Akateemikko Kustaa Vilkuna 16/8 1966

Kirje 16.8.1966

Special investigation of selected accounts at Burlington High School for the period July 1, 2004 through February 16, 2006

Special investigation of selected accounts at Burlington High School for the period July 1, 2004 through February 16, 2006

A new highly penetrant form of obesity due to deletions on chromosome 16p11.2.

Obesity has become a major worldwide challenge to public health, owing to an interaction between the Western 'obesogenic' environment and a strong genetic contribution. Recent extensive genome-wide association studies (GWASs) have identified numerous single nucleotide polymorphisms associated with obesity, but these loci together account for only a small fraction of the known heritable component. Thus, the 'common disease, common variant' hypothesis is increasingly coming under challenge. Here we report a highly penetrant form of obesity, initially observed in 31 subjects who were heterozygous for deletions of at least 593 kilobases at 16p11.2 and whose ascertainment included cognitive deficits. Nineteen similar deletions were identified from GWAS data in 16,053 individuals from eight European cohorts. These deletions were absent from healthy non-obese controls and accounted for 0.7% of our morbid obesity cases (body mass index (BMI) >or= 40 kg m(-2) or BMI standard deviation score >or= 4; P = 6.4 x 10(-8), odds ratio 43.0), demonstrating the potential importance in common disease of rare variants with strong effects. This highlights a promising strategy for identifying missing heritability in obesity and other complex traits: cohorts with extreme phenotypes are likely to be enriched for rare variants, thereby improving power for their discovery. Subsequent analysis of the loci so identified may well reveal additional rare variants that further contribute to the missing heritability, as recently reported for SIM1 (ref. 3). The most productive approach may therefore be to combine the 'power of the extreme' in small, well-phenotyped cohorts, with targeted follow-up in case-control and population cohorts.

EPI Update, May 16, 2008

Weekly newsletter for Center For Acute Disease Epidemiology of Iowa Department of Public Health.

Motor Vehicle Crash Fatalities for Week Ending, May 16, 2008

Motor Vehicle Crash Fatalities

Simple method for detection of MYH11 DNA rearrangements in patients with inv(16)(p13q22) and acute myeloid leukemia.

The pericentric inversion on chromosome 16 [inv(16)(p13q22)] and related t(16;16)(p13;q22) are recurrent aberrations associated with acute myeloid leukemia (AML) M4 Eo. Both abberations result in a fusion of the core binding factor beta (CBFB) and smooth muscle myosin heavy chain gene (MYH11). A selected genomic 6.9-kb BamHl probe detects MYH11 DNA rearrangements in 18 of 19 inv(16)/t(16;16) patients tested using HindIII digested DNA. The rearranged fragments were not detectable after remission in two cases tested, while they were present after relapse in one of these two cases tested.

Kirjailija Juhani Konkka 16/12 1963

Kirje 16.12.1963

Ambassadör Ralph Enckell 16.12.1965 Stockholm

Kirje

Exploración del área marina Supe - Pucusana efectuada durante los periodos 9-13 y 16-18 de agosto de 1965, a bordo del "Explorador"

Describe la exploración bio oceanografía efectuada a bordo del "Explorador" tuvo como principal objetivo el comportamiento de los cardúmenes de anchoveta y determinar desove, relacionándolos con los principales factores abioticos en la zona Supe - Pisco, hasta una distancia de 60 millas náuticas de ka cista, El crucero comprendió un rastreo entre Supe Callao - Pucusana con un total de 49 estaciones distribuidas en 6 perfiles y un zig zag costero.