Power management is one of the key research challenges on the path to exascale. Supercomputers today are designed to be worst-case power provisioned, leading to two main problems-limited application performance and under-utilization of procured power. In this paper, we propose RMAP, a practical, low-overhead resource manager targeted at future power-constrained clusters. The goals for RMAP are to improve application performance as well as system power utilization, and thus minimize the average turnaround time for all jobs. Within RMAP, we design and analyze an adaptive policy, which derives job-level power bounds in a fair-share manner and supports overprovisioning and power-aware backfilling. Our results show that our new policy increases system power utilization while adhering to strict job-level power bounds and leads to 31.2% (18.5% on average) and 53.8% (36.07% on average) faster average turnaround time when compared to worst-case provisioning and naive overprovisioning respectively.

Picornaviruses including Enterovirus species A-D (EV) and Parechovirus species A (PeV-A) are the leading reported causes of pediatric central nervous system infections in the United States. We investigated the molecular epidemiology of EV and PeV-A over 10 years, in cerebrospinal fluid (CSF) collected from children seen at Children’s Mercy -Kansas City (CMKC) during 2007 through 2016. The overall prevalence for EV was 16% (862/5362) and 7% (271/4016) for PeV. Among all picornavirus CSF detections EV was 76% and PeV-A was 24%. Multiple EV types co-circulated each year with a total of 31 EV types detected in the 10-year period; majority belonged to EV-B species (96%). Two PeV-A types were detected; PeV-A3 was the dominant PeV-A type (95%). Top five picornaviruses (PeV-A3, 26%; E30, 11%; E6 10%; E18 9%, E9 7%) in the CSF of infants accounted for two-third of all detections and PeV-A3 was the leading picornavirus detected. Routine testing and reporting of PeV-A in addition to EV, especially in children under 6 months old with acute febrile illnesses, could reduce hospital stays and antibiotic usage.

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Pediatric saliva specimen demonstrated high sensitivity (93%) and specificity (96.2%) compared to paired nasopharyngeal swabs (NPS) by Aptima SARS-CoV-2 Assay (Aptima). Viral loads were comparable in both specimen types. Saliva is a safe, noninvasive, and acceptable alternative specimen for SARS-CoV-2 detection in children.

Background Enterovirus (EV) and Parechovirus type A3 (PeV-A3) cause infections ranging from asymptomatic to life-threatening. Host immune responses in children, particularly innate responses to PeV-A3, remain largely unknown. The aim of this study was to determine aspects of the cytokine/chemokine responses to EV and PeV-A3 in cerebrospinal fluid (CSF) and plasma obtained from children with systemic/central nervous system infection. Methods A total of 74 salvaged CSF samples (27 with EV, 23 PeV-A3, and 24 neither EV nor PeV-A3) and 35 paired blood samples (10 EV, 14 PeV-A3, and 11 neither) were studied. Concentrations of cytokines and chemokines were measured using a customized 21-plex MILLIPLEX MAP® Human Cytokine/Chemokine Magnetic Bead Panel. Additionally, clinical characteristics data for all the patients were collected from Electronic Medical Records to evaluate the potential association between the immune response and presentations. Results We demonstrate that EV and PeV-A3 infections induce different cytokine/chemokine immune responses in children. EV induces more robust responses in CSF with significantly elevated levels of fractalkine, IFN-α2, IFN-γ, IL-1Rα, IL-4, IL-8, and TNF-α ; PeV-A3 induces less robust or absent responses in CSF but robust responses in plasma with significantly higher concentrations of IFN-α2, IL-15, IL-1Rα, IP-10, and MCP-1 . Conclusions High cytokine/chemokine concentrations in plasma of PeV-A3 patients compared to EV patients could explain higher/more prolonged fever in PeV-A3 patients, whereas relatively low cytokine/chemokine concentrations in PeV-A3 CSF might explain the absence of CSF pleocytosis.