Stroke treatment academic industry roundtable: research priorities in the assessment of neurothrombectomy devices.

Background And Purpose: The goal of the Stroke Treatment Academic Industry Roundtable (STAIR) meetings is to advance the development of stroke therapies. At STAIR VIII, consensus recommendations were developed for clinical trial strategies to demonstrate the benefit of endovascular reperfusion therapies for acute ischemic stroke.

Summary Of Review: Prospects for success with forthcoming endovascular trials are robust, because new neurothrombectomy devices have superior reperfusion efficacy compared with earlier-generation interventions.

Heat shock protein 90 inhibition by 17-DMAG lessens disease in the MRL/lpr mouse model of systemic lupus erythematosus.

Elevated expression of heat shock protein 90 (HSP90) has been found in kidneys and serum of systemic lupus erythematosus (SLE) patients and MRL/Mp-Fas(lpr)/Fas(lpr) (MRL/lpr) autoimmune mice. We investigated if inhibition of HSP90 would reduce disease in MRL/lpr mice. In vitro, pretreatment of mesangial cells with HSP90 inhibitor Geldanamycin prior to immune-stimulation showed reduced expression of IL-6, IL-12 and NO.

HSP90 inhibition by 17-DMAG reduces inflammation in J774 macrophages through suppression of Akt and nuclear factor-κB pathways.

Objective: This study was designed to determine whether inhibition of heat shock protein 90 (HSP90) reduces pro-inflammatory mediator production by decreasing the nuclear factor (NF)-κB and Akt signaling pathways in immune-stimulated macrophages.

Methods: J774A.1 murine macrophages were treated with the HSP90 inhibitor 17-DMAG (0.

Deletion of PPAR-γ in immune cells enhances susceptibility to antiglomerular basement membrane disease.

Activation of the nuclear hormone receptor peroxisome proliferator-activated receptor gamma (PPAR-γ) has been shown to be immunoregulatory in autoimmune diseases by inhibiting production of a number of inflammatory mediators. We investigated whether PPAR-γ gene deletion in hematopoietic cells would alter disease pathogenesis in the antiglomerular basement membrane (anti-GBM) mouse model. PPAR-γ(+/+) and PPAR-γ(-/-) mice were immunized with rabbit antimouse GBM antibodies and lipopolysaccharide and evaluated for two weeks.