Onko laskettavaisuus yhä kauppaoikeuden perustunnusmerkki?

Virkaanastujaisesitelmä Turun yliopistossa 12.2.2003

Répertoire des procès-verbaux des preuves de la noblesse des jeunes gentilshommes admis aux écoles royales militaires, 1751-1792 / par Stéphane Geoffray. Liste des admis, la date et le lieu de leur naissance, l'année de leur admission... / par Messire d'Hozier de Sérigny

Comprend : Liste des admis, la date et le lieu de leur naissance, l'année de leur admission, l'indication du numéro ou de la page du procès-verbal des preuves de leur noblesse

Kirjallisuutta

Pääosa virallisen vastaväittäjän Turun yliopiston oikeustieteelliselle tiedekunnalle antamasta 11.8.2003 päivätystä lausunnosta

Koneihminen suomalaisessa kulttuurissa

Kirjoitus perustuu esitelmään Tieteen päivillä 8.-12.1.2003 sekä artikkeliin "Pi-pirskatti! S-ehän on tohtori Capran r-ruputti!" Robottien kotoistaminen 1920-luvulta 1960-luvulle" (teoksessa "Arki ja läheisyys. Juhlakirja Ulla Heinon täyttäessä 60 vuotta". toim. Terhi Kivistö. Turun historiallinen arkisto 55. Turun historiallinen yhdistys. Turku 2002.)

Haudatut muistot : rituaalisen kuoleman merkitykset Kannaksen muistitiedoissa

Lectio praecursoria Turun yliopistossa 15.5.2004

Stuorra-Jovnnan jäljillä

Lectio praecursoria Turun yliopistossa maailman ympäristöpäivänä 5.6.2004

Axial spondylometaphyseal dysplasia: Additional reports.

Axial spondylometaphyseal dysplasia (SMD) (OMIM 602271) is an uncommon skeletal dysplasia characterized by metaphyseal changes of truncal-juxtatruncal bones, including the proximal femora, and retinal abnormalities. The disorder has not attracted much attention since initially reported; however, it has been included in the nosology of genetic skeletal disorders [Warman et al. (2011); Am J Med Genet Part A 155A:943-968] in part because of a recent publication of two additional cases [Isidor et al. (2010); Am J Med Genet Part A 152A:1550-1554]. We report here on the clinical and radiological manifestations in seven affected individuals from five families (three sporadic cases and two familial cases). Based on our observations and Isidor's report, the clinical and radiological hallmarks of axial SMD can be defined: The main clinical findings are postnatal growth failure, rhizomelic short stature in early childhood evolving into short trunk in late childhood, and thoracic hypoplasia that may cause mild to moderate respiratory problems in the neonatal period and later susceptibility to airway infection. Impaired visual acuity comes to medical attention in early life and function rapidly deteriorates. Retinal changes are diagnosed as retinitis pigmentosa or pigmentary retinal degeneration on fundoscopic examination and cone-rod dystrophy on electroretinogram. The radiological hallmarks include short ribs with flared, cupped anterior ends, mild spondylar dysplasia, lacy iliac crests, and metaphyseal irregularities essentially confined to the proximal femora. Equally affected sibling pairs of opposite gender and parental consanguinity are strongly suggestive of autosomal recessive inheritance. © 2011 Wiley-Liss, Inc.

Autophagosome maturation is impaired in Fabry disease.

Fabry disease is a lysosomal storage disorder (LSD) caused by a deficiency in alpha-galactosidase A. The disease is characterized by severe major organ involvement, but the pathologic mechanisms responsible have not been elucidated. Disruptions of autophagic processes have been reported for other LSDs, but have not yet been investigated in Fabry disease. Renal biopsies were obtained from five adult male Fabry disease patients before and after three years of enzyme replacement therapy (ERT) with agalsidase alfa. Vacuole accumulation was seen in renal biopsies from all patients compared with control biopsies. Decreases in the number of vacuoles were seen after three years of ERT primarily in renal endothelial cells and mesangial cells. Measurement of the levels of LC3, a specific autophagy marker, in cultured cells from Fabry patients revealed increased basal levels compared to cells from non-Fabry subjects and a larger increase in response to starvation than seen in non-Fabry cells. Starvation in the presence of protease inhibitors did not result in a significant increase in LC3 in Fabry cells, whereas a further increase in LC3 was observed in non-Fabry cells, an observation that is consistent with impaired autophagic flux in Fabry disease. Overexpression of LC3 mRNA in Fabry fibroblasts compared to control cells is consistent with an upregulation of autophagy. Furthermore, LC3 and p62/SQSTM1 (that binds to LC3) staining in renal tissues and in cultured fibroblasts from Fabry patients supports impairment of autophagic flux. These findings suggest that Fabry disease is linked to a deregulation of autophagy.