38 research outputs found
The European Union, borders and conflict transformation: the case of Cyprus
Much of the existing literature on the European Union (EU), conflict transformation and border dynamics has been premised on the assumption that the nature of the border determines EU intervention and the consequences that flow from this in terms of EU impact. The article aims to transcend this literature through assessing how domestic interpretations influence EU border transformation in conflict situations, taking Cyprus as a case study. Moreover, the objective is to fuse the literature on EU bordering impact and perceptions of the EUâs normative projection in conflict resolution. Pursuing this line of inquiry is an attempt to depart from the notion of borders being constructed solely by unidirectional EU logics of engagement or bordering practices to a conceptualization of the border as co-constituted space, where the interpretations of the EUâs normative projections by conflict parties, and the strategies that they pursue, can determine the relative openness of the EU border
CP Violation in the Heavy Neutrinos Production Process
The problem of CP conservation and CP violation for two heavy neutrinos
production in interaction is considered. Very convenient way of
parametrization of the neutrino mass matrix, from which necessary and
sufficient condition for CP conservation easily follows, is presented. Contrary
to the Kobayashi-Maskawa mechanism, the effects of CP violation in the lepton
sector with Majorana neutrinos can be very large. Change of the total cross
section caused by CP violation can be much larger then the cross section
itself.Comment: LATEX,12 page
Systematic review of influenza resistance to the neuraminidase inhibitors
<p>Abstract</p> <p>Background</p> <p>Antivirals play a critical role in the prevention and the management of influenza. One class of antivirals, neuraminidase inhibitors (NAIs), is effective against all human influenza viruses. Currently there are two NAI drugs which are licensed worldwide: oseltamivir (Tamiflu<sup>Âź</sup>) and zanamivir (Relenza<sup>Âź</sup>); and two drugs which have received recent approval in Japan: peramivir and laninamivir. Until recently, the prevalence of antiviral resistance has been relatively low. However, almost all seasonal H1N1 strains that circulated in 2008-09 were resistant to oseltamivir whereas about 1% of tested 2009 pandemic H1N1 viruses were found to be resistant to oseltamivir. To date, no studies have demonstrated widespread resistance to zanamivir. It seems likely that the literature on antiviral resistance associated with oseltamivir as well as zanamivir is now sufficiently comprehensive to warrant a systematic review.</p> <p>The primary objectives were to systematically review the literature to determine the incidence of resistance to oseltamivir, zanamivir, and peramivir in different population groups as well as assess the clinical consequences of antiviral resistance.</p> <p>Methods</p> <p>We searched MEDLINE and EMBASE without language restrictions in September 2010 to identify studies reporting incidence of resistance to oseltamivir, zanamivir, and peramivir. We used forest plots and meta-analysis of incidence of antiviral resistance associated with the three NAIs. Subgroup analyses were done across a number of population groups. Meta-analysis was also performed to evaluate associations between antiviral resistance and clinical complications and symptoms.</p> <p>Results</p> <p>We identified 19 studies reporting incidence of antiviral resistance. Meta-analysis of 15 studies yielded a pooled incidence rate for oseltamivir resistance of 2.6% (95%CI 0.7% to 5.5%). The incidence rate for all zanamivir resistance studies was 0%. Only one study measured incidence of antiviral resistance among subjects given peramivir and was reported to be 0%. Subgroup analyses detected higher incidence rates among influenza A patients, especially for H1N1 subtype influenza. Considerable heterogeneity between studies precluded definite inferences about subgroup results for immunocompromised patients, in-patients, and children. A meta-analysis of 4 studies reporting association between oseltamivir-resistance and pneumonia yielded a statistically significant risk ratio of 4.2 (95% CI 1.3 to 13.1, p = 0.02). Oseltamivir-resistance was not statistically significantly associated with other clinical complications and symptoms.</p> <p>Conclusion</p> <p>Our results demonstrate that that a substantial number of patients may become oseltamivir-resistant as a result of oseltamivir use, and that oseltamivir resistance may be significantly associated with pneumonia. In contrast, zanamivir resistance has been rarely reported to date.</p
Medial subtalar dislocation from a low-energy trauma. A case report and review of the literature
Subtalar dislocation is a rare injury characterized by a simultaneous dislocation of the talocalcaneal and talonavicular joints. The most common type is caused by high-energy trauma with medial dislocation of the foot. This injury is frequently associated with fractures, but isolated dislocations are also reported
G-protein-coupled receptor 30/adenylyl cyclase/protein kinase A pathway is involved in estradiol 17Ă-D-glucuronide-induced cholestasis
Estradiol-17Ă-D-glucuronide (E17G) activates different signaling pathways (e.g., Ca21-
dependent protein kinase C, phosphoinositide 3-kinase/protein kinase B, mitogenactivated
protein kinases [MAPKs] p38 and extracellular signal-related kinase 1/2, and
estrogen receptor alpha) that lead to acute cholestasis in rat liver with retrieval of the
canalicular transporters, bile salt export pump (Abcb11) and multidrug resistanceassociated
protein 2 (Abcc2). E17G shares with nonconjugated estradiol the capacity to
activate these pathways. G-protein-coupled receptor 30 (GPR30) is a receptor implicated
in nongenomic effects of estradiol, and the aim of this study was to analyze the potential
role of this receptor and its downstream effectors in E17G-induced cholestasis. In
vitro, GPR30 inhibition by G15 or its knockdown with small interfering RNA strongly
prevented E17G-induced impairment of canalicular transporter function and localization.
E17G increased cyclic adenosine monophosphate (cAMP) levels, and this increase
was blocked by G15, linking GPR30 to adenylyl cyclase (AC). Moreover, AC inhibition
totally prevented E17G insult. E17G also increased protein kinase A (PKA) activity,
which was blocked by G15 and AC inhibitors, connecting the links of the pathway,
GPR30-AC-PKA. PKA inhibition prevented E17G-induced cholestasis, whereas exchange
protein activated directly by cyclic nucleotide/MAPK kinase, another cAMP downstream
effector, was not implicated in cAMP cholestatic action. In the perfused rat liver model,
inhibition of the GPR30-AC-PKA pathway totally prevented E17G-induced alteration in
Abcb11 and Abcc2 function and localization. Conclusion: In conclusion, activation of
GPR30-AC-PKA is a key factor in the alteration of canalicular transporter function and
localization induced by E17G. Interaction of E17G with GPR30 may be the first event
in the cascade of signaling activation.Fil: Zucchetti, AndrĂ©s E. Universidad Nacional de Rosario. Facultad de Ciencias BioquĂmicas y FarmacĂ©uticas. Instituto de FisiologĂa Experimental (IFISE-CONICET); Argentina.Fil: Barosso, Ismael R. Universidad Nacional de Rosario. Facultad de Ciencias BioquĂmicas y FarmacĂ©uticas. Instituto de FisiologĂa Experimental (IFISE-CONICET); Argentina.Fil: Boaglio, Andrea C. Universidad Nacional de Rosario. Facultad de Ciencias BioquĂmicas y FarmacĂ©uticas. Instituto de FisiologĂa Experimental (IFISE-CONICET); Argentina.Fil: Basiglio, Cecilia Lorena. Universidad Nacional de Rosario. Facultad de Ciencias BioquĂmicas y FarmacĂ©uticas. Instituto de FisiologĂa Experimental (IFISE-CONICET); Argentina.Fil: Miszczuk, Gisel Sabrina. Universidad Nacional de Rosario. Facultad de Ciencias BioquĂmicas y FarmacĂ©uticas. Instituto de FisiologĂa Experimental (IFISE-CONICET); Argentina.Fil: Larocca, MarĂa Cecilia. Universidad Nacional de Rosario. Facultad de Ciencias BioquĂmicas y FarmacĂ©uticas. Instituto de FisiologĂa Experimental (IFISE-CONICET); ArgentinaFil: Ruiz, M. Laura. Universidad Nacional de Rosario. Facultad de Ciencias BioquĂmicas y FarmacĂ©uticas. Instituto de FisiologĂa Experimental (IFISE-CONICET); Argentina.Fil: Davio, Carlos A. Universidad de Buenos Aires. Facultad de Farmacia y BioquĂmica. Departamento de FarmacologĂa. Laboratorio de FarmacologĂa de Receptores; Argentina.Fil: Roma, Marcelo Gabriel. Universidad Nacional de Rosario. Facultad de Ciencias BioquĂmicas y FarmacĂ©uticas. Instituto de FisiologĂa Experimental (IFISE-CONICET); Argentina.Fil: Crocenzi, Fernando A. Universidad Nacional de Rosario. Facultad de Ciencias BioquĂmicas y FarmacĂ©uticas. Instituto de FisiologĂa Experimental (IFISE-CONICET); Argentina.Fil: SĂĄnchez Pozzi, Enrique J. Universidad Nacional de Rosario. Facultad de Ciencias BioquĂmicas y FarmacĂ©uticas. Instituto de FisiologĂa Experimental (IFISE-CONICET); Argentina
Prevention of estradiol 17ÎČ-d-glucuronideâinduced canalicular transporter internalization by hormonal modulation of cAMP in rat hepatocytes
Glucagon- and salbutamol-derived cAMP prevents estrogen-induced alteration of canalicular transporter localization and function via different pathways. Glucagon-derived protection depends on PKA activation, whereas salbutamol protection is exerted through a pathway that depends on Epac/MEK and microtubules