PSV and Vr appear to have a significant role in predicting in-stent stenosis. To determine >or=80% stenosis, combining PSV >or=275 cm/s and Vr >or=3.50 is highly specific and predictive.

Mild traumatic brain injury afflicts over 2 million people annually and little can be done for the underlying injury. The Food and Drug Administration-approved drugs Minocycline plus N-acetylcysteine (MINO plus NAC) synergistically improved cognition and memory in a rat mild controlled cortical impact (mCCI) model of traumatic brain injury. The underlying cellular and molecular mechanisms of the drug combination are unknown. This study addressed the effect of the drug combination on white matter damage and neuroinflammation after mCCI. Brain tissue from mCCI rats given either sham-injury, saline, MINO alone, NAC alone, or MINO plus NAC was investigated via histology and qPCR at four time points (2, 4, 7, and 14 days post-injury) for markers of white matter damage and neuroinflammation. MINO plus NAC synergistically protected resident oligodendrocytes and decreased the number of oligodendrocyte precursor cells. Activation of microglia/macrophages (MP/MG) was synergistically increased in white matter two days post-injury after MINO plus NAC treatment. Patterns of M1 and M2 MP/MG were also altered after treatment. The modulation of neuroinflammation is a potential mechanism to promote remyelination and improve cognition and memory. These data also provide new and important insights into how drug treatments can induce repair after traumatic brain injury.

Endovascular interventions for TASC II B and C lesions are associated with restenosis/occlusion rates that are at least as good as those of open femoropopliteal bypass surgery from historical, previously published series. Furthermore, overall assisted-patency rates are excellent, although low preoperative ABIs continue to be associated with worse outcomes.

confidence interval, 0.203-0.802; P Ͻ .01). Treatment with anakinra starting 3 or 7 days after elastase exposure significantly reduced aortic dilation compared with vehicle alone. Treatment starting 3 days after elastase resulted in 43.7% Ϯ 8.3% dilation vs 86.4% Ϯ 3.5% dilation with vehicle alone (P Ͻ .0005). Anakinra treatment starting 7 days after elastase exposure reduced aortic dilation from 82.4% Ϯ 6.9% with vehicle alone to 52.9% Ϯ 1.4% (P Ͻ .005). Aortas treated with anakinra demonstrated less macrophage and neutrophil infiltration, less elastin degradation, and less IL-1␤.Conclusions: IL-1␤ signaling was critical for AAA formation, and inhibition of its corresponding receptor through receptor antagonism with anakinra attenuated AAA formation, macrophage and neutrophil infiltration, and elastin degradation. Furthermore, delayed initiation of IL-1R antagonism after early aneurysm formation inhibited AAA progression, suggesting that IL-1␤ pathway antagonism may function as a novel treatment strategy for AAAs. Introduction:Intimal hyperplasia is an overactive healing response that leads to failure of half of all vascular interventions in Ͻ5 years. Increasing evidence suggests that circulating progenitor cells expressing the marker CD34 play an important role in this disease. Several studies have highlighted either a direct cellular contribution to intimal lesions or by fostering a favorable environment for restenosis. Despite their evolving importance in this clinically important disease, the kinetics of CD34 cell mobilization after vascular injury are not known. In addition, there is no way to specifically intervene on these cells. In this study, we investigated the timecourse of CD34-positive progenitor cells after vascular injury and examined whether an affinity pheresis approach could mediate systemic depletion of CD34positive cells at the time of vascular injury in a large-animal model.Methods: An ovine model underwent placement of an arteriovenous polytetrafluorethylene graft between the carotid and jugular veins. The contralateral carotid underwent balloon angioplasty. Endothelial injury in this model was confirmed by scanning electron microscopy. The first groups of animals underwent flow cytometric assessment of CD34/vascular endothelial factor receptor 2-positive cells after vascular (n ϭ 3) and a control, nonvascular surgery (n ϭ 3). Next, separate groups underwent vascular injury, and over 14 days, the model underwent serial depletion using affinity pheresis toward the progenitor cell marker CD34 (n ϭ 3) or a mock control (n ϭ 4). Cells bound to the affinity system were eluted enzymatically and examined by flow cytometry. Finally, complete blood counts were compared between the study groups for changes after affinity pheresis.Results: Our findings suggest a surge of CD34-positive cells after vascular intervention that is not observed after control surgical procedures (Fig 1). Our pheresis group revealed that the surge can be attenuated by a CD34 affinity pheresis but not by a mock control (Fig 2)...

Objectives: Pediatric mandibular distraction osteogenesis (MDO) is an increasingly common surgical procedure used to lengthen the mandible. Little is known about the long-term effects of MDO on dental development. This retrospective study sought to identify dental abnormalities at mixed dentition and early permanent dentition stages in patients who had undergone MDO. Methods: All pediatric patients who underwent MDO with imaging and clinical exams at mixed dentition and early permanent dentition stages were evaluated identify pathology. Data included demographic information, medical and surgical history, complications, and dental exam information. Descriptive statistics were reported. Results: Twenty-two hemimandibles at mixed dentition stage and 24 at early permanent stage were included. Mean age at initial MDO was 7.95 years with a mean follow-up time of 15.1 years. Nine patients required more than 1 distraction. At the mixed dentition stage, all patients showed abnormalities. The most common abnormalities were absent, dysplastic, or ectopic molars. At early permanent dentition stage, 87.5% of patients had dental abnormalities. The most common abnormality was missing molars (third, second, and first), but dysplastic, impacted, and ectopic teeth were also noted. At both mixed and early permanent dentition stages, some patients were noted to have abnormal V-shaped sigmoid notching of the mandibular ramus of undetermined clinical significance. Buccal mucosal scarring that interfered with orthodontic treatment was observed in a subset of patients. Conclusions: This study provides long-term dental analyses of patients undergoing MDO for mandibular hypoplasia. Dental abnormalities were seen at both mixed and early permanent dentition stages. Molars were the most commonly affected with absence the most commonly seen abnormality. Dysplastic, ectopic, and impacted teeth were also seen in posterior and anterior dentition, and abnormalities in buccal soft tissue and the mandibular ramus were also seen. MDO remains a crucial tool for functional and aesthetic improvement in children with hypoplastic mandibles. Dental abnormalities as a consequence of MDO should be considered as part of surgical planning process.

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Background Intimal hyperplasia (restenosis) is an exaggerated healing response leading to failure of half of vascular interventions. Increasing evidence suggests that circulating progenitor cells contribute to intimal pathology, and clinical studies have demonstrated a correlation between progenitor cells and the incidence of restenosis after cardiovascular interventions. The aims of this study were to characterize the temporal response of CD34+ progenitors following vascular injury in an ovine model and to evaluate an affinity pheresis approach to attenuate this response. Methods An ovine model underwent either operative vascular injury or a nonvascular surgery (n = 3 per group). Blood was examined perioperatively over 2 weeks by flow cytometry. Next, an affinity pheresis approach to mediate systemic depletion of CD34 progenitors was designed. Custom agarose pheresis matrix with antibody affinity toward CD34 or an isotype control was evaluated in vitro. Next, following vascular injury, sheep underwent perioperative whole blood volume pheresis toward either the progenitor cell marker CD34 (n = 3) or an isotype control (n = 4) for 14 days. Animals were monitored by physical exam as well as complete blood counts. Cells recovered by pheresis were eluted and examined by flow cytometry. Results Flow cytometry revealed a focal surge of circulating CD34 cells after vascular injury but not among surgical controls (P = .05). Toward the goal of an approach to attenuate the surge of CD34 progenitors, an evaluation of high-flow affinity matrix revealed efficacy in removal of progenitors from ovine blood in vitro. Next, a separate group of animals undergoing affinity pheresis after vascular injury was evaluated to mediate systemic depletion of CD34+ cells. Again, a surge of CD34+ cells was observed among isotype pheresis animals following vascular intervention but was attenuated over 20-fold by a CD34 pheresis approach (P = .029). Furthermore, an average of 77 million CD34-positive cells were eluted from the CD34 pheresis matrix. Despite multiple sessions of pheresis, complete blood counts remained essentially unchanged over 2 weeks. Conclusions Despite evidence suggesting a role for CD34+ circulating progenitor cells in restenotic pathology, the temporal pattern of CD34 progenitors after vascular injury has not been previously defined. We have demonstrated a surge among circulating CD34+ cells that appears confined to procedures involving vascular injury and that this event seems to occur early after vascular injury. We further conclude that CD34 affinity pheresis attenuates the surge. This approach for direct depletion of progenitors may have important implications for the study of progenitors in vascular restenosis.