The strong inverse association between plasma concentrations of soluble tumor necrosis factor receptors type 1 with adiponectin/leptin ratio in older women.

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; ß = -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.

Circulating c-Met-Expressing Memory T Cells Define Cardiac Autoimmunity.

BACKGROUND: Autoimmunity is increasingly recognized as a key contributing factor in heart muscle diseases. The functional features of cardiac autoimmunity in humans remain undefined because of the challenge of studying immune responses in situ. We previously described a subset of c-mesenchymal epithelial transition factor (c-Met)-expressing (c-Met+) memory T lymphocytes that preferentially migrate to cardiac tissue in mice and humans. METHODS: In-depth phenotyping of peripheral blood T cells, including c-Met+ T cells, was undertaken in groups of patients with inflammatory and noninflammatory cardiomyopathies, patients with noncardiac autoimmunity, and healthy controls. Validation studies were carried out using human cardiac tissue and in an experimental model of cardiac inflammation. RESULTS: We show that c-Met+ T cells are selectively increased in the circulation and in the myocardium of patients with inflammatory cardiomyopathies. The phenotype and function of c-Met+ T cells are distinct from those of c-Met-negative (c-Met-) T cells, including preferential proliferation to cardiac myosin and coproduction of multiple cytokines (interleukin-4, interleukin-17, and interleukin-22). Furthermore, circulating c-Met+ T cell subpopulations in different heart muscle diseases identify distinct and overlapping mechanisms of heart inflammation. In experimental autoimmune myocarditis, elevations in autoantigen-specific c-Met+ T cells in peripheral blood mark the loss of immune tolerance to the heart. Disease development can be halted by pharmacologic c-Met inhibition, indicating a causative role for c-Met+ T cells. CONCLUSIONS: Our study demonstrates that the detection of circulating c-Met+ T cells may have use in the diagnosis and monitoring of adaptive cardiac inflammation and definition of new targets for therapeutic intervention when cardiac autoimmunity causes or contributes to progressive cardiac injury.

Neurological consequences of exercise during prenatal Zika virus exposure to mice pups.

PURPOSE/AIM: Zika virus (ZIKV) infection during the pregnancy period is related to microcephaly and neurobehavioral disorders at birth, while prenatal exercise is supposed to provide neuroprotection in newborns pups. The aim of this study was to investigate the neurological consequences of exercise during prenatal ZIKV exposure to mice pups. MATERIAL AND METHODS: Twelve weeks female mice were randomly assigned into three groups: Control group, intraperitoneally injected with saline (Control); untrained group, intraperitoneally injected with ZIKV (ZIKV); and trained group, intraperitoneally injected with ZIKV (ZIKV/swim). There was one familiarization week prior to the beginning of the swimming training. Dams swam for 60 min/session, 5 days/week, during 4 weeks. Mating occurred between the fifth and seventh day of the first week of the swimming training. ZIKV 106 plaque-forming units/100 µl (106 PFUs/100 µl) or an equal volume of saline was intraperitoneally injected in the pregnant mice at embryonic day 10.5. Pup's body mass and brain weight were measured at postnatal day 1 (P1). Behavioral tests were performed from P30 to P35. Thereafter, hippocampal levels of syntaxin-1, GFAP, IBA-1, and BDNF were measured. RESULTS: Exercise during prenatal ZIKV exposure prevented brain atrophy, development of depression, anxiety, and disruption of social behavior. Exercise during prenatal ZIKV exposure inhibited the overexpression of microglia (IBA-1) and astrocytes (GFAP), with reduction of BDNF levels in the hippocampi of female and male mice pups. No significant changes were seen in syntaxin-1 levels. CONCLUSION: Our findings reveal beneficial effects of exercise during pregnancy exposure to ZIKV in mice pups.

Photobiomodulation therapy on expression of HSP70 protein and tissue repair in experimental acute Achilles tendinitis.

The aim of the present study was to investigate the effects of photobiomodulation (PBM) therapy on the expression of heat shock protein 70 (HSP70) and tissue repair in an experimental model of collagenase-induced Achilles tendinitis. Thirty Wistar rats (aged 12 weeks) were randomly distributed among control group (n = 8), tendinitis group (n = 11), and LED group (n = 11). Tendinitis was induced in the tendinitis and LED groups through a peritendinous injection of collagenase (100 µl). The LED group animals received the first irradiation 1 h after injury. A 630 ± 20 nm, 300-mW continuous wave light-emitting diode (LED), spot size 1 cm2, was placed in contact with the skin. One point over the tendon was irradiated for 30 s, delivering 9 J (9 J/cm2). LED irradiation was performed once daily for 7 days, with the total energy delivered being 63 J. The tendons were surgically removed and expression of the HSP70 protein was calculated using semi-quantitative analyses of immunohistochemistry (HSCORE). Number of fibroblasts and amount of collagen were measured using histological and histochemical analyses. An increase in the mean HSCORE for HSP70, in the number of fibroblasts, and in the amount of collagen were found in the LED group compared with those in the tendinitis and control group (P ≤ 0.05). PBM therapy increased the expression of the HSP70, number of fibroblasts, and amount of collagen in the acute Achilles tendinitis in rats.

High-intensity interval training reduces monocyte activation in obese adults.

Alterations in the distribution and activation of monocyte subsets are frequently observed in individuals with obesity and their participation in the pathological complications of obesity is proposed. High-intensity interval training (HIIT) can be a time-efficient alternative to counteract the inflammatory outcomes of obesity, but so far, its effects on monocytes in obesity has not been fully explored. In this study, we investigated whether 8 weeks of HIIT can modify the distribution and activation of the three monocyte subsets (classical, intermediate and non-classical monocytes) in individuals with obesity. Our data show that individuals with obesity have a higher percentage of non-classical monocytes compared to control, lean individuals, and consequently an imbalance among the CD16+ monocyte subsets. Also, the expression of HLA-DR by intermediate monocytes is higher in insulin-resistant obese individuals, which indicates monocyte activation in obesity. After 8 weeks of HIIT, the percentage of non-classical monocytes was reduced in individuals with obesity, restoring the balance among the CD16+ monocytes. Also, the expression of HLA-DR by intermediate monocytes in insulin-resistant obese subjects was lower after HIIT. Both findings indicate that monocyte activation in individuals with obesity was reduced by HIIT. These modifications were observed in the absence of changes in weight and body composition, although they were accompanied by the improvement in the metabolic status (reduced insulin levels). Our findings indicate that HIIT can be considered a time-efficient strategy to manage obesity-related monocyte alterations and strengthen the immunomodulatory potential of HIIT.

IL-33 in obesity: where do we go from here?

IL-33 is a cytokine that belongs to the IL-1 family and is classically associated with type 2-like immune responses. In the adipose tissue, IL-33 is related to the beiging of adipocytes and to the maintenance of adipose tissue-resident immune cells, such as innate lymphoid cells 2, alternatively activated macrophages and regulatory T cells, which contribute to the maintenance of adipose tissue homeostasis. In the obese adipose tissue, the number of these cells is diminished, unlike the expression of IL-33, which is up-regulated. However, despite its increased expression, IL-33 is not able to maintain the homeostasis of the obese adipose tissue. IL-33 treatment, on the other hand, highly improves obesity-related inflammatory and metabolic alterations. The evidence that exogenous IL-33, but not adipose tissue-driven IL-33, regulates the inflammatory process in obesity leaves a gap in the understanding of IL-33 biology. Thus, in this review we discuss the potential mechanisms associated with the impaired action of IL-33 in obesity.

Late Neutrophil Priming Following a Single Session of High-intensity Interval Exercise.

This study evaluated the effect of an acute high-intensity interval exercise (HIIE) session on the function of human neutrophils. Twelve sedentary men performed a HIIE session (8 bouts of 60 s at 90% of peak power, intercalated with 75 s of active recovery at 30 W). Neutrophils were collected before, 30 min and 24 h after the exercise session for the evaluation of phagocytic capacity, expression of phagocytic receptors, reactive oxygen species generation, and redox status. 24 h after the HIIE session, an increase was observed in both neutrophil phagocytic capacity and yeast-induced generation of reactive oxygen species, which indicates neutrophil priming in response to an acute HIIE session. Neutrophils also presented an increase in superoxide dismutase activity 24 h after the exercise. Improvement in neutrophil function was accompanied by increased serum levels of IL-8 and increased concentration of plasma lactate dehydrogenase. Our findings show a late activating effect of one HIIE session on neutrophils. We propose that priming of neutrophils by HIIE may play a role in skeletal muscle inflammation after exercise.

Infrared photobiomodulation (PBM) therapy improves glucose metabolism and intracellular insulin pathway in adipose tissue of high-fat fed mice.

Obesity represents a continuously growing global epidemic and is associated with the development of type 2 diabetes mellitus. The etiology of type 2 diabetes is related to the resistance of insulin-sensitive tissues to its action leading to impaired blood glucose regulation. Photobiomodulation (PBM) therapy might be a non-pharmacological, non-invasive strategy to improve insulin resistance. It has been reported that PBM therapy in combination with physical exercise reduces insulin resistance. Therefore, the aim of this study was to investigate the effects of PBM therapy on insulin resistance in obese mice. Male Swiss albino mice received low-fat control diet (n = 16, LFC) or high-fat diet (n = 18, HFD) for 12 weeks. From 9th to 12th week, the mice received PBM therapy (LASER) or Sham (light off) treatment and were allocated into four groups: LFC Sham (n = 8), LFC PBM (n = 8), HFD Sham (n = 9), and HFD PBM (n = 9). The PBM therapy was applied in five locations: to the left and right quadriceps muscle, upper limbs and center of the abdomen, during 40 s at each point, once a day, 5 days a week, for 4 weeks (780 nm, 250 mW/cm2, 10 J/cm2, 0.4 J per site; 2 J total dose per day). Insulin signaling pathway was evaluated in the epididymal adipose tissue. PBM therapy improved glucose tolerance and phosphorylation of Akt (Ser473) and reversed the HFD-induced reduction of GLUT4 content and phosphorylation of AS160 (Ser588). Also, PBM therapy reversed the increased area of epididymal and mesenteric adipocytes. The results showed that chronic PBM therapy improved parameters related to obesity and insulin resistance in HFD-induced obesity in mice.

The effect of insulin resistance and exercise on the percentage of CD16(+) monocyte subset in obese individuals.

UNLABELLED: Obesity is a low-grade chronic inflammation condition, and macrophages, and possibly monocytes, are involved in the pathological outcomes of obesity. Physical exercise is a low-cost strategy to prevent and treat obesity, probably because of its anti-inflammatory action. We evaluated the percentage of CD16(-) and CD16(+) monocyte subsets in obese insulin-resistant individuals and the effect of an exercise bout on the percentage of these cells. Twenty-seven volunteers were divided into three experimental groups: lean insulin sensitive, obese insulin sensitive and obese insulin resistant. Venous blood samples collected before and 1 h after an aerobic exercise session on a cycle ergometer were used for determination of monocyte subsets by flow cytometry. Insulin-resistant obese individuals have a higher percentage of CD16(+) monocytes (14.8 ± 2.4%) than the lean group (10.0 ± 1.3%). A positive correlation of the percentage of CD16(+) monocytes with body mass index and fasting plasma insulin levels was found. One bout of moderate exercise reduced the percentage of CD16(+) monocytes by 10% in all the groups evaluated. Also, the absolute monocyte count, as well as all other leukocyte populations, in lean and obese individuals, increased after exercise. This fact may partially account for the observed reduction in the percentage of CD16(+) cells in response to exercise. Insulin-resistant, but not insulin-sensitive obese individuals, have an increased percentage of CD16(+) monocytes that can be slightly modulated by a single bout of moderate aerobic exercise. These findings may be clinically relevant to the population studied, considering the involvement of CD16(+) monocytes in the pathophysiology of obesity. Copyright © 2016 John Wiley & Sons, Ltd. SIGNIFICANCE OF THE STUDY: Obesity is now considered to be an inflammatory condition associated with many pathological consequences, including insulin resistance. It is proposed that insulin resistance contributes to the aggravation of the inflammatory dysfunction in obesity. The effect of obesity on the percentage of monocytes was previously observed in class II and III obese individuals who presented other alterations in addition to insulin resistance. In this study we observed that insulin-resistant obese individuals, but not insulin-sensitive ones, had an increased percentage of CD14(+) CD16(+) monocytes. This fact shows that a dysfunction of the monocyte percentage in class I obese individuals is only seen when this condition is associated with insulin resistance.

The in vitro exposure to cypermethrin does not inhibit the proliferative response of peripheral blood mononuclear cells.

This study evaluated the effect of in vitro exposure to cypermethrin on peripheral blood mononuclear cells proliferative response, considering reduced peripheral blood mononuclear cells proliferative response observed in individuals occupationally exposed to pyrethroids. Peripheral blood mononuclear cells were obtained from 21 healthy subjects (28.0 ± 9.0 years old). The effect of cypermethrin (at 0.5, 1.0 and 5.0 mg/ml) on cell viability was evaluated by flow cytometry using an apoptosis detection kit. Cell proliferation (PI) was evaluated by 5-(and 6)-carboxyfluorescein diacetate succinimidyl ester (CFSE) fluorescence decay using flow cytometry. Cells labeled with CFSE were exposed, in vitro, to cypermethrin (0.5, 1.0, 2.0, 2.5 and 4 µg/ml) and stimulated with phytohemagglutinin (PHA 1.0 or 5.0 µg/ml) for 5 d (37 °C, 5% CO2). The in vitro treatment of peripheral blood mononuclear cells with cypermethrin did not induce apoptosis or necrosis after 5 d in culture. Stimulation by PHA induced cell proliferation (PI = 1.29 ± 1.09 and 2.01 ± 0.62, PHA at 1.0 and 5.0 µg/ml, respectively, mean ± SD) and in vitro exposure to cypermethrin did not alter cellular proliferative response to PHA (PI = 1.80 ± 0.50, 2.60 ± 0.05 and 2.10 ± 1.20 for cypermethrin at 1.0, 2.0 and 4.0 µg/ml, respectively, and PHA at 5.0 µg/ml). In vitro treatment of peripheral blood mononuclear cells with cypermethrin, at the doses tested, does not affect cell viability or proliferation. These findings suggest that the reduction of proliferation observed on lymphocytes derived from individuals occupationally exposed to pesticides may be related to other mechanisms than direct action of cypermethrin on lymphocytes.

Increased Migratory and Activation Cell Markers of Peripheral Blood Lymphocytes in an Experimental Model of Nephrotic Syndrome.

The present study aimed to evaluate the expression of CD80 and CD18 in subpopulations of peripheral blood leukocytes and oxidative kidney damage in rats with nephrotic syndrome (NS) induced by doxorubicin (Dox) in comparison to control animals at different time points. Male adult Wistar rats were submitted to 24-hour urine and blood collection for biochemical and immunological analysis at 7, 14, 21, and 28 days after Dox injection. After euthanasia, the kidneys were removed for histological analysis and the evaluation of oxidative stress. The phenotypic characterization of leukocytes was performed using flow cytometry. Dox-injected animals exhibited increased CD18 expression in cytotoxic T lymphocytes, NK cells, and monocytes and high CD80 expression in monocytes. Kidney oxidative damage was positively correlated with CD80 expression in monocytes and serum levels of creatinine. These results suggest that phagocytic and cytotoxic cells are preferentially recruited to the tissue injury site, which may contribute to kidney dysfunction in this animal model of NS. The blockade of integrin and costimulatory molecules may provide new therapeutic opportunities for NS.

A MUFA/carotenoid-rich oil ameliorated insulin resistance by improving inflammation and oxidative stress in obese rats.

Obesity is associated with low-grade inflammation and oxidative stress, leading to insulin resistance and type II diabetes. Caryocar brasiliense pulp oil (pequi oil - PO) is rich in oleic acid and carotenoids and positively implicated in regulating inflammation and oxidative stress. This study investigated PO's antioxidant and anti-inflammatory effects in a diet-induced obesity model. Male Wistar rats were allocated into three experimental groups: Control (CD), Western Diet (WD), and Western Diet, with 27% of lard switched by PO (WDP). Metabolic, inflammatory, and oxidative stress biomarkers were evaluated after 12 weeks of diet protocols in liver and adipose tissue. WDP rats gained less body mass and epididymal fat, had less hepatic fat infiltration, and were more glucose-tolerant and insulin-sensitive than WD (p < 0.05). In the liver, the WDP group had the highest non-enzymatic antioxidant capacity, SOD and GPx activities, CAT, SOD II, and HSP72 expression compared to WD (p < 0.05). Adipose tissue IL-6 and TNF were reduced, and IL-10 was increased in WDP compared to WD (p < 0.05). Our data suggest that the partial replacement of lard by PO in a Western diet prevented visceral fat accumulation and contributed to reducing inflammation in adipose tissue and liver oxidative stress, improving obesity-related insulin resistance.

Association between Anti-DENV IgM Serum Prevalence and CD11b Expression by Classical Monocytes in Obesity.

Dengue and obesity are currently highly prevalent conditions worldwide and the association between these two conditions may result in greater risk for DENV infection and disease severity. In this study the association between obesity and recent, inapparent dengue was investigated. Serum DENV IgM and NS1 were evaluated in 49 adult volunteers (15 lean and 34 individuals with obesity, according to body mass index), between September 2017 and June 2018. Adiposity, endocrine, metabolic, and immune data of the participants were also obtained. None of the study participants tested positive for the DENV NS1 antigen. DENV IgM was detected in 33.3% of the lean individuals, and in 44.1% of those with obesity; the presence of DENV IgM was not associated with body mass index (OR = 1.32, 95% CI = 0.59-2.98, p = 0.48). However, body fat index was higher in obese individuals who had recent inapparent dengue (14.7 ± 3.1 versus 12.7 ± 2.1 kg/m2, p = 0.04), as was the expression of CD11b by classical (CD14++CD16-) monocytes (1103.0 ± 311.3 versus 720.3 ± 281.1 mean fluoresce intensity). Our findings suggest an association between adiposity and recent inapparent dengue and the involvement of classical monocytes in this association.

SARS-CoV-2 genome incidence on the inanimate surface of the material used in the flow of biological samples from the collection point to the testing unit.

Despite the undeniable effect of vaccination against COVID-19 in reducing disease severity, there is still a need to monitor and limit SARS-CoV-2 circulation and transmission. Thus, this study evaluated the presence of the SARS-CoV-2 genome on the surfaces of highly touched objects manipulated in the biological sample collection point and at the reception unit of the diagnostic laboratory. Surfaces were sampled once a week, for 6 weeks, between September 18th and October 23rd, 2020. RT-qPCR was used for SARS-CoV-2 detection. The coolers for biological sample transportation and the envelope containing the patient form were the objects with the highest occurrence of viral genome detection, although it was detected in each object in only two of the 6 evaluations. And the SARS-CoV-2 genome was detected just once on the vehicle steering wheel, computer keyboard, bathroom door handle and disinfection bench. The virus genome was not detected in any object on three of the six evaluations. And eight was the largest number of surfaces contaminated by the virus genome on one occasion. The reduced incidence of object contamination by the SARS-CoV-2 genome can be explained by the exposure of the objects to environmental conditions and the adoption of virus-spread containment measures. It can also reflect the low incidence of SARS-CoV-2 during the study's development period. Despite the low frequency of SARS-CoV-2 genome detection, our findings show that the virus was present in the environment at some point. This highlights the importance of adopting personal preventive measures to reduce respiratory virus spread, especially during epidemics and outbreaks.

Seroprevalence of Dengue, Chikungunya, and Zika viruses antibodies in a cohort of asymptomatic pregnant women in a low-income region of Minas Gerais, Brazil, 2018-2019.

Dengue, Chikungunya, and Zika viruses are arthropod-borne viruses (arboviruses) that infect millions of individuals in tropical and subtropical regions. In the Americas, arboviruses represent a major public health problem, especially among vulnerable groups such as the elderly, children, and pregnant women. In this study, the seroprevalence of IgM or IgG against these arboviruses in pregnant, young women in the city of Diamantina, Minas Gerais, Brazil, and the influence of sociodemographic factors on the incidence/prevalence of infection in this group were investigated. A cross-sectional investigation was conducted on a total of 135 pregnant women for Dengue and Chikungunya IgM and 88 pregnant women for Zika IgG. Dengue IgM was found on the serum of twenty participants (14.8%) and only one woman (0.7%) tested positive for Chikungunya IgM. Zika IgG was found in three (3.4%) participants and 2 women who tested positive for Zika virus were also positive for Dengue virus IgM. Although the arboviruses seroprevalence was higher frequency among young (20-25 years old), brown and high school women, with a monthly income of 1-3 minimum wages, no association between these sociodemographic factors and arboviruses seroprevalence was found.

A comprehensive evaluation of heat stress and heat strain in a sample of sugarcane cutters in Brazil.

Sugarcane cutters are vulnerable to extreme heat and are at risk for heat-related illness and chronic kidney disease, potentially due to high heat strain. We performed a comprehensive assessment of the physiological demands of sugarcane cutters via measurements of metabolic, thermal, and cardiovascular responses. In addition, we assessed cross-shift changes in markers of kidney function. Nine male sugarcane cutters were monitored while working during the spring harvest season in Brazil. Core temperature (Tcore) and heart rate (HR) were continuously recorded, and oxygen consumption was measured during the work shift. Urine and blood samples were collected pre- and postwork shifts. Total sweat loss was calculated using body weight changes and adjusting for water ingestion and urine output. A wet-bulb globe temperature (WBGT) station was used to monitor environmental heat stress. WBGT was ≥30°C on 7 of the 8 study days. Mean and peak Tcore during the work shift were 37.96 ± 0.47°C and 38.60 ± 0.41°C, respectively, with all participants surpassing a Tcore of 38°C. Mean and peak HR during the work shift were 137 ± 14 and 164 ± 11 beats/min, respectively. Percent of maximal oxygen consumption was, on average, 53 ± 11%. Workers had a total sweat loss of 7.63 ± 2.31 L and ingested 6.04 ± 1.95 L of fluid. Kidney function (estimated glomerular filtration rate) was reduced from pre- to postwork shift (Δ -20 ± 18 mL·min·1.73 m2). We demonstrated that sugarcane cutters performing prolonged work during a period of high environmental heat stress display high levels of heat strain, high water turnover, and reduced kidney function.NEW & NOTEWORTHY We demonstrate that a shift of sugarcane cutting performed outdoors during the spring harvest season results in a high level of heat strain. In fact, all the studied workers sustained core temperatures above 38°C and heart rates above 75% of the measured maximum heart rate. Additionally, workers displayed a high water turnover with sweat loss close to 10% of their body weight. Finally, we report elevated muscle damage and reductions in kidney function following the work shift.

Swim training does not protect mice from skeletal muscle oxidative damage following a maximum exercise test.

We investigated whether swim training protects skeletal muscle from oxidative damage in response to a maximum progressive exercise. First, we investigated the effect of swim training on the activities of the antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), in the gastrocnemius muscle of C57Bl/6 mice, 48 h after the last training session. Mice swam for 90 min, twice a day, for 5 weeks at 31°C (± 1°C). The activities of SOD and CAT were increased in trained mice (P < 0.05) compared to untrained group. However, no effect of training was observed in the activity of GPx. In a second experiment, trained and untrained mice were submitted to a maximum progressive swim test. Compared to control mice (untrained, not acutely exercised), malondialdehyde (MDA) levels were increased in the skeletal muscle of both trained and untrained mice after maximum swim. The activity of GPx was increased in the skeletal muscle of both trained and untrained mice, while SOD activity was increased only in trained mice after maximum swimming. CAT activity was increased only in the untrained compared to the control group. Although the trained mice showed increased activity of citrate synthase in skeletal muscle, swim performance was not different compared to untrained mice. Our results show an imbalance in the activities of SOD, CAT and GPx in response to swim training, which could account for the oxidative damage observed in the skeletal muscle of trained mice in response to maximum swim, resulting in the absence of improved exercise performance.

Detection of SARS-CoV-2 genome on inanimate surfaces in COVID-19 intensive care units and emergency care cohort.

INTRODUCTION: Understanding the different transmission routes of SARS-CoV-2 is crucial in planning effective interventions in healthcare institutions. This study aimed to evaluate the presence of SARS-Cov-2 genome on inanimate surfaces in COVID-19 intensive care unit and emergency care cohorts. METHODS: This is a prospective cross-sectional study. Samples of the environmental surface of objects and furniture were collected between July 15 and October 15, 2020, at COVID-19 intensive and emergency care units. The presence of SARS-CoV-2 genome was determined by quantitative RT-qPCR. The positivity rate for SARS-Cov-2 genome is presented as the arithmetic mean of the sum of the values obtained in each collection. Values of 1.0, 0.5, and 0.0 were assigned for positive, indeterminate, and negative events, respectively. RESULTS: In the intensive care unit, 86% of samples collected at the stethoscope and bed rail surfaces were positive. In the emergency care unit, 43% of bathroom tap, bed rails, and bedside table samples were positive. SARS-CoV-2 genome was not detected at the computer mouse and keyboard. At the emergency care unit, 14.3% of the samples from the collection room armchair were positive. CONCLUSIONS: SARS-CoV-2 genome can be found at the environmental surface of objects and furniture at COVID-19 care units. They can represent a potential source of indirect transmission pathway for COVID-19, especially within health service institutions.

Prenatal LPS exposure increases hippocampus IL-10 and prevents short-term memory loss in the male adolescent offspring of high-fat diet fed dams.

Lipopolysaccharide (LPS) tolerance can reduce the neuroinflammation caused by high fat maternal diets; however, there are no reports that have evaluated the effects of prenatal LPS exposure on the memories of the offspring of high-fat diet fed dams. This study evaluated the effects of prenatal LPS exposure on the inflammatory parameters and redox status in the brain, as well as the object recognition memory of adolescent offspring of Wistar rat dams that were treated with a high-fat diet during gestation and lactation. Female pregnant Wistar rats randomly received a standard diet (17.5% fat) or a high-fat diet (45.0% fat) during gestation and lactation. On gestation days 8, 10, and 12, half of the females in each group were intraperitoneally treated with LPS (0.1 mg.kg-1). After weaning, the male offspring were placed in cages in standard conditions, and at 6 weeks old, animals underwent the novel object recognition test (for short- and long-term memory). The offspring of the high-fat diet fed dams showed increased hippocampus IL-6 levels (21-days-old) and impaired short-term memories. These effects were avoided in the offspring of high-fat diet fed dams submitted to prenatal LPS exposure, which showed greater hippocampus IL-10 levels (at 21- and 50-days-old), increased antioxidant activity (50-days-old) in the hippocampus and prefrontal cortex, without memory impairments (short- and long-term memory). IL-6 has been consistently implicated in memory deficits and as an endogenous mechanism for limiting plasticity, while IL-10 regulates glial activation and has a strong association with improvements in cognitive function. Prenatal LPS exposure preventing the increase of IL-6 in the hippocampus and the impairment to short-term object recognition memory caused by the high-fat maternal diet.

Storage Duration Affects the Quantification of Oxidative Stress Markers in the Gastrocnemius, Heart, and Brain of Mice Submitted to a Maximum Exercise.

This study investigated the effect of sample storage duration on the quantification of oxidative stress markers in the gastrocnemius, heart, and brain of mice submitted to a maximum swimming exercise. Thiobarbituric acid reactive substances (TBARSs), protein carbonyl derivatives, total antioxidant capacity (TAC), and the activity of superoxide dismutase (SOD) and catalase (CAT) were quantified in fresh tissues and in samples stored at -80°C for 1, 3, or 6 months, from exercised (n = 13) and nonexercised mice (n = 13). Except for protein carbonyl derivatives in the heart, the exercise resulted in the modification of all markers in all fresh-evaluated samples (p < 0.001). The storage duration did not modify the effect of exercise on protein carbonyl derivatives and TAC. TBARS was stable for 3 months in the gastrocnemius and for 1 month in frozen heart and brain. Accordingly, the exercise effect on TBARS levels observed in fresh samples was absent in the gastrocnemius frozen for 6 months (p = 0.98) and in the heart and brain frozen for 3 months (p = 0.07 and 0.28, respectively) or more (p = 0.21 for heart and p > 0.99 for brain). In addition, CAT and SOD activities were reduced by storage duration in all tissues evaluated (p < 0.05). Our findings show that sample storage duration alters the quantification of oxidative stress markers in mice submitted to maximum exercise, and its effect is tissue and marker dependent. Some recommendations to achieve more accurate and reproducible data in the exercise physiology and oxidative stress markers field are presented.