Ainasta Sariin ja Otosta Kimmoon : Suomenkielistä homonyymiparista etunimistä 1800-luvun lopulta noin vuoteen 1980

Tutkielma selvittää homonyymiparisten suomalaisten etunimien suosionvaihtelua eri aikoina eri alueilla. Tarkastelu rajoittuu ajanjaksoon 1800-luvun lopulta noin vuoteen 1980. Tarkoituksenani on kuvata myös sitä ympäristöä, jossa nimenantajat ovat valintansa tehneet. Nimen on hyväksytyksi tullakseen noudatettava yhteisön senhetkisiä nimimalleja. Kulttuurissa tapahtuvat muutokset heijastuvat henkilönnimistöön, esimerkiksi varsinaisista etunimistä voi puhua vasta sitten, kun nimijärjestelmään kuuluu lisäksi sukunimi tai säännöllisesti käytetty lisänimi. Homonyymiparisella etunimellä tarkoitan sellaista etunimenä käytettyä tai sellaiseksi tarkoitettua propria, jolla on Nykysuomen sanakirjan mukaan yleiskielessä sitä äänteellisesti vastaava ei-proprinen, merkityksellinen sana. Tätä kutsun proprin homonyymipariksi. Nimen rinnalla olevan homonyymin merkitys ei useinkaan sinänsä ole vakiinnuttanut nimeä, mutta on nimiryhmiä, joiden homonyymiparit muodostavat merkityskenttiä: Ilta (< Mathilda) on saanut tukea nimistä Aamu ja Päivä. (Huom. *Yö ei ole etunimi.) Ajanjaksojen homonyymipariset suosikkinimet muistuttavat toisiaan ja ovat rakenteeltaan toistensa ja samaan aikaan suosiossa olleiden muiden nimien kanssa samankaltaisia.

Tumorigenesis in celiac disease

Celiac disease is life-long autoimmune disorder of the small intestine, which is caused by a reaction to gliadin found in wheat, rye and barley in genetically predisposed individuals. Proline- and glutamine -rich proteins cause villous atrophy and crypt hyperplasia with extensive inflammation in the epithelium and lamina propria. Symptoms of celiac disease vary considerably and elimination of gluten from diet is the only way to treat disease. In small intestine of celiac disease patient transglutaminase 2 (TG2) modifies gluten peptides, which causes T-cell activation and inflammation in the epithelium of mucosa. T-cell activation induces development of celiac disease specific antibodies. These celiac disease specific antibodies recognise TG2 and interfere in vitro and in vivo in angiogenesis. Abnormal angiogenesis is typical in many disorders, such in cancer, in which TG2 has a crucial role in the development and growth of tumor. Overexpression of TG2 has been shown to correlate with accelerated growth of tumor. TG2-specific antibodies are suggested to inhibit differentation of epithelial cell, increase their proliferation, decrease their barrier-function and increase the permeability of blood vessels. The aims of the pilot study were to establish whether celiac disease TG2 antibodies affect in vivo tumorigenesis and tumorangiogenesis as well as to try to clarify the mechanism behind the phenomenon. Tumor xenograft model was used in severe combined immunodeficient (SCID) mice. Human oesophageal carcinoma (OE-19) cancer cells were incubated with celiacs TG2 miniautoantibody (mini 2.8), non-celiac miniautoantibody (mini 6.2) or PBS before cancer cells were injected to mice subcutaneously. During the experiment mice were weighted and tumor size was measured couple of times per week. To estimate the volumes of tumors the following formula was used: π/6 * L* W* H. Experiment lasted for four weeks after which the mice were euthanized, cardiac blood and tissue samples taken and tumours were excised and weighted. Sections were made from tumors and immunohistochemical stainings were done to compare blood vessel areas and to study general tumors´morphology and other parameters. Western blot -analyse were performed to cancer cells. The masses and volumes were clearly smaller in mini 2.8-group compared to control groups and the necrotic area of tumor in mini 2.8 was smallest as percentage compared to control groups. Blood vessel area were smallest in mini 2.8 group. Results suggest that celiac disease anti-TG2-autoantibodies inhibit tumor growth, but the number of animals is insufficient to give an accurate outcome.