Constraining the Warm Dark Matter Particle Mass through Ultra-Deep UV Luminosity Functions at z=2

We compute the mass function of galactic dark matter halos for different values of the Warm Dark Matter (WDM) particle mass m_X and compare it with the abundance of ultra-faint galaxies derived from the deepest UV luminosity function available so far at redshift z~2. The magnitude limit M_UV=-13 reached by such observations allows us to probe the WDM mass functions down to scales close to or smaller than the half-mass mode mass scale ~10^9 M_sun. This allowed for an efficient discrimination among predictions for different m_X which turn out to be independent of the star formation efficiency adopted to associate the observed UV luminosities of galaxies to the corresponding dark matter masses. Adopting a conservative approach to take into account the existing theoretical uncertainties in the galaxy halo mass function, we derive a robust limit m_X>1.8 keV for the mass of thermal relic WDM particles when comparing with the measured abundance of the faintest galaxies, while m_X>1.5 keV is obtained when we compare with the Schechter fit to the observed luminosity function. The corresponding lower limit for sterile neutrinos depends on the modeling of the production mechanism; for instance m_sterile > 4 keV holds for the Shi-Fuller mechanism. We discuss the impact of observational uncertainties on the above bound on m_X. As a baseline for comparison with forthcoming observations from the HST Frontier Field, we provide predictions for the abundance of faint galaxies with M_UV=-13 for different values of m_X and of the star formation efficiency, valid up to z~4.Comment: 14 pages, 3 figures. Accepted for publication in The Astrophysical Journa

Spontaneous perforation of small intestine followed by rupture of the cystic artery: the natural history of Vascular Ehlers-Danlos Syndrome

Vascular Ehlers-Danlos Syndrome (VEDS) is a rare autosomal dominant disorder caused by mutations in the COL3A1 or COL1A1 genes. Its mortality is secondary to sudden and spontaneous rupture of arteries or hollow organs. The genotype influences the distribution of arterial pathology with aneurysms of intra-abdominal visceral arteries being relatively uncommon. We describe the case of a young man with probable VEDS who died of a spontaneous rupture and dissection of the cystic artery. The patient initially presented with abdominal pain due to an unrecognized spontaneous perforation of the small intestine complicated by sepsis. We postulate that inflammatory mediators may have triggered the arterial rupture due to remodeling and weakening of vessel walls. The phenotype of the patient’s vascular damage included bilateral spontaneous carotid-cavernous sinus fistulae and dissection with pseudoaneurysm formation of large- and medium-sized arteries, predominantly the abdominal aorta and its branches. The autopsy uncovered a long history of vascular events that may have been asymptomatic. These findings along with a positive family history supported the VEDS diagnosis. Loeys-Dietz, Marfan, and familial thoracic aortic aneurysm and dissection syndromes were ruled out based on the absence of arterial tortuosity, eye abnormalities, bone overgrowth, and the distribution of vascular damage among other features. Interestingly, microscopic examination of the hippocampus revealed a focus of neuronal heterotopia, commonly associated with epilepsy; however, the patient had no history of seizures. The natural course of VEDS involves the rupture and dissection of arteries that, if unrecognized, can lead to a rapid death after bleeding into free spaces

Opinion dynamics model with domain size dependent dynamics: novel features and new universality class

A model for opinion dynamics (Model I) has been recently introduced in which the binary opinions of the individuals are determined according to the size of their neighboring domains (population having the same opinion). The coarsening dynamics of the equivalent Ising model shows power law behavior and has been found to belong to a new universality class with the dynamic exponent $z=1.0 \pm 0.01$ and persistence exponent $\theta \simeq 0.235$ in one dimension. The critical behavior has been found to be robust for a large variety of annealed disorder that has been studied. Further, by mapping Model I to a system of random walkers in one dimension with a tendency to walk towards their nearest neighbour with probability $\epsilon$, we find that for any $\epsilon > 0.5$, the Model I dynamical behaviour is prevalent at long times.Comment: 12 pages, 10 figures. To be published in "Journal of Physics : Conference Series" (2011

Neonatal acute liver failure with pulmonary yellow hyaline membrane and kernicterus

Background: Neonatal acute liver failure (NALF) is a rare and life-threatening condition. It causes bilirubin to accumulate to a dangerous level in the body, causing permanent damage to vital organs such as the brain and lungs. In many cases, the etiology of NALF remains unknown. Case presentation: We described a case of an 8-day-old baby girl who presented with poor oral intake, lethargy, and jaundice. Her clinical condition rapidly deteriorated with progression to multi-organ failure, and despite intensive resuscitation efforts, she expired. At autopsy, the most significant findings were liver necrosis, yellow hyaline membrane deposition in the lungs, and bilirubin deposition in the brain (kernicterus). Conclusions: NALF is a rare and potentially fatal condition necessitating prompt recognition and disease-specific treatment approaches. Toxic accumulation of bilirubin in the lungs can lead to hypoxia and precipitate further ischemic injury to the liver

Chronic IL-10 overproduction disrupts microglia-neuron dialogue similar to aging, resulting in impaired hippocampal neurogenesis and spatial memory

Altres ajuts: Acord transformatiu CRUE-CSICThis work was supported by the Spanish Ministry of Economy and Business (BFU2014-55459 and BFU2017-87843-R).The subgranular zone of the dentate gyrus is an adult neurogenic niche where new neurons are continuously generated. A dramatic hippocampal neurogenesis decline occurs with increasing age, contributing to cognitive deficits. The process of neurogenesis is intimately regulated by the microenvironment, with inflammation being considered a strong negative factor for this process. Thus, we hypothesize that the reduction of new neurons in the aged brain could be attributed to the age-related microenvironmental changes towards a pro-inflammatory status. In this work, we evaluated whether an anti-inflammatory microenvironment could counteract the negative effect of age on promoting new hippocampal neurons. Surprisingly, our results show that transgenic animals chronically overexpressing IL-10 by astrocytes present a decreased hippocampal neurogenesis in adulthood. This results from an impairment in the survival of neural newborn cells without differences in cell proliferation. In parallel, hippocampal-dependent spatial learning and memory processes were affected by IL-10 overproduction as assessed by the Morris water maze test. Microglial cells, which are key players in the neurogenesis process, presented a different phenotype in transgenic animals characterized by high activation together with alterations in receptors involved in neuronal communication, such as CD200R and CX3CR1. Interestingly, the changes described in adult transgenic animals were similar to those observed by the effect of normal aging. Thus, our data suggest that chronic IL-10 overproduction mimics the physiological age-related disruption of the microglia-neuron dialogue, resulting in hippocampal neurogenesis decrease and spatial memory impairment

Genetic deficiency of apolipoprotein D in the mouse is associated with nonfasting hypertriglyceridemia and hyperinsulinemia

Producción CientíficaApolipoprotein D (ApoD) is an atypical apolipoprotein with an incompletely understood function in the regulation of triglyceride and glucose metabolism. We have demonstrated that elevated ApoD production in mice results in improved postprandial triglyceride clearance. This work studies the role of ApoD deficiency in the regulation of triglyceride and glucose metabolism and its dependence on aging. We used ApoD knockout (ApoD-KO) mice of 3 and 21 months of age. Body weight and food intake were measured. Hepatic histology, triglyceride content, lipoprotein lipase levels, and plasma metabolites were studied. Phenotypic characterization of glucose metabolism was performed using glucose tolerance test. β-Cell mass, islet volume, and islet number were analyzed by histomorphometry. Apolipoprotein D deficiency results in nonfasting hypertriglyceridemia in young (P = .01) and aged mice (P = .002). In young ApoD-KO mice, hypertriglyceridemiawas associated with 30% to 50% increased food intake in nonfasting and fasting conditions, respectively, without changes in body weight. In addition, lipoprotein lipase levels were reduced by 35% in adipose tissue (P = .006). In aged ApoD-KO mice, hypertriglyceridemia was not associated with changes in food intake or body weight, whereas hepatic triglyceride levels were reduced by 35% (P = .02). Furthermore, nonfasting plasma insulin levels were elevated by 2-fold in young (P = .016) and aged (P = .004) ApoD-KO mice, without changes in blood glucose levels, glucose tolerance, β-cell mass, or islet number. These findings underscore the importance of ApoD in the regulation of plasma insulin levels and triglyceride metabolism, suggesting that ApoD plays an important role in the pathogenesis of dyslipidemia

Continuous opinion model in small world directed networks

In the compromise model of continuous opinions proposed by Deffuant et al, the states of two agents in a network can start to converge if they are neighbors and if their opinions are sufficiently close to each other, below a given threshold of tolerance $\epsilon$. In directed networks, if agent i is a neighbor of agent j, j need not be a neighbor of i. In Watts-Strogatz networks we performed simulations to find the averaged number of final opinions and their distribution as a function of $\epsilon$ and of the network structural disorder. In directed networks exhibits a rich structure, being larger than in undirected networks for higher values of $\epsilon$, and smaller for lower values of $\epsilon$.Comment: 15 pages, 6 figure

The genes encoding Arabidopsis ORC subunits are E2F targets and the two ORC1 genes are differently expressed in proliferating and endoreplicating cells

Initiation of eukaryotic DNA replication depends on the function of pre-replication complexes (pre-RC), one of its key component being the six subunits origin recognition complex (ORC). In spite of a significant degree of conservation among ORC proteins from different eukaryotic sources, the regulation of their availability varies considerably in different model systems and cell types. Here, we show that the six ORC genes of Arabidopsis thaliana are regulated at the transcriptional level during cell cycle and development. We found that Arabidopsis ORC genes, except AtORC5, contain binding sites for the E2F family of transcription factors. Expression of AtORC genes containing E2F binding sites peaks at the G1/S-phase. Analysis of AtORC gene expression in plants with reduced E2F activity, obtained by expressing a dominant negative version of DP, the E2F heterodimerization partner, and with increased E2F activity, obtained by inactivation of the retinoblastoma protein, led us to conclude that all AtORC genes, except AtORC5 are E2F targets. Interestingly, Arabidopsis contains two AtORC1 (a and b) genes, highly conserved at the amino acid level but with unrelated promoter sequences. AtORC1b expression is restricted to proliferating cells. However, AtORC1a is preferentially expressed in endoreplicating cells based on our analysis in endoreplicating tissues and in a mutant with altered endocycle pattern. This suggests a differential expression of the two ORC1 genes in Arabidopsis

From Mouse To Human : Comparative Analysis Between Grey And White Matter By Synchrotron-Fourier Transformed Infrared Microspectroscopy

Fourier Transform Infrared microspectroscopy (μFTIR) is a very useful method to analyze the biochemical properties of biological samples in situ. Many diseases affecting the central nervous system (CNS) have been studied using this method, to elucidate alterations in lipid oxidation or protein aggregation, among others. In this work, we describe in detail the characteristics between grey matter (GM) and white matter (WM) areas of the human brain by μFTIR, and we compare them with the mouse brain (strain C57BL/6), the most used animal model in neurological disorders. Our results show a clear different infrared profile between brain areas in the lipid region of both species. After applying a second derivative in the data, we established a 1.5 threshold value for the lipid/protein ratio to discriminate between GM and WM areas in non-pathological conditions. Furthermore, we demonstrated intrinsic differences of lipids and proteins by cerebral area. Lipids from GM present higher C=CH, C=O and CH3 functional groups compared to WM in humans and mice. Regarding proteins, GM present lower Amide II amounts and higher intramolecular β-sheet structure amounts with respect to WM in both species. However, the presence of intermolecular β-sheet structures, which is related to β-aggregation, was only observed in the GM of some human individuals. The present study defines the relevant biochemical properties of non-pathological human and mouse brains by μFTIR as a benchmark for future studies involving CNS pathological samples