Åtgärdsprogram för vattenvården för åren 2022–2027 i Södra Österbotten, Österbotten och Mellersta Österbotten.

Det centrala syftet med vattenvården är att hindra att tillståndet i vattendragen, sjöarna och kustvattnen försämras och att sträva efter att alla vatten uppnår åtminstone god status. Tillståndet i vatten som bedömts ha hög eller god status får inte försämras. För att nå målet planerar och vidtar man åtgärder som förbättrar vattnens status samt följer upp effekterna. I vattenvården beaktar man också målen för havsvården, för hanteringen av översvämnings-risker och för naturskyddet. Vattenvården planeras enligt vattenförvaltningsområden, av vilka det finns sju i Fastlandsfinland. Ett vattenför-valtningsområde bildas av ett eller flera vattendragsområden. Planeringen av vattenvården framskrider i sexårspe-rioder. De första åtgärdsprogrammen som sträcker sig fram till 2015 utarbetades i ett brett samarbete under 2008–2009. Mer information om vattenvården och organiseringen av den inom vattenförvaltningsområdet finns på https://www.ymparisto.fi/sv-FI/Vatten/Vattenskydd/Vattenvardsplanering_och_samarbete/Vattenforvaltningsomraden/Kumo_alvSkargardshavetBottenhavet och i förvaltningsplanen för Kumo älvs-Skärgårdshavets-Bottenhavets vattenförvaltningsområde. I förvaltningsplanen för vattenvården beskrivs lagstiftningen och andra planer och strategier som rör vattenvården mer i detalj. Dessutom har man i vattenförvaltningsplanen gjort en granskning av alternativ för vattenvårdsåtgär-derna i hela vattenförvaltningsområdet

Airport emission particles:Exposure characterization and toxicity following intratracheal instillation in mice

Background: Little is known about the exposure levels and adverse health effects of occupational exposure to airplane emissions. Diesel exhaust particles are classified as carcinogenic to humans and jet engines produce potentially similar soot particles. Here, we evaluated the potential occupational exposure risk by analyzing particles from a non-commercial airfield and from the apron of a commercial airport. Toxicity of the collected particles was evaluated alongside NIST standard reference diesel exhaust particles (NIST2975) in terms of acute phase response, pulmonary inflammation, and genotoxicity after single intratracheal instillation in mice. Results: Particle exposure levels were up to 1 mg/m3 at the non-commercial airfield. Particulate matter from the non-commercial airfield air consisted of primary and aggregated soot particles, whereas commercial airport sampling resulted in a more heterogeneous mixture of organic compounds including salt, pollen and soot, reflecting the complex occupational exposure at an apron. The particle contents of polycyclic aromatic hydrocarbons and metals were similar to the content in NIST2975. Mice were exposed to doses 6, 18 and 54 μg alongside carbon black (Printex 90) and NIST2975 and euthanized after 1, 28 or 90 days. Dose-dependent increases in total number of cells, neutrophils, and eosinophils in bronchoalveolar lavage fluid were observed on day 1 post-exposure for all particles. Lymphocytes were increased for all four particle types on 28 days post-exposure as well as for neutrophil influx for jet engine particles and carbon black nanoparticles. Increased Saa3 mRNA levels in lung tissue and increased SAA3 protein levels in plasma were observed on day 1 post-exposure. Increased levels of DNA strand breaks in bronchoalveolar lavage cells and liver tissue were observed for both particles, at single dose levels across doses and time points. Conclusions: Pulmonary exposure of mice to particles collected at two airports induced acute phase response, inflammation, and genotoxicity similar to standard diesel exhaust particles and carbon black nanoparticles, suggesting similar physicochemical properties and toxicity of jet engine particles and diesel exhaust particles. Given this resemblance as well as the dose-response relationship between diesel exhaust exposure and lung cancer, occupational exposure to jet engine emissions at the two airports should be minimized.publishedVersionPeer reviewe

Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis.

Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis

Common Inflammation-Related Candidate Gene Variants and Acute Kidney Injury in 2647 Critically Ill Finnish Patients

Acute kidney injury (AKI) is a syndrome with high incidence among the critically ill. Because the clinical variables and currently used biomarkers have failed to predict the individual susceptibility to AKI, candidate gene variants for the trait have been studied. Studies about genetic predisposition to AKI have been mainly underpowered and of moderate quality. We report the association study of 27 genetic variants in a cohort of Finnish critically ill patients, focusing on the replication of associations detected with variants in genes related to inflammation, cell survival, or circulation. In this prospective, observational Finnish Acute Kidney Injury (FINNAKI) study, 2647 patients without chronic kidney disease were genotyped. We defined AKI according to Kidney Disease: Improving Global Outcomes (KDIGO) criteria. We compared severe AKI (Stages 2 and 3, n = 625) to controls (Stage 0, n = 1582). For genotyping we used iPLEX(TM) Assay (Agena Bioscience). We performed the association analyses with PLINK software, using an additive genetic model in logistic regression. Despite the numerous, although contradictory, studies about association between polymorphisms rs1800629 in TNFA and rs1800896 in IL10 and AKI, we found no association (odds ratios 1.06 (95% CI 0.89-1.28, p = 0.51) and 0.92 (95% CI 0.80-1.05, p = 0.20), respectively). Adjusting for confounders did not change the results. To conclude, we could not confirm the associations reported in previous studies in a cohort of critically ill patients.Peer reviewe

Nanomateriaalit osana yhteiskuntaa : Kohti turvallista nanoteknologian tulevaisuutta

Katsaus sisältää tietoa nanomateriaalien käytöstä, turvallisuuteen liittyvistä kysymyksistä, sääntelystä, sekä tutkimuksesta Suomessa. Nanomateriaaleissa vähintään yksi niiden ulottuvuus on välillä 1–100 nanometriä. Aineella voi nanokoossa olla kemiallisia, fysikaalisia, sähköisiä ja mekaanisia erityisominaisuuksia. Nanoteknologiaa käytetään tuotteiden ominaisuuksien parantamiseen. Teollisesti tuotettuja nanomateriaaleja käytetään lähes kaikilla teollisuuden aloilla. Ihmistoiminnan seurauksena syntyy myös tahattomasti poltto- ja prosessiperäisiä nanohiukkasia. Nanomateriaalien terveydelle tai ympäristölle aiheuttamia vaikutuksia ei vielä täysin tunneta. Terveys- ja ympäristöriskien arviointi perustuu tietoihin nanomateriaalien vaaraominaisuuksista ja altistumistasoista. Teollisesti tuotetuille nanomateriaaleille on mahdollista altistua valmistuksessa ja käytössä. Altistuminen kuluttajatuotteista on pääsääntöisesti vähäistä. Nanomateriaalien sääntelyssä sovelletaan EU- ja kansallisia säädöksiä, jotka koskevat kemikaaleja, elintarvikkeita tai lääkkeitä. Lisäksi EU:ssa on sektorikohtaisia säädöksiä nanomateriaalien turvalliselle käytölle. Euroopan komissio rahoittaa yhä enemmän nanomateriaalien turvallisuuteen liittyvää tutkimista. Suomen yliopistoissa ja valtion tutkimuslaitoksissa tehdään ansiokasta nanomateriaaleja koskevaa materiaali- ja turvallisuustutkimusta

Nanomaterials as part of society : Towards a safe future of nanotechnology

Nanomaterials as part of society : Towards a safe future of nanotechnologyThe review contains information on the use of nanomaterials and safety issues, regulation and research related to nanomaterials in Finland. Nanomaterials have at least one dimension between 1–100 nanometers. At the nanoscale, materials can exhibit unique chemical, physical, electronic and mechanical properties. Nanotechnology is used to improve the properties of materials. Manufactured nanomaterials are used in nearly all industrial sectors. As a result of human activity, nanoparticles are also generated unintentionally through various processes and combustion. The impact that nanomaterials have on health or the environment is not yet fully understood. The assessment of health and environmental risks is based on information on the hazardous properties and exposure levels of nanomaterials. Exposure to manufactured nanomaterials may occur during the production process or the use of these products. However, as a rule, the risk of exposure to manufactured nanomaterials in consumer products is minimal. The regulation of nanomaterials builds on EU and national legislation concerning chemicals, food and medicines. The EU also has sector-specific legislation on the safe use of nanomaterials. The European Commission is directing more and more funding to the research on the safety of nanomaterials. In Finland, universities and government research institutes conduct valuable safety and material-related research on nanomaterials

Genome-wide meta-analysis for Alzheimer's disease cerebrospinal fluid biomarkers

Amyloid-beta 42 (A beta 42) and phosphorylated tau (pTau) levels in cerebrospinal fluid (CSF) reflect core features of the pathogenesis of Alzheimer's disease (AD) more directly than clinical diagnosis. Initiated by the European Alzheimer & Dementia Biobank (EADB), the largest collaborative effort on genetics underlying CSF biomarkers was established, including 31 cohorts with a total of 13,116 individuals (discovery n = 8074; replication n = 5042 individuals). Besides the APOE locus, novel associations with two other well-established AD risk loci were observed; CR1 was shown a locus for A beta 42 and BIN1 for pTau. GMNC and C16orf95 were further identified as loci for pTau, of which the latter is novel. Clustering methods exploring the influence of all known AD risk loci on the CSF protein levels, revealed 4 biological categories suggesting multiple A beta 42 and pTau related biological pathways involved in the etiology of AD. In functional follow-up analyses, GMNC and C16orf95 both associated with lateral ventricular volume, implying an overlap in genetic etiology for tau levels and brain ventricular volume.Peer reviewe

Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease

We identified rare coding variants associated with Alzheimer’s disease (AD) in a 3-stage case-control study of 85,133 subjects. In stage 1, 34,174 samples were genotyped using a whole-exome microarray. In stage 2, we tested associated variants (P<1×10-4) in 35,962 independent samples using de novo genotyping and imputed genotypes. In stage 3, an additional 14,997 samples were used to test the most significant stage 2 associations (P<5×10-8) using imputed genotypes. We observed 3 novel genome-wide significant (GWS) AD associated non-synonymous variants; a protective variant in PLCG2 (rs72824905/p.P522R, P=5.38×10-10, OR=0.68, MAFcases=0.0059, MAFcontrols=0.0093), a risk variant in ABI3 (rs616338/p.S209F, P=4.56×10-10, OR=1.43, MAFcases=0.011, MAFcontrols=0.008), and a novel GWS variant in TREM2 (rs143332484/p.R62H, P=1.55×10-14, OR=1.67, MAFcases=0.0143, MAFcontrols=0.0089), a known AD susceptibility gene. These protein-coding changes are in genes highly expressed in microglia and highlight an immune-related protein-protein interaction network enriched for previously identified AD risk genes. These genetic findings provide additional evidence that the microglia-mediated innate immune response contributes directly to AD development

Common variants in Alzheimer’s disease and risk stratification by polygenic risk scores

Funder: Funder: Fundación bancaria ‘La Caixa’ Number: LCF/PR/PR16/51110003 Funder: Grifols SA Number: LCF/PR/PR16/51110003 Funder: European Union/EFPIA Innovative Medicines Initiative Joint Number: 115975 Funder: JPco-fuND FP-829-029 Number: 733051061Genetic discoveries of Alzheimer's disease are the drivers of our understanding, and together with polygenetic risk stratification can contribute towards planning of feasible and efficient preventive and curative clinical trials. We first perform a large genetic association study by merging all available case-control datasets and by-proxy study results (discovery n = 409,435 and validation size n = 58,190). Here, we add six variants associated with Alzheimer's disease risk (near APP, CHRNE, PRKD3/NDUFAF7, PLCG2 and two exonic variants in the SHARPIN gene). Assessment of the polygenic risk score and stratifying by APOE reveal a 4 to 5.5 years difference in median age at onset of Alzheimer's disease patients in APOE ɛ4 carriers. Because of this study, the underlying mechanisms of APP can be studied to refine the amyloid cascade and the polygenic risk score provides a tool to select individuals at high risk of Alzheimer's disease