A standard source for high energy neutrino astronomy

A standard source of high energy neutrinos composed of a source of accelerated particles imbedded in a cloud of low density gas is described. The main mechanism of neutrino production in the source is pp-collision, and the main process of detection is through muons produced underground by the neutrions. The flux of neutrino-produced muons is computed for sources with different spectral index

A search for cosmic sources of high energy neutrinos with small underground detectors

On the basis of standard source calculations of high energy neutrino fluxes, some models of astrophysical object (single stars and binary systems) are discussed from which a detectable muon flux is expected in small underground detectors

Climate change and migration: Is agriculture the main channel?

Migration and climate change are two of the most important challenges the world currently faces. They are connected as climate change may stimulate or hinder migration. One of the sectors strongly affected by climate change is agriculture, which is the source of income for most of the world's poor. Climate change may affect agricultural productivity and hence migration because of its impact on average temperatures and rainfall and because it increases the frequency and intensity of weather shocks. In this paper we use data on 108 countries from 1960 to 2010 to analyze the relationship between weather variations, changes in agricultural productivity and international migration. We find that negative shocks to agricultural productivity caused by climate fluctuations significantly increase emigration from developing countries, an especially strong impact in poor countries but less so in middle income countries. These results are robust to the definitions of the poor country sample, and to several checks and alternative explanations suggested by the literature. Importantly, our results point to a causal interpretation of the agricultural channel to explain the climate change-migration nexus

Contribution of G inhibitory protein alpha subunits in paradoxical hyperalgesia elicited by exceedingly low doses of morphine in mice.

Aims: Although morphine, at higher doses, induces analgesia, it may also enhance sensitivity to pain at extremely low doses as shown in studies for testing an animal's sensitivity to pain. We used an antisense approach capable of selectively down-regulating in vivo G(i)(G inhibitory protein),G(o) and G(s) members of the G(alpha), sub-family protein subunits in order to establish if these proteins might be implicated in the effects induced by extremely low morphine doses on acute thermonociception. Main methods: Mice pretreated with a morphine hyperalgesic dose (1 mu g/kg) were submitted to hot plate test after pre-treatment with antisense oligodeoxynucleotides (aODNs) targeting G(i alpha), G(o alpha) and G(s alpha) regulatory proteins. The association of G-protein (guanine nucleotide-binding regulatory protein) coupled receptors with G protein was investigated using co-immunoprecipitation procedure. Key findings: The downregulation of the G(i alpha 1-3) and G(o alpha 1) proteins reversed the licking latency responses induced by 1 mu g/kg morphine administration toward the basal value whereas downregulation of the G(o alpha 2) and G(s alpha) proteins did not significantly modify the hyperalgesic response. Significance: These results suggest that G inhibitory proteins play a role in the production of low dose evoked morphine hyperalgesia in mouse. Immunoprecipitation studies revealed that both mu opioid receptor (mu OR) and alpha(2) adrenoreceptor (alpha(2) AR) are bound to G inhibitory proteins in hyperalgesic response to morphine extremely low dose. Both mu OR and alpha(2) AR appear to be necessary for low morphine dose induced hyperalgesic response through G inhibitory proteins. (C) 2011 Elsevier Inc. All rights reserved

Conceivable difference in the anti-inflammatory mechanisms of lipocortins 1 and 5

Human recombinant lipocortins (LCT) 1 and 5 have been expressed in a yeast secretion vector and purified by ion exchange chromatography. The action of the proteins has been investigated in two models of experimental acute inflammation in the rat: carrageenin induced paw oedema and zymosan induced pleurisy. The effects of the proteins on PGE2 release in vitro by rat macrophages stimulated with zymosan and on rat neutrophil chemotaxis induced by FMLP have also been assessed. LCT-1 significantly inhibited both paw swelling in carrageenin oedema and leukocyte migration in zymosan pleurisy. Moreover it showed a dose dependent, inhibitory effect on PGE2 release. Neutrophil chemotaxis was only weakly affected by LCT-1. Conversely LCT-5 did not reduce carrageenin oedema and slightly inhibited PGE2 release, but showed profound, dose dependent inhibitory activity on leukocyte migration in zymosan pleurisy and on neutrophil chemotaxis. These data suggest that LCT-1 acts mainly by interfering with arachidonic acid metabolism via the inhibition of phospholipase A2. The anti-inflammatory activity of LCT-5, at variance with LCT-1, may be due to a direct effect on cell motility in addition to the interference with arachidonic acid metabolism

Role of potassium channels in the antinociception induced by agonists of alpha2-adrenoceptors

1. The effect of the administration of pertussis toxin (PTX) as well as modulators of different subtypes of K(+) channels on the antinociception induced by clonidine and guanabenz was evaluated in the mouse hot plate test. 2. Pretreatment with pertussis toxin (0.25 μg per mouse i.c.v.) 7 days before the hot-plate test, prevented the antinociception induced by both clonidine (0.08–0.2 mg kg(−1), s.c.) and guanabenz (0.1–0.5 mg kg(−1), s.c.). 3. The administration of the K(ATP) channel openers minoxidil (10 μg per mouse, i.c.v.), pinacidil (25 μg per mouse, i.c.v.) and diazoxide (100 mg kg(−1), p.o.) potentiated the antinociception produced by clonidine and guanabenz whereas the K(ATP) channel blocker gliquidone (6 μg per mouse, i.c.v.) prevented the α(2) adrenoceptor agonist-induced analgesia. 4. Pretreatment with an antisense oligonucleotide (aODN) to mKv1.1, a voltage-gated K(+) channel, at the dose of 2.0 nmol per single i.c.v. injection, prevented the antinociception induced by both clonidine and guanabenz in comparison with degenerate oligonucleotide (dODN)-treated mice. 5. The administration of the Ca(2+)-gated K(+) channel blocker apamin (0.5–2.0 ng per mouse, i.c.v.) never modified clonidine and guanabenz analgesia. 6. At the highest effective doses, none of the drugs used modified animals' gross behaviour nor impaired motor coordination, as revealed by the rota-rod test. 7. The present data demonstrate that both K(ATP) and mKv1.1 K(+) channels represent an important step in the transduction mechanism underlying central antinociception induced by activation of α(2) adrenoceptors

Results of low energy background measurements with the Liquid Scintillation Detector (LSD) of the Mont Blanc Laboratory

The 90 tons liquid scintillation detector (LSD) is fully running since October 1984, at a depth of 5,200 hg/sq cm of standard rock underground. The main goal is to search for neutrino bursts from collapsing stars. The experiment is very sensitive to detect low energy particles and has a very good signature to gamma-rays from (n,p) reaction which follows the upsilon e + p yields n + e sup + neutrino capture. The analysis of data is presented and the preliminary results on low energy measurements are discussed