Highlights d Gene expression profiling mapped systemic macrophage responses to sepsis, MI, and stroke d The tissue microenvironment determined phenotypic adaptions following remote injury d Local proliferation dominated over recruitment in expanding tissue macrophage numbers d Alveolar macrophage priming post MI increased resilience against subsequent pneumonia

The Amplatzer Vascular Plug allows for a cost-effective method to occlude the internal iliac artery in patients undergoing endograft repairs of aortoiliac aneurysms. The use of a single device with a precise placement at the origin of the artery minimizes cost and avoids ischemic complications.

Lymphoscintigraphy (LS), performed with technetium 99m-labeled antimony trisulfide colloid (Cadema Medical Products, Inc., Middletown, N.Y.), was used as a noninvasive diagnostic examination to evaluate the lymphatic circulation in 190 extremities of 115 patients. Forty-six patients had primary lymphedema, 48 had secondary lymphedema, and 21 patients had other causes of limb swelling. To determine the value of LS in surgical decision making, preoperative and postoperative LS of 16 patients who underwent surgical repair of the lymphatic abnormality were studied separately. Semiquantitative evaluation of the lymphatic drainage and visual interpretation of the image patterns were reliable to differentiate lymphedema from edemas of other origin (sensitivity: 92%, specificity: 100%). Although certain image patterns were characteristic of either primary or secondary lymphedema, LS could not consistently differentiate between the two types. Episodes of cellulitis in lymphedema clearly delayed lymph transport. LS was helpful in patient selection and follow-up after lymphatic surgery, but it did not prove patency of lymphovenous anastomoses. It was diagnostic in the evaluation of lymphangiectasia and was used to document successful surgical treatment of reflux of chyle. LS is safe and reliable and has no side effects. It should replace contrast lymphangiography in the routine evaluation of the swollen extremity.

Sterile tissue injury is thought to locally activate innate immune responses via damage-associated molecular patterns (DAMPs). Whether innate immune pathways are remotely activated remains relatively unexplored. Here, by analyzing ~145,000 single-cell transcriptomes at steady state and after myocardial infarction (MI) in mice and humans, we show that the type I interferon (IFN) response, characterized by expression of IFN-stimulated genes (ISGs), begins far from the site of injury, in neutrophil and monocyte progenitors within the bone marrow. In the peripheral blood of patients, we observed defined subsets of ISG-expressing neutrophils and monocytes. In the bone marrow and blood of mice, ISG expression was detected in neutrophils and monocytes and their progenitors, intensified with maturation at steady-state and after MI, and was controlled by Tet2 and Irf3 transcriptional regulators. Within the infarcted heart, ISG-expressing cells were negatively regulated by Nrf2 activation in Ccr2− steady-state cardiac macrophages. Our results show that IFN signaling begins in the bone marrow, implicate multiple transcriptional regulators (Tet2, Irf3, and Nrf2) in governing ISG expression, and provide a clinical biomarker (ISG score) for studying IFN signaling in patients.