Emissions of transboundary air pollutants in the Netherlands 1990-2012 : Informative Inventory Report 2014

Emissies Nederland blijven in 2012 onder nationale plafonds De uitstoot van stikstofoxiden (NOx), ammoniak, zwaveldioxide en niet-methaan vluchtige organische stoffen (NMVOS) is in 2012 in Nederland licht gedaald. Daarmee bleef de uitstoot onder de maxima die de Europese Unie daaraan sinds 2010 stelt. Nederland voldoet daardoor, net als in 2011, aan de vier 'nationale emissieplafonds' (NEC) voor deze stoffen. Dit blijkt uit de Nederlandse emissiecijfers van grootschalige luchtverontreinigende stoffen. Het RIVM verzamelt en analyseert deze cijfers. Behalve bovengenoemde stoffen gaat het om de uitstoot van koolmonoxide, fijn stof (PM10), zware metalen en persistente organische stoffen (POP's). De uitstoot van al deze stoffen is tussen 1990 en 2012 gedaald. Dit komt vooral door schonere auto's en brandstoffen en door emissiebeperkende maatregelen van industriële sectoren. Meer kilometers door bromfietsen Door de jaren heen zijn de methoden om de emissies te berekenen verbeterd, wat nu resulteert in nauwkeurigere cijfers. De emissies van bromfietsen en motorfietsen zijn afhankelijk van het aantal gereden kilometers per jaar en daar is nu beter inzicht in. Het totale aantal gereden kilometers door bromfietsen blijkt in de afgelopen jaren bijna twee keer zo hoog is als werd gedacht. Daarmee is de uitstoot van schadelijke stoffen navenant hoger. Ten opzichte van andere typ voertuigen blijven bromfietsen echter een relatief kleine emissiebron en dragen ze beperkt bij aan de totale nationale emissies. In steden zijn ze wel een relevante bron. Het aantal gereden kilometers door motorfietsen, en daarmee de uitstoot, blijft in lijn met eerdere inzichten. Vrachtauto's zwaarder beladen De uitstoot van schadelijke stoffen door vrachtauto's is voor het eerst berekend op basis van recente inzichten in het gewicht van vrachtauto's. Trekker-opleggers blijken zwaarder beladen dan tot nu toe werd verondersteld. Ook rijden vrachtauto's vaker met een aanhanger dan tot nu toe werd aangenomen, waardoor ze zwaarder zijn. Een hoger gewicht betekent een hoger brandstofverbruik, en veelal ook een hogere uitstoot per gereden kilometer. De uitstoot van PM10 door vrachtauto's is hierdoor circa 5 procent hoger dan in de vorige IIR-rapportage. Hogere emissies ammoniak De uitstoot van ammoniak blijkt hoger dan eerder werd verondersteld vanwege enkele nieuwe inzichten; de cijfers zijn hierdoor vanaf 1997 bijgesteld. Zo worden luchtwassers, die voornamelijk op varkensstallen zitten, niet altijd gebruikt. Ook is vanaf 2002 in melkveestallen het leefoppervlak per dier toegenomen. Door het grotere contactoppervlak van mest met lucht wordt meer ammoniak uitgestoten. Door de aangepaste aannames is het nationale totaal met 6,6 kiloton verhoogd ten opzichte van 2011.Emissions the Netherlands in 2012 remain under national ceilings Emissions of nitrogen oxides (NOx), ammonia, sulphur dioxide and non-methane volatile organic compounds (NMVOC) in the Netherlands have slightly decreased in 2012. Consequently, the emissions stayed below the caps the European Union has set from 2010. Herewith, the Netherlands comply with all four so-called emission ceilings (NEC). This has become apparent from the emission data on air pollutants from the Netherlands. RIVM collects and reports these data. Besides above-mentioned substances, emissions of carbon monoxide, particulate matter (PM10), heavy metals and persistent organic pollutants (POPs) have been reported. The emissions of all substances have decreased in the 1990 - 2012 period. The downward trend may in particular be attributed to cleaner fuels, cleaner car engines and to emission reductions in the industrial sectors. More kilometres by mopeds Over the years emission calculation methods have been improved, resulting in higher data accuracy. In 2012, the emissions from mopeds and motorcycles have been calculated, based on improved knowledge of the mileages. The total number of kilometres driven by mopeds appears to have been nearly twice as high in recent years. As a result, the emissions of pollutants are proportionally higher. In relation to the total number of vehicles, the number of mopeds however remains relatively low and their contribution to the total national emissions is limited. In cities, they are a relevant source. The mileages by motorcycles, and consequently their emissions remain in line with previous insights. Heavy-duty vehicles carry heavier loads Emissions of pollutants by heavy-duty trucks have for the first time been calculated on the basis of recent insights in truck loads. Tractor-trailer combinations appear to carry heavier loads and the fraction of trailers behind rigid trucks is larger than previously assumed. A heavier load means a higher fuel use and for most substances a higher emission per kilometre driven. PM10 emissions by heavy-duty trucks are about 5 percent higher than in the previous IIR report. Higher agricultural ammonia emissions Agricultural ammonia emissions appear to be higher than previously assumed because of new insights. Air scrubbers on animal housing (predominantly pigs) were not always in use or even employed. Since 2002, the living space per animal has increased for dairy cattle housing. This resulted in a higher contact surface manure-air and thus more ammonia emitted. The new insights have raised the national total of ammonia emissions by about 6 percent compared to 2011

Measuring every particle's size from three-dimensional imaging experiments

Often experimentalists study colloidal suspensions that are nominally monodisperse. In reality these samples have a polydispersity of 4-10%. At the level of an individual particle, the consequences of this polydispersity are unknown as it is difficult to measure an individual particle size from microscopy. We propose a general method to estimate individual particle radii within a moderately concentrated colloidal suspension observed with confocal microscopy. We confirm the validity of our method by numerical simulations of four major systems: random close packing, colloidal gels, nominally monodisperse dense samples, and nominally binary dense samples. We then apply our method to experimental data, and demonstrate the utility of this method with results from four case studies. In the first, we demonstrate that we can recover the full particle size distribution {\it in situ}. In the second, we show that accounting for particle size leads to more accurate structural information in a random close packed sample. In the third, we show that crystal nucleation occurs in locally monodisperse regions. In the fourth, we show that particle mobility in a dense sample is correlated to the local volume fraction.Comment: 7 pages, 5 figure

Effect of Global Cardiac Ischemia on Human Ventricular Fibrillation: Insights from a Multi-scale Mechanistic Model of the Human Heart

Acute regional ischemia in the heart can lead to cardiac arrhythmias such as ventricular fibrillation (VF), which in turn compromise cardiac output and result in secondary global cardiac ischemia. The secondary ischemia may influence the underlying arrhythmia mechanism. A recent clinical study documents the effect of global cardiac ischaemia on the mechanisms of VF. During 150 seconds of global ischemia the dominant frequency of activation decreased, while after reperfusion it increased rapidly. At the same time the complexity of epicardial excitation, measured as the number of epicardical phase singularity points, remained approximately constant during ischemia. Here we perform numerical studies based on these clinical data and propose explanations for the observed dynamics of the period and complexity of activation patterns. In particular, we study the effects on ischemia in pseudo-1D and 2D cardiac tissue models as well as in an anatomically accurate model of human heart ventricles. We demonstrate that the fall of dominant frequency in VF during secondary ischemia can be explained by an increase in extracellular potassium, while the increase during reperfusion is consistent with washout of potassium and continued activation of the ATP-dependent potassium channels. We also suggest that memory effects are responsible for the observed complexity dynamics. In addition, we present unpublished clinical results of individual patient recordings and propose a way of estimating extracellular potassium and activation of ATP-dependent potassium channels from these measurements

Determining the genome-wide kinship coefficient seems unhelpful in distinguishing consanguineous couples with a high versus low risk for adverse reproductive outcome

Background: Offspring of consanguineous couples are at increased risk of congenital disorders. The risk increases as parents are more closely related. Individuals that have the same degree of relatedness according to their pedigree, show variable genomic kinship coefficients. To investigate whether we can differentiate between couples with high- and low risk for offspring with congenital disorders, we have compared the genomic kinship coefficient of consanguineous parents with a child affected with an autosomal recessive disorder with that of consanguineous parents with only healthy children, corrected for the degree of pedigree relatedness. Methods: 151 consanguineous couples (73 cases and 78 controls) from 10 different ethnic backgrounds were genotyped on the Affymetrix platform and passed quality control checks. After pruning SNPs in linkage disequilibrium, 57,358 SNPs remained. Kinship coefficients were calculated using three different toolsets: PLINK, King and IBDelphi, yielding five different estimates (IBDelphi, PLINK (all), PLINK (by population), King robust (all) and King homo (by population)). We performed a one-sided Mann Whitney test to investigate whether the median relative difference regarding observed and expected kinship coefficients is bigger for cases than for controls. Furthermore, we fitted a mixed effects linear model to correct for a possible population effect. Results: Although the estimated degrees of genomic relatedness with the different toolsets show substantial variability, correlation measures between the different estimators demonstrated moderate to strong correlations. Controls have higher point estimates for genomic kinship coefficients. The one-sided Mann Whitney test did not show any evidence for a higher median relative difference for cases compared to controls. Neither did the regression analysis exhibit a positive association between case–control status and genomic kinship coefficient. Conclusions: In this case–control setting, in which we compared consanguineous couples corrected for degree of pedigree relatedness, a higher degree of genomic relatedness was not significantly associated with a higher likelihood of having an affected child. Further translational research should focus on which parts of the genome and which pathogenic mutations couples are sharing. Looking at relatedness coefficients by determining genome-wide SNPs does not seem to be an effective measure for prospective risk assessment in consanguineous parents

Molecular diagnostics of intestinal parasites in returning travellers

A new diagnostic strategy was assessed for the routine diagnosis of intestinal parasites in returning travellers and immigrants. Over a period of 13 months, unpreserved stool samples, patient characteristics and clinical data were collected from those attending a travel clinic. Stool samples were analysed on a daily basis by microscopic examination and antigen detection (i.e. care as usual), and compared with a weekly performed multiplex real-time polymerase chain reaction (PCR) analysis on Entamoeba histolytica, Giardia lamblia, Cryptosporidium and Strongyloides stercoralis. Microscopy and antigen assays of 2,591 stool samples showed E. histolytica, G. lamblia, Cryptosporidium and S. stercoralis in 0.3, 4.7, 0.5 and 0.1% of the cases, respectively. These detection rates were increased using real-time PCR to 0.5, 6.0, 1.3 and 0.8%, respectively. The prevalence of ten additional pathogenic parasite species identified with microscopy was, at most, 0.5%. A pre-selective decision tree based on travel history or gastro-intestinal complaints could not be made. With increased detection rates at a lower workload and the potential to extend with additional parasite targets combined with fully automated DNA isolation, molecular high-throughput screening could eventually replace microscopy to a large extent

Acute left ventricular dysfunction secondary to right ventricular septal pacing in a woman with initial preserved contractility: a case report

<p>Abstract</p> <p>Introduction</p> <p>Right ventricular apical pacing-related heart failure is reported in some patients after long-term pacing. The exact mechanism is not yet clear but may be related to left ventricular dyssynchrony induced by right ventricular apical pacing. Right ventricular septal pacing is thought to deteriorate left ventricular function less frequently because of a more normal left ventricular activation pattern.</p> <p>Case presentation</p> <p>We report the case of a 55-year-old Tunisian woman with preserved ventricular function, implanted with a dual-chamber pacemaker for complete atrioventricular block. Right ventricular septal pacing induced a major ventricular dyssynchrony, severe left ventricular ejection fraction deterioration and symptoms of congestive heart failure. Upgrading to a biventricular device was associated with a decrease in the symptoms and the ventricular dyssynchrony, and an increase of left ventricular ejection fraction.</p> <p>Conclusion</p> <p>Right ventricular septal pacing can induce reversible left ventricular dysfunction and heart failure secondary to left ventricular dyssynchrony. This complication remains an unpredictable complication of right ventricular septal pacing.</p

Cellular Imaging of Human Atherosclerotic Lesions by Intravascular Electric Impedance Spectroscopy

Background: Newer techniques are required to identify atherosclerotic lesions that are prone to rupture. Electric impedance spectroscopy (EIS) is able to provide information about the cellular composition of biological tissue. The present study was performed to determine the influence of inflammatory processes in type Va (lipid core, thick fibrous cap) and Vc (abundant fibrous connective tissue while lipid is minimal or even absent) human atherosclerotic lesions on the electrical impedance of these lesions measured by EIS. Methods and Results: EIS was performed on 1 aortic and 3 femoral human arteries at 25 spots with visually heavy plaque burden. Severely calcified lesions were excluded from analysis. A highly flexible micro-electrode mounted onto a balloon catheter was placed on marked regions to measure impedance values at 100 kHz. After paraffin embedding, visible marked cross sections (n = 21) were processed. Assessment of lesion types was performed by Movats staining. Immunostaining for CD31 (marker of neovascularisation), CD36 (scavenger cells) and MMP-3 (matrix metalloproteinase-3) was performed. The amount of positive cells was assessed semi-quantitatively. 15 type Va lesions and 6 type Vc lesions were identified. Lesions containing abundant CD36-, CD31- and MMP-3-positive staining revealed significantly higher impedance values compared to lesions with marginal or without positive staining (CD36+455650 V vs. CD36- 346653 V, p = 0.001; CD31+436643 V vs. CD31- 340655 V, p = 0.001; MMP-3+ 400668 V vs. MMP-3- 323633 V, p = 0.03)

Coagulation Factor Xa Induces Proinflammatory Responses in Cardiac Fibroblasts via Activation of Protease-Activated Receptor-1

Coagulation factor (F) Xa induces proinflammatory responses through activation of protease-activated receptors (PARs). However, the effect of FXa on cardiac fibroblasts (CFs) and the contribution of PARs in FXa-induced cellular signalling in CF has not been fully characterised. To answer these questions, human and rat CFs were incubated with FXa (or TRAP-14, PAR-1 agonist). Gene expression of pro-fibrotic and proinflammatory markers was determined by qRT-PCR after 4 and 24 h. Gene silencing of F2R (PAR-1) and F2RL1 (PAR-2) was achieved using siRNA. MCP-1 protein levels were measured by ELISA of FXa-conditioned media at 24 h. Cell proliferation was assessed after 24 h of incubation with FXa ± SCH79797 (PAR-1 antagonist). In rat CFs, FXa induced upregulation of Ccl2 (MCP-1; >30-fold at 4 h in atrial and ventricular CF) and Il6 (IL-6; ±7-fold at 4 h in ventricular CF). Increased MCP-1 protein levels were detected in FXa-conditioned media at 24 h. In human CF, FXa upregulated the gene expression of CCL2 (>3-fold) and IL6 (>4-fold) at 4 h. Silencing of F2R (PAR-1 gene), but not F2RL1 (PAR-2 gene), downregulated this effect. Selective activation of PAR-1 by TRAP-14 increased CCL2 and IL6 gene expression; this was prevented by F2R (PAR-1 gene) knockdown. Moreover, SCH79797 decreased FXa-induced proliferation after 24 h. In conclusion, our study shows that FXa induces overexpression of proinflammatory genes in human CFs via PAR-1, which was found to be the most abundant PARs isoform in this cell type