MOLYBDENUM CATALYZED ACID PEROXIDE BLEACHING OF EUCALYPTUS KRAFT PULP

Molybdenum catalyzed peroxide bleaching (PMo Stage) consists of pulp treatment with hydrogen peroxide under acidic conditions in the presence of a molybdenum catalyst. Molybdenum is applied in catalytic doses (50-200 mg/kg pulp) and may originate from various sources, including (NH4)6Mo7O24.4H2O, Na2MoO4.2H2O, siliconmolybdate, etc. This work is aimed at optimizing the PMo stage and evaluating its industrial application in the OAZDP sequence. Optimum PMo stage conditions for bleaching eucalyptus pulp were 90 ºC, pH 3.5, 2 h, 0.1 kg/adt Mo and 5 kg/adt H2O2. The PMo stage was more efficient to remove pulp hexenuronic acids than lignin. Its efficiency decreased with increasing pH in the range of 1.5-5.5, while it increased with increasing temperature and peroxide and molybdenum doses. The application of the PMo stage as replacement for the A-stage of the AZDP sequence significantly decreased chlorine dioxide demand. The PMo stage caused a decrease of 20-30% in the generation of organically bound chlorine. The quality parameters of the pulp produced during the PMo stage mill trial were comparable to those obtained with the reference A-stage

Schmallenberg virus pathogenesis, tropism and interaction with the innate immune system of the host

Schmallenberg virus (SBV) is an emerging orthobunyavirus of ruminants associated with outbreaks of congenital malformations in aborted and stillborn animals. Since its discovery in November 2011, SBV has spread very rapidly to many European countries. Here, we developed molecular and serological tools, and an experimental in vivo model as a platform to study SBV pathogenesis, tropism and virus-host cell interactions. Using a synthetic biology approach, we developed a reverse genetics system for the rapid rescue and genetic manipulation of SBV. We showed that SBV has a wide tropism in cell culture and “synthetic” SBV replicates in vitro as efficiently as wild type virus. We developed an experimental mouse model to study SBV infection and showed that this virus replicates abundantly in neurons where it causes cerebral malacia and vacuolation of the cerebral cortex. These virus-induced acute lesions are useful in understanding the progression from vacuolation to porencephaly and extensive tissue destruction, often observed in aborted lambs and calves in naturally occurring Schmallenberg cases. Indeed, we detected high levels of SBV antigens in the neurons of the gray matter of brain and spinal cord of naturally affected lambs and calves, suggesting that muscular hypoplasia observed in SBV-infected lambs is mostly secondary to central nervous system damage. Finally, we investigated the molecular determinants of SBV virulence. Interestingly, we found a biological SBV clone that after passage in cell culture displays increased virulence in mice. We also found that a SBV deletion mutant of the non-structural NSs protein (SBVΔNSs) is less virulent in mice than wild type SBV. Attenuation of SBV virulence depends on the inability of SBVΔNSs to block IFN synthesis in virus infected cells. In conclusion, this work provides a useful experimental framework to study the biology and pathogenesis of SBV

Nanotechnology in hormone replacement therapy: Safe and efficacy of transdermal estriol and estradiol nanoparticles after 5 Years Follow-Up Study

This study aimed to evaluate the safety and efficacy of a novel protocol of transdermal Hormone Replacement Therapy (HRT) based on a nanostructured formulation of Estriol (0.1 %) + Estradiol (0.25 %) restoring serum levels and relieving menopausal symptoms. We evaluated 122 women with mean age of 56.88 (± 6.27) as part a longitudinal prospective study on post-menopausal women with natural menopause, received in the right forearm a transdermal formulation of (EE) daily for 60 months. Clinical parameters including the degree of satisfaction with symptomatic relief, serum concentrations of estradiol, weight, blood pressure, and bilateral mammography BI-RADS were compared between the baseline and five years after treatment. New evidence regarding this HRT protocol was assessed. The transdermal nanoformulation estradiol improved clinical parameters. Satisfaction with treatment was 92 %. Serum concentrations of estradiol changed significantly after treatment (p 0.05) over the years. No vaginal bleeding was observed. Bilateral mammography assessment of the breasts following 60 months of HRT with bioidentical estradiol treatment found normal results in all women. This paper shows for the first time the effectiveness of a nanostructured transdermal formulation enhancer on the delivery of estradiol and estriol measured in vivo using Raman Confocal Spectroscopy. The Nanostructured formulation is safe and effective in reestablishing estradiol serum levels and relieving menopausal symptoms. The nanoformulation may serve as a good choice for hormone replacement therapy to protect against other post-menopausal symptoms.Colegio de Farmacéuticos de la Provincia de Buenos Aire

Elliptic flow of charged particles in Pb-Pb collisions at 2.76 TeV

We report the first measurement of charged particle elliptic flow in Pb-Pb collisions at 2.76 TeV with the ALICE detector at the CERN Large Hadron Collider. The measurement is performed in the central pseudorapidity region (|$\eta$|<0.8) and transverse momentum range 0.2< $p_{\rm T}$< 5.0 GeV/$c$. The elliptic flow signal v$_2$, measured using the 4-particle correlation method, averaged over transverse momentum and pseudorapidity is 0.087 $\pm$ 0.002 (stat) $\pm$ 0.004 (syst) in the 40-50% centrality class. The differential elliptic flow v$_2(p_{\rm T})$ reaches a maximum of 0.2 near $p_{\rm T}$ = 3 GeV/$c$. Compared to RHIC Au-Au collisions at 200 GeV, the elliptic flow increases by about 30%. Some hydrodynamic model predictions which include viscous corrections are in agreement with the observed increase.Comment: 10 pages, 4 captioned figures, published version, figures at http://aliceinfo.cern.ch/ArtSubmission/node/389

Two-pion Bose-Einstein correlations in central Pb-Pb collisions at sNN\sqrt{s_{\rm NN}} = 2.76 TeV

The first measurement of two-pion Bose-Einstein correlations in central Pb-Pb collisions at $\sqrt{s_{\rm NN}} = 2.76$ TeV at the Large Hadron Collider is presented. We observe a growing trend with energy now not only for the longitudinal and the outward but also for the sideward pion source radius. The pion homogeneity volume and the decoupling time are significantly larger than those measured at RHIC.Comment: 17 pages, 5 captioned figures, 1 table, authors from page 12, published version, figures at http://aliceinfo.cern.ch/ArtSubmission/node/388

DRhoGEF2 Regulates Cellular Tension and Cell Pulsations in the Amnioserosa during Drosophila Dorsal Closure

Coordination of apical constriction in epithelial sheets is a fundamental process during embryogenesis. Here, we show that DRhoGEF2 is a key regulator of apical pulsation and constriction of amnioserosal cells during Drosophila dorsal closure. Amnioserosal cells mutant for DRhoGEF2 exhibit a consistent decrease in amnioserosa pulsations whereas overexpression of DRhoGEF2 in this tissue leads to an increase in the contraction time of pulsations. We probed the physical properties of the amnioserosa to show that the average tension in DRhoGEF2 mutant cells is lower than wild-type and that overexpression of DRhoGEF2 results in a tissue that is more solid-like than wild-type. We also observe that in the DRhoGEF2 overexpressing cells there is a dramatic increase of apical actomyosin coalescence that can contribute to the generation of more contractile forces, leading to amnioserosal cells with smaller apical surface than wild-type. Conversely, in DRhoGEF2 mutants, the apical actomyosin coalescence is impaired. These results identify DRhoGEF2 as an upstream regulator of the actomyosin contractile machinery that drives amnioserosa cells pulsations and apical constriction

The association of depression and all-cause and cause-specific mortality: an umbrella review of systematic reviews and meta-analyses

Background: Depression is a prevalent and disabling mental disorder that frequently co-occurs with a wide range of chronic conditions. Evidence has suggested that depression could be associated with excess all-cause mortality across different settings and populations, although the causality of these associations remains unclear. Methods: We conducted an umbrella review of systematic reviews and meta-analyses of observational studies. PubMed, PsycINFO, and Embase electronic databases were searched through January 20, 2018. Systematic reviews and meta-analyses that investigated associations of depression and all-cause and cause-specific mortality were selected for the review. The evidence was graded as convincing, highly suggestive, suggestive, or weak based on quantitative criteria that included an assessment of heterogeneity, 95% prediction intervals, small-study effects, and excess significance bias. Results: A total of 26 references providing 2 systematic reviews and data for 17 meta-analytic estimates met inclusion criteria (19 of them on all-cause mortality); data from 246 unique studies (N = 3,825,380) were synthesized. All 17 associations had P < 0.05 per random effects summary effects, but none of them met criteria for convincing evidence. Associations of depression and all-cause mortality in patients after acute myocardial infarction, in individuals with heart failure, in cancer patients as well as in samples from mixed settings met criteria for highly suggestive evidence. However, none of the associations remained supported by highly suggestive evidence in sensitivity analyses that considered studies employing structured diagnostic interviews. In addition, associations of depression and all-cause mortality in cancer and post-acute myocardial infarction samples were supported only by suggestive evidence when studies that tried to adjust for potential confounders were considered. Conclusions: Even though associations between depression and mortality have nominally significant results in all assessed settings and populations, the evidence becomes weaker when focusing on studies that used structured interviews and those that tried to adjust for potential confounders. A causal effect of depression on all-cause and cause-specific mortality remains unproven, and thus interventions targeting depression are not expected to result in lower mortality rates at least based on current evidence from observational studies