Measuring and mapping the effectiveness of the European Air Quality Directive in reducing N and S deposition at the ecosystem level

To protect human health and the environment (namely ecosystems), international air quality protocols and guidelines, like the Gothenburg protocol (1999) and the 2001 EU Air Quality Directive (NECD), conveyed national emission ceilings for atmospheric pollutants (Directive 2001/81/EC), including the reduction of sulfur (S) and nitrogen (N) emissions by 2010. However, to what degree this expected reduction in emissions had reflections at the ecosystem level (i.e. pollutant levels reaching and impacting ecosystems and their organisms) remains unknown. Here, we used lichens as ecological indicators, together with reported air and precipitation pollutant concentrations, to determine and map the consequences of the S and N atmospheric emission's reduction, during the implementation of the 2001 Directive (in 2002 and 2011), due primarily to the industrial-sector. The study area is a mixed-land-use industrialized Mediterranean agroforest ecosystem, in southwest Europe. The reduction of S emissions (2002-2011) was reflected at the ecosystem level, as the same S-declining trend was observed in atmospheric measurement stations and lichens alike (-70%), indicating that most S deposited to the ecosystem had an industrial origin. However, this was not the case for N with a slight N-reduction near industrial facilities, but mostly N-deposition in lichens increased in areas dominated by agricultural land-uses. Taken together, these results highlight the importance of going beyond emissions estimation and modeling, to assess the success of the implementation of the NECD in lowering pollutant accumulation in living organisms and their environment. This can only be achieved by measuring pollutant deposition at the ecosystem level (e.g. living organisms). By doing so, we were able to show that the 2001 NECD was successful in reducing S concentrations from Industry, whereas N remains a challenge. Despite the small reduction in N-emissions, deposition into ecosystems did not reflect these changes as agriculture and transport sectors must reduce NH3 and NOx emissions. (C) 2018 Published by Elsevier B.V.The research was supported by project GISA [funded by private companies: GALP, Repsol, APS, AdSA, AICEP, CARBOGAL, EDP, EuroResinas, KIMAXTRA, REN and GENERG; and managed by local authorities: CCDRA, ARSA and Municipalities of Sines, Santiago do Cacem, Grandola, Alcacer do Sal and Odemira]; article preparation was supported by project NitroPortugal [European Union's Horizon 2020 research and innovation programme under grant agreement No 692331]. NitroPortugal is a co-financer for the project Towards INMS, implemented by UN Environment. Concentration of pollutants in precipitation available in the EBAS database has largely been funded by the UN-ECE CLRTAP (EMEP) and through NILU internal resources

Autologous stem cell transplantation for the treatment of pediatric solid tumors in Brazil

Hosp Clin, Pediat Oncol Unit, Porto Alegre, RS, BrazilUniversidade Federal de São Paulo, GRAACC, Pediat Oncol Inst, São Paulo, BrazilHosp AC Camargo Fund Antonio Prudente, Dept Pediat, São Paulo, BrazilSanta Casa de São Paulo, Pediat Hematol & Bone Marrow Transplantat Unit, São Paulo, BrazilUniversidade Federal de São Paulo, GRAACC, Pediat Oncol Inst, São Paulo, BrazilWeb of Scienc

Cosmogenic neutron production at the Sudbury Neutrino Observatory

Neutrons produced in nuclear interactions initiated by cosmic-ray muons present an irreducible background to many rare-event searches, even in detectors located deep underground. Models for the production of these neutrons have been tested against previous experimental data, but the extrapolation to deeper sites is not well understood. Here we report results from an analysis of cosmogenically produced neutrons at the Sudbury Neutrino Observatory. A specific set of observables are presented, which can be used to benchmark the validity of geant4 physics models. In addition, the cosmogenic neutron yield, in units of 10-4 cm2/(g·μ), is measured to be 7.28±0.09(stat)-1.12+1.59(syst) in pure heavy water and 7.30±0.07(stat)-1.02+1.40(syst) in NaCl-loaded heavy water. These results provide unique insights into this potential background source for experiments at SNOLAB

Genetics of human hydrocephalus

Human hydrocephalus is a common medical condition that is characterized by abnormalities in the flow or resorption of cerebrospinal fluid (CSF), resulting in ventricular dilatation. Human hydrocephalus can be classified into two clinical forms, congenital and acquired. Hydrocephalus is one of the complex and multifactorial neurological disorders. A growing body of evidence indicates that genetic factors play a major role in the pathogenesis of hydrocephalus. An understanding of the genetic components and mechanism of this complex disorder may offer us significant insights into the molecular etiology of impaired brain development and an accumulation of the cerebrospinal fluid in cerebral compartments during the pathogenesis of hydrocephalus. Genetic studies in animal models have started to open the way for understanding the underlying pathology of hydrocephalus. At least 43 mutants/loci linked to hereditary hydrocephalus have been identified in animal models and humans. Up to date, 9 genes associated with hydrocephalus have been identified in animal models. In contrast, only one such gene has been identified in humans. Most of known hydrocephalus gene products are the important cytokines, growth factors or related molecules in the cellular signal pathways during early brain development. The current molecular genetic evidence from animal models indicate that in the early development stage, impaired and abnormal brain development caused by abnormal cellular signaling and functioning, all these cellular and developmental events would eventually lead to the congenital hydrocephalus. Owing to our very primitive knowledge of the genetics and molecular pathogenesis of human hydrocephalus, it is difficult to evaluate whether data gained from animal models can be extrapolated to humans. Initiation of a large population genetics study in humans will certainly provide invaluable information about the molecular and cellular etiology and the developmental mechanisms of human hydrocephalus. This review summarizes the recent findings on this issue among human and animal models, especially with reference to the molecular genetics, pathological, physiological and cellular studies, and identifies future research directions

Cesarean and Vbac Rates Among Immigrant vs. Native-Born Women: A Retrospective Observational Study From Taiwan Cesarean Delivery and Vbac Among Immigrant Women in Taiwan

Background Cultural and ethnic roots impact women\u27s fertility and delivery preferences This study investigated whether the likelihood of cesarean delivery, primary cesarean, and vaginal delivery after cesarean (VBAC) varies by maternal national origin. Methods We conducted a nation-wide, population-based, observational study using secondary data from Taiwan. De-identified data were obtained on all 392,246 singleton live births (≥500 g; ≥20 weeks) born to native-born Taiwanese, Vietnamese and mainland Chinese-born mothers between January 1 2006 and December 31 2007 from Taiwan\u27s nation-wide birth certificate data. Our analytic samples consisted of the following: for overall cesarean likelihood 392,246 births, primary cesarean 336,766 (excluding repeat cesarean and VBAC), and VBAC 55,480 births (excluding primary cesarean and vaginal births without previous cesarean). Our main outcome measures were the odds of cesarean delivery, primary cesarean delivery and VBAC for Vietnamese and Chinese immigrant mothers relative to Taiwanese mothers, using multiple regression analyses to adjust for maternal and neonatal characteristics, paternal age, institutional setting, and major obstetric complications. Results Unadjusted overall cesarean, primary cesarean, and VBAC rates were 33.9%, 23.0% and 4.0% for Taiwanese, 27.6%, 20.1% and 5.0% for mainland Chinese, and 19.3%, 13.9 and 6.1% for Vietnamese respectively. Adjusted for confounders, Vietnamese mothers were less likely than native-born Taiwanese to have overall and primary cesarean delivery (OR = 0.59 and 0.58 respectively), followed by Chinese mothers (both ORs = 0.90 relative to native-born Taiwanese). Vietnamese mothers were most likely to have successful VBAC (OR = 1.58), followed by Chinese mothers (OR = 1.25). Conclusion Immigrant Vietnamese and Chinese mothers have lower odds of cesarean and higher VBAC odds than native-born Taiwanese, consistent with lower cesarean rates prevailing in their home countries (Vietnam 10.1%; mainland China 20% - 50% rural and urban respectively)

Silencing cytokeratin 18 gene inhibits intracellular replication of Trypanosoma cruzi in HeLa cells but not binding and invasion of trypanosomes

<p>Abstract</p> <p>Background</p> <p>As an obligatory intracellular parasite, <it>Trypanosoma cruzi</it>, the etiological agent of Chagas' disease, must invade and multiply within mammalian cells. Cytokeratin 18 (CK18) is among the host molecules that have been suggested as a mediator of important events during <it>T. cruzi</it>-host cell interaction. Based on that possibility, we addressed whether RNA interference (RNAi)-mediated down regulation of the CK18 gene could interfere with the parasite life cycle <it>in vitro</it>. HeLa cells transiently transfected with CK18-RNAi had negligible levels of CK18 transcripts, and significantly reduced levels of CK18 protein expression as determined by immunoblotting or immunofluorescence.</p> <p>Results</p> <p>CK18 negative or positive HeLa cells were invaded equally as well by trypomastigotes of different <it>T. cruzi </it>strains. Also, in CK18 negative or positive cells, parasites recruited host cells lysosomes and escaped from the parasitophorous vacuole equally as well. After that, the growth of amastigotes of the Y or CL-Brener strains, was drastically arrested in CK18 RNAi-treated cells. After 48 hours, the number of amastigotes was several times lower in CK18 RNAi-treated cells when compared to control cells. Simultaneous staining of parasites and CK18 showed that in HeLa cells infected with the Y strain both co-localize. Although the amastigote surface protein-2 contains the domain VTVXNVFLYNR previously described to bind to CK18, in several attempts, we failed to detect binding of a recombinant protein to CK-18.</p> <p>Conclusion</p> <p>The study demonstrates that silencing CK18 by transient RNAi, inhibits intracellular multiplication of the Y and CL strain of <it>T. cruzi </it>in HeLa cells, but not trypanosome binding and invasion.</p