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BACKGROUND Transcarotid artery revascularization (TCAR) with cerebral flow reversal is an emerging treatment option for carotid artery stenosis in patients with high risk for traditional endarterectomy. The purpose of this study was to compare real-world, procedure-related outcomes in similarly comorbid patients undergoing TCAR or carotid endarterectomy (CEA). METHODS A retrospective review of all patients receiving either TCAR or CEA outside of clinical trial regulations at our institution was performed. Participants were propensity-matched by age, gender, body mass index, smoking status, presence of restenosis, history of neck radiation, presence of contralateral carotid occlusion, history of previous neck dissection, and symptom status. Bivariate analysis was followed by a penalized Firth logistic regression to compare treatments. RESULTS Between January 2011 and July 2018, 342 CEAs and 109 TCARs were captured for analysis. After matching, 87 distinct treatment pairs were created without evidence of variathorter operative time and less blood loss. BACKGROUND We hypothesized that administration of cilostazol may clarify the occult atrial fibrillation (AF) during hospitalization in mild stroke patients, who has no history of AF. METHODS From our prospective non-cardioembolic stroke study, randomized to dual antiplatelet therapy using cilostazol and aspirin or aspirin alone trial (ADS), data on the presence or absence of AF were retrospectively analyzed. In the ADS, during hospitalization, as a routine examination, presence of AF was investigated using electrocardiogram (ECG), ECG monitoring and Holter ECG. Multivariate regression analysis was conducted to evaluate the independent parameters related to the AF. Clinical outcome at 3&nbsp;months was evaluated using modified Rankin Scale (mRS) score. RESULTS Data on 1194 patients (793 [66%] men; median age [interquartile range] of 69 [61-77] years, National Institutes of Health Stroke Scale score 2 [1-4], onset-to-admission 10.8 [4.7-20.5] hours) were retrospectively analyzed. AF was newly detected in 41 (3%) patients (3 by ECG, 21 by the ECG monitoring and 17 by the Holter ECG) during hospitalization. Patients treated with combined cilostazol and aspirin therapy frequently had the AF than those took aspirin alone (5% vs. 2%, p&nbsp;=&nbsp;.007). Multivariate regression analysis showed that cilostazol administration was one of the independent factors for new-AF (odds ratio 2.672, 95%CI 1.205-5.927, p&nbsp;=&nbsp;.016). The frequency of mRS 0-1 was 68% in the new-AF group and 67% in the non-AF group (p&nbsp;=&nbsp;1.000). CONCLUSION Cilostazol therapy may increase the detectability of AF in acute non-cardioembolic stroke, though the new-AF was not related to clinical outcome at 3&nbsp;months. V.BACKGROUND Children with congenital heart disease (CHD) have an increased risk of neurocognitive impairment. No prior studies have evaluated the role of obstructive sleep apnea (OSA), which is associated with neurocognitive impairment in children without CHD. RESEARCH QUESTION Is OSA is associated with neurocognitive impairment in children with CHD? STUDY DESIGN AND METHODS Children age 6-17 years with corrected moderate-complex CHD without syndromes that may affect neurocognition were recruited from the pediatric cardiology clinic. Participants underwent home sleep testing and neurocognitive testing including a validated IQ test as well as validated tests of memory (Paired Associates Learning test), executive function (Intra-Extra Dimensional set shift test) and attention (Simple Reaction Test) from the CANTAB neurocognitive testing battery. RESULTS Complete results were available for 30 children. Seventeen children (57%) were found to have OSA. Total IQ was markedly lower in children with CHD and comorbid OSA compared to children with CHD without comorbid OSA (mean 86 ± 12, vs 98 ± 11, p=0.01). Children with CHD and OSA did significantly worse on the Paired Associates Learning test, with a median of 8 total errors (interquartile range [IQR] 2.25-15) compared to children with CHD without OSA (median total errors 2, IQR 1-8), p=0.02. INTERPRETATION Children with CHD and comorbid OSA have impaired neurocognition compared to children with CHD without comorbid OSA. OSA may be a reversible cause of neurocognitive impairment in children with CHD. Further research is needed to evaluate the effects of OSA treatment on neurocognitive impairment in children with CHD. Methamphetamine (METH) is a major public health and safety problem worldwide. METH is psychostimulant that activates microglia via the toll-like receptor (TLR) 4/MD2 complex, modulating the abundant production of pro-inflammatory cytokines in the central nervous system (CNS). The TLR4/MD2 complex on the surface of microglia recognizes pathogen-associated molecular patterns such as lipopolysaccharide (LPS) resulting in brain tissue inflammation and neuronal damage. Since METH has been associated with microglia-induced neurotoxicity, we hypothesized that METH impairs the expression of TLR4 and activation of NF-κB in NR-9460 microglia-like cells after LPS challenge. We demonstrated that METH decreases the distribution and expression of TLR4 receptors on the surface of microglia-like cells after incubation with endotoxin. Moreover, METH impairs the TLR4/MD2 complex signaling pathways, compromises the activation of NF-κB, and reduces the production of pro-inflammatory mediators in microglia-like cells upon LPS stimulation. Interestingly, microglia-like cells treated with METH and challenged with LPS showed considerable cellular morphological changes including enlarged nuclei and ruffled surface. Our results suggest that METH may have a significant impact on microglial-induced neuroinflammation, neurotoxicity, and the CNS defense against infection. It also highlights the importance of studying the effects of METH on the molecular and cellular components of users' CNS immunity. Finally, animal studies exploring the role of METH on the effectors functions of microglia after antigenic exposure are necessary to understand drug-related inflammation and neural damage in users. Most of therapeutic monoclonal antibodies belong to the immunoglobulin G1 (IgG1) family; they interact with the Fcγ receptors (FcγRs) at the surface of immune cells to trigger effector functions. The IgG1-Fc N-glycans impact the interaction with FcγRs and are considered a critical quality attribute. Pioneer studies on FcγR N-glycans have unveiled an additional complexity in that the N-glycan linked on the Asn-162 of FcγRIIIa was shown to be directly involved in the strong affinity for afucosylated IgG1. The last few years have thus seen the emergence of many studies investigating the complex influence of FcγRIIIa N-glycans on the interaction with IgG1 through their glycosylation sites or their glycoprofiles. In this context, we performed site-directed mutagenesis along with glycoengineering on FcγRs (FcγRI, FcγRIIaH131/b and FcγRIIIaV158/F158) in an effort to elucidate the impact of FcγRs N-glycans on the interaction with IgG1. [https://www.selleckchem.com/products/dorsomorphin-2hcl.html BML-275 2HCl] Furthermore, we assessed their binding to various trastuzumab glycoforms with an enhanced surface plasmon resonance assay.