Relative age effects in political selection

We exploit a regression discontinuity design to provide causal evidence of the relative age effect (RAE) on a long-run adult age outcome: Political selection. We find strong evidence of the RAE in politics in Finland. However, the effect is heterogeneous: We find that male candidates born early in the calendar year have a significantly higher probability of getting elected to the parliament but no similar RAE applies to female candidates nor to municipal elections. Moreover, this effect only takes place in the most competitive parliamentary districts and is present only for some parties. We also find that in all the groups where the RAE does not exist, early-born candidates are under-represented suggesting attrition of talent in the candidate placement. Overall, our results show that seemingly artificial cutoffs imposed by the government have persistent consequences even on the selection to the highest positions of power within a society

Database-assisted spectrum sharing in satellite communications:A survey

This survey paper discusses the feasibility of sharing the spectrum between satellite telecommunication networks and terrestrial and other satellite networks on the basis of a comprehensive study carried out as part of the European Space Agency's (ESA) Advanced Research in Telecommunications Systems (ARTES) programme. The main area of investigation is the use of spectrum databases to enable a controlled sharing environment. Future satellite systems can largely benefit from the ability to access spectrum bands other than the dedicated licensed spectrum band. Potential spectrum sharing scenarios are classified as: a) secondary use of the satellite spectrum by terrestrial systems, b) satellite system as a secondary user of spectrum, c) extension of a terrestrial network by using the satellite network, and d) two satellite systems sharing the same spectrum. We define practical use cases for each scenario and identify suitable techniques. The proposed scenarios and use cases cover several frequency bands and satellite orbits. Out of all the scenarios reviewed, owing to the announcement of many different mega-constellation satellite networks, we focus on analysing the feasibility of spectrum sharing between geostationary orbit (GSO) and non-geostationary orbit (NGSO) satellite systems. The performance is primarily analysed on the basis of widely accepted recommendations of the Radiocommunications Sector of the International Telecommunications Union (ITU-R). Finally, future research directions are identified

Monoterpene pollution episodes in a forest environment : indication of anthropogenic origin and association with aerosol particles

We used a monoterpene volume mixing ratio dataset measured from 12 June 2006 to 24 September 2007 and from 1 June 2008 to 3 March 2009 at the SMEAR II station to quantify the magnitude of anthropogenic monoterpene emissions aside from biogenic origins, to examine the anthropogenic sources, and to look at other associated pollutants. We discuss the relations between increased monoterpene mixing ratios and particle concentrations. We also characterize chemical properties of aerosol particles during two monoterpene pollution episodes in case studies. Out of 580 days analyzed, anthropogenic monoterpene pollution episodes were found on 341 (58.8%) days. The average monoterpene mixing ratio increased from 0.19 to 0.26 ppbv due to the presence of anthropogenic monoterpenes, which is equal to an increase of 36.8%. The observed anthropogenic monoterpenes were mostly from the Korkeakoski sawmill. Other gas pollutants might occasionally be emitted during the episodes, but did not show clear association with anthropogenic monoterpenes. Aerosol particle concentrations substantially increased during episodes, and monoterpene mixing ratios showed strong connections with Aitken mode particles both in number and volume concentrations. Particles associated with monoterpene episodes reached a CCN (cloud concentration nucleus) size. The chemical characterizations of aerosol particles in case studies show that the increase in aerosol particle mass was mainly from secondary organic aerosol

Association of lifetime blood pressure with adulthood exercise blood pressure response: the cardiovascular risk in young Finns study

PurposeElevated blood pressure (BP) in childhood has been associated with increased adulthood BP. However, BP and its change from childhood to adulthood and the risk of exaggerated adulthood exercise BP response are largely unknown. Therefore, we studied the association of childhood and adulthood BP with adulthood exercise BP response.Materials and methodsThis investigation consisted of 406 individuals participating in the ongoing Cardiovascular Risk in Young Finns Study (baseline in 1980, at age of 6-18 years; follow-up in adulthood in 27-29 years since baseline). In childhood BP was classified as elevated according to the tables from the International Child Blood Pressure References Establishment Consortium, while in adulthood BP was considered elevated if systolic BP was >= 120 mmHg or diastolic BP was >= 80 mmHg or if use of antihypertensive medications was self-reported. A maximal cardiopulmonary exercise test with BP measurements was performed by participants in 2008-2009, and exercise BP was considered exaggerated (EEBP) if peak systolic blood pressure exceeded 210 mmHg in men and 190 mmHg in women.ResultsParticipants with consistently high BP from childhood to adulthood and individuals with normal childhood but high adulthood BP had an increased risk of EEBP response in adulthood (relative risk [95% confidence interval], 3.32 [2.05-5.40] and 3.03 [1.77-5.17], respectively) in comparison with individuals with normal BP both in childhood and adulthood. Interestingly, individuals with elevated BP in childhood but not in adulthood also had an increased risk of EEBP [relative risk [95% confidence interval], 2.17 [1.35-3.50]).ConclusionsThese findings reinforce the importance of achieving and sustaining normal blood pressure from childhood through adulthood.</p

Determinants of exercise peak arterial blood pressure, circulatory power, and exercise cardiac power in a population based sample of Finnish male and female aged 30 to 47 years: the Cardiovascular Risk in Young Finns Study

Background Novel parameters derived from peak maximal oxygen uptake (VO2) and exercise arterial blood pressure, such as peak circulatory power (CP) and exercise cardiac power (ECP), can be used in the risk assessment of cardiovascular disease and stroke. However, the determinants of these factors are poorly characterized in the general population. Methods We assessed peak arterial blood pressure, CP and ECP with standardized cardiopulmonary exercise test (CPET) on 281 female and 257 male participants of the Cardiovascular Risk in Young Finns Study. The subjects were aged 30–47 years. Peak VO2 as well as systolic and diastolic arterial blood pressures were measured to calculate peak mean arterial pressure, CP and ECP. These parameters were assessed for correlation with sex, age, height, weight, waist-to-hip ratio, smoking, physical activity index (PAI), fasting insulin and glucose levels as well as the use of antihypertensive treatment. Results Sex, age and weight explained 36% of the variation in peak systolic blood pressure, and these factors in combination with height and the use of antihypertensive treatment explained 13% of the variation in peak diastolic blood pressure. Sex, height, weight, waist-to-hip ratio, PAI and smoking explained 49% − 52% of the variation in peak CP. Sex, age, height, weight, waist-to-hip ratio, PAI, smoking and insulin levels explained 21% − 49% of variation in ECP. Conclusions Subject demographics and lifestyle-related factors should be taken into account when exercise blood pressure response, CP and ECP are used to evaluate patients’ cardiac function in CPET.BioMed Central open acces

Inflammatory cytokines and cytokine gene polymorphisms in chronic lymphocytic leukaemia, in primary Sjögren's syndrome and in healthy subjects

Sytokiinit ovat joukko liukoisia tulehdusvälittäjäaineita, joiden keskinäinen tasapaino on häiriintynyt monissa sairauksissa. Sytokiinien geenit ovat polymorfisia, ja tämän geneettisen vaihtelun on kuvattu liittyvän vaihteluun yksittäisten sytokiinien tuotantokyvyssä. Tässä poikkileikkaustutkimuksessa tutkittiin sytokiinituotannon häiriöiden ja sytokiinigeenien polymorfismin osuutta kahteen etiologialtaan tuntemattomaan sairauteen, krooniseen lymfaattiseen B-soluleukemiaan (B-KLL) ja primääriin Sjögrenin syndroomaan (pSS). Lisäksi sytokiinigeenien jakautumia ja vaikutuksia terveessä väestössä tutkittiin 400 SPR:n verenluovuttajan aineistossa. Tutkimuksessa havaittiin, että interleukiini-6 (IL-6) proteiinin plasmapitoisuudet olivat koholla sekä B-KLL:ssa että pSS:ssa. Plasman IL-6 pitoisuudet olivat riippuvaisia B-KLL:n vaikeusasteesta siten, että korkeimmat pitoisuudet tavattiin potilailla joilla oli vaikeusasteluokittelun mukaan lyhin ennuste. Korkea plasman IL-6 liittyi potilailla esiintyvään anemiaan, mataliin hemoglobiinitasoihin sekä korkeaan laskoon. IL-6:sta poiketen interleukiini-1 perheen sytokiinien IL-1b ja IL-1Ra plasmatasot olivat madaltuneet B-KLL:ssä. Korkea plasman IL-1b taso ja matala IL-1Ra/IL-1b suhde liittyivät B-KLL:ssa ei-etenevään tautimuotoon. Kuten B-KLL:ssa, myös pSS:ssa plasman IL-6 tasot vaihtelivat taudin ilmenemismuodoista ja taudin vaikeusasteesta riippuen. Plasman IL-6 pitoisuudet korreloivat lähes lineaarisesti pienten sylkirauhasten histopatologiseen lymfosyytti-infiltraatioon, jota on pidetty taudin vaikeusasteen yhtenä tärkeimpänä mittarina. Lisäksi korkea plasman IL-6 pitoisuus liittyi pSS-potilailla esiintyvään pleuriittiin, perifeerisen hermoston oireisiin ja keliakiaan. IL-1 geeniperheen ja IL-6 geenin alleelijakaumat eivätkä alleelien vaikutukset ko.sytokiinien tuotantoihin poikenneet B-CLL-potilaiden ja normaaliväestön välillä toisistaan. IL-1 geeniperheen alleelivaikutus IL-1b plasmatasoihin selittyi normaaliväestössä tämän geeniperheen eri haplotyyppien yhteisvaikutuksen kautta, ja harvinaisimman IL-1 haplotyypin omaavilla kohdehenkilöillä tavattiin ko. proteiinin korkeimmat plasmatasot. IL-6 geenin promoottorialueen polymorfia sääteli IL-6 tasoja pSS:ssä, mutta tämän polymorfian alleelijakauma ei poikennut pSS potilaiden ja normaaliväestön välillä. IL-10 geenin alleelijakauma sen sijaan poikkesi pSS potilailla normaaliväestöstä siten, että korkeaan IL-10 tuotantoon liittyvien IL-10 geenin promoottorialueen haplotyyppien esiintymistiheys oli potilailla noussut. Nämä ennakkotulokset vahvistavat oletusta, että IL-6 plasmatasojen mittausta voitaisiin käyttää apuna B-CLL:n ja pSS:n vaikeusasteen määrittämisessä ja plasman IL-1Ra/IL-1b suhteen määritystä B-CLL:n etenemisnopeutta ennustavana laboratorioparametrina. Tulokset viittaavat myös siihen, että korkealla IL-1b aktiivisuudella saattaa olla B-KLL:n etenemiseltä suojaava vaikutus. IL-1 geeniperheen tai IL-6 geenin promoottorialueen polymorfioita ei kuitenkaan voida käyttää B-KLL:n riskinarvioinnissa, eikä näiden geenien alleelinen epätasapaino aiheuta taudissa tavattavia sytokiinituotannon häiriöitä. Tämä negatiivinen tulos pätee myös IL-6 geenin polymorfiaan pSS:ssä. IL-10 geenin haplotyyppien jakautumien poikkeavuus pSS:ssa viittaa siihen, että IL-10 geenin määrätyt haplotyypit, tai näihin kytkeytynyt toistaiseksi vielä tunnistamaton geneettinen tekijä altistaa potilaita pSS:lle. IL-10 haplotyyppien ja IL-10 proteiinituotannon välisten yhteyksien vuoksi on todennäköistä, että tautiriskin lisääntyminen ainakin osin välittyy lisääntyneen IL-10 tuotannon kautta. Yksittäisen poikkileikkaustutkimuksen antama informaatio tässä suhteessa on kuitenkin rajallinen, ja kontrolloitujen pitkäaikaistutkimusten tarve on ilmeinen.In this dissertation we studied two aetiologically unknown disorders (B cell chronic lymphocytic leukaemia and primary Sjögren's syndrome) with imbalanced cytokine production in order to find out whether these imbalances have an effect on disease phenotype or severity. Several cytokine gene polymorphisms were studied in these patients in order to find out whether the allelic imbalance of these genes predisposes patients to disease, or whether disturbed cytokine profiles are caused by these genetic factors. Moreover, circulating cytokines and polymorphisms of corresponding genes were studied in a cohort of healthy subjects. The role of in vitro IL-6 and TNF-a production was studied in 24 patients with B-CLL. The role of circulating IL-1b, IL-1Ra and IL-6 and several polymorphic sites of corresponding genes were studied in 36 patients with B-CLL. Circulating IL-6 and IL-10 and the genetic polymorphism of these genes were studied in cohorts of 66 and 62 patients with pSS. The cytokine gene polymorphisms of IL-1a, IL-1b, IL-1Ra, IL-6 and IL-10 were studied in a cohort of 400 healthy Finnish Red Cross Transfusion Service blood donors, who also served as controls for allele frequency analyses and cytokine production studies. The in vitro and in vivo production of IL-6 was stage dependent in B-CLL. The cellular release of IL-6 (and to a lesser extent TNF-a) was decreased in Binet C stage patients, who by contrast have the highest circulating IL-6 levels. The overall plasma IL-6 was increased in B-CLL compared to levels of normal subjects. Plasma IL-6 was shown to be associated with anaemia, haemoglobin levels and with ESRs in B-CLL patients. In contrast to IL-6, baseline plasma concentrations of IL-1b and IL-1Ra were diminished in B-CLL. High circulating IL-1b was associated with non-progressive disease and the plasma IL-1Ra/IL-1b ratio was strikingly low in the patients with non-progressive B-CLL. High plasma IL-1b was associated with atypical B-CLL immunophenotype in B-CLL. The allele distributions of IL-1 family genes and IL-6 gene were similar in B-CLL patients and in healthy control subjects. These data suggest that other mechanisms than allelic imbalance cause the distinct IL-1b, IL-1Ra and IL-6 profiles in B-CLL. The normal allelic distribution of corresponding genes in B-CLL exclude the possibility that the polymorphic loci of these genes could be used in the risk-assessment of B-CLL. The association of high IL-1b activity in non-progressive disease indicates that high IL-1b has a protective role in the disease. These results also suggest that high plasma IL-6 is a good potential candidate marker for inferior prognosis in B-CLL. Moreover, high plasma IL-1b and low plasma IL-1Ra/IL-1b ratios are potential candidate markers for non-progressive B-CLL. These preliminary results emphasize the need for longitudinal studies concerning the role of these proteins in B-CLL. The plasma levels of IL-6 were increased in pSS and high plasma IL-6 was associated with lymphocyte focus score and specific extraglandular manifestations such as coeliac disease, pleuritis and peripheral nervous system symptoms of the disease. The circulating IL-10 levels were also higher in pSS patients than in control subjects, but this difference was not statistically significant. The plasma IL-6 and IL-10 concentrations were dependent on the IL-6 or IL-10 allelic status of the pSS patients. The allelic distribution of IL-6 -174 polymorphism was similar in patients and controls. In contrast to IL-6 alleles, the frequency of IL-10 gene GCC haplotype increased, and the frequency of ACC haplotype decreased in pSS when compared with the control population. Plasma IL-10 was not associated with disease phenotype or disease activity markers in pSS. The complementary histological and clinical findings concerning IL-6 strongly suggest that IL-6 may be used as a surrogate marker for severity of pSS. These findings also suggest that IL-6 may be involved in the development of some of extraglandular disease manifestations in pSS. The normal IL-6 allele distribution in pSS excludes the possibility that allelic imbalance of this gene is a primary cause for the overall increase of plasma IL-6 in pSS. In contrast to IL-6 polymorphism, polymorphism of the IL-10 gene seems to be a predisposing factor for pSS. The increase of GCC, IL-10 "high producer" haplotype may partly explain increased IL-10 observed earlier in pSS. Due to the subtle nature of allelic effects, larger cohorts and longitudinal studies are needed to find phenotypic effects of allelic imbalance in IL-10 gene. We also demonstrated that the baseline plasma levels of IL-1b are genetically regulated in healthy subjects by IL-1a polymorphism. This genetic effect could be observed only in those subjects who were homozygous for allele 2 of the IL-1a gene. Moreover, IL-1b (-511) allele 2 had a cumulative effect on the IL-1a allele 2.2 homozygosity-associated high IL-1b. These results suggest that IL-1a allele 2 regulates IL-1b production indirectly by IL-1a production, or that this allele contains or codes for a regulative element enhancing the transcription of itself and the adjacent genes. No statistically significant differences in plasma IL-6 or IL-10 were observed, when healthy controls were categorized on the basis of IL-10 haplotypes. This suggests that IL-10 and IL-6 polymorphisms regulate primarily inducible cytokine responses or that basal and induced responses of these cytokines are differently regulated

Inflammatory cytokines and cytokine gene polymorphisms in chronic lymphocytic leukaemia, in primary Sjögren's syndrome and in healthy subjects

Sytokiinit ovat joukko liukoisia tulehdusvälittäjäaineita, joiden keskinäinen tasapaino on häiriintynyt monissa sairauksissa. Sytokiinien geenit ovat polymorfisia, ja tämän geneettisen vaihtelun on kuvattu liittyvän vaihteluun yksittäisten sytokiinien tuotantokyvyssä. Tässä poikkileikkaustutkimuksessa tutkittiin sytokiinituotannon häiriöiden ja sytokiinigeenien polymorfismin osuutta kahteen etiologialtaan tuntemattomaan sairauteen, krooniseen lymfaattiseen B-soluleukemiaan (B-KLL) ja primääriin Sjögrenin syndroomaan (pSS). Lisäksi sytokiinigeenien jakautumia ja vaikutuksia terveessä väestössä tutkittiin 400 SPR:n verenluovuttajan aineistossa. Tutkimuksessa havaittiin, että interleukiini-6 (IL-6) proteiinin plasmapitoisuudet olivat koholla sekä B-KLL:ssa että pSS:ssa. Plasman IL-6 pitoisuudet olivat riippuvaisia B-KLL:n vaikeusasteesta siten, että korkeimmat pitoisuudet tavattiin potilailla joilla oli vaikeusasteluokittelun mukaan lyhin ennuste. Korkea plasman IL-6 liittyi potilailla esiintyvään anemiaan, mataliin hemoglobiinitasoihin sekä korkeaan laskoon. IL-6:sta poiketen interleukiini-1 perheen sytokiinien IL-1b ja IL-1Ra plasmatasot olivat madaltuneet B-KLL:ssä. Korkea plasman IL-1b taso ja matala IL-1Ra/IL-1b suhde liittyivät B-KLL:ssa ei-etenevään tautimuotoon. Kuten B-KLL:ssa, myös pSS:ssa plasman IL-6 tasot vaihtelivat taudin ilmenemismuodoista ja taudin vaikeusasteesta riippuen. Plasman IL-6 pitoisuudet korreloivat lähes lineaarisesti pienten sylkirauhasten histopatologiseen lymfosyytti-infiltraatioon, jota on pidetty taudin vaikeusasteen yhtenä tärkeimpänä mittarina. Lisäksi korkea plasman IL-6 pitoisuus liittyi pSS-potilailla esiintyvään pleuriittiin, perifeerisen hermoston oireisiin ja keliakiaan. IL-1 geeniperheen ja IL-6 geenin alleelijakaumat eivätkä alleelien vaikutukset ko.sytokiinien tuotantoihin poikenneet B-CLL-potilaiden ja normaaliväestön välillä toisistaan. IL-1 geeniperheen alleelivaikutus IL-1b plasmatasoihin selittyi normaaliväestössä tämän geeniperheen eri haplotyyppien yhteisvaikutuksen kautta, ja harvinaisimman IL-1 haplotyypin omaavilla kohdehenkilöillä tavattiin ko. proteiinin korkeimmat plasmatasot. IL-6 geenin promoottorialueen polymorfia sääteli IL-6 tasoja pSS:ssä, mutta tämän polymorfian alleelijakauma ei poikennut pSS potilaiden ja normaaliväestön välillä. IL-10 geenin alleelijakauma sen sijaan poikkesi pSS potilailla normaaliväestöstä siten, että korkeaan IL-10 tuotantoon liittyvien IL-10 geenin promoottorialueen haplotyyppien esiintymistiheys oli potilailla noussut. Nämä ennakkotulokset vahvistavat oletusta, että IL-6 plasmatasojen mittausta voitaisiin käyttää apuna B-CLL:n ja pSS:n vaikeusasteen määrittämisessä ja plasman IL-1Ra/IL-1b suhteen määritystä B-CLL:n etenemisnopeutta ennustavana laboratorioparametrina. Tulokset viittaavat myös siihen, että korkealla IL-1b aktiivisuudella saattaa olla B-KLL:n etenemiseltä suojaava vaikutus. IL-1 geeniperheen tai IL-6 geenin promoottorialueen polymorfioita ei kuitenkaan voida käyttää B-KLL:n riskinarvioinnissa, eikä näiden geenien alleelinen epätasapaino aiheuta taudissa tavattavia sytokiinituotannon häiriöitä. Tämä negatiivinen tulos pätee myös IL-6 geenin polymorfiaan pSS:ssä. IL-10 geenin haplotyyppien jakautumien poikkeavuus pSS:ssa viittaa siihen, että IL-10 geenin määrätyt haplotyypit, tai näihin kytkeytynyt toistaiseksi vielä tunnistamaton geneettinen tekijä altistaa potilaita pSS:lle. IL-10 haplotyyppien ja IL-10 proteiinituotannon välisten yhteyksien vuoksi on todennäköistä, että tautiriskin lisääntyminen ainakin osin välittyy lisääntyneen IL-10 tuotannon kautta. Yksittäisen poikkileikkaustutkimuksen antama informaatio tässä suhteessa on kuitenkin rajallinen, ja kontrolloitujen pitkäaikaistutkimusten tarve on ilmeinen.In this dissertation we studied two aetiologically unknown disorders (B cell chronic lymphocytic leukaemia and primary Sjögren's syndrome) with imbalanced cytokine production in order to find out whether these imbalances have an effect on disease phenotype or severity. Several cytokine gene polymorphisms were studied in these patients in order to find out whether the allelic imbalance of these genes predisposes patients to disease, or whether disturbed cytokine profiles are caused by these genetic factors. Moreover, circulating cytokines and polymorphisms of corresponding genes were studied in a cohort of healthy subjects. The role of in vitro IL-6 and TNF-a production was studied in 24 patients with B-CLL. The role of circulating IL-1b, IL-1Ra and IL-6 and several polymorphic sites of corresponding genes were studied in 36 patients with B-CLL. Circulating IL-6 and IL-10 and the genetic polymorphism of these genes were studied in cohorts of 66 and 62 patients with pSS. The cytokine gene polymorphisms of IL-1a, IL-1b, IL-1Ra, IL-6 and IL-10 were studied in a cohort of 400 healthy Finnish Red Cross Transfusion Service blood donors, who also served as controls for allele frequency analyses and cytokine production studies. The in vitro and in vivo production of IL-6 was stage dependent in B-CLL. The cellular release of IL-6 (and to a lesser extent TNF-a) was decreased in Binet C stage patients, who by contrast have the highest circulating IL-6 levels. The overall plasma IL-6 was increased in B-CLL compared to levels of normal subjects. Plasma IL-6 was shown to be associated with anaemia, haemoglobin levels and with ESRs in B-CLL patients. In contrast to IL-6, baseline plasma concentrations of IL-1b and IL-1Ra were diminished in B-CLL. High circulating IL-1b was associated with non-progressive disease and the plasma IL-1Ra/IL-1b ratio was strikingly low in the patients with non-progressive B-CLL. High plasma IL-1b was associated with atypical B-CLL immunophenotype in B-CLL. The allele distributions of IL-1 family genes and IL-6 gene were similar in B-CLL patients and in healthy control subjects. These data suggest that other mechanisms than allelic imbalance cause the distinct IL-1b, IL-1Ra and IL-6 profiles in B-CLL. The normal allelic distribution of corresponding genes in B-CLL exclude the possibility that the polymorphic loci of these genes could be used in the risk-assessment of B-CLL. The association of high IL-1b activity in non-progressive disease indicates that high IL-1b has a protective role in the disease. These results also suggest that high plasma IL-6 is a good potential candidate marker for inferior prognosis in B-CLL. Moreover, high plasma IL-1b and low plasma IL-1Ra/IL-1b ratios are potential candidate markers for non-progressive B-CLL. These preliminary results emphasize the need for longitudinal studies concerning the role of these proteins in B-CLL. The plasma levels of IL-6 were increased in pSS and high plasma IL-6 was associated with lymphocyte focus score and specific extraglandular manifestations such as coeliac disease, pleuritis and peripheral nervous system symptoms of the disease. The circulating IL-10 levels were also higher in pSS patients than in control subjects, but this difference was not statistically significant. The plasma IL-6 and IL-10 concentrations were dependent on the IL-6 or IL-10 allelic status of the pSS patients. The allelic distribution of IL-6 -174 polymorphism was similar in patients and controls. In contrast to IL-6 alleles, the frequency of IL-10 gene GCC haplotype increased, and the frequency of ACC haplotype decreased in pSS when compared with the control population. Plasma IL-10 was not associated with disease phenotype or disease activity markers in pSS. The complementary histological and clinical findings concerning IL-6 strongly suggest that IL-6 may be used as a surrogate marker for severity of pSS. These findings also suggest that IL-6 may be involved in the development of some of extraglandular disease manifestations in pSS. The normal IL-6 allele distribution in pSS excludes the possibility that allelic imbalance of this gene is a primary cause for the overall increase of plasma IL-6 in pSS. In contrast to IL-6 polymorphism, polymorphism of the IL-10 gene seems to be a predisposing factor for pSS. The increase of GCC, IL-10 "high producer" haplotype may partly explain increased IL-10 observed earlier in pSS. Due to the subtle nature of allelic effects, larger cohorts and longitudinal studies are needed to find phenotypic effects of allelic imbalance in IL-10 gene. We also demonstrated that the baseline plasma levels of IL-1b are genetically regulated in healthy subjects by IL-1a polymorphism. This genetic effect could be observed only in those subjects who were homozygous for allele 2 of the IL-1a gene. Moreover, IL-1b (-511) allele 2 had a cumulative effect on the IL-1a allele 2.2 homozygosity-associated high IL-1b. These results suggest that IL-1a allele 2 regulates IL-1b production indirectly by IL-1a production, or that this allele contains or codes for a regulative element enhancing the transcription of itself and the adjacent genes. No statistically significant differences in plasma IL-6 or IL-10 were observed, when healthy controls were categorized on the basis of IL-10 haplotypes. This suggests that IL-10 and IL-6 polymorphisms regulate primarily inducible cytokine responses or that basal and induced responses of these cytokines are differently regulated

Diminished production of interleukin-6 in chronic lymphocytic leukaemia (B-CLL) cells from patients at advanced stages of disease.

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Generating alpha with AI in the stock markets : Towards understanding the process

Artificial intelligence (AI) is a high-profile topic – it is currently impossible to avoid in the media. It is said that a technological arms race exists in the field of finance, regarding AI. The subject of this thesis has been researched relatively little with a qualitative approach. Therefore, this thesis was written with a qualitative approach to explore the phenomenon of AI in stock investing more broadly than usually seen in the literature, from the perspectives of experts on the subject. The purpose of this thesis is to provide clarity to the process of generating alpha with AI in the stock markets and also to the main aspects to take into account when trying to or considering to use AI in stock investing effectively. The empirical research methods used in this study have been semi-structured interviews and content analysis. Four experts were interviewed, and five different online contents (text, audio, and video) based on the views of experts on the subject were analyzed. The most recurring and relevant themes regarding the process of generating alpha with AI in the stock markets were (abbreviated): recruiting suitable, high skilled personnel, choosing the suitable stock investing and AI techniques, acquiring and refining suitable data, choosing a suitable computing strategy, and after the project has started, developing the AI stock investing solution. The main aspects to take into account when trying to, or considering to use AI in stock investing effectively, were found to be black boxes and how to treat them, how to execute backtesting and avoid overfitting, considering how autonomous an AI system should be, and if the considered business can survive in the near future without AI’s help. It seems that the practical results of AI-based stock investing have not been strong, probably because the practice appears to still be in its beginning. However, the sector is growing actively, research results are promising, and some speculate that the financial markets might change because of AI. Thus, researchers and practitioners should familiarize themselves with the subject