Fate of soil organic carbon and polycyclic aromatic hydrocarbons in a vineyard soil treated with biochar

The effect of biochar addition on the levels of black carbon (BC) and polcyclic aromatic hydrocarbons (PAHs) in a vineyard soil in central Italy was investigated within a two year period. Hydropyrolysis (HyPy) was used to determine the contents of BC (BCHyPy) in the amended and control soils while the hydrocarbon composition of the semi-labile (non-BCHyPy) fraction released by HyPy was determined by gas chromatography-mass spectrometry, together with the solvent-extractable PAHs. The concentrations of these three polycyclic aromatic carbon reservoirs, changed and impacted differently on the soil organic carbon over the period of the trial. The addition of biochar (33 ton dry biochar ha-1) gave rise to a sharp increase in soil organic carbon which could be accounted for by an increase of BCHyPy. Over time, the concentration of BCHyPy decreased significantly from 36 to 23 mg g-1, and as a carbon percentage from 79% to 61%. No clear time trends were observed for the non-BCHyPy PAHs varying from 39 to 34 µg g-1 in treated soils, not significantly different from control soils. However, the concentrations of extractable PAHs increased markedly in the amended soils, and decreased with time from 153 to 78 ng g-1 remaining always higher than those in untreated soil. The extent of the BCHyPy loss was more compatible with physical rather than chemical processes

Which service interfaces fit the model web?

Ponència presentada a The Fourth International Conference on Advanced Geographic Information Systems, Applications, and Services, GEOProcessing 2012, celebrat a València del 30 de gener al 4 de febrer de 2012The Model Web has been proposed as a concept for integrating scientific models in an interoperable and collaborative manner. However, four years after the initial idea was formulated, there is still no stable long term solution. Multiple authors propose Web Service based approaches to model publication and chaining, but current implementations are highly case specific and lack flexibility. This paper discusses the Web Service interfaces, which are required for supporting integrated environmental modeling in a sustainable manner. We explore ways to expose environmental models and their components using Web Service interfaces. Our discussions present work in progress for establishing the Web Services technological grounds for simp lifying information publication and exchange within the Model We b. As a main outcome, this contribution identifies challenges in respect to the required geo- processing and relates them to currently available Web Service standards

Bacterial and Fungal Communities Are Specifically Modulated by the Cocoa Bean Fermentation Method

Cocoa bean fermentation is carried out in different production areas following various methods. This study aimed to assess how the bacterial and fungal communities were affected by box, ground or jute fermentation methods, using high-throughput sequencing (HTS) of phylogenetic amplicons. Moreover, an evaluation of the preferable fermentation method was carried out based on the microbial dynamics observed. Box fermentation resulted in higher bacterial species diversity, while beans processed on the ground had a wider fungal community. Lactobacillus fermentum and Pichia kudriavzevii were observed in all three fermentation methods studied. Moreover, Acetobacter tropicalis dominated box fermentation and Pseudomonas fluorescens abounded in ground-fermented samples. Hanseniaspora opuntiae was the most important yeast in jute and box, while Saccharomyces cerevisiae prevailed in the box and ground fermentation. PICRUST analysis was performed to identify potential interesting pathways. In conclusion, there were noticeable differences between the three different fermentation methods. Due to its limited microbial diversity and the presence of microorganisms that guarantee good fermentation, the box method was found to be preferable. Moreover, the present study allowed us to thoroughly explore the microbiota of differently treated cocoa beans and to better understand the technological processes useful to obtain a standardized end-product

Two-Phase Stefan Problem as the Limit Case of Two-Phase Stefan Problem with Kinetic Condition

AbstractBoth one-dimensional two-phase Stefan problem with the thermodynamic equilibrium condition u(R(t),t)=0 and with the kinetic rule uε(Rε(t),t)=εRε′(t) at the moving boundary are considered. We prove, when ε approaches zero, Rε(t) converges to R(t) in C1+δ/2[0,T] for any finite T>0, 0<δ<1

Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead.

Lifestyle factors are responsible for a considerable portion of cancer incidence worldwide, but credible estimates from the World Health Organization and the International Agency for Research on Cancer (IARC) suggest that the fraction of cancers attributable to toxic environmental exposures is between 7% and 19%. To explore the hypothesis that low-dose exposures to mixtures of chemicals in the environment may be combining to contribute to environmental carcinogenesis, we reviewed 11 hallmark phenotypes of cancer, multiple priority target sites for disruption in each area and prototypical chemical disruptors for all targets, this included dose-response characterizations, evidence of low-dose effects and cross-hallmark effects for all targets and chemicals. In total, 85 examples of chemicals were reviewed for actions on key pathways/mechanisms related to carcinogenesis. Only 15% (13/85) were found to have evidence of a dose-response threshold, whereas 59% (50/85) exerted low-dose effects. No dose-response information was found for the remaining 26% (22/85). Our analysis suggests that the cumulative effects of individual (non-carcinogenic) chemicals acting on different pathways, and a variety of related systems, organs, tissues and cells could plausibly conspire to produce carcinogenic synergies. Additional basic research on carcinogenesis and research focused on low-dose effects of chemical mixtures needs to be rigorously pursued before the merits of this hypothesis can be further advanced. However, the structure of the World Health Organization International Programme on Chemical Safety 'Mode of Action' framework should be revisited as it has inherent weaknesses that are not fully aligned with our current understanding of cancer biology

Causes of genome instability: the effect of low dose chemical exposures in modern society.

Genome instability is a prerequisite for the development of cancer. It occurs when genome maintenance systems fail to safeguard the genome's integrity, whether as a consequence of inherited defects or induced via exposure to environmental agents (chemicals, biological agents and radiation). Thus, genome instability can be defined as an enhanced tendency for the genome to acquire mutations; ranging from changes to the nucleotide sequence to chromosomal gain, rearrangements or loss. This review raises the hypothesis that in addition to known human carcinogens, exposure to low dose of other chemicals present in our modern society could contribute to carcinogenesis by indirectly affecting genome stability. The selected chemicals with their mechanisms of action proposed to indirectly contribute to genome instability are: heavy metals (DNA repair, epigenetic modification, DNA damage signaling, telomere length), acrylamide (DNA repair, chromosome segregation), bisphenol A (epigenetic modification, DNA damage signaling, mitochondrial function, chromosome segregation), benomyl (chromosome segregation), quinones (epigenetic modification) and nano-sized particles (epigenetic pathways, mitochondrial function, chromosome segregation, telomere length). The purpose of this review is to describe the crucial aspects of genome instability, to outline the ways in which environmental chemicals can affect this cancer hallmark and to identify candidate chemicals for further study. The overall aim is to make scientists aware of the increasing need to unravel the underlying mechanisms via which chemicals at low doses can induce genome instability and thus promote carcinogenesis

Chemical compounds from anthropogenic environment and immune evasion mechanisms: potential interactions

An increasing number of studies suggest an important role of host immunity as a barrier to tumor formation and progression. Complex mechanisms and multiple pathways are involved in evading innate and adaptive immune responses, with a broad spectrum of chemicals displaying the potential to adversely influence immunosurveillance. The evaluation of the cumulative effects of low-dose exposures from the occupational and natural environment, especially if multiple chemicals target the same gene(s) or pathway(s), is a challenge. We reviewed common environmental chemicals and discussed their potential effects on immunosurveillance. Our overarching objective was to review related signaling pathways influencing immune surveillance such as the pathways involving PI3K/Akt, chemokines, TGF-β, FAK, IGF-1, HIF-1α, IL-6, IL-1α, CTLA-4 and PD-1/PDL-1 could individually or collectively impact immunosurveillance. A number of chemicals that are common in the anthropogenic environment such as fungicides (maneb, fluoxastrobin and pyroclostrobin), herbicides (atrazine), insecticides (pyridaben and azamethiphos), the components of personal care products (triclosan and bisphenol A) and diethylhexylphthalate with pathways critical to tumor immunosurveillance. At this time, these chemicals are not recognized as human carcinogens; however, it is known that they these chemicals can simultaneously persist in the environment and appear to have some potential interfere with the host immune response, therefore potentially contributing to promotion interacting with of immune evasion mechanisms, and promoting subsequent tumor growth and progression.The publisher and the author(s) have made this article open access. This is the publisher’s final pdf. The published article is copyrighted by the author(s) and published by Oxford University Press. The published article can be found at: http://carcin.oxfordjournals.org

Disruptive chemicals, senescence and immortality

Cell death is a process of dying within biological cells that are ceasing to function. This process is essential in regulating organism development, tissue homeostasis, and to eliminate cells in the body that are irreparably damaged. In general, dysfunction in normal cellular death is tightly linked to cancer progression. Specifically, the up-regulation of prosurvival factors, including oncogenic factors and antiapoptotic signaling pathways, and the down-regulation of proapoptotic factors, including tumor suppressive factors, confers resistance to cell death in tumor cells, which supports the emergence of a fully immortalized cellular phenotype. This review considers the potential relevance of ubiquitous environmental chemical exposures that have been shown to disrupt key pathways and mechanisms associated with this sort of dysfunction. Specifically, bisphenol A, chlorothalonil, dibutyl phthalate, dichlorvos, lindane, linuron, methoxychlor and oxyfluorfen are discussed as prototypical chemical disruptors; as their effects relate to resistance to cell death, as constituents within environmental mixtures and as potential contributors to environmental carcinogenesis.The publisher and the author(s) have made this article open access. This is the publisher’s final pdf. The published article is copyrighted by the author(s) and published by Oxford University Press. The published article can be found at: http://carcin.oxfordjournals.org

Metabolic reprogramming and dysregulated metabolism: cause, consequence and/or enabler of environmental carcinogenesis?

Environmental contributions to cancer development are widely accepted, but only a fraction of all pertinent exposures have probably been identified. Traditional toxicological approaches to the problem have largely focused on the effects of individual agents at singular endpoints. As such, they have incompletely addressed both the pro-carcinogenic contributions of environmentally relevant low-dose chemical mixtures and the fact that exposures can influence multiple cancer-associated endpoints over varying timescales. Of these endpoints, dysregulated metabolism is one of the most common and recognizable features of cancer, but its specific roles in exposure-associated cancer development remain poorly understood. Most studies have focused on discrete aspects of cancer metabolism and have incompletely considered both its dynamic integrated nature and the complex controlling influences of substrate availability, external trophic signals and environmental conditions. Emerging high throughput approaches to environmental risk assessment also do not directly address the metabolic causes or consequences of changes in gene expression. As such, there is a compelling need to establish common or complementary frameworks for further exploration that experimentally and conceptually consider the gestalt of cancer metabolism and its causal relationships to both carcinogenesis and the development of other cancer hallmarks. A literature review to identify environmentally relevant exposures unambiguously linked to both cancer development and dysregulated metabolism suggests major gaps in our understanding of exposure-associated carcinogenesis and metabolic reprogramming. Although limited evidence exists to support primary causal roles for metabolism in carcinogenesis, the universality of altered cancer metabolism underscores its fundamental biological importance, and multiple pleiomorphic, even dichotomous, roles for metabolism in promoting, antagonizing or otherwise enabling the development and selection of cancer are suggested