Rationale Fetal cells enter the maternal circulation during pregnancy and may persist in maternal tissue for decades as microchimeras. Objective Based on clinical observations of peripartum cardiomyopathy patients and the high rate of recovery they experience from heart failure, our objective was to determine whether fetal cells can migrate to the maternal heart and differentiate to cardiac cells. Methods and Results We report that fetal cells selectively home to injured maternal hearts and undergo differentiation into diverse cardiac lineages. Utilizing enhanced green fluorescent protein (eGFP) tagged fetuses, we demonstrate engraftment of multipotent fetal cells in injury zones of maternal hearts. In vivo, eGFP+ fetal cells form endothelial cells, smooth muscle cells, and cardiomyocytes. In vitro, fetal cells isolated from maternal hearts recapitulate these differentiation pathways, additionally forming vascular tubes and beating cardiomyocytes in a fusion-independent manner. ~40% of fetal cells in the maternal heart express Caudal-related homeobox2 (Cdx2), previously associated with trophoblast stem (TS) cells, thought to solely form placenta. Conclusions Fetal maternal stem cell transfer appears to be a critical mechanism in the maternal response to cardiac injury. Furthermore, we have identified Cdx2 cells as a novel cell type for potential use in cardiovascular regenerative therapy.

Staphylococcus aureus is a leading cause of ventricular assist device–related infections. This study evaluated the protective effect against S. aureus infection of active and passive immunization that targeted 3 proteins involved in bacterial attachment to a murine intra-aortic polyurethane patch. Active immunization of mice with a combination of the A domains of clumping factor A (ClfA), fibronectin-binding protein A (FnBPA) and fibronectin-binding protein B or passive immunization with monoclonal antibodies against ClfA and FnBPA resulted in a higher level of protection than that obtained by vaccination with either protein or antibody alone. The combination of antibodies or protein antigens appears to provide enhanced protection against prosthetic-device infection.

Fetal cells enter the maternal circulation during pregnancies and can persist in blood and tissues for decades, creating a state of physiologic microchimerism. Microchimerism refers to acquisition of cells from another individual and can be due to bi-directional cell traffic between mother and fetus during pregnancy. Peripartum cardiomyopathy, a rare cardiac disorder associated with high mortality rates has the highest recovery rate amongst all etiologies of heart failure although the reason is unknown. Collectively, these observations led us to hypothesize that fetal cells enter the maternal circulation and may be recruited to the sites of myocardial disease or injury. The ability to genetically modify mice makes them an ideal system for studying the phenomenon of microchimerism in cardiac disease. Described here is a mouse model for ischemic cardiac injury during pregnancy designed to study microchimerism. Wild-type virgin female mice mated with eGFP male mice underwent ligation of the left anterior descending artery to induce a myocardial infarction at gestation day 12. We demonstrate the selective homing of eGFP cells to the site of cardiac injury without such homing to nonfinjured tissues suggesting the presence of precise signals sensed by fetal cells enabling them to target diseased myocardium specifically.

A 66-year-old man was transferred to our hospital with the diagnosis of a large thoracoabdominal aneurysm. Computed tomography showed thoracic vertebral erosion, suggesting a chronic contained rupture. He was hemodynamically stable with no neurological complication preoperatively. He underwent successful surgical replacement of the descending aorta. During surgery, the 6th and 7th thoracic vertebral bones adjacent to the thoracic aneurysm were found to be eroded. The postoperative course was uneventful.

Cardiac tumours are relatively rare and are difficult to diagnose merely with imaging techniques. We demonstrated an unusual case of left atrial myxoma, displaying the successful detection by positron emission tomography using 2-deoxy-2-[18 F] fluoro-D-glucose (18 F-FDG PET), correlated closely to more intense and enhanced immunoreactivity with glucose transporter-1 (GLUT-1) in a substantial number of cardiac myxoma cells. Further prospective studies are needed to validate the significance of 18 F-FDG PET findings for cardiac myxoma and the association with immunohistochemical GLUT-1 expression in its tumour cells, after collecting and investigating a larger number of surgical cases examined with both of them.Virtual slidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/2991481941253449