Cerebrovascular injuries after blunt or penetrating head and neck trauma often lead to significant disability from ischemic stroke, hemorrhagic stroke and uncontrolled extracranial hemorrhage. Trauma causes carotid or vertebral dissection, occlusion, pseudoaneurysm, arteriovenous fistula, vessel transection, traumatic epistaxis, venous sinus thrombosis and carotid cavernous fistula. The rapid development of neuroendovascular techniques over the past two decades has led to effective therapies for each of these injuries. Controlled lesion embolization may use coils, liquid embolics (onyx or n-butyl cyanoarcrylate), polyvinyl alcohol particles or detachable balloons; there is stent angioplasty with uncovered, overlapping and covered stents or mechanical thrombolysis using stent-retrievers or aspiration catheters and the use of balloon occlusion tests and supraselective angiography to delineate safety of vessel sacrifice and to diagnose occult lesions respectively. Furthermore, the proliferation of stroke centers has increased local availability of rapid neuroendovascular expertise at many major trauma centers. Neuroendovascular therapies are less invasive than surgery, can often preserve the injured parent vessels and aid in treating conditions where surgery may be limited. In the absence of randomized controlled trials we present a narrative review of current endovascular therapeutic applications for each of these injuries. This expands the therapies at trauma teams' disposal in the continued effort to control bleeding, reduce secondary injury and prevent disability after trauma. Further research is necessary to inform the role of endovascular techniques after trauma. In particular, comparative studies are necessary to quantify the risk and benefits in conditions where surgical options also exist.

BackgroundAn issue associated with efficient bioethanol production is the fact that the desired product is toxic to the biocatalyst. Among other effects, ethanol has previously been found to influence the membrane of E. coli in a dose-dependent manner and induce changes in the lipid composition of the plasma membrane. We describe here the characterization of a collection of ethanol-tolerant strains derived from the ethanologenic Escherichia coli strain FBR5.ResultsMembrane permeability assays indicate that many of the strains in the collection have alterations in membrane permeability and/or responsiveness of the membrane to environmental changes such as temperature shifts or ethanol exposure. However, analysis of the strains by gas chromatography and mass spectrometry revealed no qualitative changes in the acyl chain composition of membrane lipids in response to ethanol or temperature. To determine whether these strains contain any mutations that might contribute to ethanol tolerance or changes in membrane permeability, we sequenced the entire genome of each strain. Unexpectedly, none of the strains displayed mutations in genes known to control membrane lipid synthesis, and a few strains carried no mutations at all. Interestingly, we found that four independently-isolated strains acquired an identical C → A (V244 V) silent mutation in the ferric citrate transporter gene fecA. Further, we demonstrated that either a deletion of fecA or over-expression of fecA can confer increased ethanol survival, suggesting that any misregulation of fecA expression affects the cellular response to ethanol.ConclusionsThe fact that no mutations were observed in several ethanol-tolerant strains suggested that epigenetic mechanisms play a role in E. coli ethanol tolerance and membrane permeability. Our data also represent the first direct phenotypic evidence that the fecA gene plays a role in ethanol tolerance. We propose that the recurring silent mutation may exert an effect on phenotype by altering RNA-mediated regulation of fecA expression.Electronic supplementary materialThe online version of this article (10.1186/s12866-018-1180-1) contains supplementary material, which is available to authorized users.