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Partial discharges (PD) are localized breakdowns in the insulation within high-voltage (HV) equipment and can be a warning sign of potential future failure. Regular PD monitoring through preventive maintenance is essential to the reliability of many expensive HV apparatuses. Hence, the purpose of this work is to assess the performance of a novel class of multi-turn inductive loop sensors based on printed circuit board (PCB) to detect PD in free space. Based on their topology, three distinct inductive sensors, named meander, non-spiral, and spiral, are evaluated towards detecting in-lab corona, internal, and surface PDs. Through simulations and measurements, the low-frequency lumped-element circuit model for each of the three magnetic field probes was extracted. Experimental PRPD patterns showed that the three evaluated inductive loops could be effectively applied for online monitoring and recognition of PDs. The experimental results show that the single PD pulses detected by the three sensors have a typical PD pulse shape that is a damped sinusoidal function with frequency spectra spanning from 14.84 MHz to 46 MHz. The spiral sensor yielded the maximum sensitivity, while the meander topology produced the lowest.

The circadian rhythms originate within the organism and synchronize with cyclic fluctuations in the external environment. It has been demonstrated that part of the human genome is under control of the circadian clock and that a synchronizer that helps to maintain daily rhythms is Melatonin, a neuro-hormone primarily synthesized by the pineal gland during the night. The chronic disruption of circadian rhythm has been linked to many conditions such as obesity, metabolic syndrome, type 2 diabetes, cancer, and neurodegenerative diseases. Studies in the mice showed that the disruption of the retinal circadian rhythm increases the decline during the aging of photoreceptors, accelerating age-related disruption of cone cell structure, function, and viability and that the melatonin receptor deletion seems to influence the health of retinal cells, speeding up their aging. In conclusion, preserving the circadian rhythms could be to add to the prevention and treatment of age-related degenerative retinal diseases, and although additional studies are needed, melatonin could be a valid support to favor this “chronoprotection action”.

ABSTRACTChampetais themusic from the Colombian Caribbean coast and extremely popular in Afro-descendant communities of any age, increasingly fancied by non-black people as well. Despite being highly celebrated on the coast, in the capital of Bogotá and other big cities of the country’s interior, champetais still marginalized and not recognized as a music suitable for the rest of Colombian society. This article reviews the history of champetamusic from the late 1960s to the late 1990s, with a particular focus on the diverging developments in Cartagena and Barranquilla, respectively. It analyzes factors that may explain the local and regional popularity as well as the national rejection of champeta, and concludes that the elements which made champetaregionally successful are precisely those elements which hindered its acceptance on a national level: namely, the focus on blackness and the African Diaspora, distinct class-based tastes, a loud claim to space by the lower classes, and the high regional stratification of the Colombian society.

Context. AGILE is an Italian Space Agency mission dedicated to observing the gamma-ray Universe. The AGILE's very innovative instrumentation for the first time combines a gamma-ray imager (sensitive in the energy range 30 MeV–50 GeV), a hard X-ray imager (sensitive in the range 18–60 keV), a calorimeter (sensitive in the range 350 keV–100 MeV), and an anticoincidence system. AGILE was successfully launched on 2007 April 23 from the Indian base of Sriharikota and was inserted in an equatorial orbit with very low particle background.

Many recent studies have demonstrated that CO2increase is driving the climate in Mediterranean areas towards important changes, mainly represented by a temperature increase and a contemporaneous rainfall reduction. Starting from this premise, the primary aim of the present study is to investigate the effects of potential climatic changes on vegetational stress in Mediterranean ecosystems. Particular attention is here focussed only on the plants' water stress in water controlled ecosystems, mainly related to soil water balance. The interactions among climate, soil and vegetation are evaluated numerically by means of an ecohydrological model. In this work, different future climatic scenarios and their effects on woody and grassy vegetation are analysed, and the results show an increase in water stress for woody and grass vegetations: trees could suffer more because of the higher evapotranspiration rates and the decrease of the winter recharge. Results are strictly dependent on the future rainfall seasonal distribution and the possible modification in rainfall frequency and intensity. Copyright © 2010 John Wiley & Sons, Ltd.

Diacylglycerol kinases (Dgk) phosphorylate diacylglycerol (DG) to phosphatidic acid (PA), thus turning off and on, respectively, DG-mediated and PA-mediated signaling pathways. We previously showed that hepatocyte growth factor (HGF), vascular endothelial growth factor, and anaplastic lymphoma kinase activate Dgkα in endothelial and leukemia cells through a Src-mediated mechanism and that activation of Dgkα is required for chemotactic, proliferative, and angiogenic signaling in vitro. Here, we investigate the downstream events and signaling pathways regulated by Dgkα, leading to cell scatter and migration upon HGF treatment and v-Src expression in epithelial cells. We report that specific inhibition of Dgkα, obtained either pharmacologically by R59949 treatment, or by expression of Dgkα dominant-negative mutant, or by small interfering RNA-mediated down-regulation of endogenous Dgkα, impairs 1) HGF- and v-Src-induced cell scatter and migration, without affecting the loss of intercellular adhesions; 2) HGF-induced cell spreading, lamellipodia formation, membrane ruffling, and focal adhesions remodeling; and 3) HGF-induced Rac activation and membrane targeting. In summary, we provide evidence that Dgkα, activated downstream of tyrosine kinase receptors and Src, regulates crucial steps directing Rac activation and Rac-dependent remodeling of actin cytoskeleton and focal contacts in migrating epithelial cells.

Diacylglycerol kinases (Dgk) phosphorylate diacylglycerol (DG) to phosphatidic acid (PA), thus turning off and on, respectively, DG-mediated and PA-mediated signaling pathways. We previously showed that hepatocyte growth factor (HGF), vascular endothelial growth factor, and anaplastic lymphoma kinase activate Dgkα in endothelial and leukemia cells through a Src-mediated mechanism and that activation of Dgkα is required for chemotactic, proliferative, and angiogenic signaling in vitro. Here, we investigate the downstream events and signaling pathways regulated by Dgkα, leading to cell scatter and migration upon HGF treatment and v-Src expression in epithelial cells. We report that specific inhibition of Dgkα, obtained either pharmacologically by R59949 treatment, or by expression of Dgkα dominant-negative mutant, or by small interfering RNA-mediated down-regulation of endogenous Dgkα, impairs 1) HGF- and v-Src-induced cell scatter and migration, without affecting the loss of intercellular adhesions; 2) HGF-induced cell spreading, lamellipodia formation, membrane ruffling, and focal adhesions remodeling; and 3) HGF-induced Rac activation and membrane targeting. In summary, we provide evidence that Dgkα, activated downstream of tyrosine kinase receptors and Src, regulates crucial steps directing Rac activation and Rac-dependent remodeling of actin cytoskeleton and focal contacts in migrating epithelial cells.

Ghrelin is an acylated peptidyl gastric hormone acting on the pituitary and hypothalamus to stimulate appetite, adiposity, and growth hormone release, through activation of growth hormone secretagogue receptor (GHSR)-1a receptor. Moreover, ghrelin features several activities such as inhibition of apoptosis, regulation of differentiation, and stimulation or inhibition of proliferation of several cell types. Ghrelin acylation is absolutely required for both GHSR-1a binding and its central endocrine activities. However, the unacylated ghrelin form, des-acyl ghrelin, which does not bind GHSR-1a and is devoid of any endocrine activity, is far more abundant than ghrelin in plasma, and it shares with ghrelin some of its cellular activities. Inhere we show that both ghrelin and des-acyl ghrelin stimulate proliferating C2C12 skeletal myoblasts to differentiate and to fuse into multinucleated myotubes in vitro through activation of p38. Consistently, both ghrelin and des-acyl ghrelin inhibit C2C12 proliferation in growth medium. Moreover, the ectopic expression of ghrelin in C2C12 enhances differentiation and fusion of these myoblasts in differentiation medium. Finally, we show that C2C12 cells do not express GHSR-1a, but they do contain a common high-affinity binding site recognized by both acylated and des-acylated ghrelin, suggesting that the described activities on C2C12 are likely mediated by this novel, yet unidentified receptor for both ghrelin forms.

Ghrelin is an acylated peptidyl gastric hormone acting on the pituitary and hypothalamus to stimulate appetite, adiposity, and growth hormone release, through activation of growth hormone secretagogue receptor (GHSR)-1a receptor. Moreover, ghrelin features several activities such as inhibition of apoptosis, regulation of differentiation, and stimulation or inhibition of proliferation of several cell types. Ghrelin acylation is absolutely required for both GHSR-1a binding and its central endocrine activities. However, the unacylated ghrelin form, des-acyl ghrelin, which does not bind GHSR-1a and is devoid of any endocrine activity, is far more abundant than ghrelin in plasma, and it shares with ghrelin some of its cellular activities. Inhere we show that both ghrelin and des-acyl ghrelin stimulate proliferating C2C12 skeletal myoblasts to differentiate and to fuse into multinucleated myotubes in vitro through activation of p38. Consistently, both ghrelin and des-acyl ghrelin inhibit C2C12 proliferation in growth medium. Moreover, the ectopic expression of ghrelin in C2C12 enhances differentiation and fusion of these myoblasts in differentiation medium. Finally, we show that C2C12 cells do not express GHSR-1a, but they do contain a common high-affinity binding site recognized by both acylated and des-acylated ghrelin, suggesting that the described activities on C2C12 are likely mediated by this novel, yet unidentified receptor for both ghrelin forms.

Substrate access to the active-site cavity of squalene-hopene cyclase from Alicyclobacillus acidocaldarious and lanosterol synthase [OSC (oxidosqualene cyclase)] from Saccharomyces cerevisiae was studied by an inhibition, mutagenesis and homology-modelling approach. Crystal structure and homology modelling indicate that both enzymes possess a narrow constriction that separates an entrance lipophilic channel from the active-site cavity. The role of the constriction as a mobile gate that permits substrate passage was investigated by experiments in which critically located Cys residues, either present in native protein or inserted by site-directed mutagenesis, were labelled with specifically designed thiol-reacting molecules. Some amino acid residues of the yeast enzyme, selected on the basis of sequence alignment and a homology model, were individually replaced by residues bearing side chains of different lengths, charges or hydrophobicities. In some of these mutants, substitution severely reduced enzymatic activity and thermal stability. Homology modelling revealed that in these mutants some critical stabilizing interactions could no longer occur. The possible critical role of entrance channel and constriction in specific substrate recognition by eukaryotic OSC is discussed.

To report the estimated incidence, probability, risk factors, and 1-year outcomes of rhegmatogenous retinal detachment (RRD) in eyes receiving intravitreal injections (IVTs) of VEGF inhibitors for various retinal conditions in routine clinical practice.

Two pairs of isomers (18Z)- (8), (18E)-29-methylidene-2,3-oxidohexanorsqualene (21), and (18Z)- (31), (18E)-29-methylidene-2,3-oxidosqualene (34), have been obtained in a fully stereospecific manner, as inhibitors of rat and yeast oxidosqualene cyclase. A new method for the synthesis of C22 squalene aldehyde 2,3-epoxide is reported, as well as that of other 19-modified 2,3-oxidosqualene analogues.We found that the activity is the opposite in the two series:  the (E)-hexanormethylidene 21 and the (Z)-methylidene 31 are potent and irreversible inhibitors of oxidosqualene cyclase, while (Z)-hexanormethylidene 8 and (E)-methylidene 34 are almost completely inactive. Reduction of the 18,19-double bond, such as in 39, eliminates the activity, while removal of both of the 19-linked groups such as in heptanor derivative 40 greatly reduces inhibition of the enzyme. (E)-Hexanormethylidene 21 results the first irreversible inhibitor of the series toward the yeast enzyme.

Effects of chlorpromazine and d-amphetamine on food dominance were studied in 18 purebred dogs over a 10-wk. period. Dominance was determined by time spent at a common food dish. Trials were conducted each week with no drugs to determine the dominance relationships, followed by each dominant and submissive member receiving either saline, d-amphetamine, or chlorpromazine. New pairings were created on the following week with a total of 72 pairings and 144 drug treatments. Dominance (dominant or submissive) was a function of particular pairings. Amphetamine altered dominance relationships only when administered to the dominant animal. Chlorpromazine altered the dominance relationship only when administered to the submissive animal.

The metabolic fate of anti-inflammatory agent 2-(5-ethylpyridin-2-yl)benzimidazole (KB-1043) was studied in rats after oral administration. An average of 12.2±1.5% of the dose was excreted in the urine in the course of 0–48 h; 56.7±2.6% with feces. Two metabolites were also detected in the urine and isolated by reverse phase HPLC. Structures have been given after identification by comparison with authentic samples.

The metabolism of phenelzine (2-phenylethylhydrazine) by rat liver microsomes yields phenylacetaldehyde, 2-phenylethanol, and ethylbenzene. A carbon radical is formed during the oxidative metabolism of phenelzine that reacts with the prosthetic heme of cytochrome P-450 and irreversibly inactivates the enzyme. The radical has been spin-trapped, isolated, and shown by mass spectrometry to be the 2-phenylethyl radical. The metal-free pophyrin derived from the prosthetic heme group has been isolated and identified as N-(2-phenylethyl)protoporphyrin IX. The metabolism of phenelzine, an alkyl hydrazine, thus yields a carbon radical that inactivates cytochrome P-450, is converted to a hydrocarbon by hydrogen atom abstraction, and reacts with spin traps or (presumably) alternative cellular targets.

The abilities of 22,23-epoxy-2-aza-2,3-dihydrosqualene and the corresponding N-oxide, 22,23-epoxy-2-aza-2,3-dihydrosqualene-N-oxide, to inhibit sterol biosynthesis were studied in microsomes and cells of Saccharomyces cerevisiae and Candida albicans. 22,23-Epoxy-2-aza-2,3-dihydrosqualene, which differs from the other inhibitor only in lacking oxygen at position 2, exhibited higher inhibitory properties in all preparations tested. The different levels of effectiveness of the two azasqualene derivatives were evident mostly in microsomes from S. cerevisiae (the 50 inhibitory concentrations of the 2-aza derivative and the corresponding N-oxide on oxidosqualene cyclase were 30 and 120 microM respectively) and in cell cultures of the same strain (1 order of magnitude separated the inhibitory activities of the two compounds on sterol biosynthesis). A possible explanation for the differences between 22,23-epoxy-2-aza-2,3-dihydrosqualene and the corresponding N-oxide arose from the study of their metabolic fates in vivo and in vitro. While the 2-aza derivative did not undergo any transformation, the N-oxide compound was actively reduced to the corresponding amine in microsomes and in cells of both yeast strains. 22,23-Epoxy-2-aza-2,3-dihydrosqualene-N-oxide seems to behave as a proinhibitor of sterol biosynthesis, becoming active only after transformation into the active form 22,23-epoxy-2-aza-2,3-dihydrosqualene.

Mutations in lamin A/C and emerin change myogenic cell fate by disrupting heterochromatin tethering to the nuclear envelope.