A 'Darboux Theorem' for shifted symplectic structures on derived Artin stacks, with applications

This is the fifth in a series arXiv:1304.4508, arXiv:1305,6302, arXiv:1211.3259, arXiv:1305.6428 on the '$k$-shifted symplectic derived algebraic geometry' of Pantev, Toen, Vaquie and Vezzosi, arXiv:1111.3209. This paper extends the previous three from (derived) schemes to (derived) Artin stacks. We prove four main results: (a) If $(X,\omega)$ is a $k$-shifted symplectic derived Artin stack for $k<0$ in the sense of arXiv:1111.3209, then near each $x\in X$ we can find a 'minimal' smooth atlas $\varphi:U\to X$ with $U$ an affine derived scheme, such that $(U,\varphi^*(\omega))$ may be written explicitly in coordinates in a standard 'Darboux form'. (b) If $(X,\omega)$ is a $-1$-shifted symplectic derived Artin stack and $X'$ the underlying classical Artin stack, then $X'$ extends naturally to a 'd-critical stack' $(X',s)$ in the sense of arXiv:1304.4508. (c) If $(X,s)$ is an oriented d-critical stack, we can define a natural perverse sheaf $P^\bullet_{X,s}$ on $X$, such that whenever $T$ is a scheme and $t:T\to X$ is smooth of relative dimension $n$, then $T$ is locally modelled on a critical locus Crit$(f:U\to{\mathbb A}^1)$ for $U$ smooth, and $t^*(P^\bullet_{X,s})[n]$ is locally modelled on the perverse sheaf of vanishing cycles $PV_{U,f}^\bullet$ of $f$. (d) If $(X,s)$ is a finite type oriented d-critical stack, we can define a natural motive $MF_{X,s}$ in a ring of motives $\bar{\mathcal M}^{st,\hat\mu}_X$ on $X$, such that whenever $T$ is a finite type scheme and $t:T\to X$ is smooth of dimension $n$, then $T$ is locally modelled on a critical locus Crit$(f:U\to{\mathbb A}^1)$ for $U$ smooth, and ${\mathbb L}^{-n/2}\odot t^*(MF_{X,s})$ is locally modelled on the motivic vanishing cycle $MF^{mot,\phi}_{U,f}$ of $f$ in $\bar{\mathcal M}^{st,\hat\mu}_T$. Our results have applications to categorified and motivic extensions of Donaldson-Thomas theory of Calabi-Yau 3-foldsComment: (v2) 61 pages. Minor corrections, foundational material on perverse sheaves shortene

Magnetoelectric Effects on Composite Nano Granular Fe/TiO2−δFe/TiO_{2-\delta} Films

Employing a new experimental technique to measure magnetoelectric response functions, we have measured the magnetoelectric effect in composite films of nano granular metallic iron in anatase titanium dioxide at temperatures below 50 K. A magnetoelectric resistance is defined as the ratio of a transverse voltage to bias current as a function of the magnetic field. In contrast to the anomalous Hall resistance measured above 50 K, the magnetoelectic resistance below 50 K is significantly larger and exhibits an even symmetry with respect to magnetic field reversal $H\to -H$. The measurement technique required attached electrodes in the plane of the film composite in order to measure voltage as a function of bias current and external magnetic field. To our knowledge, the composite films are unique in terms of showing magnetoelectric effects at low temperatures, $<$ 50 K, and anomalous Hall effects at high temperatures, $>$ 50 K.Comment: ReVTeX, 2 figures, 3 page

Transcriptional Regulation of the Mitochondrial Citrate and Carnitine/Acylcarnitine Transporters: Two Genes Involved in Fatty Acid Biosynthesis and E-oxidation

Transcriptional regulation of genes involved in fatty acid metabolism is considered the major long-term regulatory mechanism controlling lipid homeostasis. By means of this mechanism, transcription factors, nutrients, hormones and epigenetics control not only fatty acid metabolism, but also many metabolic pathways and cellular functions at the molecular level. The regulation of the expression of many genes at the level of their transcription has already been analyzed. This review focuses on the transcriptional control of two genes involved in fatty acid biosynthesis and oxidation: the citrate carrier (CIC) and the carnitine/ acylcarnitine/carrier (CAC), which are members of the mitochondrial carrier gene family, SLC25. The contribution of tissue-specific and less tissue-specific transcription factors in activating or repressing CIC and CAC gene expression is discussed. The interaction with drugs of some transcription factors, such as PPAR and FOXA1, and how this interaction can be an attractive therapeutic approach, has also been evaluated. Moreover, the mechanism by which the expression of the CIC and CAC genes is modulated by coordinated responses to hormonal and nutritional changes and to epigenetics is highlighte

Is mass loss along the red giant branch of globular clusters sharply peaked? The case of M3

There is a growing evidence that several globular clusters must contain multiple stellar generations, differing in helium content. This hypothesis has helped to interpret peculiar unexplained features in their horizontal branches. In this framework we model the peaked distribution of the RR Lyr periods in M3, that has defied explanation until now. At the same time, we try to reproduce the colour distribution of M3 horizontal branch stars. We find that only a very small dispersion in mass loss along the red giant branch reproduces with good accuracy the observational data. The enhanced and variable helium content among cluster stars is at the origin of the extension in colour of the horizontal branch, while the sharply peaked mass loss is necessary to reproduce the sharply peaked period distribution of RR Lyr variables. The dispersion in mass loss has to be <~ 0.003 Msun, to be compared with the usually assumed values of ~0.02 Msun. This requirement represents a substantial change in the interpretation of the physical mechanisms regulating the evolution of globular cluster stars.Comment: Accepted for publication in The Astrophysical Journa

Magnetic fields from inflation?

We consider the possibility of generation of the seeds of primordial magnetic field on inflation and show that the effect of the back reaction of this field can be very important. Assuming that back reaction does not spoil inflation we find a rather strong restriction on the amplitude of the primordial seeds which could be generated on inflation. Namely, this amplitude recalculated to the present epoch cannot exceed $10^{-32}G$ in $Mpc$ scales. This field seems to be too small to be amplified to the observable values by galactic dynamo mechanism.Comment: 10 page

Hyperhomocysteinemia: related genetic diseases and congenital defects, abnormal DNA methylation and newborn screening issues

Homocysteine, a sulfur-containing amino acid derived from the methionine metabolism, is located at the branch point of two pathways of the methionine cycle, i.e. remethylation and transsulfuration. Gene abnormalities in the enzymes catalyzing reactions in both pathways lead to hyperhomocysteinemia. Hyperhomocysteinemia is associated with increased risk for congenital disorders, including neural tube closure defects, heart defects, cleft lip/palate, Down syndrome, and multi-system abnormalities in adults. Since hyperhomocysteinemia is known to affect the extent of DNA methylation, it is likely that abnormal DNA methylation during embryogenesis, may be a pathogenic factor for these congenital disorders. In this review we highlight the importance of homocysteinemia by describing the genes encoding for enzymes of homocysteine metabolism relevant to the clinical practice, especially cystathionine-β-synthase and methylenetetrahydrofolate reductase mutations, and the impairment of related metabolites levels. Moreover, a possible correlation between hyperhomocysteine and congenital disorders through the involvement of abnormal DNA methylation during embryogenesis is discussed. Finally, the relevance of present and future diagnostic tools such as tandem mass spectrometry and next generation sequencing in newborn screening is highlighted

A key role of the mitochondrial citrate carrier (SLC25A1) in TNFα- and IFNγ-triggered inflammation

The chronic induction of inflammation underlies multiple pathological conditions, including metabolic, autoimmune disorders and cancer. The mitochondrial citrate carrier (CIC), encoded by the SLC25A1 gene, promotes the export of citrate from the mitochondria to the cytoplasm, a process that profoundly influences energy balance in the cells. We have previously shown that SLC25A1 is a target gene for lipopolysaccharide signaling and promotes the production of inflammatory mediators. We now demonstrate that SLC25A1 is induced at the transcriptional level by two key pro-inflammatory cytokines, tumor necrosis factor-α (TNFα) and interferon-γ (IFNγ), and such induction involves the activity of the nuclear factor kappa B and STAT1 transcription factors. By studying the down-stream events following SLC25A1 activation during signals that mimic inflammation, we demonstrate that CIC is required for regulating the levels of nitric oxide and of prostaglandins by TNFα or IFNγ. Importantly, we show that the citrate exported from mitochondria via CIC and its downstream metabolic intermediate, acetyl-coenzyme A, are necessary for TNFα or IFNγ to induce nitric oxide and prostaglandin production. These findings provide the first line of evidence that the citrate export pathway, via CIC, is central for cytokine-induced inflammatory signals and shed new light on the relationship between energy metabolism and inflammation

TRANSCRIPTION OF THE MITOCHONDRIAL CITRATE CARRIER GENE: ROLE OF SREBP-1, UPREGULATION BY INSULIN AND DOWNREGULATION BY PUFA

In this study we investigated the transcriptional role of the sterol regulatory element (SRE) present in the promoter of the mitochon- drial citrate carrier (CIC). We show that wild-type (but not mutated) CIC SRE cloned in front of the luciferase promoter confers tran- scriptional activation of the gene reporter. We also demonstrate that insulin activates, and polyunsaturated fatty acids (PUFA) inhibit, the gene reporter activity driven by the CIC promoter containing wild-type (but not mutated) SRE. Finally, both insulin treatment and overexpression of SRE binding protein (SREBP-1) increase the CIC transcript and protein levels, whereas PUFA have an opposite effect. These results show that SRE/SREBP-1 play a role in the transcriptional regulation of CIC by insulin and PUFA

Effect of layered double hydroxide intercalated with fluoride ions on the physical, biological and release properties of a dental composite resin

OBJECTIVES: The aim of this work was the preparation of a new fluoride-releasing dental material characterized by a release of fluoride relatively constant over time without any initial toxic burst effect. This type of delivery is obtained by a matrix controlled elution and elicits the beneficial effect of a low amount of fluoride on human dental pulp stem cells (hDPSCs) towards mature phenotype. METHODS: The modified hydrotalcite intercalated with fluoride ions (LDH-F), used as filler, was prepared via ion exchange procedure and characterized by X-ray diffraction and FT-IR spectroscopy. The LDH-F inorganic particles (0.7, 5, 10, 20wt.%) were mixed with a photo-activated Bis-GMA/TEGDMA (45/55wt/wt) matrix and novel visible-light cured composites were prepared. The dynamic thermo-mechanical properties were determined by dynamic mechanical analyzer. The release of fluoride ions in physiological solution was determined using a ionometer. Total DNA content was measured by a PicoGreen dsDNA quantification kit to assess the proliferation rate of hDPSCs. Alkaline phosphatase activity (ALP) was measured in presence of fluoride resins. RESULTS: Incorporation of even small mass fractions (e.g. 0.7 and 5wt.%) of the fluoride LDH in Bis-GMA/TEGDMA dental resin significantly improved the mechanical properties of the pristine resin, in particular at 37°C. The observed reinforcement increases on increasing the filler concentration. The release of fluoride ions resulted very slow, lasting months. ALP activity gradually increased for 28 days in hDPSCs cell grown, demonstrating that low concentrations of fluoride contributed to the cell differentiation. CONCLUSIONS: The prepared composites containing different amount of hydrotalcite filler showed improved mechanical properties, slow fluoride release and promoted hDPSCs cell proliferation and cell differentiation