Atrial Natriuretic Peptide Induces Postprandial Lipid Oxidation in Humans

OBJECTIVE—Atrial natriuretic peptide (ANP) regulates arterial blood pressure. In addition, ANP has recently been shown to promote human adipose tissue lipolysis through cGMP-mediated hormone-sensitive lipase activation. We hypothesized that ANP increases postprandial free fatty acid (FFA) availability and energy expenditure while decreasing arterial blood pressure

Correlations and Characterization of Emitting Sources

Dynamical and thermal characterizations of excited nuclear systems produced during the collisions between two heavy ions at intermediate incident energies are presented by means of a review of experimental and theoretical work performed in the last two decades. Intensity interferometry, applied to both charged particles (light particles and intermediate mass fragments) and to uncharged radiation (gamma rays and neutrons) has provided relevant information about the space-time properties of nuclear reactions. The volume, lifetime, density and relative chronology of particle emission from decaying nuclear sources has been extensively explored and has provided valuable information about the dynamics of heavy-ion collisions. Similar correlation techniques applied to coincidences between light particles and complex fragments are also presented as a tool to determine the internal excitation energy of excited primary fragments as it appears in secondary-decay phenomena.Comment: To appear on Euorpean Physics Journal A as part of the Topical Volume "Dynamics and Thermodynamics with Nuclear Degrees of Freedom

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This study was funded by the Norwegian Ministry of Climate and the Environment. TAM is grateful for partial support by Centro de Estatística e Aplicações da Universidade de Lisboa, funded by the Fundação para a Ciência e a Tecnologia, Portugal, through the project UID/MAT/00006/2013.Polar bears have experienced a rapid loss of sea-ice habitat in the Barents Sea. Monitoring this subpopulation focuses on the effects on polar bear demography. In August 2015, we conducted a survey in the Norwegian Arctic to estimate polar bear numbers and reveal population substructure. DNA profiles from biopsy samples and ear tags identified on photographs revealed that about half of the bears in Svalbard, compared to only 4.5% in the pack ice north of the archipelago, were recognized recaptures. The recaptured bears had originally been marked in Svalbard, mostly in spring. The existence of a local Svalbard stock, and another ecotype of bears using the pack ice in autumn with low likelihood of visiting Svalbard, support separate population size estimation for the two areas. Mainly by aerial survey line transect distance sampling methods, we estimated that 264 (95% CI = 199 - 363) bears were in Svalbard, close to 241 bears estimated for August 2004. The pack ice area had an estimated 709 bears (95% CI = 334 - 1026). The pack ice and the total (Svalbard + pack ice, 973 bears, 95% CI = 334 - 1026) both had higher estimates compared to August 2004 (444 and 685 bears, respectively), but the increase was not significant. There is no evidence that the fast reduction of sea-ice habitat in the area has yet led to a reduction in population size. The carrying capacity is likely reduced significantly, but recovery from earlier depletion up to 1973 may still be ongoing.Publisher PDFPeer reviewe

Температурное поле в кристалле иттрий-алюминиевого граната при двухстадийном выращивании

Установлено существование оптимального значения теплопроводности, при котором достигается наиболее равномерное распределение модуля температурного градиента на фронте кристаллизации

Frequency of GAA-FGF14 Ataxia in a Large Cohort of Brazilian Patients With Unsolved Adult-Onset Cerebellar Ataxia

OBJECTIVES: Intronic FGF14 GAA repeat expansions have recently been found to be a common cause of hereditary ataxia (GAA-FGF14 ataxia; SCA27B). The global epidemiology and regional prevalence of this newly reported disorder remain to be established. In this study, we investigated the frequency of GAA-FGF14 ataxia in a large cohort of Brazilian patients with unsolved adult-onset ataxia. METHODS: We recruited 93 index patients with genetically unsolved adult-onset ataxia despite extensive genetic investigation and genotyped the FGF14 repeat locus. Patients were recruited across 4 different regions of Brazil. RESULTS: Of the 93 index patients, 8 (9%) carried an FGF14 (GAA)≥250 expansion. The expansion was also identified in 1 affected relative. Seven patients were of European descent, 1 was of African descent, and 1was of admixed American ancestry. One patient carrying a (GAA)376 expansion developed ataxia at age 28 years, confirming that GAA-FGF14 ataxia can occur before the age of 30 years. One patient displayed episodic symptoms, while none had downbeat nystagmus. Cerebellar atrophy was observed on brain MRI in 7 of 8 patients (87%). DISCUSSION: Our results suggest that GAA-FGF14 ataxia is a common cause of adult-onset ataxia in the Brazilian population, although larger studies are needed to fully define its epidemiology

Age-related shift in LTD is dependent on neuronal adenosine A(2A) receptors interplay with mGluR5 and NMDA receptors

Synaptic dysfunction plays a central role in Alzheimer's disease (AD), since it drives the cognitive decline. An association between a polymorphism of the adenosine A2A receptor (A2AR) encoding gene-ADORA2A, and hippocampal volume in AD patients was recently described. In this study, we explore the synaptic function of A2AR in age-related conditions. We report, for the first time, a significant overexpression of A2AR in hippocampal neurons of aged humans, which is aggravated in AD patients. A similar profile of A2AR overexpression in rats was sufficient to drive age-like memory impairments in young animals and to uncover a hippocampal LTD-to-LTP shift. This was accompanied by increased NMDA receptor gating, dependent on mGluR5 and linked to enhanced Ca(2+) influx. We confirmed the same plasticity shift in memory-impaired aged rats and APP/PS1 mice modeling AD, which was rescued upon A2AR blockade. This A2AR/mGluR5/NMDAR interaction might prove a suitable alternative for regulating aberrant mGluR5/NMDAR signaling in AD without disrupting their constitutive activity