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Articoli di riviste sul tema "Inflammation"

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Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 20 luglio 2024

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1

Vijayendranath, Nayak S., Gunasheela S, Karthik M e Hegde Aparna. "Healing by Inflammation - Prolotherapy". Case Reports in Dental Science 1, n. 1 (30 giugno 2020): 9–14. http://dx.doi.org/10.46619/crds.2020.1-1003.

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Temporomandibular disorder (TMD) is a collective term used to describe a group of disorders related to temporomandibular region. It’s considered to be the common cause for orofacial pain. With the advancement of research, prolotherapy is considered to be the one of the treatment modalities to treat TMD, when the conservative management fails.

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2

J, Mancini-Filho. "Natural Antioxidants and Tissue Inflammation". Bioequivalence & Bioavailability International Journal 7, n. 2 (4 luglio 2023): 1–3. http://dx.doi.org/10.23880/beba-16000203.

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The phenolic compounds present in food cover a wide range of structures that have different biological properties. Highlighting its antioxidant properties and the presence mainly of spices, herbs and other foods. Some compounds present in spices can be listed for their antioxidant activity, such as: cloves have eugenol, pinene in their composition, cinnamon also has eugenol, limonene, pinene, catechins and other phenolic compounds in their composition, anise has pinene, rutin, apigenin, oregano has apigenin, quercecin, rosmarinic, caffeic, p-coumaric acids, and others. Rosemary presents the carnosic, rosmarinic, caffeic and hydroxycinnamic. The tissue inflammatory process normally starts with the presence of free radicals that are associated with the oxidative process activated by reactive oxygen species represented by peroxides, superoxide ion, presence of hydroxyl radical, singlet oxygen, among others. The highlighted phenolic compounds have in their structure one or more hydroxyls that have the property of donating a hydrogen atom to free radical structures, which can block the triggering of the oxidative process and thus inflammation.

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Djaldetti, Meir. "Piperine – An Immunomodulator and Inflammation Mitigator". Journal of Clinical and Laboratory Research 2, n. 5 (3 giugno 2021): 01–04. http://dx.doi.org/10.31579/2768-0487/027.

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Black pepper, one of the most widespread spices, gained the entitlement “King of spices” founded on its peculiar pungent test and therapeutic properties, both owed to its active alkaloid - piperine. Mounting evidence indicates that piperine possesses immunomodulatory and therapeutic activities. The aim of this mini review was to summarize the role of piperine in abolishing inflammation, its part in the immune activity of peripheral blood mononuclear- and a number of other cells, its capacity to elicit production of inflammatory cytokines and its function as a synergist endorsing the beneficial therapeutic effect of conventional anti-inflammatory drugs.

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H, Khazaei. "Overview of Orbital Inflammation/Unmet Needs". Open Access Journal of Ophthalmology 7, n. 2 (1 luglio 2022): 1–6. http://dx.doi.org/10.23880/oajo-16000245.

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Diseases of the orbit and periorbital eye tissues manifest in a wide variety of clinical presentations. Space occupying lesions in the orbit include infections, inflammations, vascular malformations, and malignancies. The significant variation in presentations is due to the complex anatomy of the orbit and the heterogeneous nature of the multiple disease processes that present themselves as orbital inflammatory processes. Additionally, although specific disease entities often show similar patterns of orbital tissue involvement, there is still a spectrum of clinical presentations within disease processes, which furthermore overlap with other inflammatory etiologies. This heterogeneity creates a significant challenge in determining specific diagnoses and subsequently instituting timely medical and surgical management of patients with orbital inflammation. Despite advances in imaging, physical examination, and laboratory tests, a biopsy is often needed for diagnosis and to guide treatment. Unfortunately, the biopsy is too often read as non-specific or idiopathic inflammation, a term that gives minimal guidance to the patient or to the clinician. There is clearly a need for developing more specific and sensitive clinical diagnostic testing.

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5

Narula, Jagat, e Eloisa Arbustini. "Inflammation, Superadded Inflammation, and Out-of-Proportion Inflammation in Atherosclerosis". JAMA Cardiology 3, n. 10 (1 ottobre 2018): 912. http://dx.doi.org/10.1001/jamacardio.2018.2760.

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6

Alderton, Gemma, e Seth Thomas Scanlon. "Inflammation". Science 374, n. 6571 (26 novembre 2021): 1068–69. http://dx.doi.org/10.1126/science.abn1721.

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7

Miyamoto, Terumasa. "Inflammation". Ensho 13, n. 2 (1993): 99–100. http://dx.doi.org/10.2492/jsir1981.13.99.

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8

Miyamoto, Terumasa. "Inflammation". Ensho 9, n. 5 (1989): 357. http://dx.doi.org/10.2492/jsir1981.9.357.

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9

Lederer, Katy. "Inflammation". Colorado Review 43, n. 3 (2016): 128–30. http://dx.doi.org/10.1353/col.2016.0094.

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10

Weiss, Ursula. "Inflammation". Nature 454, n. 7203 (luglio 2008): 427. http://dx.doi.org/10.1038/454427a.

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11

Weiss, Ursula. "Inflammation". Nature 420, n. 6917 (dicembre 2002): 845. http://dx.doi.org/10.1038/nature01319x.

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12

Vergnolle, N., e P. Andrade-Gordon. "Inflammation". Journal of Pain 5, n. 3 (aprile 2004): S23. http://dx.doi.org/10.1016/j.jpain.2004.02.060.

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13

Parnes, Ohad. "Inflammation". Lancet 372, n. 9639 (agosto 2008): 621. http://dx.doi.org/10.1016/s0140-6736(08)61262-3.

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14

Cone, John B. "Inflammation". American Journal of Surgery 182, n. 6 (dicembre 2001): 558–62. http://dx.doi.org/10.1016/s0002-9610(01)00822-4.

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15

Penn, Audrey S. "Inflammation". Current Opinion in Neurology 9, n. 3 (giugno 1996): 219–20. http://dx.doi.org/10.1097/00019052-199606000-00012.

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16

Johnston, Craig A. "Inflammation". American Journal of Lifestyle Medicine 6, n. 1 (14 ottobre 2011): 18–20. http://dx.doi.org/10.1177/1559827611425023.

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17

Mantovani, A. "Inflammation". Research in Immunology 143, n. 8 (gennaio 1992): 850–52. http://dx.doi.org/10.1016/0923-2494(92)80104-s.

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18

Ado, A. A. "Allergic inflammation". Kazan medical journal 29, n. 11-12 (12 gennaio 2022): 966–83. http://dx.doi.org/10.17816/kazmj90287.

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Abstract (sommario):

Relatively not so long ago, the doctrine of the inflammatory response was enriched by the concept of "allergic inflammation" (von Pirquet 1907-08). However, the subsequent experimental and clinical study of these inflammatory forms has deepened our understanding of the pathogenesis of each inflammatory reaction so much that it can rightfully be called a stage in the new history of inflammation. From time immemorial, the doctor knew the variety of forms of development and course of inflammation. The construction of these numerous modifications of inflammation in most cases remained unclear. In his practice, each doctor encounters forms of extremely rapidly developing inflammation. Notae verae inflammationis is especially prominent in these cases. Tissue lesions end in necrosis. This one symptom already indicates the rapid development of this form of inflammation. But the rate of its formation can also be registered when studying other inflammatory signs preceding necrosis. A characteristic feature of the development of a normal skin test in an allergic person is the appearance within the first half an hour, literally "before the eyes" of the observer, hyperemia, edema on the periphery of the injection and even infiltration at the injection site.

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19

Johnkennedy, Nnodim, e Okafor Chibuzor Mercy. "Perspective of Inflammation and Inflammation Markers". Journal La Medihealtico 3, n. 1 (31 marzo 2022): 16–26. http://dx.doi.org/10.37899/journallamedihealtico.v3i1.620.

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Progression and occurrence of coronary heart disease can be attributed in part to the presence of inflammation. As a result of our understanding of inflammation's molecular underpinnings, we have identified markers that may also serve as new treatment targets for atherosclerosis. Individuals with and without a history of cardiovascular disease can benefit from monitoring their C-reactive protein (CRP) levels (CVD). The anti-inflammatory characteristics of statins have lately been explored, and they have been shown to significantly lower cardiovascular morbidity and death. C-reactive protein, adiponectin, CD40 ligand, and lipoprotein-associated phospholipase A were the focus of this review, which also looked at statins' effect on these biomarkers and their potential link to cardiovascular events, all of which are thought to be involved in the inflammatory process that leads to atherothrombosis and other cardiovascular diseases.

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20

Strukova, Svetlana. "Blood coagulation-dependent inflammation. Coagulation-dependent inflammation and inflammation-dependent thrombosis". Frontiers in Bioscience 11, n. 1 (2006): 59. http://dx.doi.org/10.2741/1780.

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21

Kuzenko, Yevhen, Anatoly Romanyuk e Antonina Politun. "Macrophage in periodontal inflammation". Journal of Stomatology 69, n. 6 (31 dicembre 2016): 674–79. http://dx.doi.org/10.5604/00114553.1230588.

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Aim of the study. To investigate the expression of CD68 and HSP90AA1 in periodontal inflammation. Methods. A total of twenty-seven patients (giant-cell epulis) and thirty patients (acute and chronic inflammations) have been examined for expression of CD68 and HSP90AA1 by hematoxylin – eosin and immunohistochemistry. Results. Strong giant-cell positivity for CD68 was observed in 100% of patients whereas only 85.31% of giant-cell was positive for HSP90AA1 (p lower than 0.05). Strong macrophage immunoreactivity for CD68 was figured in acute 23.2±1.3%, and in chronic 83.1±5.6% (p lower than 0.05) inflammation. Immunoreactivity for HSP90AA1 was fixed in acute and chronic inflammation 98.2±1.79%. Conclusion. Inflammatory macrophages are a group of cells with protective functions, macrophages being more set up in chronic inflammation. Central giant cell epulis is the multinucleated macrophages, formed as a result of chronic inflammation. Population of macrophages resulted in bone resorption.

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22

Aarabi, Ghazal, Renate Schnabel, Guido Heydecke e Udo Seedorf. "Potential Impact of Oral Inflammations on Cardiac Functions and Atrial Fibrillation". Biomolecules 8, n. 3 (1 agosto 2018): 66. http://dx.doi.org/10.3390/biom8030066.

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Inflammation may be a risk factor for atrial fibrillation (AF). Oral infections frequently lead to chronic inflammation, such as gingivitis, periodontitis, and endodontic lesions. In this narrative review, we consider five basic pathogenic mechanisms that involve oral infections and inflammations in the pathogenesis of AF: (1) low level bacteremia by which oral bacteria enter the blood stream at inflamed sites of the oral cavity and invade the heart; (2) Systemic inflammation induced by inflammatory mediators, which are released from the sites of oral inflammation into the blood stream, affecting cardiac remodeling; (3) autoimmunity against molecular structures expressed in the heart caused by the host immune response to specific components of oral pathogens; (4) potentially arrhythmic effects mediated by activation of the autonomous nervous system triggered by oral inflammations; and (5) arrhythmic effects resulting from specific bacterial toxins that are produced by oral pathogenic bacteria. A number of studies support the involvement of all five mechanisms, suggesting a potentially complex contribution of oral inflammations to the pathogenesis of AF.

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23

Titus, Anto Sam Crosslee Louis Sam. "Macrophage Polarization in Tissue Inflammation and Fibrosis". Clinical Pathology & Research Journal 7, n. 1 (2023): 1–3. http://dx.doi.org/10.23880/cprj-16000175.

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Macrophages are mononuclear phagocytic cells, which have varied phenotypes and perform diverse intricate functions ranging from inflammation to their role in onset and progression of fibrotic diseases

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24

Klepikov, Igor. "Pseudosepsis in Acute Inflammation of the Lung". Open Access Journal of Pulmonary & Respiratory Sciences 8, n. 1 (2024): 1–5. http://dx.doi.org/10.23880/oajprs-16000162.

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Sepsis has become one of the global problems in the healthcare system in recent decades. According to the World Health Organization (WHO), 49 million people suffer from sepsis every year, treatment of which leads to death in 11 million cases [1].

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25

John Edward, Nagar, e Elmo Ado. "Curcumin in Turmeric as Treatment for Eye Inflammation". Journal of Optometry, Eye and Health Research 4, n. 2 (12 gennaio 2023): 7. http://dx.doi.org/10.57002/joehr.v4i2.301.

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AbstractThe research wants to find out if curcumin in turmeric is effective in treating inflammations of the eye. Theresearch also aims to determine if curcumin is an irritant. To answer these questions, curcumin wasextracted and eyedrops were made to be tested on animal models of eye inflammation. Results show thatsigns of inflammation was alleviated with the use of the eyedrops made from curcumin. The study alsofound out that curcumin is practically non-irritative. The study shows the potential use of curcumin as anophthalmic drop, capable of eliminating eye inflammations.

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26

Kondapalli, Lavanya, Javid Moslehi e Marc P. Bonaca. "Inflammation begets inflammation: cancer and acute MI". European Heart Journal 41, n. 23 (18 febbraio 2020): 2194–96. http://dx.doi.org/10.1093/eurheartj/ehz951.

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27

Meirovitz, Amichay, Rachel Goldberg, Adi Binder, Ariel M. Rubinstein, Esther Hermano e Michael Elkin. "Heparanase in inflammation and inflammation-associated cancer". FEBS Journal 280, n. 10 (4 marzo 2013): 2307–19. http://dx.doi.org/10.1111/febs.12184.

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28

White, Raymond P. "Third Molar Oral Inflammation and Systemic Inflammation". Journal of Oral and Maxillofacial Surgery 63, n. 8 (agosto 2005): 5–6. http://dx.doi.org/10.1016/j.joms.2005.05.013.

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Fehér, János, Illés Kovács e Corrado Balacco Gabrieli. "Role of gastrointestinal inflammations in the development and treatment of depression". Orvosi Hetilap 152, n. 37 (settembre 2011): 1477–85. http://dx.doi.org/10.1556/oh.2011.29166.

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Abstract (sommario):

Recent studies have revealed that inflammation, among other factors, may be involved in the pathogenesis of depression. One line of studies has shown that depression is frequently associated with manifest gastrointestinal inflammations and autoimmune diseases as well as with cardiovascular diseases, neurodegenerative diseases, type 2-diabetes and also cancer, in which chronic low-grade inflammation is a significant contributing factor. Thus depression may be a neuropsychiatric manifestation of a chronic inflammatory syndrome. Another line of studies has shown that the primary cause of inflammation may be the dysfunction of the “gut-brain axis”. Although, this is a bidirectional mechanism, life style factors may primarily affect the symbiosis between host mucous membrane and the microbiota. Local inflammation through the release of cytokines, neuropeptides and eicosanoids may also influence the function of the brain and of other organs. Role of metabolic burst due to inflammation represents a new aspect in both pathophysiology and treatment of the depression. Finally, an increasing number of clinical studies have shown that treating gastrointestinal inflammations with probiotics, vitamin B, D and omega 3 fatty acids, through attenuating proinflammatory stimuli to brain, may also improve depression symptoms and quality of life. All these findings justify an assumption that treating gastrointestinal inflammations may improve the efficacy of the currently used treatment modalities of depression and related diseases. However, further studies are certainly needed to confirm these findings. Orv. Hetil., 2011, 152, 1477–1485.

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Chukwuedozie Francis Nwachukwu. "Inflammatory reaction - A posit to the double-edged sword". International Journal of Biological and Pharmaceutical Sciences Archive 1, n. 2 (30 maggio 2021): 197–209. http://dx.doi.org/10.30574/ijbpsa.2021.1.2.0036.

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Response by inflammation is triggered by arrays of causes, which include disrupted cells, toxins, germs, and others. It underlies a wide variety of pathophysiological changes. Many aspects of inflammation as it relates to the pathology of various inflammations are very much understood. Yet the healthy roles of inflammation are widely unknown. Inflammation has a controversial role in health and its meanings are, a matter of viewpoint. It has critical roles in protecting organisms from pathogens and injurious substances likewise causing a driving variety of disease progression. On this ground the research aimed at prescribing the essential needs for effective regulations of inflammatory responses. Efficient control of the inflammatory process will avert a plethora of diseases. Articles used for this review were obtained using appropriate keywords on six electronic databases including nature, advantage, disadvantage, and immune response regarding inflammation and immunological response. Inflammation is self-perpetuating though no disease is caused by inflammation as it is not self-triggering. Additionally, the research did weigh up the merits alongside the demerit of inflammation to advocate for effective regulation of inflammation. Essentially, inflammation is a required mechanism in healthy and unhealthy status in humans hence there is a need for importunate reconsideration, exploring its therapeutic benefits.

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Arulselvan, Palanisamy, Masoumeh Tangestani Fard, Woan Sean Tan, Sivapragasam Gothai, Sharida Fakurazi, Mohd Esa Norhaizan e S. Suresh Kumar. "Role of Antioxidants and Natural Products in Inflammation". Oxidative Medicine and Cellular Longevity 2016 (2016): 1–15. http://dx.doi.org/10.1155/2016/5276130.

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Inflammation is a comprehensive array of physiological response to a foreign organism, including human pathogens, dust particles, and viruses. Inflammations are mainly divided into acute and chronic inflammation depending on various inflammatory processes and cellular mechanisms. Recent investigations have clarified that inflammation is a major factor for the progression of various chronic diseases/disorders, including diabetes, cancer, cardiovascular diseases, eye disorders, arthritis, obesity, autoimmune diseases, and inflammatory bowel disease. Free radical productions from different biological and environmental sources are due to an imbalance of natural antioxidants which further leads to various inflammatory associated diseases. In this review article, we have outlined the inflammatory process and its cellular mechanisms involved in the progression of various chronic modern human diseases. In addition, we have discussed the role of free radicals-induced tissue damage, antioxidant defence, and molecular mechanisms in chronic inflammatory diseases/disorders. The systematic knowledge regarding the role of inflammation and its associated adverse effects can provide a clear understanding in the development of innovative therapeutic targets from natural sources that are intended for suppression of various chronic inflammations associated diseases.

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Fleischman, Angela G. "Inflammation as a Driver of Clonal Evolution in Myeloproliferative Neoplasm". Mediators of Inflammation 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/606819.

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Our understanding of inflammation’s role in the pathogenesis of myeloproliferative neoplasm (MPN) is evolving. The impact of chronic inflammation, a characteristic feature of MPN, likely goes far beyond its role as a driver of constitutional symptoms. An inflammatory response to the neoplastic clone may be responsible for some pathologic aspects of MPN. Moreover,JAK2V617Fmutated hematopoietic stem and progenitor cells are resistant to inflammation, and this gives the neoplastic clone a selective advantage allowing for its clonal expansion. Because inflammation plays a central role in MPN inflammation is a logical therapeutic target in MPN.

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Shi, Xuan-Zheng, John H. Winston e Sushil K. Sarna. "Differential immune and genetic responses in rat models of Crohn's colitis and ulcerative colitis". American Journal of Physiology-Gastrointestinal and Liver Physiology 300, n. 1 (gennaio 2011): G41—G51. http://dx.doi.org/10.1152/ajpgi.00358.2010.

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Crohn's disease and ulcerative colitis are clinically, immunologically, and morphologically distinct forms of inflammatory bowel disease (IBD). However, smooth muscle function is impaired similarly in both diseases, resulting in diarrhea. We tested the hypothesis that differential cellular, genetic, and immunological mechanisms mediate smooth muscle dysfunction in two animal models believed to represent the two diseases. We used the rat models of trinitrobenzene sulfonic acid (TNBS)- and dextran sodium sulfate (DSS)-induced colonic inflammations, which closely mimic the clinical and morphological features of Crohn's disease and ulcerative colitis, respectively. DSS inflammation induced oxidative stress initially in mucosa/submucosa, which then propagated to the muscularis externa to impair smooth muscle function. The muscularis externa showed no increase of cytokines/chemokines. On the other hand, TNBS inflammation almost simultaneously induced oxidative stress, recruited or activated immune cells, and generated cytokines/chemokines in both mucosa/submucosa and muscularis externa. The generation of cytokines/chemokines did not correlate with the recruitment and activation of immune cells. Consequently, the impairment of smooth muscle function in DSS inflammation was primarily due to oxidative stress, whereas that in TNBS inflammation was due to both oxidative stress and proinflammatory cytokines. The impairment of smooth muscle function in DSS inflammation was due to suppression of Gαq protein of the excitation-contraction coupling. In TNBS inflammation, it was due to suppression of the α1C1b subunit of Cav1.2b channels, CPI-17 and Gαq. TNBS inflammation increased IGF-1 and TGF-β time dependently in the muscularis externa. IGF-1 induced smooth muscle hyperplasia; both IGF-1 and TGF-β induced hypertrophy. In conclusion, both TNBS and DSS induce transmural inflammation, albeit with different types of inflammatory mediators. The recruitment or activation of immune cells does not correlate directly with the intensity of generation of inflammatory mediators. The inflammatory mediators in TNBS and DSS inflammations target different genes to impair smooth muscle function.

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Brito, T. de, e M. F. Franco. "Granulomatous inflammation". Revista do Instituto de Medicina Tropical de São Paulo 36, n. 2 (aprile 1994): 185–92. http://dx.doi.org/10.1590/s0036-46651994000200016.

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Natsume, Midori. "Polyphenols: Inflammation". Current Pharmaceutical Design 24, n. 2 (5 aprile 2018): 191–202. http://dx.doi.org/10.2174/1381612823666171109104141.

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Background: Polyphenols widely distributed in plants, fruits and vegetables have received considerable attention on account of their physiological functions, including their antioxidant and anti-inflammatory properties. Some antioxidant components of cacao liquor prepared from fermented and roasted cacao beans, which is a major ingredient of cocoa and chocolate products, have been characterized as flavan-3-ols and procyanidin oligomers. Methods: This review focuses on a specific group of (-)-epicatechins and their oligomers, the procyanidins, in cacao products. Dietary polyphenols in cacao products have been shown to reduce hypertension, reduce platelet aggregation, improve serum lipids, and lower the incidence of atherosclerosis in animal studies and clinical trials. Conclusion: The intake of cacao products reduces hypertension and atherosclerosis on account of their physiological functions as antioxidants and anti-inflammation agents, indicating the mechanisms of prevention of hypertension and atherosclerosis by polyphenols.

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Hussain, Mazhar, Muhammad Bilal Ghafoor, Muhammad Shahbaz Hussain e Lubna Akhtar. "SUBCLINICAL INFLAMMATION". Professional Medical Journal 23, n. 09 (10 settembre 2016): 1132–37. http://dx.doi.org/10.29309/tpmj/2016.23.09.1710.

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Objectives: To evaluate the anti-inflammatory effects of sitagliptin in type 2diabetic hyperlipidemic patients. Period: 25 August 2015 to 25 November 2015 (12 weeks).Study Design: Randomized clinical trials. Setting: Outdoor of diabetic clinic of Sheikh ZayedMedical College/Hospital, Rahim Yar Khan. Materials and Methods: Diabetic patients (n=46)with poor glycemic control(HbA1c > 7.2%) and deranged lipid profile were selected. The patientreceived sitagliptin 50mg twice daily for 12 weeks. Results: A total of 46 patients completed thestudy. After 12 weeks treatment with sitagliptin, there was a significant reduction in the value ofHbA1c from 8.26±0.73% at baseline to 7.33±0.62% (p <0.01). Body mass index also decreasedsignificantly from 31.90±1.57 kg/m2 at baseline to 27.31±1.60 kg/m2 at 12 weeks (p<0.01).There was also significant reduction in the serum level of total Cholesterol (TC), triglycerides(TG) and Low density lipoprotein cholesterol( LDL-C) were detected( TC: 255.35±13.89to 220.76±14.65 mg/dl, TG: 188.80±11.62 to 153.39±9.24 mg/dl,; LDL-C 169.89±12.06 to147.11±8.1 mg/dl with p-value <0.01. High density lipoprotein cholesterol (HDL-C) increasedsignificantly from 41.21±3.11 mg/dl at baseline to 50.21±2.37 mg/dl (p <0.01) at 12 weeks.There is also significant reduction in the value of inflammatory markers after 12 weeks treatmentwith sitagliptin, ESR: 27.04±4.07 vs 11.43±1.74 mm/hr, WBC count: 6.90±0.51 vs 5.65±0.34109/L and hs-CRP: 4.21±0.37 vs 2.16±0.23 mg/L with p-value <0.01. Conclusion: Seeing themultiple benefits of sitagliptin on risk factors and markers of inflammation it is concluded that itshould be started early in diabetic patients to prevent micro and macro vascular complicationsin future.

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Gilroy, Derek W. "Resolving inflammation". Nature Reviews Immunology 21, n. 10 (27 settembre 2021): 620–21. http://dx.doi.org/10.1038/s41577-021-00597-w.

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Aikawa, Masanori, Ichiro Manabe, Adrian Chester e Elena Aikawa. "Cardiovascular Inflammation". International Journal of Inflammation 2012 (2012): 1–2. http://dx.doi.org/10.1155/2012/904608.

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Wang, Miao, Weijun Jin, Austin Meng Guo e Jane Stubbe. "Cardiovascular Inflammation". Mediators of Inflammation 2013 (2013): 1–2. http://dx.doi.org/10.1155/2013/123513.

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David, Rachel. "Manipulating inflammation". Nature Reviews Microbiology 8, n. 2 (11 gennaio 2010): 90. http://dx.doi.org/10.1038/nrmicro2303.

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Meuwissen, Martijn, Allard C. van der Wal, Robbert J. de Winter, Karel T. Koch, Anton E. Becker e Jan J. Piek. "Stent Inflammation". Circulation 106, n. 9 (27 agosto 2002): 1176–77. http://dx.doi.org/10.1161/01.cir.0000029209.89156.88.

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Maciel, T. T., E. Merle, A. Fricot, R. Monteiro, I. C. Moura, G. Seleznik, H. Seeger et al. "PATHOLOGY INFLAMMATION". Nephrology Dialysis Transplantation 29, suppl 3 (1 maggio 2014): iii25—iii26. http://dx.doi.org/10.1093/ndt/gfu119.

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43

Flower, Roderick J., e Mauro Perretti. "Controlling inflammation". Journal of Experimental Medicine 201, n. 5 (7 marzo 2005): 671–74. http://dx.doi.org/10.1084/jem.20050222.

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Abstract (sommario):

The inflammatory response protects the body against infection and injury but can itself become deregulated with deleterious consequences to the host. It is now clear that several endogenous biochemical pathways activated during defense reactions can counterregulate inflammation. New experimental evidence adds resolvin E1 to this group of endogenous inhibitors and provides further rationale for the beneficial effects of dietary supplementation with fish oils. It also highlights an unexpected twist in the pharmacology of aspirin.

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44

Huerva, Valentín, Francisco J. Ascaso e Andrzej Grzybowski. "Ocular Inflammation". Mediators of Inflammation 2015 (2015): 1–2. http://dx.doi.org/10.1155/2015/398076.

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45

SMITH, LUCILLE L. "Acute inflammation". Medicine and Science in Sports and Exercise 23, n. 5 (maggio 1991): 542???551. http://dx.doi.org/10.1249/00005768-199105000-00006.

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46

Hurtley, Stella M. "Activating Inflammation". Science 353, n. 6294 (30 giugno 2016): 40.4–41. http://dx.doi.org/10.1126/science.353.6294.40-d.

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47

Flemming, Alexandra. "DAMPening inflammation". Nature Reviews Drug Discovery 10, n. 6 (giugno 2011): 416. http://dx.doi.org/10.1038/nrd3468.

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48

Kugelberg, Elisabeth. "Starving inflammation". Nature Reviews Drug Discovery 14, n. 4 (aprile 2015): 237. http://dx.doi.org/10.1038/nrd4590.

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49

Durham, S. R. "Allergic inflammation". Pediatric Allergy and Immunology 4, S4 (28 giugno 2008): 7–12. http://dx.doi.org/10.1111/j.1399-3038.1993.tb00332.x.

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50

Clerck, L. S. De. "Chronic Inflammation". Acta Clinica Belgica 52, n. 6 (gennaio 1997): 388–93. http://dx.doi.org/10.1080/17843286.1997.11718605.

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