Fossil versus contemporary sources of fine elemental and organic carbonaceous particulate matter during the DAURE campaign in Northeast Spain

We present results from the international field campaign DAURE (Detn. of the sources of atm. Aerosols in Urban and Rural Environments in the Western Mediterranean), with the objective of apportioning the sources of fine carbonaceous aerosols. Submicron fine particulate matter (PM1) samples were collected during Feb.-March 2009 and July 2009 at an urban background site in Barcelona (BCN) and at a forested regional background site in Montseny (MSY). We present radiocarbon (14C) anal. for elemental and org. carbon (EC and OC) and source apportionment for these data. We combine the results with those from component anal. of aerosol mass spectrometer (AMS) measurements, and compare to levoglucosan-based ests. of biomass burning OC, source apportionment of filter data with inorg. compn. + EC + OC, submicron bulk potassium (K) concns., and gaseous acetonitrile concns. At BCN, 87 % and 91 % of the EC on av., in winter and summer, resp., had a fossil origin, whereas at MSY these fractions were 66 % and 79 %. The contribution of fossil sources to org. carbon (OC) at BCN was 40 % and 48 %, in winter and summer, resp., and 31 % and 25 % at MSY. The combination of results obtained using the 14C technique, AMS data, and the correlations between fossil OC and fossil EC imply that the fossil OC at Barcelona is ∼47 % primary whereas at MSY the fossil OC is mainly secondary (∼85 %). Day-to-day variation in total carbonaceous aerosol loading and the relative contributions of different sources predominantly depended on the meteorol. transport conditions. The estd. biogenic secondary OC at MSY only increased by ∼40 % compared to the order-of-magnitude increase obsd. for biogenic volatile org. compds. (VOCs) between winter and summer, which highlights the uncertainties in the estn. of that component. Biomass burning contributions estd. using the 14C technique ranged from similar to slightly higher than when estd. using other techniques, and the different estns. were highly or moderately correlated. Differences can be explained by the contribution of secondary org. matter (not included in the primary biomass burning source ests.), and/or by an over-estn. of the biomass burning OC contribution by the 14C technique if the estd. biomass burning EC/OC ratio used for the calcns. is too high for this region. Acetonitrile concns. correlate well with the biomass burning EC detd. by 14C. K is a noisy tracer for biomass burning. [on SciFinder(R)]

Life cycle complexity, environmental change and the emerging status of salmonid proliferative kidney disease

P>1. Proliferative kidney disease (PKD) is a disease of salmonid fish caused by the endoparasitic myxozoan, Tetracapsuloides bryosalmonae, which uses freshwater bryozoans as primary hosts. Clinical PKD is characterised by a temperature-dependent proliferative and inflammatory response to parasite stages in the kidney.;2. Evidence that PKD is an emerging disease includes outbreaks in new regions, declines in Swiss brown trout populations and the adoption of expensive practices by fish farms to reduce heavy losses. Disease-related mortality in wild fish populations is almost certainly underestimated because of e.g. oversight, scavenging by wild animals, misdiagnosis and fish stocking.;3. PKD prevalences are spatially and temporally variable, range from 0 to 90-100% and are typically highest in juvenile fish.;4. Laboratory and field studies demonstrate that (i) increasing temperatures enhance disease prevalence, severity and distribution and PKD-related mortality; (ii) eutrophication may promote outbreaks. Both bryozoans and T. bryosalmonae stages in bryozoans undergo temperature- and nutrient-driven proliferation.;5. Tetracapsuloides bryosalmonae is likely to achieve persistent infection of highly clonal bryozoan hosts through vertical transmission, low virulence and host condition-dependent cycling between covert and overt infections. Exploitation of fish hosts entails massive proliferation and spore production by stages that escape the immune response. Many aspects of the parasite's life cycle remain obscure. If infectious stages are produced in all hosts then the complex life cycle includes multiple transmission routes.;6. Patterns of disease outbreaks suggest that background, subclinical infections exist under normal environmental conditions. When conditions change, outbreaks may then occur in regions where infection was hitherto unsuspected.;7. Environmental change is likely to cause PKD outbreaks in more northerly regions as warmer temperatures promote disease development, enhance bryozoan biomass and increase spore production, but may also reduce the geographical range of this unique multihost-parasite system. Coevolutionary dynamics resulting from host-parasite interactions that maximise fitness in previous environments may pose problems for sustainability, particularly in view of extensive declines in salmonid populations and degradation of many freshwater habitats.

Periodontal healing after application of enamel matrix derivative in surgical supra/infrabony periodontal defects in rats with streptozotocin-induced diabetes

BACKGROUND AND OBJECTIVE Epidemiologic and clinical studies have indicated that diabetes is a risk factor for periodontal disease progression and healing. The aim of the present study was to evaluate short-term healing after enamel matrix derivative (EMD) application in combined supra/infrabony periodontal defects in diabetic rats. MATERIAL AND METHODS Thirty male Wistar rats were initially divided into two groups, one with streptozotocin-induced diabetes and another one with healthy (non-diabetic) animals. Bony defects were surgically created on the mesial root of the first maxillary molars. After root surface planing and EDTA conditioning, EMD was applied to the roots at one side of the maxillae, while those on the contralateral sides were left untreated. Animals were killed 3 wk after surgery, and block sections were prepared for histologic and histomorphometric analysis. RESULTS There was statistically significant more gingival recession in diabetic animals than in non-diabetic animals. The length of the junctional epithelium was significantly shorter in the EMD-treated sites in both diabetic and normoglycemic rats. Sulcus depth and length of supracrestal soft connective tissue showed no statistically significant differences between groups. In all animals, new bone formation was observed. Although new bone occurred more frequently in healthy animals, the extent of new bone was not significantly different between groups. In none of the teeth, a layer of new cementum was detectable. EMD had no influence on bone or cementum regeneration. Adverse reactions such as excessive inflammation due to bacterial root colonization, ankylosis and bone fractures were exclusively observed in diabetic animals, irrespective of EMD treatment. CONCLUSION Within the limits of the present study, it can be concluded that periodontal healing was impaired in streptozotocin-induced diabetic rats. EMD had no beneficial effects on new bone and cementum formation during short-term healing in this defect model and could not ameliorate the adverse effects in the systemically compromised animals.