Sustainability of sunflower cultivation for biodiesel production in central Italy according to the Renewable Energy Directive methodology

The use of renewable energies as alternative to fossil fuels has value from different points of view and has effects at environmental, social and economic level. These aspects are often connected to each other and together define the overall sustainability of bioenergy. At European level, the Directive 2009/28/EC gives the basic criteria for the estimation of sustainability of biofuels and indicates a minimum threshold of 35% of greenhouse gas saving for a biofuel in order to be considered sustainable. The Directive gives the possibility to identify standard regional values for the cultivation steps that could be utilized for the certification. This paper aims to give a contribution to the definition of these values considering the RED methodology applied to the sunflower cropped in central Italy which is characterized by a hilly landscape and not-irrigated crops. To determine input and output of sunflower cultivation in the central Italy, the results of PROBIO project, carried out by the Authors, were used. The sustainability of biodiesel produced from sunflower grown in central Italy is variable and depends on the nitrogen input and seasonal climatic conditions that affect the yields. The greenhouse gases savings of the Italian chain is 40% in average, greater than the required 35% and would be possible to assign this value as standard to the biofuel chain biodiesel from sunflower cultivated in central Italy. Using an averaged regional standard value guards against the possibility of considering unsustainable harvesting in unfavourable years and seeing it overestimated in the favourable ones

Solid biofuels production from agricultural residues and processing by-products by means of torrefaction treatment: the case of sunflower chain

The high heterogeneity of some residual biomasses makes rather difficult their energy use. Their standardisation is going to be a key aspect to get good quality biofuels from those residues. Torrefaction is an interesting process to improve the physical and chemical properties of lignocellulosic biomasses and to achieve standardisation. In the present study torrefaction has been employed on residues and by-products deriving from sunflower production chain, in particular sunflower stalks, husks and oil press cake. The thermal behaviour of these materials has been studied at first by thermogravimetric analysis in order to identify torrefaction temperatures range. Afterwards, different residence time and torrefaction temperatures have been tested in a bench top torrefaction reactor. Analyses of raw and torrefied materials have been carried out to assess the influence of the treatment. As a consequence of torrefaction, the carbon and ash contents increase while the volatilisation range reduces making the material more stable and standardised. Mass yield, energy yield and energy densification reach values of about 60%, 80% and 1.33 for sunflower stalks and 64%, 85% and 1.33 for sunflower oil press cake respectively. As highlighted by the results, torrefaction is more interesting for sunflower stalks than oil cake and husks due to their different original characteristics. Untreated oil press cake and husks, in fact, already show a good high heating value and, for this reason, their torrefaction should be mild to avoid an excessive ash concentration. On the contrary, for sunflower stalks the treatment is more useful and could be more severe

Zerovalent Fe, Co and Ni nanoparticle toxicity evaluated on SKOV-3 and U87 cell lines

ABSTRACT:We have considered nanoparticles (NPs) of Fe, Co and Ni, three transition metals sharing similar chemical properties. NP dissolution, conducted by radioactive tracer method and inductively coupled plasmamass spectrometry, indicated that NiNPs and FeNPs released in the medium a much smaller amount of ions than that released by Co NPs. The two considered methodological approaches, however, gave comparable but not identical results. All NPs are readily internalized by the cells, but their quantity inside the cells is less than 5%. Cytotoxicity and gene expression experimentswere performed on SKOV-3 and U87 cells. In both cell lines, CoNPs and NiNPs were definitely more toxic than FeNPs. Real-time polymerase chain reaction experiments aimed to evaluatemodifications of the expression of genes involved in the cellular stress response (HSP70, MT2A), or susceptible to metal exposure (SDHB1 and MLL), or involved in specific cellular processes (caspase3, IQSEC1 and VMP1), gave different response patterns in the two cell lines. HSP70, for example, was highly upregulated by CoNPs and NiNPs, but only in SKOV-3 cell lines. Overall, this work underlines the difficulties in predicting NP toxicological properties based only on their chemical characteristics. We, consequently, think that, at this stage of our knowledge, biological effects induced by metal-based NPs should be examined on a case-by-case basis following studies on different in vitro models. Moreover, with the only exception of U87 exposed to Ni, our results suggest thatmetallic NPs have caused, on gene expression, similar effects to those caused by their cor- Q2 responding ions

005_Foppa_Pedretti(567)_35

___________ 1 A Google search for "renewable energy" (with the string in inverted commas in order to search for the words in this sequence) yields more than 17 million (M) hits; a search for "energy" produces more than 350 M hits, placing it in reassuring competition with "food" (over 600 m hits). However, when limited to PDF files (i.e. documents available for download, which are likely to be reports of a certain value), the search yields more than 3 M hits for "renewable energy" and less than 55 M for "food". These data, confined to the English language, are partial but highlight various questions, in particular the huge amount of material available on the Web. Its sheer quantity would require a summarizing effort directed at identifying relevant material for teaching purposes and for spreading research results. 2 This view is widely held, with Hubbert a major points of reference (http://www.hubbertpeak.com). Given the scarcity of fossil resources, some authors propose focusing EU university curricula on "renewable energy sources" and "agricultural engineering". 3 This view has a narrower following but the literature is usually highly qualified. 4 Among various actions, one in particular deserves to be mentioned -the setting up of the Intergovernmental Panel for Climate Change (IPCC), whose remit is to study climate change and its causes. At the EU level the IPCC reports have led to an articulated body of rules aimed at reducing CO 2 emissions that will become increasingly restrictive over time

Metabolic control of DNA methylation in naive pluripotent cells.

Naive epiblast and embryonic stem cells (ESCs) give rise to all cells of adults. Such developmental plasticity is associated with genome hypomethylation. Here, we show that LIF-Stat3 signaling induces genomic hypomethylation via metabolic reconfiguration. Stat3-/- ESCs show decreased α-ketoglutarate production from glutamine, leading to increased Dnmt3a and Dnmt3b expression and DNA methylation. Notably, genome methylation is dynamically controlled through modulation of α-ketoglutarate availability or Stat3 activation in mitochondria. Alpha-ketoglutarate links metabolism to the epigenome by reducing the expression of Otx2 and its targets Dnmt3a and Dnmt3b. Genetic inactivation of Otx2 or Dnmt3a and Dnmt3b results in genomic hypomethylation even in the absence of active LIF-Stat3. Stat3-/- ESCs show increased methylation at imprinting control regions and altered expression of cognate transcripts. Single-cell analyses of Stat3-/- embryos confirmed the dysregulated expression of Otx2, Dnmt3a and Dnmt3b as well as imprinted genes. Several cancers display Stat3 overactivation and abnormal DNA methylation; therefore, the molecular module that we describe might be exploited under pathological conditions

Metabolic control of DNA methylation in naive pluripotent cells.

Naive epiblast and embryonic stem cells (ESCs) give rise to all cells of adults. Such developmental plasticity is associated with genome hypomethylation. Here, we show that LIF-Stat3 signaling induces genomic hypomethylation via metabolic reconfiguration. Stat3-/- ESCs show decreased α-ketoglutarate production from glutamine, leading to increased Dnmt3a and Dnmt3b expression and DNA methylation. Notably, genome methylation is dynamically controlled through modulation of α-ketoglutarate availability or Stat3 activation in mitochondria. Alpha-ketoglutarate links metabolism to the epigenome by reducing the expression of Otx2 and its targets Dnmt3a and Dnmt3b. Genetic inactivation of Otx2 or Dnmt3a and Dnmt3b results in genomic hypomethylation even in the absence of active LIF-Stat3. Stat3-/- ESCs show increased methylation at imprinting control regions and altered expression of cognate transcripts. Single-cell analyses of Stat3-/- embryos confirmed the dysregulated expression of Otx2, Dnmt3a and Dnmt3b as well as imprinted genes. Several cancers display Stat3 overactivation and abnormal DNA methylation; therefore, the molecular module that we describe might be exploited under pathological conditions

Author Correction: Mutant p53 sustains serine-glycine synthesis and essential amino acids intake promoting breast cancer growth

Reprogramming of amino acid metabolism, sustained by oncogenic signaling, is crucial for cancer cell survival under nutrient limitation. Here we discovered that missense mutant p53 oncoproteins stimulate de novo serine/glycine synthesis and essential amino acids intake, promoting breast cancer growth. Mechanistically, mutant p53, unlike the wild-type counterpart, induces the expression of serine-synthesis-pathway enzymes and L-type amino acid transporter 1 (LAT1)/CD98 heavy chain heterodimer. This effect is exacerbated by amino acid shortage, representing a mutant p53-dependent metabolic adaptive response. When cells suffer amino acids scarcity, mutant p53 protein is stabilized and induces metabolic alterations and an amino acid transcriptional program that sustain cancer cell proliferation. In patient-derived tumor organoids, pharmacological targeting of either serine-synthesis-pathway and LAT1-mediated transport synergizes with amino acid shortage in blunting mutant p53-dependent growth. These findings reveal vulnerabilities potentially exploitable for tackling breast tumors bearing missense TP53 mutation

Mutant p53 sustains serine-glycine synthesis and essential amino acids intake promoting breast cancer growth

Reprogramming of amino acid metabolism, sustained by oncogenic signaling, is crucial for cancer cell survival under nutrient limitation. Here we discovered that missense mutant p53 oncoproteins stimulate de novo serine/glycine synthesis and essential amino acids intake, promoting breast cancer growth. Mechanistically, mutant p53, unlike the wild-type counterpart, induces the expression of serine-synthesis-pathway enzymes and L-type amino acid transporter 1 (LAT1)/CD98 heavy chain heterodimer. This effect is exacerbated by amino acid shortage, representing a mutant p53-dependent metabolic adaptive response. When cells suffer amino acids scarcity, mutant p53 protein is stabilized and induces metabolic alterations and an amino acid transcriptional program that sustain cancer cell proliferation. In patient-derived tumor organoids, pharmacological targeting of either serine-synthesis-pathway and LAT1-mediated transport synergizes with amino acid shortage in blunting mutant p53-dependent growth. These findings reveal vulnerabilities potentially exploitable for tackling breast tumors bearing missense TP53 mutations.Mutant p53 induces serine/glycine synthesis and essential amino acids intake. Under amino acid restriction, mutant p53 is stabilized and activates a transcriptional program that sustains a metabolic adaptive response promoting breast cancer cells growt