Статті в журналах: "Inflammation-related factors"

1

Limasset, B., F. Michel, R. Rey, G. Guarrigues, and A. Crastes De Paulet. "Inflammation-Related Factors in Haemorrhoids." Phlebology: The Journal of Venous Disease 9, no. 1_suppl (January 1994): 30–33. http://dx.doi.org/10.1177/0268355594009001s10.

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Objective: To establish whether eicosanoid production characterizes the inflammatory processes of the haemorrhoidal plexus. Design: Open, single patient group study. Setting: Private practice. Patients: Fourteen patients selected for haemorrhoidectomy. Interventions: Specimens were obtained during either the acute (five patients, group I) or chronic (nine patients, group II) phase of the disease. We assayed the concentrations of prostaglandins E2 (PGE2) and F2α (PGF2α) and of leukotriene B4 (LTB4) in the vascular and mucosal tissues of the anterior and posterior haemorrhoidal plexus. Results: Very high levels of prostaglandins were recorded (up to 1445 <g/g fresh tissue of PGE2 in group I), which were consistently higher in group II than group I ( p <0.05, Wilcoxon distribution free test) for 10 out of 18 parameters measured. Four to 20 times more PGE2 than PGF2α was produced. These two eicosanoids were strongly correlated (0.73–0.93 according to sample). LTB4 production was up to 20 times lower than that of PGE2 (6–10 ng/g, group II; 17–52 ng/g, group I). Conclusions: PGF2α and LTB4 seem to be valuable independent study parameters to be included in the design of protocols investigating the action of anti-inflammatory agents on haemorrhoids.

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2

Chang, Wen-Jun. "Inflammation-related factors predicting prognosis of gastric cancer." World Journal of Gastroenterology 20, no. 16 (2014): 4586. http://dx.doi.org/10.3748/wjg.v20.i16.4586.

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Reid-Lombardo, Kaye M., Brooke L. Fridley, William R. Bamlet, Julie M. Cunningham, Michael G. Sarr, and Gloria M. Petersen. "Inflammation-Related Gene Variants as Risk Factors for Pancreatic Cancer." Cancer Epidemiology Biomarkers & Prevention 20, no. 6 (April 5, 2011): 1251–54. http://dx.doi.org/10.1158/1055-9965.epi-11-0264.

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Ravindran, Vinod, and P. P. Anoof. "Traditional and inflammation related cardiovascular risk factors in rheumatoid arthritis." Indian Journal of Rheumatology 9, no. 1 (March 2014): 2–3. http://dx.doi.org/10.1016/j.injr.2014.01.009.

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Soto, Ileana, Mark P. Krebs, Alaina M. Reagan, and Gareth R. Howell. "Vascular Inflammation Risk Factors in Retinal Disease." Annual Review of Vision Science 5, no. 1 (September 15, 2019): 99–122. http://dx.doi.org/10.1146/annurev-vision-091517-034416.

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Inflammation of the blood vessels that serve the central nervous system has been increasingly identified as an early and possibly initiating event among neurodegenerative conditions such as Alzheimer's disease and related dementias. However, the causal relevance of vascular inflammation to major retinal degenerative diseases is unresolved. Here, we describe how genetics, aging-associated changes, and environmental factors contribute to vascular inflammation in age-related macular degeneration, diabetic retinopathy, and glaucoma. We highlight the importance of mouse models in studying the underlying mechanisms and possible treatments for these diseases. We conclude that data support vascular inflammation playing a central if not primary role in retinal degenerative diseases, and this association should be a focus of future research.

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Bilash, S. М., M. M. Koptev, N. I. Vynnyk, O. М. Pronina, and L. M. Shylkina. "INFLAMMATION-RELATED MORPHOLOGICAL ALTERATIONS IN THE MICROVASCULATURE." Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії 21, no. 1 (March 21, 2021): 155–59. http://dx.doi.org/10.31718/2077-1096.21.1.155.

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Microvasculature is a complex structural and functional system that regulates blood supply of body organs, provides transcapillary exchange of fluid and supports the tissue homeostasis. The human microvasculature is represented by the system of small vessels: arterioles, capillaries, venules and arteriolovenular anastomoses. The vessels of this complex become flexible in the altered blood flow; they can deposit the blood corpuscles, get affected by spasms and pass plasma only, change their permeability for tissue fluid. Microvasculature is extremely sensitive to the insults of various factors. Microvascular dysfunction coexists or precedes the macrovascular diseases probably due to joint mechanisms of damage to vessels such as oxidative stress and inflammation. Disorders of microcirculation are one of the main components of inflammation. This article is aimed at the analysis of the scientific publications on the study of morphological alterations in the microvasculature in response to inflammation. The bibliosemantic method was used. The findings of current publications on the morphological alterations that occur in the microcirculation in response to inflammation have been investigated. The analysis has shown significant morphological alterations in the microvessels in response to the proinflammatory factors. Inflammatory processes are accompanied by the events of microvascular dysfunction, associated with hyperpermeability of capillaries, destruction of microvascular endothelial barrier, loss of antiadhesive function of endothelium, etc. In response to inflammation, the marked morphofunctional alterations in the microvasculature of the various organs are observed that are dependent on the time course of inflammation. Early onset is manifested mainly by the spasm of the vascular resistance and dilatation of the capacitance vessels. Disorders of blood rheological properties are manifested by stasis, sludge, microthrombosis.

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Philippou, Anastassios. "Systemic Responses of Inflammation-Related Factors Following Eccentric Exercise in Humans." American Journal of Sports Science 6, no. 2 (2018): 32. http://dx.doi.org/10.11648/j.ajss.20180602.11.

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Goldstein, Gregory P., Stephanie A. Leonard, Peiyi Kan, Euna B. Koo, Henry C. Lee, and Suzan L. Carmichael. "Prenatal and postnatal inflammation-related risk factors for retinopathy of prematurity." Journal of Perinatology 39, no. 7 (April 1, 2019): 964–73. http://dx.doi.org/10.1038/s41372-019-0357-2.

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9

Bower, Julienne E., and Donald M. Lamkin. "Inflammation and cancer-related fatigue: Mechanisms, contributing factors, and treatment implications." Brain, Behavior, and Immunity 30 (March 2013): S48—S57. http://dx.doi.org/10.1016/j.bbi.2012.06.011.

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MOSHFEGHI, DARIUS M., and MARK S. BLUMENKRANZ. "ROLE OF GENETIC FACTORS AND INFLAMMATION IN AGE-RELATED MACULAR DEGENERATION." Retina 27, no. 3 (March 2007): 269–75. http://dx.doi.org/10.1097/iae.0b013e31802e3e9b.

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Parmeggiani, Francesco, Mario R. Romano, Ciro Costagliola, Francesco Semeraro, Carlo Incorvaia, Sergio D’Angelo, Paolo Perri, Paolo De Palma, Katia De Nadai, and Adolfo Sebastiani. "Mechanism of Inflammation in Age-Related Macular Degeneration." Mediators of Inflammation 2012 (2012): 1–16. http://dx.doi.org/10.1155/2012/546786.

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Age-related macular degeneration (AMD) is a multifactorial disease that represents the most common cause of irreversible visual impairment among people over the age of 50 in Europe, the United States, and Australia, accounting for up to 50% of all cases of central blindness. Risk factors of AMD are heterogeneous, mainly including increasing age and different genetic predispositions, together with several environmental/epigenetic factors, that is, cigarette smoking, dietary habits, and phototoxic exposure. In the aging retina, free radicals and oxidized lipoproteins are considered to be major causes of tissue stress resulting in local triggers for parainflammation, a chronic status which contributes to initiation and/or progression of many human neurodegenerative diseases such as AMD. Experimental and clinical evidences strongly indicate the pathogenetic role of immunologic processes in AMD occurrence, consisting of production of inflammatory related molecules, recruitment of macrophages, complement activation, microglial activation and accumulation within those structures that compose an essential area of the retina known as macula lutea. This paper reviews some attractive aspects of the literature about the mechanisms of inflammation in AMD, especially focusing on those findings or arguments more directly translatable to improve the clinical management of patients with AMD and to prevent the severe vision loss caused by this disease.

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12

Okada, Futoshi, Runa Izutsu, Keisuke Goto, and Mitsuhiko Osaki. "Inflammation-Related Carcinogenesis: Lessons from Animal Models to Clinical Aspects." Cancers 13, no. 4 (February 22, 2021): 921. http://dx.doi.org/10.3390/cancers13040921.

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Inflammation-related carcinogenesis has long been known as one of the carcinogenesis patterns in humans. Common carcinogenic factors are inflammation caused by infection with pathogens or the uptake of foreign substances from the environment into the body. Inflammation-related carcinogenesis as a cause for cancer-related death worldwide accounts for approximately 20%, and the incidence varies widely by continent, country, and even region of the country and can be affected by economic status or development. Many novel approaches are currently available concerning the development of animal models to elucidate inflammation-related carcinogenesis. By learning from the oldest to the latest animal models for each organ, we sought to uncover the essential common causes of inflammation-related carcinogenesis. This review confirmed that a common etiology of organ-specific animal models that mimic human inflammation-related carcinogenesis is prolonged exudation of inflammatory cells. Genotoxicity or epigenetic modifications by inflammatory cells resulted in gene mutations or altered gene expression, respectively. Inflammatory cytokines/growth factors released from inflammatory cells promote cell proliferation and repair tissue injury, and inflammation serves as a “carcinogenic niche”, because these fundamental biological events are common to all types of carcinogenesis, not just inflammation-related carcinogenesis. Since clinical strategies are needed to prevent carcinogenesis, we propose the therapeutic apheresis of inflammatory cells as a means of eliminating fundamental cause of inflammation-related carcinogenesis.

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13

Crauciuc, Dragos Valentin, Allia Sindilar, Madalina Diac, Daniel Tabian, Sofia Mihaela David, Diana Bulgaru-Iliescu, and Eduard Grabriel Crauciuc. "Immune Inflammation Related to Obesity in Pregnant Women." Revista de Chimie 70, no. 5 (June 15, 2019): 1812–17. http://dx.doi.org/10.37358/rc.19.5.7221.

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Although there are many conditions to be met for the disease to occur (genetic predisposition, environmental factors, stress, exposure to pollutants, noxes, xenobiotics, diet), chronic inflammation is the way how the body responds to these substances. Excess weight leads to an alteration of the immune response, to an increased oxidative stress, and damage to the cellular Deoxyribonucleic acid (DNA) structure. The study aims to evaluate inflammation in obese mothers. The study group consisted of 30 pregnant women in which inflammation was analysed, with a mean age of 30.80 � 6,94 years old divided in 2 groups depending on their weight, that is 25 pregnant women with obesity and 5 normoponderal pregnant women. From the markers found in the blood samples, only CRP (AUC=0.740; IC95%: 0.466-1.014), leptin (AUC=0.616; IC95%: 0.296-0.936) and glycaemia (AUC=0.648; IC95%: 0.369-0.927) were good indicators of immune inflammation. The estimated risk of immune inflammation is 5 times higher in obese pregnancies with CRP levels above 6.

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von Scholten, Bernt J., Erik N. Andresen, Thorkild IA Sørensen, and Tine Jess. "Aetiological factors behind adipose tissue inflammation: an unexplored research area." Public Health Nutrition 16, no. 1 (April 2, 2012): 27–35. http://dx.doi.org/10.1017/s1368980012000894.

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AbstractObjectiveDespite extensive research into the biological mechanisms behind obesity-related inflammation, knowledge of environmental and genetic factors triggering such mechanisms is limited. In the present narrative review we present potential determinants of adipose tissue inflammation and suggest ways ahead for future research in the field.DesignWe searched the literature for potential determinants of obesity with inflammation through MEDLINE by applying the MeSH headings ‘obesity’ and ‘inflammation’ in combination with specific terms for a series of environmental and genetic factors.ResultsNumerous articles reported on the association between environmental or genetic factors and respectively obesity and inflammation, whereas only a few studies assessed obesity and inflammation as a combined outcome. Among suggested determinants for obesity with inflammation were Adenovirus-36, the gut microbiota,trans-fatty acids, and the four genesFTO,MC4R,TNF-αandLEPR.ConclusionsWe present a limited number of factors potentially contributing to the development of obesity with inflammation, while concluding that overall the area is indeed sparsely investigated. We present ideas for future studies that can identify relevant aetiological factors. This identification is essential for targeted prevention of obesity with inflammation and the clinical consequences thereof.

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15

Li, Lu, Huaibin Zou, Manman Xu, Shuang Li, Yunxia Zhu, Sujun Zheng, Zhongping Duan, and Yu Chen. "Risk factors related to postpartum hepatic inflammation in pregnant women with chronic hepatitis B." Journal of International Medical Research 48, no. 11 (November 2020): 030006052096643. http://dx.doi.org/10.1177/0300060520966439.

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Objectives To investigate liver function after pregnancy in women with chronic hepatitis B virus (HBV) and factors related to postpartum abnormalities. Methods A total of 317 pregnant women were included in this study and 138 had an HBV DNA level. In this trial, the highest number and proportion of hepatitis B surface antigen-positive mothers with postpartum hepatic inflammation were at 1 month after delivery. Results Baseline liver function of postpartum women with hepatic inflammation was significantly higher than that in those before delivery. The rates of hepatitis B e-antigen (HBeAg)-positive status, baseline HBV DNA levels, gestational diabetes mellitus, and antiviral therapy during pregnancy were significantly higher in the hepatic inflammation group than in the control group. Among the 138 women who received antiviral therapy, 83 withdrew from antiviral therapy immediately after delivery and 55 continued antiviral therapy for at least 1 month after delivery. Multivariate logistic regression analysis showed that HBeAg-positivity and gestational diabetes mellitus were associated with hepatic inflammation after delivery. Postpartum hepatic inflammation occurred mostly at 1 month after delivery in pregnant women with HBV infection. Conclusions Close monitoring of women with HBV during pregnancy is required, especially for those who are HBeAg-positive and have gestational diabetes mellitus.

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Cormier, Yvon, and Evelyne Israël-Assayag. "Chronic inflammation induced by organic dust and related metabolic cardiovascular disease risk factors." Scandinavian Journal of Work, Environment & Health 30, no. 6 (December 2004): 438–44. http://dx.doi.org/10.5271/sjweh.832.

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Ness, Roberta B., Jeane Ann Grisso, Carrie Cottreau, Jennifer Klapper, Ron Vergona, James E. Wheeler, Mark Morgan, and James J. Schlesselman. "Factors Related to Inflammation of the Ovarian Epithelium and Risk of Ovarian Cancer." Epidemiology 11, no. 2 (March 2000): 111–17. http://dx.doi.org/10.1097/00001648-200003000-00006.

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Lavrovsky, Y. "Role of redox-regulated transcription factors in inflammation, aging and age-related diseases." Experimental Gerontology 35, no. 5 (August 1, 2000): 521–32. http://dx.doi.org/10.1016/s0531-5565(00)00118-2.

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Kubota, Toshinobu, Masao Katayama, Suzuko Moritani, and Tadashi Yoshino. "Serologic Factors in Early Relapse of IgG4-Related Orbital Inflammation After Steroid Treatment." American Journal of Ophthalmology 155, no. 2 (February 2013): 373–79. http://dx.doi.org/10.1016/j.ajo.2012.07.024.

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Suo, Zhanwei, Ye Liu, Miro Ferreri, Tao Zhang, Zhongjie Liu, Xiang Mu, and Bo Han. "Impact of matrine on inflammation related factors in rat intestinal microvascular endothelial cells." Journal of Ethnopharmacology 125, no. 3 (September 2009): 404–9. http://dx.doi.org/10.1016/j.jep.2009.07.023.

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Suh, Sung-Hyeok. "Changes in Muscle Hypertrophy-Related Factors and Vascular Inflammation-Related Factors Associated with 12-Weeks Weight Training and Supplementation of Protein Supplements." Journal of the Korean society for Wellness 13, no. 4 (November 30, 2018): 411–20. http://dx.doi.org/10.21097/ksw.2018.11.13.4.411.

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Lv, Qing, Qinghua Xia, Anshu Li, and Zhiyong Wang. "The Potential Role of IL1RAP on Tumor Microenvironment-Related Inflammatory Factors in Stomach Adenocarcinoma." Technology in Cancer Research & Treatment 20 (January 1, 2021): 153303382199528. http://dx.doi.org/10.1177/1533033821995282.

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This study was performed to investigate the role of interleukin-1 receptor accessory protein (IL1RAP) in stomach carcinoma in vitro and in vivo, determine whether IL1RAP knockdown could regulate the development of stomach carcinoma, and elucidate the relationship between IL1RAP knockdown and inflammation by tumor microenvironment-related inflammatory factors in stomach carcinoma. We first used TCGA and GEPIA systems to predict the potential function of IL1RAP. Second, western blot and RT-PCR were used to analyze the expression, or mRNA level, of IL1RAP at different tissue or cell lines. Third, the occurrence and development of stomach carcinoma in vitro and in vivo were observed by using IL1RAP knockdown lentivirus. Finally, the inflammation of stomach carcinoma in vitro and in vivo was observed. Results show that in GEPIA and TCGA systems, IL1RAP expression in STAD tumor tissue was higher than normal, and high expression of IL1RAP in STAD patients had a worse prognostic outcome. Besides, GSEA shown IL1RAP was negative correlation of apopopsis, TLR4 and NF-κB signaling pathway. We also predicted that IL1RAP may related to IL-1 s, IL-33, and IL-36 s in STAD. The IL1RAP expression and mRNA level in tumor, or MGC803, cells were increased. Furthermore, IL1RAP knockdown by lentivirus could inhibit stomach carcinoma development in vitro and in vivo through weakening tumor cell proliferation, migration, invasion, therefore reducing tumor volume, weight, and biomarker levels, and increasing apoptotic level. Finally, we found IL1RAP knockdown could increase inflammation of tumor microenvironment-related inflammatory factors of stomach carcinoma, in vitro and in vivo. Our study demonstrates that IL1RAP is possibly able to regulate inflammation and apoptosis in stomach carcinoma. Furthermore, TLR4, NF-κB, IL-1 s, IL-33, and IL-36 s maybe the downstream target factor of IL1RAP in inflammation. These results may provide a new strategy for stomach carcinoma development by regulating inflammation.

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Ohnishi, Shiho, Ning Ma, Raynoo Thanan, Somchai Pinlaor, Olfat Hammam, Mariko Murata, and Shosuke Kawanishi. "DNA Damage in Inflammation-Related Carcinogenesis and Cancer Stem Cells." Oxidative Medicine and Cellular Longevity 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/387014.

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Infection and chronic inflammation have been recognized as important factors for carcinogenesis. Under inflammatory conditions, reactive oxygen species (ROS) and reactive nitrogen species (RNS) are generated from inflammatory and epithelial cells and result in oxidative and nitrative DNA damage, such as 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG) and 8-nitroguanine. The DNA damage can cause mutations and has been implicated in the initiation and/or promotion of inflammation-mediated carcinogenesis. It has been estimated that various infectious agents are carcinogenic to humans (IARC group 1), including parasites (Schistosoma haematobium(SH) andOpisthorchis viverrini(OV)), viruses (hepatitis C virus (HCV), human papillomavirus (HPV), and Epstein-Barr virus (EBV)), and bacteriumHelicobacter pylori(HP). SH, OV, HCV, HPV, EBV, and HP are important risk factors for bladder cancer, cholangiocarcinoma, hepatocellular carcinoma, cervical cancer, nasopharyngeal carcinoma, and gastric cancer, respectively. We demonstrated that 8-nitroguanine was strongly formed via inducible nitric oxide synthase (iNOS) expression at these cancer sites of patients. Moreover, 8-nitroguanine was formed in Oct3/4-positive stem cells in SH-associated bladder cancer tissues and in Oct3/4- and CD133-positive stem cells in OV-associated cholangiocarcinoma tissues. Therefore, it is considered that oxidative and nitrative DNA damage in stem cells may play a key role in inflammation-related carcinogenesis.

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Lv, Tingxia, Wei Cao, and Taisheng Li. "HIV-Related Immune Activation and Inflammation: Current Understanding and Strategies." Journal of Immunology Research 2021 (September 29, 2021): 1–13. http://dx.doi.org/10.1155/2021/7316456.

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Although antiretroviral therapy effectively controls human immunodeficiency virus (HIV) replication, a residual chronic immune activation/inflammation persists throughout the disease. This aberrant immune activation and inflammation are considered an accelerator of non-AIDS-related events and one of the driving forces of CD4+ T cell depletion. Unfortunately, HIV-associated immune activation is driven by various factors, while the mechanism of excessive inflammation has not been formally clarified. To date, several clinical interventions or treatment candidates undergoing clinical trials have been proposed to combat this systemic immune activation/inflammation. However, these strategies revealed limited results, or their nonspecific anti-inflammatory properties are similar to previous interventions. Here, we reviewed recent learnings of immune activation and persisting inflammation associated with HIV infection, as well as the current directions to overcome it. Of note, a more profound understanding of the specific mechanisms for aberrant inflammation is still imperative for identifying an effective clinical intervention strategy.

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Rodríguez-Hernández, Heriberto, Luis E. Simental-Mendía, Gabriela Rodríguez-Ramírez, and Miguel A. Reyes-Romero. "Obesity and Inflammation: Epidemiology, Risk Factors, and Markers of Inflammation." International Journal of Endocrinology 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/678159.

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Obesity is a public health problem that has reached epidemic proportions with an increasing worldwide prevalence. The global emergence of obesity increases the risk of developing chronic metabolic disorders. Thus, it is an economic issue that increased the costs of the comorbidities associated. Moreover, in recent years, it has been demonstrated that obesity is associated with chronic systemic inflammation, this status is conditioned by the innate immune system activation in adipose tissue that promotes an increase in the production and release of pro-inflammatory cytokines that contribute to the triggering of the systemic acute-phase response which is characterized by elevation of acute-phase protein levels. On this regard, low-grade chronic inflammation is a characteristic of various chronic diseases such as metabolic syndrome, cardiovascular disease, diabetes, hypertension, non-alcoholic fatty liver disease, and some cancers, among others, which are also characterized by obesity condition. Thus, a growing body of evidence supports the important role that is played by the inflammatory response in obesity condition and the pathogenesis of chronic diseases related.

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Teixeira, Antonio L., Lais B. Martins, Michael Berk, and Moisés E. Bauer. "Severe psychiatric disorders and general medical comorbidities: inflammation-related mechanisms and therapeutic opportunities." Clinical Science 136, no. 17 (September 2022): 1257–80. http://dx.doi.org/10.1042/cs20211106.

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Abstract Individuals with severe psychiatric disorders, such as mood disorders and schizophrenia, are at increased risk of developing other medical conditions, especially cardiovascular and metabolic diseases. These medical conditions are underdiagnosed and undertreated in these patients contributing to their increased morbidity and mortality. The basis for this increased comorbidity is not well understood, possibly reflecting shared risks factors (e.g. lifestyle risk factors), shared biological mechanisms and/or reciprocal interactions. Among overlapping pathophysiological mechanisms, inflammation and related factors, such as dysbiosis and insulin resistance, stand out. Besides underlying the association between psychiatric disorders and cardiometabolic diseases, these mechanisms provide several potential therapeutic targets.

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Yoshida, Hiroki. "Preventive and Ameliorating Effects of Food Factors on Obesity-related Diseases by Regulating Inflammation." YAKUGAKU ZASSHI 141, no. 10 (October 1, 2021): 1161–71. http://dx.doi.org/10.1248/yakushi.21-00121.

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Luna-Moreno, Dalia, Raúl Aguilar-Roblero, and Mauricio Díaz-Muñoz. "RESTRICTED FEEDING ENTRAINS RHYTHMS OF INFLAMMATION-RELATED FACTORS WITHOUT PROMOTING AN ACUTE-PHASE RESPONSE." Chronobiology International 26, no. 7 (October 2009): 1409–29. http://dx.doi.org/10.3109/07420520903417003.

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Slattery, Martha L., and F. A. Fitzpatrick. "Convergence of Hormones, Inflammation, and Energy-Related Factors: A Novel Pathway of Cancer Etiology." Cancer Prevention Research 2, no. 11 (November 2009): 922–30. http://dx.doi.org/10.1158/1940-6207.capr-08-0191.

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Chen, Liping, Qi Zhang, Wenjun Chang, Yan Du, Hongwei Zhang, and Guangwen Cao. "Viral and host inflammation-related factors that can predict the prognosis of hepatocellular carcinoma." European Journal of Cancer 48, no. 13 (September 2012): 1977–87. http://dx.doi.org/10.1016/j.ejca.2012.01.015.

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Wang, Song-zi, Min Wu, Ke-ji Chen, Yue Liu, Jing Sun, Zhuo Sun, He Ma, and Long-tao Liu. "Hawthorn Extract Alleviates Atherosclerosis through Regulating Inflammation and Apoptosis Related Factors: An Experimental Study." Chinese Journal of Integrative Medicine 25, no. 2 (December 5, 2018): 108–15. http://dx.doi.org/10.1007/s11655-018-3020-4.

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Adachi, Saeko, Takahiro Hamoya, Gen Fujii, Takumi Narita, Masami Komiya, Shingo Miyamoto, Yurie Kurokawa, et al. "Theracurmin inhibits intestinal polyp development in Apc ‐mutant mice by inhibiting inflammation‐related factors." Cancer Science 111, no. 4 (February 22, 2020): 1367–74. http://dx.doi.org/10.1111/cas.14329.

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Purnichi, Traian, Alina E. Rosca, Ana Giurgiuca, Alexandru N. Pavel, and Valentin P. Matei. "Neuro-inflammation and its effects on cognition: A review of literature." Romanian Journal of Psychiatry and Psychotherapy 20, no. 3 (September 30, 2018): 100–103. http://dx.doi.org/10.37897/rjpp.2018.3.2.

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Introduction: More and more evidence suggests that inflammation is positively associated with age-related cognitive decline and may play a role in the development of dementia. Method: Physiological pathways linking the immune system to the central nervous system are reviewed in this article and studies regarding the association between inflammation and neurocognitive function are reviewed from literature. Results: Recent studies show that midlife inflammation is related to cognitive function and brain morphology. Human studies combining different markers of inflammation, neuroimaging methods and cognitive tests are consistent with studies on animal models which conclude that inflammation contributes to lowering cognitive performance over and above more traditional cardiovascular risk factors such as: hypertension, metabolic factors, smoking and subclinical atherosclerosis. The studies reviewed had limitations by not estimating the impact of multiple factors known to affect circulating levels of inflammatory mediators such as: acute inflammatory disease, psychological stress or physical activity. Conclusions: Circulating markers of inflammation predict future risk of cognitive decline and possibly contribute to the pathophysiology of preclinical neurocognitive decline.

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Kumar, Sushil, Girijesh Kumar Patel, and Uday C. Ghoshal. "Helicobacter pylori-Induced Inflammation: Possible Factors Modulating the Risk of Gastric Cancer." Pathogens 10, no. 9 (August 29, 2021): 1099. http://dx.doi.org/10.3390/pathogens10091099.

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Chronic inflammation and long-term tissue injury are related to many malignancies, including gastric cancer (GC). Helicobacter pylori (H. pylori), classified as a class I carcinogen, induces chronic superficial gastritis followed by gastric carcinogenesis. Despite a high prevalence of H. pylori infection, only about 1–3% of people infected with this bacterium develop GC worldwide. Furthermore, the development of chronic gastritis in some, but not all, H. pylori-infected subjects remains unexplained. These conflicting findings indicate that clinical outcomes of aggressive inflammation (atrophic gastritis) to gastric carcinogenesis are influenced by several other factors (in addition to H. pylori infection), such as gut microbiota, co-existence of intestinal helminths, dietary habits, and host genetic factors. This review has five goals: (1) to assess our current understanding of the process of H. pylori-triggered inflammation and gastric precursor lesions; (2) to present a hypothesis on risk modulation by the gut microbiota and infestation with intestinal helminths; (3) to identify the dietary behavior of the people at risk of GC; (4) to check the inflammation-related genetic polymorphisms and role of exosomes together with other factors as initiators of precancerous lesions and gastric carcinoma; and (5) finally, to conclude and suggest a new direction for future research.

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Jeong, Junhui, Ji Hyuk Han, Hyun Seung Choi, and In Seok Moon. "Immunoinflammatory and vascular inflammatory factors can be potential disease biomarkers of age-related hearing loss." European Journal of Inflammation 20 (January 2022): 1721727X2211100. http://dx.doi.org/10.1177/1721727x221110078.

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Objectives: The relationship between age-related diseases and chronic inflammation associated with aging has recently been investigated. This study aimed to investigate how chronic inflammation is associated with age-related hearing loss (ARHL). Methods: Twenty ARHL patients aged ≥65 years were prospectively enrolled from July 1 to 31 December 2015. Audiological tests and serological tests, such as C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), immunoglobulin G (IgG), interleukin 6 (IL-6), white blood cell (WBC) counts, neutrophil counts, lymphocyte counts, and platelet counts, were performed. The patients were divided into two groups: mild hearing loss group (n = 7) and moderate to profound hearing loss group (n = 13). Results: Immunoinflammatory biomarkers, such as CRP, ESR, and IL-6, and vascular inflammatory biomarkers, such as neutrophil-to-lymphocyte ratio and platelet-to-lymphocyte ratio, were higher in the moderate to profound hearing loss group. IgG, WBC counts, and neutrophil counts were similar in both groups. Conclusion: The present preliminary pilot study demonstrated that high levels of inflammatory biomarkers may be associated with ARHL. The results suggest a possible association between chronic inflammation and ARHL. Further well-designed studies of ARHL, based on a new perspective of chronic inflammation, should be performed.

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Scholand, Kaitlin K., Alexis F. Mack, Gary U. Guzman, Michael E. Maniskas, Ritu Sampige, Gowthaman Govindarajan, Louise D. McCullough, and Cintia S. de Paiva. "Heterochronic Parabiosis Causes Dacryoadenitis in Young Lacrimal Glands." International Journal of Molecular Sciences 24, no. 5 (March 3, 2023): 4897. http://dx.doi.org/10.3390/ijms24054897.

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Aging is associated with inflammation and oxidative stress in the lacrimal gland (LG). We investigated if heterochronic parabiosis of mice could modulate age-related LG alterations. In both males and females, there were significant increases in total immune infiltration in isochronic aged LGs compared to that in isochronic young LGs. Male heterochronic young LGs were significantly more infiltrated compared to male isochronic young LGs. While both females and males had significant increases in inflammatory and B-cell-related transcripts in isochronic and heterochronic aged LGs compared to levels isochronic and heterochronic young LGs, females had a greater fold expression of some of these transcripts than males. Through flow cytometry, specific subsets of B cells were increased in the male heterochronic aged LGs compared to those in male isochronic aged LGs. Our results indicate that serum soluble factors from young mice were not enough to reverse inflammation and infiltrating immune cells in aged tissues and that there were specific sex-related differences in parabiosis treatment. This suggests that age-related changes in the LG microenvironment/architecture participate in perpetuating inflammation, which is not reversible by exposure to youthful systemic factors. In contrast, male young heterochronic LGs were significantly worse than their isochronic counterparts, suggesting that aged soluble factors can enhance inflammation in the young host. Therapies that aim at improving cellular health may have a stronger impact on improving inflammation and cellular inflammation in LGs than parabiosis.

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Poredoš, Pavel, Peter Poredoš, and Mateja Kaja Jezovnik. "Factors influencing recanalization of thrombotic venous occlusions." Vasa 49, no. 1 (January 1, 2020): 17–22. http://dx.doi.org/10.1024/0301-1526/a000800.

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Summary. The outcome of a thrombotic vessel occlusion is related to the resolution of thrombus and restitution of blood flow. Thrombus formation simultaneously activates an enzymatic process that mediates endogenous fibrinolysis to maintain vessel patency. The balance between coagulation and fibrinolysis determines the extent of thrombus formation, its resolution, and clinical outcome. Endogenic fibrinolysis is frequently unable to overcome coagulation and to resolve the thrombus. Therefore, for a complete resolution of thrombus in an acute phase, exogenic fibrinolytic agents are needed. Currently, tissue plasminogen activator (tPA) is most frequently used for therapeutic thrombolysis. Also, heparins, particularly low-molecular-weight heparins and direct oral anticoagulants which are known as anticoagulant drugs, have some pro-fibrinolytic properties. Besides the extent and age of a clot, different other factors influence the lysis of thrombus. Thrombus structure is one of the most important determinants of thrombus lysis. The concentration of thrombolytic agent (tPA) around and inside of thrombus importantly determines clot lysis velocity. Further, flow-induced mechanical forces which stimulate the transport of thrombolytic agent into the clot influence thrombolysis. Inflammation most probably represents a basic pathogenetic mechanism of activation of coagulation and influences the activity of the fibrinolytic system. Inflammation increases tissue factor release, platelet activity, fibrinogen concentration and inhibits fibrinolysis by increasing plasminogen activator inhibitor 1. Therefore, recanalization of a thrombotic vessel occlusion is inversely related to levels of some circulating inflammatory agents. Consequently, inhibition of inflammation with anti-inflammatory drugs may improve the efficacy of prevention of thromboembolic events and stimulate recanalization of thrombotic occlusions of veins.

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Fortes, Paulo C., Priscilla H. Versari, Andréa E. M. Stinghen, and Roberto Pecoits–Filho. "Controlling Inflammation in Peritoneal Dialysis: The Role of PD-Related Factors as Potential Intervention Targets." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 27, no. 2_suppl (June 2007): 76–81. http://dx.doi.org/10.1177/089686080702702s14.

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Cardiovascular (CV) disease is the main cause of death in peritoneal dialysis (PD) patients, but the mechanisms mediating the increased CV risk observed in this group of patients are still largely unknown, which limits the perspective on effective therapeutic strategies. Patients on PD are already exposed to a number of traditional risk factors from the start of their chronic kidney disease (CKD), because many of those risk factors are common to CV disease and CKD alike. As renal dysfunction progresses, CKD-related risk factors are introduced, changing the profile of both the CV disease and the markers of risk. In this phase, which usually starts when glomerular filtration rate falls below 60 mL/min, the list of risk factors is expanded to include disturbances of mineral metabolism, anemia, fluid overload, uremic toxicity, and increased signs of oxidative stress and inflammation. Although many of the risk factors linked to CV burden are not related to the dialytic procedure, additional harm is introduced after the initiation of PD—with, for example, the presence of chronic infections and factors related to PD fluids, particularly reabsorption of glucose. In the present article, we review the impact of the novel risk factors introduced with the initiation of PD therapy, and we propose potential therapeutic strategies (which remain to be tested) for reducing CV mortality in this group of patients.

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Masehi-Lano, Jacqueline J., Maya Deyssenroth, Sandra W. Jacobson, Joseph L. Jacobson, Christopher D. Molteno, Neil C. Dodge, Helen C. Wainwright, et al. "Alterations in Placental Inflammation-Related Gene Expression Partially Mediate the Effects of Prenatal Alcohol Consumption on Maternal Iron Homeostasis." Nutrients 15, no. 19 (September 22, 2023): 4105. http://dx.doi.org/10.3390/nu15194105.

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Prenatal alcohol exposure (PAE) is associated with alterations in maternal and infant iron homeostasis that are consistent with changes seen in the setting of inflammation. We hypothesized that PAE leads to alterations in the placental expression of genes related to iron metabolism and inflammation that play functional roles in the teratogenic effects of alcohol on iron homeostasis. A total of 126 heavy-drinking women (≥1 oz (30 mL) absolute alcohol/day (~1.67 standard drinks/day) or women reporting binge drinking (≥2 drinks/occasion)) and 80 control women (<0.5 oz AA per day, no binging) in Cape Town, South Africa were interviewed prenatally regarding demographics, and alcohol, smoking, and drug use around conception and during pregnancy. Prenatal/maternal and infant hemoglobin and ferritin were measured. Whole-transcriptome RNA sequencing analysis was performed on flash-frozen transplacental tissue samples. Gene sets related to iron metabolism (n = 398) and inflammation (n = 467) were constructed by searching the Molecular Signatures Database for related ontology terms. Principal component analysis (PCA) yielded 59 factors for each theme. In multivariable regression models, PAE was related to 2 iron metabolism PCA factors (PCs) and 5 inflammation PCs, among which 2 iron metabolism and 4 inflammation factors were related to at least 1 key maternal or infant iron outcome. In causal inference analyses based on marginal structural models and the product method, the alterations in the expression profile of genes with functions in immune cell regulation, cytokine activity, angiogenesis, hematopoiesis, and ubiquitous cell processes appeared to partially mediate the relation of prenatal drinking frequency (days/week) around conception to a lower maternal hemoglobin-to-log(ferritin) ratio (proportion mediation = 51.35%). These findings suggest that placental inflammation may be partly responsible for the differences in alcohol-related iron homeostasis patterns between pregnant and non-pregnant adults.

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Hirabara, Sandro M., Renata Gorjão, Marco A. Vinolo, Alice C. Rodrigues, Renato T. Nachbar, and Rui Curi. "Molecular Targets Related to Inflammation and Insulin Resistance and Potential Interventions." Journal of Biomedicine and Biotechnology 2012 (2012): 1–16. http://dx.doi.org/10.1155/2012/379024.

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Inflammation and insulin resistance are common in several chronic diseases, such as obesity, type 2diabetes mellitus, metabolic syndrome, cancer, and cardiovascular diseases. Various studies show a relationship between these two factors, although the mechanisms involved are not completely understood yet. Here, we discuss the molecular basis of insulin resistance and inflammation and the molecular aspects on inflammatory pathways interfering in insulin action. Moreover, we explore interventions based on molecular targets for preventing or treating correlated disorders, advances for a better characterization, and understanding of the mechanisms and mediators involved in the different inflammatory and insulin resistance conditions. Finally, we address biotechnological studies for the development of new potential therapies and interventions.

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Sakkinen, Pamela A., Patricia Wahl, Mary Cushman, Michael R. Lewis, and Russell P. Tracy. "Clustering of Procoagulation, Inflammation, and Fibrinolysis Variables with Metabolic Factors in Insulin Resistance Syndrome." American Journal of Epidemiology 152, no. 10 (November 15, 2000): 897–907. http://dx.doi.org/10.1093/aje/152.10.897.

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Abstract The known metabolic cardiovascular disease risk factors associated with insulin resistance syndrome (IRS) do not adequately explain the excess cardiovascular disease risk attributed to this syndrome, and abnormalities in hemostatic variables may contribute to this excess risk. Using data from 322 nondiabetic elderly men and women (aged 65–100 years) participating in the Cardiovascular Health Study during 1989–1990, the authors performed factor analysis on 10 metabolic risk factors associated with IRS and 11 procoagulation, inflammation, and fibrinolysis variables to examine the clustering of the metabolic and hemostatic risk markers. Factor analysis of the metabolic variables confirmed four uncorrelated factors: body mass, insulin/glucose, lipids, and blood pressure. Adding the hemostatic variables yielded three new factors interpreted as inflammation, vitamin K-dependent proteins, and procoagulant activity. Plasminogen activator inhibitor-1 clustered with the body mass factor, supporting the hypothesis that obesity is related to impaired fibrinolysis. Fibrinogen clustered with the inflammation summary factor rather than procoagulant activity, supporting the position that fibrinogen principally reflects underlying inflammation rather than procoagulant potential. The authors conclude that should hemostatic variables be shown to contribute to IRS-related cardiovascular disease, apart from plasminogen activator inhibitor-1, they may do so independently of the established metabolic abnormalities. Am J Epidemiol 2000;152:897–907.

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Oh, Sang-Rog, Jonathan D. Tung, Ayelet Priel, Leah Levi, David B. Granet, Bobby S. Korn, and Don O. Kikkawa. "Reduction of Orbital Inflammation following Decompression for Thyroid-Related Orbitopathy." BioMed Research International 2013 (2013): 1–6. http://dx.doi.org/10.1155/2013/794984.

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Purpose. Thyroid-related orbitopathy (TRO) is associated with inflammation, expansion of orbital fat, enlargement of extraocular muscles, and optic neuropathy (ON). We examined the effects of orbital decompression on the inflammatory and congestive signs of TRO in patients who underwent emergent orbital decompression.Methods. This retrospective, consecutive study included patients with ON from TRO who underwent orbital decompression. Pre- and postoperative orbital inflammatory signs in the operated and nonoperated, contralateral eyes were graded with the 10-item clinical activity score (CAS).Results. Thirty-one orbits were included. Postoperatively, 22 patients and 29 orbits had resolution of ON while the remaining 2 patients had improvement in visual acuity. Mean preoperative CAS was 9.5 ± 0.4. At 12 months, postoperative CAS was 2.1 ± 0.6 (P<0.01) in the operated eye and 3.2 ± 0.5 (P<0.05) in the nonoperated, contralateral eye.Conclusion. In our series, 94% of orbits had resolution of ON. There was also a statistically significant postoperative reduction in the CAS in both the operated and nonoperated, contralateral eyes. This phenomenon may be due to lowered venous congestion, decreased intraorbital pressure, and diminution in inflammatory factors.

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Hernández, Domingo, Juana Alonso-Titos, Ana Maria Armas-Padrón, Veronica Lopez, Mercedes Cabello, Eugenia Sola, Laura Fuentes, et al. "Waiting List and Kidney Transplant Vascular Risk: An Ongoing Unmet Concern." Kidney and Blood Pressure Research 45, no. 1 (December 4, 2019): 1–27. http://dx.doi.org/10.1159/000504546.

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Background: Chronic kidney disease (CKD) is an important independent risk factor for adverse cardiovascular events in patients waitlisted for kidney transplantation (KT). Although KT reduces cardiovascular risk, these patients still have a higher all-cause and cardiovascular mortality than the general population. This concerning situation is due to a high burden of traditional and nontraditional risk factors as well as uremia-related factors and transplant-specific factors, leading to 2 differentiated processes under the framework of CKD, atherosclerosis and arteriosclerosis. These can be initiated by insults to the vascular endothelial endothelium, leading to vascular calcification (VC) of the tunica media or the tunica intima, which may coexist. Several pathogenic mechanisms such as inflammation-related endothelial dysfunction, mineral metabolism disorders, activation of the renin-angiotensin system, reduction of nitric oxide, lipid disorders, and the fibroblast growth factor 23-klotho axis are involved in the pathogenesis of atherosclerosis and arteriosclerosis, including VC. Summary: This review focuses on the current understanding of atherosclerosis and arteriosclerosis, both in patients on the waiting list as well as in kidney transplant recipients, emphasizing the cardiovascular risk factors in both populations and the inflammation-related pathogenic mechanisms. Key Message: The importance of cardiovascular risk factors and the pathogenic mechanisms related to inflammation in patients waitlisted for KT and kidney transplant recipients.

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Chen, Li, Rui Chen, Hua Wang, and Fengxia Liang. "Mechanisms Linking Inflammation to Insulin Resistance." International Journal of Endocrinology 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/508409.

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Obesity is now widespread around the world. Obesity-associated chronic low-grade inflammation is responsible for the decrease of insulin sensitivity, which makes obesity a major risk factor for insulin resistance and related diseases such as type 2 diabetes mellitus and metabolic syndromes. The state of low-grade inflammation is caused by overnutrition which leads to lipid accumulation in adipocytes. Obesity might increase the expression of some inflammatory cytokines and activate several signaling pathways, both of which are involved in the pathogenesis of insulin resistance by interfering with insulin signaling and action. It has been suggested that specific factors and signaling pathways are often correlated with each other; therefore, both of the fluctuation of cytokines and the status of relevant signaling pathways should be considered during studies analyzing inflammation-related insulin resistance. In this paper, we discuss how these factors and signaling pathways contribute to insulin resistance and the therapeutic promise targeting inflammation in insulin resistance based on the latest experimental studies.

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Rupankar Barik and Pritha Pal. "Study of Impact of Dietary Factors on Prevalence of Colon Cancer." Journal of Advanced Zoology 44, S6 (December 8, 2023): 1674–83. http://dx.doi.org/10.17762/jaz.v44is6.2590.

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The third most frequent cancer worldwide is colorectal cancer. Globally, 1.5 million new cases of colorectal cancer were reported in 2023, making up 10% of all new cancer cases. According to estimates, colorectal cancer is the fourth most prevalent cancer-related cause of death.be accountable for about 700,000 cancer-related deaths. Survival from colorectal cancer depends on the stage of the disease, with later-stage diagnoses having a worse prognosis. 90% of colorectal cancer patients who receive an early diagnosis survive five years. Western Africa has the lowest estimated rates, while Australia and New Zealand have the highest. Men and women worldwide experience colorectal cancer in similar ways. More than 2.2 million colorectal cancer cases are anticipated to be diagnosed during the next 15 years, a 60% rise. It is one of the malignancies whose incidence is rising globally. The diet has a direct connection with the colon cancer because inflammation in the bowels and gut is influenced by what we consume, and inflammation is a risk factor for the development of colorectal cancer. Researchers have identified sugar, animal fats, red and processed meats as the key food ingredients that produce inflammation in the body and may raise the risk of colon cancer.

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Mukai, Ryo, Hidetaka Matsumoto, and Hideo Akiyama. "Risk factors for emerging intraocular inflammation after intravitreal brolucizumab injection for age-related macular degeneration." PLOS ONE 16, no. 12 (December 6, 2021): e0259879. http://dx.doi.org/10.1371/journal.pone.0259879.

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Purpose To analyze the risk factors associated with emerging intraocular inflammation (IOI) after intravitreal brolucizumab injection (IVBr) to treat age-related macular degeneration (AMD). Methods This study included 93 eyes of 90 patients. The incidence of emerging IOI was analyzed. The patients were classified into IOI or non-IOI groups, and background clinical characteristics in each group were compared. Results IOI occurred in 14 eyes of 14 cases (16%; five women, nine men [5:9]; IOI group) after IVBr; contrastingly, no IOI occurred in 76 patients (10 women, 66 men [10:66]; non-IOI group). The mean ages in IOI and non-IOI groups were 79.4 ± 8.1 and 73.8 ± 8.9 years old, respectively, and the average age in the IOI group was significantly higher than that in the non-IOI group (P = 0.0425). In addition, the percentages of females in the IOI and non-IOI groups were 43% and 13%, respectively, and IOI occurred predominantly in females (odds ratio: 4.95, P = 0.0076). Moreover, the prevalence of diabetes in the IOI and non-IOI groups was 64% and 32%, respectively, with a significant difference (odds ratio: 3.90, P = 0.0196). In contrast, the prevalence of hypertension in the IOI and non-IOI groups was 36% and 57%, respectively, with no significant difference (P = 0.15). Conclusion The comparison of clinical profiles of IOI or non-IOI cases in IVBr treatment for AMD suggests that the risk factors for IOI are old age, female sex, and history of diabetes; however, IOI with vasculitis or vascular occlusion in this cohort does not seem to cause severe visual impairment. Further studies are required to investigate potential risk factors for IOI.

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Tsuchiya, Yuya, Hiroki Sakai, Akihiro Hirata, and Tokuma Yanai. "Brazilian green propolis suppresses acetaminophen-induced hepatocellular necrosis by modulating inflammation-related factors in rats." Journal of Toxicologic Pathology 31, no. 4 (2018): 275–82. http://dx.doi.org/10.1293/tox.2018-0027.

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Gori, Elizabeth, Takafira Mduluza, Mudavanhu Nyagura, Babill Stray-Pedersen, and Zvenyika Alfred Gomo. "Inflammation-modulating cytokine profile and lipid interaction in HIV-related risk factors for cardiovascular diseases." Therapeutics and Clinical Risk Management Volume 12 (November 2016): 1659–66. http://dx.doi.org/10.2147/tcrm.s117980.

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Matsuo, Kentaro, Eita Sasaki, Satonori Higuchi, Shohei Takai, Koichi Tsuneyama, Tatsuki Fukami, Miki Nakajima, and Tsuyoshi Yokoi. "Involvement of oxidative stress and immune- and inflammation-related factors in azathioprine-induced liver injury." Toxicology Letters 224, no. 2 (January 2014): 215–24. http://dx.doi.org/10.1016/j.toxlet.2013.10.025.

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Cao, Linghui, Feiyu Huang, Isaac Yaw Massey, Cong Wen, Shuilin Zheng, Shuaishuai Xu, and Fei Yang. "Effects of Microcystin-LR on the Microstructure and Inflammation-Related Factors of Jejunum in Mice." Toxins 11, no. 9 (August 21, 2019): 482. http://dx.doi.org/10.3390/toxins11090482.

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The increasing cyanobacterial blooms have recently been considered a severe environmental problem. Microcystin-leucine arginine (MC-LR) is one of the secondary products of cyanobacteria metabolism and most harmful cyanotoxins found in water bodies. Studies show MC-LR negatively affects various human organs when exposed to it. The phenotype of the jejunal chronic toxicity induced by MC-LR has not been well described. The aim of this paper was to investigate the effects of MC-LR on the jejunal microstructure and expression level of inflammatory-related factors in jejunum. Mice were treated with different doses (1, 30, 60, 90 and 120 μg/L) of MC-LR for six months. The microstructure and mRNA expression levels of inflammation-related factors in jejunum were analyzed. Results showed that the microstructure of the jejunum was destroyed and expression levels of inflammation-related factors interleukin (IL)-1β, interleukin (IL)-8, tumor necrosis factor alpha, transforming growth factor-β1 and interleukin (IL)-10 were altered at different MC-LR concentrations. To the best of our knowledge, this is the first study that mice were exposed to a high dose of MC-LR for six months. Our data demonstrated MC-LR had the potential to cause intestinal toxicity by destroying the microstructure of the jejunum and inducing an inflammatory response in mice, which provided new insight into understanding the prevention and diagnosis of the intestinal diseases caused by MC-LR.

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