Tavallisia tarinoita : rivikansalaiset television uutisjutuissa

Tässä opinnäytetyössä käsittelen tavallisia ihmisiä televisiouutisten jutuissa käyttäen esimerkkeinä uutisjuttuja Nelosen ja MTV3:n kotimaan uutisista. Tavoitteeni on tutkia tavallisen ihmisen rooleja ja tehtäviä television uutisjutuissa, sekä tarkastella ”rivikansalaisten” käyttämistä uutisjutuissa toimittajantyön kannalta. Valotan sitä, mitä MTV3 ja Nelonen uutisillaan tavoittelevat, millaisista lähtökohdista kanavat toimivat ja miten kanavien arvot vaikuttavat tavallisten ihmisen esiintymiseen uutisjutuissa. Esittelen ja analysoin erilaisia juttutyyppejä, joissa tavallisia ihmisiä uutisissa esiintyy, pohdin millaisia tarinoita ja sisältöjä heidän kannaltaan kerrotaan ja millaisissa rooleissa he esiintyvät. Pohdin myös sitä, mitä lisäarvoa tavallisilla ihmisillä uutisjuttuihin haetaan ja sitä, voisiko arjen näkökulmaa laajentaa niistä juttutyypeistä, joissa se nyt jo esiintyy. Tarkastelen omien kokemuksieni pohjalta myös, millaisia käytännöllisiä, moraalisia ja journalistisia pulmia ja mahdollisuuksia tavallisten ihmisten käyttämiseen television uutisjutuissa liittyy. Käsittelen myös sitä, mihin tavalliset ihmiset asettuvat uutisten hierarkiassa, ja miten heidän esiintymisensä uutisjutuissa vaikuttaa uutisen objektiivisuuteen. Tavallinen ihminen on uutisjutussa elävöittävä kokija, toimija tai passiivinen toiminnan kohde. Hän voi esiintyä lähes minkä tahansa tyyppisessä uutisjutussa kuvittajana, kommentoijana, uutiskuorman keventäjänä tai jutulle rakenteen antavana tapauksena. Tavalliset ihmiset esiintyvät televisiouutisten gallupeissa tai avaamassa keskustelunaiheita elämäntilanteellaan. Usein he esiintyvät toimittajan tai toimituksen alter egoina, ottavat kantaa asioihin vapaina uutishuoneen objektiivisen totuuden oletusarvosta. Televisio on arkinen, perhekeskeinen ja tasa-arvoinen väline, joka joutuu taistelemaan huomiosta kodin muiden tapahtumien kanssa. Viihtymisen kannalta on olennaista kuvata ihmiskasvoja, tehdä uutisista tarinoita ja tarjota samaistuttavia elementtejä katsojalle. Vaikka monet tutkijat sijoittavat tavallisen ihmisen uutishierarkian alimmalle portaalle, heillä on uutisjutuissa viihdyttäjän osan ohella tärkeä tehtävä totuudenpuhujina.

New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk.

Levels of circulating glucose are tightly regulated. To identify new loci influencing glycemic traits, we performed meta-analyses of 21 genome-wide association studies informative for fasting glucose, fasting insulin and indices of beta-cell function (HOMA-B) and insulin resistance (HOMA-IR) in up to 46,186 nondiabetic participants. Follow-up of 25 loci in up to 76,558 additional subjects identified 16 loci associated with fasting glucose and HOMA-B and two loci associated with fasting insulin and HOMA-IR. These include nine loci newly associated with fasting glucose (in or near ADCY5, MADD, ADRA2A, CRY2, FADS1, GLIS3, SLC2A2, PROX1 and C2CD4B) and one influencing fasting insulin and HOMA-IR (near IGF1). We also demonstrated association of ADCY5, PROX1, GCK, GCKR and DGKB-TMEM195 with type 2 diabetes. Within these loci, likely biological candidate genes influence signal transduction, cell proliferation, development, glucose-sensing and circadian regulation. Our results demonstrate that genetic studies of glycemic traits can identify type 2 diabetes risk loci, as well as loci containing gene variants that are associated with a modest elevation in glucose levels but are not associated with overt diabetes.

Genome-wide association analyses identify 18 new loci associated with serum urate concentrations.

Elevated serum urate concentrations can cause gout, a prevalent and painful inflammatory arthritis. By combining data from >140,000 individuals of European ancestry within the Global Urate Genetics Consortium (GUGC), we identified and replicated 28 genome-wide significant loci in association with serum urate concentrations (18 new regions in or near TRIM46, INHBB, SFMBT1, TMEM171, VEGFA, BAZ1B, PRKAG2, STC1, HNF4G, A1CF, ATXN2, UBE2Q2, IGF1R, NFAT5, MAF, HLF, ACVR1B-ACVRL1 and B3GNT4). Associations for many of the loci were of similar magnitude in individuals of non-European ancestry. We further characterized these loci for associations with gout, transcript expression and the fractional excretion of urate. Network analyses implicate the inhibins-activins signaling pathways and glucose metabolism in systemic urate control. New candidate genes for serum urate concentration highlight the importance of metabolic control of urate production and excretion, which may have implications for the treatment and prevention of gout.

Parent-of-origin-specific allelic associations among 106 genomic loci for age at menarche.

Age at menarche is a marker of timing of puberty in females. It varies widely between individuals, is a heritable trait and is associated with risks for obesity, type 2 diabetes, cardiovascular disease, breast cancer and all-cause mortality. Studies of rare human disorders of puberty and animal models point to a complex hypothalamic-pituitary-hormonal regulation, but the mechanisms that determine pubertal timing and underlie its links to disease risk remain unclear. Here, using genome-wide and custom-genotyping arrays in up to 182,416 women of European descent from 57 studies, we found robust evidence (P < 5 × 10(-8)) for 123 signals at 106 genomic loci associated with age at menarche. Many loci were associated with other pubertal traits in both sexes, and there was substantial overlap with genes implicated in body mass index and various diseases, including rare disorders of puberty. Menarche signals were enriched in imprinted regions, with three loci (DLK1-WDR25, MKRN3-MAGEL2 and KCNK9) demonstrating parent-of-origin-specific associations concordant with known parental expression patterns. Pathway analyses implicated nuclear hormone receptors, particularly retinoic acid and γ-aminobutyric acid-B2 receptor signalling, among novel mechanisms that regulate pubertal timing in humans. Our findings suggest a genetic architecture involving at least hundreds of common variants in the coordinated timing of the pubertal transition.

Gene-Age Interactions in Blood Pressure Regulation: A Large-Scale Investigation with the CHARGE, Global BPgen, and ICBP Consortia.

Although age-dependent effects on blood pressure (BP) have been reported, they have not been systematically investigated in large-scale genome-wide association studies (GWASs). We leveraged the infrastructure of three well-established consortia (CHARGE, GBPgen, and ICBP) and a nonstandard approach (age stratification and metaregression) to conduct a genome-wide search of common variants with age-dependent effects on systolic (SBP), diastolic (DBP), mean arterial (MAP), and pulse (PP) pressure. In a two-staged design using 99,241 individuals of European ancestry, we identified 20 genome-wide significant (p ≤ 5 × 10(-8)) loci by using joint tests of the SNP main effect and SNP-age interaction. Nine of the significant loci demonstrated nominal evidence of age-dependent effects on BP by tests of the interactions alone. Index SNPs in the EHBP1L1 (DBP and MAP), CASZ1 (SBP and MAP), and GOSR2 (PP) loci exhibited the largest age interactions, with opposite directions of effect in the young versus the old. The changes in the genetic effects over time were small but nonnegligible (up to 1.58 mm Hg over 60 years). The EHBP1L1 locus was discovered through gene-age interactions only in whites but had DBP main effects replicated (p = 8.3 × 10(-4)) in 8,682 Asians from Singapore, indicating potential interethnic heterogeneity. A secondary analysis revealed 22 loci with evidence of age-specific effects (e.g., only in 20 to 29-year-olds). Age can be used to select samples with larger genetic effect sizes and more homogenous phenotypes, which may increase statistical power. Age-dependent effects identified through novel statistical approaches can provide insight into the biology and temporal regulation underlying BP associations.