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Quantitative electroencephalography (qEEG) refers to the numerical analysis and/or visual transformations of raw electroencephalography (EEG) signals. Evaluation of qEEG in intensive care units (ICU) faces unique challenges that warrant investigation separate from those conducted in other settings. Additionally, the pathophysiology, management, and EEG patterns of critically ill conditions often significantly differ between adults and children. Thus, it is important to distinguish the literature on qEEGs specifically performed in adult ICUs. The aim of this review is to summarize the studies using qEEG for clinical evaluation of patients in adult ICUs performed over the past decade (since 2010), and to present the state of the art of these techniques. Overall, these studies have reported that qEEG can reveal important information faster than typically possible with traditional methods of reviewing the raw EEG only, with reasonable accuracy. However, it is crucial to emphasize that qEEG must be reviewed in conjunction with raw EEG and in context of understanding the patients' clinical status. Because each qEEG panel only focuses on a few aspects of the entire EEG, different combinations of qEEG panels may be required for optimal analyses of each medical condition and individual patient. Currently in practical terms, qEEG can serve as a complementary, valuable tool for portions of the EEG that require more detailed review. Further multi-center collaborative studies are needed to ultimately develop standardized methods of employing qEEG that are generalizable across institutions. As qEEG techniques continue to advance, including those involving machine learning, qEEG will further benefit from algorithms specifically suited for ICUs.

We aimed to identify continuous electroencephalogram (cEEG) markers associated with survival and death in patients with extracorporeal membrane oxygenation (ECMO) support under standardized sedation cessation protocol.Prospectively collected records of adult patients (age ≥ 18 years) who were started on ECMO support in July 2016 to December 2020 at a single tertiary center were analyzed. cEEGs were performed on patients on the basis of inclusion and exclusion criteria. Patients receiving sedation that affect cEEG reactivity at the start of cEEG recording, including propofol, ketamine, or benzodiazepines, were excluded. We allowed fentanyl and dexmedetomidine during cEEG monitoring. cEEGs were evaluated for frequency, amplitude, variability, reactivity, and state changes.Of 290 patients, 40 underwent cEEG in the absence of confounding sedation (median age 60 years, 85% venoarterial-ECMO, 15% venovenous-ECMO). The median length of ECMO support and analyzable cEEG were 143 h and 24 h, respectively. A total of 27 patients underwent withdrawal of life-sustaining therapies (WOLST) during ECMO support. Of the 13 who weaned off ECMO, 9 underwent WOLST later in the hospitalization and 4 survived at hospital discharge. Decisions of WOLST were not influenced by cEEG features' results. Proportions of present EEG reactivity, present state changes, and fair/good variability were significantly higher in patients who survived compared with those who died (odds ratios infinity, infinity, and 13.57, respectively; p values 0.001, 0.001, and 0.0299, respectively). Sensitivity and specificity for survival at discharge were 100% and 91.67% for intact reactivity, 100% and 97.20% for present state changes, and 75% and 83.3% for fair/good variability.Although future multicenter studies with larger patient cohorts are certainly warranted, we were able to validate the feasibility of protocolized sedation cessation and cEEG analyses in the absence of a confounding effect from sedating medications. Moreover, we demonstrate some evidence that cEEG features of intact reactivity, present state changes, and fair/good variability in comatose patients on ECMO may be associated with survival at hospital discharge.

A necessary-sufficient condition for the existence or nonexistence of global solutions to the following reaction-diffusion equations { u t = Δ u + ψ ( t ) u p , in R N ×( 0 , t ∗ ) , u ( ⋅ , 0 )= u 0 ≥ 0 , in R N , has not been known and remained as an open problem for a few decades. The purpose of this paper is to resolve this problem completely, even for more general source ψ( t) f( u) as follows: There is a global solution to the equation if and only if ∫ 0 ∞ ψ ( t ) f ( ‖ S ( t ) u 0 ‖ ∞ ) ‖ S ( t ) u 0 ‖ ∞ dt < ∞ for some nonnegative and nontrivial u 0 ∈ C 0 ( R N ) . Here, ( S ( t ) ) t ≥ 0 is the heat semigroup on R N .

The purpose of this paper is to give a necessary and sufficient condition for the existence and non-existence of global solutions of the following semilinear parabolic equations u t = Δ u + ψ ( t ) f ( u ) , in Ω × ( 0 , t ∗ ) , under the Dirichlet boundary condition on a bounded domain. In fact, this has remained as an open problem for a few decades, even for the case f ( u ) = u p . As a matter of fact, we prove: there is no global solution for any initial data if and only if ∫ 0 ∞ ψ ( t ) f ( ‖ S ( t ) u 0 ‖ ∞ ) ‖ S ( t ) u 0 ‖ ∞ dt = ∞ for every nonnegative nontrivial initial data u 0 ∈ C 0 ( Ω ) . Here, ( S ( t ) ) t ≥ 0 is the heat semigroup with the Dirichlet boundary condition.

The purpose of this paper is to give a necessary and sufficient condition for the existence and non-existence of global solutions of the following semilinear parabolic equations \[ u_{t}=\Delta u+\psi(t)f(u),\,\,\mbox{ in }\Omega\times (0,t^{*}), \] under the Dirichlet boundary condition on a bounded domain. In fact, this has remained as an open problem for a few decades, even for the case $f(u)=u^{p}$. As a matter of fact, we prove: \[ \begin{aligned} &\mbox{there is no global solution for any initial data if and only if } &\mbox{the function } f \mbox{ satisfies} &\hspace{20mm}\int_{0}^{\infty}\psi(t)\frac{f\left(\lVert S(t)u_{0}\rVert_{\infty}\right)}{\lVert S(t)u_{0}\rVert_{\infty}}dt=\infty &\mbox{for every }\,\epsilon>0\,\mbox{ and nonnegative nontrivial initial data }\,u_{0}\in C_{0}(\Omega). \end{aligned} \] Here, $(S(t))_{t\geq 0}$ is the heat semigroup with the Dirichlet boundary condition., Comment: 12 pages

In this paper, we study long-time behaviours of solutions to the discrete reaction-diffusion equations u t = Δ ω u + ψ ( t ) f ( u ) with nontrivial and nonnegative initial data, under the mixed bo...

Introduction: Schizophrenia, a devastating disorder with onset in adolescence or young adulthood, afflicts 1% of the population leading to severe social, educational, and occupational impai...

How the glioma immune microenvironment fosters tumorigenesis remains incompletely defined. Here, we use single-cell RNA-sequencing and multiplexed tissue-imaging to characterize the composition, spatial organization, and clinical significance of extracellular purinergic signaling in glioma. We show that microglia are the predominant source of CD39, while tumor cells principally express CD73. In glioblastoma, CD73 is associated with EGFR amplification, astrocyte-like differentiation, and increased adenosine, and is linked to hypoxia. Glioblastomas enriched for CD73 exhibit inflammatory microenvironments, suggesting that purinergic signaling regulates immune adaptation. Spatially-resolved single-cell analyses demonstrate a strong spatial correlation between tumor-CD73 and microglial-CD39, with proximity associated with poor outcomes. Similar spatial organization is present in pediatric high-grade gliomas including H3K27M-mutant diffuse midline glioma. These data reveal that purinergic signaling in gliomas is shaped by genotype, lineage, and functional state, and that core enzymes expressed by tumor and myeloid cells are organized to promote adenosine-rich microenvironments potentially amenable to therapeutic targeting.

ObjectiveTo test the hypothesis that myoclonus in patients with multiple system atrophy with predominant cerebellar ataxia (MSA-C) is associated with a heavier burden of α-synuclein deposition in the motor regions of the spinal cord, we compared the degree of α-synuclein deposition in spinal cords of 3 patients with MSA-C with myoclonus and 3 without myoclonus.MethodsAll human tissue was obtained by the Massachusetts General Hospital Department of Pathology with support from and according to neuropathology guidelines of the Massachusetts Alzheimer's Disease Research Center. Tissue was stained with Luxol fast blue and hematoxylin & eosin for morphologic evaluation, and with a mouse monoclonal antibody to α-synuclein and Vectastain DAB kit. Images of the spinal cord sections were digitized using a 10× objective lens. Grayscale versions of these images were transferred to ImageJ software for quantitative analysis of 8 different regions of interest (ROIs) in the spinal cord: dorsal column, anterior white column, left and right dorsal horns, left and right anterior horns, and left and right lateral corticospinal tracts. A mixed-effect, multiple linear regression model was constructed to determine if patients with and without myoclonus had significantly different distributions of α-synuclein deposition across the various ROIs.ResultsPatients with myoclonus had more α-synuclein in the anterior horns (p < 0.001) and lateral corticospinal tracts (p = 0.02) than those without myoclonus.ConclusionsIn MSA-C, myoclonus appears to be associated with a higher burden of α-synuclein deposition within spinal cord motor regions. Future studies with more patients will be needed to confirm these findings.

In this paper, we study the discrete eigenvalue problems for the p -Schrodinger equations under the mixed boundary conditions defined on networks as follows: − Δ p , ω ϕ ( x ) + q ( x ) | ϕ ( x ) | p − 2 ϕ ( x ) = λ | ϕ ( x ) | p − 2 ϕ ( x ) , x ∈ S , μ ( z ) ∂ ϕ ∂ p n ( z ) + σ ( z ) | ϕ ( z ) | p − 2 ϕ ( z ) = 0 , z ∈ ∂ S , where p > 1 , q is a real-valued function on a network S , and μ , σ are nonnegative functions on the boundary ∂ S of S , with μ ( z ) + σ ( z ) > 0 , z ∈ ∂ S . Next, we use the above result to provide the existence of a positive solution to the discrete Poisson equation − Δ p , ω u ( x ) + q ( x ) | u ( x ) | p − 2 u ( x ) = f ( x ) , x ∈ S , μ ( z ) ∂ u ∂ p n ( z ) + σ ( z ) | u ( z ) | p − 2 u ( z ) = 0 , z ∈ ∂ S .

In this paper, we consider the following discrete p-Laplacian nonlinear parabolic equations with q-nonlocal reaction { u t ( x , t ) = Δ p , ω u ( x , t ) + λ ∑ y ∈ S | u ( y , t ) | q − 1 u ( y , t ) , ( x , t ) ∈ S × ( 0 , ∞ ) , u ( x , t ) = 0 , ( x , t ) ∈ ∂ S × ( 0 , ∞ ) , u ( x , 0 ) = u 0 ≥ 0 , x ∈ S ‾ . Here, S is a network with boundary ∂S. The goal of this paper is to characterize completely the parameters p > 1 and q > 0 to see when the solution blows up, vanishes, or exists globally. Indeed, the blow-up rates for the blow-up solutions are derived.

Pelvic bone fractures may cause extensive bleeding; however, the efficacy of tranexamic acid (TXA) usage in pelvic fracture surgery remains unclear. In this systematic review and meta-analysis, we aimed to evaluate the efficacy of TXA in open reduction and internal fixation surgery for pelvic and acetabular fracture.MEDLINE, Embase, and Cochrane Library databases were systematically searched for studies published before April 22, 2020, that investigated the effect of TXA in the treatment of pelvic and acetabular fracture with open reduction and internal fixation. A pooled analysis was used to identify the differences between a TXA usage group and a control group in terms of estimated blood loss (EBL), transfusion rates, and postoperative complications.We included 6 studies involving 764 patients, comprising 293 patients who received TXA (TXA group) and 471 patients who did not (control group). The pooled analysis showed no differences in EBL between the groups (mean difference -64.67, 95% confidence interval [CI] -185.27 to -55.93, P = .29). The study period transfusion rate showed no significant difference between the groups (odds ratio [OR] 0.77, 95% CI 0.19-3.14, P = .71, I2 = 82%), nor in venous thromboembolism incidence (OR 1.53, 95% CI 0.44-5.25, P = .50, I2 = 0%) or postoperative infection rates (OR 1.15, 95% CI 0.13-9.98, P = .90, I2 = 48%).Despite several studies having recommended TXA administration in orthopedic surgery, our study did not find TXA usage to be more effective than not using TXA in pelvic and acetabular fracture surgery, especially in terms of EBL reduction, transfusion rates, and the risk of postoperative complications.

A low-cost quantitative structured office measurement of movements in the extremities of people with Parkinson's disease [1,2] was performed on people with Parkinson's disease, multiple system atrophy, and age-matched healthy volunteers. Participants underwent twelve videotaped procedures rated by a trained examiner while connected to four accelerometers [1,2] generating a trace of the three location dimensions expressed as spreadsheets [3,4]. The signals of the five repetitive motion items [1,2] underwent processing to fast Fourier [5] and continuous wavelet transforms [6]. The dataset [7] includes the coding form with scores of the live ratings [1,2], the raw files [3], the converted spreadsheets [4], and the fast Fourier [5] and continuous wavelet transforms [6]. All files are unfiltered. The data also provide findings suitable to compare and contrast with data obtained by investigators applying the same procedure to other populations. Since this is an inexpensive procedure to quantitatively measure motions in Parkinson's disease and other movement disorders, this will be a valuable resource to colleagues, particularly in underdeveloped regions with limited budgets. The dataset will serve as a template for other investigations to develop novel techniques to facilitate the diagnosis, monitoring, and treatment of Parkinson's disease, other movement disorders, and other nervous and mental conditions. The procedure will provide the basis to obtain objective quantitative measurements of participants in clinical trials of new agents.

The purpose of this paper is to investigate a condition \begin{equation*} (C_{p}) \hspace{1cm} \alpha \int_{0}^{u}f(s)ds \leq uf(u)+\beta u^{p}+\gamma,\,\,u>0 \end{equation*} for some $\alpha>2$, $\gamma>0$, and $0\leq\beta\leq\frac{\left(\alpha-p\right)\lambda_{p,0}}{p}$, where $p>1$ and $\lambda_{p,0}$ is the first eigenvalue of the discrete $p$-Laplacian $\Delta_{p,\omega}$. Using the above condition, we obtain blow-up solutions to discrete $p$-Laplacian parabolic equations \begin{equation*} \begin{cases} u_{t}\left(x,t\right)=\Delta_{p,\omega}u\left(x,t\right)+f(u(x,t)), & \left(x,t\right)\in S\times\left(0,+\infty\right), \mu(z)\frac{\partial u}{\partial_{p} n}(x,t)+\sigma(z)|u(x,t)|^{p-2}u(x,t)=0, & \left(x,t\right)\in\partial S\times\left[0,+\infty\right), u\left(x,0\right)=u_{0}\geq0(nontrivial), & x\in S, \end{cases} \end{equation*} on a discrete network $S$, where $\frac{\partial u}{\partial_{p}n}$ denotes the discrete $p$-normal derivative. Here, $\mu$ and $\sigma$ are nonnegative functions on the boundary $\partial S$ of $S$, with $\mu(z)+\sigma(z)>0$, $z\in \partial S$. In fact, it will be seen that the condition $(C_{p})$, the generalized version of the condition $(C)$, improves the conditions known so far., Comment: 22 pages. arXiv admin note: substantial text overlap with arXiv:1706.03494

Autism spectrum disorder (ASD) is a condition with onset in early childhood characterized by marked deficits in interpersonal interactions and communication and by a restricted and repetitive range of interests and activities. This review points out key recent findings utilizing molecular imaging including magnetic resonance spectroscopy (MRS) and nuclear neuroimaging techniques such as positron emission tomography (PET) and single-photon emission computed tomography (SPECT). MRS indicates an excitatory/inhibitory imbalance in high-functioning autism. Dysfunction of neurotransmitter and glucose metabolism has been demonstrated by PET and SPECT. Levels of serotonin synthesis in typically developing children are approximately twice those of adults; after the age of 5 years, levels decrease to those of adults. In contrast, levels of serotonin synthesis of children with ASD increase between ages 2 and 15 to 1.5-times adult values. The dopamine transporter is increased in the orbitofrontal cortex of men with ASD. The serotonin transporter is reduced in the brains of children, adolescents, and adults with ASD. Reduced serotonin receptors in the thalamus of adults with ASD are associated with communication difficulties. Glucose metabolism is reduced in the brains of people with ASD. Molecular imaging will provide the preliminary data for promising therapeutic interventions.

INTRODUCTION Purinergic signaling plays critical roles in the regulation of tumor growth and anti-tumor immunity via autocrine/paracrine binding of metabolites to receptors on neoplastic and non-neoplastic populations. Extracellular purine concentrations are mediated by the ectonucleotidase enzymes CD39 and CD73, which catabolize ATP to adenosine. Within tumors such as glioblastoma, neoplastic, immune, and stromal cells expressing these enzymes may co-localize to generate immunosuppressive adenosine-rich environments. However, the composition, architecture, and phenotypic properties of these tumor ecosystems and their relationship to tumor genotype are poorly characterized. METHODS We quantified CD73 expression by immunohistochemistry in a cohort of CNS tumors [meningiomas(n=222), gliomas(n=244), ependymomas(n=44), medulloblastomas(n=24), and craniopharyngiomas(n=38)]. We used publicly-available single-cell RNA-seq data and 36-marker multiplexed tissue imaging (t-CyCIF) of 139 clinically and genomically annotated glioblastoma resections to characterize CD39 and CD73-expressing populations, define the immune architecture and tumor cell-states at single cell resolution, and identify markers of clinical outcome. We used mass spectrometry imaging (MALDI-MSI) to generate spatially-resolved quantification of purine metabolite levels in glioblastoma resections (n=10). RESULTS CD73 exhibited strong expression in a subset of gliomas and meningiomas but was typically not expressed in ependymomas or medulloblastomas. CD73 expression correlated with poor progression-free-survival in IDH-wildtype glioblastoma (p=0.04). scRNA-seq and t-CyCIF in glioblastoma showed CD73 expression in tumor cells, and CD39 expression in macrophages and endothelial cells. MALDI-MSI showed significantly greater adenosine concentrations (3.5-fold;p=0.04) in glioblastomas with high CD73 expression. scRNA-seq showed direct correlations between stem-like mRNA expression, proliferation, and CD73 expression in DIPG. CD73 expression significantly correlated with EGFR amplification, interferon signaling, and PD-L1 expression in glioblastoma. CONCLUSIONS Phenogenomic analysis of purinergic immunomodulatory signaling revealed significant interplay between CD73 activity and genotype, adenosine concentration, differentiation-state, clinical outcome, and possible interaction between CD39-positive macrophages and CD73-positive neoplastic cells. Anti-CD73 therapy may provide therapeutic benefits in glioblastoma by blunting immunosuppressive and oncogenic adenosine signaling.

INTRODUCTION: Extracellular purinergic signaling plays critical roles in the regulation of tumor growth and anti-tumor immunity via autocrine/paracrine binding of metabolites to receptors on neoplastic and non-neoplastic populations. Extracellular purine concentrations are principally mediated by the ectonucleotidase enzymes CD39 and CD73, which catabolize ATP to adenosine. Within the tumor microenvironment, neoplastic, immune, and stromal cells expressing these enzymes may co-localize to generate an immunosuppressive adenosine-rich niche. However, the cellular composition, spatial architecture and phenotypic properties of these tumor ecosystems and their relationship to tumor genotype have been poorly characterized. METHODS: We quantified CD73 expression by immunohistochemistry (IHC) in a cohort of CNS tumors [meningiomas(N=222), gliomas(N=244), ependymomas(N=44), medulloblastomas(N=24), craniopharyngiomas(N=38)]. We used publicly-available single-cell RNA-seq data and 36 marker multiplexed tissue imaging (t-CyCIF) of 139 clinically and genomically annotated glioblastomas to characterize CD39 and CD73 expressing populations, define immune architecture and tumor cell states at single cell resolution, evaluate spatial correlations, and identify markers of clinical outcome. Mass spectrometry imaging (MALDI-MSI) was employed to generate spatially-resolved quantification of purine metabolite levels in glioblastoma resections (N=9). RESULTS: IHC revealed strong CD73 expression in meningiomas and gliomas. Tumor CD73 expression was associated with poor progression-free-survival in IDH-wildtype glioblastoma (p=0.04). scRNA-seq in glioblastoma revealed that CD73 is predominantly expressed by tumor cell populations, while CD39 is predominantly expressed by monocytic (macrophage, microglial) populations. t-CyCIF showed enrichment of EGFR, Ki-67, and TP53 expression in CD73-high tumor cells at a single cell level independent of genotype, as well as significant spatial correlation between CD73 expression in tumor cells and CD39 expression in macrophages. MALDI-MSI showed significantly greater adenosine concentrations in glioblastomas with high CD73 expression. CD73 expression significantly correlated with EGFR amplification or C-terminal deletion (EGFRvIII or variants), type-II interferon signaling, and PD-L1 expression in glioblastoma. CONCLUSIONS: Phenogenomic analysis of purinergic signaling in glioblastoma revealed correlations between CD73 expression and genotype, adenosine concentration, and clinical outcome. Spatial analysis revealed interaction between macrophages CD39 expression and tumor cell CD73 expression, suggesting that these populations may interact to suppress anti-tumor immunity. Anti-CD73 therapy may provide therapeutic benefits in glioblastoma by blunting immunosuppressive and oncogenic adenosine signaling. Citation Format: Shannon Coy, Jia-Ren Lin, Shu Wang, Sylwia Stopka, Rumana Rashid, Jaeho Hwang, Prasidda Khadka, Philipp Euskirchen, Pratiti Bandopadhayay, Patrick Y. Wen, Peter K. Sorger, Nathalie Agar, Keith L. Ligon, Mehdi Touat, Sandro Santagata. Phenogenomic characterization of immunomodulatory purinergic signaling in glioblastoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 1816.

Muscular dystrophy is a group of genetic disorders characterised by degeneration of muscles. Different forms of muscular dystrophy can show varying phenotypes with a wide range of age, severity and location of muscle deterioration. Many palliative care options are available for muscular dystrophy patients, but no curative treatment is available. Exon-skipping therapy aims to induce skipping of exons with disease-causing mutations and/or nearby exons to restore the reading frame, which results in an internally truncated, partially functional protein. In antisense-mediated exon-skipping synthetic antisense oligonucleotide binds to pre-mRNA to induce exon skipping. Recent advances in exon skipping have yielded promising results; the US Food and Drug Administration (FDA) approved eteplirsen (Exondys51) as the first exon-skipping drug for the treatment of Duchenne muscular dystrophy, and in vivo exon skipping has been demonstrated in animal models of dysferlinopathy, limb-girdle muscular dystrophy type 2C and congenital muscular dystrophy type 1A. Novel methods that induce exon skipping utilizing Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) are also being developed where splice site mutations are created within the genome to induce exon skipping. Challenges remain as exon-skipping agents can have deleterious non-specific effects and different in-frame deletions show phenotypic variance. This article reviews the state of the art of exon skipping for treating muscular dystrophy and discusses challenges and future prospects.

Supplemental Digital Content is available in the text., Objectives: Current studies lack robust information on the prevalence and associated factors of cerebral microbleeds in patients who underwent extracorporeal membrane oxygenation. Design: Retrospective analysis. Setting: We reviewed patients who underwent (extracorporeal membrane oxygenation) and subsequent brain autopsy with gross and microscopic examinations from January 2009 to December 2018 from a single tertiary center. Patients: Twenty-five extracorporeal membrane oxygenation patients (median age, 53 yr; interquartile range, 36–61 yr; 17 women and 8 men) underwent brain autopsy. Interventions: Descriptive analysis of neuropathologic findings. Cerebral microbleed was defined as a small focus (< 10 mm diameter) of accumulation of blood product in the brain tissue. Macrohemorrhage was defined as any of the grossly identifiable epidural, subdural, subarachnoid, or intraparenchymal hemorrhages larger than 10 mm. Measurement and Main Results: Of 25 (22 venoarterial extracorporeal membrane oxygenation; three venovenous extracorporeal membrane oxygenation), 15 patients (60%) were found to have cerebral microbleeds, whereas 13 (52%) had macrohemorrhages, of whom five (20%) had both. Overall, 92% of brains demonstrated the presence of either cerebral microbleeds or macrohemorrhages after extracorporeal membrane oxygenation support. Of the patients with cerebral microbleeds, lobar cerebral microbleeds (80%) occurred more frequently than deep cerebral microbleeds (60%), with 40% of patients having both types. The cases of macrohemorrhages consisted of one epidural (8%), two subdural (15%), and 10 subarachnoid hemorrhages (77%). In univariate analyses, the presence of macrohemorrhages was significantly associated with the presence of cerebral microbleeds (p = 0.03) with odds ratio of 0.13 (CI, 0.02–0.82). Age, sex, extracorporeal membrane oxygenation duration, extracorporeal membrane oxygenation type, use of aspirin or dialysis during extracorporeal membrane oxygenation support, bloodstream infections, hemoglobin, platelets, and coagulopathy profiles were not associated with cerebral microbleeds. Conclusions: In patients with postmortem neuropathologic evaluation, 92% sustained acute cerebral microbleeds or macrohemorrhages after extracorporeal membrane oxygenation support. Cerebral microbleeds were commonly present in the majority of extracorporeal membrane oxygenation nonsurvivors. Further research is necessary to study the long-term sequelae, such as cognitive outcome of extracorporeal membrane oxygenation-associated cerebral microbleeds in extracorporeal membrane oxygenation survivors.

In order to comply with the Federal Motor Vehicle Safety Standard(FMVSS) No. 208 that has been in force since September 2003, an automatic airbag suppression system has become an essential option for detecting and protecting infants and children seated in the front passenger seat of vehicles in the U.S. market. MOBIS has developed the world’s first weight-based OCS under the name NWCS. NWCS is composed of two sensors and ECU. It is sub-packaged in order to minimize the seat structure deviation. In this paper, technical features, robustness and performance of NWCS are summarized and discussed.

Disseminated glioneuronal tumors of childhood are rare. We present a retrospective IRB-approved review of the clinical course and frequency of BRAF mutations in disseminated glioneuronal tumors at two institutions. Defining features of our cohort include diffuse leptomeningeal-spread, often with a discrete spinal cord nodule and oligodendroglioma-like histologic features. Patients were identified through a pathology database search of all cases with disseminated low-grade neoplasms with an oligodendroglioma-like component. De-identified clinical information was collected by chart review and all imaging was reviewed. We retrieved the results of targeted genomic analyses for alterations in BRAF. Ten patients (aged 2-14 years) were identified from the Dana-Farber/Boston Children's Hospital and the Royal Children's Hospital, Melbourne pathology databases. Nine patients received chemotherapy. Eight patients are alive, although three have had episodes of progressive disease. We identified genomic alterations affecting the MAPK pathway in six patients. One patient had a germline RAF1 mutation and a clinical diagnosis of cardio-facio-cutaneous syndrome. BRAF duplications were identified in four and BRAF V600E mutation was identified in one. These data support the presence of targetable genomic alterations in this disease.

In this paper, a novel data link layer protocol adopted in the ATSC 3.0 terrestrial broadcast standard is described. The data link layer is a protocol layer between the physical layer and the network layer. The data link layer transports data from the network layer to the physical layer at the sending side and transports data from the physical layer to the network layer at the receiving side. The data link layer protocol in ATSC 3.0 is called the ATSC link-layer protocol (ALP). The major function of ALP is to take multiple input formats, not only IP packets but also legacy broadcast formats such as MPEG-2 TS packets, and output them in a common format to the physical layer. ALP provides overhead reduction mechanisms to achieve efficient transmission, particularly the compression of IP/UDP packet headers. The protocol and operation of ALP, as well as efficiency analysis and evaluation of ALP are presented.

Reoperation after breast-conserving surgery (BCS) is common and has been partially associated with the lack of consensus on margin definition. We sought to investigate factors associated with reoperations and variation in reoperation rates across breast surgeons at our cancer center. Retrospective analyses of patients with clinical stage I–II breast cancer who underwent BCS between January and December 2014 were conducted prior to the recommendation of ‘no ink on tumor’ margin. Patient demographics and tumor and surgical data were extracted from medical records. A multivariate regression model was used to identify factors associated with reoperation. Overall, 490 patients with stage I (n = 408) and stage II (n = 89) breast cancer underwent BCS; seven patients had bilateral breast cancer and underwent bilateral BCS procedures. Median invasive tumor size was 1.1 cm, reoperation rate was 22.9% (n = 114) and varied among surgeons (range 15–40%), and, in 100 (88%) patients, the second procedure was re-excision, followed by unilateral mastectomy (n = 7, 6%) and bilateral mastectomy (n = 7, 6%). Intraoperative margin techniques (global cavity or targeted shaves) were utilized in 50.1% of cases, while no specific margin technique was utilized in 49.9% of cases. Median total specimen size was 65.8 cm3 (range 24.5–156.0). In the adjusted model, patients with multifocal disease were more likely to undergo reoperation [odds ratio (OR) 5.78, 95% confidence interval (CI) 2.17–15.42]. In addition, two surgeons were found to have significantly higher reoperation rates (OR 6.41, 95% CI 1.94–21.22; OR 3.41, 95% CI 1.07–10.85). Examination of BCS demonstrated variability in reoperation rates and margin practices among our breast surgeons. Future trials should look at surgeon-specific factors that may predict for reoperations.