29 research outputs found

    Neotropical freshwater fisheries : A dataset of occurrence and abundance of freshwater fishes in the Neotropics

    No full text
    The Neotropical region hosts 4225 freshwater fish species, ranking first among the world's most diverse regions for freshwater fishes. Our NEOTROPICAL FRESHWATER FISHES data set is the first to produce a large-scale Neotropical freshwater fish inventory, covering the entire Neotropical region from Mexico and the Caribbean in the north to the southern limits in Argentina, Paraguay, Chile, and Uruguay. We compiled 185,787 distribution records, with unique georeferenced coordinates, for the 4225 species, represented by occurrence and abundance data. The number of species for the most numerous orders are as follows: Characiformes (1289), Siluriformes (1384), Cichliformes (354), Cyprinodontiformes (245), and Gymnotiformes (135). The most recorded species was the characid Astyanax fasciatus (4696 records). We registered 116,802 distribution records for native species, compared to 1802 distribution records for nonnative species. The main aim of the NEOTROPICAL FRESHWATER FISHES data set was to make these occurrence and abundance data accessible for international researchers to develop ecological and macroecological studies, from local to regional scales, with focal fish species, families, or orders. We anticipate that the NEOTROPICAL FRESHWATER FISHES data set will be valuable for studies on a wide range of ecological processes, such as trophic cascades, fishery pressure, the effects of habitat loss and fragmentation, and the impacts of species invasion and climate change. There are no copyright restrictions on the data, and please cite this data paper when using the data in publications

    Health-status outcomes with invasive or conservative care in coronary disease

    No full text
    BACKGROUND In the ISCHEMIA trial, an invasive strategy with angiographic assessment and revascularization did not reduce clinical events among patients with stable ischemic heart disease and moderate or severe ischemia. A secondary objective of the trial was to assess angina-related health status among these patients. METHODS We assessed angina-related symptoms, function, and quality of life with the Seattle Angina Questionnaire (SAQ) at randomization, at months 1.5, 3, and 6, and every 6 months thereafter in participants who had been randomly assigned to an invasive treatment strategy (2295 participants) or a conservative strategy (2322). Mixed-effects cumulative probability models within a Bayesian framework were used to estimate differences between the treatment groups. The primary outcome of this health-status analysis was the SAQ summary score (scores range from 0 to 100, with higher scores indicating better health status). All analyses were performed in the overall population and according to baseline angina frequency. RESULTS At baseline, 35% of patients reported having no angina in the previous month. SAQ summary scores increased in both treatment groups, with increases at 3, 12, and 36 months that were 4.1 points (95% credible interval, 3.2 to 5.0), 4.2 points (95% credible interval, 3.3 to 5.1), and 2.9 points (95% credible interval, 2.2 to 3.7) higher with the invasive strategy than with the conservative strategy. Differences were larger among participants who had more frequent angina at baseline (8.5 vs. 0.1 points at 3 months and 5.3 vs. 1.2 points at 36 months among participants with daily or weekly angina as compared with no angina). CONCLUSIONS In the overall trial population with moderate or severe ischemia, which included 35% of participants without angina at baseline, patients randomly assigned to the invasive strategy had greater improvement in angina-related health status than those assigned to the conservative strategy. The modest mean differences favoring the invasive strategy in the overall group reflected minimal differences among asymptomatic patients and larger differences among patients who had had angina at baseline

    Initial invasive or conservative strategy for stable coronary disease

    No full text
    BACKGROUND Among patients with stable coronary disease and moderate or severe ischemia, whether clinical outcomes are better in those who receive an invasive intervention plus medical therapy than in those who receive medical therapy alone is uncertain. METHODS We randomly assigned 5179 patients with moderate or severe ischemia to an initial invasive strategy (angiography and revascularization when feasible) and medical therapy or to an initial conservative strategy of medical therapy alone and angiography if medical therapy failed. The primary outcome was a composite of death from cardiovascular causes, myocardial infarction, or hospitalization for unstable angina, heart failure, or resuscitated cardiac arrest. A key secondary outcome was death from cardiovascular causes or myocardial infarction. RESULTS Over a median of 3.2 years, 318 primary outcome events occurred in the invasive-strategy group and 352 occurred in the conservative-strategy group. At 6 months, the cumulative event rate was 5.3% in the invasive-strategy group and 3.4% in the conservative-strategy group (difference, 1.9 percentage points; 95% confidence interval [CI], 0.8 to 3.0); at 5 years, the cumulative event rate was 16.4% and 18.2%, respectively (difference, 121.8 percentage points; 95% CI, 124.7 to 1.0). Results were similar with respect to the key secondary outcome. The incidence of the primary outcome was sensitive to the definition of myocardial infarction; a secondary analysis yielded more procedural myocardial infarctions of uncertain clinical importance. There were 145 deaths in the invasive-strategy group and 144 deaths in the conservative-strategy group (hazard ratio, 1.05; 95% CI, 0.83 to 1.32). CONCLUSIONS Among patients with stable coronary disease and moderate or severe ischemia, we did not find evidence that an initial invasive strategy, as compared with an initial conservative strategy, reduced the risk of ischemic cardiovascular events or death from any cause over a median of 3.2 years. The trial findings were sensitive to the definition of myocardial infarction that was used

    Current contribution of diffusion tensor imaging in the evaluation of diffuse axonal injury

    No full text
    <div><p>ABSTRACT Traumatic brain injury (TBI) is the number one cause of death and morbidity among young adults. Moreover, survivors are frequently left with functional disabilities during the most productive years of their lives. One main aspect of TBI pathology is diffuse axonal injury, which is increasingly recognized due to its presence in 40% to 50% of all cases that require hospital admission. Diffuse axonal injury is defined as widespread axonal damage and is characterized by complete axotomy and secondary reactions due to overall axonopathy. These changes can be seen in neuroimaging studies as hemorrhagic focal areas and diffuse edema. However, the diffuse axonal injury findings are frequently under-recognized in conventional neuroimaging studies. In such scenarios, diffuse tensor imaging (DTI) plays an important role because it provides further information on white matter integrity that is not obtained with standard magnetic resonance imaging sequences. Extensive reviews concerning the physics of DTI and its use in the context of TBI patients have been published, but these issues are still hazy for many allied-health professionals. Herein, we aim to review the current contribution of diverse state-of-the-art DTI analytical methods to the understanding of diffuse axonal injury pathophysiology and prognosis, to serve as a quick reference for those interested in planning new studies and who are involved in the care of TBI victims. For this purpose, a comprehensive search in Pubmed was performed using the following keywords: “traumatic brain injury”, “diffuse axonal injury”, and “diffusion tensor imaging”.</p></div

    Responsiveness of pituitary to galanin throughout the reproductive cycle of male European sea bass (Dicentrarchus labrax)

    Get PDF
    The neuropeptide galanin (Gal) is a putative factor regulating puberty onset and reproduction through its actions on the pituitary. The present study investigated the pituitary responsiveness to galanin and the patterns of galanin receptors (Galrs) expression throughout the reproductive cycle of two years old male European sea bass (Dicentrarchus labrax), an important aquaculture species. Quantitative analysis of pituitary and hypothalamus transcript expression of four galr subtypes revealed differential regulation according to the testicular developmental stage, with an overall decrease in expression from the immature stage to the mid-recrudescence stage. Incubation of pituitary cells with mammalian 1-29 Gal peptide induced significant changes in cAMP concentration, with sensitivities that varied according to the testicular development stages. Furthermore 1-29 Gal was able to stimulate both follicle stimulating hormone (Fsh) and luteinizing hormone (Lh) release from pituitary cell suspensions. The magnitude of the effects and effective concentrations varied according to reproductive stage, with generalized induction of Fsh and Lh release in animals sampled in January (full spermiation). The differential expression of galrs in pituitary and hypothalamus across the reproductive season, together with the differential effects of Gal on gonadotropins release in vitro strongly suggests the involvement of the galaninergic system in the regulation the hypothalamus-pituitary-gonad axis of male sea bass. This is to our knowledge the first clear evidence for the involvement of galanin in the regulation of reproduction in non-mammalian vertebrates. (C) 2017 Elsevier Inc. All rights reserved.European Union Seventh Framework Programme [262336]Spanish Ministry of Science and Innovation (MICINN)Spanish Ministry of the Economy and Competitiveness (MINECO) [AGL2009-11086]Spanish Ministry of the Economy and CompetitivenessRegional Government of Valencia [PROME-TEOH/2014/051]info:eu-repo/semantics/acceptedVersio

    Extratemporal abnormalities in phosphorus magnetic resonance spectroscopy of patients with mesial temporal sclerosis

    No full text
    ABSTRACT Objective We evaluated extratemporal metabolic changes with phosphorus magnetic resonance spectroscopy (31P-MRS) in patients with unilateral mesial temporal sclerosis (MTS). Method 31P-MRS of 33 patients with unilateral MTS was compared with 31 controls. The voxels were selected in the anterior, posterior insula-basal ganglia (AIBG, PIBG) and frontal lobes (FL). Relative values of phosphodiesters- PDE, phosphomonoesters-PME, inorganic phosphate - Pi, phosphocreatine- PCr, total adenosine triphosphate [ATPt = γ- + a- + b-ATP] and the ratios PCr/ATPt, PCr/γ-ATP, PCr/Pi and PME/PDE were obtained. Results We found energetic abnormalities in the MTS patients compared to the controls with Pi reduction bilaterally in the AIBG and ipsilaterally in the PIBG and the contralateral FL; there was also decreased PCr/γ-ATP in the ipsilateral AIBG and PIBG. Increased ATPT in the contralateral AIBG and increased γ-ATP in the ipsilateral PIBG were detected. Conclusion Widespread energy dysfunction was detected in patients with unilateral MTS

    Phosphorus magnetic resonance spectroscopy in malformations of cortical development

    No full text
    Introduction Malformations of cortical development (MCD) result from disruptions in the dynamic process of cerebral corticogenesis and are important causes of epilepsy, motor deficits and cognitive impairment. Objectives The aim of this study was to evaluate phospholipids metabolism in vivo in a series of patients with epilepsy and MCD. Methods Thirty-seven patients with MCD and 31 control subjects were studied using three-dimensional phosphorus magnetic resonance spectroscopy (31P-MRS) at a 3.0 T scanner. Quantification methods were applied to the following resonances: phosphoethanolamine (PE), phosphocholine (PC), glycerophosphoethanolamine (GPE), glycerophosphocholine (GPC), inorganic phosphate (Pi), phosphocreatine (PCr), and a-, b-, and g-adenosine triphosphate (ATP). The magnesium (Mg2+) levels and pH were calculated based on PCr, Pi and b-ATP chemical shifts. Results Compared to controls, the MCD lesions exhibited lower pH values and higher Mg2+ levels (p<0.05). The lesions also presented significant reduction of GPC and PDE, and an increased PME/PDE ratio. The otherwise normal appearing parenchyma also demonstrated lower pH values in the frontoparietal cortex and bilateral centrum semiovale. Conclusions Our data support the idea that metabolic impairments occur in the lesions of MCD, with propagation to remote normal appearing parenchyma. The results also suggest that there are membrane turnover disturbances in MCD lesions

    Phosphorus magnetic resonance spectroscopy in malformations of cortical development

    No full text
    INTRODUÇÃO: As malformações do desenvolvimento cortical (MDC) resultam de distúrbios no dinâmico processo de corticogênese cerebral e são importante causa de epilepsia grave, atraso do desenvolvimento, déficits motores e cognitivos. O papel do metabolismo na epilepsia humana tem sido extensamente debatido, e há inúmeras evidências que apontam para disfunções bioenergéticas como fatores-chave na ictogênese. Distúrbios metabólicos foram identificados nas malformações corticais com outras modalidades de neuroimagem, tais como a espectroscopia de prótons por ressonância magnética. Para o nosso conhecimento, entretanto, o metabolismo de fósforo em pacientes com epilepsia secundária a MDC não foi extensamente investigado até o momento. OBJETIVOS: O objetivo deste estudo foi avaliar o metabolismo de fosfolipídios in vivo em uma série de pacientes com epilepsia e MDC. MÉTODO: Trinta e sete pacientes com MDC e 31 voluntários foram estudados usando espectroscopia de fósforo por ressonância magnética (31P-ERM) tridimensional em aparelho de 3,0 Tesla. Os voxels nas lesões foram comparados ao córtex frontoparietal dos controles (volumes efetivos de 12,5 cm3). O parênquima aparentemente normal foi avaliado em voxels homólogos de pacientes e controles, abrangendo cinco regiões cerebrais: regiões nucleocapsulares direita e esquerda, córtex frontoparietal parassagital, e centros semiovais direito e esquerdo. Foram utilizados métodos de quantificação para ajustar os dados no domínio do tempo para as seguintes ressonâncias: fosfoetanolamina (PE), fosfocolina (PC), glicerofosfoetanolamina (GPE), glicerofosfocolina (GPC), fosfato inorgânico (Pi), fosfocreatina (PCr), e a-, b- e g-adenosina trifosfato (ATP). Também foram calculados o ATP total (ATPt=a-+b-+g-ATP), fosfodiésteres (PDE=GPC+GPE), fosfomonoésteres (PME=PE+PC), e as razões PME/PDE, PCr/ATPt, e PCr/Pi. O magnésio (Mg2+) e os níveis de pH foram calculados com base nos desvios químicos da PCr, Pi, e -ATP. RESULTADOS: Comparativamente aos controles, e assumindo um valor de p < 0,05 estatisticamente significativo, as lesões apresentaram redução dos valores de pH e aumento de Mg2+. Também foram encontrados redução significativa de GPC e PDE, e aumento da relação PME/PDE nas MDC. O parênquima aparentemente normal também demonstrou redução dos valores de pH no córtex frontoparietal e no centro semioval bilateral. As diferenças nos valores de pH, tanto nas lesões como no parênquima aparentemente normal, permaneceram estatisticamente significativas nos subgrupos individuais de MDC (displasia cortical ou hemimegalencefalia; heterotopia; polimicrogiria e/ou esquizencefalia). Não houve correlação entre o tempo da última convulsão e as alterações do pH. CONCLUSÕES: O Mg2+ e o pH são parâmetros muito importantes na regulação bioenergética e estão envolvidos em múltiplas vias da atividade elétrica cerebral. Nossos dados corroboram a ideia de que distúrbios metabólicos ocorrem nas lesões focais de MDC, com propagação para áreas remotas aparentemente normais. As anormalidades de GPC, PDE, e da razão PME/PDE sugerem que há deficiências na renovação das membranas celulares nas lesões dos pacientes com epilepsia e MDC.INTRODUCTION: Malformations of cortical development (MCD) result from disruptions in the dynamic process of cerebral corticogenesis and are important causes of severe epilepsy, neurodevelopmental delay, motor deficits and cognitive impairment. Metabolism in human epilepsy has been intensely debated, and there are several evidences pointing to brain bioenergetic disturbances as key factors in ictogenesis. Metabolic impairments in cortical malformations have been identified with other neuroimaging tools, such as proton magnetic resonance spectroscopy. To our knowledge, however, phosphorus metabolism in epilepsy caused by MCD has not been thoroughly investigated hitherto. OBJECTIVES: The aim of this study was to evaluate phospholipids metabolism in vivo in a series of patients with epilepsy and MCD. METHODS: Thirty-seven patients with MCD and 31 control subjects were studied using three-dimensional phosphorus magnetic resonance spectroscopy (31P-MRS) at a 3.0 T scanner. The voxels in the lesions were compared to the frontoparietal cortex of the control subjects (the effective volumes were 12.5 cm3). Normal appearing parenchyma was evaluated in homologous voxels of patients and controls encompassing five cerebral regions: right and left nucleocapsular regions, midline frontoparietal cortex and right and left semioval centers. Quantification methods were applied to fit the time-domain data to the following resonances: phosphoethanolamine (PE), phosphocholine (PC), glycerophosphoethanolamine (GPE), glycerophosphocholine (GPC), inorganic phosphate (Pi), phosphocreatine (PCr), and a-, b-, and g-adenosine triphosphate (ATP). We also estimated the total ATP (ATPt=a-+b-+g-ATP), phosphodiesters (PDE=GPC+ GPE), phosphomonoesters (PME=PE+PC), and the PME/PDE, PCr/ATPt, and PCr/Pi ratios. The magnesium (Mg2+) levels and pH were calculated based on PCr, Pi, and -ATP chemical shifts. RESULTS: Compared to controls and assuming that a p-value < 0.05 indicates significance, the MCD lesions exhibited lower pH values and higher Mg2+ levels. The lesions also presented significant reduction of GPC and PDE, and an increased PME/PDE ratio. The otherwise normal appearing parenchyma also demonstrated lower pH values in the frontoparietal cortex and bilateral centrum semiovale. The differences in pH values, both in the lesions and in the normal appearing parenchyma, remained statistically significant in individual subgroups of MCD (hemimegalencephaly or cortical dysplasia; heterotopia; polymicrogyria and/or schizencephaly). There was no correlation between the time of the last seizure and the pH abnormalities. CONCLUSIONS: Mg2+ and pH are very important in the regulation of bioenergetics and are involved in many electrical activity pathways in the brain. Our data support the idea that metabolic impairments occur in the lesions of MCD, with propagation to remote normal appearing parenchyma. The GPC, PDE, and PME/PDE abnormalities suggest that there are membrane turnover disturbances in MCD lesions
    corecore