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.

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.

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)...

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New Jersey was among the first states impacted by the COVID-19 pandemic, with one of the highest overall death rates in the nation. Nevertheless, relatively few reports have been published focusing specifically on New Jersey. Here we report on molecular, clinical, and epidemiologic observations from the largest healthcare network in the state, in a cohort of vaccinated and unvaccinated individuals with laboratory-confirmed SARS-CoV-2 infection. We conducted molecular surveillance of SARS-CoV-2-positive nasopharyngeal swabs collected in nine hospitals from December 2020 through June 2022, using both whole genome sequencing (WGS) and a real-time RT-PCR screening assay targeting spike protein mutations found in variants of concern (VOC) within our region. De-identified clinical data were obtained retrospectively, including demographics, COVID-19 vaccination status, ICU admission, ventilator support, mortality, and medical history. Statistical analyses were performed to identify associations between SARS-CoV-2 variants, vaccination status, clinical outcomes, and medical risk factors. A total of 5,007 SARS-CoV-2-positive nasopharyngeal swabs were successfully screened and/or sequenced. Variant screening identified three predominant VOC, including Alpha (n =714), Delta (n =1,877), and Omicron (n =1,802). Omicron isolates were further sub-typed as BA.1 (n =899), BA.2 (n =853), and BA.4/BA.5 (n =50); the remaining 614 isolates were classified as “Other”. Approximately 31.5% (1,577/5,007) of the samples were associated with vaccine breakthrough infections, which increased in frequency following the emergence of Delta and Omicron. Severe clinical outcomes included ICU admission (336/5007 = 6.7%), ventilator support (236/5007 = 4.7%), and mortality (430/5007 = 8.6%), with increasing age being the most significant contributor to each (p <0.001). Unvaccinated individuals accounted for 79.7% (268/336) of ICU admissions, 78.3% (185/236) of ventilator cases, and 74.4% (320/430) of deaths. Highly significant (p <0.001) increases in mortality were observed in individuals with cardiovascular disease, hypertension, cancer, diabetes, and hyperlipidemia, but not with obesity, thyroid disease, or respiratory disease. Significant differences (p <0.001) in clinical outcomes were also noted between SARS-CoV-2 variants, including Delta, Omicron BA.1, and Omicron BA.2. Vaccination was associated with significantly improved clinical outcomes in our study, despite an increase in breakthrough infections associated with waning immunity, greater antigenic variability, or both. Underlying comorbidities contributed significantly to mortality in both vaccinated and unvaccinated individuals, with increasing risk based on the total number of comorbidities. Real-time RT-PCR-based screening facilitated timely identification of predominant variants using a minimal number of spike protein mutations, with faster turnaround time and reduced cost compared to WGS. Continued evolution of SARS-CoV-2 variants will likely require ongoing surveillance for new VOCs, with real-time assessment of clinical impact.