Diffuse Idiopathic Skeletal Hyperostosis (DISH): New evidence from micro-XCT scanning.

Objective: To observe and describe the development and underlying structure of the spinal manifestations of individuals osteologically diagnosed with DISH (Diffuse Idiopathic Skeletal Hyperostosis), using micro-XCT imaging.

Materials: A total of 72 individuals with DISH were identified in two modern skeletal collections in South Africa.

Methods: Vertebral columns affected by DISH were scanned at the micro-focus x-ray computed tomography facility at the Nuclear Energy Corporation of South Africa.

Telomerase therapy reverses vascular senescence and extends lifespan in progeria mice.

Aims: Hutchinson-Gilford progeria syndrome (HGPS) is an accelerated ageing syndrome associated with premature vascular disease and death due to heart attack and stroke. In HGPS a mutation in lamin A (progerin) alters nuclear morphology and gene expression. Current therapy increases the lifespan of these children only modestly.

Selective blood-brain barrier permeabilization of brain metastases by a type 1 receptor-selective tumor necrosis factor mutein.

Background: Metastasis to the brain is a major challenge with poor prognosis. The blood-brain barrier (BBB) is a significant impediment to effective treatment, being intact during the early stages of tumor development and heterogeneously permeable at later stages. Intravenous injection of tumor necrosis factor (TNF) selectively induces BBB permeabilization at sites of brain micrometastasis, in a TNF type 1 receptor (TNFR1)-dependent manner.

Redefining IL11 as a regeneration-limiting hepatotoxin and therapeutic target in acetaminophen-induced liver injury.

Acetaminophen (-acetyl--aminophenol; APAP) toxicity is a common cause of liver damage. In the mouse model of APAP-induced liver injury (AILI), interleukin 11 (IL11) is highly up-regulated and administration of recombinant human IL11 (rhIL11) has been shown to be protective. Here, we demonstrate that the beneficial effect of rhIL11 in the mouse model of AILI is due to its inhibition of endogenous mouse IL11 activity.