For the past couple of decades, clinicians have watched the stem-cell field with a mixture of anticipation and skepticism. No group of patients has been more expectant than those with spinal cord injuries. Therapies for spinal cord injury have been ...

The accrual of cholesterol-laden macrophages in the atherosclerotic plaque is a critical event that precedes plaque rupture. The guidance molecule netrin-1 mediates this accrual in a mouse model of atherosclerosis.

A recent study reveals a biochemical mechanism that underlies the effect of exercise on glucose metabolism and weight loss. The mechanism involves irisin, a molecule secreted by skeletal muscle in response to exercise.

Thiazolidinediones activate the nuclear receptor PPAR-γ, which brings about increased glucose tolerance and glucose sensitivity. Endogenous ligand can achieve the same effect under certain conditions, suggesting a different approach to activating the same pathway.

Autophagy, a programmed cell-survival strategy that allows cells to sustain themselves by digesting their own contents, turns out to be a critical link between chemotherapy-induced cell death and the triggering of an antitumor immune response.

The protein BRD4 binds acetylated histones (mediators of chromatin structure), which, when bound, can activate the MYC oncogene. A recent study implicated BRD4 in sustaining cells in AML. Treating these cells with a BRD4 inhibitor reduced MYC expression and elicited cell death.

A signal feature of spinal muscular atrophy (SMA) is the dying back of motor neurons. This is caused by a loss-of-function mutation in SMN1. Administration of an oligonucleotide that modifies the processing of SMN2, a homologous gene, extends the life span in a mouse model of SMA.

The holy grail of gene therapy is the treatment of disease caused by genetic mutations. A recent study in mice provides proof of principle that alpha₁-antitrypsin deficiency can be corrected, if not cured, by the infusion of autologous induced pluripotent stem cells.

Ferroportin permits the uptake of dietary iron by cells of the intestinal epithelium into the circulation. Hepcidin targets ferroportin for lysosomal destruction. A recent study shows that an engineered minihepcidin reduces levels of iron in the serum and liver.

Cruciform vegetables may be critical to intestinal health and immunity. It turns out that these vegetables contain ligands of the aryl hydrogen receptor which, when bound, turn on genes that mediate intestinal immune defense.

Obtaining hematopoietic stem cells (HSCs) for transplantation depends on effective egress of HSCs from bone marrow into the peripheral circulation on induction. This process is impaired in a mouse model of diabetes and in patients undergoing autologous transplantation.

Understanding the function of proteins rendered mutant in disease provides insight into the mechanism of disease. Recent studies implicate the axonal cytoskeleton in neuropathies.

There is growing evidence that acute injury of the central nervous system, including stroke, impairs the immune system. A recent study implicates the postischemic activation of a particular type of lymphocyte, by noradrenergic signaling, as a mediator of impairment.

CDKAL1, a gene implicated in susceptibility to type 2 diabetes, has been found to mediate a fundamental event in protein translation that affects proinsulin processing.

Heart failure has been attributed to a deficiency in a calcium ATPase. A recent study shows that tweaking this enzyme may boost its levels and thus guard against heart failure.

The genetic shifts and drifts of the influenza virus pose an obstacle to designing antiviral agents and vaccines that are effective over the long term. However, a recent study suggests that this goal is attainable.

Many older adults believe that their memory is not as good as it was when they were younger. An epidemiologic study in Finland documented that 76% of persons over the age of 60 years reported problems with their memory.¹ Age-associated memory decline has ...

Eliciting mucosal immunity through vaccination has been problematic. Two recent studies suggest a strategy to achieve this goal.

A recent study suggests that regulatory T cells are relevant in reducing the need for immunosuppressive drugs and in overcoming the limitations of a genetic mismatch between donor and recipient in allogeneic hematopoietic-cell transplantation.

Recent studies implicate a peculiar form of neutrophil death and its extracellular sequelae in mediating inflammation in patients with systemic lupus erythematosus.