Right Coronary Artery Button Pseudoaneurysm After the Modified Bentall Procedure.

Anastomoses of the coronary buttons are the Achilles' heel of the modified Bentall procedure (MBP) for the repair of the aortic root and ascending aorta. We present a rare case of post-MBP right coronary artery button pseudoaneurysm in a 30-year-old man. The contained leak, attributed to a pseudoknot in the polypropylene suture, was visualized via computed tomography angiography and transesophageal echocardiogram and repaired under deep hypothermic circulatory arrest.

Effect of left ventricular diastolic dysfunction on development of primary graft dysfunction after lung transplant.

PURPOSE OF REVIEW: Primary graft dysfunction (PGD) is one of the most common complications after lung transplant and is associated with significant early and late morbidity and mortality. The cause of primary graft dysfunction is often multifactorial involving patient, donor, and operational factors. Diastolic dysfunction is increasingly recognized as an important risk factor for development of PGD after lung transplant and here we examine recent evidence on the topic. RECENT FINDINGS: Patients with end-stage lung disease are more likely to suffer from cardiovascular disease including diastolic dysfunction. PGD as result of ischemia-reperfusion injury after lung transplant is exacerbated by increased left atrial pressure and pulmonary venous congestion impacted by diastolic dysfunction. Recent studies on relationship between diastolic dysfunction and PGD after lung transplant show that patients with diastolic dysfunction are more likely to develop PGD with worse survival outcome and complicated hospital course. SUMMARY: Patients with diastolic dysfunction is more likely to suffer from PGD after lung transplant. From the lung transplant candidate selection to perioperative and posttransplant care, thorough evaluation and documentation diastolic dysfunction to guide patient care are imperative.

Comparisons of social interaction and activities of daily living between long-term care facility and community-dwelling stroke patients.

[Purpose] This study was conducted to compare the correlation between social interaction and activities of daily living (ADL) between community-dwelling and long-term care facility stroke patients. [Subjects and Methods] The Subjects were 65 chronic stroke patients (32 facility-residing, 33 community-dwelling). The Evaluation Social Interaction (ESI) tool was used to evaluate social interaction and the Assessment of Motor and Process Skills (AMPS) measure was used to evaluate ADL. [Results] Both social interaction and ADL were higher in community-dwelling than facility-residing stroke patients. There was a correlation between ESI and ADL for both motor and process skills among facility-residing patients, while only ADL process skills and ESI correlated among community-dwelling patients. In a partial correlation analysis using ADL motor and process skills as control variables, only process skills correlated with ESI. [Conclusion] For rehabilitation of stroke patients, an extended treatment process that combines ADL and social activities is likely to be required. Furthermore, treatment programs and institutional systems that can improve social interaction and promote health maintenance for community-dwelling and facility-residing chronic stroke patients are needed throughout the rehabilitation process.

The neurogenic basic helix-loop-helix transcription factor NeuroD6 concomitantly increases mitochondrial mass and regulates cytoskeletal organization in the early stages of neuronal differentiation.

Mitochondria play a central role during neurogenesis by providing energy in the form of ATP for cytoskeletal remodelling, outgrowth of neuronal processes, growth cone activity and synaptic activity. However, the fundamental question of how differentiating neurons control mitochondrial biogenesis remains vastly unexplored. Since our previous studies have shown that the neurogenic bHLH (basic helix-loop-helix) transcription factor NeuroD6 is sufficient to induce differentiation of the neuronal progenitor-like PC12 cells and that it triggers expression of mitochondrial-related genes, we investigated whether NeuroD6 could modulate the mitochondrial biomass using our PC12-ND6 cellular paradigm. Using a combination of flow cytometry, confocal microscopy and mitochondrial fractionation, we demonstrate that NeuroD6 stimulates maximal mitochondrial mass at the lamellipodia stage, thus preceding axonal growth. NeuroD6 triggers remodelling of the actin and microtubule networks in conjunction with increased expression of the motor protein KIF5B, thus promoting mitochondrial movement in developing neurites with accumulation in growth cones. Maintenance of the NeuroD6-induced mitochondrial mass requires an intact cytoskeletal network, as its disruption severely reduces mitochondrial mass. The present study provides the first evidence that NeuroD6 plays an integrative role in co-ordinating increase in mitochondrial mass with cytoskeletal remodelling, suggestive of a role of this transcription factor as a co-regulator of neuronal differentiation and energy metabolism.