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Introduction: Sudden sensorineural hearing loss (SSNHL) is a common emergency symptom in otolaryngology that requires immediate diagnosis and treatment. SSNHL has a multifactorial etiology, and its pathophysiologic mechanisms may be associated with inflammatory and metabolic changes that may affect the cochlear microenvironment or its nervous component, thus triggering the process or hindering hearing recovery. Therefore, the aim of this study was to assess metabolic and inflammatory changes to identify systemic parameters that could serve as prognostic factors for hearing recovery in patients with SSNHL. Materials and methods: Thirty patients with a sudden hearing loss of at least 30 dB in three contiguous frequencies were enrolled in this study. Patients were followed up for 4 months and peripheral blood samples were collected at 7 days (V1), 30 days (V2) and 120 days (V3). Interleukins (IL)-1F7, IL-2, IL-4, IL-5, IL-6, IL-10, interferon γ (IFN-γ), tumor necrosis factor α (TNF-α) and adiponectin were quantified in serum. In addition, lipid and glycemic profiles as well as concentration of creatinine, uric acid, fructosamine, peroxide, total proteins and albumin were analyzed. Patients underwent weekly ear-specific hearing tests with standard pure tone thresholds for frequencies of 250-8,000 Hz, speech recognition threshold and word recognition score. Results: Patients with SSNHL were divided into a group of patients who did not achieve hearing recovery (n = 14) and another group who achieved complete and significant recovery (n = 16). Most serologic parameters showed no significant changes or values indicating clinical changes. However, IFN-γ levels decreased by 36.3% between V1 and V2. The cytokine TNF-α showed a statistically significant decrease from V1 to V3 (from 22.91 to 10.34 pg./mL). Adiponectin showed a decrease from 553.7 ng/mL in V1 to 454.4 ng/mL in V3. Discussion: Our results show that serologic cytokine levels change in the acute phase of manifestation of SSNHL and establish a parallel between systemic changes and improvements in hearing, especially TNF-α, which showed differences in hearing recovery. The use of IFN-γ, TNF-α and adiponectin may elucidate the clinical improvement in these patients. [ABSTRACT FROM AUTHOR]

Running economy (RE), expresses the relationship between the energy cost of running (Cr) and the work performed by a runner and is an predictor of performance. Given the intense effort of marathon runners during training and competition and the dearth of studies that address performance and cytokines in this population, the objective of the current study was to investigate the relationship between RE and cytokines in marathon runners.

Introduction: Although it is broadly known that monocyte recruitment is involved in atherosclerosis development and that, in accordance with the microenvironment, these cells can be modulated into three well-known subpopulations: Classical (CD14++CD16-), intermediate (CD14++CD16+), and non-classical (CD14+CD16++), the effects of treatment with different pharmacological strategies (based on lipid-lowering and antiplatelets) after acute myocardial infarction upon the monocytes modulation and the role of the chemokine receptors CCR2, CCR5 and CX3CR1 in this context, are poorly understood. Methods: In this study, patients [n = 148, both men (n = 105, 71%) and women (n = 43, 29%)] submitted to treatment with a 2x2 factorial design, in which they received rosuvastatin 20 mg or simvastatin 40 mg plus ezetimibe 10 mg, as well as ticagrelor 90 mg or clopidogrel 75 mg were enrolled. Monocyte subsets were analyzed by flow cytometry at baseline (BL), and after one (1-M) and 6 months (6-M) of treatment. Results: Firstly, our results showed that, regardless of the treatment received, higher percentages of classical monocytes and lower of non-classical monocytes were found at the 6-M time point than BL values, whilst the percentage of intermediate monocytes was higher in all time points assessed than the other subsets. There were reductions in the CCR2 expression by non-classical and intermediate monocytes, without differences for the classical subtype. Concerning the CCR5 expression, there were reductions in the three monocyte subtypes, whereas the CX3CR1 expression increased both in intermediate and classical monocytes, without differences for non-classical monocytes. In relation to the treatment received, a higher percentage of intermediate monocytes at the 6-M time point than the values BL was observed in the group treated with simvastatin + ezetimibe + clopidogrel. No significant differences were found concerning non-classical, intermediate, and classical monocytes, for CCR2, CCR5, and CX3CR1 in the four treatment arms. Conclusion: Taken together, our results demonstrated that even under lipid-lowering and antiplatelet therapy for 6 months, the inflammatory phenotype of monocytes still persisted in the patients enrolled in this study. [ABSTRACT FROM AUTHOR]

Human Endogenous Retroviruses (HERVs) are derived from ancient exogenous retroviral infections that have infected our ancestors' germline cells, underwent endogenization process, and were passed throughout the generations by retrotransposition and hereditary transmission. HERVs comprise 8% of the human genome and are critical for several physiological activities. Yet, HERVs reactivation is involved in pathological process as cancer and autoimmune diseases. In this review, we summarize the multiple aspects of HERVs' role within the human genome, as well as virological and molecular aspects, and their fusogenic property. We also discuss possibilities of how the HERVs are possibly transactivated and participate in modulating the inflammatory response in health conditions. An update on their role in several autoimmune, inflammatory, and aging-related diseases is also presented. [ABSTRACT FROM AUTHOR]

Introduction Combination of chronic inflammation and an altered tissue remodeling process are involved in the development of Chronic Rhinosinusitis with Nasal Polyps (CRSwNP). Studies demonstrated that mesenchymal stem cells expressing the progenitor gene CD133 were involved in a significant reduction of the chronic inflammatory process in the polypoid tissue. Objective To evaluate the levels of CD133 (Prominin-1) in nasal polypoid tissue and its correlation with interleukin-8 (IL-8) and transforming growth factor β1 (TGF-β1). Methods A total of 74 subjects were divided in the following groups: control group (n=35); chronic rhinosinusitis with nasal polyps nonpresenting comorbid asthma and aspirin intolerance (CRSwNPnonAI) group (n=27); and chronic rhinosinusitis with nasal polyps presenting comorbid asthma and aspirin intolerance (CRSwNPAI) group (n=12). Histologic analysis and also evaluation of the concentration of CD133, IL-8, and TGF-β1 by enzyme-linked immunosorbent assay (ELISA) kits were performed in nasal tissue obtained from nasal polypectomy or from middle turbinate tissue. Results Higher eosinophilic infiltration was found in both CRSwNP groups by histologic analysis. Lower levels of TGF-β1 and IL-8 were observed in both CRSwNP groups when compared with the control group,whereas theCD133levelswere significantly reduced only in the CRSwNPnonAI group compared with the control group. Conclusion It was demonstrated that the nasal mucosa presenting polyposis showed a significant reduction of CD133 levels, and also that this reduction was significantly correlated with the reduction of TGF-β1 levels, but not with IL-8 levels. Therefore, these findings may be involved in the altered inflammatory and remodeling processes observed in the nasal polyposis. [ABSTRACT FROM AUTHOR]

Introduction/Purpose Obesity increases significantly every year worldwide. Since 1980, the prevalence of individuals with obesity has practically doubled. Obesity plays an important role in the pathophysiology of diseases that arise from a complex interaction of nutritional, genetic, and metabolic factors, characterizing a chronic inflammatory state. This study aimed to verify the systemic inflammatory response through the analysis of IGF-1, IL-23, and resistin levels and the lipid profile in severely obese women undergoing surgery for obesity and weight-related diseases. Materials and Methods This randomized controlled clinical trial includes female patients clinically diagnosed with severe obesity with an indication for bariatric surgery. Results In the initial evaluation, no significant difference was observed between the control (CG) and bariatric surgery (BSG) groups. The weight, BMI, systolic and diastolic blood pressures, total cholesterol, LDL, HDL, total non-HDL cholesterol, and glucose in BSG patients showed a significant change after surgery. Pre- and post-surgery levels of resistin, IGF-1, and IL-23 showed a significant difference in the BSG group, but only IL-23 was changed after 6 months in the CG. Conclusion The results of this study confirmed that weight loss induced by surgery for obesity and weight-related diseases improved the lipid profile and reduced the chronic inflammatory status in women with severe obesity. [ABSTRACT FROM AUTHOR]

Purpose: This study aimed to evaluate whether supplementation with L-arginine alone or in combination with physical exercise training can modulate rats' lipid and inflammatory profiles after a single intense exercise session. Methods: Male Wistar rats were divided into four different groups: control (C), trained (T), supplemented with L-arginine (C + A) and trained and supplemented (T + A). Animals from supplemented groups (C + A and T + A groups) received 300 mg/kg animal body weight L-arginine diluted in 30 mL of drinking water for 8 weeks. Exercise training protocol (moderate intensity--70% achieved in the maximum effort test) was held 5 days/week for 8 weeks. Results: Exercise training induced a decrease in the amount of plasma, cholesterol and triglyceride totals, and skeletal muscle VEGF and CINC. Supplementation alone showed a benefit by reducing LDL levels. Conclusion: Training combined with supplementation showed a pronounced reduction in skeletal muscle VEGF and CINC amount. L-arginine supplementation, especially when associated with the regular aerobic physical exercise at moderate intensity was able to improve not only plasma lipid profile but also the inflammatory response of skeletal muscle immediately after an exhaustive physical exercise session. [ABSTRACT FROM AUTHOR]

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Desalination of seawater is becoming an important means to address the increasing scarcity of freshwater resources in the world. Seawater has been used as drinking water in the health, food, and medical fields and various beneficial effects have been suggested, although not confirmed. Given the presence of 63 minerals and trace elements in drinking desalinated seawater (63 DSW), we evaluated their effects on the behavior of tumorigenic and nontumorigenic cells through the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay and annexin-V-fluorescein isothiocyanate/propidium iodide staining. Our results showed that cell viability and proliferation in the presence of 63 DSW were significantly greater than in mineral water and in the presence of fetal bovine serum in a dose-dependent manner. Furthermore, 63 DSW showed no toxic effect on murine embryonic fibroblast (NIH-3T3) and murine melanoma (B16-F10) cells. In another assay, we also showed that pre-treatment of non-adherent THP-1 cells with 63 DSW reduces apoptosis incidence, suggesting a protective effect against cell death. We conclude that cell viability and proliferation were improved by the mineral components of 63 DSW and this effect can guide further studies on health effects associated with DSW consumption. [ABSTRACT FROM AUTHOR]

Background: Bone marrow is an accessible source of progenitor cells, which have been investigated as treatment for neurological diseases in a number of clinical trials. Here we evaluated the potential benefit of bone marrow cells in protecting against convulsive seizures induced by maximum electroconvulsive shock (MES), a widely used model for screening of anti-epileptic drugs. Behavioral and inflammatory responses were measured after MES induction in order to verify the effects promoted by transplantation of bone marrow cells. To assess the anticonvulsant effects of bone marrow cell transplantation, we measured the frequency and duration of tonic seizure, the mortality rate, the microglial expression and the blood levels of cytokine IL-1, IL-6, IL-10 and TNF-α after MES induction. We hypothesized that these behavioral and inflammatory responses to a strong stimulus such as a convulsive seizure could be modified by the transplantation of bone marrow cells. Results: Bone marrow transplanted cells altered the convulsive threshold and showed anticonvulsant effect by protecting from tonic seizures. Bone marrow cells modified the microglial expression in the analyzed brain areas, increased the IL-10 and attenuate IL-6 levels. Conclusions: Bone marrow cells exert protective effects by blocking the course of electroconvulsive seizures. Additionally, electroconvulsive seizures induced acute inflammatory responses by altering the pattern of microglia expression, as well as in IL-6 and IL-10 levels. Our findings also indicated that the anticonvulsant effects of these cells can be tested with the MES model following the same paradigm used for drug testing in pharmacological screening. Studies on the inflammatory reaction in response to acute seizures in the presence of transplanted bone marrow cells might open a wide range of discussions on the mechanisms relevant to the pathophysiology of epilepsies. [ABSTRACT FROM AUTHOR]

There is evidence that the platelet-activating factor receptor (PAFR) is involved in the clearance of apoptotic cells by macrophages, and that this is associated with anti-inflammatory phenotype. Our group has previously shown that coinjection of a large number of apoptotic cells can promote tumor growth from a subtumorigenic dose of melanoma cells. Here, we studied the involvement of the PAFR in the tumor growth promoting effect of apoptotic cells. A sub-tumorigenic dose of melanoma cells (Tm1) was coinjected with apoptotic Tm1 cells, subcutaneously in the flank of C57Bl/6 mice, and the volume was monitored for 30 days. Animals received the PAFR antagonists, WEB2170 or PCA4248 (5 mg/kg body weight) or vehicle, by peritumoral daily injection for 5 days. Results showed that PAFR antagonists significantly inhibited the tumor growth induced by the coinjection of a subtumorigenic dose of melanoma cells together with apoptotic cells. This was accompanied by inhibition of early neutrophil and macrophage infiltration. Addition of (platelet-activating factor) to this system has no significant effect. PAFR antagonists did not affect the promoting effect of carrageenan. We suggest that the recognition of apoptotic cells by phagocytes leads to activation of PAFR pathways, resulting in a microenvironment response favorable to melanoma growth. [ABSTRACT FROM AUTHOR]