Maj Lind 1973 : Alkuerä [Raekallio, Luolajan-Mikkola]

Soitinnus: piano.

Arkistoluettelo 141: Eino Linnala

Luettelo Kansalliskirjastossa olevan Eino Linnalan arkiston sisällöstä

Arkistoluettelo 740: Eino Roiha

Luettelo Kansalliskirjastossa olevan Eino Roihan arkiston sisällöstä

Kaksi laulua Eino Leinon "Tuonelan joutsenesta"

Soitinnus: lauluääni, piano.

Leino, Eino

Eino Leino eg. Armas Einar Leopold Lönnbohm f. 6.7.1878 på Hövelö gård i Paltamo d. 10.1.1926 i Nuppulinna, Tusby Som diktare representerar Eino Leino den nationella nyromantiken, och hans lyrik har blivit gemensam egendom bland finländarna. Finsk folkdiktning och europeiska litterära strömningar möts framför allt i hans två samlingar av Helkavirsiä (sv. Helkasånger) från 1903 och 1916. I dem smälter en ny, levande bildlighet ihop med en mytisk värld, som bottnar i folkdiktningen. Från år 1906 skriver Leino även prosa. Hans trilogi från ofärdsåren, bestående av romanerna Tuomas Vitikka, Jaana Rönty och Olli Suurpää (utgivna mellan 1906 och 1908), representerar ett brytningsskede i skildringen av folket. i sin dramatik behandlar Leino framför allt historiska ämnen. I sin tid blev Leino även känd som självständig essäist, teater- och litteraturkritiker samt politisk kåsör. http://www.blf.fi/artikel.php?id=2833 http://www.kansallisbiografia.fi/kb/artikkeli/2833/

Ectodysplasin A1 promotes placodal cell fate during early morphogenesis of ectodermal appendages.

Organs developing as appendages of the ectoderm are initiated from epithelial thickenings called placodes. Their formation is regulated by interactions between the ectoderm and underlying mesenchyme, and several signalling molecules have been implicated as activators or inhibitors of placode formation. Ectodysplasin (Eda) is a unique signalling molecule in the tumour necrosis factor family that, together with its receptor Edar, is necessary for normal development of ectodermal organs both in humans and mice. We have shown previously that overexpression of the Eda-A1 isoform in transgenic mice stimulates the formation of several ectodermal organs. In the present study, we have analysed the formation and morphology of placodes using in vivo and in vitro models in which both the timing and amount of Eda-A1 applied could be varied. The hair and tooth placodes of K14-Eda-A1 transgenic embryos were enlarged, and extra placodes developed from the dental lamina and mammary line. Exposure of embryonic skin to Eda-A1 recombinant protein in vitro stimulated the growth and fusion of placodes. However, it did not accelerate the initiation of the first wave of hair follicles giving rise to the guard hairs. Hence, the function of Eda-A1 appears to be downstream of the primary inductive signal required for placode initiation during skin patterning. Analysis of BrdU incorporation indicated that the formation of the epithelial thickening in early placodes does not involve increased cell proliferation and also that the positive effect of Eda-A1 on placode expansion is not a result of increased cell proliferation. Taken together, our results suggest that Eda-A1 signalling promotes placodal cell fate during early development of ectodermal organs.

Ectodysplasin regulates hormone-independent mammary ductal morphogenesis via NF-κB.

Ductal growth of the mammary gland occurs in two distinct stages. The first round of branching morphogenesis occurs during embryogenesis, and the second round commences at the onset of puberty. Currently, relatively little is known about the genetic networks that control the initial phases of ductal expansion, which, unlike pubertal development, proceeds independent of hormonal input in female mice. Here we identify NF-κB downstream of the TNF-like ligand ectodysplasin (Eda) as a unique regulator of embryonic and prepubertal ductal morphogenesis. Loss of Eda, or inhibition of NF-κB, led to smaller ductal trees with fewer branches. On the other hand, overexpression of Eda caused a dramatic NF-κB-dependent phenotype in both female and male mice characterized by precocious and highly increased ductal growth and branching that correlated with enhanced cell proliferation. We have identified several putative transcriptional target genes of Eda/NF-κB, including PTHrP, Wnt10a, and Wnt10b, as well as Egf family ligands amphiregulin and epigen. We developed a mammary bud culture system that allowed us to manipulate mammary development ex vivo and found that recombinant PTHrP, Wnt3A, and Egf family ligands stimulate embryonic branching morphogenesis, suggesting that these pathways may cooperatively mediate the effects of Eda.