Magnetic anisotropy reveals Acadian transpressional fabrics in an Appalachian ophiolite (Thetford Mines, Canada)

SUMMARY Magnetic anisotropy has proved effective in characterizing primary, spreading-related magmatic fabrics in Mesozoic (Tethyan) ophiolites, for example in documenting lower oceanic crustal flow. The potential for preservation of primary magnetic fabrics has not been tested, however, in older Palaeozoic ophiolites, where anisotropy may record regional strain during polyphase deformation. Here, we present anisotropy of magnetic susceptibility results from the Ordovician Thetford Mines ophiolite (Canada) that experienced two major phases of post-accretion deformation, during the Taconian and Acadian orogenic events. Magnetic fabrics consistent with modal layering in gabbros are observed at one locality, suggesting that primary fabrics may survive deformation locally in low strain zones. However, at remaining sites rocks with different magmatic origins have consistent magnetic fabrics, reflecting structurally controlled shape preferred orientations of iron-rich phases. Subhorizontal NW-SE-oriented minimum principal susceptibility axes correlate with poles to cleavage observed in overlying post-obduction, pre-Acadian sedimentary formations, indicating that the magnetic foliation in the ophiolite formed during regional NW-SE Acadian shortening. Maximum principal susceptibility axes plunging steeply to the NE are orthogonal to the orientation of regional Acadian fold axes, and are consistent with subvertical tectonic stretching. This magnetic lineation is parallel to the shape preferred orientation of secondary amphibole crystals and is interpreted to reflect grain growth during Acadian dextral transpression. This structural style has been widely reported along the Appalachian orogen, but the magnetic fabric data presented here provide the first evidence for transpression recorded in an Appalachian ophiolite.</jats:p

Transcript profiling of chitosan-treated Arabidopsis seedlings

In nature, plants can recognize potential pathogens, thus activating intricate networks of defense signals and reactions. Inducible defense is often mediated by the detection of microbe or pathogen associated molecular pattern elicitors, such as flagellin and chitin. Chitosan, the deacetylated form of chitin, plays a role in inducing protection against pathogens in many plant species. We evaluated the ability of chitosan to confer resistance to Botrytis cinerea in Arabidopsis leaves. We subsequently treated Arabidopsis seedlings with chitosan and carried out a transcript profiling analysis using both ATH1 GeneChip microarrays and quantitative RT-PCR. The results showed that defense response genes, including camalexin biosynthesis genes, were up-regulated by chitosan, both in wild-type and in the chitin-insensitive cerk1 mutant, indicating that chitosan is perceived through a CERK1-independent pathway

May Adiponectin be considered as a Novel Cardiometabolic Biomarker?

This study was designed to evaluate the interaction between total adiponectin (ADPN) and metabolic syndrome (MetS) on cardiac changes in 135 subjects with and without MetS, subgrouped according to normal or low ADPN. Left ventricular internal diameter (LVID/h), LV mass (LVM), LVM index (LVMI), interventricular septal thickness (IVST), relative wall thickness (RWT) and LV ejection fraction (EF) by echocardiography and diastolic parameters, by pulsed-wave Doppler were calculated. BMI, LVM, LVMI, LVID/h, IVST and RWT values were significantly (p<0.05) higher in both groups with low ADPN. Prevalence of left ventricular hypertrophy (p<0.001) and coronary artery disease (p<0.01) was significantly higher in both low ADPN groups. LVMI correlated directly with BMI (p<0.001), (p<0.001), MetS (p<0.001) and inversely with ADPN (p<0.0001). ADPN and BMI resulted independently associated with LVMI. In conclusion, our data suggest that hypoadiponectinemia might be considered a novel “cardiometabolic biomarker”. Accordingly, circulating ADPN might become a new target in the management of cardiometabolic syndrome

Pathogenesis and molecular mechanisms of anderson–fabry disease and possible new molecular addressed therapeutic strategies

Anderson–Fabry disease (AFD) is a rare disease with an incidenceof approxi-mately 1:117,000 male births. Lysosomal accumulation of globotriaosylceramide (Gb3) is the element characterizing Fabry disease due to a hereditary deficiency α-galactosidase A (GLA) enzyme. The accumulation of Gb3 causes lysosomal dysfunction that compromises cell signaling pathways. Deposition of sphingolipids occurs in the autonomic nervous system, dorsal root ganglia, kidney epithelial cells, vascular system cells, and myocardial cells, resulting in organ failure. This manuscript will review the molecular pathogenetic pathways involved in Anderson–Fabry disease and in its organ damage. Some studies reported that inhibition of mitochondrial function and energy metabolism plays a signif-icant role in AFD cardiomyopathy and in kidney disease of AFD patients. Furthermore, mitochondrial dysfunction has been reported as linked to the dysregulation of the au-tophagy–lysosomal pathway which inhibits the mechanistic target of rapamycin kinase (mTOR) mediated control of mitochondrial metabolism in AFD cells. Cerebrovascular complications due to AFD are caused by cerebral micro vessel stenosis. These are caused by wall thickening resulting from the intramural accumulation of glycolipids, luminal oc-clusion or thrombosis. Other pathogenetic mechanisms involved in organ damage linked to Gb3 accumulation are endocytosis and lysosomal degradation of endothelial calcium-activated intermediate-conductance potassium ion channel 3.1 (KCa3.1) via a clathrin-de-pendent process. This process represents a crucial event in endothelial dysfunction. Several studies have identified the deacylated form of Gb3, globotriaosylsphingosine (Lyso-Gb3), as the main catabolite that increases in plasma and urine in patients with AFD. The mean concentrations of Gb3 in all organs and plasma of Galactosidase A knockout mice were significantly higher than those of wild-type mice. The distributions of Gb3 isoforms vary from organ to organ. Various Gb3 isoforms were observed mainly in the kidneys, and kidney-specific Gb3 isoforms were hydroxylated. Furthermore, the action of Gb3 on the KCa3.1 channel suggests a possible contribution of this interaction to the Fabry disease process, as this channel is expressed in various cells, including endothelial cells, fibro-blasts, smooth muscle cells in proliferation, microglia, and lymphocytes. These molecular pathways could be considered a potential therapeutic target to correct the enzyme in ad-dition to the traditional enzyme replacement therapies (ERT) or drug chaperone therapy

Il valore del patrimonio. Studi per Giulio Mondini

È con vero piacere che la collana della Scuola accoglie, nel suo terzo volume, una miscellanea di scritti che è di fatto un "festschrift", una raccolta di saggi in onore di Giulio Mondini, per diversi anni Vicedirettore dell’istituzione al fianco di Vera Comoli, quindi Direttore vicario al momento della sua improvvisa e tragica scomparsa, e quindi Direttore. Da sempre al fianco della Scuola, al cui prestigio ha contribuito anche con la titolarità della UNESCO Chair "New paradigms and instruments for the management of Bio-Cultural Landscape", egli rimane, con il suo magistero, un punto di riferimento per la nostra Istituzione ed è quindi con riconoscenza che colleghi, amici, collaboratori, specialisti e dottorandi, tutti assieme, gli dedicano queste pagine di studi, in grande misura con un legame diretto a suoi scritti o a esperienze di lavoro comune. Nonostante l’apparente eterogeneità dei contributi, tra di essi spicca un filo comune, rappresentato dal patrimonio, alle scale più varie, trattato con due linee prevalenti di indirizzo, esplicitate dalle stesse due sezioni del volume: da un lato storia e "mise en valeur" e dall’altra valutazione, ma senza che questa ripartizione sia nulla di più che una struttura di comodo, visto il costante intreccio e richiamo di temi. Al di là dunque della miscellanea, è davvero possibile ravvisare un elemento di continuità e di omogeneità che lega questi studi: è il richiamo – talvolta esplicitato, talaltra sotteso – al valore (nel suo senso più ampio e alto) del patrimonio. Tra storia, memoria, protezione, valutazione ed espedienti per la valorizzazione, il Patrimonio appare a tratti grandioso, in altri contesti più soggiacente, sempre comunque alla ribalta, nella consapevolezza che rappresenti la nostra prima ricchezza

Quercetin Reduces Lipid Accumulation in a Cell Model of NAFLD by Inhibiting De Novo Fatty Acid Synthesis through the Acetyl‐CoA Carboxylase 1/AMPK/PP2A Axis

none6noDysregulation of de novo lipogenesis (DNL) has recently gained strong attention as being one of the critical factors that contribute to the assessment of non‐alcoholic fatty liver disease (NAFLD). NAFLD is often diagnosed in patients with dyslipidemias and type 2 diabetes; thus, an interesting correlation can be deduced between high hematic free fatty acids and glucose excess in the DNL dysregulation. In the present study, we report that, in a cellular model of NAFLD, the coexistence of elevated glucose and FFA conditions caused the highest cellular lipid accumulation. Deepening the molecular mechanisms of the DNL dysregulation—RT‐qPCR and immunoblot analysis demonstrated increased expression of mitochondrial citrate carrier (CiC), cytosolic acetyl‐ CoA carboxylase 1 (ACACA), and diacylglycerol acyltransferase 2 (DGAT2) involved in fatty acids and triglycerides synthesis, respectively. XBP‐1, an endoplasmic reticulum stress marker, and SREBP‐1 were the transcription factors connected to the DNL activation. Quercetin (Que), a flavonoid with strong antioxidant properties, and noticeably reduced the lipid accumulation and the expression of SREBP‐1 and XBP‐1, as well as of their lipogenic gene targets in steatotic cells. The anti‐lipogenic action of Que mainly occurs through a strong phosphorylation of ACACA, which catalyzes the committing step in the DNL pathway. The high level of ACACA phosphorylation in Que‐treated cells was explained by the intervention of AMPK together with the reduction of enzymatic activity of PP2A phosphatase. Overall, our findings highlight a direct anti‐lipogenic effect of Que exerted through inhibition of the DNL pathway by acting on ACACA/AMPK/PP2A axis; thus, suggesting this flavonoid as a promising molecule for the NAFLD treatment.openGnoni A.; Di Chiara Stanca B.; Giannotti L.; Gnoni G.V.; Siculella L.; Damiano F.Gnoni, A.; Di Chiara Stanca, B.; Giannotti, L.; Gnoni, G. V.; Siculella, L.; Damiano, F