Understanding of the mechanism of ultraviolet (UV)‐mediated cutaneous damages is far from complete. The cancer‐specific expression of Survivin, a member of the inhibitor of apoptosis family of proteins, coupled with its importance in inhibiting cell death and in regulating cell division, makes it a target for cancer treatment. This study was designed to investigate the modulation of Survivin during UV response, both in vitro and in vivo. We used UV‐B‐mediated damages in normal human epidermal keratinocytes (NHEK) cells as an in vitro model and SKH‐1 hairless mouse model for the in vivo studies. For in vitro studies, NHEK were treated with UV‐B and samples were processed at 5, 15, 30 min, 1,3,6,12 and 24 h after treatment. Our data demonstrated that UV‐B exposure (50 mJ/cm2) to NHEK resulted in a significant upregulation in Survivin messenger RNA (mRNA) and protein levels. We also observed that UV‐B exposure to NHEK resulted in significant (1) decrease in Smac/DIABLO and (2) increase in p53. For in vivo studies, the SKH‐1 hairless mice were subjected to a single exposure of UV‐B (180 mJ/cm2), and samples were processed at 3, 6, 12 and 24 h after UV‐B exposure, UV‐B treatment resulted in a significant increase in protein or mRNA levels (or both) of Survivin, phospho‐Survivin and p53 and a concomitant decrease in Smac/DIABLO in mouse skin. This study demonstrated, for the first time, the involvement of Survivin (and the associated events) in UV‐B response in vitro and in vivo in experimental models regarded to have relevance to human situations.

Dysfunction of different components within continuous-flow (CF) left ventricular assist device (LVAD) systems may cause adverse cardiovascular and end-organ sequelae. Outflow graft obstruction is a recognized type of LVAD component dysfunction. Ten patients were admitted and treated for LVAD outflow graft obstruction. Two of these patients subsequently developed recurrent outflow graft obstruction requiring reintervention; however, each reoccurrence was at a different site than the original obstruction. Thus, a total of 12 cases of obstruction were analyzed. The most common reasons for hospital admission were low flow LVAD alarms or decompensated heart failure. Presentation with outflow graft obstruction occurred an average of 3.0 years after LVAD implantation. Patients underwent echocardiographic evaluation at the time of admission. Left ventricular assist device component dysfunction was suspected based on echocardiographic findings, and follow-up contrast studies were used to establish the specific diagnosis of outflow graft stenosis. The majority of stenotic lesions (10/12) were treated percutaneously with balloon angioplasty and stenting with balloon-expandable endovascular prostheses. Postintervention, all patients had significant improvement in LVAD flow rates.

Introduction Erdheim–Chester disease is a rare, multisystem hematologic disease. Cardiovascular involvement is seen in patients with Erdheim–Chester disease and can lead to increased morbidity and mortality. In this series, we report various cardiovascular manifestations of patients with Erdheim–Chester disease. Methods This study includes patients with Erdheim–Chester disease who were referred to our institution from 12/3/2009 through 12/13/2017. All patients had biopsy‐proven Erdheim–Chester disease. Clinical data, multimodality imaging, and cardiac tests were reviewed. Results Cardiovascular findings in 24 patients with Erdheim–Chester disease were included in the study. We reviewed available transthoracic echocardiograms, whole body PET/CT scans, and CMR studies. Most patients were male and mean age at the time of diagnosis was 58 years. Pericardial involvement (13%), myocardial infiltration (25%), endocardial involvement (4%), valvular disease (17%), aortic/vascular disease (17%), conduction system infiltration (8%), and coronary artery disease (25%) were present. At a median follow‐up of 5.5 years, mortality was 17%. Conclusions Erdheim–Chester disease can involve various cardiovascular structures and is frequently diagnosed on an imaging modality. Some patients had asymptomatic involvement, but others presented with ischemic heart disease, heart failure, valvular disease, and conduction system abnormalities. Early recognition of cardiovascular involvement of Erdheim–Chester disease is needed because of high morbidity and mortality.

Hematological markers of hemolysis, but not echocardiographic or pump parameters, reliably changed during LVAD thrombosis. Markers of hemolysis are the best early predictors of LVAD thrombosis.