Ram B Singh, Toru Takahashi, G. Fatima, Rie Horiuchi, J. Fedacko, Zuzana Hůzová, D. Gurín
{"title":"Effects of Antioxidant-rich Indo-mediterranean Foods on Pre-heart Failure: Results from the Meta-analysis of Randomized Controlled Trials.","authors":"Ram B Singh, Toru Takahashi, G. Fatima, Rie Horiuchi, J. Fedacko, Zuzana Hůzová, D. Gurín","doi":"10.2174/1875041902008010001","DOIUrl":"https://doi.org/10.2174/1875041902008010001","url":null,"abstract":"Halberg Hospital and Research Institute, Civil Lines, Moradabad, India, Graduate School of Human Environmental Medicine, Fukuoka University, Fukuoka, Japan, Era Medical College, Lucknow, India, Mukogawa Women’s University, Nishinomiyacity, Hyogo Prefecture, Japan, Department of Medicine, Faculty of Medicine, PJ Safaric University, Kosice, Slovakia Department of Biology, Trnava university, Trnava, Slovakia Department of Biology, Faculty of Medicine, Trnava University, Trnava, Slovakia","PeriodicalId":89637,"journal":{"name":"The open inflammation journal","volume":"8 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2020-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68107890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
E. Namba, Thiago Otávio Nawick, Mariele Jung Thome, P. Trevilatto, M. Machado, L. Azevedo-Alanis, Antonio Adilson Soares de Lima, A. Johann, E. A. Rosa, S. Ignácio, A. M. Grégio
{"title":"Effect of Physical Activity on the Lesion Repair Process in the Gastrocnemius Muscle of Rats","authors":"E. Namba, Thiago Otávio Nawick, Mariele Jung Thome, P. Trevilatto, M. Machado, L. Azevedo-Alanis, Antonio Adilson Soares de Lima, A. Johann, E. A. Rosa, S. Ignácio, A. M. Grégio","doi":"10.2174/1875041901407010001","DOIUrl":"https://doi.org/10.2174/1875041901407010001","url":null,"abstract":"The present study aimed to evaluate the effect of a progressive load of physical activity on a musculoskeletal injury in rats. Sixty-four rates were divided into two groups: experimental group (EG), which underwent physical activity (swimming) with a progressive load, and the control group (CG), which was not submitted to this program. The training was carried out according to an adapted version of the Goncalves (1999) swimming system. Injuries were caused to the gastrocnemic muscle by inducing 40% NaOH. On days 2, 7, 14, and 21 after inducing muscle injury, the animals from both EC and CG were sacrificed. The injured area was removed and processed. The neutrophils, macrophages, lymphocytes, and plasmocytes were quantified by hematoxylin and eosin (HE GC=2.48±1.00; p=0.006) and lymphocytes (GE=2.12±0.82; GC=0.06±0.82; p=0.037) after 2 days, and of macrophages (GE=15.74±3.00; GC=6.02±1.95; p=0.007) and lymphocytes (GE=2.01±0.78; GC=0.14±0.09; p=0.044) after 7 days, could be observed in the EG when compared to the CG; however, the opposite was true for neutrophils (GE=48.12±17.04; GC=105.54±12.25; p=0.005). After 14 days, a smaller quantity of neutrophils (GE= 32.70±10.26; GC= 90.96±17.62; p= 0.044) and a larger quantity of plasmocytes (GE=9.06±3.84; GC=0.68±0.53; p=0.028) could be observed in the EG as compared to the CG. A greater area of type III collagen could be observed in the EG when compared to the CG over a 14-day period (GE=44.90±16.15; GC=0.74±0.40; p=0.000) and a 21-day period (GE=13.19±9.09; GC=1.02±0.94; p=0.029), whereas the opposite could be observed for type I collagen. The physical activity promoted an increase in the deposition of type III collagen in the muscle injury. This activity accelerated the repair process after 14 days, possibly moderated by the larger number of inflammatory cells, while after 21 days, the lesion presented a lesser resistance.","PeriodicalId":89637,"journal":{"name":"The open inflammation journal","volume":"7 1","pages":"1-5"},"PeriodicalIF":0.0,"publicationDate":"2014-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68107852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Recurrence of Kawasaki Disease in a Young Child","authors":"J. Bangert, Georgios Meridis, E. Strehle","doi":"10.2174/1875041920130710001","DOIUrl":"https://doi.org/10.2174/1875041920130710001","url":null,"abstract":"A diagnosis of Kawasaki disease (KD) is mainly based on clinical criteria. We discuss the case of a young boy who presented at the ages of 7 months and 13 months with signs and symptoms suggestive of Kawasaki disease. At the first episode he was treated for Kawasaki disease and at the second episode for lymphadenitis and fever. A diagnosis of recurrent KD was only made retrospectively when he developed thrombocytosis and desquamation of the extremities. Subsequent echocardiograms revealed no abnormalities. It is important that a diagnosis of KD is considered in any child presenting with a fever of more than 5 days irrespective of the previous medical history.","PeriodicalId":89637,"journal":{"name":"The open inflammation journal","volume":"6 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2013-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68107907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Kawasaki Disease: Time for Change","authors":"E. Strehle","doi":"10.2174/1875041920130710002","DOIUrl":"https://doi.org/10.2174/1875041920130710002","url":null,"abstract":"The first cases of mucocutaneous lymph node syndrome (MLNS) were reported by Dr Tomisaku Kawasaki in 1967. His surname was later assigned to this new disease entity, and I was fortunate to meet him at the 100 Annual Conference of the German Paediatric Association in Berlin in 2004 [1]. According to our current understanding Kawasaki disease (KD) is a systemic autoimmune vasculitis which occurs in genetically susceptible people following an acute infection. Outside Japan KD has a low incidence and is notoriously difficult to diagnose because of its similarity to common infective childhood illnesses and a lack of specific and sensitive laboratory tests. The case report of KD by Bangert et al. [2] illustrates these difficulties aptly and calls for prompt diagnosis and treatment of this condition to avoid serious cardiovascular complications.","PeriodicalId":89637,"journal":{"name":"The open inflammation journal","volume":"6 1","pages":"4-5"},"PeriodicalIF":0.0,"publicationDate":"2013-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68107426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Definition of Inflammation, Causes of Inflammation and PossibleAnti-inflammatory Strategies","authors":"S. Stankov","doi":"10.2174/1875041901205010001","DOIUrl":"https://doi.org/10.2174/1875041901205010001","url":null,"abstract":"Current definition of inflammation by its cardinal signs is obsolete and unsuitable for guiding adequate therapeutic strategies. Furthermore, present theory of the inflammatory process regarding vascular phenomena as essential for generation of cardinal signs is invalid and unable to explain well established empirical facts, particularly the extent of the osmotic pressure and temperature variations within the inflamed tissue. From five cardinal signs, there is actually just one specific macroscopic sign of inflammation, namely localized edema. Further, the driving force for tissue fluid accumulation is defined in biochemical terms and as such taken for the definition of the inflammatory process. Inflammation may be defined as a degenerative process which is intense enough to cause local accumulation of low molecular weight catabolic products, which in turn elevates tissue osmotic pressure that attracts extra fluid, with or without heat release sufficient for significant elevation of tissue temperature. This process is in a sharp contrast to the pathogenesis of burns, where externally applied heat causes a process that is in essence opposite to inflammation, bearing only some superficial similarities with the latter. The inflammatory process is itself a pathological process, whereas the natural anti-inflammatory response that ensues after acute inflammation tends to reverse tissue homeostasis towards normality and should therefore be regarded as a true defensive reaction of the affected tissue. Based on the therapeutic principle of reverse thermodynamics, heat application to the inflamed tissue is an obvious, yet non-exclusive therapeutic choice that follows from the given universal definition of inflammation.","PeriodicalId":89637,"journal":{"name":"The open inflammation journal","volume":"5 1","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"2012-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68107840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Biomarkers in Pediatric Sepsis","authors":"Kristen A. Smith, M. Bigham","doi":"10.2174/1875041901104010024","DOIUrl":"https://doi.org/10.2174/1875041901104010024","url":null,"abstract":"Sepsis is a leading killer of both adult and pediatric patients, and delays in recognition and treatment significantly increase the risk of morbidity and mortality [2, 3]. The concept of early detection serves as the foundation for the search for clinically viable indicators of severe sepsis and septic shock – hence the interest in sepsis biomarkers. A biomarker is defined as the biological parameters associated with the presence and severity of specific disease states. Biomarkers are detectable and measurable by a variety of methods including physical examination, laboratory assays, and medical imaging. Specifically, a biomarker is a characteristic that is objectively measured and evaluated in a normal biologic process, in a pathologic process, or as a pharmacologic response to a therapeutic intervention [4]. For sepsis, a “good” biomarker may permit earlier diagnosis, earlier treatment, and thus reduced morbidity and mortality.","PeriodicalId":89637,"journal":{"name":"The open inflammation journal","volume":"4 1","pages":"24-30"},"PeriodicalIF":0.0,"publicationDate":"2011-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68107598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Annia Maslash-Hubbard, Nidal El-wiher, T. Shanley, Timothy T. Cornell
{"title":"Negative Regulators of the Host Response in Sepsis","authors":"Annia Maslash-Hubbard, Nidal El-wiher, T. Shanley, Timothy T. Cornell","doi":"10.2174/1875041901104010061","DOIUrl":"https://doi.org/10.2174/1875041901104010061","url":null,"abstract":"The inflammatory response of the innate immune system to invading pathogen is complex and requires precise regulation in order to eradicate the organism while protecting the surrounding host tissues. Two main signal transduction pathways, the NFB and mitogen activated protein kinase (MAPK) pathways, are activated by the invading pathogens requiring a set of negative regulatory processes once the pathogen is eradicated. In this review we focus on three key negative regulatory processes: intracellular inhibitors, regulatory phosphatases and epigenetic mechanisms.","PeriodicalId":89637,"journal":{"name":"The open inflammation journal","volume":"18 1","pages":"61-66"},"PeriodicalIF":0.0,"publicationDate":"2011-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68107658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Oxidative Stress in Critically Ill Children with Sepsis.","authors":"Derek S Wheeler","doi":"10.2174/1875041901104010074","DOIUrl":"10.2174/1875041901104010074","url":null,"abstract":"<p><p>Sepsis is one of the leading causes of death in critically ill patients in the intensive care unit. Sepsis accounts for significant morbidity and mortality in critically ill children as well. The pathophysiology of sepsis is characterized by a complex systemic inflammatory response, endothelial dysfunction, and alterations in the coagulation system, which lead to perturbations in the delivery of oxygen and metabolic substrates to the tissues, end-organ dysfunction, and ultimately death. Oxidative stress plays a crucial role as both a promoter and mediator of the systemic inflammatory response, suggesting potential targets for the treatment of critically ill children with the sepsis syndrome. Herein, we will provide a brief review of the role of oxidative and nitrosative stress in the pathophysiology of sepsis.</p>","PeriodicalId":89637,"journal":{"name":"The open inflammation journal","volume":"4 s1","pages":"74-81"},"PeriodicalIF":0.0,"publicationDate":"2011-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3563065/pdf/nihms352219.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31221157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
John S Giuliano, Patrick M Lahni, Hector R Wong, Derek S Wheeler
{"title":"Pediatric Sepsis - Part V: Extracellular Heat Shock Proteins: Alarmins for the Host Immune System.","authors":"John S Giuliano, Patrick M Lahni, Hector R Wong, Derek S Wheeler","doi":"10.2174/1875041901104010049","DOIUrl":"10.2174/1875041901104010049","url":null,"abstract":"<p><p>Heat shock proteins (HSPs) are molecular chaperones that facilitate the proper folding and assembly of nascent polypeptides and assist in the refolding and stabilization of damaged polypeptides. Through these largely intracellular functions, the HSPs maintain homeostasis and assure cell survival. However, a growing body of literature suggests that HSPs have important effects in the extracellular environment as well. Extracellular HSPs are released from damaged or stressed cells and appear to act as local \"danger signals\" that activate stress response programs in surrounding cells. Importantly, extracellular HSPs have been shown to activate the host innate and adaptive immune response. With this in mind, extracellular HSPs are commonly included in a growing list of a family of proteins known as danger-associated molecular patterns (DAMPs) or alarmins, which trigger an immune response to tissue injury, such as may occur with trauma, ischemia-reperfusion injury, oxidative stress, etc. Extracellular HSPs, including Hsp72 (HSPA), Hsp27 (HSPB1), Hsp90 (HSPC), Hsp60 (HSPD), and Chaperonin/Hsp10 (HSPE) are especially attractrive candidates for DAMPs or alarmins which may be particularly relevant in the pathophysiology of the sepsis syndrome.</p>","PeriodicalId":89637,"journal":{"name":"The open inflammation journal","volume":"4 ","pages":"49-60"},"PeriodicalIF":0.0,"publicationDate":"2011-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3995031/pdf/nihms-352211.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32289230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Sepsis-induced Innate and Adaptive Immune Suppression","authors":"Jennifer A. Muszynski, M. Hall","doi":"10.2174/1875041901104010067","DOIUrl":"https://doi.org/10.2174/1875041901104010067","url":null,"abstract":"The inflammatory response to sepsis has classically been characterized by an overactive innate immune response. Recent adult and pediatric evidence suggests that the immune response is quite dynamic in this setting, often with endogenous innate and adaptive immunosuppression following the onset of sepsis. Sepsis-induced innate immune dysfunction can include reduction in antigen presenting capacity (as evidenced by decreased monocyte HLA-DR expression) and low pro-inflammatory cytokine production capacity (as evidenced by reduced ex vivo LPS-induced tumor necrosis factor-� production). The term immunoparalysis describes a state of severe reduction in these parameters and has been associated with increased risks for the development of nosocomial infection and death in septic adults and children. Intriguing evidence suggests that immunoparalysis may be reversible with beneficial effects on outcomes. Adaptive immune dysfunction has also been reported following the onset of sepsis. Lymphopenia, lymphocyte apoptosis, and skewing toward anti-inflammatory T cell subtypes (such as regulatory T cells) have all been associated with adverse outcomes from sepsis. Without specific testing, most aspects of sepsis-related immune dysfunction are occult. Accordingly, the development of robust immune monitoring and modulation protocols should be a high priority in the battle to improve outcomes from sepsis in critically ill adults and children.","PeriodicalId":89637,"journal":{"name":"The open inflammation journal","volume":"4 1","pages":"67-73"},"PeriodicalIF":0.0,"publicationDate":"2011-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68107705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}