Minä sulle homonyymit näytän. Kielellinen leikittely Pertti Jarlan Fingerpori-sarjakuvassa

Tutkielmassa tarkastellaan kielellistä leikittelyä Pertti Jarlan Fingerporistrippisarjakuvissa. Fingerpori on ilmestynyt mm. Helsingin Sanomissa vuodesta 2007 alkaen. Useat Fingerporin vitsit perustuvat kielenaineksilla leikittelyyn. Mukaan tähän tutkimukseen valikoitui 122 strippiä 748 stripistä, jotka on julkaistu Helsingin Sanomissa helmikuun 2007 ja elokuun 2009 välillä. Stripit on valittu siten, että ne tarjoavat mahdollisimman monipuolisen otoksen eri leikittelykeinoista. Fingerporin kielelliseen leikittelyyn perustuvissa stripeissä käytetään niin sana-, lauseke- kuin lausetason leikittelykeinoja. Analysoin työssäni tällaisia strippejä suomen kielen deskriptiivistä muoto-, sananmuodotus- ja lauseoppia apuna käyttäen. Analysoin strippejä myös semanttisista ja pragmaattisista näkökulmista käsin. Oman sijansa saa myös sarjakuvan kontekstuaalinen tulkinta. Työni tutkimusosassa analysoin lähinnä mikrotasolla erilaisia leikittelykeinoja. Käyn läpi kvalitatiivisesti kielellisiä leikittelykeinoja esimerkkien valossa. Tarkkoja esiintymismääriä en työssäni esittele. Esittelen kuitenkin karkean jaottelun strippien leikittelykeinoista. Fingerporissa esiintyvä kielellinen leikittely rakentuu pääosin monitulkintaisista ilmauksista, jotka tavallisesti poikkeavat suomen kielen konventionaalisista merkityksistä. Suuri osa kielellisestä leikittelystä perustuu yksittäisten sanojen polysemian ja homonymian varaan. Käyn läpi myös monisanaisten kielen yksiköiden monimerkityksisyyksiä, kuten leksikaalistuneiden idiomien, fraasien ja sananparsien käyttöä leksikaalistumattomissa muodoissaan. Fingerporissa rikotaan normatiivisen yleiskielen ja pragmaattisen odotuksenmukaisuuden rajoja. Sarjakuvassa pyritään kielellisellä leikittelyllä luomaan humoristisia vaikutelmia. Fingerporin maailma tarjoaakin monipuolisen kehyksen tällaiselle leikittelylle.

Maj Lind [1976] : [alkuerä] : Tuula Hanhinen, Pertti Eerola

Soitinnus: piano.

Maj Lind [1976] : [välierä] : Pertti Eerola

Soitinnus: piano.

The Thrombin Receptor Antagonist for Clinical Event Reduction in Acute Coronary Syndrome (TRA.CER) trial: study design and rationale

Background The protease-activated receptor 1 (PAR-1), the main platelet receptor for thrombin, represents a novel target for treatment of arterial thrombosis, and SCH 530348 is an orally active, selective, competitive PAR-1 antagonist. We designed TRA.CER to evaluate the efficacy and safety of SCH 530348 compared with placebo in addition to standard of care in patients with non-ST-segment elevation (NSTE) acute coronary syndromes (ACS) and high-risk features. Trial design TRA.CER is a prospective, randomized, double-blind, multicenter, phase III trial with an original estimated sample size of 10,000 subjects. Our primary objective is to demonstrate that SCH 530348 in addition to standard of care will reduce the incidence of the composite of cardiovascular death, myocardial infarction (MI), stroke, recurrent ischemia with rehospitalization, and urgent coronary revascularization compared with standard of care alone. Our key secondary objective is to determine whether SCH 530348 will reduce the composite of cardiovascular death, MI, or stroke compared with standard of care alone. Secondary objectives related to safety are the composite of moderate and severe GUSTO bleeding and clinically significant TIMI bleeding. The trial will continue until a predetermined minimum number of centrally adjudicated primary and key secondary end point events have occurred and all subjects have participated in the study for at least I year. The TRA.CER trial is part of the large phase III SCH 530348 development program that includes a concomitant evaluation in secondary prevention. Conclusion TRA.CER will define efficacy and safety of the novel platelet PAR-1 inhibitor SCH 530348 in the treatment of high-risk patients with NSTE ACS in the setting of current treatment strategies. (Am Heart J 2009; 158:327-34.)

Convergence of singular integrals with general measures

We show that L2-bounded singular integrals in metric spaces with respect to general measures and kernels converge weakly. This implies a kind of average convergence almost everywhere. For measures with zero density we prove the almost everywhere existence of principal values.

Meta-analysis identifies 13 new loci associated with waist-hip ratio and reveals sexual dimorphism in the genetic basis of fat distribution.

Waist-hip ratio (WHR) is a measure of body fat distribution and a predictor of metabolic consequences independent of overall adiposity. WHR is heritable, but few genetic variants influencing this trait have been identified. We conducted a meta-analysis of 32 genome-wide association studies for WHR adjusted for body mass index (comprising up to 77,167 participants), following up 16 loci in an additional 29 studies (comprising up to 113,636 subjects). We identified 13 new loci in or near RSPO3, VEGFA, TBX15-WARS2, NFE2L3, GRB14, DNM3-PIGC, ITPR2-SSPN, LY86, HOXC13, ADAMTS9, ZNRF3-KREMEN1, NISCH-STAB1 and CPEB4 (P = 1.9 × 10⁻⁹ to P = 1.8 × 10⁻⁴⁰) and the known signal at LYPLAL1. Seven of these loci exhibited marked sexual dimorphism, all with a stronger effect on WHR in women than men (P for sex difference = 1.9 × 10⁻³ to P = 1.2 × 10⁻&supl;³). These findings provide evidence for multiple loci that modulate body fat distribution independent of overall adiposity and reveal strong gene-by-sex interactions.

Singular integrals on Ahlfors-David regular subsets of the Heisenberg group

"Vegeu el resum a l'inici del document del fitxer adjunt."

Novel loci for adiponectin levels and their influence on type 2 diabetes and metabolic traits: a multi-ethnic meta-analysis of 45,891 individuals.

Circulating levels of adiponectin, a hormone produced predominantly by adipocytes, are highly heritable and are inversely associated with type 2 diabetes mellitus (T2D) and other metabolic traits. We conducted a meta-analysis of genome-wide association studies in 39,883 individuals of European ancestry to identify genes associated with metabolic disease. We identified 8 novel loci associated with adiponectin levels and confirmed 2 previously reported loci (P = 4.5×10(-8)-1.2×10(-43)). Using a novel method to combine data across ethnicities (N = 4,232 African Americans, N = 1,776 Asians, and N = 29,347 Europeans), we identified two additional novel loci. Expression analyses of 436 human adipocyte samples revealed that mRNA levels of 18 genes at candidate regions were associated with adiponectin concentrations after accounting for multiple testing (p<3×10(-4)). We next developed a multi-SNP genotypic risk score to test the association of adiponectin decreasing risk alleles on metabolic traits and diseases using consortia-level meta-analytic data. This risk score was associated with increased risk of T2D (p = 4.3×10(-3), n = 22,044), increased triglycerides (p = 2.6×10(-14), n = 93,440), increased waist-to-hip ratio (p = 1.8×10(-5), n = 77,167), increased glucose two hours post oral glucose tolerance testing (p = 4.4×10(-3), n = 15,234), increased fasting insulin (p = 0.015, n = 48,238), but with lower in HDL-cholesterol concentrations (p = 4.5×10(-13), n = 96,748) and decreased BMI (p = 1.4×10(-4), n = 121,335). These findings identify novel genetic determinants of adiponectin levels, which, taken together, influence risk of T2D and markers of insulin resistance.