Analysis of data from a large, multistate outbreak of fungal infections showed substantial morbidity and mortality. The infections were associated with injection of a contaminated glucocorticoid medication from a single compounding pharmacy. Rapid public health actions included prompt recall of the implicated product, notification of exposed persons, and early outreach to clinicians.
Background and Purpose-To investigate the incidence of retrograde flow from complex plaques (Ն4-mm-thick, ulcerated, or superimposed thrombi) of the descending aorta (DAo) and its potential role in embolic stroke. Methods-Ninety-four consecutive acute stroke patients with aortic plaques Ն3-mm-thick in transesophageal echocardiography were prospectively included. MRI was performed to localize complex plaques and to measure time-resolved 3-dimensional blood flow within the aorta. Three-dimensional visualization was used to evaluate if diastolic retrograde flow connected plaque location with the outlet of the left subclavian artery, left common carotid artery, or brachiocephalic trunk. Complex DAo plaques were considered an embolic source if retrograde flow reached a supra-aortic vessel that supplied the territory of visible acute and embolic retinal or cerebral infarction. Results-Only decreasing heart rate was correlated (PϽ0.02) with increasing flow reversal to the aortic arch. Retrograde flow from complex DAo plaques reached the left subclavian artery in 55 (58.5%), the left common carotid artery in 23 (24.5%), and the brachiocephalic trunk in 13 patients (13.8%). Based on routine diagnostics and MRI of the ascending aorta/aortic arch, stroke etiology was determined in 57 and cryptogenic in 37 patients. Potential embolization from DAo plaques was then identified in 19 of 57 patients (33.3%) with determined and in 9 of 37 patients (24.3%) with cryptogenic stroke. Conclusions-Retrograde flow from complex DAo plaques was frequent in both determined and cryptogenic stroke and could explain embolism to all brain territories. These findings suggest that complex DAo plaques should be considered a new source of stroke. (Stroke. 2010;41:1145-1150.)Key Words: acute stroke Ⅲ aorta Ⅲ atherosclerosis Ⅲ magnetic resonance Ⅲ pathogenesis C omplex aortic plaques defined as Ն4-mm-thick, ulcerated or containing mobile thrombi are considered a major source of stroke. 1 Although their incidence is highest in the proximal descending aorta (DAo), such plaques are only considered an embolic source of stroke in the unlikely coincidence of severe aortic valve insufficiency causing retrograde flow and embolization in case of plaque rupture. 1,2 However, there is growing evidence that diastolic retrograde flow in the DAo may be a frequent phenomenon in the presence of atherosclerosis and thus an overlooked mechanism of retrograde embolization in stroke patients. Oscillating thrombus mobility 3 and Doppler flow curves in the DAo in transesophageal echocardiography (TEE) indirectly proved the existence of flow reversal. 4 In contrast to TEE, flowsensitive 4-dimensional MRI permits the precise analysis of individual 3-dimensional flow patterns at the site of complex DAo plaques. [5][6][7] Moreover, it allows for a more reliable detection and characterization of aortic plaques compared to TEE. 8,9 In this context, retrograde embolization from complex DAo plaques was recently described as a proof-ofprinciple and constituted the only proba...
Microglial erythrophagocytosis is crucial in injury response to hemorrhagic stroke. We hypothesized that regulation of microglial erythrophagocytosis via HO‐1/CO depends on a pathway involving reactive oxygen species (ROS) and CD36 surface‐expression. The microglial BV‐2 cell line and primary microglia (PMG) were incubated +/−blood and +/−CO‐exposure. PMG isolated from tissue‐specific HO‐1‐deficient (LyzM‐Cre‐Hmox1 fl/fl) and CD36 −/− mice or siRNA against AMPK (AMP‐activated protein kinase) were used to test our hypothesis. In a murine subarachnoid hemorrhage (SAH) model, we compared neuronal injury in wild‐type and CD36 −/− mice. Readouts included vasospasm, microglia activation, neuronal apoptosis, and spatial memory. We observed increased microglial HO‐1‐expression after blood‐exposure. A burst in ROS‐production was seen after CO‐exposure, which led to increased amounts of phosphorylated AMPK with subsequently enhanced CD36 surface‐expression. Naïve PMG from LyzM‐Cre‐Hmox1 fl/fl mice showed reduced ROS‐production and CD36 surface‐expression and failed to respond to CO with increased CD36 surface‐expression. Lack of HO‐1 and CD36 resulted in reduced erythrophagocytosis that could not be rescued with CO. Erythrophagocytosis was enhanced in BV‐2 cells in the presence of exogenous CO, which was abolished in cells treated with siRNA to AMPK. CD36 −/− mice subjected to SAH showed enhanced neuronal cell death, which resulted in impaired spatial memory function. We demonstrate that microglial phagocytic function partly depends on a pathway involving HO‐1 with changes in ROS‐production, phosphorylated AMPK, and surface expression of CD36. CD36 was identified as a crucial component in blood clearance after hemorrhage that ultimately determines neuronal outcome. These results demand further investigations studying the potential neuroprotective properties of CO.
Introduction:Resection of anorectal malignancies may result in extensive perineal/pelvic defects that require an interdisciplinary surgical approach involving reconstructive surgery. The myocutaneous gracilis flap (MGF) and the gluteal fold flap (GFF) are common options for defect coverage in this area. Here we report our experience with the MGF/GFF and compare the outcome regarding clinical key parameters. Methods: In a retrospective chart review, we collected data from the Department of Plastic Surgery of the University of Freiburg from December 2008-18 focusing on epidemiological, oncological, and therapy-related data including comorbidities (ASA Classification) and peri-/postoperative complications (Clavien-Dindo-System). Results: Twenty-nine patients were included with a mean follow-up of 17 months. Of the cases, 19 (65.5%) presented with recurrent disease, 21 (72.4%) received radiochemotherapy preoperatively, 2 (6.9%) received chemotherapy alone. Microscopic tumor free margins were achieved in 25 cases (86.2%). 17 patients (7 men, 10 women, rectal adenocarcinoma n = 11; anal squamous cell carcinoma n = 6; mean age 58.5 ± 10.68, mean BMI 23.1, mean ASA score 2.8) received a MGF (unilateral n = 10; bilateral n = 7). Twelve patients (7 men, 5 women, rectal adenocarcinoma n = 7; anal squamous cell carcinoma n = 4, proctodeal gland carcinoma n = 1, mean age 66.2 ± 9.2, mean BMI 23.6, mean ASA score 2.6) received coverage with a GFF (unilateral n = 4; bilateral n = 8). Mean operation time of coverage was 105 ± 9 min for unilateral and 163 ± 11 for bilateral MGFs, 70 ± 13 min for unilateral and 107 ± 14 for bilateral GFFs. Complications affected 62%. There was no significant difference in the complication rate between the MGF-and GFF-group. Complications were mainly wound healing disorders that did not extend the hospital stay. No flap loss and no complication that lead to long-lasting disability was documented (both groups). Pain-free sitting took more time in the GFF-group due to the location of the donor site. Conclusion: MG-flaps and GF-flaps prove to be reliable and robust techniques for perineal/pelvic reconstruction. Though flap elevation is significantly faster for GF-flaps, Thiele et al. Gracilis/Gluteal Fold for Perineal Coverage preoperative planning and intraoperative Doppler confirmation are advisable. With comparable complication rates, we suggest a decision-making based on distribution of adipose tissue for dead space obliteration, intraoperative patient positioning, and perforator vessel quality/distribution.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.