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Whole body vibration training (WBVT) has been identified as an alternative intervention to improve exercise capacity and quality of life of patients with chronic obstructive pulmonary disease (COPD). However, the effect of WBVT on inflammatory-oxidative biomarkers remains unknown. The aim of this trial was to investigate the effects of WBVT on quality of life and physical and inflammatory-oxidative parameters in patients with COPD. Twenty patients were equally divided into 1) an intervention group (IG) that performed the WBVT, and 2) a control group (CG) that did not receive any intervention. Intervention consisted in performing static squatting on a vibrating platform, in six series of 30 s, 3 days/wk, for 12 wk. Patients were evaluated for plasma levels of IL-6, IL-8, IFN-γ, soluble receptors of TNF-α; white cell count; plasma levels of oxidant and antioxidant markers; 6-min walking distance (6MWD); peak oxygen uptake (V̇o 2peak ); handgrip strength; quality of life; timed 5-chair sit-to-stand (5STS); and timed get-up and go test (TUG). After WBVT, patients from IG showed a significant increase in the 6MWD, V̇o 2peak , and handgrip strength ( P < 0.05). Furthermore, patients from the IG reached minimal clinically important difference regarding quality of life. No significant differences were found in 5STS, TUG, inflammatory-oxidative biomarkers, and white cell count in the IG. The CG did not show significant improvement in all assessments ( P > 0.05). Taken together, our results demonstrated that the WBVT induced clinically significant benefits regarding exercise capacity, muscle strength, and quality of life in patients with COPD that were not related to inflammatory-oxidative biomarker changes. NEW & NOTEWORTHY Whole body vibration training is a new option for nonpharmacological treatment of chronic obstructive pulmonary disease (COPD). This study showed the potential of this training to improve exercise capacity, quality of life, and muscle strength in patients with COPD. Furthermore, to our knowledge this was the first study showing that vibration exercise does not modify the plasma levels of inflammatory-oxidative biomarkers, suggesting that the beneficial effects on physical measures and quality of life are independent of changes in biomarkers.

This study aims to evaluate the analgesic and modulating effect of Curcuma longa and Miconia albicans herbal medicines in knee's osteoarthritis (OA) treatment. This longitudinal study evaluated 24 patients with OA. The patients were divided into three groups: ibuprofen (1200 mg/day), C. longa (1000 mg/day) and M. albicans (1000 mg/day). The medications were applied orally for 30 days. The synovial fluid of the knee joint was collect at the first (day 0) and the last medical (day 30) consultation. The groups treated with herbal medicines presented the same results when compared to Ibuprofen. The comparison of the means of Total WOMAC for M. albicans before and after treatment presented a statistically significant difference (mean day 0 = 57.19; mean day 30 = 31.02) as well as variation of Total WOMAC for C. longa (mean day 0 = 54.79; mean day 30 = 37.08). The WOMAC Total and the VASP were compared, it was found that there was a significant decrease in the means in the C. longa and M. albicans groups, as well as in the Ibuprofen group after treatment. The study demonstrated that the treatment of knee OA with C. longa or M. albicans positively interferes with patients pain and functionality, decreased WOMAC and VASP scores, leading to functional improvement of these patients. This is the first clinical study demonstrating the analgesic and anti-inflammatory effect on knee osteoarthritis from M. albicans comparable to Ibuprofen drug. [ABSTRACT FROM AUTHOR]

Objective: Evaluate and compare the isolated and combined effects of Inspiratory Muscle Training (IMT) and Aerobic Training (AT) on respiratory and functional parameters, inflamatory biomarkers, redox status and health-related quality of life (HRQoL) in hemodialysis patients. Methods: A randomised controlled trial with factorial allocation and intention-to-treat analysis was performed in hemodialysis patients. Volunteers were randomly assigned to performe 8-weeks of IMT at 50% of maximal inspiratory pressure (MIP), low intensity AT or combined training (CT). Before the interventions, all the volunteers went 8-weeks through a control period (without training). Measures are taken at baseline, 8-week (after control period) and 16-week (after the interventions). Primary outcomes were functional capacity (incremental shuttle walk test), MIP and lower limbs strength (Sit-to-Stand test of 30 seconds). Plasma levels of interleukin-6 (IL-6), soluble tumor necrosis factor receptor 1 (sTNFR1) and 2 (sTNFR2), adiponectin, resistin and leptin, redox status parameters and HRQoL (KDQOL-SF questionnaire) were the scondary outcomes. Data analyses were performed by two-way repeated measurements ANOVA. Results: 37 hemodialysis patients aged 48.2 years old (IC95% 43.2–54.7) were randomized. Increase of MIP, functional capacity, lower limbs strength and resistin levels, and reduction of sTNFR2 levels in 16-week, compared to baseline and 8-week, were observed in all the groups (p<0.001). IMT improved functional capacity, MIP and lower limbs strength in 96.7m (IC95% 5.6–189.9), 34.5cmH2O (IC95% 22.4–46.7) and 2.2repetitions (IC95% 1.1–3.2) respectively. Increase in resistin leves and reduction in sTNFR2 leves after IMT was 0.8ng/dL (IC95% 0.5–1.1) and 0.8ng/dL (IC95% 0.3–1.3), respectively, without between-group differences. Compared to baseline and 8-week, adiponectin levels (p<0.001) and fatigue domain of the HRQoL (p<0.05) increased in 16-week only in CT. Conclusion: IMT, AT and CT improved functional parameters and modulated inflammatory biomarkers, in addition, IMT provoked a similar response to low intensity AT in hemodialysis patients. Trial registration: Registro Brasileiro de Ensaios clínicos RBR-4hv9rs. [ABSTRACT FROM AUTHOR]

Childhood obesity is related to a cascade of neuroendocrine inflammatory changes. However, there remains a gap in the current literature regarding the possible occurrence of these changes in overweight/obese infants. The objective of this study was to evaluate adipokines, cortisol, brain-derived neurotrophic factor (BDNF) and redox status in overweight/obese infants versus normal-weight peers. A cross-sectional study was conducted with 50 infants (25 in the overweight/obese group and 25 in the normal-weight group) between 6 and 24 months. Plasma levels of leptin, adiponectin, resistin, soluble tumor necrosis factor (TNF) receptors, chemokines, BDNF, serum cortisol and redox status were measured. Unpaired Student's t-test was used to analyze the results and a probability of p<0.05 was acceptable for rejection of the null hypothesis. The Pearson correlation was used to verify the association between the biomarkers analyzed in each group. Plasma levels of leptin (p = 0.0001), adiponectin (p = 0.0007) and BDNF (p = 0.003), and serum cortisol (p = 0.048) were significantly higher in overweight/obese infants than normal-weight infants. In contrast, the concentration of thiobarbituric acid reactive substances (TBARS) (p = 0.004), and catalase (p = 0.045) and superoxide dismutase activity (p = 0.02) were lower in overweight/obese infants than normal-weight peers. All the results together indicate neuroendocrine inflammatory response changes in overweight/obese infants between 6 and 24 months. Although there is already an environment that predisposes for a subsequent pro-inflammatory response, neuroendocrine secretion changes that permit the control of the inflammatory process in this age interval can be observed. [ABSTRACT FROM AUTHOR]

The aim of the study was to analyze the concentrations of sTNFR1 and sTNFR2 in both plasma and synovial fluid of patients with primary knee osteoarthritis (OA) and to determine their relationship to self-reported pain, stiffness and physical function. Twenty-seven patients with knee OA and 19 healthy subjects were enrolled in the study. The Western Ontario and McMaster University Osteoarthritis Index questionnaire was used to evaluate self-reported physical function, pain and stiffness. The sTNFR1 and sTNFR2 levels in the plasma and synovial fluid were measured by enzyme-linked immunosorbent assay. The sTNFR1 levels in synovial fluid of OA patients (2,587 ± 66.12 pg/mL) were 2.5-fold higher than in corresponding blood samples and were 1.5-fold higher than in the plasma of healthy controls. The plasma sTNFR2 levels in the patients with knee OA were lower than in healthy controls (2,249 ± 126.3 vs. 2,700 ± 126.3 pg/mL, p < 0.05), and sTNFR2 levels in synovial fluid of knee OA patients (2,021 ± 107.0 pg/mL) were lower than in the plasma of healthy controls. Synovial fluid sTNFR1 levels were negatively correlated with pain and physical function self-reported ( r − 0.6785, p < 0.0001 and r − 0.4194, p = 0.03, respectively). Synovial fluid sTNFR2 levels were negatively correlated with pain and joint stiffness ( r − 0.5433, p = 0.01 and r − 0.4249, p = 0.02, respectively). The findings of this study demonstrated the presence of soluble receptors for TNF-alpha, particularly sTNFR1, in the synovial fluid of patients with primary knee OA and the relationship of these receptors with clinical parameters. [ABSTRACT FROM AUTHOR]

The aim of this study was to analyze the levels of brain-derived neurotrophic factor (BDNF) in both the plasma and synovial fluid of patients with primary knee osteoarthritis compared with control individuals and to investigate the relationship between BDNF levels and self-reported pain. Twenty-seven patients with knee osteoarthritis (OA) and 19 healthy subjects were enrolled in the study. Anteroposterior knee radiographs were taken to determine the disease severity of the affected knee. Radiographic grading of OA in the knee was performed using the Kellgren-Lawrence criteria. The BDNF levels in the plasma and synovial fluid were measured by enzyme-linked immunosorbent assay. The mean plasma BDNF levels of the knee OA patients were significantly higher than that of the healthy controls (2,378 ± 1,067.2 vs. 1,756 ± 804.3 pg/mL, p < 0.05). BDNF levels in the synovial fluid of OA patients (358.9 ± 178.4 pg/mL) were sixfold lower than in corresponding blood samples ( p < 0.0001) and fourfold lower than in the plasma of healthy controls ( p < 0.0001). Subsequent analyses showed that the plasma BDNF levels significantly correlated with self-reported pain (Western Ontario and McMaster Universities Osteoarthritis Index) ( r = 0.39, p = 0.04). Furthermore, no correlation was found between the plasma and synovial fluid BDNF concentrations and knee OA severity. The findings of this study suggest that systemic BDNF levels are most likely associated with the mechanism of joint pain in knee OA in the acute stage of joint inflammatory process. Further studies are necessary to address the functional role of BDNF in the modulation of pain to establish new therapeutic implications. [ABSTRACT FROM AUTHOR]

The activation of inflammatory cascades has been consistently demonstrated in the pathophysiology of Alzheimer's disease (AD). Among several putative neuroinflammatory mechanisms, the tumor necrosis factor α (TNF-α) signaling system has a central role in this process. Recent evidence indicates that the abnormal production of inflammatory factors may accompany the progression from mild cognitive impairment (MCI) to dementia. We aimed to examine serum levels of TNF-α and its soluble receptors (sTNFR1 and sTNFR2) in patients with MCI and AD as compared to cognitively unimpaired elderly subjects. We further aimed to investigate whether abnormal levels of these cytokines predict the progression from MCI to AD upon follow-up. We utilized cross-sectional determination of serum levels of TNF-α, sTNFR1, and sTNFR2 (ELISA method) in a test group comprising 167 older adults (31 AD, 72 MCI, and 64 healthy controls), and longitudinal reassessment of clinical status after 18.9 ± 10.0 months. At baseline, there were no statistically significant differences in serum TNF-α, sTNFR1, and sTNFR2 between patients with MCI and AD as compared to controls. Nevertheless, patients with MCI who progressed to AD had significantly higher serum sTNFR1 levels as opposed to patients who retained the diagnosis of MCI upon follow-up (p=0.03). Cox regression analysis showed that high serum sTNFR1 levels predicted the conversion from MCI to AD (p=0.003), whereas no significant differences were found with respect to serum levels of TNF-α and sTNFR2. Abnormal activation of TNF-α signaling system, represented by increased expression of sTNFR1, is associated with a higher risk of progression from MCI to AD. [ABSTRACT FROM AUTHOR]

• An proportional inverse relationship was observed between the A/L ratio and sTNFr-1. • sTNFr-1 causes an inflammatory effect that affect cross-talk between muscle and adipose tissue. • Higher concentration of sTNFr-1 can result in more inflammation and related physical-functional consequences. Complex inflammatory crosstalk between muscular and adipose organs during ageing is controlled by adipokines and myokines. The Adiponectin/Leptin ratio (A/L ratio) has proven to be a promising biomarker for identifying insulin sensitivity, cardiovascular risk and adipose tissue inflammation. Although the A/L ratio has been related to inflammatory conditions, its ability to associate with or indicate the behavior of other inflammatory mediators remains unknown. The present study aimed to verify the association between the A/L ratio and a panel of inflammatory biomarkers in community-dwelling older women. The plasmatic concentrations of adiponectin, leptin, resistin, brain-derived neurotrophic factor (BDNF), interferon-gamma (IFN-γ), interleukins 2, 4, 5, 6, 8 and 10, tumour necrosis factor (TNF) and its soluble receptors (sTNF-r) 1 and 2 were evaluated in 71 community-dwelling older women with 75 (±7) years. The A/L ratio was negative and inverse correlated with BNDF (r = −0.29; p = 0.01), IL-8 (r = −0.37; p = 0.001) and sTNFr- 1 (r = −0.98; p < 0.001) levels. A strong and inverse association, with proportional effect, between A/L ratio and sTNFr-1 concentrations was found (Adjusted R2 = 0.22; β = −0.48; p > 0.001). It suggests that the presence of sTNFr-1 causes an inflammatory effect that affect cross-talk between muscle and adipose tissue, contributing to pro-inflammatory imbalance, which may have molecular and functional consequences. In addition, we provide insights into diagnostic biomarkers for inflammation, especially related to muscle wasting and intrinsic capacity in older people. [ABSTRACT FROM AUTHOR]

The soluble receptors tumor necrosis factor-alpha (sTNFRs) can lead to an increase in the expression of tumor necrosis factor, increasing its detrimental to systemic inflammatory activation in Chagas cardiomyopathy (ChC). However, the correlation between sTNFRs levels, echocardiographic, and functional levels in patients with ChC remains unknown. This study aimed to verify the correlation between the plasma sTNFRs levels, echocardiographic, and NYHA functional levels in patients with ChC. Sixty-four patients with ChD (54 ± 2 years, 44% males, NYHA I-II) were evaluated by anamnesis protocol, echocardiography, and plasma sTNFR1 and sTNFR2 measurement. Linear regression analysis and Student's t -test were used as appropriate. Higher plasma sTNFR1 and sTNFR2 levels were associate with worse systolic function (R2 = 0.10; p = 0.008 and R2 = 0.44; p < 0.001) and cardiac dilation (R2 = 0.13; p = 0.002 and R2 = 0.43; p < 0.001). Patients with systolic dysfunction and cardiac dilatation had higher sTNFRs levels (p < 0.001). There were no significant differences among NYHA functional classes for both sTNFRs. Plasma sTNFR1 and sTNFR2 levels are associated with greater cardiac dilation and poor systolic function in ChC patients. • Plasma sTNFRs levels are related to poor prognosis in patients with heart disease. • Cardiac dysfunction was associated with higher plasma sTNFRs levels in ChC patients. • Plasma sTNFRs levels were similar among the ChC patients with NYHA classes I and II. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the plasma levels of CCL2, CCL3, CCL11, CCL24, tumor necrosis factor alpha, sTNFR1, and sTNFR2 in subjects exposed to silica (SES) with and without silicosis compared with unexposed reference control group, and their associations with the radiological severity and duration of exposure to silica. Methods: Fifty-seven SES; 36 with silicosis and 22 subjects in control group, were included in the study. Results: CCL3, CCL24, sTNFR1, and sTNFR2 were increased in SES and in SES with silicosis than in controls. There were no differences in the levels of CCL2, CCL11, or tumor necrosis factor alpha. The sTNFR2 level was greater in SES with silicosis than in SES without silicosis. There was a positive correlation between sTNFR1and sTNFR2 and the radiological severity and time of exposure to silica. sTNFR2 was associated with all categories of radiological severity. Conclusion: sTNFR2 is associated with silicosis severity and early exposure to silica. [ABSTRACT FROM AUTHOR]

Abstract: Increased pro-inflammatory state has been implicated in the pathophysiology of major depressive disorder. The aim of this study was to determine serum levels of TNF-α and soluble TNF-α receptors 1 and 2 (sTNFR1 and sTNFR2) in anti-depressant free depressed elderly patients as compared to healthy controls. Sixty-seven older adults (28 with major depression and 39 controls) were enrolled to this study. Participants were assessed by the SCID and diagnosis of major depressive episode was made according to the DSM-IV criteria. Serum TNF-α, sTNFR1 and sTNFR2 were determined by ELISA. Anti-depressant free patients with late-life depression showed an increased level of the sTNFR2 as compared to controls (p = 0.03). No significant differences were found in serum TNF-α and sTNFR1 levels (p = 0.1 and p = 0.4, respectively). There was no correlation between serum levels of these inflammatory markers and the severity of depression. Our findings provide additional evidence of the involvement of abnormal pro-inflammatory state in late-life depression. [ABSTRACT FROM AUTHOR]

• Intense physical training is suggested to be harmful to cognitive function. • HIIT was used to assess redox state, behavior and cognitive function in rats. • HIIT did not change the anxious profile or locomotor activity. • Lipid peroxidation, and antioxidant mechanisms were seen in cerebellar tissue. • HIIT had no deleterious effects on rats' cognitive function. High-intensity interval training (HIIT) is associated with better physical performance, but there is limited information about the effects of HIIT on redox state of cerebellar tissue, cerebral cortex, and cognition. The aim of this study was to evaluate the effects of HIIT on redox state parameters in cerebellar tissue, cerebral cortex, and cognitive function of Wistar rats. Forty-three young male Wistar rats were housed under controlled environmental conditions with food, and water ad libitum. Animals were assigned to HIIT or Non-trained groups. HIIT protocol was performed during six weeks. Speed was determined through the assesstment of the maximum oxygen consumption (VO 2max). HIIT consisted of short bouts (1 min) running on a treadmill at 10° inclination (85–100% of VO 2max) with 2 min of active recovery (60% of VO 2max , without inclination). Non-trained group was daily exposed to a disconnected treadmill for the same amount of time as HITT group. Both groups were submitted to the open field, and novel object recognition tasks after six weeks. Malondialdehyde concentration (MDA), superoxide dismutase (SOD) activity, and non-enzymatic antioxidant capacity (FRAP) were quantified to determine the redox state. HIIT presented increased levels of MDA, SOD, and FRAP (p < 0.05) in the cerebellar tissue, but no differences were seen in cerebral cortex. These results indicated an improved antioxidant capacity, despite increased MDA levels in the cerebellar tissue. Both groups did not present impairment in locomotor activity, development of anxious behavior or cognitive decline. HIIT enhanced the antioxidant defenses on cerebellar tissue with no deleterious effects on rats' cognition. [ABSTRACT FROM AUTHOR]

It is known that a single session of high-intensity interval exercise (HIIE) contributes to the increase of the reactive species of oxygen, accompanied by a greater antioxidant activity. However, it is poorly understood if a single session of HIIE has similar effects on the brain tissue. This study evaluated the effects of a single HIIE on the hippocampal redox status. Sixteen males Wistar rats were allocated into HIIE (n = 8) and control (n = 8) groups. Maximum oxygen consumption (VO 2max) was evaluated using a treadmill at 10° inclination in a metabolic chamber. HIIE group was submitted to a single run on the treadmill composed by 10 bouts of high-intensity exercise of 1 min each (85–100% of VO 2max), at 28 m/min, 10° inclination, interspersed by 2 min of active recovery, at 10 m/min, with no inclination. Analysis of the redox status at the hippocampus were conducted 24 h after the HIIE session. It was not identified lipid peroxidation in the hippocampus of the HIIE group (Control 1.9 ± 0.31, vs HIIT 2.2 ± 0.53 nmol MDA/mg protein (p >.05). However, the activity of the superoxide dismutase (Control 2.614 ± 0.225 vs HIIT 3.718 ± 0.4589 U/mg protein), and the non-enzymatic total antioxidant capacity (Control 1584 ± 75.88 vs HIIT 1984 ± 137.7 nM FeSO4/mg protein) were enhanced (p <.05) after the exercise session. These results indicate that the antioxidant mechanisms are enhanced even after a single session of HIIE. A single session of HIIE does not induce lipid peroxidation and improves the antioxidant defenses in Wistar rats' hippocampus. • Antioxidant capacity is enhanced after a single session of high-intensity interval exercise (HIIE) on rats' hippocampus. • A single session of HIIE does not induce lipid peroxidation on rats' hippocampus. • A single session of HIIE improves enzymatic and non-enzymatic total antioxidant capacity in Wistar rats' hippocampus. [ABSTRACT FROM AUTHOR]