Luonnonmuistomerkit Suomessa

Tässä tutkimuksessa selvitellään luonnonsuojelulain nojalla rauhoitettujen luonnonmuistomerkkien vaiheita Suomessa ensimmäisen luonnonsuojelulain voimaantulosta tähän päivään asti ja etsitään syitä siihen, miksi nämä aiemmin arvokkaat luonnonmonumentit ovat jääneet nykyään lähes unohduksiin. Ensimmäinen luonnonsuojelulaki vuonna 1923 mahdollisti yksittäisten luontokohteiden eli luonnonmuistomerkkien rauhoittamispäätökset. Rauhoituksista päätti yksityisillä mailla Lääninhallitukset maanomistajan aloitteesta eli rauhoitusanomusten perusteella. Julkisilla alueilla päätöksiä tekivät ne virastot, joiden hallinnoimilla alueilla kohteet sijaitsivat. 1990-luvun alussa luonnonsuojelulakia muutettiin siten, että kunnat saivat päättää omilla alueillaan kohteiden rauhoituksista ja 1996 koko luonnonsuojelulaki uudistettiin ja luonnonmuistomerkkien suojeluun tuli lisäksi pykälä 29§ eli luontotyyppisuojelu, jonka kohdassa 9. on maininta avointa maisemaa hallitsevista suurista yksittäisistä puista tai puuryhmistä. Luonnonmuistomerkkejä rauhoitettiin harvakseltaan 1923 alkaen, sotien jälkeen rauhoituspäätösten määrä alkoi hiljalleen kasvamaan ja 1960-luvulla päätöksiä tehtiin toistaiseksi eniten. Vielä 1970 ja -80 luvuilla rauhoitusmäärät pysyivät melko korkeina, mutta 1990-luvulla määrät laskivat ja 2000-luvuilla rauhoituksia on tehty hyvin vähän. Luonnonmuistomerkeistä koottiin julkaisuja eri vuosikymmeninä lähinnä Lääninhallituksiin koottujen tietojen perusteella. Viimeinen julkaisu kertoo rauhoitusmäärät ja kohteet kunnittain valtakunnallisesti vuoteen 1984 asti. Sen jälkeen valtakunnallista luetteloa ei ole julkaistu, koska velvoite rekisterin ylläpitämisestä siirtyi valtiolta kunnille. Tutkimuksessa selvitellään myös luonnonmuistomerkkien sisältämiä arvoja. Tutkimuksessa selvitellään myös sitä, mistä kaikkialta luonnonmuistomerkkejä koskevaa tietoa on saatavilla ja miten uusi luonnonmuistomerkkirekisteri olisi mahdollista koota. Aineistoina on käytetty vanhoja luonnonmuistomerkkijulkaisuja, lehtiartikkeleita ja uutisia aihepiiristä sekä kolmea ajankohtaista blogia, joissa on käsitelty luonnonmuistomerkkejä. Tutkimusmetodina on käytetty aineistojen sisällön analysointia. Tulokseksi saatiin, että luonnonmuistomerkkien rauhoitukset ovat jääneet luonnonsuojelualueiden rauhoituksien yleistymisen myötä vähemmälle huomiolle. Luonnonmuistomerkkien merkitys ihmisille ja yhteisöille on myös vähemmän merkittävä kuin ennen. Syynä merkityksen vähenemiseen on ihmisten liikkuva elämäntapa ja kaupungistuminen.Siirretty Doriast

Reproductive history and blood cell DNA methylation later in life: the Young Finns Study

Background: Women with a history of complications of pregnancy, including hypertensive disorders, gestational diabetes or an infant fetal growth restriction or preterm birth, are at higher risk for cardiovascular disease later in life. We aimed to examine differences in maternal DNA methylation following pregnancy complications.Methods: Data on women participating in the Young Finns study (n = 836) were linked to the national birth registry. DNA methylation in whole blood was assessed using the Infinium Methylation EPIC BeadChip. Epigenome-wide analysis was conducted on differential CpG methylation at 850 K sites. Reproductive history was also modeled as a predictor of four epigenetic age indices.Results: Fourteen significant differentially methylated sites were found associated with both history of pre-eclampsia and overall hypertensive disorders of pregnancy. No associations were found between reproductive history and any epigenetic age acceleration measure.Conclusions: Differences in epigenetic methylation profiles could represent pre-existing risk factors, or changes that occurred as a result of experiencing these complications.</div

Epigenome-450K-wide methylation signatures of active cigarette smoking : The Young Finns Study

Smoking as a major risk factor for morbidity affects numerous regulatory systems of the human body including DNA methylation. Most of the previous studies with genome-wide methylation data are based on conventional association analysis and earliest threshold-based gene set analysis that lacks sensitivity to be able to reveal all the relevant effects of smoking. The aim of the present study was to investigate the impact of active smoking on DNA methylation at three biological levels: 5'-C-phosphate-G-3' (CpG) sites, genes and functionally related genes (gene sets). Gene set analysis was done with mGSZ, a modern threshold-free method previously developed by us that utilizes all the genes in the experiment and their differential methylation scores. Application of such method in DNA methylation study is novel. Epigenome-wide methylation levels were profiled from Young Finns Study (YFS) participants' whole blood from 2011 follow-up using Illumina Infinium Hu-manMethylation450 BeadChips. We identified three novel smoking related CpG sites and replicated 57 of the previously identified ones. We found that smoking is associated with hypomethylation in shore (genomic regions 0-2 kilobases from CpG island). We identified smoking related methylation changes in 13 gene sets with false discovery rate (FDR)Peer reviewe

Aging-associated DNA methylation changes in middle-aged individuals: the Young Finns study

Background Chronological aging-associated changes in the human DNA methylome have been studied by multiple epigenome-wide association studies (EWASs). Certain CpG sites have been identified as aging-associated in multiple studies, and the majority of the sites identified in various studies show common features regarding location and direction of the methylation change. However, as a whole, the sets of aging-associated CpGs identified in different studies, even with similar tissues and age ranges, show only limited overlap. In this study, we further explore and characterize CpG sites that show close relationship between their DNA methylation level and chronological age during adulthood and which bear the relationship regardless of blood cell type heterogeneity. Results In this study, with a multivariable regression model adjusted for cell type heterogeneity, we identified 1202 aging-associated CpG sites (a-CpGs, FDR < 5 %), in whole blood in a population with an especially narrow age range (40 - 49 years). Repeatedly reported a-CpGs located in genes ELOVL2, FHL2, PENK and KLF14 were also identified. Regions with aging-associated hypermethylation were enriched regarding several gene ontology (GO) terms (especially in the cluster of developmental processes), whereas hypomethylated sites showed no enrichment. The genes with higher numbers of a-CpG hits were more often hypermethylated with advancing age. The comparison analysis revealed that of the 1202 a-CpGs identified in the present study, 987 were identified as differentially methylated also between nonagenarians and young adults in a previous study (The Vitality 90+ study), and importantly, the directions of changes were identical in the previous and in the present study. Conclusions Here we report that aging-associated DNA methylation features can be identified in a middle-aged population with an age range of only 9 years. A great majority of these sites have been previously reported as aging-associated in a population aged 19 to 90 years. Aging is associated with different types of changes in DNA methylation, clock-like as well as random. We speculate that the a-CpGs identified here in a population with a narrow age-range represent clock-like changes, as they showed concordant methylation behavior in population spanning whole adulthood as well.BioMed Central open acces

Obesity accelerates epigenetic aging in middle-aged but not in elderly individuals

BioMed Central open acces

Randomised double-blind phase 3 clinical study testing impact of atorvastatin on prostate cancer progression after initiation of androgen deprivation therapy : study protocol

Introduction Blood cholesterol is likely a risk factor for prostate cancer prognosis and use of statins is associated with lowered risk of prostate cancer recurrence and progression. Furthermore, use of statins has been associated with prolonged time before development of castration resistance (CR) during androgen deprivation therapy (ADT) for prostate cancer. However, the efficacy of statins on delaying castration-resistance has not been tested in a randomised placebo-controlled setting. This study aims to test statins' efficacy compared to placebo in delaying development of CR during ADT treatment for primary metastatic or recurrent prostate cancer. Secondary aim is to explore effect of statin intervention on prostate cancer mortality and lipid metabolism during ADT. Methods and analysis In this randomised placebo-controlled trial, a total of 400 men with de novo metastatic prostate cancer or recurrent disease after primary treatment and starting ADT will be recruited and randomised 1:1 to use daily 80 mg of atorvastatin or placebo. All researchers, study nurses and patients will be blinded throughout the trial. Patients are followed until disease recurrence or death. Primary outcome is time to formation of CR after initiation of ADT. Serum lipid levels (total cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL) and trigyserides) are analysed to test whether changes in serum cholesterol parameters during ADT predict length of treatment response. Furthermore, the trial will compare quality of life, cardiovascular morbidity, changes in blood glucose and circulating cell-free DNA, and urine lipidome during trial. Ethics and dissemination This study is approved by the Regional ethics committees of the Pirkanrnaa Hospital District, Science centre, Tampere, Finland (R18065M) and Tarto University Hospital, Tarto, Estonia (319/T-6). All participants read and sign informed consent form before study entry. After publication of results for the primary endpoints, anonymised summary metadata and statistical code will be made openly available. The data will not include any information that could make it possible to identify a given participant.Peer reviewe

Mitochondrial genome-wide analysis of nuclear DNA methylation quantitative trait loci

Mitochondria have a complex communication network with the surrounding cell and can alter nuclear DNA methylation (DNAm). Variation in the mitochondrial DNA (mtDNA) has also been linked to differential DNAm. Genome-wide association studies have identified numerous DNAm quantitative trait loci, but these studies have not examined the mitochondrial genome. Herein, we quantified nuclear DNAm from blood and conducted a mitochondrial genome-wide association study of DNAm, with an additional emphasis on sex- and prediabetes-specific heterogeneity. We used the Young Finns Study (n = 926) with sequenced mtDNA genotypes as a discovery sample and sought replication in the Ludwigshafen Risk and Cardiovascular Health study (n = 2317). We identified numerous significant associations in the discovery phase (P < 10(-9)), but they were not replicated when accounting for multiple testing. In total, 27 associations were nominally replicated with a P < 0.05. The replication analysis presented no evidence of sex- or prediabetes-specific heterogeneity. The 27 associations were included in a joint meta-analysis of the two cohorts, and 19 DNAm sites associated with mtDNA variants, while four other sites showed haplogroup associations. An expression quantitative trait methylation analysis was performed for the identified DNAm sites, pinpointing two statistically significant associations. This study provides evidence of a mitochondrial genetic control of nuclear DNAm with little evidence found for sex- and prediabetes-specific effects. The lack of a comparable mtDNA data set for replication is a limitation in our study and further studies are needed to validate our results.Peer reviewe

Methylation status of VTRNA2-1/nc886 is stable across populations, monozygotic twin pairs and in majority of tissues

Aims & methods: The aim of this study was to characterize the methylation level of a polymorphically imprinted gene, VTRNA2-1/nc886, in human populations and somatic tissues.48 datasets, consisting of more than 30 tissues and >30,000 individuals, were used. Results: nc886 methylation status is associated with twin status and ethnic background, but the variation between populations is limited. Monozygotic twin pairs present concordant methylation, whereas similar to 30% of dizygotic twin pairs present discordant methylation in the nc886 locus. The methylation levels of nc886 are uniform across somatic tissues, except in cerebellum and skeletal muscle. Conclusion: The nc886 imprint may be established in the oocyte, and, after implantation, the methylation status is stable, excluding a few specific tissues. Tweetable abstract Methylation status of a polymorphically imprinted gene, VTRNA2-1/nc886, is stable in human populations (48 cohorts, n > 30,000) and in somatic tissues, except in cerebellum and skeletal muscle. Twin data suggest it may already be established in the oocyte.Peer reviewe

Modular genome-wide gene expression architecture shared by early traits of osteoporosis and atherosclerosis in the Young Finns Study

We analysed whole blood genome-wide expression data to identify gene co-expression modules shared by early traits of osteoporosis and atherosclerosis. Gene expression was profiled for the Young Finns Study participants. Bone mineral density and content were measured as early traits of osteoporosis. Carotid and bulbus intima media thickness were measured as early traits of atherosclerosis. Joint association of the modules, identified with weighted co-expression analysis, with early traits of the diseases was tested with multivariate analysis. Among the six modules significantly correlated with early traits of both the diseases, two had significant (adjusted p-values (p.adj) < 0.05) and another two had suggestively significant (p.adj < 0.25) joint association with the two diseases after adjusting for age, sex, body mass index, smoking habit, alcohol consumption, and physical activity. The three most significant member genes from the significant modules were NOSIP, GXYLT2, and TRIM63 (p.adj ≤ 0.18). Genes in the modules were enriched with biological processes that have separately been found to be involved in either bone metabolism or atherosclerosis. The gene modules and their most significant member genes identified in this study support the osteoporosis-atherosclerosis comorbidity hypothesis and can provide new joint biomarkers for both diseases and their dual prevention