Publications by authors named "Érica Leandro Marciano Vieira"

65 Publications

Physiological and Biochemical Evaluation of Different Types of Recovery in National Level Paralympic Powerlifting.

Int J Environ Res Public Health 2021 May 13;18(10). Epub 2021 May 13.

Graduate Program in Physical Education, Federal University of Sergipe (UFS), São Cristovão 49100-000, Sergipe, Brazil.

Background: Recovery from training is vital as it ensures training and performance to continue at high intensities and longer durations to stimulate the body and cause further adaptations.

Objective: To evaluate different methods of post-workout recovery in Paralympic powerlifting athletes.

Methods: Twelve male athletes participated (25.4 ± 3.3 years; 70.3 ± 12.1 kg). The presence of muscle edema, pain threshold, plasma cytokines, and performance measurement were evaluated five times. The recovery methods used in this study were passive recovery (PR), dry needling (DN), and cold-water immersion (CWI).

Results: The data analysis showed that the maximal force decreased compared to the pretest value at 15 min and 2 h. The results also revealed that CWI and DN increased Interleukin 2 (IL-2) levels from 24 to 48 h more than that from 2 h to 24 h. After DN, muscle thickness did not increase significantly in any of the muscles, and after 2 h, muscle thickness decreased significantly again in the major pectoralis muscle. After CWI, pain pressure stabilized after 15 min and increased significantly again after 2 h for acromial pectoralis.

Conclusion: The strength training sessions generate several changes in metabolism and different recovery methods contribute differently to maintain homeostasis in Paralympic powerlifting athletes.
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http://dx.doi.org/10.3390/ijerph18105155DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8152222PMC
May 2021

PI3K, mTOR and GSK3 modulate cytokines' production in peripheral leukocyte in temporal lobe epilepsy.

Neurosci Lett 2021 May 9;756:135948. Epub 2021 May 9.

Neuroscience Program, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil; Department of Pharmacology, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. Electronic address:

Introduction: Epilepsy is a common pathological condition that predisposes individuals to seizures, as well as cognitive and emotional dysfunctions. Different studies have demonstrated that inflammation contributes to the pathophysiology of epilepsy. Indeed, seizures change the peripheral inflammatory pattern, which, in turn, could contribute to seizures. However, the cause of the altered production of peripheral inflammatory mediators is not known. The PI3K/mTOR/GSK3β pathway is important for different physiological and pharmacological phenomena. Therefore, in the present study, we tested the hypothesis that the PI3K/mTOR/GSK3β pathway is deregulated in immune cells from patients with epilepsy and contributes to the abnormal production of inflammatory mediators.

Methods: Patients with temporal lobe epilepsy presenting hippocampal sclerosis and controls aged between 18 and 65 years-old were selected for this study. Peripheral blood was collected for the isolation of peripheral mononuclear blood cells (PBMC). Cells were pre-incubated with different PI3K, mTOR and GSK-3 inhibitors for 30 min and further stimulated with phytohaemaglutinin (PHA) or vehicle for 24 h. The supernatant was used to evaluate the production of IL-1β, IL-6, IL-10, TNF e IL-12p70.

Results: Non-selective inhibition of PI3K, as well as inhibition of PI3Kγ and GSK-3, reduced the levels of TNF and IL-10 in PHA-stimulated cells from TLE individuals. This stimulus increased the production of IL-12p70 only in cells from TLE individuals, while the inhibition of PI3K and mTOR enhanced the production of this cytokine. On the other hand, inhibition of GSK3 reduced the PHA-induced production of IL-12p70.

Conclusions: Herein we demonstrated that the production of cytokines by immune cells from patients with TLE differs from non-epileptic patients. This differential regulation may be associated with the altered activity and responsiveness of intracellular molecules, such as PI3K, mTOR and GSK-3, which, in turn, might contribute to the inflammatory state that exists in epilepsy and its pathogenesis.
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http://dx.doi.org/10.1016/j.neulet.2021.135948DOI Listing
May 2021

Serotonin and dopamine receptors profile on peripheral immune cells from patients with temporal lobe epilepsy.

J Neuroimmunol 2021 05 5;354:577534. Epub 2021 Mar 5.

Laboratório de Neurofarmacologia, Departamento de Farmacologia, ICB, Universidade Federal de Minas Gerais, Belo Horizonte 31270-901, Brazil; Programa de Neurociências, Universidade Federal de Minas Gerais, Belo Horizonte 31270-901, Brazil. Electronic address:

The role of inflammation and immune cells has been demonstrated in neurological diseases, including epilepsy. Leukocytes, as well as inflammatory mediators, contribute to abnormal processes that lead to a reduction in seizure threshold and synaptic reorganization. In this sense, identifying different phenotypes of circulating immune cells is essential to understanding the role of these cells in epilepsy. Immune cells can express a variety of surface markers, including neurotransmitter receptors, such as serotonin and dopamine. Alteration in these receptors expression patterns may affect the level of inflammatory mediators and the pathophysiology of epilepsy. Therefore, in the current study, we evaluated the expression of dopamine and serotonin receptors on white blood cells from patients with temporal lobe epilepsy with hippocampal sclerosis (TLE-HS). Blood samples from 17 patients with TLE-HS and 21 controls were collected. PBMC were isolated and stained ex vivo for flow cytometry. We evaluated the expression of serotonin (5-HT, 5-HT, 5-HT, 5-HT, 5-HT, 5-HT, 5-HT), and dopamine receptors (D, D, D, D, and D) on the cell surface of lymphocytes and innate immune cells (monocytes and granulocytes). Our results demonstrated that innate cells and lymphocytes from patients with TLE-HS showed high mean fluorescent intensity (MFI) for 5-HT, 5-HT, 5-HT and 5-HT compared to controls. No difference was observed for 5-HT. For dopamine receptors, the expression of D, D, D and D receptors was higher on innate cells from patients with TLE-HS when compared to controls for the MFI. Regarding lymphocytes population, D expression was increased in patients with TLE-HS. In conclusion, there are alterations in the expression of serotonin and dopamine receptors on immune blood cells of patients with TLE-HS. Although the biological significance of these findings still needs to be further investigated, these changes may contribute to the understanding of TLE-HS pathophysiology.
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http://dx.doi.org/10.1016/j.jneuroim.2021.577534DOI Listing
May 2021

Tumor necrosis factor superfamily molecules are increased in behavioral variant frontotemporal dementia and correlate with cortical atrophy: An exploratory investigation.

J Neuroimmunol 2021 05 27;354:577531. Epub 2021 Feb 27.

Laboratório Interdisciplinar de Investigação Médica, Faculdade de Medicina, UFMG, Belo Horizonte, MG, Brazil; Departamento de Clínica Médica, Faculdade de Medicina, UFMG, Belo Horizonte, MG, Brazil; Programa de Pós-Graduação em Neurociências, Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, MG, Brazil. Electronic address:

Frontotemporal dementia (FTD) is the second most frequent cause of young-onset dementia. Even though immune-mediated and neuroinflammatory factors have been recognized as potential pathophysiological mechanisms, the role of specific immune molecules, such as the tumor necrosis factor (TNF) superfamily, remains elusive. The aim of this study was to investigate TNF Superfamily Molecules (TNF, TNF-related weak inducer of apoptosis [TWEAK], soluble TNF receptor type 1 [sTNFRI] and soluble TNF receptor type 2 [sTNFRII]) in patients with behavioral variant FTD (bvFTD) and controls, and to explore potential associations with clinical parameters and brain atrophy. This study included two groups of participants matched for age, sex and schooling years: patients with probable bvFTD (n = 17, mean age = 64.9 years, 6 women/11 men) and healthy controls (HC, n = 17; mean age = 63.9 years, 10 women/7 men). All participants underwent comprehensive cognitive assessment and structural brain imaging with 3 T magnetic resonance imaging. Plasma levels of TNF, TWEAK, sTNFRI and sTNFRII were determined by ELISA. We conducted voxel-based morphometry analyses to investigate correlations between grey matter (GM) atrophy and plasma levels of TNF, TWEAK, sTNFRI and sTNFRII within bvFTD group. Compared to HC, bvFTD patients had lower cognitive scores and marked frontotemporal atrophy. Patients with bvFTD had significantly higher plasma levels of TNF (p < 0.0001), sTNFRI (p < 0.001), and sTNFRII (p < 0.0001), and similar levels of TWEAK in comparison with controls. The levels of sTNFRII were positively correlated with GM atrophy involving temporal poles, precuneus and cerebellum in bvFTD patients, while the levels of TWEAK positively correlated with right superior temporal gyrus. Our results implicate TNF superfamily in the pathophysiology of FTD.
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http://dx.doi.org/10.1016/j.jneuroim.2021.577531DOI Listing
May 2021

NLRP3 and NLRP1 inflammasomes are up-regulated in patients with mesial temporal lobe epilepsy and may contribute to overexpression of caspase-1 and IL-β in sclerotic hippocampi.

Brain Res 2021 Feb 29;1752:147230. Epub 2020 Dec 29.

Neuropsychiatry Program, Department of Psychiatry and Behavioral Sciences, University of Texas Health Science Center at Houston, TX, United States.

Inflammation plays a role in the pathophysiology of mesial temporal lobe epilepsy (MTLE). Inflammasome pathways, including the NLRP1 and NLRP3-induced ones, promote neuroinflammation and pyroptosis through interleukin (IL)-1β and caspase-1 action. Evaluation of NLRP1 in sclerotic hippocampi is scarce and there are no data on NLRP3 in human TLE. The aim of this study was to evaluate the expression of these proteins alongside caspase-1 and IL-1β in the hippocampi of patients with TLE compared to control samples. We also sought to investigate peripheral levels of caspase-1 and IL-1β in an independent cohort. Sclerotic and control hippocampi were collected for both histological and immunohistochemical analyses of NLRP1, NLRP3, caspase-1 and IL-1β; plasma was sampled for the measurement of caspase-1 and IL-1β levels through enzyme-linked immunoassay (ELISA) and cytometric bead array (CBA). Sclerotic hippocampi displayed higher expression of the measured proteins than control. Both glia and neurons showed activation of these pathways. Additionally, increased expression of NLRP1 and NLRP3 was associated with elevated plasma levels of IL-1β and in TLE, and increased levels of peripheral caspase-1 were associated with bilateral hippocampal sclerosis (HS). In conclusion, NLRP1 and NLRP3 are up-regulated in sclerotic hippocampi, what may be responsible, at least in part, for the increased hippocampal expression of caspase-1 and IL-1β. Our data suggest a role for inflammasome activation in central and peripheral inflammation in TLE.
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http://dx.doi.org/10.1016/j.brainres.2020.147230DOI Listing
February 2021

Evaluation of Brain Cytokines and the Level of Brain-Derived Neurotrophic Factor in an Inflammatory Model of Depression.

Neuroimmunomodulation 2020 11;27(2):87-96. Epub 2020 Nov 11.

Department of Pharmacology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil,

Introduction: Major depressive disorder is considered a global public health problem. Inflammatory processes are likely involved in its pathophysiology, but the underlying mechanisms have remained uncertain.Here, we used the model of systemic lipopolysaccharide (LPS) injection to test the hypothesis that depressive-like behaviors occur along with changes in the levels of cytokines and brain-derived neurotrophic factor (BDNF) in the hippocampus (HC), prefrontal cortex (PFC), and hypothalamus (HT), and can be prevented by dexamethasone administration.

Methods: Adult C57Bl/6 male mice were first isolated for 10 days, and thereafter received an injection of dexamethasone (6 mg/kg, intraperitoneal [i.p.]), saline followed by LPS (0.83 mg/kg, i.p.), or saline. After 6 h, animals were subjected to the forced-swim test (FST) and open-field tests. Immediately after the behavioral tests, they were euthanized and their brains were collected for the biochemical analyses.

Results: LPS increased the immobility time and reduced the distance travelled in the FST and open-field test, respectively. Dexamethasone increased the immobility time in saline-treated mice but reduced this behavior in the LPS group. LPS increased the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6 and interferon (IFN)-γ in most of the regions evaluated. Dexamethasone prevented LPS-induced IL-6 in the HC, PFC, and HT. Interestingly, dexamethasone increased IL-4 and IL-10 levels in both the LPS- and saline-treated groups. Although dexamethasone reduced BDNF in saline-treated mice, it prevented LPS-induced reduction in this neurotrophic factor.

Conclusion: In summary, dexamethasone decreased proinflammatory and increased anti-inflammatory levels of cytokines and prevented a reduction in BDNF levels induced by the inflammatory stimulus. Thus, the attenuation of depressive-like behavior induced by dexamethasone may be related to the effects on these parameters.
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http://dx.doi.org/10.1159/000511181DOI Listing
November 2020

Corrigendum to "Two protocols of aerobic exercise modulate the counter-regulatory axis of the renin-angiotensin system" [Heliyon 6 (1) (January 2020) e03208].

Heliyon 2020 Oct 23;6(10):e05256. Epub 2020 Oct 23.

Laboratório Interdisciplinar de Investigação Médica (LIIM), Faculdade de Medicina, Universidade Federal de Minas Gerais (UFMG), Av. Prof. Alfredo Balena, 190, Room 281, Belo Horizonte, Postal Code: 30130-100, MG, Brazil.

[This corrects the article DOI: 10.1016/j.heliyon.2020.e03208.].
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http://dx.doi.org/10.1016/j.heliyon.2020.e05256DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7586090PMC
October 2020

Sleep, social behaviour and food consumption of schoolchildren of a large Brazilian city.

Public Health Nutr 2021 Apr 7;24(6):1531-1541. Epub 2020 Oct 7.

Federal University of Minas Gerais, School of Nursing, Nutrition Department, Belo Horizonte, MG, Brazil.

Objective: To explore the impact of inadequate sleep and associated factors on the social behaviour and food consumption of children and adolescents.

Design: Cross-sectional study.

Setting: Sleep information, social behaviour (Strengths and Difficulties Questionnaire), food consumption, demography, nutritional status, lifestyle, and biochemical tests were investigated.

Participants: School children in the 4th grade of the municipal school system of a large Brazilian city.

Results: Of a total of 797 schoolchildren, 50·9 % were female, with a median age of 9·7 (9·5-10·0) years old and an energy consumption of 7613·6 (5982·7-9766·2) kJ. It was determined that 31·6 % were overweight, and 76·8 % reported insufficient weekly practice of physical activity. A median of 9·6 (8·9-10·5) h of sleep (lower values on weekdays: 9·3 v. 10·5 h, P < 0·001) was recorded. In addition, 27 % of the individuals who experienced inadequate sleep (<9 h) engaged in longer screen time daily (≥2 h/d) (P = 0·05), had an inadequate bedtime (> 22 h) or adequate wake-up time (5-7 h), studied in the morning (P < 0·001) and never took a shower before school (P < 0·001). Of the entire sample, 9·9 % had poor or very poor sleep quality and a greater probability of sleep talking regularly, had difficulty falling asleep, and engaged in inadequate social behaviour while experiencing these conditions compared with those with positive sleep quality. There was no association between sleep and the other variables investigated.

Conclusions: Sleep impairment contributed to changes in sleep and social behaviour in schoolchildren. The findings of this study may reinforce the importance of developing actions to promote adequate sleep and a healthy lifestyle at school age.
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http://dx.doi.org/10.1017/S1368980020003924DOI Listing
April 2021

Effects of tDCS on neuroplasticity and inflammatory biomarkers in bipolar depression: Results from a sham-controlled study.

Prog Neuropsychopharmacol Biol Psychiatry 2021 Mar 4;105:110119. Epub 2020 Oct 4.

Laboratory of Neurosciences (LIM-27), Instituto Nacional de Biomarcadores em Neuropsiquiatria (INBioN), Department and Institute of Psychiatry, Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil; Department of Internal Medicine, Faculdade de Medicina da Universidade de São Paulo & Hospital Universitário, Universidade de São Paulo, Av. Prof Lineu Prestes 2565, 05508-000 São Paulo, Brazil. Electronic address:

Objectives: We investigated the role of peripheral biomarkers associated with neuroplasticity and immune-inflammatory processes on the effects of transcranial direct current stimulation (tDCS), a safe, affordable, and portable non-invasive neuromodulatory treatment, in bipolar depression.

Methods: This is an exploratory analysis using a dataset from the sham-controlled study the Bipolar Depression Electrical Treatment Trial (BETTER)(clinicaltrials.govNCT02152878). Participants were 52 adults with type I or II bipolar disorder in a moderate-to-severe depressive episode, randomized to 12 bifrontal active or sham tDCS sessions over a 6-week treatment course. Plasma levels of brain derived neurotrophic factor (BDNF), glial cell derived neurotrophic factor (GDNF), interleukins (IL) 2, 4, 6, 8, 10, 18, 33, 1β, 12p70, 17a, interferon gamma (IFN), tumor necrosis factor alpha (TNF) and its soluble receptors 1 and 2, ST2, and KLOTHO were investigated at baseline and endpoint. We performed analyses unadjusted for multiple testing to evaluate whether baseline biomarkers were predictive for depression improvement and changed during treatment using linear regression models.

Results: A time x group interaction (Cohen's d: -1.16, 95% CI = -1.96 to -0.3, p = .005) was found for IL-8, with greater reductions after active tDCS. Higher baseline IL-6 plasma levels was associated with symptomatic improvement after tDCS (F = 5.43; p = .025). Other associations were not significant.

Conclusions: Our exploratory findings suggested that IL-6 is a potential predictor of tDCS response and IL-8 might decrease after tDCS; although confirmatory studies are warranted due to the multiplicity of comparisons.
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http://dx.doi.org/10.1016/j.pnpbp.2020.110119DOI Listing
March 2021

Stress, anxiety, self-efficacy, and the meanings that physical therapy students attribute to their experience with an objective structured clinical examination.

BMC Med Educ 2020 Sep 10;20(1):296. Epub 2020 Sep 10.

Department of Physical Therapy, Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, MG, Brazil.

Background: Excessive stress and anxiety can impair learning. The objective structured clinical examination (OSCE) is a valuable tool to assess and promote the acquisition of clinical skills. However, significant OSCE-related stress and anxiety are frequently reported. The aim of this study was to investigate the relationships between physiological stress, self-reported levels of anxiety due to an OSCE, self-efficacy, and the meanings that physical therapy students attribute to their experience with the exam.

Design: Concurrent mixed methods study.

Methods: A total of 32 students took part in this study. All were enrolled in the third semester of a 10-semester Physical Therapy Bachelor Program. Salivary cortisol levels, self-reported anxiety (State-Trait Anxiety Inventory, STAI) were measured before the OSCE. Exam scores and self-efficacy ratings were also recorded. Correlations between variables were tested with the Pearson correlation, with ɑ at 0.05. Semi-structured interviews were used to explore the personal perspectives of students. Thematic analysis was used to investigate emergent themes.

Results: Trait anxiety scores were significantly higher than normative values (p < 0.001). A high proportion of students showed high (STAI> 49) state anxiety (37.5%) and trait anxiety (65.6%). Salivary cortisol was not associated anxiety (p > 0.05). Neither stress nor anxiety correlated with OSCE scores. A moderate and significant direct correlation was found for self-efficacy scores and OSCE scores (r = 0.475, p = 0.007). Students reported that confidence had a calming effect and led to better self-perceived performance. They also reported that the OSCE can provide meaningful learning experiences despite being stressful.

Conclusions: A high proportion of our students reported a stable/lingering negative affect. However, neither stress nor anxiety related to OSCE scores. Students' confidence in their capabilities was correlated with their performance. Their subjective reports suggest that self-confidence may have protected them from the negative effects of stress and anxiety on academic performance.
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http://dx.doi.org/10.1186/s12909-020-02202-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7488334PMC
September 2020

Peripheral levels of sST2 are increased in patients with temporal lobe epilepsy: Additional evidence of low-grade inflammation.

Epilepsy Behav 2020 11 23;112:107351. Epub 2020 Aug 23.

Santa Casa BH Instituto de Ensino e Pesquisa, Belo Horizonte, MG, Brazil; Neuropsychiatry Program, Department of Psychiatry and Behavioral Sciences, School of Medicine, University of Texas Health Science Center at Houston, TX, USA.

Inflammation plays a pivotal role in temporal lobe epilepsy (TLE) pathophysiology. IL-33 can act as a transcription factor or as a cytokine, the latter through the transmembrane ST2 receptor or its soluble isoform (sST2), presenting a dual role in neurological diseases. The aim of this study was to determine the plasma levels of IL-33 and sST2 in parallel with clinical features in patients with TLE. Peripheral blood from patients and controls was sampled for the measurement of plasma levels of IL-33 and sST2 by enzyme-linked immunoassay (ELISA). While there were similar levels of IL-33 between controls and patients, sST2 were increased in patients. IL33 and sST2 plasma levels were not associated with TLE-related clinical features. In a subgroup analysis, IL-33 levels correlated with memory performance. In conclusion, our results reinforce the concept of chronic low-grade inflammation in patients with TLE.
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http://dx.doi.org/10.1016/j.yebeh.2020.107351DOI Listing
November 2020

Comparison of Inflammatory Mediators in Patients With Atrial Fibrillation Using Warfarin or Rivaroxaban.

Front Cardiovasc Med 2020 24;7:114. Epub 2020 Jul 24.

Neurofar Laboratory, Departamento de Farmacologia, ICB, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.

Atrial fibrillation (AF) is the most common arrhythmia associated with high risk of venous thromboembolism. Inflammatory mechanisms may be involved in the pathophysiology of AF and in the AF-related thrombogenesis, and patients with AF might benefit from the use of anticoagulants with anti-inflammatory properties. However, the evidence is still scarce, and it points out the need of trials seeking to investigate the levels of inflammatory mediators in patients with AF under different anticoagulant therapies. Therefore, this study was designed to define whether patients with AF treated either with an activated coagulation factor X (FXa) inhibitor (rivaroxaban) or with a vitamin K inhibitor (warfarin) present changes in peripheral levels of inflammatory mediators, mainly cytokines and chemokines. A total of 127 subjects were included in this study, divided into three groups: patients with non-valvular atrial fibrillation (NVAF) using warfarin ( = 42), patients with NVAF using rivaroxaban ( = 29), and controls ( = 56). Plasma levels of inflammatory mediators were quantified by immunoassays. Patients with AF (both warfarin and rivaroxaban groups) presented increased levels of inflammatory cytokines in comparison with controls. The use of rivaroxaban was associated with decreased levels of inflammatory cytokines in comparison with warfarin. On the other hand, patients with AF using rivaroxaban presented increased levels of the chemokines (MCP-1 in comparison with warfarin users; MIG and IP-10 in comparison with controls). AF is associated with an inflammatory profile that was less pronounced in patients on rivaroxaban in comparison with warfarin users. Further studies are necessary to assess the clinical implications of our results and whether patients with AF would benefit from rivaroxaban anti-inflammatory effects.
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http://dx.doi.org/10.3389/fcvm.2020.00114DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7393940PMC
July 2020

Role of gut microbiota in the GBR12909 model of mania-like behavior in mice.

J Neuroimmunol 2020 Jun 16;346:577292. Epub 2020 Jun 16.

Neuropsychiatry Program, Department of Psychiatry and Behavioral Sciences, McGovern Medical School, University of Texas Health Science Center at Houston, TX, USA.

Growing evidence suggests a role for brain-gut-microbiota axis in affective disorders including major depression and bipolar disorder (BD). Herein, we aim to explore, by employing germ-free (GF) mice, the effect of the indigenous microbiota in the development of mania-like behavior. Conventional and GF mice were evaluated for the hyperlocomotion induced by the dopamine transporter inhibitor GBR12909 (15 mg/Kg), a validated model for mania-like behavior. Inflammatory mediators and neurotrophic factors were quantified in the prefrontal cortex, hippocampus and striatum. Mice lacking indigenous microbiota were less susceptible to the mania-like behavior induced by GBR12909. This effect was associated with decreased levels of inflammatory cytokines such as IL-6 and TNF-α, along with increased concentrations of anti- inflammatory cytokines (IL-10) and of neurotrophins (BDNF and NGF). We provided the first evidence that gut-microbiota-brain axis participates in the development of mania-like behavior in rodents, possibly through neuroimmunepathways.
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http://dx.doi.org/10.1016/j.jneuroim.2020.577292DOI Listing
June 2020

Factors associated with functional capacity in the elderly enrolled in the Family Health Strategy.

Cien Saude Colet 2020 Jun 30;25(6):2041-2050. Epub 2018 Sep 30.

Instituto de Ciências da Motricidade, Universidade Federal de Alfenas. Av. Jovino Fernandes Sales 2600, Santa Clara. 37133-840, Alfenas, MG, Brasil.

The study investigated the prevalence of functional capacity decline and its associated factors in the older people enrolled in the Family Health Strategy (ESF) in a city in the south of Minas Gerais. This is an observational, cross-sectional, population-based study with 406 elderly (70.49 years ± 6.77). The functional capacity was evaluated by the Short Physical Performance Battery (SPPB), and its associated factors were evaluated by a structured questionnaire including sociodemographic, economic, clinical and physical aspects. The analysis of plasma levels of inflammatory mediators was performed by the ELISA method. Multiple linear regression was used for the analyses (p < 0.05). The prevalence of functional decline in the sample was 57.6% and factors associated with functional capacity were advanced age, female gender, number of medications, depressive symptoms, high plasma concentrations of the soluble receptor of tumor necrosis factor alpha 1 (sTNFR1) and low handgrip strength. The results demonstrated that functional capacity was associated with a network of multidimensional factors. This study contributes to the practice of ESF professionals by indicating the main factors that can guide actions to promote and prevent the decline of functional capacity in the elderly population.
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http://dx.doi.org/10.1590/1413-81232020256.26092018DOI Listing
June 2020

Clinical and molecular correlates of the ASPECTS in the acute phase of stroke.

Arq Neuropsiquiatr 2020 05 29;78(5):262-268. Epub 2020 May 29.

Laboratório Interdisciplinar de Investigação Médica, Faculdade de Medicina, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.

Background: The Alberta Stroke Program Early CT Score (ASPECTS) scale was developed for monitoring early ischemic changes on CT, being associated with clinical outcomes. The ASPECTS can also associate with peripheral biomarkers that reflect the pathophysiological response of the brain to the ischemic stroke.

Objective: To investigate the association between peripheral biomarkers with the Alberta Stroke Program Early CT Score (ASPECTS) in individuals after ischemic stroke.

Methods: Patients over 18 years old with acute ischemic stroke were enrolled in this study. No patient was eligible for thrombolysis. The patients were submitted to non-contrast CT in the first 24 hours of admission, being the Alberta Stroke Program Early CT Score and clinical and molecular evaluations applied on the same day. The National Institutes of Health Stroke Scale (NIHSS), modified Rankin scale and the Mini-Mental State Examination for clinical evaluation were also applied to all subjects. Plasma levels of BDNF, VCAM-1, VEGF, IL-1β, sTNFRs and adiponectin were determined by ELISA.

Results: Worse neurological impairment (NIHSS), cognitive (MEEM) and functional (Rankin) performance was observed in the group with changes in the NCTT. Patients with NCTT changes also exhibited higher levels of IL-1β and adiponectin. In the linear multivariate regression, an adjusted R coefficient of 0.515 was found, indicating adiponectin and NIHSS as independent predictors of ASPECTS.

Conclusion: Plasma levels of adiponectin are associated with the ASPECTS scores.
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http://dx.doi.org/10.1590/0004-282x20200001DOI Listing
May 2020

Renin-angiotensin system molecules are associated with subclinical atherosclerosis and disease activity in rheumatoid arthritis.

Mod Rheumatol 2021 Jan 30;31(1):119-126. Epub 2020 Mar 30.

Interdisciplinary Laboratory of Medical Investigation, Federal University of Minas Gerais, Belo Horizonte, Brazil.

Objectives: To compare serum levels of RAS components in women with RA versus healthy females and to investigate the association between these molecules and subclinical atherosclerosis.

Methods: A cross-sectional study involving female RA patients without ischemic CVD. Disease activity was assessed using the DAS28 and the CDAI. IMT of the common carotid artery was evaluated by ultrasonography. Serum levels of Ang II, Ang-(1-7), ACE and ACE2 were determined by enzyme immunoassay.

Results: Fifty women with RA, mean 48.2 (7.3) years, were compared to 30 healthy women, paired by age. RA patients had higher plasma levels of Ang II ( < .01), Ang-(1-7) ( < .01), and ACE ( < .01) than controls. The ratios of ACE to ACE2 were higher in RA patients, whereas Ang II/Ang-(1-7) ratios were lower in RA patients. The presence of hypertension and the treatment with ACE inhibitors did not significantly modify serum levels of Ang II, Ang-(1-7), ACE and ACE2 in patients with RA. Seven RA patients had altered IMT, and eight patients exhibited atherosclerotic plaque. There was a negative correlation between ACE2 levels and IMT ( = .041). IMT positively correlated with age ( = .022), disease duration ( = .012) and overall Framingham risk score ( = .008). Ang II concentrations positively correlated with DAS28 ( = .034) and CDAI ( = .040).

Conclusion: Patients with RA had an activation of the RAS, suggesting an association with disease activity and cardiovascular risk. Rheumatological key messages Imbalance of both RAS axes may be associated with cardiovascular risk and disease activity in rheumatoid arthritis. Ultrasonography of the carotid arteries can identify early, subclinical atherosclerotic disease in rheumatoid arthritis patients. Angiotensin-converting enzyme inhibition or angiotensin 1 receptor blockade may be beneficial for rheumatoid arthritis patients.
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http://dx.doi.org/10.1080/14397595.2020.1740418DOI Listing
January 2021

Two protocols of aerobic exercise modulate the counter-regulatory axis of the renin-angiotensin system.

Heliyon 2020 Jan 16;6(1):e03208. Epub 2020 Jan 16.

Laboratório Interdisciplinar de Investigação Médica (LIIM), Faculdade de Medicina, Universidade Federal de Minas Gerais (UFMG), Av. Prof. Alfredo Balena, 190, Room 281, Belo Horizonte, Postal Code: 30130-100, MG, Brazil.

Aims: The renin-angiotensin system (RAS) is a dual system with two opposite arms: i) the classical one formed by the angiotensin converting enzyme (ACE), angiotensin (Ang) II and angiotensin type 1 (AT1) receptors; ii) the counter-regulatory arm consisting of ACE2, Ang-(1-7) and Mas receptor. Physical exercise can modulate this system, however, only animal studies have compared the effects of different intensity protocols on the RAS. No data with humans were provided. Therefore, we investigated the acute effect of two protocols of isowork aerobic exercise [High-Intensity Interval Exercise (HIIE) and Moderate-Intensity Continuous Exercise (MICE)] in plasma and urinary levels of RAS components in physically active men.

Main Methods: The HIIE protocol included a 5-minute warm-up cycling at 60-70% of heart rate peak (HRp) intensity followed by 10 sets of 30 s above 90% with 1 min of recovery and 3 min of cool down. The MICE protocol was performed at a constant power corresponding to 60-70% of HRp and finalized at the same total work of HIIE. Blood and urine samples were collected before and after the protocols. Plasma and urinary levels of ACE, ACE2, Ang-(1-7) and Ang II were analyzed by enzyme-linked immunoassay.

Key Findings: While the HIIE protocol significantly increased urinary levels of ACE and plasma levels of ACE2, the MICE protocol elevated urinary concentrations of ACE2 and of Ang-(1-7). A greater increase of urine concentrations of Ang-(1-7) occurred in the MICE if compared with the HIIE protocol.

Significance: Aerobic physical exercise acutely increases the activity of the counter-regulatory RAS axis, mostly the MICE protocol.
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http://dx.doi.org/10.1016/j.heliyon.2020.e03208DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6970173PMC
January 2020

Mechanisms underlying fat pad remodeling induced by fasting: role of PAF receptor.

Nutrition 2020 03 30;71:110616. Epub 2019 Oct 30.

Department of Nutrition, Nursing School, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil. Electronic address:

Objectives: Fasting has long been practiced for political and religious reasons and to lose weight. However, biological responses during fasting have yet to be fully understood. Previous studies have shown that cytokines may control fat pad expansion, at least in part, owing to the induction of lipolysis. Indeed, we have previously shown that mice with a lower inflammatory response, such as platelet-activating factor receptor knockout mice (PAFR), are prone to gain weight and adiposity. The aims of this study were to determine whether adipose tissue becomes inflamed after fasting and to evaluate whether the PAF signaling is a factor in the fat loss induced by fasting.

Methods: Wild-type (WT) and PAFR mice were fasted for 24 h. Adiposity, leukocyte recruitment, and cytokine levels were evaluated. Multiple comparisons were performed using two-way analysis of variance and post hoc Fisher exact test.

Results: After fasting, male WT mice showed lower adiposity (P < 0.001), higher recruitment of immune cells (P < 0.001), and increased cytokine levels (P < 0.05) in adipose tissue. Although WT mice lost ~79% of their adipose tissue mass, PAFR mice lost only 36%. Additionally, PAFR mice did not show enhanced cytokine and chemokine levels after fasting (P > 0.05).

Conclusion: Despite low-grade inflammation being associated with metabolic syndrome, at least in part, the inflammatory milieu is also important to induce proper fat mobilization and remodeling of adipose tissue.
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http://dx.doi.org/10.1016/j.nut.2019.110616DOI Listing
March 2020

Microgliosis is associated with visual memory decline in patients with temporal lobe epilepsy and hippocampal sclerosis: A clinicopathologic study.

Epilepsy Behav 2020 01 2;102:106643. Epub 2019 Dec 2.

Neuropsychiatry Program and Immuno-Psychiatry Lab, Department of Psychiatry and Behavioral Sciences, University of Texas Health Science Center at Houston, TX, United States.

Hippocampal sclerosis (HS) is characterized by neuronal loss and gliosis. The intensity and distribution of these histopathological findings over the Cornu Ammonis (CA) subfields are important for the classification of HS and prognostication of patients with temporal lobe epilepsy (TLE). Several studies have associated the neuronal density reduction in the hippocampus with cognitive decline in patients with TLE. The current study aimed at investigating whether the expression of glial proteins in sclerotic hippocampi is associated with presurgical memory performance of patients with TLE. Before amygdalohippocampectomy, patients were submitted to memory tests. Immunohistochemical and morphometric analyses with glial fibrillary acidic protein (GFAP) for astrogliosis and human leucocyte antigen DR (HLA-DR) for microgliosis were performed in paraffin-embedded HS and control hippocampi. Sclerotic hippocampi exhibited increased gliosis in comparison with controls. In patients with TLE, the area and intensity of staining for HLA-DR were associated with worse performance in the memory tests. Glial fibrillary acidic protein was neither associated nor correlated with memory test performance. Our data suggest association between microgliosis, but not astrogliosis, with visual memory decline in patients with TLE.
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http://dx.doi.org/10.1016/j.yebeh.2019.106643DOI Listing
January 2020

NVP-BEZ235 (Dactolisib) Has Protective Effects in a Transgenic Mouse Model of Alzheimer's Disease.

Front Pharmacol 2019 13;10:1345. Epub 2019 Nov 13.

Department of Pharmacology, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.

Alzheimer's disease (AD) is a neurodegenerative disease and the main cause of dementia. Its major symptom is memory loss, which is a result of neuronal cell death, which is accompanied by neuroinflammation. Some studies indicate the overactivation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanistic target of rapamycin (mTOR) pathway in this disease, being, thus, a potential target for pharmacological treatment. Here, we used a transgenic mouse model of AD that expresses a mutant amyloid-β precursor protein (T41 mice) to investigate the effects of dactolisib (alternative name: NVP-BEZ235, abbreviation BEZ), a dual PI3K/mTOR inhibitor. Ten-months-old T41 animals were treated for 14 days with BEZ or vehicle oral gavage and then submitted to social memory, open field and contextual conditioned fear tests. Hippocampal slices were prepared and Aβ content, NeuN, Iba-1, CD68 and GFAP were evaluated. Tissues were further processed to evaluate cytokines levels through cytometric bead array. The treatment with BEZ (5 mg/kg) reduced social memory impairment in T41 mice. However, BEZ did not have any effect on altered Aβ levels, NeuN, or GFAP staining. The drug reduced the CD68/Iba-1 ratio in CA3 region of hippocampus. Finally, BEZ diminished IL-10 levels in T41 mice. Thus, although its mechanisms are not clear, BEZ protects against memory impairment, reduces microglial activation and reestablishes IL-10 levels, revealing beneficial effects, which should be further investigated for the treatment of AD.
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http://dx.doi.org/10.3389/fphar.2019.01345DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6864823PMC
November 2019

Minocycline treatment prevents depression and anxiety-like behaviors and promotes neuroprotection after experimental ischemic stroke.

Brain Res Bull 2020 02 19;155:1-10. Epub 2019 Nov 19.

Laboratório de Patologia Celular e Molecular do Departamento de Patologia Geral, Instituto de Ciências Biológicas, UFMG, Brazil; Laboratório Interdisciplinar de Investigação Médica, Faculdade de Medicina, Universidade Federal de Minas Gerais, MG, Brazil. Electronic address:

Depression and anxiety have been reported as the major neuropsychiatric consequences following stroke. Minocycline, a neuroprotective drug has minimized depressive symptoms in patients with major depressive disorders and anxiety-like symptoms. In addition, minocycline demonstrated efficacy and seemed a promising neuroprotective agent in acute stroke patients. The present studied evaluated the effects of minocycline treatment on the depression and anxiety-like behaviors, brain damage and expression of inflammatory and neuroprotective mediators after transient global cerebral ischemia in C57BL/6 mice. Brain ischemia was induced by bilateral occlusion of the common carotids (BCCAo) for 25 min and subsequent reperfusion. Sham and BCCAo animals received minocycline at a dose of 30 mg/kg by intraperitoneal injection during 14 days. The locomotor activity, depression and anxiety-like behaviors were assessed by open field, forced swim and elevated plus maze tests, respectively. Then, the brains were removed and processed to evaluate brain damage by histological and morphometric analysis, hippocampal neurodegeneration using Fluoro-Jade C histochemistry, microglial activity using iba-1 immunohistochemistry, brain levels of TNF, IFN-γ, IL-6, IL-10, IL-12p70 and CCL2 by CBA, CX3CL1 and BDNF by ELISA assays. The animals developed depression and anxiety-like behaviors post-stroke and minocycline treatment prevented those neurobehavioral changes. Moreover, minocycline-treated BCCAo animals showed less intense brain damage in the cerebral cortex, brainstem and cerebellum as well as significantly reduced hippocampal neurodegeneration. BCCAo groups exhibited up-regulation of some cytokines at day 14 after ischemia and brain levels of CX3CL1 and BDNF remained unaltered. Our data indicate that the depression and anxiety-like behavioral improvements promoted by minocycline treatment might be related to its neuroprotective effect after brain ischemia in mice.
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http://dx.doi.org/10.1016/j.brainresbull.2019.11.009DOI Listing
February 2020

A positive allosteric modulator of mGluR5 promotes neuroprotective effects in mouse models of Alzheimer's disease.

Neuropharmacology 2019 12 18;160:107785. Epub 2019 Sep 18.

Department of Pharmacology, Universidade Federal de Minas Gerais, Belo Horizonte, 31270-901, Brazil. Electronic address:

Alzheimer's Disease (AD) is the most prevalent neurodegenerative disorder. Despite advances in the understanding of its pathophysiology, none of the available therapies prevents disease progression. Excess glutamate plays an important role in excitotoxicity by activating ionotropic receptors. However, the mechanisms modulating neuronal cell survival/death via metabotropic glutamate receptors (mGluRs) are not completely understood. Recent data indicates that CDPPB, a positive allosteric modulator of mGluR5, has neuroprotective effects. Thus, this work aimed to investigate CDPPB treatment effects on amyloid-β (Aβ) induced pathological alterations in vitro and in vivo and in a transgenic mouse model of AD (T41 mice). Aβ induced cell death in primary cultures of hippocampal neurons, which was prevented by CDPPB. Male C57BL/6 mice underwent stereotaxic surgery for unilateral intra-hippocampal Aβ injection, which induced memory deficits, neurodegeneration, neuronal viability reduction and decrease of doublecortin-positive cells, a marker of immature neurons and neuronal proliferation. Treatment with CDPPB for 8 days reversed neurodegeneration and doublecortin-positive cells loss and recovered memory function. Fourteen months old T41 mice presented cognitive deficits, neuronal viability reduction, gliosis and Aβ accumulation. Treatment with CDPPB for 28 days increased neuronal viability (32.2% increase in NeuN cells) and reduced gliosis in CA1 region (Iba-1 area by 31.3% and GFAP area by 37.5%) in transgenic animals, without inducing hepatotoxicity. However, it did not reverse cognitive deficit. Despite a four-week treatment did not prevent memory loss in aged transgenic mice, CDPPB is protective against Aβ stimulus. Therefore, this drug represents a potential candidate for further investigations as AD treatment.
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http://dx.doi.org/10.1016/j.neuropharm.2019.107785DOI Listing
December 2019

Evidence for interactions between inflammatory markers and renin-angiotensin system molecules in the occurrence of albuminuria in children with sickle cell anemia.

Cytokine 2020 01 20;125:154800. Epub 2019 Aug 20.

Laboratório Interdisciplinar de Investigação Médica, Faculdade de Medicina, Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Minas Gerais 30130-100, Brazil. Electronic address:

Sickle cell anemia (SCA) is an important cause of chronic kidney disease, but its pathophysiology is not completely understood. The aim of this study was to compare inflammatory biomarkers in urine samples of SCA children with and without albuminuria, and to explore correlations with renin-angiotensin system (RAS) molecules. A cross-sectional study of 213 children selected from the Minas Gerais state cohort were assigned to two groups: Group 1-89 children with SCA who had albuminuria; Group 2-124 children with SCA and normal albuminuria matched by age and sex with group 1. A subset of 89 children was prospectively followed for a median time of 1.1 year. Inflammatory biomarkers (chemokines and cytokines) in urine were measured using cytometric beads array, and RAS molecules were measured by ELISA. Children with albuminuria had significantly higher urinary levels of IP-10/CXCL10, MCP-1/CCL2, MIG/CXCL9, IL-8/CXCL8, IL-12p70, TNF, IL-10, and IL-6 than patients with normal albuminuria. In the correlation analysis, albumin/creatinine ratio was significantly and positively correlated with IP-10/CXCL10, MCP-1/CCL2, MIG/CXCL9, IL-8/CXCL8, TNF, IL-10, and IL-6. Significant correlations were found between inflammatory and RAS molecules. In the prospective analysis, cumulative risk of persistent albuminuria was higher for children with urinary levels of IP-10/CXCL10 or IL-6 above the 50th percentile. Our data showed that inflammatory markers and RAS molecules might contribute to the occurrence of albuminuria in children with SCA, suggesting that both pathways interact in sickle cell nephropathy.
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http://dx.doi.org/10.1016/j.cyto.2019.154800DOI Listing
January 2020

Inflammatory changes in peripheral organs in the BACHD murine model of Huntington's disease.

Life Sci 2019 Sep 11;232:116653. Epub 2019 Jul 11.

Departamento de Morfologia, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil; Laboratório Interdisciplinar de Investigação Médica, Faculdade de Medicina, UFMG, Belo Horizonte, Minas Gerais, Brazil. Electronic address:

Huntington's disease (HD) is a neurodegenerative disease caused by a CAG repeat expansion in the gene encoding the huntingtin protein (HTT). This expansion leads to the formation of mutant huntingtin protein (mHTT) that is expressed in many body tissue cells. The mHTT interacts with several molecular pathways within different cell types, affecting the regulation of the immune system cells. It is still very limited the understanding of the immune changes in peripheral tissues in HD. Herein, we investigated the levels of inflammatory and regulatory cytokines in peripheral organs (i.e. kidney, heart, liver and spleen) of the 12-month-old BACHD model of HD. This robust murine model closely resembles the human disease. We found significant changes in cytokine levels in all organs analyzed. Increased levels of IL-6 were found in the kidney, while levels of IL-6 and IL-12p70 were increased in the heart of BACHD mice in comparison with wild-type (WT) animals. In the liver, we observed enhanced IL-12p70 and TNF-α levels. In the spleen, there was an increase in the levels of IL-4 and a decrease in the levels of IL-5 and IL-6 in BACHD compared to WT. Our findings provide the first evidence that the BACHD model also exhibits immune changes in peripheral organs, opening an avenue for the investigation of the potential role played by peripheral inflammatory response in HD. Further studies are needed to systematically address the mechanisms and pathways underlying immune signaling in peripheral organs in HD.
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http://dx.doi.org/10.1016/j.lfs.2019.116653DOI Listing
September 2019

T-lymphocytes response persists following Plasmodium berghei strain Anka infection resolution and may contribute to later experimental cerebral malaria outcomes.

J Neuroimmunol 2019 05 7;330:5-11. Epub 2019 Feb 7.

Neuropsychiatry Program, Department of Psychiatry and Behavioral Sciences, McGovern Medical School, University of Texas Health Science Center at Houston, USA.

Several studies have proposed cerebral malaria (CM) as a CD4+ and CD8+ T lymphocyte-mediated disease. However, there are no data regarding the recruitment and/or persistence of these cells in the CNS following the phase of infection resolution. Glutamate-mediate excitotoxicity has also been implicated in CM. Blockade of glutamate NMDA receptors by its noncompetitive antagonist MK801 modulates cytokine and neurotrophic factors expression preventing cognitive and depressive-like behavior in experimental CM. Herein, we aim to investigate the role of T lymphocytes in later outcomes in CM, and whether the protective role of MK801 is associated with T lymphocytes response.
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http://dx.doi.org/10.1016/j.jneuroim.2019.02.002DOI Listing
May 2019

Relationship between Sarcopenia and mTOR Pathway in Patients with Colorectal Cancer: Preliminary Report.

Nutr Cancer 2019 20;71(1):172-177. Epub 2019 Jan 20.

a Universidade Federal de Minas Gerais , Belo Horizonte , Brazil.

Sarcopenia is a syndrome characterized by loss of muscle mass and strength that impacts clinical outcomes and mortality in cancer patients. Although the molecular pathways involved in sarcopenia are not fully elucidated, the decrease in protein synthesis rate appears to be one of the most important events. The objective of this study was to investigate the relationship between sarcopenia and mTOR signaling pathway in patients undergoing colorectal resection surgery. Three groups of patients were assessed: 1) the control group (no cancer, no sarcopenia), 2) the cancer non-sarcopenic group and 3) the cancer sarcopenic group. All individuals were evaluated in relation to presence of sarcopenia and mTOR signaling pathway. Sarcopenia was evaluated by the combination of low muscle mass and low muscle strength, measured using computerized tomography images, and hand grip strength, respectively. Rectus abdominis muscle biopsy was performed at the time of surgery. mTOR pathway was analyzed by MILLIPLEX Map Kit Phospho/total mTOR 2-Plex Magnetic Bead Panel. Results were presented by phosphor/total mTOR ratio. Independent T test, Kruskal-Wallis test, and Dunn-Bonferroni post hoc were performed for statistical analysis and P < 0.05 was considered. Thirty-six patients and five controls were evaluated. A total of 13 cancer patients (36.1%) had sarcopenia. The phospho/total mTOR ratio was different between the control group (0.167 MFI) and the cancer non-sarcopenic group (0.055 MFI) (P = 0.026) as well as between the control group (0.167 MFI) and the cancer sarcopenic group (0.0049 MFI) (P = 0.041). No difference was observed on the median phospho/total mTOR ratio between the cancer groups (P > 0.05). More research is needed to extrapolate these results.
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http://dx.doi.org/10.1080/01635581.2018.1540716DOI Listing
May 2020

Role of interleukin-3 as a prognostic marker in septic patients.

Rev Bras Ter Intensiva 2018 Oct-Dec;30(4):443-452. Epub 2019 Jan 10.

Programa de Pós-graduação em Ciências da Saúde, Infectologia e Medicina Tropical, Departamento de Clínica Médica, Hospital das Clínicas, Faculdade de Medicina, Universidade Federal de Minas Gerais - Belo Horizonte (MG), Brasil.

Objective: To evaluate the accuracy of IL-3 to predict the outcome of septic patients.

Methods: Prospective cohort study with adult patients in an intensive care unit with sepsis or septic shock diagnosed within the previous 48 hours. Circulating IL-3 levels were measured upon inclusion (day 1) and on days 3 and 7. The primary outcome was hospital mortality.

Results: One hundred and twenty patients were included. Serum levels of IL-3 on day 1 were significantly higher among patients who died than among patients who survived the hospital stay (91.2pg/mL versus 36pg/mL, p = 0.024). In a Cox survival model considering the IL-3 levels at inclusion, age and sequential SOFA, IL-3 values remained independently associated with mortality (HR 1.032; 95%CI 1.010 - 1.055; p = 0.005). An receiver operating characteristic curve was built to further investigate the accuracy of IL-3, with an area under the curve of 0.62 (95%CI 0.51 - 0.73; p = 0.024) for hospital mortality. A cutoff initial IL-3 value above 127.5pg/mL was associated with hospital mortality (OR 2.97; 95%CI: 1.27 - 6.97; p = 0.0019) but with a low performance (82% for specificity, 39% for sensibility, 53% for the positive predictive value, 72% for the negative predictive value, 0.73 for the negative likelihood and 2.16 for the positive likelihood ratio).

Conclusion: Higher levels of IL-3 are shown to be independently associated with hospital mortality in septic patients but with poor clinical performance.
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http://dx.doi.org/10.5935/0103-507X.20180064DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6334479PMC
May 2019

Plasma Levels of Brain-Derived Neurotrophic Factor are Associated with Prognosis in the Acute Phase of Ischemic Stroke.

J Stroke Cerebrovasc Dis 2019 Mar 3;28(3):735-740. Epub 2018 Dec 3.

Interdisciplinary Laboratory of Medical Investigation, School of Medicine, University of Minas Gerais (UFMG), Belo Horizonte, Minas Gerais, Brazil.

Context: Brain-derived neurotrophic factor (BDNF) is a neurotrophin involved in neuronal survival, differentiation, and maturation.

Purpose: To evaluate the levels of BDNF in the acute phase of stroke and their potential association with neurological impairment.

Methods: Patients in the acute phase of ischemic stroke were evaluated with the following clinical tools: National Institutes of Health Stroke Scale, modified Rankin scale, Gugging Swallowing Screen and Alberta Stroke Program Early CT Score. Blood samples were collected at 3 different moments of hospital stay. BDNF was measured through enzyme-linked immunosorbent assay.

Results: Patients who were discharged after 10 days had worse clinical outcomes and higher levels of BDNF since admission. There was correlation between BDNF levels and clinical parameters.

Conclusion: BDNF levels were associated with clinical prognosis in the acute phase of ischemic stroke.
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http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2018.11.013DOI Listing
March 2019

Circulating levels of adipokines are altered in patients with temporal lobe epilepsy.

Epilepsy Behav 2019 01 7;90:137-141. Epub 2018 Dec 7.

Laboratório Interdisciplinar de Investigação Médica, Medical School, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil; Neuropsychiatry Program, Department of Psychiatry and Behavioral Sciences, School of Medicine, University of Texas Health Science Center at Houston, TX, United States.

Objective: A persistent low-grade inflammatory state has been described in patients with temporal lobe epilepsy (TLE) in the interictal period. Adipokines are cytokines produced by the adipose tissue that can influence inflammatory response. The purpose of this study was to evaluate the plasma levels of adipokines in patients with TLE in comparison with controls. In addition, we sought to investigate whether the levels of adipokines were associated with clinical parameters in TLE.

Methods: Forty patients with TLE and 40 controls were enrolled in this study. All participants were subjected to clinical assessment that included the Mini International Neuropsychiatric Interview (MINI) and the Hamilton Depression Rating Scale (HAM-D). Peripheral blood was drawn, and plasma levels of adipokines (adiponectin, leptin, and resistin) were measured by enzyme-linked immunoassay (ELISA).

Results: People with TLE presented higher leptin and lower adiponectin and resistin levels in comparison with controls. The levels of these adipokines correlated negatively with illness length but not with other clinical parameters. In a binary logistic regression model, higher leptin and lower adiponectin levels remained as significant predictors of TLE diagnosis.

Conclusions: These results corroborate the view that TLE is a multisystemic condition associated with low-grade inflammation.
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http://dx.doi.org/10.1016/j.yebeh.2018.11.023DOI Listing
January 2019

Evidence for a role of angiotensin converting enzyme 2 in proteinuria of idiopathic nephrotic syndrome.

Biosci Rep 2019 01 3;39(1). Epub 2019 Jan 3.

Interdisciplinary Laboratory of Medical Investigation, Faculty of Medicine, Universidade Federal de Minas Gerais (UFMG), Brazil

Renin angiotensin system (RAS) plays a role in idiopathic nephrotic syndrome (INS). Most studies investigated only the classical RAS axis. Therefore, the aims of the present study were to evaluate urinary levels of RAS molecules related to classical and to counter-regulatory axes in pediatric patients with INS, to compare the measurements with levels in healthy controls and to search for associations with inflammatory molecules, proteinuria and disease treatment. This cross-sectional study included 31 patients with INS and 19 healthy controls, matched for age and sex. Patients and controls were submitted to urine collection for measurement of RAS molecules [Ang II, Ang-(1-7), ACE and ACE2] by enzyme immunoassay and cytokines by Cytometric Bead Array. Findings in INS patients were compared according to proteinuria: absent (<150 mg/dl, = 15) and present (≥150 mg/dl, = 16). In comparison to controls, INS patients had increased Ang II, Ang-(1-7) and ACE, levels while ACE2 was reduced. INS patients with proteinuria had lower levels of ACE2 than those without proteinuria. ACE2 levels were negatively correlated with 24-h-proteinuria. Urinary concentrations of MCP-1/CCL2 were significantly higher in INS patients, positively correlated with Ang II and negatively with Ang-(1-7). ACE2 concentrations were negatively correlated with IP-10/CXCL-10 levels, which, in turn, were positively correlated with 24-h-proteinuria. INS patients exhibited changes in RAS molecules and in chemokines. Proteinuria was associated with low levels of ACE2 and high levels of inflammatory molecules.
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http://dx.doi.org/10.1042/BSR20181361DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6328887PMC
January 2019