Volume 22 Issue 2, February 2016

A new study has located 'hot spots' in the rat spinal cord that are associated with leg flexion and extension in rats. Electrical stimulation applied in an alternating pattern between these hot spots facilitated locomotion after the hindlimbs were paralyzed as a result of spinal cord injury (SCI).

A new study of the pathogenesis of systemic lupus erythematosus (SLE) highlights the importance of mitochondria and mitochondrial reactive oxygen species (ROS) in the generation of neutrophil extracellular traps (NETs) that have the enhanced potential to elicit interferon-induced gene expression.

Roberts and Kim discuss the mechanistic roles played by EZH2 in cancer as well as efforts to therapeutically target this epigenetic modifier.

In Alzheimer's disease, PD-1 immune checkpoint blockade reduces pathology and improves memory in mice with established disease.

Analysis of synergistic muscle activations during locomotion and anatomical tracing of muscle synergy representations in the rodent spinal cord guide the development of a new spinal implant for neuromodulation therapy. In multiple rodent models of spinal cord injury, spatiotemporal stimulation that mimics naturalistic muscle activation patterns promotes improved functional recovery over previously described continuous stimulation protocols.

Lupus-like disease is driven by NETs enriched in mitochondrial DNA.

Pulmonary fibrosis induced by repetitive chemical injury in mice involves cross talk among macrophages, endothelial cells and fibroblasts. Macrophages induce expression of the Notch ligand Jag1 in pulmonary capillary endothelial cells, leading to Notch pathway activation in perivascular fibroblasts and fibrosis.

Reducing levels of mitochondrial iron by diet or pharmacological chelation ameliorates symptoms of cigarette smoke–induced chronic obstructive pulmonary disease in mice.

Myocardial injury induced by ischemia-reperfusion or doxorubicin leads to cardiomyocyte necroptosis via RIP3-mediated phosphorylation of CaMKII and opening of the mitochondrial permeability transition pore.

A KIM-1–AIM interaction promotes clearance of cellular debris in renal tubules after acute kidney injury to improve disease outcome.

c-Met binds to and phosphorylates PARP1 in cancer cells, thereby reducing PARP1 binding to a PARP inhibitor; c-Met and PARP inhibitor combination therapy shows improved efficacy in preclinical models of breast and lung cancer.

Blocking the enzyme KMO with a small molecule reduces the levels of toxic tryptophan metabolites and reduces multiple extrapancreatic organ failure in a rat model of acute pancreatitis.

Judy Lieberman and colleagues show that intracellular parasites are eradicated by lymphocyte delivery of cytotoxic granule contents—perforin, granulysin and granzymes—into infected cells.