Status of Salerno Laboratory (Measurements in Nuclear Emulsion)

A report on the analysis work in the Salerno Emulsion Laboratory is presented. It is related to the search for nu_mu->nu_tau oscillations in CHORUS experiment, the calibrations in the WANF (West Area Neutrino Facility) at Cern and tests and preparation for new experiments.Comment: Proc. The First International Workshop of Nuclear Emulsion Techniques (12-24 June 1998, Nagoya, Japan), 15 pages, 11 figure

La0.8Sr0.2Ga0.8Mg0.2O3-δ thin films for IT-SOFCs: Microstructure and transport properties correlation.

Highly textured La0.8Sr0.2Ga0.8Mg0.2O3 (LSGM) films with columnar structure were grown by pulsed laser deposition on (001) NdGaO3 and SrTiO3 buffered (001) MgO substrates. Combined analysis of the films structure and morphology and EIS measurements showed that the transport properties are mainly limited by perpendicular grain boundaries effects. Increasing the film thickness, columnar nanosized grains tend to coalesce leading to a decrease of grain boundary concentration, hence to enhanced conductivity

Field emission properties of as-grown multiwalled carbon nanotube films

Multiwalled carbon nanotubes have been produced by ethylene catalytic chemical vapor deposition and used to fabricate thick and dense freestanding films ("buckypapers") by membrane filtering. Field emission properties of buckypapers have been locally studied by means of high vacuum atomic force microscopy with a standard metallic cantilever used as anode to collect electrons emitted from the sample. Buckypapers showed an interesting linear dependence in the Fowler-Nordheim plots demonstrating their suitability as emitters. By precisely tuning the tip-sample distance in the submicron region we found out that the field enhancement factor is not affected by distance variations up to 2um. Finally, the study of current stability showed that the field emission current with intensity of about 3,3*10-5A remains remarkably stable (within 5% fluctuations) for several hours.Comment: 18 pages, 5 figure

Use of the frozen elephant trunk technique for type B aortic dissection and aberrant right subclavian artery: an anatomic repair of the “arteria lusoria”

Retrograde extension into the aortic arch occurs in 16.5% of patients with type B aortic dissection (TBAD) (1). This cohort of patients may be eligible for a radical repair using the frozen elephant trunk (FET) technique. The combination of surgical replacement of the aortic arch and deployment of the stent graft allows complete exclusion of the false lumen in aortic dissections. In the case of aneurysm or residual dissection, patients undergoing FET are ready for subsequent endovascular or surgical treatment (2)

Inhibition of Bromodomain and Extraterminal Domain (BET) Proteins by JQ1 Unravels a Novel Epigenetic Modulation to Control Lipid Homeostasis

The homeostatic control of lipid metabolism is essential for many fundamental physiological processes. A deep understanding of its regulatory mechanisms is pivotal to unravel prospective physiopathological factors and to identify novel molecular targets that could be employed to design promising therapies in the management of lipid disorders. Here, we investigated the role of bromodomain and extraterminal domain (BET) proteins in the regulation of lipid metabolism. To reach this aim, we used a loss-of-function approach by treating HepG2 cells with JQ1, a powerful and selective BET inhibitor. The main results demonstrated that BET inhibition by JQ1 efficiently decreases intracellular lipid content, determining a significant modulation of proteins involved in lipid biosynthesis, uptake and intracellular trafficking. Importantly, the capability of BET inhibition to slow down cell proliferation is dependent on the modulation of cholesterol metabolism. Taken together, these data highlight a novel epigenetic mechanism involved in the regulation of lipid homeostasis

mTOR inhibition leads to SRC-mediated EGFR internalisation and degradation in glioma cells

Epidermal Growth Factor receptor (EGFR) is a tyrosine kinase receptor widely expressed on the surface of numerous cell types, which activates several downstream signalling pathways involved in cell proliferation, migration and survival. EGFR alterations, such as overexpression or mutations, have been frequently observed in several cancers, including glioblastoma (GBM), and are associated to uncontrolled cell proliferation. Here we show that the inhibition of mammalian target of Rapamycin (mTOR) mediates EGFR delivery to lysosomes for degradation in GBM cells, independently of autophagy activation. Coherently with EGFR internalisation and degradation, mTOR blockade negatively affects the mitogen activated protein/extracellular signal-regulated kinase (MAPK)/ERK pathway. Furthermore, we provide evidence that Src kinase activation is required for EGFR internaliation upon mTOR inhibition. Our results further support the hypothesis that mTOR targeting may represent an effective therapeutic strategy in GBM management, as its inhibition results in EGFR degradation and in proliferative signal alteration

mTOR inhibition leads to SRC-mediated EGFR internalisation and degradation in glioma cells

Epidermal Growth Factor receptor (EGFR) is a tyrosine kinase receptor widely expressed on the surface of numerous cell types, which activates several downstream signalling pathways involved in cell proliferation, migration and survival. EGFR alterations, such as overexpression or mutations, have been frequently observed in several cancers, including glioblastoma (GBM), and are associated to uncontrolled cell proliferation. Here we show that the inhibition of mammalian target of Rapamycin (mTOR) mediates EGFR delivery to lysosomes for degradation in GBM cells, independently of autophagy activation. Coherently with EGFR internalisation and degradation, mTOR blockade negatively affects the mitogen activated protein/extracellular signal-regulated kinase (MAPK)/ERK pathway. Furthermore, we provide evidence that Src kinase activation is required for EGFR internaliation upon mTOR inhibition. Our results further support the hypothesis that mTOR targeting may represent an effective therapeutic strategy in GBM management, as its inhibition results in EGFR degradation and in proliferative signal alteration