High velocity blue-shifted FeII absorption in the dwarf star-forming galaxy PHL293B: Evidence for a wind driven supershell?

X-shooter and ISIS WHT spectra of the starforming galaxy PHL 293B also known as A2228-00 and SDSS J223036.79-000636.9 are presented in this paper. We find broad (FWHM = 1000km/s) and very broad (FWZI = 4000km/s) components in the Balmer lines, narrow absorption components in the Balmer series blueshifted by 800km/s, previously undetected FeII multiplet (42) absorptions also blueshifted by 800km/s, IR CaII triplet stellar absorptions consistent with [Fe/H] < -2.0 and no broad components or blushifted absorptions in the HeI lines. Based on historical records, we found no optical variability at the 5 sigma level of 0.02 mag between 2005 and 2013 and no optical variability at the level of 0.1mag for the past 24 years. The lack of variability rules out transient phenomena like luminous blue variables or SN IIn as the origin of the blue shifted absorptions of HI and FeII. The evidence points to either a young and dense expanding supershell or a stationary cooling wind, in both cases driven by the young cluster wind.Comment: Accepted for publication in MNRAS; 15 pages, 10 figure

p38(MAPK)/p53 signalling axis mediates neuronal apoptosis in response to tetrahydrobiopterin-induced oxidative stress and glucose uptake inhibition: implication for neurodegeneration.

BH4 (tetrahydrobiopterin) induces neuronal demise via production of ROS (reactive oxygen species). In the present study we investigated the mechanisms of its toxicity and the redox signalling events responsible for the apoptotic commitment in SH-SY5Y neuroblastoma cells and in mouse primary cortical neurons. We identified in p38(MAPK)/p53 a BH4-responsive pro-apoptotic signalling axis, as demonstrated by the recovery of neuronal viability achieved by gene silencing or pharmacological inhibition of both p38(MAPK) and p53. BH4-induced oxidative stress was characterized by a decrease in the GSH/GSSG ratio, an increase in protein carbonylation and DNA damage. BH4 toxicity and the redox-activated apoptotic pathway were counteracted by the H2O2-scavengers catalase and N-acetylcysteine and enhanced by the GSH neo-synthesis inhibitor BSO (buthionine sulfoximine). We also demonstrated that BH4 impairs glucose uptake and utilization, which was prevented by catalase administration. This effect contributes to the neuronal demise, exacerbating BH4-induced nuclear damage and the activation of the pro-apoptotic p38(MAPK)/p53 axis. Inhibition of glucose uptake was also observed upon treatment with 6-hydroxydopamine, another redox-cycling molecule, suggesting a common mechanism of action for auto-oxidizable neurotoxins

THE CHURCH OF SANT'ANDREA IN BERGAMO: AN INTEGRATED SURVEY FOR KNOWLEDGE AND CONSERVATION

Abstract. The church dedicated to Sant'Andrea (St. Andrew) in Porta Dipinta street in Bergamo city is a treasure that keep inside it a rich heritage of great historical and cultural value, both from the architectural and from the artistic point of view. Lacking of the façade (left unfinished), it is often neglected, despite being on the main road leading to the old town from Sant'Agostino Gate. The approach to an historical building like this requires a multi-disciplinary integration, in order to join the technical competence of engineering sciences to the sensitivity of human and fine arts sciences. For a better understanding of the structural performances of the building, historical research, measurement survey, material and decay condition study have to complement each other.</p

Under the ROS…thiol network is the principal suspect for autophagy commitment.

Low molecular weight and protein sulphydryls undergo reactive oxygen species (ROS)-mediated oxidation. However, in contrast to the irreversible damages that oxidative conditions yield on biomolecules, the oxidation of reactive cysteines frequently results in reversible modifications, which represent the prototype of the molecular mechanisms underlying redox signaling. Many proteins involved in a wide range of cellular processes have been classified as “redoxsensitive,” thereby modulating their function/activity dependent on the redox state of their critical thiols. Growing evidence from the past few years supports the idea that ROS production also correlates with the occurrence of autophagy. Nonetheless, the cysteine protease Atg4 remains the sole example of a protein whose redox regulation has been completely characterized and demonstrated to be necessary for the progression of autophagy. The principal aim of this commentary is to draw attention to the remarkable number of proteins that can fit the double role of: (i) being involved in autophagy, especially in autophagosome formation and (ii) sensing alterations of the cellular redox state by means of reactive cysteine residues. We will also attempt to provide a hypothetical model to explain the possible functional role of thiols in the occurrence of autophagy and outline a network of redox reactions likely concurring to allow the correct initiation and completion of autophagosomes

Carcinoma cells activate AMP-activated protein kinase-dependent autophagy as survival response to kaempferol-mediated energetic impairment.

Kaempferol, a dietary cancer chemopreventive polyphenol, has been reported to trigger apoptosis in several tumor histotypes, but the mechanism underlying this phenomenon is not fully understood. Here, we demonstrate that in HeLa cells, kaempferol induces energetic failure due to inhibition of both glucose uptake and Complex I of the mitochondrial respiratory chain. As adaptive response, cells activate autophagy, the occurrence of which was established cytofluorometrically, upon acridine orange staining, and immunochemically, by following the increase of the autolysosome-associated form of the microtubule-associated protein light chain 3 (LC3-II). Autophagy is an early and reversible process occurring as survival mechanisms against apoptosis. Indeed, chemical inhibition of autophagy, by incubations with monensin, wortmannin, 3-methyladenine, or by silencing Atg5, significantly increases the extent of apoptosis, which takes place via the mitochondrial pathway, and shortens the time in which the apoptotic markers are detectable. We also demonstrate that autophagy depends on the early activation of the AMP-activated protein kinase (AMPK)/mTOR-mediated pathway. The overexpression of dominant negative AMPK results in a decrease of autophagic cells, a decrement of LC3-II levels, and a significant increase of apoptosis. Experiments performed with another carcinoma cell line yielded the same results, suggesting for kaempferol a unique mechanism of action

Rapid onset of bronchodilation with formoterol/beclomethasone Modulite and formoterol/budesonide Turbuhaler as compared to formoterol alone in patients with COPD

In the present study, we examined whether there is a difference in the onset of bronchodilatation between formoterol/beclomethasone 12/200 μg Modulite and formoterol/budesonide 9/320 μg Turbuhaler in patients with COPD. We enrolled 28 patients with stable COPD. Both formoterol/beclomethasone and formoterol/budesonide elicited a larger mean FEV1–AUC0−15min than formoterol alone, whereas there was no significant difference between their FEV1–AUC0−15min. Also the change in FEV1 15 min after inhalation of formoterol/beclomethasone combination or formoterol/budesonide combination was greater than that induced by formoterol alone. This study confirms the rapid effect of the inhaled corticosteroid component when combined with formoterol and indicates that the onset of bronchodilation of formoterol/beclomethasone Modulite and formoterol/budesonide Turbuhaler are similar and greater than formoterol alone in patients with COPD

Does attentional style moderate the relationship between time perspective and social network addiction? A cross‐sectional study on a sample of social networking sites users

The present study investigates the role of attentional style as a moderator variable between temporal perspective and social network addiction, since little is known about users’ cognitive variables involved in this kind of addictive behavior. To achieve this goal, a sample of 186 volunteers and anonymous social networking sites users (M = 34%; F = 66%; Mage = 22.54 years; SD = 3.94; range: 18 ÷ 45 years) participated in a cross‐sectional study. All participants filled out self-report instruments measuring temporal perspective, internal vs. external attentional style, and social network addiction. The results align with the previous literature and show that present fatalistic and past negative time orientations are associated with social network addiction, whereas the future is a negative precursor. Moreover, a four‐step hierarchical regression analysis showed that internal attentional style is a significant moderator of the relationship between high levels of temporal perspective and a high level of social network addiction. This result suggests that social network‐addicted users are oriented toward internal stimuli such as their intrusive thoughts or feelings and that social network addiction is similar to obsessive compulsive disorders, depression, or anxiety. Despite its limitations, the present study could contribute to the efforts of clinicians, psychiatrists, psychologists, teachers, and all those who seek to combat social network addiction in developing treatment programs to reduce its harmful effects