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    Preditores de mortalidade e anos de vida perdidos ajustados por incapacidade (DALY) no traumatismo cranioencefálico grave em uma capital do sudeste do Brasil: um estudo observacional prospectivo
    (Universidade Federal do Espírito Santo, 2025-08-21) Grobério, Rodrigo Miranda; Arêas, Fernando Zanela da Silva; https://orcid.org/0000-0002-2068-2606; http://lattes.cnpq.br/2219697069216192; https://orcid.org/0009-0007-0005-7209; http://lattes.cnpq.br/7464873031004308; Salarolli, Luciane Bresciani; https://orcid.org/0000-0002-1881-0306; http://lattes.cnpq.br/3503255904138561; Schwarzbold, Marcelo Liborio; https://orcid.org/0000-0002-7260-7704; http://lattes.cnpq.br/0866862539864076; Gouvêa, Sônia Alves; https://orcid.org/0000-0001-5180-471X; http://lattes.cnpq.br/7268228122543743
    Severe traumatic brain injury (TBI) is a highly complex clinical condition and one of the leading causes of premature death and long-term functional disability worldwide. In Brazil, the lack of region-specific studies with robust data limits the understanding of its actual magnitude, especially in understudied areas. This study aimed to identify the main predictors of mortality and estimate the burden of disease—expressed in disability-adjusted life years (DALY) —in patients with severe TBI treated at a referral hospital in the metropolitan area of Vitória, Espírito Santo. This was a prospective, observational cohort study including 737 adult patients diagnosed with severe TBI (Glasgow Coma Scale ≤ 8), conducted between May 2021 and May 2023. Clinical, sociodemographic, laboratory, and neurosurgical variables were analyzed using binary logistic regression. The burden of disease was calculated based on the sum of years of life lost due to premature death (YLL) and years lived with disability (YLD). The overall mortality rate was 52.1%, predominantly affecting young men (81.4%), with a mean age of 44.4 years. Falls from standing height were the most frequent cause of injury (32.8%). In the acute phase (up to 7 days), mortality was independently associated with decompressive craniectomy, use of vasoactive drugs, and the presence of associated trauma. In the subacute phase (8 to 112 days), intracranial pressure monitoring (ICP) and thrombocytopenia were significant predictors of death. In the chronic phase (after 113 days), age over 65 years was the main predictor. The total burden of disease was estimated at 22,322.23 DALYs over 24 months, with a mean of 30.28 DALYs per patient and 593.41 DALYs per 100,000 inhabitants/year. The findings highlight the substantial impact of severe TBI on regional public health, emphasizing the urgent need for targeted prevention, care, and rehabilitation strategies focused on high-risk populations.
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    Análise dos níveis de espécies reativas de oxigênio, biomarcadores inflamatórios e imunológicos, e da função pulmonar em crianças e adolescentes com asma em Vitória – ES
    (Universidade Federal do Espírito Santo, 2025-09-25) Ferreira, Maiane Fernandes; Mill, José Geraldo; https://orcid.org/0000-0002-0987-368X; http://lattes.cnpq.br/2497419234600362; Meyrelles, Silvana Santos; https://orcid.org/0000-0003-0167-4093; http://lattes.cnpq.br/7731215198101947; https://orcid.org/0000-0002-2348-8323; http://lattes.cnpq.br/9367628468946101; Leite, Camila Ferreira; https://orcid.org/0000-0001-6375-8845; http://lattes.cnpq.br/7052858599464930; Nascimento, Lucas Rodrigues; https://orcid.org/0000-0002-6792-0819; http://lattes.cnpq.br/4634873197928322
    INTRODUCTION: Given the inflammatory effects triggered by the inhalation of pollutants that promote the production of reactive oxygen species (ROS), it is important to investigate the impact of exposure to air pollution on respiratory health, especially among children and adolescents with asthma, a particularly vulnerable group due to the ongoing development of their respiratory system. OBJECTIVES: To evaluate systemic levels of ROS, inflammatory and immunological biomarkers, as well as pulmonary function, in children and adolescents with and without a diagnosis of asthma residing in Vitória, Brazil. MATERIALS AND METHODS: This was an observational, cross-sectional study including 110 children and adolescents of both sexes, aged 6 to 15 years, with (n = 83) and without (n = 27) a previous diagnosis of asthma according to medical records from a Primary Health Care Unit. On a scheduled day, clinical assessments for pulmonary function (spirometry) were performed, and fasting blood samples were collected for complete blood count, basic biochemistry, and immunoglobulin measurements. A blood aliquot was stored at −80 °C for later quantification of ROS (superoxide anion and hydrogen peroxide) by flow cytometry. The study was approved by the Research Ethics Committee of CCS/UFES (Approval No. 3.546.535). Statistical analyses were performed using GraphPad Prism 9.0. Data were expressed as mean ± standard deviation, median and interquartile range (IQR), or percentage (%). Group comparisons were conducted using the Mann–Whitney test, Student’s t test, and Chi-square test, with significance set at p < 0.05. RESULTS: Patients with asthma showed higher eosinophil counts (447 [223–682] vs. 237 [157–410] N/mm³; p < 0.01) and higher IgE levels (548 [212–1091] vs. 138 [49.4–480] KU/L; p < 0.01) compared to controls. Regarding ROS production, there was a significant increase in superoxide anion levels (MIF) in the asthma group, with a median of 1295 [1162–1416], compared to the control group (1129 [973–1302]; p < 0.01). On the other hand, no significant difference was detected in hydrogen peroxide levels (MIF) between the asthma and control groups (3039 [1751–4293] vs. 2849 [1910–3403]; p = 0.34). Concerning pulmonary function, the asthma group presented lower Forced Expiratory Volume in the first second (FEV₁; %pred) compared to the non-asthma group (95.4 ± 15.9 vs. 105.0 ± 12.0; p < 0.01). Similarly, Forced Vital Capacity (FVC; %pred) was lower in the asthma group (100.4 ± 16.8 vs. 109.9 ± 15.2; p < 0.05). CONCLUSION: Children and adolescents with mild to moderate asthma exhibited greater inflammatory and oxidative activity, along with reduced pulmonary function, although still within normal clinical limits. Systemic quantification of ROS, particularly superoxide anion, proved sensitive in detecting oxidative activation, suggesting its potential as a complementary biomarker in the monitoring of asthma.
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    O ácido elágico melhora o padrão funcional hemodinâmico e previne o remodelamento cardíaco após infarto agudo do miocárdio em ratas ovariectomizadas
    (Universidade Federal do Espírito Santo, 2024-03-27) Gonçalves, Laís Lopes; Simões, Simone Alves de Almeida; https://orcid.org/0000-0002-9905-509X; http://lattes.cnpq.br/4036865618615755; Abreu, Glaucia Rodrigues de; https://orcid.org/0009-0008-8772-8470; http://lattes.cnpq.br/0229590907405570; https://orcid.org/0000-0002-8603-8354; http://lattes.cnpq.br/0964569425731887; Gouvea, Sônia Alves; https://orcid.org/0000-0001-5180-471X; http://lattes.cnpq.br/7268228122543743; Lemos, Virgínia Soares; https://orcid.org/0000-0003-1234-9325; http://lattes.cnpq.br/6575569264319071
    Postmenopausal women have a higher incidence of acute myocardial infarction (MI) and a worse prognosis. The main cause of fibrosis and heart failure is MI. We previously demonstrated that Ellagic acid (EA) attenuates diastolic dysfunction by reducing cardiac oxidative stress. Here, we examined the effect of the administration of EA on cardiac fibrosis and other pathological effects induced by MI in female rats that have been exposed to estrogen deprivation. Ovariectomized Wistar rats were subjected to coronary artery ligation to induce MI. The EA (30 mg/kg) was administered by oral gavage daily for four weeks. Hemodynamic parameters were measured through cannulation of the carotid artery. Picrosirius red staining was used to evaluate collagen deposition and to determine the size of the infarction. MMP-8 expression was measured by immunofluorescence. Nitric oxide (NO) and reactive oxygen species (ROS) production were quantified by the DAF-2 and DHE probes, respectively. ELISA was used for the quantification of inflammatory cytokines. MI promoted ventricular dysfunction and cardiac fibrosis. Oral administration of EA reduced the size of the myocardial lesion, improved hemodynamic parameters, decreased the deposition of total collagen, and type I collagen, and increased the deposition of type III collagen. MMP-8 expression and IL-6 production were increased in the heart after MI and EA decreased them. Finally, the administration of EA increased the production of in situ NO and decreased the production of ROS. These data highlight that oral treatment with EA may be a potential natural therapeutic for menopausal women under cardiac stress.
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    Preditores de mortalidade e recuperação funcional após traumatismo cranioencefálico grave: um estudo observacional prospectivo do tipo coorte
    (Universidade Federal do Espírito Santo, 2023-10-06) Goncalves, Jéssica Vaz; Arêas, Fernando Zanela da Silva; https://orcid.org/0000-0002-2068-2606; http://lattes.cnpq.br/2219697069216192; https://orcid.org/0000000157960043; http://lattes.cnpq.br/9396185941965261; Nascimento, Lucas Rodrigues; https://orcid.org/0000-0002-6792-0819; http://lattes.cnpq.br/4634873197928322
    Severe Traumatic Brain Injury (TBI) is a significant global public health issue, considered the leading cause of mortality and disability in young adults. Some clinical, neurosurgical, and sociodemographic factors have already been described as predictors of higher risks of in-hospital mortality and lower levels of functional recovery after the traumatic event. Identifying these predictive factors is crucial for guiding treatment and prognosis strategies, as well as shaping public health policies for this population. The aim of this study was to identify predictors of mortality and functional recovery from hospital admission up to 12 months after severe TBI. This was a prospective observational cohort study conducted at a trauma referral hospital in the state of Espírito Santo, Brazil. All individuals diagnosed with severe TBI over the age of 18 admitted within a one-year period were included. The analyzed outcomes were in-hospital mortality and functional recovery assessed using the Extended Glasgow Outcome Scale (GOSE) at the time of hospital discharge, 3, 6, and 12 months after TBI. After applying the inclusion criteria, 383 patients were included, of which 211 (55%) died, and 172 (45%) survived hospitalization. Among these, 145 completed the one-year follow-up. The mean age was 49 years, 80% were male, and falls (46.5%) were the main cause of injury. In the final binomial logistic regression model, age over 65 years, days on mechanical ventilation, and low educational level were strong predictors of unfavorable functional recovery over the 12 months following the trauma. Pupillary changes, such as anisocoria and mydriasis, high respiratory rate, decreased body temperature, ISS scores >25, and the performance of decompressive craniectomy were associated with a higher risk of in-hospital mortality. This study was the first to investigate predictors of mortality and functional recovery one year after severe Traumatic Brain Injury in the Brazilian population. The higher mortality rate in TBI patients compared to both high-income countries (HICs) and low- and middleincome countries (LMICs) underscores the importance of considering regional disparities when developing and implementing TBI management strategies worldwide.
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    A PRIVAÇÃO ANDROGÊNICA DE LONGO PRAZO MODULA A REATIVIDADE VASCULAR POR VIAS DEPENDENTES DE ALDOSTERONA E ANGIOTENSINA II
    (Universidade Federal do Espírito Santo, 2022-08-31) Costa, Anna Karolina Nascimento; Stefanon, Ivanita; https://orcid.org/0000-0003-2638-5183; http://lattes.cnpq.br/8456612999765726; https://orcid.org/; http://lattes.cnpq.br/0575590472541198; Bissoli, Nazare Souza; https://orcid.org/; http://lattes.cnpq.br/8865368585732583; Davel, Ana Paula Couto; https://orcid.org/; http://lattes.cnpq.br/
    Testosterone is a vasoactive hormone, which acts by genomic and non-genomic mechanisms. Acutely, it may have endothelium-dependent vasodilatory actions. However, the long-term modulation of testosterone on the regulation of vascular tone remains unclear. The hypothesis of this study is that, in the long term, testosterone participates in the vascular reactivity regulation, dependent on the renin-angiotensin- aldosterone system. Wistar rats (N=128), at 12 weeks of age, were divided into male Control (SHAM) and orchiectomy surgery (OQT), treated for 3 months with losartan, an angiotensin II receptor blocker (SHAM+LOS and OQT+ LOS), 15 mg/kg, s.c); spironolactone (SHAM+SPI and OQT+SPI, 80 mg/kg, gavage), mineralocorticoid receptor antagonist and apocynin, NADPH oxidase inhibitor (SHAM+APO and OQT+APO, 30 mg/kg, drinking water), Vascular reactivity was analysed in isolated aortic rings, as the percentage of response to KCl (75 mM), superfused with modified Krebs pH 7.4, 36.5oC. The presence of vascular presence was observed in vitro as curves-response to phenylephrine (10-11 to 10-3 M) and absence of: L-NAME, 100 μM; indomethacin (INDO, 10 μM) and endothelium-denuded rings (E-). Plasma lipid peroxidation was measured using the TBARS technique. (CEUA-UFES 017/2020). Results were expressed as mean ± SEM and using Student's t test, analysis of variance (ANOVA), one way. The OQT groups, untreated and OQT treated with APO and LOS, had lower body weight at the end of the 3 months (SHAM 231 ± 11g; OQT= 158,4 ± 13,0g*; OQT+APO 208,3 ± 15,4g; OQT+LOS 156,0 ± 23,0g *p<0,05). The Rmax for phenylephrine was the same between the SHAM and OQT groups. Treatments for 3 months with LOS and APO did not change Rmax to phenylephrine. However, LOS treatment reduced the pD2 of the OQT group (log EC50: OQT= -6.240 ± 0.15 vs OQT+LOS= -7.218 ± 0.23 *p<0.01). Inhibition of MR receptors with spironolactone determined a lower maximal contraction to phenylephrine in the OQT group than in the SHAM, suggesting that this pathway could be testosterone dependent. (SHAM+SPI =120.4 ± 7.56% n=10 vs OQT+SPI= 93.3 ± 10.2% n=10; *p<0.05). Phenylephrine reactivity increased in the presence of L-NAME and in the absence of E, similarly between the groups. Inhibition of the COX pathway with indomethacin determined a reduction in Rmax in both groups (Rmax SHAM= 118.3 ± 8.04 vs SHAM+INDO = 56.27 ± 6.61, p <0.01 and OQT= 119.8 ± 8.41 vs OQT+INDO= 72.64 ± 9.34, p<0.01). There was no difference in reactivity between the groups incubated with indomethacin (SHAM+INDO and OQT+INDO). There was a reduction in RMax, in the presence of indomethacin, only in the OQT+SPI group. This result suggests the participation of aldosterone in the COX activation pathway, possibly of a vasoconstrictor, since in the SHAM+SPI group, indomethacin reduced the maximum contraction (Rmax: SHAM+SPI = 120.4 ± 7.56; OQT+ SPI= 93.28 ± 10.18; SHAM+SPI+INDO = 89.99 ± 8.45; OQT+SPI+INDO = 74.15 ± 7.92, * p <0.05). Endothelial NO bioavaliability seems to have been modified in the group treated with losartan, especially in the OQT+LOS- LN group, suggesting the importance of the testosterone pathway in the production of NO mediated by angiotensin II receptors. These data suggest that testosterone participates in the production of NO mediated by angio II, because when we remove the production of NO, through the LN, in the OQT group, there was a reduction in Rmax in relation to its control. Is suggests the importance of testosterone in the contractile response. mediated by the AT1 angiotensin receptor (Rmax: SHAM+LOS = 127.5 ± 5.63; OQT+LOS = 135.6 ± 4.74; SHAM+LOS LN = 183.4 ± 10.50; OQT+LOS LN = 151.8 ± 8.311; * p<0.05). The effects of treatment with the angiotensin II inhibitor, losartan, on rings without endothelium, showed that the endothelium injury caused an increase in the response to phenylephrine in the SHAM group. However, there was no difference between the OQT+LOS E- and OQT+LOS CT groups, suggesting a vasoconstrictor positive modulation that depends on the presence of angiotensin II. These data suggest that testosterone participates in the production of NO mediated by angio II, because when we remove the production of NO, through the LN, in the castrated group there is a reduction in Rmax in relation to its control, suggesting the importance of testosterone in the contractile response. mediated by the AT1 angiotensin receptor (Rmax: SHAM+LOS = 127.5 ± 5.63; OQT+LOS = 135.6 ± 4.74; SHAM+LOS LN = 183.4 ± 10.50; OQT+LOS LN = 151.8 ± 8.311; * p<0.05). The effects of treatment with the angiotensin II inhibitor, losartan, on rings without endothelium, showed that the endothelium injury caused an increase in the response to phenylephrine in the SHAM group. However, there was no difference between the OQT+LOS E- and OQT+LOS CT groups, suggesting a vasoconstrictor positive modulation that depends on the presence of angiotensin II. Orchidectomy modified the endothelium-dependent response during treatment with losartam (Rmax: SHAM+LOS = 127.5 ± 5.63; OQT+LOS = 135.6 ± 4.74; SHAM+LOS E- = 217.3 ± 217.3 ± 26.77; OQT+LOS E- = 145.3 ± 7.90. * p<0.05). In conclusion, the set of these results suggest the long term participation of testosterone and aldosterone in the modulation of vascular contraction induced by phenylephrine.