Sosiaalisten vaikutusten arviointi voimajohtohankkeissa

Verkkoversion ISBN 951-33-1410-3, ISSN 1795-810

Global warming will affect the maximum potential abundance of boreal plant species

Forecasting the impact of future global warming on biodiversity requires understanding how temperature limits the distribution of species. Here we rely on Liebig's Law of Minimum to estimate the effect of temperature on the maximum potential abundance that a species can attain at a certain location. We develop 95%‐quantile regressions to model the influence of effective temperature sum on the maximum potential abundance of 25 common understory plant species of Finland, along 868 nationwide plots sampled in 1985. Fifteen of these species showed a significant response to temperature sum that was consistent in temperature‐only models and in all‐predictors models, which also included cumulative precipitation, soil texture, soil fertility, tree species and stand maturity as predictors. For species with significant and consistent responses to temperature, we forecasted potential shifts in abundance for the period 2041–2070 under the IPCC A1B emission scenario using temperature‐only models. We predict major potential changes in abundance and average northward distribution shifts of 6–8 km yr−1. Our results emphasize inter‐specific differences in the impact of global warming on the understory layer of boreal forests. Species in all functional groups from dwarf shrubs, herbs and grasses to bryophytes and lichens showed significant responses to temperature, while temperature did not limit the abundance of 10 species. We discuss the interest of modelling the ‘maximum potential abundance’ to deal with the uncertainty in the predictions of realized abundances associated to the effect of environmental factors not accounted for and to dispersal limitations of species, among others. We believe this concept has a promising and unexplored potential to forecast the impact of specific drivers of global change under future scenarios.202

The value of scientific information on climate change: a choice experiment on Rokua esker, Finland

This article presents an application of the choice experiment method in order to provide estimates of economic values generated by water quantity improvements in the environment. More importantly, this is the first choice experiment study valuing scientific information and in particular scientific information on climate change. The case study of interest is Rokua in Northern Finland, a groundwater dependent ecosystem very sensitive to climate change and natural variability. The study deals with the uncertainty about the actual dynamics of the system and the effect of future climate change by exploring whether the public values sustained provision of resources for scientific research to better understand long-term environmental changes in Rokua. Data are analysed using a nested multinomial logit and an error component model. Evidence from this study suggests that individuals are willing to pay in order to assure scientific research so as to better understand long-term environmental changes. As a result, policy should consider investing in and supporting related research. Other aspects of water management policy valued by the public are water quantity, recreation, and total land income. We gratefully acknowledge the financial support from the European Union via the 7th Framework Program GENESIS: Groundwater and dependent ecosystems: New Scientific basis on climate change and land-use impact for the update of the EU Groundwater Directive; WP-6 Groundwater systems management: scenarios, risk assessment, cost-efficient measures and legal aspects. We finally thank two anonymous referees for constructive and insightful comments Koundouri, P.; Kougea, E.; Stithoua, M.; Ala-Ahob, P.; Eskelinenb, R.; Karjalainenc, T.; Klove, B.... (2012). The Value of Scientific Information on Climate Change: A Choice Experiment on Rokua esker, Finland. Journal of Environmental Economics and Policy. 1(1):85-102. doi:10.1080/21606544.2011.647450 Senia 85 102 1

Radium-223 dichloride treatment in metastatic castration-resistant prostate cancer in Finland: A real-world evidence multicenter study

Background: Radium-233 dichloride is an alpha emitter that specifically targets bone metastases in prostate cancer. Results of a previously reported phase III randomized trial showed survival benefit for radium-223 compared to best supportive care in castration-resistant prostate cancer (CRPC) with bone metastases. However, real-world data are also needed with wider inclusion criteria.Methods: We report results of a retrospective multicenter study including all patients with metastatic CRPC treated with radium-223 in all five university hospitals in Finland since the introduction of the treatment. We identified 160 patients who had received radium-223 in Finland in 2014-2019.Results: The median overall survival (OS) was 13.8 months (range 0.5-57 months), and the median real-world progression-free survival (rwPFS) was 4.9 months (range 0.5-29.8 months). Alkaline phosphatase (ALP) values within the normal range before and during the radium-223 treatment or the reduction of elevated ALP to normal range during treatment were associated with better OS when compared to elevated ALP values before and during treatment (p Conclusion: Radium-223 was well tolerated in routine clinical practice, and most patients achieved pain relief. Pain relief, ALP normalization, lower baseline PSA, and PSA decrease during radium-223 treatment were prognostic for better survival. The efficacy of radium-223 in mCRPC as estimated using OS was comparable to earlier randomized trial in this retrospective real-world study. Our results support using radium-223 for mCRPC patients with symptomatic bone metastases even in the era of new-generation androgen receptor-targeted agents.</p

Diabetes and heart failure associations in women and men: results from the MORGAM consortium

Background: Diabetes and its cardiovascular complications are a growing concern worldwide. Recently, some studies have demonstrated that relative risk of heart failure (HF) is higher in women with type 1 diabetes (T1DM) than in men. This study aims to validate these findings in cohorts representing five countries across Europe. Methods: This study includes 88,559 (51.8% women) participants, 3,281 (46.3% women) of whom had diabetes at baseline. Survival analysis was performed with the outcomes of interest being death and HF with a follow-up time of 12 years. Sub-group analysis according to sex and type of diabetes was also performed for the HF outcome. Results: 6,460 deaths were recorded, of which 567 were amongst those with diabetes. Additionally, HF was diagnosed in 2,772 individuals (446 with diabetes). A multivariable Cox proportional hazard analysis showed that there was an increased risk of death and HF (hazard ratio (HR) of 1.73 [1.58–1.89] and 2.12 [1.91–2.36], respectively) when comparing those with diabetes and those without. The HR for HF was 6.72 [2.75–16.41] for women with T1DM vs. 5.80 [2.72–12.37] for men with T1DM, but the interaction term for sex differences was insignificant (p for interaction 0.45). There was no significant difference in the relative risk of HF between men and women when both types of diabetes were combined (HR 2.22 [1.93–2.54] vs. 1.99 [1.67–2.38] respectively, p for interaction 0.80). Conclusion: Diabetes is associated with increased risks of death and heart failure, and there was no difference in relative risk according to sex

High-precision mass measurements for the isobaric multiplet mass equation at A=52

Masses of Co-52, (52)Com, Fe-52, Fe-52(m), and Mn-52 have been measured with the JYFLTRAP double Penning trap mass spectrometer. The isobaric multiplet mass equation for the T = 2 quintet at A = 52 has been studied employing the new mass values. No significant breakdown (beyond the 3 sigma level) of the quadratic form of the IMME was observed (chi(2)/n = 2.4). The cubic coefficient was 6.0(32) keV (chi(2)/n = 1.1). The excitation energies for the isomer and the T = 2 isobaric analog state in Co-52 have been determined to be 374(13) keV and 2922(13) keV, respectively. The measured mass values for Co-52 and (52)Com are 29(10) keV and 16(15) keV higher, respectively, than obtained in a recent storage-ring experiment, and significantly lower than predicted by extrapolations. Consequently, this has an impact on the proton separation energies for Co-52 and Ni-53 relevant for the astrophysical rapid proton capture process. The Q value for the proton decay from the 19/2(-) isomer in Co-53 has been determined with an unprecedented precision, Q(p) = 1558.8(17) keV.Peer reviewe

Identification of Kinases Regulating Prostate Cancer Cell Growth Using an RNAi Phenotypic Screen

As prostate cancer progresses to castration-resistant disease, there is an increase in signal transduction activity. Most castration-resistant prostate tumors continue to express the androgen receptor (AR) as well as androgen-responsive genes, despite the near absence of circulating androgen in these patients. The AR is regulated not only by its cognate steroid hormone, but also by interactions with a constellation of co-regulatory and signaling molecules. Thus, the elevated signaling activity that occurs during progression to castration resistance can affect prostate cancer cell growth either through the AR or independent of the AR. In order to identify signaling pathways that regulate prostate cancer cell growth, we screened a panel of shRNAs targeting 673 human kinases against LNCaP prostate cancer cells grown in the presence and absence of hormone. The screen identified multiple shRNA clones against known and novel gene targets that regulate prostate cancer cell growth. Based on the magnitude of effect on growth, we selected six kinases for further study: MAP3K11, DGKD, ICK, CIT, GALK2, and PSKH1. Knockdown of these kinases decreased cell growth in both androgen-dependent and castration-resistant prostate cancer cells. However, these kinases had different effects on basal or androgen-induced transcriptional activity of AR target genes. MAP3K11 knockdown most consistently altered transcription of AR target genes, suggesting that MAP3K11 affected its growth inhibitory effect by modulating the AR transcriptional program. Consistent with MAP3K11 acting on the AR, knockdown of MAP3K11 inhibited AR Ser 650 phosphorylation, further supporting stress kinase regulation of AR phosphorylation. This study demonstrates the applicability of lentiviral-based shRNA for conducting phenotypic screens and identifies MAP3K11, DGKD, ICK, CIT, GALK2, and PSKH1 as regulators of prostate cancer cell growth. The thorough evaluation of these kinase targets will pave the way for developing more effective treatments for castration-resistant prostate cancer