Directed Random Markets: Connectivity determines Money

Boltzmann-Gibbs distribution arises as the statistical equilibrium probability distribution of money among the agents of a closed economic system where random and undirected exchanges are allowed. When considering a model with uniform savings in the exchanges, the final distribution is close to the gamma family. In this work, we implement these exchange rules on networks and we find that these stationary probability distributions are robust and they are not affected by the topology of the underlying network. We introduce a new family of interactions: random but directed ones. In this case, it is found the topology to be determinant and the mean money per economic agent is related to the degree of the node representing the agent in the network. The relation between the mean money per economic agent and its degree is shown to be linear.Comment: 14 pages, 6 figure

Ultra-processed food consumption and risk of obesity: a prospective cohort study of UK Biobank

Objective: To examine the associations between ultra-processed food consumption and risk of obesity among UK adults. Methods: Participants aged 40-69 years at recruitment in the UK Biobank (2006-2019) with dietary intakes collected using 24-hour recall and repeated measures of adiposity - body mass index (BMI), waist circumference (WC) and percentage of body fat (% BF) - were included (N=22,659; median follow-up: 5 years). Ultra-processed foods were identified using the NOVA classification and their consumption was expressed as a percentage of total energy intake. Multivariable Cox proportional hazards regression models were used to estimate hazard ratios (HR) of several indicators of obesity according to ultra-processed food consumption. Models were adjusted for sociodemographic and lifestyle characteristics. Results: 947 incident cases of overall obesity (BMI≥30 kg/m2) and 1,900 incident cases of abdominal obesity (men: WC≥102cm, women: WC≥88cm) were identified during follow-up. Participants in the highest quartile of ultra-processed food consumption had significantly higher risk of developing overall obesity (HR: 1.79; 95%CI: 1.06─3.03) and abdominal obesity (HR: 1.30; 95%CI: 1.14─1.48). They had higher risk of experiencing a ≥5% increase in BMI (HR: 1.31; 95%CI: 1.20─1.43), WC (HR: 1.35; 95%CI: 1.25─1.45) and %BF (HR: 1.14; 95%CI: 1.03─1.25), than those in the lowest quartile of consumption. Conclusions: Our findings provide evidence that higher consumption of ultra-processed food is strongly associated with a higher risk of multiple indicators of obesity in the UK adult population. Policy makers should consider actions that promote consumption of fresh or minimally processed foods and reduce consumption of ultra-processed foods

A importância da meso e macrofauna do solo na fertilidade e como bioindicadores.

Made available in DSpace on 2011-06-06T17:15:31Z (GMT). No. of bitstreams: 1 aimportanciadamesoemacrofaunadosolo.pdf: 438843 bytes, checksum: 8c3a7d588fad2f7d7f84dd3352828641 (MD5) Previous issue date: 2009-09-2

Copy number variation arising from gene conversion on the human Y chromosome

We describe the variation in copy number of a ~ 10 kb region overlapping the long intergenic noncoding RNA (lincRNA) gene, TTTY22, within the IR3 inverted repeat on the short arm of the human Y chromosome, leading to individuals with 0–3 copies of this region in the general population. Variation of this CNV is common, with 266 individuals having 0 copies, 943 (including the reference sequence) having 1, 23 having 2 copies, and two having 3 copies, and was validated by breakpoint PCR, fbre-FISH, and 10× Genomics Chromium linked-read sequencing in subsets of 1234 individuals from the 1000 Genomes Project. Mapping the changes in copy number to the phylogeny of these Y chromosomes previously established by the Project identifed at least 20 mutational events, and investigation of fanking paralogous sequence variants showed that the mutations involved fanking sequences in 18 of these, and could extend over > 30 kb of DNA. While either gene conversion or double crossover between misaligned sister chromatids could formally explain the 0–2 copy events, gene conversion is the more likely mechanism, and these events include the longest non-allelic gene conversion reported thus far. Chromosomes with three copies of this CNV have arisen just once in our data set via another mechanism: duplication of 420 kb that places the third copy 230 kb proximal to the existing proximal copy. Our results establish gene conversion as a previously under-appreciated mechanism of generating copy number changes in humans and reveal the exceptionally large size of the conversion events that can occur

Dinâmica de liberação de nutrientes disponibilizados por diferentes tipos de rochas em colunas de lixiviação.

Rochas moídas podem suprir parcial ou totalmente a aplicação de fertilizantes solúveis com a vantagem de proporcionar uma liberação de nutrientes gradual, favorecendo o equilíbrio do solo e de plantas. O presente experimento foi desenvolvido em colunas de lixiviação para determinar a capacidade de diferentes tipos de rochas em alterar o pH e a condutividade elétrica bem como de disponibilizar e liberar para a água de percolação Ca, Mg e K em dois tipos de solo

Smoking-induced aggravation of experimental arthritis is dependent of aryl hydrocarbon receptor activation in Th17 cells.

Background: Epidemiologic studies have highlighted the association of environmental factors with the development and progression of autoimmune and chronic inflammatory diseases. Among the environmental factors, smoking has been associated with increased susceptibility and poor prognosis in rheumatoid arthritis (RA). However, the immune and molecular mechanism of smoking-induced arthritis aggravation remains unclear. The transcription factor aryl hydrocarbon receptor (AHR) regulates the generation of Th17 cells, CD4 T cells linked the development of autoimmune diseases. AHR is activated by organic compounds including polycyclic aromatic hydrocarbons (PAHs), which are environmental pollutants that are also present in cigarette smoke. In this study, we investigated the role of AHR activation in the aggravation of experiment arthritis induced by exposure to cigarette smoke. Methods: Mice were exposed to cigarette smoke during the developmental phase of antigen-induced arthritis and collagen-induced arthritis to evaluate the effects of smoking on disease development. Aggravation of articular inflammation was assessed by measuring neutrophil migration to the joints, increase in articular hyperalgesia and changes in the frequencies of Th17 cells. In vitro studies were performed to evaluate the direct effects of cigarette smoke and PAH on Th17 differentiation. We also used mice genetically deficient for AHR (Ahr KO) and IL-17Ra (Il17ra KO) to determine the in vivo mechanism of smoking-induced arthritis aggravation. Results: We found that smoking induces arthritis aggravation and increase in the frequencies of Th17 cells. The absence of IL-17 signaling (Il17ra KO) conferred protection to smoking-induced arthritis aggravation. Moreover, in vitro experiments showed that cigarette smoke can directly increase Th17 differentiation of T cells by inducing AHR activation. Indeed, Ahr KO mice were protected from cigarette smoke-induced arthritis aggravation and did not display increase in TH17 frequencies, suggesting that AHR activation is an important mechanism for cigarette smoke effects on arthritis. Finally, we demonstrate that PAHs are also able to induce arthritis aggravation. Conclusions: Our data demonstrate that the disease-exacerbating effects of cigarette smoking are AHR dependent and environmental pollutants with AHR agonist activity can induce arthritis aggravation by directly enhancing Th17 cell development