Interactions among systems of finite size en predictive relativistic mechanics III. Short-range interaction and second-order terms

We compute up to and including all the c-2 terms in the dynamical equations for extended bodies interacting through electromagnetic, gravitational, or short-range fields. We show that these equations can be reduced to those of point particles with intrinsic angular momentum assuming spherical symmetry.

Percolation and epidemic thresholds in clustered networks

We develop a theoretical approach to percolation in random clustered networks. We find that, although clustering in scale-free networks can strongly affect some percolation properties, such as the size and the resilience of the giant connected component, it cannot restore a finite percolation threshold. In turn, this implies the absence of an epidemic threshold in this class of networks, thus extending this result to a wide variety of real scale-free networks which shows a high level of transitivity. Our findings are in good agreement with numerical simulations.

Short-eared Owl Asio flammeus, 2011

Data sheet produced by the Iowa Department of Natural Resources is about different times of animals, insects, snakes, birds, fish, butterflies, etc. that can be found in Iowa.

Organizações multilaterais, estado e políticas de educação infantil: history repeats

As políticas brasileiras de educação infantil (EI) nas últimas quatro décadas apresentam-se como resposta a várias tensões. Nos anos 70, o despertar dos novos movimentos sociais trouxe o tema para a agenda de suas reivindicações. Nos anos 80, pressões em diferentes sentidos provocaram, de um lado, a expansão da EI seguindo, de modo geral, um modelo "a baixo custo" e, de outro, a consciência social da EI como um direito das crianças pequenas à educação e um direito de assistência aos filhos de pais e mães trabalhadores (Constituição de 1988). O artigo descreve e analisa as tensões presentes, e suas conseqüências, em três momentos da história da EI brasileira contemporânea: a fase de expansão durante o governo militar; as inovações trazidas pela Constituição de 1988; o impacto das reformas educacionais contemporâneas sob a égide do "Consenso de Washington". A descrição e análise desses momentos serão efetuadas no contexto dos modelos propugnados pelas organizações multilaterais.

Short-term overexpression of a constitutively active form of AMP-activated protein kinase in the liver leads to mild hypoglycemia and fatty liver.

AMP-activated protein kinase (AMPK) is a major therapeutic target for the treatment of diabetes. We investigated the effect of a short-term overexpression of AMPK specifically in the liver by adenovirus-mediated transfer of a gene encoding a constitutively active form of AMPKalpha2 (AMPKalpha2-CA). Hepatic AMPKalpha2-CA expression significantly decreased blood glucose levels and gluconeogenic gene expression. Hepatic expression of AMPKalpha2-CA in streptozotocin-induced and ob/ob diabetic mice abolished hyperglycemia and decreased gluconeogenic gene expression. In normal mouse liver, AMPKalpha2-CA considerably decreased the refeeding-induced transcriptional activation of genes encoding proteins involved in glycolysis and lipogenesis and their upstream regulators, SREBP-1 (sterol regulatory element-binding protein-1) and ChREBP (carbohydrate response element-binding protein). This resulted in decreases in hepatic glycogen synthesis and circulating lipid levels. Surprisingly, despite the inhibition of hepatic lipogenesis, expression of AMPKalpha2-CA led to fatty liver due to the accumulation of lipids released from adipose tissue. The relative scarcity of glucose due to AMPKalpha2-CA expression led to an increase in hepatic fatty acid oxidation and ketone bodies production as an alternative source of energy for peripheral tissues. Thus, short-term AMPK activation in the liver reduces blood glucose levels and results in a switch from glucose to fatty acid utilization to supply energy needs.

Hundreds of variants clustered in genomic loci and biological pathways affect human height.

Most common human traits and diseases have a polygenic pattern of inheritance: DNA sequence variants at many genetic loci influence the phenotype. Genome-wide association (GWA) studies have identified more than 600 variants associated with human traits, but these typically explain small fractions of phenotypic variation, raising questions about the use of further studies. Here, using 183,727 individuals, we show that hundreds of genetic variants, in at least 180 loci, influence adult height, a highly heritable and classic polygenic trait. The large number of loci reveals patterns with important implications for genetic studies of common human diseases and traits. First, the 180 loci are not random, but instead are enriched for genes that are connected in biological pathways (P = 0.016) and that underlie skeletal growth defects (P < 0.001). Second, the likely causal gene is often located near the most strongly associated variant: in 13 of 21 loci containing a known skeletal growth gene, that gene was closest to the associated variant. Third, at least 19 loci have multiple independently associated variants, suggesting that allelic heterogeneity is a frequent feature of polygenic traits, that comprehensive explorations of already-discovered loci should discover additional variants and that an appreciable fraction of associated loci may have been identified. Fourth, associated variants are enriched for likely functional effects on genes, being over-represented among variants that alter amino-acid structure of proteins and expression levels of nearby genes. Our data explain approximately 10% of the phenotypic variation in height, and we estimate that unidentified common variants of similar effect sizes would increase this figure to approximately 16% of phenotypic variation (approximately 20% of heritable variation). Although additional approaches are needed to dissect the genetic architecture of polygenic human traits fully, our findings indicate that GWA studies can identify large numbers of loci that implicate biologically relevant genes and pathways.

The expansion of amino-acid repeats is not associated to adaptive evolution in mammalian genes.

BACKGROUND: The expansion of amino acid repeats is determined by a high mutation rate and can be increased or limited by selection. It has been suggested that recent expansions could be associated with the potential of adaptation to new environments. In this work, we quantify the strength of this association, as well as the contribution of potential confounding factors. RESULTS: Mammalian positively selected genes have accumulated more recent amino acid repeats than other mammalian genes. However, we found little support for an accelerated evolutionary rate as the main driver for the expansion of amino acid repeats. The most significant predictors of amino acid repeats are gene function and GC content. There is no correlation with expression level. CONCLUSIONS: Our analyses show that amino acid repeat expansions are causally independent from protein adaptive evolution in mammalian genomes. Relaxed purifying selection or positive selection do not associate with more or more recent amino acid repeats. Their occurrence is slightly favoured by the sequence context but mainly determined by the molecular function of the gene.

Oligoanalgesia in the emergency department: short-term beneficial effects of an education program on acute pain.

STUDY OBJECTIVE: Acute pain is the most frequent complaint in emergency department (ED) admissions, but its management is often neglected, placing patients at risk of oligoanalgesia. We evaluate the effect of the implementation of guidelines for pain management in ED patients with pain at admission or anytime during their stay in our ED. METHODS: This prospective pre-post intervention cohort study included data collection both before and after guideline implementation. Consecutive adult patients admitted with acute pain from any cause or with pain at any time after admission were enrolled. The quality of pain management was evaluated according to information in the ED medical records by using a standardized collection form, and its impact on patients was recorded with a questionnaire at discharge. RESULTS: Two hundred forty-nine and 192 patients were included during pre- and postintervention periods. Pain was documented in 61% and 76% of nurse and physician notes, respectively, versus 78% and 85% after the intervention (difference 17%/9%; 95% confidence interval [CI] 8% to 26%/2% to 17%, respectively). Administration of analgesia increased from 40% to 63% (difference 23%; 95% CI 13% to 32%) and of morphine from 10% to 27% (difference 17%; 95% CI 10% to 24%). Mean doses of intravenous morphine increased from 2.4 mg (95% CI 1.9 to 2.9 mg) to 4.6 mg (95% CI 3.9 to 5.3 mg); administration of nonsteroidal antiinflammatory drugs and acetaminophen increased as well. There was a greater reduction of visual analogue scale score after intervention: 2.1 cm (95% CI 1.7 to 2.4 cm) versus 2.9 cm (95% CI 2.5 to 3.3 cm), which was associated with improved patient satisfaction. CONCLUSION: Education program and guidelines implementation for pain management lead to improved pain management, analgesia, and patient satisfaction in the ED.

Short-term oleoyl-estrone treatment affects capacity to manage lipids in rat adipose tissue

Background: Short-term OE (oleoyl-estrone) treatment causes significant decreases in rat weight mainly due to adipose tissue loss. The aim of this work was to determine if OE treatment affects the expression of genes that regulate lipid metabolism in white adipose tissue. Results: Gene expression in adipose tissue from female treated rats (48 hours) was analysed by hybridization to cDNA arrays and levels of specific mRNAs were determined by real-time PCR. Treatment with OE decreased the expression of 232 genes and up-regulated 75 other genes in mesenteric white adipose tissue. The use of real-time PCR validate that, in mesenteric white adipose tissue, mRNA levels for Lipoprotein Lipase (LPL) were decreased by 52%, those of Fatty Acid Synthase (FAS) by 95%, those of Hormone Sensible Lipase (HSL) by 32%, those of Acetyl CoA Carboxylase (ACC) by 92%, those of Carnitine Palmitoyltransferase 1b (CPT1b) by 45%, and those of Fatty Acid Transport Protein 1 (FATP1) and Adipocyte Fatty Acid Binding Protein (FABP4) by 52% and 49%, respectively. Conversely, Tumour Necrosis Factor (TNF¿) values showed overexpression (198%). Conclusion: Short-term treatment with OE affects adipose tissue capacity to extract fatty acids from lipoproteins and to deal with fatty acid transport and metabolism.

Changes in sleeping and basal energy expenditure and substrate oxidation induced by short term thyroxin administration in man.

The present study was designed to explore the thermogenic effect of thyroid hormone administration and the resulting changes in nitrogen homeostasis. Normal male volunteers (n = 7) received thyroxin during 6 weeks. The first 3-week period served to suppress endogenous thyroid secretion (180 micrograms T4/day). This dose was doubled for the next 3 weeks. Sleeping energy expenditure (respiratory chamber) and BMR (hood) were measured by indirect calorimetry, under standardized conditions. Sleeping heart rate was continuously recorded and urine was collected during this 12-hour period to assess nitrogen excretion. The changes in energy expenditure, heart rate and nitrogen balance were then related to the excess thyroxin administered. After 3 weeks of treatment, serum TSH level fell to 0.15 mU/L, indicating an almost complete inhibition of the pituitary-thyroid axis. During this phase of treatment there was an increase in sleeping EE and sleeping heart rate, which increased further by doubling the T4 dose (delta EE: +8.5 +/- 2.3%, delta heart rate +16.1 +/- 2.2%). The T4 dose, which is currently used as a substitutive dose, lead to a borderline hyperthyroid state, with an increase in EE and heart rate. Exogenous T4 administration provoked a significant increase in urinary nitrogen excretion averaging 40%. It is concluded that T4 provokes an important stimulation of EE, which is mostly mediated by an excess protein oxidation.