Neointimal dissection – a rare complication to endovascular treatment in grafts and stent grafts

Abstract Background Neointima formation and hyperplasia in vascular grafts may lead to graft complications threatening the patency of the vascular reconstruction. A rare complication to endovascular treatment of grafts and stent grafts is dissection inside the graft. Case report We present here a case of a 69-year-old female with acute occlusion of the limb of an aorto-bifemoral graft for the third time, 16 years after the primary operation. As at the first two occasions, catheter-based intra-arterial thrombolysis was performed, but with residual stenosis inside the graft. During stent placement, dissection of the neointima or fibrin sheet occluded the inflow to the stent. The complication was resolved with placement of kissing stents. Conclusions It is important to recognize iatrogenic neointima dissection inside graft and stent grafts, as continued thrombolysis will not solve this, but increase the risk of hemorrhagic complications

Coupled luminescence and cosmogenic nuclide dating of postglacial deflation surfaces and sand drift on a raised ice-contact delta at Veinge, SW Sweden

Wind-abraded cobbles (ventifacts) and aeolian sand are known from the sandy-gravelly coastal areas of south-western Sweden, especially in association with raised deltas. Ventifacts are recorded on at least two different stratigraphic levels, at some sites atop glaciofluvial sediment, at other sites atop littoral deposits, and in some places at both levels, while aeolian sand usually forms a surficial cover. The formation of ventifacts has usually been coupled to abrasion due to katabatic winds from the retreating ice sheet or with periglacial climate during the Younger Dryas stadial (12.8–11.7 ka). To determine the timing of these deflation events, we have applied a combination of dating methods to ventifacts and associated sediments on top of an ice-contact delta at Veinge, south-western Sweden. Quartz and feldspar luminescence dating as well as portable luminescence profiling has been used for littoral and aeolian sediments over- and underlying deflation surfaces, while rock surface luminescence burial dating and paired 14C–10Be cosmogenic nuclide dating were conducted on ventifacts. The results show that a first deflation event occurred c. 16.5 ka, just after deglaciation and prior to a regional transgression that peaked around 15.7 ka. At 12.4–11.4 ka, during the Younger Dryas stadial, a new set of ventifacts formed on the surface of the exposed littoral sands and gravels. Some wind abrasion also occurred in the early Holocene, but at c. 8.5 ka the surface was covered by aeolian sand, up to 2.5 m thick. The combination of different dating methods have allowed us to draw more informed conclusions on the timing and duration of these wind abrasion/transport events than would have been possible from the use of only single-method dating. It has also made it possible to infer some environmental conditions during deposition. For example, both glaciofluvial and littoral deposits show evidence of incomplete bleaching of the luminescence signal. This suggests short subaerial transport and brief reworking by waves, respectively, though bleaching conditions improved during shore regression. Rock surface burial luminescence profiles reveal that some ventifacts were repeatedly exposed, but that later event(s) were shorter in duration as indicated by quartz-feldspar age comparisons.</p

Browning of human adipocytes requires KLF11 and reprogramming of PPARγ superenhancers

Long-term exposure to peroxisome proliferator-activated receptor γ (PPARγ) agonists such as rosiglitazone induces browning of rodent and human adipocytes; however, the transcriptional mechanisms governing this phenotypic switch in adipocytes are largely unknown. Here we show that rosiglitazone-induced browning of human adipocytes activates a comprehensive gene program that leads to increased mitochondrial oxidative capacity. Once induced, this gene program and oxidative capacity are maintained independently of rosiglitazone, suggesting that additional browning factors are activated. Browning triggers reprogramming of PPARγ binding, leading to the formation of PPARγ “superenhancers” that are selective for brown-in-white (brite) adipocytes. These are highly associated with key brite-selective genes. Based on such an association, we identified an evolutionarily conserved metabolic regulator, Kruppel-like factor 11 (KLF11), as a novel browning transcription factor in human adipocytes that is required for rosiglitazone-induced browning, including the increase in mitochondrial oxidative capacity. KLF11 is directly induced by PPARγ and appears to cooperate with PPARγ in a feed-forward manner to activate and maintain the brite-selective gene program