Acute ophthalmoplegia in a patient with anti-GQ1b antibody and chronic facial diplegia.

A 56-year-old man with a remote history of bilateral recurrent facial palsies presented with a week of ophthalmoplegia with intact deep tendon reflexes and lack of ataxia, cerebrospinal fluid with albuminocytologic dissociation and elevated serum anti-ganglioside Q1b (GQ1b) IgG antibody. We diagnosed the patient with acute ophthalmoplegia without ataxia, a condition under the spectrum of anti-GQ1b antibody syndromes which also includes Miller Fisher syndrome. Given the rarity of recurrent facial palsies and anti-GQ1b antibody syndromes as well as reports associating facial palsies and this syndrome, we suggest that our case may be an unusual presentation of an anti-GQ1b antibody syndrome beginning with recurrent facial palsies several years prior to ophthalmoplegia.

Loss of CX3CR1 increases accumulation of inflammatory monocytes and promotes gliomagenesis.

The most abundant populations of non-neoplastic cells in the glioblastoma (GBM) microenvironment are resident microglia, macrophages and infiltrating monocytes from the blood circulation. The mechanisms by which monocytes infiltrate into GBM, their fate following infiltration, and their role in GBM growth are not known. Here we tested the hypothesis that loss of the fractalkine receptor CX3CR1 in microglia and monocytes would affect gliomagenesis.

Progress in gene therapy for heart failure.

Recent advances in our understanding of the pathophysiology of myocardial dysfunction in the setting of congestive heart failure have created a new opportunity in developing nonpharmacological approaches to treatment. Gene therapy has emerged as a powerful tool in targeting the molecular mechanisms of disease by preventing the ventricular remodeling and improving bioenergetics in heart failure. Refinements in vector technology, including the creation of recombinant adeno-associated viruses, have allowed for safe and efficient gene transfer.

Cardiac gene therapy with SERCA2a: from bench to bedside.

While progress in conventional treatments is making steady and incremental gains to reduce mortality associated with heart failure, there remains a need to explore potentially new therapeutic approaches. Heart failure induced by different etiologies such as coronary artery disease, hypertension, diabetes, infection, or inflammation results generally in calcium cycling dysregulation at the myocyte level. Recent advances in understanding of the molecular basis of these calcium cycling abnormalities, together with the evolution of increasingly efficient gene transfer technology, have placed heart failure within reach of gene-based therapy.