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Gotowe bibliografie tematyczne / Peripheral inflammation

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Gotowa bibliografia na temat „Peripheral inflammation”

Autor: Grafiati

Data publikacji: 31 sierpnia 2024

Data aktualizacji: 12 lipca 2025

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Artykuły w czasopismach na temat "Peripheral inflammation"

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De Kock, Marc, Sebastien Loix, and Patricia Lavand'homme. "Ketamine and Peripheral Inflammation." CNS Neuroscience & Therapeutics 19, no. 6 (2013): 403–10. http://dx.doi.org/10.1111/cns.12104.

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Träger, Ulrike, and Sarah J. Tabrizi. "Peripheral inflammation in neurodegeneration." Journal of Molecular Medicine 91, no. 6 (2013): 673–81. http://dx.doi.org/10.1007/s00109-013-1026-0.

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Poutler, L. W. "Central inflammation is more important than peripheral inflammation." Respiratory Medicine 91 (November 1997): 9–10. http://dx.doi.org/10.1016/s0954-6111(97)90097-4.

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Hamid, Q. A. "Peripheral inflammation is more important than central inflammation." Respiratory Medicine 91 (November 1997): 11–12. http://dx.doi.org/10.1016/s0954-6111(97)90098-6.

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Groven, N., E. A. Fors, V. C. Iversen, L. R. White, and S. K. Reitan. "Peripheral inflammation in fibromyalgia syndrome." European Neuropsychopharmacology 27 (October 2017): S634. http://dx.doi.org/10.1016/s0924-977x(17)31194-x.

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Lisney, S. J. W. "The development of peripheral inflammation." Pain Forum 4, no. 3 (1995): 153–54. http://dx.doi.org/10.1016/s1082-3174(11)80047-4.

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Brevetti, Gregorio, Giuseppe Giugliano, Linda Brevetti, and William R. Hiatt. "Inflammation in Peripheral Artery Disease." Circulation 122, no. 18 (2010): 1862–75. http://dx.doi.org/10.1161/circulationaha.109.918417.

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Signorelli, Salvatore, Elisa Marino, and Salvatore Scuto. "Inflammation and Peripheral Arterial Disease." J 2, no. 2 (2019): 142–51. http://dx.doi.org/10.3390/j2020012.

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Peripheral arterial disease (PAD) is an atherosclerotic disease closely associated with high morbidity and mortality in cardiac events. Inflammation is crucial in atherosclerosis both at triggering and in progression. Numerous inflammatory biomarkers (cytokines, matrix metalloproteinases (MMPs), selectin, intracellular adhesion molecule (ICAM), vascular cell adhesion molecule (VCAM) C-reactive protein (CRP), fibrinogen) have been measured in atherosclerotic diseases including PAD. This paper summarizes the data on the inflammatory biomarkers for PAD pathophysiology and highlights the most useful markers in monitoring PAD outcomes.

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Callas, Peter, Matthew Allison, Michael Criqui, and Mary Cushman. "Inflammation and peripheral venous disease." Thrombosis and Haemostasis 112, no. 09 (2014): 566–72. http://dx.doi.org/10.1160/th13-10-0860.

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SummaryThe inflammatory response to healing in venous thrombosis might cause vein damage and post-thrombotic syndrome. Inflammation may also be involved in venous insufficiency apart from deep-vein thrombosis. We studied the association of inflammation markers with venous insufficiency in a general population sample. We characterised 2,404 men and women in a general population cohort for peripheral venous disease and its severity using physical exam, symptom assessment, and venous ultrasound. Inflammation markers, C-reactive protein (CRP), fibrinogen, interleukin 1-beta (IL-1-beta), IL-8, IL-10, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, monocyte chemoattractant-1 (MCP-1) and vascular endothelial cell growth factor (VEGF) were compared in 352 case participants with peripheral venous disease and 352 controls with no venous abnormalities frequency matched to cases by age, sex and race. Associations were also evaluated including a subset of 108 cases of severe venous disease, as previously defined. Odds ratios (95% CI), for peripheral venous disease for biomarkers in the top quartile (adjusting for age, race, sex, body mass index and history of venous thrombosis) were 1.8 (1.1–3.0), 1.6 (1.0–2.5) and 1.5 (0.9–2.3) for CRP, fibrinogen and IL-10, respectively. Associations were larger considering cases of severe venous disease, with odds ratios for these three analytes of 2.6 (1.2–5.9), 3.1 (1.3–7.3) and 2.2 (1.1–4.4), and for IL-8: 2.4 (1.1–5.2). There was no association of IL-1-beta, ICAM-1, VCAM-1, E-selectin, MCP-1 or VEGF with overall cases or severe venous disease. In conclusion, a subset of inflammation markers were associated with increased risk of peripheral venous disease, suggesting potential therapeutic targets for treatment.

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Schafer, M., Y. Imai, S. Mousa, I. Antonijevic, G. R. Uhl, and C. Stein. "Peripheral Opioid Analgesia in Inflammation." Anesthesiology 81, SUPPLEMENT (1994): A920. http://dx.doi.org/10.1097/00000542-199409001-00919.

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Rozprawy doktorskie na temat "Peripheral inflammation"

1

Chapman, Katie. "Peripheral inflammation after experimental stroke." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.518434.

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McColl, Alison. "The brain response to peripheral inflammation." Thesis, University of Glasgow, 2015. http://theses.gla.ac.uk/6764/.

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Communication between the immune system and the central nervous system (CNS) is becoming increasingly topical as evidence suggests the two systems are intricately linked. Although the brain is considered an ‘immune-specialised’ tissue, it is not free from the influences of the periphery. Recent data indicate that peripheral immune stimulation can significantly affect the CNS, and patients with chronic inflammatory diseases, including rheumatoid arthritis (RA) and psoriasis, are often further burdened by the onset of neuropsychiatric conditions such as major depressive disorder (MDD), schizophrenia and anxiety. However, despite increases in our understanding, the precise mechanisms underpinning this relationship remain unclear. Therefore, the aim of this thesis is to investigate the communication pathways that exist between the immune system and the nervous system and to enhance our understanding of this bidirectional relationship. Using a well-characterised animal model of psoriasis-like skin inflammation, I have investigated the effects of cutaneous, peripheral inflammation on the brain. Psoriasis-like skin inflammation was induced in female C57BL/6 mice via the repeated application of Aldara cream to the shaved dorsal skin. Twenty-four hours after the fifth application, the transcriptional response in the brain was assessed and compared with mice treated with an aqueous control cream, using Affymetrix GeneChip arrays. The induction of target genes, identified using microarray analysis, was confirmed in an independent model using QPCR and was compared to the gene induction following a number of other inflammatory models, including a sterile model of cutaneous inflammation. Transcriptional profiling techniques allowed me to identify a number of differentially expressed genes in the brains of Aldara- and Imiquimod (IMQ)- treated mice when compared with the brains of control mice. This response included a range of interferon-stimulated genes (ISGs) and chemokines that were not induced in the peripheral blood leukocytes (PBL), and occurred independently of an overt cytokine response in the PBL. The brain ISG and chemokine response was not detected following a sterile model of cutaneous inflammation or following the intraperitoneal administration of Imiquimod. The central induction of a number of chemokines prompted the evaluation of immune cell infiltration into the brain parenchyma. In addition, the functional consequences of topical Aldara treatment, and the involvement of inflammatory chemokines, were determined by assessing dentate neurogenesis and burrowing behaviour in wild-type and ACKR2-deficient mice. The transcriptional response following cutaneous IMQ-induced inflammation is indicative of a peripherally triggered inflammatory response in the brain. In addition, the data described in this thesis demonstrate a functional consequence of peripheral immune stimulation and suggest that cutaneous inflammation could modulate the recruitment of leukocytes to the brain. These data highlight a potential mechanism of TLR-dependent communication between the periphery and the brain that could be mediated through the activation of the afferent vagus nerve.

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Adeoye, Opeolu M. D. "Peripheral Leukocytes and Intracerebral Hemorrhage." University of Cincinnati / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1353100438.

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Jiang, Yanyan. "The role of peripheral TNF in acute brain inflammation." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.496980.

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Barr, Laura Caroline. "Peripheral blood mononuclear cell depletion for experimental human lung inflammation." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/23705.

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Acute lung injury (ALI) affects a significant proportion of patients requiring critical care and is associated with high morbidity and mortality. Treatment is currently only supportive, with no pharmacological treatment yet shown to definitively improve outcome. There is evidence from murine models of ALI that monocytes play a key role in the development of the neutrophilic lung infiltration characteristic of ALI. Depletion of blood monocytes in mice given intra-tracheal lipopolysaccharide (LPS) significantly reduces pulmonary neutrophil influx, systemic neutrophilia and other markers of lung injury. In humans, monocyte-like cells have been documented in the bronchoalveolar lavage (BAL) fluid of patients with a variety of inflammatory lung conditions, including ALI. This thesis describes novel work performed in healthy human subjects to test whether, in an experimental model of human lung inflammation, depletion of circulating blood monocytes can ameliorate systemic and pulmonary inflammation. LPS inhalation is an established method of modelling ALI in healthy human subjects as it safely and consistently induces mild and self-limiting systemic and pulmonary inflammation. A preliminary study in a group of 12 healthy subjects confirmed the safety and efficacy of LPS inhalation compared to saline placebo. LPS inhalation induced a marked blood neutrophilia together with a rise in body temperature and heart rate and elevated BAL neutrophil and pro-inflammatory cytokine concentrations. This study also used flow cytometry to confirm the presence of pulmonary monocyte-like cells (PMLCs) in BAL fluid, which, although distinct from blood monocytes, could be clearly divided into two separate sub-types according to CD14/CD16 expression. LPS inhalation caused a rise in the number of circulating classical monocytes in blood and an expansion in the CD14++CD16- 'inducible' iPMLC subtype (reminiscent of classical blood monocytes), compared to the CD14++CD16+ 'resident' rPMLC subtype. This may represent transmigration of classical monocytes from blood across the pulmonary endothelium. In humans, mononuclear cell (MNC) leukapheresis provides a readily available method of depleting circulating blood monocytes. A second preliminary study, performed in a separate group of 6 healthy subjects, demonstrated that leukapheresis of four total blood volumes could be safely employed to deplete large numbers of circulating blood monocytes. Active recruitment of monocytes into circulating blood during leukapheresis did, however, limit the reduction in total circulating blood monocyte counts. This study also investigated, for the first time, the potential pulmonary effects of leukapheresis. Despite a relative prominence of iPMLCs in BAL fluid after leukapheresis, there was no evidence of significant neutrophil influx or a clinically important pro-inflammatory effect in the alveolar space. A randomised, double blind, placebo-controlled trial was then performed in a third group of 30 healthy human subjects who all inhaled LPS at baseline. There was no evidence that MNC leukapheresis (depletion group, n=15), compared to a sham procedure (sham group, n=15), attenuated the systemic and pulmonary inflammation induced by LPS inhalation, as measured by: blood neutrophil and plasma C-reactive protein (CRP) levels; by the neutrophil, protein and pro-inflammatory cytokine content of BAL fluid; and by [18F]fluorodeoxyglucose positron emission tomography ([18F]FDG PET)-derived measures of global lung inflammation. MNC leukapheresis temporarily prevented the LPS-induced rise in circulating classical monocytes and was also associated with a small reduction in the estimated numbers of MNCs in BAL fluid. It did not, however, appear to affect the LPS-induced expansion in the iPMLC subtype. Further characterisation of the PMLC subtypes by flow cytometry/sorting and cell culture demonstrated that the iPMLC subtype was more pro-inflammatory but less mature and with a lower proliferation potential than the rPMLC subtype. In summary, this work did not support a role for circulating blood monocytes in the evolution of LPS-induced systemic or pulmonary neutrophilia in man. The rise in circulating levels of classical blood monocytes and the dramatic expansion of pro-inflammatory, immature iPMLCs in BAL fluid after LPS inhalation do, however, suggest that monocytes migrate to the lung and are to some extent involved in the pathogenesis of lung inflammation. Compared to murine methods of monocyte depletion, leukapheresis could not achieve such an extensive or sustained reduction in circulating blood monocyte counts, nor was it likely to have influenced other (specifically patrolling or splenic) monocyte pools. Future work in the drive to find treatments for ALI should therefore investigate the potential of pre-emptive leukapheresis or the efficacy and safety of other methods of human monocyte depletion in experimental lung inflammation.

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Karim, Salman. "Peripheral and central markers of inflammation in mild cognitive impairment." Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/peripheral-and-central-markers-of-inflammation-in-mild-cognitive-impairment(bd21dafe-65c1-42c9-949b-733abfc71037).html.

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There has been accumulating scientific evidence, over the last three decades, of the role of inflammatory processes in the development of Alzheimer's disease (AD). Population based studies suggest that plasma levels of inflammatory markers are raised in peripheral blood of people with AD. People on long term use of non-steroidal anti-inflammatory drugs have a lower prevalence of AD. Moreover, both animal and human histopathology studies have reported localization of inflammation in brain areas primarily affected by AD pathology. Areas of increased inflammation can be visualized in vivo by Positron Emission Tomography (PET) scans using the PK11195 ligand that binds with the benzodiazepine receptor sites of activated microglial cells. Cognitive decline in AD has been shown to correlate with levels of microglial activation using PK11195 PET scans. People with amnestic mild cognitive impairment (MCI) are known to be at high risk of developing AD.We aimed to investigate the association between peripheral and central markers of inflammation and cognitive decline in a group of people with amnestic MCI.MCI subjects (n=70) underwent cognitive testing, IL-6 and CRP in peripheral blood were measured and repeated after 1 year. A sub group (n=15) was followed up for another year and central brain microglial activation was measured by PET using PK11195 along with cognitive and peripheral inflammatory marker measurement. The mean CRP and IL-6 levels of the cohort increased over one year but the rise was only significant for CRP. No association was detected between inflammatory markers levels and cognition as measured by a battery of cognitive instruments. Group comparisons of the PET cohort with healthy controls (n=5) showed increased PK11195 binding (mean binding potential) in frontal lobe, temporal lobe, parietal lobe, putamen, occipital lobes and significantly increased binding in posterior cingulate gyrus. This study, to our knowledge, is unique in studying makers of inflammation in amnestic MCI participants both in peripheral blood and brain. The results of this study, in the light of current literature, add to the importance of recognition of inflammatory processes in people at risk of developing AD. The results suggest that CRP levels rise significantly over time and are detectable in peripheral blood by using practically simple laboratory techniques. The results also suggest that activated microglia in amnestic MCI patients can be visualized in vivo by using PK11195 PET scans and show higher levels of activation as compared to healthy controls. These finding could be useful in identifying people with malactivated (pro-inflammatory) microglia as potential targets for prevention/early treatment strategies. Further studies with larger samples sizes and long term follow-up are needed to investigate whether these peripheral and central inflammatory markers could shed light on the aetiology of AD and be useful in monitoring disease progression.

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Thomson, Carolyn. "Peripheral inflammation remotely triggers global gene expression changes in the brain." Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/5390/.

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Although the central nervous system (CNS) was once considered an immunologically privileged site, in recent years it has become increasingly evident that cross talk between the immune system and the CNS does occur. As a result, patients with chronic inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease or psoriasis are often further burdened with neuropsychiatric symptoms such as depression, anxiety and fatigue. Despite the recent advances in our understanding of neuroimmune communication pathways, the precise effect peripheral immune activation has on neural circuitry remains unclear. Therefore, the primary aim of this thesis was to develop a better understanding of the bidirectional relationship, and communication pathways, that exist between the immune system and the nervous system. By utilising transcriptomics in a well-characterised murine model of systemic inflammation, I have investigated the molecular mechanisms by which inflammation originating in the periphery can induce transcriptional modulation in the brain. Systemic inflammation was induced in male C57BL/6 mice via intraperitoneal injection of lipopolysaccharide (LPS). After 48 hours, whole brain transcriptional profiles were assessed, and compared to that of a vehicle- treated control group, using Affymetrix GeneChip microarrays. Target gene induction, identified by microarray analysis was validated independently using QPCR. Expression of the same panel of target genes was then investigated, in the brains of mice, following the induction of different sterile, and TLR- dependent, models of peripheral inflammation. Microarray analysis of whole brains collected 48hr after LPS challenge revealed increased transcription of a range of interferon-stimulated genes (ISGs) in the brain, including a significant upregulation of the classic interferon-induced chemokine CXCL10. This transcriptional profile could not be reproduced by the systemic administration of TNFα, or following lipoteichoic acid-induced systemic inflammation. However, target genes remained induced in the brain following daily LPS injections, in the absence of a detectable inflammatory cytokine response in the periphery. 1 The central induction of CXCL10 suggests that acute exposure to LPS in the periphery may prime the brain for T cell infiltration. This prompted an investigation into whether leukocytes infiltrated the brain following daily systemic LPS injections. First, the inflammatory chemokine repertoire in the brains of LPS treated mice was systematically characterised. In addition to Cxcl10, repeated injection of LPS in the periphery triggered a transient increase in the transcription of a number of other inflammatory chemokines in the brain. Chemokine induction was associated with an influx of leukocytes from the periphery, and an increase in mRNA encoding the relevant chemokine receptors. Therefore, chemokine induction in the brain following daily systemic LPS injections may mediate the recruitment of leukocytes from the periphery. The transcriptional response in the brain following systemic LPS challenge is indicative of a peripherally triggered inflammatory response in the brain. The data described in this thesis highlight a potential mechanism of gene modulation in the brain which may be dependent on a TLR-induced type I interferon response. Considerable evidence links type I interferons to psychiatric disorders, and consequently, interferon production in the brain could represent an important mechanism linking peripheral TLR-induced inflammation with behavioural changes. In addition, the data described in this thesis demonstrate that chronic exposure to LPS in the periphery may remotely modulate the recruitment of leukocytes to the brain. This highlights a potential protective mechanism that could prevent a chronic bacterial infection from spreading from the periphery to the brain.

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Tzoulaki, Ioanna. "Inflammation and haemostasis in the development and progression of peripheral atherosclerotic disease." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/2148.

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Peripheral arterial disease (PAD) defines atherosclerotic disease of the arteries to the legs. PAD begins early in life and remains asymptomatic over long periods. The ankle brachial index (ABI) is an important diagnostic test which can identify asymptomatic individuals and serve as a good marker of the underlying peripheral and systemic atherosclerosis. Recent advances in vascular biology proposed a role of inflammatory and haemostatic mechanisms in atherosclerotic disease. Although inflammatory and haemostatic markers have been associated with coronary atherosclerosis in large scale epidemiological studies their role in PAD development is not well established and for many markers unknown. Also, their relationship with the progression of early asymptomatic disease has not been studied before. The aim of this thesis was to examine 12 markers of inflammation and haemostasis in relation to peripheral atherosclerotic progression and incident PAD. The Edinburgh Artery Study was used for this analysis. This is a population based cohort study of 1,592 men and women recruited in 1987. ABI was measured at baseline and at two follow up examinations which were conducted after 5 and after 12 years. Also, subjects were followed up for cardiovascular events for 17 years. Conventional cardiovascular risk factors, C-reactive protein (CRP), interleukin-6 (IL-6), intercellular adhesion molecule 1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), E-selectin, fibrinogen, D-dimer, tissue plasminogen activator (t-PA), vonWillebrand factor (vWF), factor VII, fibrinopeptide A (FpA) and prothrombin fragments 1+2 (F1+2) were measured at baseline. Valid ABI measurements were available for 1,582 subjects at baseline, for 1,081 subjects at the 5 year follow up and for 816 subjects at the 12 year follow up. The population showed a progression in atherosclerotic disease assessed by the mean ABI decline over time. The mean change in ABI was -0.04 (0.18) after 5 years and -0.06 (0.19) after 12 years. From inflammatory markers, CRP (p <0.01), IL-6 (p <0.001) and ICAM-1 (p <0.01) were associated with atherosclerotic progression after 12 years, independently of baseline ABI and of conventional cardiovascular risk factors. Also, from haemostatic markers, fibrinogen (p =0.05) and D-dimer (p ≤ 0.05) were significantly associated with atherosclerotic progression independently of baseline ABI and cardiovascular risk factors. Moreover, subjects with higher levels of both D-dimer and IL-6 at baseline had the greatest ABI decline. Also, IL-6 showed the stronger independent effect on atherosclerotic progression and retained statistical significance after adjustments for all inflammatory markers and for fibrinogen and D-dimer. Approximately 26% of the baseline population developed at least one event of major CVD and 14% of the baseline population developed symptomatic PAD after 17 years of follow up. Inflammatory markers, CRP and IL-6 showed modest associations with PAD which lost statistical significance in the multivariable model. On the other hand, these markers were associated with incident major CVD with hazard ratios (95% CI) 1.6 (1.2, 2.3) and 1.8 (1.3, 2.6) respectively (top vs. bottom tertile) in the multivariable model. ICAM-1 showed weak associations with incident CVD, however, was significantly associated with PAD with hazard ratio (95% CI) 1.8 (1.2, 2.7) (top vs. bottom tertile) after adjustments for cardiovascular risk factors and CVD at baseline. Haemostatic markers, fibrinogen and D-dimer were associated with 2.2 (95% CI: 1.5, 3.2) and 1.7 (1.2, 2.6) increase in the risk of PAD development and 1.8 (1.3, 2.3) and 1.6 (1.2, 2.1) increase in the risk of CVD independently of cardiovascular risk factors and history of CVD at baseline, respectively. This analysis showed a major role of inflammatory markers, CRP, IL-6 and ICAM-1 in atherosclerotic development and progression. In addition, fibrinogen and D-dimer, but not other haemostatic factors, were associated with progressive and incident peripheral atherosclerosis. Since D-dimer and fibrinogen are acute phase reactants, these data support the hypothesis that inflammation is more related to atherosclerosis than is hypercoagulation. Most importantly, the majority of the reported associations were not explained by increased levels of cardiovascular risk factors or pre-existing clinical or subclinical arterial disease. Thus these markers are more likely to have a causal than a consequential role in atherosclerotic disease.

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Parmar, Jiteshkumar H. "The role of inflammation in ischaemia reperfusion injury due to peripheral arterial revascularisation." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.509840.

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Hau, Vincent Sinh. "EFFECT OF PERIPHERAL INFLAMMATORY PAIN ON THE BLOOD-BRAIN BARRIER." Diss., Tucson, Arizona : University of Arizona, 2005. http://etd.library.arizona.edu/etd/GetFileServlet?file=file:///data1/pdf/etd/azu%5Fetd%5F1071%5F1%5Fm.pdf&type=application/pdf.

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Książki na temat "Peripheral inflammation"

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Schäfer, Michael, and Christoph Stein, eds. Mind over Matter - Regulation of Peripheral Inflammation by the CNS. Birkhäuser Basel, 2003. http://dx.doi.org/10.1007/978-3-0348-8039-8.

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De Leo, Joyce A., 1960-, Sorkin Linda S. 1953-, Watkins Linda R. 1954-, and International Association for the Study of Pain., eds. Immune and glial regulation of pain. IASP Press, 2007.

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Fatima Shad, Kaneez, ed. Erythrocyte - A Peripheral Biomarker For Infection and Inflammation. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.92510.

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Shad, Kaneez Fatima. Erythrocyte: A Peripheral Biomarker for Infection and Inflammation. IntechOpen, 2021.

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Jacoby, Dr Richard, and Raquel Baldelomar. Sugar Crush: How to Reduce Inflammation, Reverse Nerve Damage, and Reclaim Good Health. Harper Wave, 2016.

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Baldelomar, Raquel, and Richard Jacoby. Sugar Crush: How to Reduce Inflammation, Reverse Nerve Damage, and Reclaim Good Health. HarperCollins Publishers, 2015.

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(Editor), Michael Schäfer, and Christoph Stein (Editor), eds. Mind over Matter - Regulation of Peripheral Inflammation by the CNS (Progress in Inflammation Research). Birkhäuser Basel, 2004.

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Stein, Christoph, and Michael Schäfer. Mind over Matter - Regulation of Peripheral Inflammation by the CNS. Birkhauser Verlag, 2012.

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Schäfer, Michael. Mind over Matter - Regulation of Peripheral Inflammation by the Cns. Springer, 2012.

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Siebert, Stefan, Sengupta Raj, and Alexander Tsoukas. Peripheral musculoskeletal involvement in axial spondyloarthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198755296.003.0007.

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In addition to the axial diseases that characterizes axial spondyloarthritis (axSpA), many patients also develop peripheral musculoskeletal involvement. This can include peripheral joint synovitis, enthesitis, and dactylitis. Peripheral musculoskeletal involvement is an important component of the disease with significant impact on function and quality of life. Many of the features may also be subtle and overlooked, unless specifically evaluated and examined. In particular, hip disease is a bad prognostic feature and, if present, may require more aggressive therapy or surgical intervention. On occasion, further imaging may be required to detect enthesitis or subtle joint inflammation in order to inform treatment decisions.

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Części książek na temat "Peripheral inflammation"

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Olszewski, Waldemar L., and Marzanna T. Zaleska. "Inflammation." In Peripheral Lymphedema. Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-3484-0_15.

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Gupta, Noopur, Yogita Gupta, M. Vanathi, and Radhika Tandon. "Peripheral Ulcerative Keratitis." In Corneal Infection and Inflammation. CRC Press, 2021. http://dx.doi.org/10.1201/9781003024897-10.

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Lim, Alvin, Katarina Krajina, and Anna L. Marsland. "Peripheral Inflammation and Cognitive Aging." In Inflammation in Psychiatry. S. KARGER AG, 2013. http://dx.doi.org/10.1159/000346362.

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Murta, Verónica, and Carina Ferrari. "Peripheral Inflammation and Demyelinating Diseases." In Advances in Experimental Medicine and Biology. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-40764-7_13.

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Griffith, James F., and Roman Guggenberger. "Peripheral Nerve Imaging." In IDKD Springer Series. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-71281-5_18.

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AbstractThis chapter reviews the basics and practicalities of imaging the peripheral nerves with ultrasound and MRI. Nerve entrapment, tumours, trauma, and inflammation are covered. The complimentary role of ultrasound and MRI in imaging peripheral nerve disorders is stressed.

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Lever, Isobel. "Inflammation, Modulation by Peripheral Cannabinoid Receptors." In Encyclopedia of Pain. Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_1943.

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Carlton, Susan M. "Inflammation, Role of Peripheral Glutamate Receptors." In Encyclopedia of Pain. Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_1945.

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Shaikh, Sikandar. "PET-CT in Peripheral Vascular Pathologies." In PET-CT in Infection and Inflammation. Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-9801-2_9.

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Kamer, Angela R., Ronald G. Craig, and Mony J. de Leon. "Peripheral Inflammation and Alzheimer’s Disease: Periodontal Disease." In A Clinician's Guide to Systemic Effects of Periodontal Diseases. Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-49699-2_8.

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Ago, Yukio, Michael C. Condro, Abha K. Rajbhandari, et al. "PACAP Modulation of CNS and Peripheral Inflammation." In Current Topics in Neurotoxicity. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-35135-3_38.

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Streszczenia konferencji na temat "Peripheral inflammation"

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Machado, Luiza, Camila Santos, Bianca Leonardi, 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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Rotman, Oren, Dalit Shav, Uri Zaretsky, and Shmuel Einav. "Bio-Mechanical Aspects of Short Peripheral Catheter Thrombophlebitis." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-205445.

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Venflons, or Short Peripheral Catheters (SPC), are the most common intravenous devices being used in medical practice, particularly in hospitals and intensive care units. SPC is usually inserted into veins of the upper extremities to administer fluids, medications, blood products or for prophylactic use before procedures. It has been reported that 40–80% of hospitalized patients were treated with SPCs [1, 2]. Short Peripheral Catheter Thrombophlebitis (SPCT) is the most frequent complication of treatment with, characterized by pain, tenderness, warmth, erythema, swelling and palpable thrombosis of the cannulated vein. SPCT causes patients discomfort and generally leads to catheter removal and insertion of a new catheter at a different site [3]. SPCT is a sterile inflammation [2, 3], and its pathogenesis is not well understood. Several mechanisms have been suggested for SPCT pathogenesis, such as chemical irritation of the endothelium due to infusate or catheter material, or that vein wall injury combined with stasis cause an inflammation response and thrombosis [4, 5].

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Takeyama, K., A. Kurokawa, T. Akaba, et al. "Mucus Accumulation in Peripheral Airways: Comparison Between Neutrophilic and Eosinophilic Inflammation." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1324.

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cummings, steven M. "Fluorescein Isothiocyanate (FITC) Labelled Dextran As A Peripheral Marker Of Lung Inflammation." 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.a4376.

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Dürholz, K., M. Linnerbauer, E. Schmid, et al. "OP0029 GUT-SPECIFIC H3R SIGNALING ORCHESTRATES MICROGLIA-DEPENDENT RESOLUTION OF PERIPHERAL INFLAMMATION." In EULAR 2024 European Congress of Rheumatology, 12-15 June. Vienna, Austria. BMJ Publishing Group Ltd and European League Against Rheumatism, 2024. http://dx.doi.org/10.1136/annrheumdis-2024-eular.2235.

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Douglas, I. S., A. Longino, T. Hiller, et al. "CD40 Costimulatory Inhibition Modulates Immune Inflammation in Human Septic Peripheral Blood Mononuclear Cells." 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.a2824.

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Aldehmi, N., E. Naredo, J. Dale, A. Najm, and N. Basu. "AB0135 RELATING PERIPHERAL JOINT INFLAMMATION AND PAIN IN RHEUMATOID ARTHRITIS: A MUSCULOSKELETAL ULTRASOUND STUDY." In EULAR 2024 European Congress of Rheumatology, 12-15 June. Vienna, Austria. BMJ Publishing Group Ltd and European League Against Rheumatism, 2024. http://dx.doi.org/10.1136/annrheumdis-2024-eular.5271.

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Lopalco, G., L. DI Pietro, A. Privitera, et al. "AB0971 OXIDATIVE STRESS AND INFLAMMATION IN AXIAL SPONDYLOARTHRITIS: PROFILING OF PERIPHERAL BLOOD MONONUCLEAR CELLS." In EULAR 2024 European Congress of Rheumatology, 12-15 June. Vienna, Austria. BMJ Publishing Group Ltd and European League Against Rheumatism, 2024. http://dx.doi.org/10.1136/annrheumdis-2024-eular.4836.

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Shirai, Toshihiro, Masashi Mikamo, Yuichiro Shishido, et al. "Colored 3D Analyses Of Respiratory Impedance In Asthma: Association With Peripheral Airway Inflammation And Dysfunction." 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.a3939.

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Andrade, Dariana Rodrigues, Letícia Mendes de Lima, Luis Henrique Goes Hamati Rosa, and Edvaldo Cardoso. "SARS-CoV-2 infection in the development of peripheral neuropathies." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.406.

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Introduction: Although respiratory symptoms are the characteristic findings of COVID- 19, this disease may also present with neurological manifestations, since SARS-CoV- 2 showed several degrees of neurotropism. Objectives: To review the influence of SARS-CoV-2 infection on the development of peripheral neuropathies. Methods: Integrative review carried out at PUBMED with the descriptors peripheral neuropathy, SARS-CoV-2 and COVID-19, and having as inclusion criteria full texts and in English in the period from 11/2019 to 05/2021. The selection has made among those compatible with the objectives of the work. Results: Peripheral neuropathy was observed in less than 1% of patients with COVID-19. The virus can cause acute polyradiculoneuropathy regardless of pulmonary disease, and may occur due to dysregulation of the immune system caused by SARS-CoV-2. Systemic hyper-inflammation with macrophage activation syndrome has been proposed for patients with COVID-19. Such immunomediated manifestations typically occur after the decrease in the acute phase of disease. The most commonly reported symptoms in peripheral nervous system involvement are ageusia, anosmia, diplopia, facial nerve paralysis, polyneuritis, myasthenic crisis, musculoskeletal injuries, and neuralgia. Conclusion: As soon as possible recognition of peripheral neuropathy may result in better clinical goals for patients and understanding these manifestations will contribute to the development of improved treatment. Although only a small percentage of patients with COVID-19 develop peripheral neuropathy, in a pandemic this can have a major impact.

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Raporty organizacyjne na temat "Peripheral inflammation"

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Lekhanya, Portia Keabetswe, and Kabelo Mokgalaboni. Exploring the effectiveness of vitamin B12 complex and alpha-lipoic acid as a treatment for diabetic neuropathy. Protocol for systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.5.0167.

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Review question / Objective: Does Alpha-Lipoic acid increase the uptake of glucose for better glycaemic control? Does vitamin B12 and Alpha-Lipoic acid improve inflammation? The aim of the study is to explore the effectiveness of Vitamin B12 and Alpha-Lipoic Acid as a possible treatment for diabetic neuropathy with major emphasis on markers of inflammation and glucose metabolism. Condition being studied: Diabetic Neuropathy (DN) is a heterogeneous type of nerve damage associated with diabetes mellitus, the condition most often damages nerves in the legs and feet. It presents both clinically and sub-clinically affecting the peripheral nervous system as a result of an increase in glucose concentration which interferes with nerve signalling. After the discovery of insulin as a treatment for Diabetes Mellitus (DM), the prevalence of DN has since increased significantly due to DM patients having a longer life expectancy. It has been estimated that atleast 50% of DM patients will develop DN in their life, with approximately 20% of these patients experiencing neuropathic pain. Nerves are susceptible to changes in glucose concentrations and insulin makes it impossible for neurons to continue regulating glucose uptake.

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Schwartz, Bertha, Vaclav Vetvicka, Ofer Danai, and Yitzhak Hadar. Increasing the value of mushrooms as functional foods: induction of alpha and beta glucan content via novel cultivation methods. United States Department of Agriculture, 2015. http://dx.doi.org/10.32747/2015.7600033.bard.

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During the granting period, we performed the following projects: Firstly, we differentially measured glucan content in several pleurotus mushroom strains. Mushroom polysaccharides are edible polymers that have numerous reported biological functions; the most common effects are attributed to β-glucans. In recent years, it became apparent that the less abundant α-glucans also possess potent effects in various health conditions. In our first study, we explored several Pleurotus species for their total, β and α-glucan content. Pleurotuseryngii was found to have the highest total glucan concentrations and the highest α-glucans proportion. We also found that the stalks (stipe) of the fruit body contained higher glucan content then the caps (pileus). Since mushrooms respond markedly to changes in environmental and growth conditions, we developed cultivation methods aiming to increase the levels of α and β-glucans. Using olive mill solid waste (OMSW) from three-phase olive mills in the cultivation substrate. We were able to enrich the levels mainly of α-glucans. Maximal total glucan concentrations were enhanced up to twice when the growth substrate contained 80% of OMSW compared to no OMSW. Taking together this study demonstrate that Pleurotuseryngii can serve as a potential rich source of glucans for nutritional and medicinal applications and that glucan content in mushroom fruiting bodies can be further enriched by applying OMSW into the cultivation substrate. We then compared the immune-modulating activity of glucans extracted from P. ostreatus and P. eryngii on phagocytosis of peripheral blood neutrophils, and superoxide release from HL-60 cells. The results suggest that the anti-inflammatory properties of these glucans are partially mediated through modulation of neutrophileffector functions (P. eryngiiwas more effective). Additionally, both glucans dose-dependently competed for the anti-Dectin-1 and anti-CR3 antibody binding. We then tested the putative anti-inflammatory effects of the extracted glucans in inflammatory bowel disease (IBD) using the dextran sulfate sodium (DSS)–induced model in mice. The clinical symptoms of IBD were efficiently relieved by the treatment with two different doses of the glucan from both fungi. Glucan fractions, from either P. ostreatus or P. eryngii, markedly prevented TNF-α mediated inflammation in the DSS–induced inflamed intestine. These results suggest that there are variations in glucan preparations from different fungi in their anti-inflammatory ability. In our next study, we tested the effect of glucans on lipopolysaccharide (LPS)-induced production of TNF-α. We demonstrated that glucan extracts are more effective than mill mushroom preparations. Additionally, the effectiveness of stalk-derived glucans were slightly more pronounced than of caps. Cap and stalk glucans from mill or isolated glucan competed dose-dependently with anti-Dectin-and anti-CR-3 antibodies, indicating that they contain β-glucans recognized by these receptors. Using the dextran sulfate sodium (DSS)-inflammatory bowel disease mice model, intestinal inflammatory response to the mill preparations was measured and compared to extracted glucan fractions from caps and stalks. We found that mill and glucan extracts were very effective in downregulatingIFN-γ and MIP-2 levels and that stalk-derived preparations were more effective than from caps. The tested glucans were equally effective in regulating the number of CD14/CD16 monocytes and upregulating the levels of fecal-released IgA to almost normal levels. In conclusion, the most effective glucans in ameliorating some IBD-inflammatory associated symptoms induced by DSS treatment in mice were glucan extracts prepared from the stalk of P. eryngii. These spatial distinctions may be helpful in selecting more effective specific anti-inflammatory mushrooms-derived glucans. We additionally tested the effect of glucans on lipopolysaccharide-induced production of TNF-α, which demonstrated stalk-derived glucans were more effective than of caps-derived glucans. Isolated glucans competed with anti-Dectin-1 and anti-CR3 antibodies, indicating that they contain β-glucans recognized by these receptors. In conclusion, the most effective glucans in ameliorating IBD-associated symptoms induced by DSS treatment in mice were glucan extracts prepared from the stalk of P. eryngii grown at higher concentrations of OMSW. We conclude that these stress-induced growing conditions may be helpful in selecting more effective glucans derived from edible mushrooms. Based on the findings that we could enhance glucan content in Pleurotuseryngii following cultivation of the mushrooms on a substrate containing different concentrations of olive mill solid waste (OMSW) and that these changes are directly related to the content of OMSW in the growing substrate we tested the extracted glucans in several models. Using dextran sulfate sodium (DSS)–inflammatory bowel disease (IBD) mice model, we measured the colonic inflammatory response to the different glucan preparations. We found that the histology damaging score (HDS) resulting from DSS treatment reach a value of 11.8 ± 2.3 were efficiently downregulated by treatment with the fungal extracted glucans, glucans extracted from stalks cultivated at 20% OMSWdownregulated to a HDS value of 6.4 ± 0.5 and at 80% OMSW showed the strongest effects (5.5 ± 0.6). Similar downregulatory effects were obtained for expression of various intestinal cytokines. All tested glucans were equally effective in regulating the number of CD14/CD16 monocytes from 18.2 ± 2.7 % for DSS to 6.4 ± 2.0 for DSS +glucans extracted from stalks cultivated at 50% OMSW. We finally tested glucans extracted from Pleurotuseryngii grown on a substrate containing increasing concentrations of olive mill solid waste (OMSW) contain greater glucan concentrations as a function of OMSW content. Treatment of rat Intestinal epithelial cells (IEC-6) transiently transfected with Nf-κB fused to luciferase demonstrated that glucans extracted from P. eryngii stalks grown on 80% OMSWdownregulatedTNF-α activation. Glucans from mushrooms grown on 80% OMSW exerted the most significant reducing activity of nitric oxide production in lipopolysaccharide (LPS) treated J774A.1 murine macrophages. The isolated glucans were tested in vivo using the Dextran Sodium Sulfate (DSS) induced colitis in C57Bl/6 mice and found to reduce the histology damaging score resulting from DSS treatment. Expression of various intestinal cytokines were efficiently downregulated by treatment with the fungal extracted glucans. We conclude that the stress-induced growing conditions exerted by OMSW induces production of more effective anti-inflammatory glucans in P. eryngii stalks.

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