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Fibrinolysis and Inflammation
Published in Pia Glas-Greenwalt, Molecular and Hemovascular Aspects of Fibrinolysis, 2019
A combination of reactions at the site of physical or chemical injury leads to local inflammation, especially when pathogenic microorganisms have access to the site. Systemic manifestations may accompany the local inflammatory or infectious process (see Figure 1). The classical clinical signs of local inflammation, rubor, calor, dolor, tumor, and functio laesa, are — with the probable exception of pain — mainly consequences of the changes in the microvasculature. The endothelium plays an essential role in the pathogenesis of the inflammatory response, not only as a target for the agent or for antibodies (e.g., in autoimmune disease), but also as a reacting organ, releasing a number of enzymes, adhesion molecules and cytokines, and giving passage to proteins and blood corpuscles, and finally by forming new vessels (angiogenesis) in inflammatory tissue (granuloma), specially in chronic forms of inflammation.
Molecular biology of peritoneal carcinomatosis
Published in Wim P. Ceelen, Edward A. Levine, Intraperitoneal Cancer Therapy, 2015
Riom Kwakman, Nina R. Sluiter, Erienne M.V. de Cuba, Elisabeth (Lisette) A. te Velde
Inflammation is a state of an organ or tissue where the five cardinal signs of inflammation are present: rubor, calor, dolor, tumor, and functio laesa. Pathophysiologically, this is caused by a release of cytokines and inflammatory molecules, which results in increased vascular permeability, vasodilation, and edema. Although one is inclined to think that inflammation is the immune system’s appropriate reaction to the tumor, cancer cells can harness the effects of inflammation to promote their own proliferation and nutrient supply. This is why inflammation has recently been put on the map as one of the new emerging hallmarks of cancer [4]. Already described in many types of cancer, inflammation is often seen in PC, which is why it is sometimes referred to as peritonitis carcinomatosa; cancerous inflammation of peritoneum. Patients with pseudomyxoma peritonei have higher levels of CRP in their blood than normal individuals, but a higher CRP is also linked to a higher chance of having ascites [52]. Patients with PC of colorectal origin have worse prognosis if presented with high CRP concentration [53].
Clinical trials: dental pain
Published in Harald Breivik, William I Campbell, Michael K Nicholas, Clinical Pain Management, 2008
Surgical removal of mandibular impacted or incompletely erupted third molars in ambulatory patients is a common procedure, both in general dental practice and in oral surgery practice (Figure 43.1). The operative procedure results in hyperalgesia two to four hours later, with cardinal signs of inflammation (rubor, calor, tumor, dolor, functio laesa) involving the alveolar bone, surrounding mucosa, and masticatory organs. The study of pain and pain relief after this type of surgery is often referred to as “the dental pain model.” The postoperative pain experienced varies from mild to severe following dissipation of the local anesthetic block, reaching its peak within the first six hours. Following this initial period, acute pain abates and the patient requires less analgesic medication.1 Although the duration of pain and discomfort may last for more than four postoperative days, it is usually transient and is limited to one to three postoperative days.2 Other sequelae, such as trismus with reduced mouth opening and facial swelling, may also appear gradually, peaking at between 48 and 72 hours.3[II] The majority of these patients are healthy young adults (18–30 years old) without former experience of oral disability or consuming medication, which could influence pain assessment or interact with the analgesic under study.
Sirtuins: potential therapeutic targets for regulating acute inflammatory response?
Published in Expert Opinion on Therapeutic Targets, 2020
Vidula Vachharajani, Charles E. McCall
Acute inflammatory responses begin within seconds to minutes of sensing an environmental danger signal, and often become clinically evident after a few hours. The five cardinal signs of acute inflammation: calor (increased heat), rubor (redness), dolor (pain) and tumor (swelling) were described by Celcus between 30 BC–38 AD, while the fifth sign, functio laesa (loss of function), was described by Virchow in nineteenth century. Another important but less famous sign is anorexia [30]. After environmental sensing of danger (alarmins) and signaling from external membrane receptors or internal protein sensors inform cytosol and nuclear signaling pathways, the acute inflammatory response, upregulates several thousand genes that reprogram pro-inflammatory resistance responses; in monocytes or macrophages, just as many genes are repressed. Importantly, organ-specific cells expressing toll-like receptors (TLR) for sensing microbes also reprogram many genes associated with anabolism and catabolism. Adaptive immune cells also increase the expression of many overlapping and cell-specific cytokines and metabolic pathways [31]. Successful acute inflammation returns to homeostasis, but restored homeostasis epigenetically differs from that which inflammation departed [32].
Polyunsaturated fatty acids and endocannabinoids in health and disease
Published in Nutritional Neuroscience, 2018
Hércules Rezende Freitas, Alinny Rosendo Isaac, Renato Malcher-Lopes, Bruno Lourenço Diaz, Isis Hara Trevenzoli, Ricardo Augusto De Melo Reis
Prostanoids derived from cyclooxygenase-dependent metabolism of ARA are also major mediators in inflammation. PGE2, the product of PGE synthase terminal enzymes, can modulate every single classic sign of inflammation: dolor, rubor, calor, tumor, and functio laesa and its production is the main target of NSAIDs.235 PGE2 also participates in the resolution phase of inflammation to increase edema, with production of IL-10 and TGF-β, and ECM remodeling. PGD synthase-derived PGD2 also has a role in either phase of inflammation. PGD2 is a direct chemotactic and activation factor for eosinophils, monocyte/macrophages and TH2 lymphocytes, and indirectly contributes for neutrophil migration. Meanwhile, PGD2 and its metabolite, 15d-Δ12,14-PGJ2, are also able to attenuate inflammation.239