LRH-1 agonism favours an immune-islet dialogue which protects against diabetes mellitus.

Type 1 diabetes mellitus (T1DM) is due to the selective destruction of islet beta cells by immune cells. Current therapies focused on repressing the immune attack or stimulating beta cell regeneration still have limited clinical efficacy. Therefore, it is timely to identify innovative targets to dampen the immune process, while promoting beta cell survival and function.

Endo-MitoEGFP mice: a novel transgenic mouse with fluorescently marked mitochondria in microvascular endothelial cells.

Blood vessel-specific fluorescent transgenic mice are excellent tools to study the development of the vasculature and angiogenic processes. There is growing interest in the biological processes relevant to endothelial cells but limited tools exist to selectively evaluate subcellular functions of this cell type in vivo. Here, we report a novel transgenic animal model that expresses mitochondrially targeted enhanced green fluorescent protein (EGFP) via the Hb9 promoter, a homeobox transcription factor with limited known involvement in the vasculature.

The liver receptor homolog-1 (LRH-1) is expressed in human islets and protects {beta}-cells against stress-induced apoptosis.

Liver receptor homolog (LRH-1) is an orphan nuclear receptor (NR5A2) that regulates cholesterol homeostasis and cell plasticity in endodermal-derived tissues. Estrogen increases LRH-1 expression conveying cell protection and proliferation. Independently, estrogen also protects isolated human islets against cytokine-induced apoptosis.

The impact of domestic travel on estimating regional rates of human campylobacteriosis.

Residential locations of cases are often used as proxy measures for the likely place of exposure and this assumption may result in biases affecting both surveillance and epidemiological studies. This study aimed to describe the importance of domestic travel in cases of human campylobacteriosis reported during routine surveillance in Iceland from 2001 to 2005. Various measures of disease frequency were calculated based upon the cases' region of residence, adjusting location of domestic travel cases to their travel region, as well as separate estimations for travellers and non-travellers.