Role of advanced imaging with cardiac computed tomography and MRI in atrial and ventricular ablation.

PURPOSE OF REVIEW: Increasing evidence supports the use of advanced imaging with cardiac computed tomography (CCT) and cardiac magnetic resonance (CMR) in the work-up of patients with arrythmias being considered for ablation. RECENT FINDINGS: Advances in imaging technology and postprocessing are facilitating the use of advanced imaging before, during and after ablation in patients with both atrial and ventricular arrhythmias.In atrial arrythmias, quantitative assessment of left atrial wall thickness on CCT and quantification of late gadolinium enhancement (LGE) on CMR identify patients more likely to develop recurrent atrial arrythmias following ablation. In addition, in patients with recurrent arrythmia post ablation, LGE CMR can potentially identify targets for repeat ablation.In ventricular arrythmias, qualitative assessment of LGE can aide in determining the optimal ablation approach and predicts likelihood of ventricular arrythmias inducibility. Quantitative assessment of LGE can identify conduction channels that can be targeted for ablation. On CCT, quantitative assessment of left ventricular wall thickness can demonstrate myocardial ridges associated with re-entrant circuits for ablation. SUMMARY: This review focuses on the utility of CCT and CMR in identifying key anatomical components and arrhythmogenic substrate contributing to both atrial and ventricular arrhythmias in patients being considered for ablation. Advanced imaging has the potential to improve procedural outcomes, decrease complications and shorten procedural time.

Trained immunity contributes to the prevention of Mycobacterium tuberculosis infection, a novel role of autophagy.

Mycobacterium tuberculosis (M. tuberculosis) is the pathogen which causes tuberculosis (TB), a significant human public health threat. Co-infection of M. tuberculosis and the human immunodeficiency virus (HIV), emergence of drug resistant M. tuberculosis, and failure to develop highly effective TB vaccines have limited control of the TB epidemic. Trained immunity is an enhanced innate immune response which functions independently of the adaptive/acquired immune system and responds non-specifically to reinfection with invading agents. Recently, several studies have found trained immunity has the capability to control and eliminate M. tuberculosis infection. Over the past decades, however, the consensus was adaptive immunity is the only protective mechanism by which hosts inhibit M. tuberculosis growth. Furthermore, autophagy plays an essential role in the development of trained immunity. Further investigation of trained immunity, M. tuberculosis infection, and the role of autophagy in this process provide new possibilities for vaccine development. In this review, we present the general characteristics of trained immunity and autophagy. We additionally summarize several examples where initiation of trained immunity contributes to the prevention of M. tuberculosis infection and propose future directions for research in this area.

Screening of the quantum dot Förster coupling at small distances: erratum.

This erratum corrects the acronym 'ISW' as 'infinite square well'.

Screening of the quantum dot Förster coupling at small distances.

We study the near-field energy transfer rates between two finite size quantum dot disks, generalizing the result of Förster coupling between two point dipoles. In particular, we derive analytical results for the envelope of the electronic wave function for model potentials at the boundaries of quantum dot disks and demonstrate how the Förster interaction is screened as the size of the dots becomes comparable to the dot-dot separation.

Biosynthesis of the Essential Fatty Acid Oxidation Cofactor Carnitine Is Stimulated in Heart and Liver after a Single Bout of Exercise in Mice.

We determined whether one single bout of exercise stimulates carnitine biosynthesis and carnitine uptake in liver and heart. Free carnitine (FC) in plasma was assayed using acetyltransferase and [14C]acetyl-CoA in Swiss Webster mice after 1 hour of moderate-intensity treadmill running or 4 hours and 8 hours into recovery. Liver and heart were removed under the same conditions for measurement of carnitine biosynthesis enzymes (liver butyrobetaine hydroxylase, γ-BBH; heart trimethyllysine dioxygenase, TMLD), organic cation transporter-2 (OCTN2, carnitine transporter), and liver peroxisome proliferator-activated receptor-alpha (PPARα, transcription factor for γ-BBH and OCTN2 synthesis). In exercised mice, FC levels in plasma decreased while heart and liver OCTN2 protein expressed increased, reflecting active uptake of FC. During recovery, the rise in FC to control levels was associated with increased liver γ-BBH expression. Protein expression of PPARα was stimulated in liver after exercise and during recovery. Interestingly, heart TMLD protein was also detected after exercise. Acute exercise stimulates carnitine uptake in liver and heart. The rapid return of FC levels in plasma after exercise indicates carnitine biosynthesis by liver is stimulated to establish carnitine homeostasis. Our results suggest that exercise may benefit patients with carnitine deficiency syndromes.

Acute Exercise Stimulates Carnitine Biosynthesis and OCTN2 Expression in Mouse Kidney.

BACKGROUND/AIMS: Carnitine is essential for the transport of long-chain FAs (FA) into the mitochondria for energy production. During acute exercise, the increased demand for FAs results in a state of free carnitine deficiency in plasma. The role of kidney in carnitine homeostasis after exercise is not known. METHODS: Swiss Webster mice were sacrificed immediately after a 1-hour moderate intensity treadmill run, and at 4-hours and 8-hours into recovery. Non-exercising mice served as controls. Plasma was analyzed for carnitine using acetyltransferase and [14C] acetyl-CoA. Kidney was removed for gene and protein expression of butyrobetaine hydroxylase (γ-BBH), organic cation transporter (OCTN2), and peroxisome proliferator-activated receptor (PPARα), a regulator of fatty acid oxidation activated by FAs. RESULTS: Acute exercise caused a decrease in plasma free carnitine levels. Rapid return of free carnitine to control levels during recovery was associated with increased γ-BBH expression. Both mRNA and protein levels of OCTN2 were detected in kidney after exercise and during recovery, suggesting renal transport mechanisms were stimulated. These changes were accompanied with a reciprocal increase in PPARα protein expression. CONCLUSIONS: Our results show that the decrease in free carnitine after exercise rapidly activates carnitine biosynthesis and renal transport mechanism in kidney to establish carnitine homeostasis.