92 research outputs found
Online Admission Control and Embedding of Service Chains
The virtualization and softwarization of modern computer networks enables the
definition and fast deployment of novel network services called service chains:
sequences of virtualized network functions (e.g., firewalls, caches, traffic
optimizers) through which traffic is routed between source and destination.
This paper attends to the problem of admitting and embedding a maximum number
of service chains, i.e., a maximum number of source-destination pairs which are
routed via a sequence of to-be-allocated, capacitated network functions. We
consider an Online variant of this maximum Service Chain Embedding Problem,
short OSCEP, where requests arrive over time, in a worst-case manner. Our main
contribution is a deterministic O(log L)-competitive online algorithm, under
the assumption that capacities are at least logarithmic in L. We show that this
is asymptotically optimal within the class of deterministic and randomized
online algorithms. We also explore lower bounds for offline approximation
algorithms, and prove that the offline problem is APX-hard for unit capacities
and small L > 2, and even Poly-APX-hard in general, when there is no bound on
L. These approximation lower bounds may be of independent interest, as they
also extend to other problems such as Virtual Circuit Routing. Finally, we
present an exact algorithm based on 0-1 programming, implying that the general
offline SCEP is in NP and by the above hardness results it is NP-complete for
constant L.Comment: early version of SIROCCO 2015 pape
Vector Bin Packing with Multiple-Choice
We consider a variant of bin packing called multiple-choice vector bin
packing. In this problem we are given a set of items, where each item can be
selected in one of several -dimensional incarnations. We are also given
bin types, each with its own cost and -dimensional size. Our goal is to pack
the items in a set of bins of minimum overall cost. The problem is motivated by
scheduling in networks with guaranteed quality of service (QoS), but due to its
general formulation it has many other applications as well. We present an
approximation algorithm that is guaranteed to produce a solution whose cost is
about times the optimum. For the running time to be polynomial we
require and . This extends previous results for vector
bin packing, in which each item has a single incarnation and there is only one
bin type. To obtain our result we also present a PTAS for the multiple-choice
version of multidimensional knapsack, where we are given only one bin and the
goal is to pack a maximum weight set of (incarnations of) items in that bin
An EPTAS for scheduling jobs on uniform processors using an MILP relaxation with a constant number of integral variables
We present an efficient polynomial time approximation scheme (EPTAS) for scheduling on uniform processors, i.e. finding a minimum length schedule for a set of n independent jobs on m processors with different speeds (a fundamental NP-hard scheduling problem). The previous best polynomial time approximation scheme (PTAS) by Hochbaum and Shmoys has a running time of (n/\epsilon)^{O(1/\epsilon^2)}. Our algorithm, based on a new mixed integer linear programming (MILP) formulation with a constant number of integral variables and an interesting rounding method, finds a schedule whose length is within a relative error of the optimum, and has running time 2^{O(1/\epsilon^2 \log(1/\epsilon)^3)} + poly(n)
The balance of power: accretion and feedback in stellar mass black holes
In this review we discuss the population of stellar-mass black holes in our
galaxy and beyond, which are the extreme endpoints of massive star evolution.
In particular we focus on how we can attempt to balance the available accretion
energy with feedback to the environment via radiation, jets and winds,
considering also possible contributions to the energy balance from black hole
spin and advection. We review quantitatively the methods which are used to
estimate these quantities, regardless of the details of the astrophysics close
to the black hole. Once these methods have been outlined, we work through an
outburst of a black hole X-ray binary system, estimating the flow of mass and
energy through the different accretion rates and states. While we focus on
feedback from stellar mass black holes in X-ray binary systems, we also
consider the applicability of what we have learned to supermassive black holes
in active galactic nuclei. As an important control sample we also review the
coupling between accretion and feedback in neutron stars, and show that it is
very similar to that observed in black holes, which strongly constrains how
much of the astrophysics of feedback can be unique to black holes.Comment: To be published in Haardt et al. Astrophysical Black Holes. Lecture
Notes in Physics. Springer 201
Para-infectious brain injury in COVID-19 persists at follow-up despite attenuated cytokine and autoantibody responses
To understand neurological complications of COVID-19 better both acutely and for recovery, we measured markers of brain injury, inflammatory mediators, and autoantibodies in 203 hospitalised participants; 111 with acute sera (1–11 days post-admission) and 92 convalescent sera (56 with COVID-19-associated neurological diagnoses). Here we show that compared to 60 uninfected controls, tTau, GFAP, NfL, and UCH-L1 are increased with COVID-19 infection at acute timepoints and NfL and GFAP are significantly higher in participants with neurological complications. Inflammatory mediators (IL-6, IL-12p40, HGF, M-CSF, CCL2, and IL-1RA) are associated with both altered consciousness and markers of brain injury. Autoantibodies are more common in COVID-19 than controls and some (including against MYL7, UCH-L1, and GRIN3B) are more frequent with altered consciousness. Additionally, convalescent participants with neurological complications show elevated GFAP and NfL, unrelated to attenuated systemic inflammatory mediators and to autoantibody responses. Overall, neurological complications of COVID-19 are associated with evidence of neuroglial injury in both acute and late disease and these correlate with dysregulated innate and adaptive immune responses acutely
SARS-CoV-2-specific nasal IgA wanes 9 months after hospitalisation with COVID-19 and is not induced by subsequent vaccination
BACKGROUND: Most studies of immunity to SARS-CoV-2 focus on circulating antibody, giving limited insights into mucosal defences that prevent viral replication and onward transmission. We studied nasal and plasma antibody responses one year after hospitalisation for COVID-19, including a period when SARS-CoV-2 vaccination was introduced. METHODS: In this follow up study, plasma and nasosorption samples were prospectively collected from 446 adults hospitalised for COVID-19 between February 2020 and March 2021 via the ISARIC4C and PHOSP-COVID consortia. IgA and IgG responses to NP and S of ancestral SARS-CoV-2, Delta and Omicron (BA.1) variants were measured by electrochemiluminescence and compared with plasma neutralisation data. FINDINGS: Strong and consistent nasal anti-NP and anti-S IgA responses were demonstrated, which remained elevated for nine months (p < 0.0001). Nasal and plasma anti-S IgG remained elevated for at least 12 months (p < 0.0001) with plasma neutralising titres that were raised against all variants compared to controls (p < 0.0001). Of 323 with complete data, 307 were vaccinated between 6 and 12 months; coinciding with rises in nasal and plasma IgA and IgG anti-S titres for all SARS-CoV-2 variants, although the change in nasal IgA was minimal (1.46-fold change after 10 months, p = 0.011) and the median remained below the positive threshold determined by pre-pandemic controls. Samples 12 months after admission showed no association between nasal IgA and plasma IgG anti-S responses (R = 0.05, p = 0.18), indicating that nasal IgA responses are distinct from those in plasma and minimally boosted by vaccination. INTERPRETATION: The decline in nasal IgA responses 9 months after infection and minimal impact of subsequent vaccination may explain the lack of long-lasting nasal defence against reinfection and the limited effects of vaccination on transmission. These findings highlight the need to develop vaccines that enhance nasal immunity. FUNDING: This study has been supported by ISARIC4C and PHOSP-COVID consortia. ISARIC4C is supported by grants from the National Institute for Health and Care Research and the Medical Research Council. Liverpool Experimental Cancer Medicine Centre provided infrastructure support for this research. The PHOSP-COVD study is jointly funded by UK Research and Innovation and National Institute of Health and Care Research. The funders were not involved in the study design, interpretation of data or the writing of this manuscript
Large-scale phenotyping of patients with long COVID post-hospitalization reveals mechanistic subtypes of disease
One in ten severe acute respiratory syndrome coronavirus 2 infections result in prolonged symptoms termed long coronavirus disease (COVID), yet disease phenotypes and mechanisms are poorly understood1. Here we profiled 368 plasma proteins in 657 participants ≥3 months following hospitalization. Of these, 426 had at least one long COVID symptom and 233 had fully recovered. Elevated markers of myeloid inflammation and complement activation were associated with long COVID. IL-1R2, MATN2 and COLEC12 were associated with cardiorespiratory symptoms, fatigue and anxiety/depression; MATN2, CSF3 and C1QA were elevated in gastrointestinal symptoms and C1QA was elevated in cognitive impairment. Additional markers of alterations in nerve tissue repair (SPON-1 and NFASC) were elevated in those with cognitive impairment and SCG3, suggestive of brain–gut axis disturbance, was elevated in gastrointestinal symptoms. Severe acute respiratory syndrome coronavirus 2-specific immunoglobulin G (IgG) was persistently elevated in some individuals with long COVID, but virus was not detected in sputum. Analysis of inflammatory markers in nasal fluids showed no association with symptoms. Our study aimed to understand inflammatory processes that underlie long COVID and was not designed for biomarker discovery. Our findings suggest that specific inflammatory pathways related to tissue damage are implicated in subtypes of long COVID, which might be targeted in future therapeutic trials
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