Junassa 5.8.-24

Kirje 5.8.1924

Hina 10.8.1944

Kirje

Hki 8/7 1943

Kirje 8.7.1943

Iowa Community Empowerment Newsletter, August 2007, Vol.8, no.4

Monthly newsletter for the Iowa Department of Public Health

Iowa Community Empowerment Newsletter, Ocotber 2007, Vol.8, no.5

Monthly newsletter for the Iowa Department of Public Health

Iowa Community Empowerment Newsletter, December 2007, Vol.8, no.6

Monthly newsletter for the Iowa Department of Public Health

Hki 17/8 1943

Kirje 17.8.1943

Operación Eureka XXX, 7-8 agosto, 1974

Muestra un cuadro general continuo de las características del stock del recurso anchoveta, su evolución en el tiempo y espacio que posibilita dar las pautas para su adecuada administración.

Helsinki 6.8.1940

Kirje

Reduced development of CD4-8-B220+ T cells but normal autoantibody production in lpr/lpr mice lacking major histocompatibility complex class I molecules.

The lpr gene has recently been shown to encode a functional mutation in the Fas receptor, a molecule involved in transducing apoptotic signals. Mice homozygous for the lpr gene develop an autoimmune syndrome accompanied by massive accumulation of double-negative (DN) CD4-8-B220+ T cell receptor-alpha/beta+ cells. In order to investigate the origin of these DN T cells, we derived lpr/lpr mice lacking major histocompatibility complex (MHC) class I molecules by intercrossing them with beta 2-microglobulin (beta 2m)-deficient mice. Interestingly, these lpr beta 2m-/- mice develop 13-fold fewer DNT cells in lymph nodes as compared to lpr/lpr wild-type (lprWT) mice. Analysis of anti-DNA antibodies and rheumatoid factor in serum demonstrates that lpr beta 2m-/- mice produce comparable levels of autoantibodies to lprWT mice. Collectively our data indicate that MHC class I molecules control the development of DN T cells but not autoantibody production in lpr/lpr mice and support the hypothesis that the majority of DN T cells may be derived from cells of the CD8 lineage.

Statsminister Ahti Karjalainen 30.8.1971

Kirje