Anti-Sporothrix Antibody Detection in Domestic Cats as an Indicator of a Possible New Occurrence Area for Sporotrichosis in North Brazil

Mycopathologia - Feline sporotrichosis has emerged as an important public health issue in some countries, especially Brazil. Currently, zoonotic transmission of Sporothrix brasiliensis by domestic...     

Active promoters give rise to false positive ‘Phantom Peaks’ in ChIP-seq experiments

Chromatin immunoprecipitation (ChIP) is widely used to identify chromosomal binding sites. Chromatin proteins are cross-linked to their target sequences in living cells. The purified chromatin is sheared and the relevant protein is enriched by immunoprecipitation with specific antibodies. The co-purifying genomic DNA is then determined by massive parallel sequencing (ChIP-seq).We applied ChIP-seq to map the chromosomal binding sites for two ISWI-containing nucleosome remodeling factors, ACF and RSF, in Drosophila embryos. Employing several polyclonal and monoclonal antibodies directed against their signature subunits, ACF1 and RSF-1, robust profiles were obtained indicating that both remodelers co-occupied a large set of active promoters.Further validation included controls using chromatin of mutant embryos that do not express ACF1 or RSF-1. Surprisingly, the ChIP-seq profiles were unchanged, suggesting that they were not due to specific immunoprecipitation. Conservative analysis lists about 3000 chromosomal loci, mostly active promoters that are prone to non-specific enrichment in ChIP and appear as ‘Phantom Peaks’. These peaks are not obtained with pre-immune serum and are not prominent in input chromatin.Mining the modENCODE ChIP-seq profiles identifies potential Phantom Peaks in many profiles of epigenetic regulators. These profiles and other ChIP-seq data featuring prominent Phantom Peaks must be validated with chromatin from cells in which the protein of interest has been depleted.     

Preliminary analysis of reproductive success in a large mammal with alternative mating tactics,the Northern chamois,Rupicapra rupicapra

In polygynous mating systems, reproductive skew depends on the ability of males to monopolize females, which in turn may promote the development of contrasting traits in the two sexes. Although dominant individuals normally enjoy a higher reproductive success (RS) than subordinates, the use of genetic markers has shown that behavioural observations of male mating success may not provide reliable clues of RS. We report the preliminary results of the first DNA‐based paternity analysis on the Northern chamois (Rupicapra rupicapra), a scarcely dimorphic mountain ungulate described as highly polygynous, in relation to mating tactic and age. Because of sampling difficulties, the success in parentage assignment was low, and the interpretation of results requires caution. Territorial males had a greater RS than nonterritorial ones but they were unable to monopolize mating events. Age had a weak effect on paternity outcome but only males ≥ 6 years showed siring success. Although future studies are needed to assess the opportunity for sexual selection in male chamois, the concurrence of limited sexual size dimorphism, compensatory growth, unbiased sex‐specific survival, RS of alternative mating tactics and, possibly, long breeding tenure, may hint at the adoption of a conservative mating strategy in this species.     

Intravenous Immunoglobulin with Enhanced Polyspecificity Improves Survival in Experimental Sepsis and Aseptic Systemic Inflammatory Response Syndromes

Sepsis is a major cause for death worldwide. Numerous interventional trials with agents neutralizing single proinflammatory mediators have failed to improve survival in sepsis and aseptic systemic inflammatory response syndromes. This failure could be explained by the widespread gene expression dysregulation known as “genomic storm” in these patients. A multifunctional polyspecific therapeutic agent might be needed to thwart the effects of this storm. Licensed pooled intravenous immunoglobulin preparations seemed to be a promising candidate, but they have also failed in their present form to prevent sepsis-related death. We report here the protective effect of a single dose of intravenous immunoglobulin preparations with additionally enhanced polyspecificity in three models of sepsis and aseptic systemic inflammation. The modification of the pooled immunoglobulin G molecules by exposure to ferrous ions resulted in their newly acquired ability to bind some proinflammatory molecules, complement components and endogenous “danger” signals. The improved survival in endotoxemia was associated with serum levels of proinflammatory cytokines, diminished complement consumption and normalization of the coagulation time. We suggest that intravenous immunoglobulin preparations with additionally enhanced polyspecificity have a clinical potential in sepsis and related systemic inflammatory syndromes.     

The Contribution of Agriculture,Forestry and other Land Use activities to Global Warming, 1990–2012

We refine the information available through the IPCC AR5 with regard to recent trends in global GHG emissions from agriculture, forestry and other land uses (AFOLU), including global emission updates to 2012. Using all three available AFOLU datasets employed for analysis in the IPCC AR5, rather than just one as done in the IPCC AR5 WGIII Summary for Policy Makers, our analyses point to a down‐revision of global AFOLU shares of total anthropogenic emissions, while providing important additional information on subsectoral trends. Our findings confirm that the share of AFOLU emissions to the anthropogenic total declined over time. They indicate a decadal average of 28.7 ± 1.5% in the 1990s and 23.6 ± 2.1% in the 2000s and an annual value of 21.2 ± 1.5% in 2010. The IPCC AR5 had indicated a 24% share in 2010. In contrast to previous decades, when emissions from land use (land use, land use change and forestry, including deforestation) were significantly larger than those from agriculture (crop and livestock production), in 2010 agriculture was the larger component, contributing 11.2 ± 0.4% of total GHG emissions, compared to 10.0 ± 1.2% of the land use sector. Deforestation was responsible for only 8% of total anthropogenic emissions in 2010, compared to 12% in the 1990s. Since 2010, the last year assessed by the IPCC AR5, new FAO estimates indicate that land use emissions have remained stable, at about 4.8 Gt CO₂ eq yr^?1 in 2012. Emissions minus removals have also remained stable, at 3.2 Gt CO₂ eq yr^?1 in 2012. By contrast, agriculture emissions have continued to grow, at roughly 1% annually, and remained larger than the land use sector, reaching 5.4 Gt CO₂ eq yr^?1 in 2012. These results are useful to further inform the current climate policy debate on land use, suggesting that more efforts and resources should be directed to further explore options for mitigation in agriculture, much in line with the large efforts devoted to REDD+ in the past decade.     

Biologically threatened dolphins and whales

Among the several threats to which free-ranging cetaceans are exposed, a number of biological noxae are believed to represent a serious hazard to their health and conservation on a global scale, with special emphasis on the Mediterranean Sea. These pathogens include viral agents such as Morbillivirus, which during the last 25 years have caused dramatic epidemics and die-offs among several aquatic mammal species and populations worldwide, as well as Herpesvirus, protozoan agents such as Toxoplasma gondii and bacterial pathogens such as Brucella spp.     

The urban environment and mental disorders: Epigenetic links

For the first time in human history, more than half of the world''s population lives in urban areas and this is projected to increase to two-thirds by 2030. This increased urbanity of the world''s population has substantial public health implications. Nearly a century of research has shown higher risk of mental disorder among persons living in urban versus rural areas. Epidemiologic research has documented that associations between particular features of the urban environment, such as concentrated disadvantage, residential segregation and social norms, contribute to the risk of mental illness. We propose that changes in DNA methylation may be one potential mechanism through which features of the urban environment contribute to psychopathology. Recent advances in animal models and human correlation studies suggest DNA methylation as a promising mechanism that can explain how the environment “gets under the skin.” Aberrant DNA methylation signatures characterize mental disorders in community settings. Emerging evidence of associations between exposure to features of the environment and methylation patterns may lead toward the identification of mechanisms that explain the link between urban environments and mental disorders. Importantly, evidence that epigenetic changes are reversible offers new opportunities for ameliorating the impact of adverse urban environments on human health.Key words: urban environment, mental disorders, DNA methylation, epigenetics, posttraumatic stress disorder, depressionThe 20th century has been characterized by the world-wide movement of populations from rural to urban areas. For the first time in human history, more than half of the world''s population lives in urban areas and this is projected to increase to two-thirds by 2030. The movement of populations to urban environments is probably the most important demographic shift in the past century. In particular, the increased urbanity of the world''s population has substantial public health implications. A body of research has long shown that there are different burdens of disease and disability in urban vs. non-urban areas and more recent work has linked specific features of the urban environment to particular health indicators (for reviews of the literature about urban health see refs. ¹ and ²).Some of the more promising work in this area concerns research that has shown relations between urbanity and mental disorders. There is more than a century of work that has shown higher risk of most mental disorders among persons living in urban versus rural areas.^3–8 Early research proposed several factors that may explain this association including selective migration and social disorganization.³ For example, it has been proposed that persons within disadvantaged areas may have a more difficult time building and sustaining supportive social relationships, therefore increasing susceptibility to mental illness. Subsequent work has shown associations between particular features of the urban environment and risk of mental illness. Living in poorer urban neighborhoods is associated with greater risk of new episodes of depression compared to living in richer neighborhoods, even when accounting for individual income or exposure to stressful or adverse circumstances.^6,9,10 Living in neighborhoods characterized by residential racial segregation is associated with a greater risk of depression and anxiety, compared to living in less segregated neighborhoods.¹¹ Other evidence suggests that neighborhood collective efficacy and norms are associated with the risk of substance use disorders12 and suicide attempts,¹³ again when taking into account individual experiences.Coincident with the growing number of studies that have demonstrated links between features of the urban environment and mental health, there has been an increase in work that has sought to understand the mechanisms underlying these epidemiologic observations. In particular, there is an emerging interest in identifying biologic explanations that may clarify the link between features of the urban environment and individual mental health. Existing research has documented a role for changes in immune function,¹⁴ gene-environment interactions¹⁵ and psychological mechanisms,¹⁶ among others, that may explain the links between the urban environment and mental health. This paper adds to this growing field and proposes that changes in DNA methylation may be one potential mechanism through which features of the urban environment contribute to psychopathology.