Academic literature on the topic 'Local inflammatory responses'

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Journal articles on the topic "Local inflammatory responses"

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O'GRADY, NAOMI P, HUGH L PREAS, JÉRÔME PUGIN, et al. "Local Inflammatory Responses following Bronchial Endotoxin Instillation in Humans." American Journal of Respiratory and Critical Care Medicine 163, no. 7 (2001): 1591–98. http://dx.doi.org/10.1164/ajrccm.163.7.2009111.

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Leishman, Shaneen J., Gregory J. Seymour, and Pauline J. Ford. "Local and Systemic Inflammatory Responses to Experimentally Induced Gingivitis." Disease Markers 35 (2013): 543–49. http://dx.doi.org/10.1155/2013/948569.

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This study profiled the local and systemic inflammatory responses to experimentally induced gingivitis. Eight females participated in a 21-day experimental gingivitis model followed by a 14-day resolution phase. Bleeding on probing and plaque index scores were assessed before, during, and after resolution of gingival inflammation, and samples of saliva, GCF, and plasma were collected. Samples were assessed for biomarkers of inflammation using the BioPlex platform and ELISA. There were no significant changes in GCF levels of cytokines during the experimental phase; however, individual variabili
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de Jager, Saskia C. A., and Imo E. Hoefer. "Local inflammatory responses take their toll on the heart." International Journal of Cardiology 293 (October 2019): 254–55. http://dx.doi.org/10.1016/j.ijcard.2019.07.055.

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Kotzbeck, Petra, Elisabeth Hofmann, Sebastian P. Nischwitz, and Lars-Peter Kamolz. "Differentiating local and systemic inflammatory responses to burn injuries." Burns 45, no. 8 (2019): 1934–35. http://dx.doi.org/10.1016/j.burns.2018.11.006.

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Garcia-Leme, J., and Sandra P. Farsky. "Hormonal control of inflammatory responses." Mediators of Inflammation 2, no. 3 (1993): 181–98. http://dx.doi.org/10.1155/s0962935193000250.

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Almost any stage of inflammatory and immunological responses is affected by hormone actions. This provides the basis for the suggestion that hormones act as modulators of the host reaction against trauma and infection. Specific hormone receptors are detected in the reactive structures in inflamed areas and binding of hormone molecules to such receptors results in the generation of signals that influence cell functions relevant for the development of inflammatory responses. Diversity of hormonal functions accounts for recognized pro- and anti-inflammatory effects exerted by these substances. Mo
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Fiuza, C., and A. F. Suffredini. "Human models of innate immunity: local and systemic inflammatory responses." Journal of Endotoxin Research 7, no. 5 (2001): 385–88. http://dx.doi.org/10.1179/096805101101532963.

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Fiuza, Carmen, and Anthony F. Suffredini. "Human models of innate immunity: local and systemic inflammatory responses." Journal of Endotoxin Research 7, no. 5 (2001): 385–88. http://dx.doi.org/10.1177/09680519010070050701.

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Raymond, Philippe, Charles Blais, Anick Décarie, Réjean Morais, and Albert Adam. "Zidovudine Potentiates Local and Systemic Inflammatory Responses in the Rat." Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology 14, no. 5 (1997): 399–407. http://dx.doi.org/10.1097/00042560-199704150-00002.

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Bhat, Niranjan, James Gaensbauer, Richard M. Peek, et al. "Local and Systemic Immune and Inflammatory Responses to Helicobacter pylori Strains." Clinical Diagnostic Laboratory Immunology 12, no. 12 (2005): 1393–400. http://dx.doi.org/10.1128/cdli.12.12.1393-1400.2005.

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ABSTRACT Colonization with Helicobacter pylori eventuates in varied clinical outcomes, which relate to both bacterial and host factors. Here we examine the relationships between cagA status, serum and gastric juice antibody responses, and gastric inflammation in dyspeptic patients. Serum, gastric juice, and gastric biopsy specimens were obtained from 89 patients undergoing endoscopy. H. pylori colonization and cagA status were determined by histology, culture, and PCR methods, and acute inflammation and chronic inflammation in the gastric mucosa were scored by a single pathologist. Serum and g
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Beiting, Daniel P., Susan K. Bliss, Donald H. Schlafer, Victoria L. Roberts, and Judith A. Appleton. "Interleukin-10 Limits Local and Body Cavity Inflammation during Infection with Muscle-Stage Trichinella spiralis." Infection and Immunity 72, no. 6 (2004): 3129–37. http://dx.doi.org/10.1128/iai.72.6.3129-3137.2004.

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ABSTRACT The aim of this study was to characterize cellular responses to muscle-stage Trichinella spiralis. From its intracellular habitat in muscle, T. spiralis secretes potent glycoprotein antigens that elicit a strong systemic host immune response. Despite the magnitude and prolonged nature of this response, nurse cells are rarely destroyed by infiltrating cells. We tested the hypothesis that the anti-inflammatory cytokine interleukin-10 (IL-10) moderates cellular responses to muscle-stage parasites. Trichinella larvae colonize the diaphragm in large numbers, prompting us to evaluate region
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Dissertations / Theses on the topic "Local inflammatory responses"

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McKenzie, Sheppard Allen IV Paquette David W. "Local and systemic inflammatory responses in gingivitis subjects clinical trial of topical triclosan /." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,1807.

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Thesis (M.S.)--University of North Carolina at Chapel Hill, 2008.<br>Title from electronic title page (viewed Dec. 11, 2008). "... in partial fulfillment of the requirements for the degree of Master of Science in the Department of Periodontology." Discipline: Periodontology; Department/School: Dentistry.
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Richards, Colin H. "An investigation of the determinants of the local and systemic inflammatory responses in patients with colorectal cancer." Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/4857/.

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Colorectal cancer is the second most common cause of cancer death in the Western world but the factors that determine disease progression remain poorly understood. At the outset of this thesis it was recognised that tumour growth and metastases were determined by complex interactions between tumour and host. It was evident that a systemic inflammatory response was associated with poor prognosis in colorectal cancer while a strong local immune cell response conferred a favourable outcome. This thesis investigated this topic by examining the factors responsible for activating, maintaining and re
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Guthrie, Graeme J. K. "An investigation into the role of interleukin-6 in linking systemic and local inflammatory responses in patients with colorectal cancer." Thesis, University of Glasgow, 2016. http://theses.gla.ac.uk/7409/.

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Colorectal cancer is the second most common cause of cancer death in the UK. It is accepted that both tumour and host factors are important determinants of disease progression and survival. While systemic and local inflammatory responses are increasingly recognized to be of particular importance the understanding of the mechanisms linking these important inflammatory processes remains unclear. This thesis examines the prognostic importance of measures of systemic and local inflammation and proposes a hypothesis for a link between tumour necrosis, systemic and local inflammatory responses in pa
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Lunsford, Keri Elizabeth. "Analysis of Immune Pathways Which Jeopardize Long-Term Pancreatic Islet Allograft Survival in the Liver." The Ohio State University, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=osu1117561893.

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Koch, Markus [Verfasser]. "Effects of tissue specific interferon-γ [interferon-gamma] expression on local inflammatory responses / vorgelegt von Markus Koch". 2003. http://d-nb.info/969717377/34.

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Books on the topic "Local inflammatory responses"

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21-Thiosteroids Meeting (1st 1987 Paris, France). Mediators of inflammation: The local response : [proceedings of the] 1st meeting 21-Thiosteroids, Paris May 14th 1987. Edited by Henry J. F. 1932-. J. Libbey, 1987.

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Roxburgh, Campbell S. D., and Donald C. McMillan. Cancer, immunity, and inflammation. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199656103.003.0012_update_001.

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The chapter focuses on the role of immunity and inflammation in established cancer. From the evidence reviewed it is clear that immune and inflammatory responses, innate, humoral and adaptive, local and systemic, are intimately linked to the tumour and themselves and impact on cancer survival. It is also possible to identify key mediators that may be targeted in the cancer patient. However, further work is required to elucidate the mechanisms by which these immune and inflammatory responses are activated, maintained, and interact. Therapeutic intervention using non-selective anti-inflammatory
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F, Henry J., ed. Mediators of inflammation: The local response. Libbey, 1988.

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Gaston, J. S. Hill. Reactive arthritis and enteropathic arthropathy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0115_update_002.

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Reactive arthritis (ReA), and enteropathic arthritis secondary to inflammatory bowel disease, are forms of spondyloarthritis, all of which share an association with HLA B27 and can involve both axial and peripheral joints. Genetic studies strongly implicate the cytokines IL-17 and IL-23 in their pathogenesis, and evidence for autoimmunity is lacking. ReA is triggered by particular bacteria, mainly affecting the gut and genitourinary tract, though infections are sometimes asymptomatic. Classically an acute oligo- or monoarthritis with enthesitis occurs, often with inflammatory back pain, though
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Gaston, J. S. Hill. Reactive arthritis and enteropathic arthropathy. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0115.

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Reactive arthritis (ReA), and enteropathic arthritis secondary to inflammatory bowel disease, are forms of spondyloarthritis, all of which share an association with HLA B27 and can involve both axial and peripheral joints. Genetic studies strongly implicate the cytokines IL-17 and IL-23 in their pathogenesis, and evidence for autoimmunity is lacking. ReA is triggered by particular bacteria, mainly affecting the gut and genitourinary tract, though infections are sometimes asymptomatic. Classically an acute oligo- or monoarthritis with enthesitis occurs, often with inflammatory back pain, though
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van der Vlag, Johan, and Jo H. M. Berden. The patient with systemic lupus erythematosus. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0161.

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Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with various clinical manifestations. The hallmark of SLE is the presence of antibodies against nuclear constituents, such as double-stranded (ds)DNA, histones, and nucleosomes. Local deposition of antinuclear antibodies in complex with nuclear autoantigens induces serious inflammatory conditions that can affect several tissues and organs, including the kidney.The levels of antinucleosome and anti-dsDNA antibodies seem to correlate with glomerulonephritis and these autoantibodies can often be detected years before the patient
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Raju, Raghavan, and Irshad H. Chaudry. The host response to hypoxia in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0305.

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The hypoxic response of the host is complex. While the oxygen-sensing intracellular machinery attempts to restore cellular homeostasis by augmenting respiration and blood flow, events such as severe haemorrhage lead to whole body hypoxia and decreased mitochondrial function. Immunological perturbations following severe haemorrhage may result in multiple organ dysfunction and sepsis, while impaired perfusion may lead to microvascular injury and local hypoxia. Trauma-haemorrhage or hypoxic exposure in animals causes a systemic inflammatory response, decreased antigen presentation by peritoneal m
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Litell, John M., and Nathan I. Shapiro. Pathophysiology of septic shock. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0297.

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The pathophysiology of sepsis is the result of a dysregulated host response to infection. Interactions between conserved pathogenic signals and host recognition systems initiate a systemic reaction to local infection. Pro- and anti-inflammatory intermediates and associated coagulatory abnormalities lead to altered macrovascular, microvascular, and mitochondrial function. Uncorrected, these processes yield similar patterns of failure in multiple organ systems. Mortality increases with successive organ failures. Although commonly thought to be a manifestation of impaired renal circulation, septi
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McGregor, Laura, Monica N. Gupta, and Max Field. Septic arthritis in adults. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0098.

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Septic arthritis (SA) is a medical emergency with mortality of around 15%. Presentation is usually monoarticular but in more than 10% SA affects two or more joints. Symptoms include rapid-onset joint inflammation with systemic inflammatory responses but fever and leucocytosis may be absent at presentation. Treatment according to British Society of Rheumatology/British Orthopaedic Association (BSR/BOA) guidelines should be commenced if there is a suspicion of SA. At-risk patients include those with primary joint disease, previous SA, recent intra-articular surgery, exogenous sources of infectio
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Pontus, Stierna, and Jannert Magnus, eds. Current opinions on the pathogenesis of sinusitis: The importance of local inflammatory response and ostial patency : proceedings of a workshop held in Lund, Sweden on August 27, 1993. Scandinavian University Press, 1994.

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Book chapters on the topic "Local inflammatory responses"

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Zaspel, J. Z., G. G. Gradl, A. W. Wipfl, and M. S. Schürmann. "Computergestützte Venenverschlußplethysmographie-Untersuchungen zur Pathophysiologie des Posttraumatischen Complex Regional Pain Syndrome Type I (CRPS I) — ist das CRPS I ein ‘local inflammatory response syndrome’." In Deutsche Gesellschaft für Chirurgie. Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-55715-6_434.

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Roxburgh, Campbell S. D., and Donald C. McMillan. "Cancer, immunity, and inflammation." In Oxford Textbook of Oncology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199656103.003.0012.

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The chapter focuses on the role of immunity and inflammation in established cancer. From the evidence reviewed it is clear that immune and inflammatory responses, innate, humoral and adaptive, local and systemic, are intimately linked to the tumour and themselves and impact on cancer survival. It is also possible to identify key mediators that may be targeted in the cancer patient. However, further work is required to elucidate the mechanisms by which these immune and inflammatory responses are activated, maintained, and interact. Therapeutic intervention using non-selective anti-inflammatory agents is widely advocated and likely to become part of routine clinical practice in the near future. Selective therapeutic intervention directed at the immune and inflammatory responses in cancer is in its infancy. Therefore, it would appear that, at least in non-hereditary disease, immune and inflammatory responses are of key, if not of prime, importance in tumour progression and dissemination.
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Gaston, J. S. Hill. "Reactive arthritis and enteropathic arthropathy." In Oxford Textbook of Rheumatology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0115_update_003.

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Reactive arthritis (ReA), and enteropathic arthritis secondary to inflammatory bowel disease, are forms of spondyloarthritis, all of which share an association with HLA B27 and can involve both axial and peripheral joints. Genetic studies strongly implicate the cytokines IL-17 and IL-23 in their pathogenesis, and evidence for autoimmunity is lacking. ReA is triggered by particular bacteria, mainly affecting the gut and genitourinary tract, though infections are sometimes asymptomatic. Classically an acute oligo- or monoarthritis with enthesitis occurs, often with inflammatory back pain, though mild polyarthritis can also occur. Septic and crystal-induced arthritis are the principal differential diagnoses. Extra-articular features may aid diagnosis, which otherwise requires laboratory evidence of preceding infection. Bacterial components traffic to the joint (which is nevertheless sterile), and elicit local pro-inflammatory immune responses. Most ReA is self-limiting, but persistent cases may require disease-modifying anti-rheumatic drugs or even biologics.
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Gaston, J. S. Hill. "Reactive arthritis and enteropathic arthropathy." In Oxford Textbook of Rheumatology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0115_update_005.

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Reactive arthritis (ReA), and enteropathic arthritis secondary to inflammatory bowel disease, are forms of spondyloarthritis, all of which share an association with HLA B27 and can involve both axial and peripheral joints. Genetic studies strongly implicate the cytokines IL-17 and IL-23 in their pathogenesis, and evidence for autoimmunity is lacking. ReA is triggered by particular bacteria, mainly affecting the gut and genitourinary tract, though infections are sometimes asymptomatic. Classically an acute oligo- or monoarthritis with enthesitis occurs, often with inflammatory back pain, though mild polyarthritis can also occur. Septic and crystal-induced arthritis are the principal differential diagnoses. Extra-articular features may aid diagnosis, which otherwise requires laboratory evidence of preceding infection. Bacterial components traffic to the joint (which is nevertheless sterile), and elicit local pro-inflammatory immune responses. Most ReA is self-limiting, but persistent cases may require disease-modifying anti-rheumatic drugs or even biologics.
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O. Ilomuanya, Margaret, Ibilola M. Cardoso-Daodu, Uloma N. Ubani-Ukoma, and Adannaya C. Adebona. "Polymeric Biomaterials for Wound Healing Incorporating Plant Extracts and Extracellular Matrix Components." In Wound Healing [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98556.

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Biomaterials are constructed to promote or stimulate the processes of wound healing. Polymeric biomaterials can be used to hydrate the wound and serve as barrier to pathogens with plant extracts, antimicrobial agents and extracellular components incorporated to stimulate the healing process. The biological and physical augmentation provided by extracellular matrix derived implants continues facilitate innovation in biomaterials utilized in management of nonhealing wounds. Tissue-processing methodologies can birth extracellular matrix-based devices with characteristic post-implantation responses ranging from the classic foreign body encapsulation of a permanent implant, to one where the implant is degraded and resorbed, to one where the processed extracellular matrix implant is populated by local fibroblasts and supporting vasculature to produce, a viable and metabolically active tissue. Extracellular matrix components and plant extracts have been shown to possesses pharmacological properties with potential for use in the treatment of skin diseases and wound healing. Antioxidant, anti-inflammatory assays, and wound healing assays have been shown to support the dermatological and wound healing usage of these medicinal plants extracts.
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Turner, A. Neil. "Infection-associated nephropathies." In Oxford Textbook of Medicine, edited by John D. Firth. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0498.

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Infection may be a primary cause of renal disease (e.g. postinfectious glomerulonephritis) or affect the kidneys on a background of debilitating illnesses and previous medical interventions. Renal disease may arise as a consequence of immune responses to a pathogen, direct invasion by the microorganism, or the effects of infection on the systemic or local circulations. Glomerulonephritis—associated with chronic and acute bacterial infections. Shunt nephritis follows colonization of a ventriculoatrial shunt, most commonly with Staphylococcus epidermidis, leading to constitutional symptoms, an acute inflammatory response, and (most characteristically) a type 1 mesangiocapillary glomerulonephritis. Infective endocarditis and other deep-seated bacterial infections may produce a similar renal picture, but they can mimic vasculitic syndromes and outcome is dependent on the response of the infection to treatment. Interstitial nephritis—bacteria that can cause this include leptospira (Weil’s disease), Rickettsia rickettsii (Rocky Mountain spotted fever), legionella, and mycobacteria. Viral infections include hantaviruses (haemorrhagic fever with renal syndrome and nephropathia epidemica) and, almost exclusively following renal transplantation, cytomegalovirus and polyomavirus hominis type 1 (BK) virus. HIV-associated renal disorders—these include HIV nephropathy, which is a focal segmental glomerulosclerosis of ‘collapsing’ form, occurring almost exclusively in black patients. Other morphologies are more common in other races, but interstitial disease is also common as a manifestation of infection or of drug toxicity. Hepatitis B virus—chronic infection is strongly associated with membranous nephropathy; affected individuals are HBeAg and HBsAg positive, usually with coexistent hepatitis; seroconversion from HBeAg positive to HBeAb positive (naturally or induced by treatment) is associated with remission of the renal lesion. Hepatitis C virus—chronic infection is the commonest cause of mixed essential (type II) cryoglobulinaemia in most populations.
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Voljč, Tadej, and Danijela Semenič. "Contribution of Topical Agents to Wound Healing." In Wound Healing [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97170.

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The process of wound healing is often accompanied by bacterial infection or critical colonization, which leads to an extension of the inflammatory response phase and delayed epithelization. In the review of scientific articles, we found the description and mode of action of topical antiseptic agents, including silver and sodium hypochlorite solution, to control the spread of microorganisms. The value of hyaluronic acid for wound healing is described. Furthermore, a novel treatment option with microspheres is mentioned. Attachment of cells to microspheres establishes a local cytokine response that acts anti-inflammatory, cell attachment results also in morphological and functional cell changes that reactivate healing.
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McGregor, Laura, Monica N. Gupta, and Max Field. "Septic arthritis in adults." In Oxford Textbook of Rheumatology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0098_update_001.

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Septic arthritis (SA) is a medical emergency with mortality of around 15%. Presentation is usually monoarticular but in more than 10% SA affects two or more joints. Symptoms include rapid-onset joint inflammation with systemic inflammatory responses but fever and leucocytosis may be absent at presentation. Treatment according to British Society of Rheumatology/British Orthopaedic Association (BSR/BOA) guidelines should be commenced if there is a suspicion of SA. At-risk patients include those with primary joint disease, previous SA, recent intra-articular surgery, exogenous sources of infection (leg ulceration, respiratory and urinary tract), and immunosupression because of medical disorders, intravenous drug use or therapy including tumour necrosis factor (TNF) inhibitors. Synovial fluid should be examined for organisms and crystals with repeat aspiration as required. Most SA results from haematogenous spread-sources of infection should be sought and blood and appropriate cultures taken prior to antibiotic treatment. Causative organisms include staphylococcus (including meticillin-resistant Staphylococcus aureus, MRSA), streptococcus, and Gram-negative organisms (in elderly patients), but no organism is identified in 43%, often after antibiotic use before diagnosis. Antibiotics should be prescribed according to local protocols, but BSR/BOA guidelines suggest initial intravenous and subsequent oral therapy. Medical treatment may be as effective as surgical in uncomplicated native SA, and can be cost-effective, but orthopaedic advice should be sought if necessary and always in cases of infected joint prostheses. In addition to high mortality, around 40% of survivors following SA develop limitation of joint function. Guidelines provide physicians with treatment advice aiming to limit mortality and morbidity and assist future research.
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Cesar Machado, Marcel Cerqueira, and Ana Maria Mendonca Coelho. "Role of Peritoneal Macrophages on Local and Systemic Inflammatory Response in Acute Pancreatitis." In Acute Pancreatitis. InTech, 2012. http://dx.doi.org/10.5772/25639.

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Benarroch, Eduardo E. "Microenvironment in the Central Nervous System." In Neuroscience for Clinicians, edited by Eduardo E. Benarroch. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.003.0023.

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The regulation of the microenvironment in the CNS is critical for neuronal and glial survival, function, and response to injury. This regulation occurs via components of a neurovascular unit that control the functional coupling between neuronal activity and local cerebral blood flow and maintain the blood-brain barrier. Cerebrospinal fluid production, circulation, and interchange with the interstitial fluid are also major factors maintaining the cerebral microenvironment and have an important role in removal of toxic products from the CNS. Impaired regulation of the local blood flow, disruption of the blood-brain barrier, and altered cerebrospinal fluid dynamics are common pathophysiological consequences of traumatic, vascular, inflammatory disorders and have an important role in epilepsy and neurodegeneration.
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Conference papers on the topic "Local inflammatory responses"

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Berger, Marieke, Daan de Boer, Koen Van der Sluijs, et al. "Local And Systemic Inflammatory Responses Following Low-Dose Bronchial Endotoxin Instillation In Mild Asthmatics." 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.a2545.

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Roseweir, Antonia Kathryn, Arfon GNT Powell, James Park, Donald C. McMillan, and Joanne Edwards. "Abstract A106: Src family kinases modulate local inflammatory responses via STAT3 and MMP9 in colorectal cancer patients." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-a106.

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Nash, Gerard B. "Studying Inflammatory Responses of Endothelial Cells and Leukocytes in Perfused Microchannels." In ASME 4th International Conference on Nanochannels, Microchannels, and Minichannels. ASMEDC, 2006. http://dx.doi.org/10.1115/icnmm2006-96013.

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Circulating leukocytes must adhere to the endothelial cells (EC) that form the lining of blood vessels, and migrate through them to carry out their protective immune functions. During inflammation this recruitment is typically controlled by cytokines released from tissue that act on the EC. The endothelial cells respond by increasing the expression of adhesion molecules on their surface (to capture flowing leukocytes), and also by presenting chemotactic agents (to induce the captured cells to migrate). This recruitment process is influenced by the local haemodynamic milieu in several ways: int
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Hegazy, AN, N. West, MJT Stubbington, et al. "Gut microbiota induce local and systemic CD4 T cell responses in healthy individuals that are altered in inflammatory bowel diseases." In Viszeralmedizin 2017. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1604874.

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Sucosky, Philippe, Kartik Balachandran, Hanjoong Jo та Ajit P. Yoganathan. "Altered Shear Stress Stimulates Upregulation of Endothelial VCAM-1 and ICAM-1 in a BMP-4- and TGF-β1-Dependent Pathway". У ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-204693.

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Inflammation and calcification are common features of aortic valve (AV) diseases [1]. AV diseases preferentially occur in the aortic side of the valvular leaflets where they are exposed to complex and unstable hemodynamic conditions [2]. The reasons for this side-specific response, potentially associated with the local shear stress environment, are not completely understood. In addition, while it has been shown that exposure of vascular endothelial cells to oscillatory shear stress induces inflammatory responses by bone morphogenic protein (BMP)-4-dependent mechanisms [3], it is not clear whet
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Yeger-McKeever, Meira, Alice H. Huang, Ashley F. Stein, and Robert L. Mauck. "Engineered MSC-Laden Cartilage Constructs are Sensitive to Inflammatory Cytokine-Mediated Degradation." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176186.

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Degeneration of cartilage resulting from trauma or disease processes is an increasingly prevalent problem in the aging population. Intrinsic repair of cartilage is limited and few methodologies exist, short of prosthetic replacement, for restoring damaged articular surfaces. These realities engender a need for new strategies for extrinsic repair. One strategy, tissue engineering, generates replacement cartilage composed of scaffolds and differentiated chondrocytes [1]. In addition to chondrocytes, recent work has demonstrated that mesenchymal stem cells (MSCs) isolated from bone marrow may be
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Zhang, Ji, and Morton H. Friedman. "The Adaptive Response of Endothelial Transcription to Increased Shear Stress In Vitro." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19318.

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Previous studies have shown a substantial effect of shear stress on endothelial phenotype and functions such as production of nitric oxide, secretion of growth factors, inflammatory responses, production of reactive oxygen species, permeability to macromolecules and cytoskeletal remodeling [1–3]. However, the dynamics of the endothelial adaptive response to changes in shear stress are largely unknown. The response of vascular endothelial cells to alterations in shear stress is an essential component of normal endothelial physiology, since local shear stress can be altered in vivo by the global
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Williams, T. J., M. Rampart, S. Nourshargh, P. G. Hellewell, S. D. Brain, and P. J. Jose. "INTERACTION OF POLYMORPHONUCLEAR LEUKOCYTES AND ENDOTHELIAL CELLS : FUNCTIONAL CONSEQUENCES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643985.

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The mechanisms involved in the accumulation of polymorphonuclear leukocytes (PMNs) in an inflammatory reaction are complex. A key phase in this process is the attachment of the PMN to the microvascular (venular in most tissues) endothelial cell, initiated by the extravascular generation of a chemical mediator. Experiments in vitro suggest that mediators, such as C5a, may act in vivo by stimulating the increased expression of the CD18 complex on the surface of the PMN within the venule lumen (1), whereas IL-1 may act by causing the expression of an adhesive molecule on the endothelial cell (2).
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Carrell, R. W., P. D. Christey, and D. R. Boswell. "SERPINS: ANTITHROMBIN AND OTHER INHIBITORS OF COAGULATION AND FIBRINOLYSIS. EVIDENCE FROM AMINO ACID SEQUENCES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642896.

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A number of the key inhibitors of coagulation and fibrinolysis have recently been shown to be members of the same superfamily of serine protease inhibitors, the serpins. The archetypes of the group are alpha-l-antitrypsin and antithrombin and it includes antiplasmin, C1-inhibitor, heparin cofactor II and the newly recognised inhibitors of plasminogen activators and activated Protein C. Alignment of their structures shows that they have the same skeletal three-dimensional conformation and, by inference, the same general function mechanisms.The serpins have a reactive centre, primarily dependent
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10

Guegan, Eric, Tian Davis, Thomas J. Koob, and Yvonne Moussy. "Transport Characteristics of a Novel Local Drug Delivery System Using Nordihydroguaiaretic Acid (NDGA)-Polymerized Collagen Fibers." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-171428.

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Local delivery of a drug in vivo would permit high interstitial drug concentration at the desired location without producing high systemic drug levels. Previous local drug delivery systems have included biodegradable polymer implants, hydrogels, and osmotic pumps [1]. In this paper, we describe a novel local drug delivery system using nordihydroguaiaretic acid (NDGA)-polymerized collagen fibers. NDGA collagen fibers were originally developed for use as biocompatible tendon bioprostheses [2]. The NDGA collagen fibers were loaded with either: dexamethasone, a synthetic glucocorticoid with anti-i
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