ABSTRACT
Fibroelastomas are the second most common benign cardiac tumor1. They are small avascular structures with a mean size of 9mm, ranging up to 70mm, usually attached to the heart valves' surface (aortic and mitral are the most affected, followed by tricuspid and pulmonary valves). Their etiology is unclear, but the hypothesis of coalescence of microthrombus at the coaptation margins of valves is the most widely accepted theory. On echocardiography, they are pedicled, mobile, with a filamentous surface, and usually have a speckled appearance with echolucencies and a stippled pattern near the edges. Clinically, they may be associated with embolic phenomena; however, in most cases, the diagnosis is incidental. We present a series of four clinical cases with an incidental diagnosis of fibroelastomas across the four cardiac valves as assessed by transthoracic echocardiography (Video 1; Figure 1). Video 1 From left to right and top to bottom: fibroelastomas of the anterior leaflet of the tricuspid valve, anterior leaflet of the mitral valve, left cusp of the pulmonary valve and left cuspid of the aortic valve, each corresponding to a different patient. Link: http://abccardiol.org/supplementary-material/2024/12102/2023-0222_IM_video01.mp4 Figure 1 From left to right and top to bottom: fibroelastomas of the anterior leaflet of the tricuspid valve, anterior leaflet of the mitral valve, left cusp of the pulmonary valve and left cuspid of the aortic valve, each corresponding to a different patient.
Os fibroelastomas são o segundo tumor cardíaco benigno mais comum. São estruturas pequenas, avasculares, com uma dimensão média de 9mm, podendo atingir até 70mm, habitualmente aderentes à superfície das válvulas cardíacas (válvulas aórtica e mitral são as mais comumente afetadas, seguidas das válvulas tricúspide e pulmonar). A etiologia não é clara, sendo a hipótese de formação de microtrombos nas margens de coaptação das válvulas a mais aceite. Na ecocardiografia apresentam aspeto pediculado, móvel, com superfície filamentosa, tipicamente com uma aparência pontilhada nas margens e ecolucente. Do ponto de vista clínico, podem estar associados a fenómenos embólicos, no entanto, na maioria dos casos o diagnóstico é incidental. Apresentamos de seguida quatro casos de diagnóstico incidental de fibroelastomas nas quatro válvulas cardíacas, diagnosticados por ecocardiograma transtorácico (ETT) (Vídeo 1; Figura 1). Vídeo 1Da esquerda para a direita, de cima para baixo: fibroelastomas no folheto anterior da válvula tricúspide, folheto anterior da válvula mitral, cúspide esquerda da válvula pulmonar e cúspide esquerda da válvula aórtica, cada um correspondendo a um doente diferente. Em: http://abccardiol.org/supplementary-material/2024/12102/2023-0222_IM_video01.mp4 Figura 1Da esquerda para a direita, de cima para baixo: fibroelastomas no folheto anterior da válvula tricúspide, folheto anterior da válvula mitral, cúspide esquerda da válvula pulmonar e cúspide esquerda da válvula aórtica, cada um correspondendo a um doente diferente.
Subject(s)
Echocardiography , Incidental Findings , Humans , Aorta , Mitral Valve/diagnostic imaging , Tricuspid Valve/diagnostic imagingABSTRACT
Resumo Os fibroelastomas são o segundo tumor cardíaco benigno mais comum. São estruturas pequenas, avasculares, com uma dimensão média de 9mm, podendo atingir até 70mm, habitualmente aderentes à superfície das válvulas cardíacas (válvulas aórtica e mitral são as mais comumente afetadas, seguidas das válvulas tricúspide e pulmonar). A etiologia não é clara, sendo a hipótese de formação de microtrombos nas margens de coaptação das válvulas a mais aceite. Na ecocardiografia apresentam aspeto pediculado, móvel, com superfície filamentosa, tipicamente com uma aparência pontilhada nas margens e ecolucente. Do ponto de vista clínico, podem estar associados a fenómenos embólicos, no entanto, na maioria dos casos o diagnóstico é incidental. Apresentamos de seguida quatro casos de diagnóstico incidental de fibroelastomas nas quatro válvulas cardíacas, diagnosticados por ecocardiograma transtorácico (ETT) (Vídeo 1; Figura 1). Vídeo 1 Da esquerda para a direita, de cima para baixo: fibroelastomas no folheto anterior da válvula tricúspide, folheto anterior da válvula mitral, cúspide esquerda da válvula pulmonar e cúspide esquerda da válvula aórtica, cada um correspondendo a um doente diferente. Em: http://abccardiol.org/supplementary-material/2024/12102/2023-0222_IM_video01.mp4 Figura 1 Da esquerda para a direita, de cima para baixo: fibroelastomas no folheto anterior da válvula tricúspide, folheto anterior da válvula mitral, cúspide esquerda da válvula pulmonar e cúspide esquerda da válvula aórtica, cada um correspondendo a um doente diferente.
Abstract Fibroelastomas are the second most common benign cardiac tumor1. They are small avascular structures with a mean size of 9mm, ranging up to 70mm, usually attached to the heart valves' surface (aortic and mitral are the most affected, followed by tricuspid and pulmonary valves). Their etiology is unclear, but the hypothesis of coalescence of microthrombus at the coaptation margins of valves is the most widely accepted theory. On echocardiography, they are pedicled, mobile, with a filamentous surface, and usually have a speckled appearance with echolucencies and a stippled pattern near the edges. Clinically, they may be associated with embolic phenomena; however, in most cases, the diagnosis is incidental. We present a series of four clinical cases with an incidental diagnosis of fibroelastomas across the four cardiac valves as assessed by transthoracic echocardiography (Video 1; Figure 1). Video 1 From left to right and top to bottom: fibroelastomas of the anterior leaflet of the tricuspid valve, anterior leaflet of the mitral valve, left cusp of the pulmonary valve and left cuspid of the aortic valve, each corresponding to a different patient. Link: http://abccardiol.org/supplementary-material/2024/12102/2023-0222_IM_video01.mp4 Figure 1 From left to right and top to bottom: fibroelastomas of the anterior leaflet of the tricuspid valve, anterior leaflet of the mitral valve, left cusp of the pulmonary valve and left cuspid of the aortic valve, each corresponding to a different patient.
ABSTRACT
Objetivo: realizar uma revisão na literatura para caracterizar o perfil epidemiológico das lesões traumáticas provocadas pela prática dessa modalidade. Metodologia: realizou-se uma revisão narrativa da literatura acerca das lesões decorrentes da prática esportiva do kitesurf na base de dados da Scielo, Ovid MEDLINE e Google Scholar de artigos de janeiro de 2000 a dezembro de 2022. Resultados: foram eleitos 14 artigos que se ajustaram aos objetivos dessa revisão. Mediante análise dos artigos, foram encontradas discussões que direcionam os principais mecanismos de trauma, riscos de lesões, estruturas mais frequentemente acometidas e propostas para minimizar os danos e a recuperação. Conclusão: as lesões que podem acometer os praticantes deste esporte aquático, em sua maioria, são leves e principalmente nos membros inferiores; entretanto, podem ser letais, o que desperta a necessidade de maior investigação epidemiológica e clínica dos casos atendidos, bem como a adoção de medidas de prevenção.
Objective: the objective of this study is to conduct a literature review to characterize the epidemiological profile of traumatic injuries caused by the practice of this modality. Methods: a narrative review of the literature was carried out on injuries resulting from the practice of kitesurfing in the database of Scielo, Ovid MEDLINE, and Google Scholar articles from January 2000 to December 2022. Results: 14 articles were chosen that suited the objectives of this review. Through the analysis of the articles, discussions were found that guide the main mechanisms of trauma, risk of injuries, structures most frequently affected, and proposals to minimize damage and recovery. Conclusion: the injuries that can affect practitioners of this aquatic sport are mostly mild and mainly in the lower members; however, they can be lethal, which raises the need for further epidemiological and clinical investigation of the cases treated, as well as the adoption of measures of prevention.
Subject(s)
Humans , Wounds and Injuries , Accident PreventionABSTRACT
Cardiorenal syndrome (CRS) is a pathological link between the kidneys and heart, in which an insult in a kidney or heart leads the other organ to incur damage. CRS is classified into five subtypes, and type 3 (CRS3) is characterized by acute kidney injury as a precursor to subsequent cardiovascular changes. Mitochondrial dysfunction and oxidative and nitrosative stress have been reported in the pathophysiology of CRS3. It is known that vitamin C, an antioxidant, has proven protective capacity for cardiac, renal, and vascular endothelial tissues. Therefore, the present study aimed to assess whether vitamin C provides protection to heart and the kidneys in an in vivo CRS3 model. The unilateral renal ischemia and reperfusion (IR) protocol was performed for 60 min in the left kidney of adult mice, with and without vitamin C treatment, immediately after IR or 15 days after IR. Kidneys and hearts were subsequently collected, and the following analyses were conducted: renal morphometric evaluation, serum urea and creatinine levels, high-resolution respirometry, amperometry technique for NO measurement, gene expression of mitochondrial dynamic markers, and NOS. The analyses showed that the left kidney weight was reduced, urea and creatinine levels were increased, mitochondrial oxygen consumption was reduced, NO levels were elevated, and Mfn2 expression was reduced after 15 days of IR compared to the sham group. Oxygen consumption and NO levels in the heart were also reduced. The treatment with vitamin C preserved the left kidney weight, restored renal function, reduced NO levels, decreased iNOS expression, elevated constitutive NOS isoforms, and improved oxygen consumption. In the heart, oxygen consumption and NO levels were improved after vitamin C treatment, whereas the three NOS isoforms were overexpressed. These data indicate that vitamin C provides protection to the kidneys and some beneficial effects to the heart after IR, indicating it may be a preventive approach against cardiorenal insults.
Subject(s)
Ascorbic Acid/pharmacology , Cardio-Renal Syndrome/pathology , Kidney/pathology , Mitochondria/pathology , Animals , Cell Respiration/drug effects , Isoenzymes/metabolism , Kidney/drug effects , Kidney/physiopathology , Male , Mice, Inbred C57BL , Mitochondria/drug effects , Mitochondrial Dynamics/drug effects , Models, Biological , Nitric Oxide/metabolism , Nitric Oxide Synthase/metabolism , Reperfusion Injury/pathology , Reperfusion Injury/physiopathologyABSTRACT
Deforestation and habitat loss resulting from land use changes are some of the utmost anthropogenic impacts that threaten tropical birds in human-modified landscapes (HMLs). The degree of these impacts on birds' diet, habitat use, and ecological niche can be measured by isotopic analysis. We investigated whether the isotopic niche width, food resources, and habitat use of bird trophic guilds differed between HMLs and natural landscapes (NLs) using stable carbon (δ13C) and nitrogen isotopes (δ15N). We analyzed feathers of 851 bird individuals from 28 landscapes in the Brazilian Atlantic Forest. We classified landscapes into two groups according to the percentage of forest cover (HMLs ≤ 30%; NLs ≥ 47%), and compared the isotopic niche width and mean values of δ13C and δ15N for each guild between landscape types. The niches of frugivores, insectivores, nectarivores, and omnivores were narrower in HMLs, whereas granivores showed the opposite pattern. In HMLs, nectarivores showed a reduction of 44% in niche width, while granivores presented an expansion of 26%. Individuals in HMLs consumed more resources from agricultural areas (C4 plants), but almost all guilds showed a preference for forest resources (C3 plants) in both landscape types, except granivores. Degraded and fragmented landscapes typically present a lower availability of habitat and food resources for many species, which was reflected by the reduction in niche width of birds in HMLs. Therefore, to protect the diversity of guilds in HMLs, landscape management strategies that offer birds more diverse habitats must be implemented in tropical regions.
Subject(s)
Birds , Forests , Agriculture , Animals , Brazil , Ecosystem , HumansSubject(s)
Computed Tomography Angiography , Metoprolol , Angiography , Child , Heart Rate , Humans , Outpatients , Tomography, X-Ray ComputedSubject(s)
Humans , Child , Computed Tomography Angiography , Metoprolol , Outpatients , Angiography , Tomography, X-Ray Computed , Heart RateABSTRACT
Ecological restoration is a traditional option for recovering biodiversity and ecosystem functions. Birds perform pollination, seed dispersal, and pest-control services, which catalyze increases in habitat structure. Habitat complexity changes bird composition, but there is little evidence of its effects on bird functional diversity in Neotropical restorations. We tested whether bird functional diversity and composition respond to increased habitat complexity. Point-counts were performed (January-December 2015) in an area undergoing restoration (536 ha) in the Atlantic Forest of southeastern Brazil, in restorations with less and more structured vegetation and pastures and forest-fragments. The functional bird traits considered were diet, habitat, biomass, environmental sensitivity, and foraging strata. Increased habitat complexity was evaluated using plant characteristics (exotic grass, canopy, herbaceous cover, and diameter at breast height). A total of 172 bird species (5% endemic; 12% migratory) were recorded. Increased vegetation structure in both restored sites and forest-fragments drove a reorganization and addition of functional bird traits, which positively influenced functional richness, dispersion, and evenness. Shifts in plant-characteristics rearranged bird functional traits (diet-forest-dependence and diet-strata-foraging). The rapid development of vegetation structure is a key factor for restoration because it provides additional habitat for semi-dependent forest birds and enhances resilience and sustainability in new man-made forests.
Subject(s)
Ecosystem , Forests , Animals , Biodiversity , Birds , Brazil , Conservation of Natural ResourcesABSTRACT
We investigated redox homeostasis in cerebral and peripheral tissues of wild type (WT) and glutaryl-CoA dehydrogenase knockout mice (Gcdh-/-) submitted to inflammation induced by lipopolysaccharide (LPS) since patients with glutaric aciduria type I (GA I) manifest acute encephalopathy during catabolic events triggered by inflammation. WT and Gcdh-/- mice fed a low (0.9%) or high (4.7%) Lys chow were euthanized 4 h after LPS intraperitoneal injection. Cerebral cortex of Lys-restricted Gcdh-/- animals presented no alterations of redox homeostasis, whereas those fed a high Lys chow showed increased malondialdehyde (MDA) levels and superoxide dismutase (SOD) activity, compared to WT mice. Furthermore, Gcdh-/- mice receiving low Lys and injected with LPS presented elevated MDA levels and decreased reduced glutathione (GSH) concentrations, glutathione peroxidase (GPx), and glutathione reductase (GR) activities in cerebral cortex. LPS administration also decreased GSH values, as well as GPx and GR activities in cerebral cortex of Gcdh-/- mice receiving Lys overload. Further experiments performed in WT and Gcdh-/- mice injected with LPS and receiving either a low or high Lys chow revealed increased MDA levels and decreased GSH concentrations in cerebral cortex and striatum, but not in hippocampus, liver and heart of Gcdh-/- mice, suggesting a selective vulnerability of these cerebral structures to oxidative stress during an inflammatory process. LPS administration also increased S100B and NF-κF protein levels in brain of Gcdh-/- mice receiving high Lys. These data support the hypothesis that low Lys diet is beneficial in GA I by preventing redox imbalance, whereas a high Lys diet or systemic inflammation per se or combined induce oxidative stress in striatum and cerebral cortex that are mainly damaged in this disorder.
Subject(s)
Cerebral Cortex/metabolism , Corpus Striatum/metabolism , Glutaryl-CoA Dehydrogenase/deficiency , Inflammation Mediators/metabolism , Lipopolysaccharides/toxicity , Oxidative Stress/physiology , Animals , Cerebral Cortex/drug effects , Corpus Striatum/drug effects , Dose-Response Relationship, Drug , Female , Male , Mice , Mice, 129 Strain , Mice, Knockout , Oxidative Stress/drug effectsABSTRACT
Melanoma is a malignant proliferative disease originated in melanocytes, characterized by high metastatic activity and by the activation of oncogenes, such as B-RAF (40-60% of cases). Recent studies have shown that vemurafenib (a MAPK inhibitor) promoted disturbance of mitochondrial bioenergetics, although underlying mechanisms are not fully comprehended. Here we showed that MAPK inhibition by vemurafenib in B-RAFV600E-mutated human melanoma culminated in the inhibition of DRP1 phosphorylation, associated to a large mitochondrial network remodeling to the hyperfused phenotype, and increased oxidative phosphorylation capacity. Such alterations may be associated to melanoma resistance to vemurafenib, since the impairment of oxidative phosphorylation increased the vemurafenib cytotoxicity. These results point to the potential of mitochondrial dynamics as a targetable pathway in melanoma.
Subject(s)
Antineoplastic Agents/pharmacology , Gene Expression Regulation, Neoplastic , Mitochondrial Dynamics/drug effects , Mitogen-Activated Protein Kinases/genetics , Protein Kinase Inhibitors/pharmacology , Proto-Oncogene Proteins B-raf/genetics , Vemurafenib/pharmacology , Cell Line, Tumor , Drug Resistance, Neoplasm/genetics , Dynamins/antagonists & inhibitors , Dynamins/genetics , Dynamins/metabolism , Humans , Melanocytes/drug effects , Melanocytes/metabolism , Melanocytes/pathology , Mitochondria/drug effects , Mitochondria/metabolism , Mitogen-Activated Protein Kinases/metabolism , Molecular Targeted Therapy , Mutation , Oxidative Phosphorylation/drug effects , Phosphorylation/drug effects , Proto-Oncogene Proteins B-raf/metabolism , Signal TransductionABSTRACT
Scientists have long been trying to understand why the Neotropical region holds the highest diversity of birds on Earth. Recently, there has been increased interest in morphological variation between and within species, and in how climate, topography, and anthropogenic pressures may explain and affect phenotypic variation. Because morphological data are not always available for many species at the local or regional scale, we are limited in our understanding of intra- and interspecies spatial morphological variation. Here, we present the ATLANTIC BIRD TRAITS, a data set that includes measurements of up to 44 morphological traits in 67,197 bird records from 2,790 populations distributed throughout the Atlantic forests of South America. This data set comprises information, compiled over two centuries (1820-2018), for 711 bird species, which represent 80% of all known bird diversity in the Atlantic Forest. Among the most commonly reported traits are sex (n = 65,717), age (n = 63,852), body mass (n = 58,768), flight molt presence (n = 44,941), molt presence (n = 44,847), body molt presence (n = 44,606), tail length (n = 43,005), reproductive stage (n = 42,588), bill length (n = 37,409), body length (n = 28,394), right wing length (n = 21,950), tarsus length (n = 20,342), and wing length (n = 18,071). The most frequently recorded species are Chiroxiphia caudata (n = 1,837), Turdus albicollis (n = 1,658), Trichothraupis melanops (n = 1,468), Turdus leucomelas (n = 1,436), and Basileuterus culicivorus (n = 1,384). The species recorded in the greatest number of sampling localities are Basileuterus culicivorus (n = 243), Trichothraupis melanops (n = 242), Chiroxiphia caudata (n = 210), Platyrinchus mystaceus (n = 208), and Turdus rufiventris (n = 191). ATLANTIC BIRD TRAITS (ABT) is the most comprehensive data set on measurements of bird morphological traits found in a biodiversity hotspot; it provides data for basic and applied research at multiple scales, from individual to community, and from the local to the macroecological perspectives. No copyright or proprietary restrictions are associated with the use of this data set. Please cite this data paper when the data are used in publications or teaching and educational activities.
ABSTRACT
Arrhythmogenic right ventricular dysplasia is a classic form of chronic myocardial disease with a broad phenotypical spectrum. We report an atypical case of a patient with biventricular arrhythmogenic cardiomyopathy. Although the current diagnosis criteria are the most widely accepted ones, they focus solely on the right ventricular phenotype. The use of late gadolinium enhancement in cardiac magnetic resonance in this patient was essential for the diagnosis and assessment of the left ventricular involvement extent. This tool allows a broader use of current diagnosis criteria for this disease
Subject(s)
Humans , Male , Female , Middle Aged , Arrhythmias, Cardiac , Arrhythmogenic Right Ventricular Dysplasia , Cardiomyopathies , Phenotype , Stroke Volume , Magnetic Resonance Spectroscopy/methods , Electrocardiography, Ambulatory/methods , Death, Sudden, Cardiac , Electrocardiography/methods , Heart VentriclesABSTRACT
OBJECTIVE: To assess the predictors of de novo atrial fibrillation in patients in a non-cardiac intensive care unit. METHODS: A total of 418 hospitalized patients were analyzed between January and September 2016 in a non-cardiac intensive care unit. Clinical characteristics, interventions, and biochemical markers were recorded during hospitalization. In-hospital mortality and length of hospital stay in the intensive care unit were also evaluated. RESULTS: A total of 310 patients were included. The mean age of the patients was 61.0 ± 18.3 years, 49.4% were male, and 23.5% presented de novo atrial fibrillation. The multivariate model identified previous stroke (OR = 10.09; p = 0.016) and elevated levels of pro-B type natriuretic peptide (proBNP, OR = 1.28 for each 1,000pg/mL increment; p = 0.004) as independent predictors of de novo atrial fibrillation. Analysis of the proBNP receiver operating characteristic curve for prediction of de novo atrial fibrillation revealed an area under the curve of 0.816 (p < 0.001), with a sensitivity of 65.2% and a specificity of 82% for proBNP > 5,666pg/mL. There were no differences in mortality (p = 0.370), but the lengths of hospital stay (p = 0.002) and stay in the intensive care unit (p = 0.031) were higher in patients with de novo atrial fibrillation. CONCLUSIONS: A history of previous stroke and elevated proBNP during hospitalization were independent predictors of de novo atrial fibrillation in the polyvalent intensive care unit. The proBNP is a useful and easy- and quick-access tool in the stratification of atrial fibrillation risk.
OBJETIVO: Avaliar quais os preditores de fibrilação atrial de novo em doentes de uma unidade de cuidados intensivos não cardíaca. MÉTODOS: Foram analisados 418 doentes internados entre janeiro e setembro de 2016 em uma unidade de cuidados intensivos não cardíaca. Registaram-se as características clínicas, as intervenções efetuadas e os marcadores bioquímicos durante a internação. Avaliaram-se ainda a mortalidade hospitalar e o tempo de internação hospitalar e na unidade de cuidados intensivos. RESULTADOS: Foram incluídos 310 doentes, com média de idades de 61,0 ± 18,3 anos, 49,4% do sexo masculino, 23,5% com fibrilação atrial de novo. O modelo multivariável identificou acidente vascular cerebral prévio (OR de 10,09; p = 0,016) e valores aumentados de proBNP (OR de 1,28 por cada aumento em 1.000pg/mL; p = 0,004) como preditores independentes de fibrilação atrial de novo. A análise por curva Característica de Operação do Receptor do proBNP para predição de fibrilação atrial de novo revelou área sob a curva de 0,816 (p < 0,001), com sensibilidade de 65,2% e especificidade de 82% para proBNP > 5.666pg/mL. Não se verificaram diferenças na mortalidade (p = 0,370), porém a duração da internação hospitalar (p = 0,002) e na unidade de cuidados intensivos (p = 0,031) foi superior nos doentes com fibrilação atrial de novo. CONCLUSÕES: História de acidente vascular cerebral prévio e proBNP elevado em internação constituíram preditores independentes de fibrilação atrial de novo na unidade de cuidados intensivos polivalente. O proBNP pode constituir ferramenta útil, de fácil e rápido acesso na estratificação do risco de fibrilação atrial.
Subject(s)
Atrial Fibrillation/epidemiology , Hospitalization/statistics & numerical data , Intensive Care Units , Natriuretic Peptide, Brain/metabolism , Peptide Fragments/metabolism , Adult , Aged , Biomarkers/metabolism , Female , Hospital Mortality , Humans , Length of Stay , Male , Middle Aged , Multivariate Analysis , Prognosis , ROC Curve , Retrospective Studies , Risk Factors , Sensitivity and SpecificityABSTRACT
RESUMO Objetivo: Avaliar quais os preditores de fibrilação atrial de novo em doentes de uma unidade de cuidados intensivos não cardíaca. Métodos: Foram analisados 418 doentes internados entre janeiro e setembro de 2016 em uma unidade de cuidados intensivos não cardíaca. Registaram-se as características clínicas, as intervenções efetuadas e os marcadores bioquímicos durante a internação. Avaliaram-se ainda a mortalidade hospitalar e o tempo de internação hospitalar e na unidade de cuidados intensivos. Resultados: Foram incluídos 310 doentes, com média de idades de 61,0 ± 18,3 anos, 49,4% do sexo masculino, 23,5% com fibrilação atrial de novo. O modelo multivariável identificou acidente vascular cerebral prévio (OR de 10,09; p = 0,016) e valores aumentados de proBNP (OR de 1,28 por cada aumento em 1.000pg/mL; p = 0,004) como preditores independentes de fibrilação atrial de novo. A análise por curva Característica de Operação do Receptor do proBNP para predição de fibrilação atrial de novo revelou área sob a curva de 0,816 (p < 0,001), com sensibilidade de 65,2% e especificidade de 82% para proBNP > 5.666pg/mL. Não se verificaram diferenças na mortalidade (p = 0,370), porém a duração da internação hospitalar (p = 0,002) e na unidade de cuidados intensivos (p = 0,031) foi superior nos doentes com fibrilação atrial de novo. Conclusões: História de acidente vascular cerebral prévio e proBNP elevado em internação constituíram preditores independentes de fibrilação atrial de novo na unidade de cuidados intensivos polivalente. O proBNP pode constituir ferramenta útil, de fácil e rápido acesso na estratificação do risco de fibrilação atrial.
ABSTRACT Objective: To assess the predictors of de novo atrial fibrillation in patients in a non-cardiac intensive care unit. Methods: A total of 418 hospitalized patients were analyzed between January and September 2016 in a non-cardiac intensive care unit. Clinical characteristics, interventions, and biochemical markers were recorded during hospitalization. In-hospital mortality and length of hospital stay in the intensive care unit were also evaluated. Results: A total of 310 patients were included. The mean age of the patients was 61.0 ± 18.3 years, 49.4% were male, and 23.5% presented de novo atrial fibrillation. The multivariate model identified previous stroke (OR = 10.09; p = 0.016) and elevated levels of pro-B type natriuretic peptide (proBNP, OR = 1.28 for each 1,000pg/mL increment; p = 0.004) as independent predictors of de novo atrial fibrillation. Analysis of the proBNP receiver operating characteristic curve for prediction of de novo atrial fibrillation revealed an area under the curve of 0.816 (p < 0.001), with a sensitivity of 65.2% and a specificity of 82% for proBNP > 5,666pg/mL. There were no differences in mortality (p = 0.370), but the lengths of hospital stay (p = 0.002) and stay in the intensive care unit (p = 0.031) were higher in patients with de novo atrial fibrillation. Conclusions: A history of previous stroke and elevated proBNP during hospitalization were independent predictors of de novo atrial fibrillation in the polyvalent intensive care unit. The proBNP is a useful and easy- and quick-access tool in the stratification of atrial fibrillation risk.
Subject(s)
Humans , Male , Female , Adult , Aged , Peptide Fragments/metabolism , Atrial Fibrillation/epidemiology , Natriuretic Peptide, Brain/metabolism , Hospitalization/statistics & numerical data , Intensive Care Units , Prognosis , Biomarkers/metabolism , Multivariate Analysis , Retrospective Studies , Risk Factors , ROC Curve , Sensitivity and Specificity , Hospital Mortality , Length of Stay , Middle AgedABSTRACT
Bradykinin-potentiating peptides (BPPs - 5a, 7a, 9a, 10c, 11e, and 12b) of Bothrops jararaca (Bj) were described as argininosuccinate synthase (AsS) activators, improving l-arginine availability. Agmatine and polyamines, which are l-arginine metabolism products, have neuroprotective properties. Here, we investigated the neuroprotective effects of low molecular mass fraction from Bj venom (LMMF) and two synthetic BPPs (BPP-10c, Subject(s)
Argininosuccinate Synthase/metabolism
, Bradykinin/metabolism
, Hydrogen Peroxide/pharmacology
, Neuroblastoma/metabolism
, Oxidative Stress/drug effects
, Peptides/chemistry
, Peptides/pharmacology
, Animals
, Bothrops
, Cell Line, Tumor
, Cell Survival/drug effects
ABSTRACT
Bird-window collisions are a dramatic cause of bird mortality globally. In Latin America, statistics are generally very scarce and/or inaccessible so the frequency of such incidents is still poorly understood. Nevertheless, civilians have applied preventive methods (e.g. adhesive bird-of-prey decals) sparsely but, to our knowledge, no study has evaluated their effectiveness in Brazil. Here, we estimated the mortality rate of bird-window collisions and tested the effectiveness of bird-of-prey decals at preventing such accidents. We undertook daily searches for bird carcasses, presumably resulting from window collisions, near all buildings on a university campus over seven months. Adhesive bird-of-prey decals were then applied to the two buildings with the highest mortality rates and surveys continued for over 12 more months. The mortality rates before and after the application of decals and between seasons were then compared using Friedman test. We recorded 36 collisions, 29 around the two buildings with the highest collision rates 19 prior and 10 after our intervention with associated collision rates of 0.08 and 0.04 collisions/day. Although mortality was reduced by almost half, this difference was not statistically significant. The Blue-black grassquit, Volatinia jacarina (Linnaeus, 1766), and Ruddy ground dove, Columbina talpacoti (Temminck, 1810) suffered the highest number of collisions, followed by the Rufous-collared sparrow, Zonotrichia capensis (P. L. Statius Müller, 1776). Our bird-of-prey decals and efforts were insufficient to prevent or dramatically reduce the number of bird-window collisions. Therefore, we recommend that different interventions be used and additional long-term studies undertaken on their efficacy.
Subject(s)
Humans , Animals , Birds , Environment , Mortality , Accident Prevention , Urban Area , BrazilABSTRACT
Bird-window collisions are a dramatic cause of bird mortality globally. In Latin America, statistics are generally very scarce and/or inaccessible so the frequency of such incidents is still poorly understood. Nevertheless, civilians have applied preventive methods (e.g. adhesive bird-of-prey decals) sparsely but, to our knowledge, no study has evaluated their effectiveness in Brazil. Here, we estimated the mortality rate of bird-window collisions and tested the effectiveness of bird-of-prey decals at preventing such accidents. We undertook daily searches for bird carcasses, presumably resulting from window collisions, near all buildings on a university campus over seven months. Adhesive bird-of-prey decals were then applied to the two buildings with the highest mortality rates and surveys continued for over 12 more months. The mortality rates before and after the application of decals and between seasons were then compared using Friedman test. We recorded 36 collisions, 29 around the two buildings with the highest collision rates 19 prior and 10 after our intervention with associated collision rates of 0.08 and 0.04 collisions/day. Although mortality was reduced by almost half, this difference was not statistically significant. The Blue-black grassquit, Volatinia jacarina (Linnaeus, 1766), and Ruddy ground dove, Columbina talpacoti (Temminck, 1810) suffered the highest number of collisions, followed by the Rufous-collared sparrow, Zonotrichia capensis (P. L. Statius Müller, 1776). Our bird-of-prey decals and efforts were insufficient to prevent or dramatically reduce the number of bird-window collisions. Therefore, we recommend that different interventions be used and additional long-term studies undertaken on their efficacy.(AU)
Subject(s)
Humans , Animals , Birds , Mortality , Accident Prevention , Urban Area , Environment , BrazilABSTRACT
3-Methylglutaric acid (3MGA) is an organic acid that accumulates in various organic acidemias whose patients present neurodegeneration events in children coursing with metabolic acidurias. Limited evidence describes the toxic mechanisms elicited by 3MGA in the brain. Herein, we explored the effects of 3MGA on different toxic endpoints in synaptosomal and mitochondrial-enriched fractions of adult rat brains to provide novel information on early mechanisms evoked by this metabolite. At 1 and 5 mM concentration, 3MGA increased lipid peroxidation, but decreased mitochondrial function only at 5 mM concentration. Despite less intense effects were obtained at 1 mM concentration, its co-administration with the kynurenine pathway (KP) metabolite and N-methyl-D-aspartate receptor (NMDAr) agonist, quinolinic acid (QUIN, 50 and 100 µM), produced toxic synergism on markers of oxidative stress and mitochondrial function. The toxicity of 3MGA per se (5 mM) was prevented by the cannabinoid receptor agonist WIN55,212-2 and the NMDAr antagonist kynurenic acid (KYNA), suggesting cannabinoid and glutamatergic components in the 3MGA pattern of toxicity. The synergic model (3MGA + QUIN) was also sensitive to KYNA and the antioxidant S-allylcysteine, but not to the nitric oxide synthase inhibitor L-nitroarginine methyl ester. These findings suggest various underlying mechanisms involved in the neurotoxicity of 3MGA that may possibly contribute to the neurodegeneration observed in acidemias.
Subject(s)
Brain/drug effects , Meglutol/analogs & derivatives , Mitochondria/drug effects , Oxidative Stress/drug effects , Synaptosomes/drug effects , Animals , Antioxidants/pharmacology , Brain/metabolism , Lipid Peroxidation/drug effects , Male , Meglutol/pharmacology , Mitochondria/metabolism , Rats, Wistar , Reactive Oxygen Species/metabolism , Receptors, Cannabinoid/metabolism , Synaptosomes/metabolismABSTRACT
Ethylmalonic acid (EMA) accumulation occurs in various metabolic diseases with neurological manifestation, including short acyl-CoA dehydrogenase deficiency (SCADD) and ethylmalonic encephalopathy (EE). Since pathophysiological mechanisms responsible for brain damage in these disorders are still poorly understood, we investigated the ex vivo effects of acute intrastriatal administration of EMA on important parameters of energy and redox homeostasis in striatum from young rats. We evaluated CO(2) production from glucose, glucose utilization and lactate production, as well as the activities of the citric acid cycle (CAC) enzymes, the electron transfer chain (ETC) complexes II-IV (oxidative phosphorylation, OXPHOS) and synaptic Na(+),K(+)-ATPase. We also tested the effect of EMA on malondialdehyde (MDA) levels (marker of lipid oxidation) and reduced glutathione (GSH) levels. EMA significantly reduced CO(2) production, increased glucose utilization and lactate production, and reduced the activities of citrate synthase and of complexes II and II-III of the ETC, suggesting an impairment of CAC and OXPHOS. EMA injection also reduced Na(+),K(+)-ATPase activity and GSH concentrations, whereas MDA levels were increased. Furthermore, EMA-induced diminution of Na(+),K(+)-ATPase activity and reduction of GSH levels were prevented, respectively, by the antioxidants melatonin and N-acetylcysteine, indicating that reactive species were involved in these effects. Considering the importance of CAC and ETC for energy production and Na(+),K(+)-ATPase for the maintenance of the cell membrane potential, the present data indicate that EMA compromises mitochondrial homeostasis and neurotransmission in striatum. We presume that these pathomechanisms may be involved to a certain extent in the neurological damage found in patients affected by SCADD and EE.
Subject(s)
Energy Metabolism/drug effects , Homeostasis/drug effects , Malonates/pharmacology , Sodium-Potassium-Exchanging ATPase/metabolism , Acetylcysteine/pharmacology , Animals , Antioxidants/pharmacology , Carbon Dioxide/metabolism , Corpus Striatum/drug effects , Corpus Striatum/metabolism , Electron Transport Complex II/metabolism , Electron Transport Complex III/metabolism , Glucose/metabolism , Glutathione/metabolism , Injections, Intraventricular , Lactates/metabolism , Male , Malonates/administration & dosage , Malondialdehyde/metabolism , Melatonin/pharmacology , Oxidation-Reduction/drug effects , Rats, Wistar , Synapses/drug effects , Synapses/enzymologyABSTRACT
Zellweger syndrome (ZS) and some peroxisomal diseases are severe inherited disorders mainly characterized by neurological symptoms and cerebellum abnormalities, whose pathogenesis is poorly understood. Biochemically, these diseases are mainly characterized by accumulation of pristanic acid (Prist) and other fatty acids in the brain and other tissues. In this work, we evaluated the in vitro influence of Prist on redox homeostasis by measuring lipid, protein, and DNA damage, as well as the antioxidant defenses and the activities of aconitase and α-ketoglutarate dehydrogenase in cerebellum of 30-day-old rats. The effect of Prist on DNA damage was also evaluated in blood of these animals. Some parameters were also evaluated in cerebellum from neonatal rats and in cerebellum neuronal cultures. Prist significantly increased malondialdehyde (MDA) levels and carbonyl formation and reduced sulfhydryl content and glutathione (GSH) concentrations in cerebellum of young rats. It also caused DNA strand damage in cerebellum and induced a high micronuclei frequency in blood. On the other hand, this fatty acid significantly reduced α-ketoglutarate dehydrogenase and aconitase activities in rat cerebellum. We also verified that Prist-induced increase of MDA levels was totally prevented by melatonin and attenuated by α-tocopherol but not by the nitric oxide synthase inhibitor N(ω)-nitro-L-arginine methyl ester, indicating the involvement of reactive oxygen species in this effect. Cerebellum from neonate rats also showed marked alterations of redox homeostasis, including an increase of MDA levels and a decrease of sulfhydryl content and GSH concentrations elicited by Prist. Finally, Prist provoked an increase of dichlorofluorescein (DCFH) oxidation in cerebellum-cultivated neurons. Our present data indicate that Prist compromises redox homeostasis in rat cerebellum and blood and inhibits critical enzymes of the citric acid cycle that are susceptible to free radical attack. The present findings may contribute to clarify the pathogenesis of the cerebellar alterations observed in patients affected by ZS and some peroxisomal disorders in which Prist is accumulated.