Dynamic Career Models and Inequality Research: A Reexamination of the Sørensen Model

This article presents a reexamination of the Sørensen model. This model derives the pattern of individual careers from structural considerations. If longitudinal data on individual careers are available, Sørensen's model provides two methods to infer the underlying structural parameter. This structural parameter gives a useful measure for unequal career chances. An implementation of these methods, using firm data, shows, however, that they lead to contradictory conclusions; this is shown to be the result of some unrealistic assumptions Sørensen uses in his derivation. Some more realistic assumptions are suggested that produce reasonable results. Finally, it is shown that despite these modifications, the main conclusions of the Sørensen model are preserved. This seems to be promising for future work with this model

A genetically modified minipig model for Alzheimer's disease with SORL1 haploinsufficiency

The established causal genes in Alzheimer’s disease (AD), APP, PSEN1, and PSEN2, are functionally characterized using biomarkers, capturing an in vivo profile reflecting the disease’s initial preclinical phase. Mutations in SORL1, encoding the endosome recycling receptor SORLA, are found in 2%–3% of individuals with early-onset AD, and SORL1 haploinsufficiency appears to be causal for AD. To test whether SORL1 can function as an AD causal gene, we use CRISPR-Cas9-based gene editing to develop a model of SORL1 haploinsufficiency in Göttingen minipigs, taking advantage of porcine models for biomarker investigations. SORL1 haploinsufficiency in young adult minipigs is found to phenocopy the preclinical in vivo profile of AD observed with APP, PSEN1, and PSEN2, resulting in elevated levels of β-amyloid (Aβ) and tau preceding amyloid plaque formation and neurodegeneration, as observed in humans. Our study provides functional support for the theory that SORL1 haploinsufficiency leads to endosome cytopathology with biofluid hallmarks of autosomal dominant AD

Processes of Allocation to Open and Closed Positions in Social Structure

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Endringer i den sosiale rekrutteringen til høyere utdanning etter 1980

Det har i den senere tid vært hevdet, dels med dekning i enkeltstående undersøkelser, at den sosiale rekrutteringen til høyere utdanning er blitt skjevere. Formålet med denne rapporten er å belyse om så er tilfelle. I løpet av vinteren 1992-93 sammenstilte Statistisk sentralbyrå et omfattende datamateriale etter retningslinjer fra NAVFs utredningsinstitutt. Professor Aage B. Sørensen (Harvard) og professor Knud Knudsen (Høgskolesenteret i Rogaland) ble trukket inn for å forestå analysene av datamaterialet. De har skrevet denne rapporten sammen med avd.sjef Per O. Aamodt, NAVFs utredningsinstitutt. Utredningsassistent Jens-Are Enoksen har bistått i arbeidet med dataene. Prosjektet er finansiert av KUF. I denne rapporten er det bare en del hovedresultater som trekkes fram. En rekke detaljer og underliggende mønstre er det aktuelt å studere videre med utgangspunkt i det meget omfattende datamaterialet som foreligger. Datagrunnlaget er ellers omtalt i et eget avsnitt