) responses to meals with moderate-fat (8.5 kcal/kg of bodyweight) and high-fat content (17 kcal/kg of bodyweight) from baseline to six hours post-meal in a randomized crossover design. This study revealed that systemic 8-isoprostane increased from baseline to six hours post-meal (38.3%), but there was no difference between the moderate-fat meal (MFM) and HFM conditions. There were no changes in airway 8-isoprostane from baseline to six hours post-MFM or HFM, or between the MFM and HFM conditions. Lastly, in study 3 (Chapter 4), we were interested in examining 8-isoprostane responses in older adults, since 8-isoprostane has been reported to increase with age. Previous research also suggests that older women (OW) and older men (OM) have differences with regard to prevalence and severity of late-onset asthma. In this study, we sought to determine whether the airway 8-isoprostane response to a strenuous bout of exercise was different in OW compared to OM. A secondary aim was to determine whether post-exercise 8-isoprostane generation was correlated with decrements in lung function. Our results showed that the generation of 8-isoprostane from pre- to post-exercise increased ~74±77% in OW and decreased ~12±50% in OM. The decrease in 8-isoprostane generation was not correlated with improvements in lung function from pre- to post-exercise. These findings collectively contribute to the literature by enhancing our understanding of the impact of lifestyle factors, age and sex on modifying and potentially mitigating the risk of developing chronic diseases.
Miettinen, J. (Johanna). "Studies on bone marrow-derived stem cells in patients with acute myocardial infarction." Doctoral thesis, Oulun yliopisto, 2011. http://urn.fi/urn:isbn:9789514293924.
Повний текст джерелаTiivistelmä Sydäninfarktipotilaiden sepelvaltimoon pallolaajennuksen yhteydessä injektoitujen kantasolujen tiedetään parantavan hieman sydämen pumppauskykyä, mutta taustalla olevaa mekanismia ei tunneta. Kantasoluhoidon onnistumiseen vaikuttavia tekijöitä on tutkittu vasta vähän, eikä myöskään sitä tiedetä, miksi kaikki potilaat eivät hyödy kantasoluhoidosta. Tämän tutkimuksen tavoitteena oli selvittää infarktialueelle annetun kantasoluhoidon vaikutuksia äkillisen ST-nousuinfarktin (STEMI) sairastaneissa potilaissa, ja etsiä hoidon onnistumiseen vaikuttavia tekijöitä. Tutkimuksessa käytettiin potilasaineistoa, johon otettiin 78 äkilliseen sydäninfarktiin sairastunutta potilasta, jotka hoidettiin liuotushoidolla ja sen jälkeen pallolaajennuksella. Puolet potilaista satunnaistettiin saamaan lumeliuosta ja puolet omaa luuydinsolukkoaan (BMC), joka ruiskutettiin pallolaajennuksen yhteydessä sepelvaltimon kautta infarktialueelle. Hoidon vaikusta tutkittiin mittaamalla angiografian avulla vasemman kammion ejektiofraktion (LVEF) muutosta lähtötilanteen ja kuuden kuukauden seurannan välillä. Lisäksi sydämen ultraäänitutkimuksella määritettiin keuhkovaltimopainetta ja vasemman kammion systolista ja diastolista toimintaa. Potilaista otettiin lisäksi verinäytteitä, joista määritettiin erilaisia tulehdusmerkkiaineita ja natriureettisia peptidejä. Lisäksi potilaista kerättyjä luuydinkantasoluja viljeltiin laboratoriossa in vitro-analyyseja varten. Tutkimuksessa todettiin, että LVEF ennen kantasoluhoitoa oli voimakkain ennustetekijä suotuisalle LVEF:n muutokselle kantasoluhoidon jälkeen. Potilaat, joilla LVEF oli ennen kantasoluhoitoa alle mediaaniarvon (≤62.5%), hyötyivät kantasoluhoidosta enemmän kuin potilaat, joilla LVEF oli yli mediaanin. Myös natriureettisten peptidien NT-proBNP:n ja NT-proANP:n korkea taso infarktin jälkeen oli yhteydessä suurempaan LVEF:n paranemiseen BMC-potilailla. Natriureettisten peptidien ja tulehdusmerkkiaineiden pitoisuuksien muutoksissa kantasoluhoidon jälkeen ei kuitenkaan todettu eroa BMC- ja kontrolliryhmän välillä. Sydämen diastolisen toiminnan havaittiin paranevan enemmän BMC-ryhmässä kuin kontrolliryhmässä. Lisäksi BMC-ryhmässä havaittiin lievää laskua keuhkovaltimopaineessa, kun taas kontrolliryhmässä se nousi merkittävästi. In vitro-tutkimukset luuytimestä erilaistetuilla mesenkymaalisilla kantasoluilla puolestaan osoittivat, että tuumorinekroositekijä alfa (TNF-α)-altistus lisäsi solujakautumista ja monien immunosupressiivisten proteiinien tuottoa soluissa. Matala LVEF sekä natriureettisten peptidien NT-proBNP:n ja NT-proANP:n korkea taso sydäninfarktin jälkeen kuvaavat infarktivaurion aiheuttamien hemodynaamisten ja neurohumoraalisten reaktioiden vakavuutta, ja tässä tutkimuksessa niiden osoitettiin olevan vahvasti yhteydessä äkillisen ST-nousuinfarktin jälkeen annetun kantasoluhoidon hyötyyn. Kantasoluhoito saattaa myös suojata infarktipotilaita haitalliselta keuhkovaltimopaineen nousulta ja parantaa sydämen diastolista toimintaa. Tulehdusvälittäjäaine TNF-α näytti in vitro-kokeiden perusteella lisäävän luuytimen mesenkymaalisten kantasolujen jakautumista ja aktivoivan niissä monia immunosuppressiivisia puolustusmekanismeja tulehdusta vastaan
Borges, João Batista. "Regional Lung Kinetics of Ventilator-Induced Lung Injury and Protective-Ventilation Strategies Studied by Dynamic Positron Emission Tomography." Doctoral thesis, Uppsala universitet, Hedenstiernalaboratoriet, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-230022.
Повний текст джерелаPetroni, Ricardo Costa. "Papel da solução salina hipertônica (NaCl 7,5%) no remodelamento pulmonar da endotoxemia induzida por lipopolissacarídeos." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5165/tde-03122013-105443/.
Повний текст джерелаSepsis syndrome is caused by inappropriate immune activation due to bacteria and bacterial components released during infection. The respiratory failure is among the most frequent complication of severe sepsis, occurring in almost 80% of the cases. About 40% of septic patients develop acute respiratory distress syndrome (ARDS) which is characterized mainly by the change of respiratory function, interstitial lung edema and fibronectin and collagen deposition in the lung. Fluid resuscitation is normally used in the management of patients with severe sepsis and septic shock. Hypertonic saline solution (HS, NaCl 7,5%) has shown to modulates immune function and decrease pulmonary injury triggered by endotoxemic shock. Our objective was to investigate the effects of early and later HS treatment on the mechanism involved in pulmonary injury, in an experimental model of endotoxemic shock. Wistar rats received lipopolysaccharide - LPS (10mg/kg i.p.) and volume i.v. after 15 minutes (early) or 1,5 hours (later). The animals were assigned in four groups (n=10): control group (not subjected to LPS); LPS group (injected with LPS 10mg/kg i.p); HS group (treated with hypertonic saline, 4 mL/Kg i.v. after LPS) and NS group (treated with normal saline, 34 mL/kg i.v. after LPS). We evaluated mortality and at 24h after treatment, pulmonary edema and mechanics, type I and type III collagen expression, metalloproteinase 9 expression and activity, focal adhesion kinase (FAK) and nitric oxide (NO) synthesis were measured. In the early treatment NS increased pulmonary resistance and elastance, compared to other groups. HS inhibited collagen expression compared to LPS and NS groups and prevented pulmonary injury by decreasing MMP-9 activity in tissue. Expression of FAK was decreased in HS groups compared to LPS and NS groups. NO expression was decreased in HS group, compared to LPS and NS groups. The later treatment with HS did not showed improvement of previous parameters increasing mortality and pulmonary injury. We concluded that HS treatment of endotoxemic shock at the earliest possible time point maximizes its efficacy in preventing pulmonary injury probably acting on nitric oxide-induced FAK activation pathway, which could modulate the collagen deposition in pulmonary tissue, and consequently decrease the progression of pulmonary fibrosis. Later treatment with HS decreased beneficial effects of hypertonic saline observed in early infusion, showed the importance of timing in the result of fluid therapy
Bernard, Amandine. "Expression des formes membranaire et soluble (Delta 6) de CD127, chaîne alpha du récepteur à l’IL-7, chez le macaque rhésus sain ou infecté par le virus de l’immunodéficience simienne." Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015PA05T008.
Повний текст джерелаInterleukin-7 (IL-7) is a crucial cytokine for T-cell development and peripheral T-cell homeostasis. The IL-7 receptor (IL-7R) is composed by the alpha chain (or CD127) shared with the TSLP receptor and the common gamma chain (or CD132) shared with several receptors of gamma cytokines. IL-7R expression was described in T lymphocytes but was not clearly demonstrated in antigen presenting cells (APC). However, CD127 chain and gamma cytokine receptors were described in these cells suggesting a functional IL-7R expression in APC. Interestingly, the CD127 chain also exists under various soluble forms (CD127s) resulting in alternative splicing of CD127 mRNA. However, the expression and the regulation of CD127 isoforms expression have been barely studied in APC. Moreover, polymorphisms in CD127 gene were identified and associated with a strong plasmatic concentration of the soluble form CD127s ∆6 in Humans and a stronger susceptibility to develop autoimmune diseases. Some of these polymorphisms are also associated with a faster evolution to the AIDS stage for HIV patients. Finally, the capacity of this soluble form to bound IL-7 suggests an important role of CD127s ∆6 to regulate IL-7 response by acting on his availability. However, the plasmatic CD127s expression is very controversial in HIV patients in chronic phase of infection. Moreover it expression was not known in infected organs and has never been described in acute phase of infection. Finally, nobody defines its origin and its function yet. The specific quantification of CD127s ∆6 by RT-qPCR revealed a minority expression of CD127s ∆6 in PBMC, weak in gut, more important in ganglions and even more in lung. More precisely, this study highlight on isolated cells from healthy monkey’s blood and spleen, a weak expression of CD127 by monocytes characterized by a majority expression of the soluble form contrary to T lymphocytes. Afterwards, we confirmed these results in vitro in two major immune populations in lung: in primary alveolar macrophages (AM) isolated from broncho-alveolar lavages (BAL) from healthy rhesus monkey and in the NCI-H226 lineage of human lung epithelial cells (LEC). In a second part, the specific quantification of CD127s Δ6 by RT-qPCR in organs (ganglions and lung) and the determination of the CD127s plasmatic protein at the acute phase of SIVmac251 infection revealed a significant up-regulation of this expression in lung in times D7, D10 and D14 post infection and its plasmatic concentration at D10 in infected monkeys. Finally, in the last part, we also quantified the viral load and IL-7 expression from infected monkeys to understand mechanisms implicated in regulation of CD127 expression during SIVmac251 infection. Surprisingly, we found none correlation between CD127s ∆6 expression and viral load or IL-7 expression from infected monkeys and healthy monkeys after injection of a pharmacological dose of IL-7. These data suggest an indirect effect of IL-7 and virus on CD127s ∆6 expression and a role of inflammation factors in regulation of his expression. In order to better define these mechanisms of regulation, the transcripts coding for the soluble form were quantified on AM and LEC in vitro after 6H of stimulation with or without IL-7 or TSLP (ligands of CD127) alone or combined with TNFα (pro inflammatory cytokine). Surprisingly, contrary to T lymphocytes, IL-7 do not induces down regulation of CD127 expression on AM and LEC. Nevertheless, CD127s ∆6 expression is upregulated upon TNFα by AM in a dose dependent manner. Moreover, the costimulation (IL-7 + TNFα) induces CD127s ∆6 expression by LEC revealing a synergic effect of IL-7 and TNFα. Finally the polarization of macrophages derived from human monocytes (hMDM) show that activated state of macrophages impact not only expression but also regulation of CD127 expression by these cytokines. (...)
Melo, Adriana Corrêa. "Função pulmonar, estresse oxidativo e marcadores inflamatórios na lesão pulmonar aguda induzida por lipopolissacarídeo: diferentes efeitos da atorvastatina, pravastatina e simvastatina." Universidade do Estado do Rio de Janeiro, 2012. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=5985.
Повний текст джерелаTo determinate what statins could attenuate acute lung injury (ALI) induced by lipopolysaccharide (LPS) in C57BL/6 mice. Young male mice ( 23 g) were divided into 5 groups (n=6 each): injected with LPS i.p. (10 mg/kg), LPS plus atorvastatin (10 mg/kg/day; LPS+A group) or pravastatin (5 mg/kg/day; LPS+P group) or simvastatin (20 mg/kg/day; LPS+S group). Control group received saline (i.p.). In a separated group of mice (n=5) the sum of pulmonary resistive and viscoelastic pressures (DeltaPtot) and static elastance (E[st]) were measured. One day later (24 h), the animals were sacrificed, BAL performed and lungs were removed for histopathological analysis and homogenized for biochemical analyses (ELISA, catalase, superoxide dismutase, myeloperoxidase, thiobarbituric acid reactive substances, protein carbonyls and griess assay). The amount of leukocytes was lower in LPS+P (p<0.01) and LPS+S (p<0.05). Cytokine levels of MCP-1 was lower in LPS+P (p<0.01) while IL-6 was lower in LPS+P (p<0.01) and LPS+S (p <0.05). Redox markers (superoxide dismutase and catalase) were lower in LPS+A (p<0.01). Lipid peroxidation (malondialdehyde and hydroperoxides) were lower in all treated groups (p<0.05). Myeloperoxidase was lower in LPS+P (p<0.01). DeltaPtot and E(st) were significantly higher in the LPS group than in the other groups. Our results suggest that atorvastatin and pravastatin, but no simvastatin, exhibits anti-inflammatory and antioxidant actions in LPS-induced ALI.
Monsel, Antoine. "Inflammation aiguë pulmonaire en réanimation : développement d'axes diagnostiques, préventifs et de thérapies immunomodulatrices." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066248/document.
Повний текст джерелаPneumonia and acute respiratory distress syndrome (ARDS) are two facets of severe acute lunginflammation, often met in intensive care unit (ICU). Rapid diagnosis of pneumonia remains essential inorder to optimize their management. We worked on setting up a quick test diagnosis based on theintensity of alveolar neutrophils autofluorescence. The validation of this test in a multicenter cohort isunderway. Preventing microaspiration across the cuff remains a priority to prevent pneumonia inmechanically ventilated patients. Based on the results of an ex vivo study followed by a clinicalrandomized trial, we showed that tapered-cuff endotracheal tube prevented microaspiration in the exvivo model, without lowering intraoperative microaspirations and postoperative pneumonia rate aftermajor vascular surgery. Both studies yielded similar results concerning the higher variation of cuffpressureover time, which leads to the question of their safety of use in terms of potential resultingtracheal wall ischemia.Pneumonia represents 80% of the cause of ARDS, which can be viewed as lung uncontrolledinflammatory response. Cell-based therapy using mesenchymal stem cells (MSC) is a growing field ofresearch in ARDS therapy. Despite numerous beneficial effects in ARDS, their capacity of self-renewalpoints them out as a potential cancer inducer in the mid-long term. In this context, evaluating thetherapeutic effects of extracellular vesicles-released from MSC (EV-MSC) represents a novel approach.We showed therapeutic effects of EC-CSM in two murine model of ARDS induced by endotoxin or liveEscherichia coli bacteria, and in another ex vivo human lung preparation.We then focused our research on temporal and compartmental dynamics of regulatory T cells(Treg) phenotypes in ARDS patients. This prospective observational clinical study showed that Early ARDSwas characterized with an alveolar compartment fully polarized towards pro-inflammatory state andneutrophils chemotaxis. In lung compartment, and compared to control patients, ARDS patients showeda quantitative Tregs deficiency, which partially recovered over time, while activation markers wereoverexpressed in both Tregs and effectors T cells (Teff). Conversely, patients with ARDS had a higherproportion of systemic Tregs compared to controls. Significant increased proportion in circulating Th1,Th22, and ILC1 subsets, and decreased proportion in ILC3 subsets were also found in ARDS patientscompared to controls.In conclusion, we developed novel strategies to diagnose and prevent pneumonia in ICU, whichremains essential to improve patients’ outcomes. Therapeutic effects of MSC and EV-MSC, as well asTreg phenotype alterations pave the way for development of novel immunoregulatory therapies
Holms, Carla Augusto Thomaz de Aquino. "Avaliação da resposta inflamatória pulmonar de suínos submetidos a lesão pulmonar aguda induzida por ácido clorídrico e tratados com solução salina hipertônica." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/5/5152/tde-22012013-174923/.
Повний текст джерелаBACKGROUND: Acute lung injury (ALI) caused by aspiration of gastric contents is not ununsual in patients with depression of airway reflexes. The potential anti-inflammatory effects of hypertonic saline 7.5% (HS) is still controversial on pulmonary response. OBJECTIVES: This study aimed to evaluate the potential anti-inflamatory effect of hypertonic saline (HS) in a swine model of hydrochloric acid (HCl) aspiration. METHODS: 32 pigs (n=32; 8/group) were randomly divided into the following groups: Sham, the animals were only anesthetized, ventilated and observed; HS, the animals received an 7.5% hypertonic saline infusion (4ml/kg); ALI, animals were submitted to ALI with HCl infusion; ALI+HS, animals were submitted to ALI with HCl infusion and treated with 7.5% hypertonic saline (4ml/kg). Hemodynamic and ventilatory parameters were measured. Blood samples were collected for blood gas analysis and plasma levels mensuration of TNF-?. Bronchoalveolar samples were also collected for IL-1, IL-6, IL-8, IL-10 and TNF-? cytokine mensuration and oxidative burst analysis. Lung tissue was collected for histological analysis. A parametrical analysis of variance with repeated measurement (ANOVA) followed by Tukey test was done. The significance level was set at 5% (p<0,05). RESULTS: There were estatistical differences regarding to ventilatory parameters, oxigenation, oxidative burst and pulmonary histological evaluation in ALI and ALI+HS groups, when compared to Sham and HS. IL-6 and IL-8 levels were higher in ALI and ALI+HS groups. However, no statistical difference were found between groups. CONCLUSION: The ALI model was effective to promote diffuse and heterogeneous lung injury. However, the group treated with 7.5% hypertonic saline did not presented statistical difference when compared to the non treated group regarding the evaluated parameters.
Junior, Luciano Filgueiras Ribeiro. "O eixo LTB4/MYD88 na inflamação estéril e na sepse em modelos experimentais de diabetes." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/42/42133/tde-25112014-165209/.
Повний текст джерелаType 1 diabetes (T1D) is associated with sterile inflammation (SI) and increased sepsis susceptibility. Sepsis induces Systemic Inflammatory Response Syndrome (SIRS) and Acute Lung Injury (ALI). Leukotriene (LT) B4 is produced in inflammatory conditions and induces MyD88 expression in macrophages (MA). We hypothesized that T1D induce LB4 that promotes SI contributing to SIRS, sepsis susceptibility and ALI. Diabetics presented higher levels of LTB4 and e IL-1b in the serum and MA expressed more MyD88/STAT-1. STAT-1 expression was induced by c-Jun on LTB4 dependent manner. Insulin treatment restored LTB4 and STAT-1/MyD88 levels and inhibition of LTB4 restored MyD88 and IL-1b levels. During sepsis, 5LO inhibition increased diabetics survival and inhibited SIRS- lower levels of IL-1b and IL-10 in the serum and TNF-a and IL-1b in the peritoneal cavity. Lungs from diabetics presented milder ALI that correlated with high levels of SOCS-1, low levels of MyD88 and impaired NFkB activation in alveolar macrophages.
Книги з теми "Pulmonary acute inflammation"
Ware, Lorraine B. Pathophysiology of acute respiratory distress syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0108.
Повний текст джерелаGiannitsis, Evangelos, and Hugo A. Katus. Biomarkers in acute coronary syndromes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0036.
Повний текст джерелаGiannitsis, Evangelos, and Hugo A. Katus. Biomarkers in acute coronary syndromes. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0036_update_001.
Повний текст джерелаGiannitsis, Evangelos, and Hugo A. Katus. Biomarkers in acute coronary syndromes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0036_update_002.
Повний текст джерелаFrew, Anthony. Air pollution. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0341.
Повний текст джерелаЧастини книг з теми "Pulmonary acute inflammation"
An, Gary, Michael Wandling, and Scott Christley. "Agent-Based Modeling Approaches to Multi-Scale Systems Biology: An Example Agent-Based Model of Acute Pulmonary Inflammation." In Systems Biology, 429–61. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6803-1_15.
Повний текст джерелаRuigrok, Dieuwertje, and Anton Vonk Noordegraaf. "Pathophysiology of acute pulmonary embolism." In ESC CardioMed, 2756–58. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0657.
Повний текст джерелаTarı Selçuk, Kevser. "Epidemiology of Inflammation-Related Diseases." In Role of Nutrition in Providing Pro-/Anti-Inflammatory Balance, 24–44. IGI Global, 2020. http://dx.doi.org/10.4018/978-1-7998-3594-3.ch002.
Повний текст джерелаTse, Doris, and Kin-Sang Chan. "Cough and other pulmonary symptoms." In Oxford Textbook of Palliative Medicine, edited by Nathan I. Cherny, Marie T. Fallon, Stein Kaasa, Russell K. Portenoy, and David C. Currow, 604–10. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198821328.003.0059.
Повний текст джерелаDotto, Annapaola. "The Anesthesiologist Contribution to Management of Acute Pancreatitis." In Multidisciplinary Management of Pancreatitis [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105821.
Повний текст джерелаFarne, Hugo, Edward Norris-Cervetto, and James Warbrick-Smith. "Cough." In Oxford Cases in Medicine and Surgery. Oxford University Press, 2015. http://dx.doi.org/10.1093/oso/9780198716228.003.0013.
Повний текст джерелаBourke, S. J., and G. P. Spickett. "Hypersensitivity pneumonitis." In Oxford Textbook of Medicine, edited by Pallav L. Shah, 4244–56. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0424.
Повний текст джерелаLittle, Brent P., and Travis S. Henry. "Bronchiolitis." In Chest Imaging, 331–36. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780199858064.003.0057.
Повний текст джерелаDaga, Mradul Kumar, Siddharth Chand, Naresh Kumar, Govind Mawari, R. V. Raghu, and J. Aarthi. "Proinflammatory and Thrombotic Manifestations and the Therapeutic Options of COVID-19." In Coronaviruses, 49–78. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815123371123030005.
Повний текст джерелаТези доповідей конференцій з теми "Pulmonary acute inflammation"
Hilliard, Kristie L., Joseph P. Mizgerd, Eri Allen, Matthew R. Jones, and Lee J. Quinton. "The Hepatic Acute Phase Response Regulates Pulmonary Inflammation During Pneumonia." 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.a3277.
Повний текст джерелаToumpanakis, Dimitrios, Eleftheria Mizi, Vyronia Vassilakopoulou, Athanasia Chatzianastasiou, Stamatios Theocharis, and Theodoros Vassilakopoulos. "Resistive breathing aggravates pulmonary inflammation and emphysema in experimental models of chronic obstructive pulmonary disease." In Abstracts from the 17th ERS Lung Science Conference: ‘Mechanisms of Acute Exacerbation of Respiratory Disease’. European Respiratory Society, 2019. http://dx.doi.org/10.1183/23120541.lungscienceconference-2019.yi04.
Повний текст джерелаStrahan, Brian, and Patrick Arndt. "S100B Regulates Pulmonary Neutrophil Recruitment In Lipopolysaccharide-induced Acute Lung 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.a2319.
Повний текст джерелаGonzalez-Ferrer, S., H. Peñaloza, A. McCollum, R. Van Der Geest, N. Kohli, M. Tabary, Z. Xiong, et al. "STAT1 Modulates Neutrophilic Inflammation During Acute Pulmonary Infection with Klebsiella Pneumoniae." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a2189.
Повний текст джерелаShpagina, L. A., E. B. Logashenko, and O. S. Kotova. "ACUTE EXACERBATIONS OF OCCUPATIONAL CHRONIC OBSTRUCTIVE PULMONARY DISEASE DUE TO INDUSTRIAL AEROSOLS CONTAINING." In The 16th «OCCUPATION and HEALTH» Russian National Congress with International Participation (OHRNC-2021). FSBSI “IRIOH”, 2021. http://dx.doi.org/10.31089/978-5-6042929-2-1-2021-1-593-597.
Повний текст джерелаKorkmaz, F. T., E. Symer, C. Odom, W. Molina, E. Na, L. Baird, Y. Kim, et al. "Expression of LOX-1 in the Lung Modulates Acute Pulmonary Inflammation During Pneumonia." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1221.
Повний текст джерелаSaperstein, SC, HL Huyck, CJ Johnston, JN Finkelstein та GS Pryhuber. "Interleukin-1β Is Essential for Tumor Necrosis Factor-α-Induced Acute Pulmonary Inflammation in Mice." У American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1916.
Повний текст джерелаChimenti, Laura, Raquel Guillamat, Neus Gomez, Jessica Tijero, LLuis Blanch, and Antonio Artigas. "Effects of nebulized heparin on pulmonary inflammation in a rat model of acute lung injury." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2138.
Повний текст джерелаBoe, Darren M., Tiffany R. Richens, Sarah A. Horstmann, William J. Janssen, Peter M. Henson, Marc Moss, and R. W. Vandivier. "Acute And Chronic Alcohol Exposure Impair The Clearance Of Apoptotic Cells And Enhance Pulmonary 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.a1267.
Повний текст джерелаKing, BA, and PS Kingma. "Surfactant Protein D Decreases Pulmonary Inflammation in Acute Respiratory Distress Syndrome Induced by Indirect Lung Injury." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3877.
Повний текст джерелаЗвіти організацій з теми "Pulmonary acute inflammation"
Ma, He, Jifu Zhao, and Zhilei Wang. Efficacy and safety of HuaYu TongFu Method combined with acupuncture in the treatment of Acute Exacerbation of Chronic Obstructive Pulmonary Disease:A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0114.
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