Umeå universitets logga

This study follows around 500 disabled individuals over their lifespan to examine their risks of dying in 19th-century society, in comparison to a reference group of non-disabled people. The aim is to detect whether people, due to their disability, had a higher probability of meeting an untimely death. We use Sweden’s 19th-century parish registers to identify people the ministers defined as disabled, and to construct a reference group of individuals who were not affected by these disabilities. By combining the deviance theories from sociology studies with demographic sources and statistical methods, we achieve new insight into how life developed for disabled people in past societies. The results suggest that disability significantly jeopardized the survival of individuals, particularly men, but also that the type of disability had an impact. Altogether, we can demonstrate that the disabled constituted a disadvantaged but heterogeneous group of people whose demography and life courses must be further researched.

Prostate cancer is one of the most common types of cancer in men in Western countries. Chronic inflammation in the prostate, regulated by a complex network of factors including inflammatory cytokines, is one of the established risk factors for development of prostate cancer. Interleukin-6 (IL-6) is a well-known promoter of inflammation-induced carcinogenesis and disease progression in prostate cancer. Presence in the prostate and possible roles in tumor development by other members of the IL-6 family of cytokines have, however, been less studied. Here we show that the IL-6-type cytokine oncostatin M (OSM) indeed induce cellular properties associated with tumorigenesis and disease progression in non-transformed human prostate epithelial cells, including morphological changes, epithelial-to-mesenchymal transition (EMT), enhanced migration and pro-invasive growth patterns. The effects by OSM were partly mediated by activation of signal transducer and activator of transcription 3 (STAT3), a transcription factor established as driver of cancer progression and treatment resistance in numerous types of cancer. The findings presented here further consolidate IL-6-type cytokines and STAT3 as promising future treatment targets for prostate cancer.