Inference of virtual network functions' state via analysis of the CPU behavior

The on-going process of softwarization of IT networks promises to reduce the operational and management costs of network infrastructures by replacing hardware middleboxes with equivalent pieces of code executed on general-purpose servers. Alongside the benefits from the operator’s perspective, new strategies to provide the network’s resources to users are arising. Following the principle of “everything as a service”, multiple tenants can access the required resources – typically CPUs, NICs, or RAM – according to a Service-Level Agreement. However, tenants’ applications may require a complex and expensive measurement infrastructure to continuously monitor the network function’s state. Although the application’s specific behavior is unknown (and often opaque to the infrastructure owner), the software nature of (virtual) network functions (VNFs) may be the key to infer the behavior of the high-level functions by accessing low-level information, which is still under the control of the operating system and therefore of the infrastructure owner. As such, in the scenario of software VNFs executed on COTS servers, the underlying CPU’s behavior can be used as the sole predictor for the high-level VNF state without explicit in-network measurements: in this paper, we develop a novel methodology to infer high-level characteristics such as throughput or packet loss using CPU data instead of network measurements. Our methodology consists of (i) experimentally analyzing the behavior of a CPU that executes a VNF under different loads, (ii) extracting a correlation between the CPU footprint and the highlevel application state, and (iii) use this knowledge to detect the previously mentioned network metrics. Our code and datasets are publicly available

On the Learnability of Software Router Performance via CPU Measurements

In the last decade the ICT community observed a growing popularity of software networking paradigms. This trend consists in moving network applications from static, expensive, hardware equipment (e.g. router, switches, firewalls) towards flexible, cheap pieces of software that are executed on a commodity server. In this context, a server owner may provide the server resources (CPUs, NICs, RAM) for customers, following a Service-Level Agreement (SLA) about clients' requirements. The problem of resource allocation is typically solved by overprovisioning, as the clients' application is opaque to the server owner, and the resource required by clients' applications are often unclear or very difficult to quantify. This paper shows a novel approach that exploits machine learning techniques in order to infer the input traffic load (i.e., the expected network traffic condition) by solely looking at the runtime CPU footprint

MSH3 polymorphisms and protein levels affect CAG repeat instability in huntington's disease mice

Expansions of trinucleotide CAG/CTG repeats in somatic tissues are thought to contribute to ongoing disease progression through an affected individual's life with Huntington's disease or myotonic dystrophy. Broad ranges of repeat instability arise between individuals with expanded repeats, suggesting the existence of modifiers of repeat instability. Mice with expanded CAG/CTG repeats show variable levels of instability depending upon mouse strain. However, to date the genetic modifiers underlying these differences have not been identified. We show that in liver and striatum the R6/1 Huntington's disease (HD) (CAG)~100 transgene, when present in a congenic C57BL/6J (B6) background, incurred expansion-biased repeat mutations, whereas the repeat was stable in a congenic BALB/cByJ (CBy) background. Reciprocal congenic mice revealed the Msh3 gene as the determinant for the differences in repeat instability. Expansion bias was observed in congenic mice homozygous for the B6 Msh3 gene on a CBy background, while the CAG tract was stabilized in congenics homozygous for the CBy Msh3 gene on a B6 background. The CAG stabilization was as dramatic as genetic deficiency of Msh2. The B6 and CBy Msh3 genes had identical promoters but differed in coding regions and showed strikingly different protein levels. B6 MSH3 variant protein is highly expressed and associated with CAG expansions, while the CBy MSH3 variant protein is expressed at barely detectable levels, associating with CAG stability. The DHFR protein, which is divergently transcribed from a promoter shared by the Msh3 gene, did not show varied levels between mouse strains. Thus, naturally occurring MSH3 protein polymorphisms are modifiers of CAG repeat instability, likely through variable MSH3 protein stability. Since evidence supports that somatic CAG instability is a modifier and predictor of disease, our data are consistent with the hypothesis that variable levels of CAG instability associated with polymorphisms of DNA repair genes may have prognostic implications for various repeat-associated diseases

Severe leukoencephalopathy with fulminant cerebral edema reflecting immune reconstitution inflammatory syndrome during HIV infection: a case report

<p>Abstract</p> <p>Introduction</p> <p>Immune reconstitution inflammatory syndrome is a well-known complication in HIV-infected patients after initiation of highly active antiretroviral therapy resulting in rapid CD4⁺cell count recovery and suppression of viral load. Generally, immune reconstitution inflammatory syndrome is based on opportunistic infections, but rare cases of immune reconstitution inflammatory syndrome inducing demyelinization of the nervous system have also been observed.</p> <p>Case presentation</p> <p>A 37-year-old African woman with HIV infection diagnosed at 13 years of age was admitted to the emergency department after experiencing backache, severe headache, acute aphasia and psychomotor slowing for one week. Nine weeks earlier, highly active antiretroviral therapy in this patient had been changed because of loss of efficacy, and a rapid increase in CD4⁺cell count and decrease of HIV viral load were observed. Magnetic resonance imaging of the brain showed extensive white matter lesions, and analysis of cerebrospinal fluid revealed an immunoreactive syndrome. Intensive investigations detected no opportunistic infections. A salvage therapy, including osmotherapy, corticosteroids and treatment of epileptic seizures, was performed, but the patient died from brainstem herniation 48 hours after admission. Neuropathologic examination of the brain revealed diffuse swelling, leptomeningeal infiltration by CD8 cells and enhancement of perivascular spaces by CD8+ cells.</p> <p>Conclusion</p> <p>Immune reconstitution inflammatory syndrome in this form seems to represent a severe autoimmunologic disease of the brain with specific histopathologic findings. This form of immune reconstitution inflammatory syndrome did not respond to therapy, and extremely rapid deterioration led to death within two days. Immune reconstitution inflammatory syndrome may also occur as severe leukoencephalopathy with fulminant cerebral edema during HIV infection with rapid immune reconstitution.</p

Isometry of medial collateral ligament reconstruction

The purpose of this study was to determine the femoral and tibial fixation sites that would result in the most isometric MCL reconstruction technique. Seven cadaveric knees were used in this study. A navigation system was utilized to determine graft isometry continuously from 0º to 90º. Five points on the medial side of the femur and four on the tibia were tested. A graft positioned in the center of the MCL femoral attachment (FC) and attached in the center of the superficial MCL attachment on the tibia led to the best isometry (2.7 ± 1.1 mm). Movement of the origin superiorly only 4 mm (FS) led to graft excursion of greater than 10 mm (P < 0.01). MCL reconstruction performed with the origin of the MCL within the femoral footprint and the insertion in tibial footprint of the superficial MCL results in the least graft excursion when the knee is cycled between 0º and 90º. Although the MCL often heals without surgical intervention, surgical reconstruction is occasionally in Grade III MCL and combined ligamentous injuries to the knee. This study demonstrates the optimal position of the MCL reconstruction to reproduce the kinematics of the native knee

High-intensity mechanical therapy for loss of knee extension for worker's compensation and non-compensation patients

<p>Abstract</p> <p>Background</p> <p>Knee flexion contractures have been associated with increased pain and a reduced ability to perform activities of daily living. Contractures can be treated either surgically or conservatively, but these treatment options may not be as successful with worker's compensation patients. The purposes of retrospective review were to 1) determine the efficacy of using adjunctive high-intensity stretch (HIS) mechanical therapy to treat flexion contractures, and 2) compare the results between groups of worker's compensation and non-compensation patients.</p> <p>Methods</p> <p>Fifty-six patients (19 women, 37 men, age = 51.5 ± 17.0 years) with flexion contractures were treated with HIS mechanical therapy as an adjunct to outpatient physical therapy. Mechanical therapy was only prescribed for those patients whose motion had reached a plateau when treated with physical therapy alone. Patients were asked to perform six, 10-minute bouts of end-range stretching per day with the ERMI Knee Extensionater^(r)(ERMI, Inc., Atlanta, GA). Passive knee extension was recorded during the postoperative visit that mechanical therapy was prescribed, 3 months after beginning mechanical therapy, and at the most recent follow-up. We used a mixed-model 2 × 3 ANOVA (group × time) to evaluate the change in passive knee extension between groups over time.</p> <p>Results</p> <p>Regardless of group, the use of adjunctive HIS mechanical therapy resulted in passive knee extension deficits that significantly improved from 10.5° ± 5.2° at the initial visit to 2.6° ± 3.5° at the 3 month visit (p < 0.001). The degree of extension was maintained at the most recent follow-up (2.0° ± 2.9°), which was significantly greater than the initial visit (p < 0.001), but did not differ from the 3 month visit (p = 0.23). The gains in knee extension did not differ between worker's compensation and non-compensation patients (p = 0.56).</p> <p>Conclusions</p> <p>We conclude that the adjunctive use of HIS mechanical therapy is an effective treatment option for patients with knee flexion contractures, regardless of whether the patient is being treated as part of a worker's compensation claim or not.</p

Minimum joint space width and tibial cartilage morphology in the knees of healthy individuals: A cross-sectional study

<p>Abstract</p> <p>Background</p> <p>The clinical use of minimum joint space width (mJSW) and cartilage volume and thickness has been limited to the longitudinal measurement of disease progression (i.e. change over time) rather than the diagnosis of OA in which values are compared to a standard. This is primarily due to lack of establishment of normative values of joint space width and cartilage morphometry as has been done with bone density values in diagnosing osteoporosis. Thus, the purpose of this pilot study is to estimate reference values of medial joint space width and cartilage morphometry in healthy individuals of all ages using standard radiography and peripheral magnetic resonance imaging.</p> <p>Design</p> <p>For this cross-sectional study, healthy volunteers underwent a fixed-flexion knee X-ray and a peripheral MR (pMR) scan of the same knee using a 1T machine (ONI OrthOne™, Wilmington, MA). Radiographs were digitized and analyzed for medial mJSW using an automated algorithm. Only knees scoring ≤1 on the Kellgren-Lawrence scale (no radiographic evidence of knee OA) were included in the analyses. All 3D SPGRE fat-sat sagittal pMR scans were analyzed for medial tibial cartilage morphometry using a proprietary software program (Chondrometrics GmbH).</p> <p>Results</p> <p>Of 119 healthy participants, 73 were female and 47 were male; mean (SD) age 38.2 (13.2) years, mean BMI 25.0 (4.4) kg/m². Minimum JSW values were calculated for each sex and decade of life. Analyses revealed mJSW did not significantly decrease with increasing decade (p > 0.05) in either sex. Females had a mean (SD) medial mJSW of 4.8 (0.7) mm compared to males with corresponding larger value of 5.7 (0.8) mm. Cartilage morphometry results showed similar trends with mean (SD) tibial cartilage volume and thickness in females of 1.50 (0.19) μL/mm²and 1.45 (0.19) mm, respectively, and 1.77 (0.24) μL/mm²and 1.71 (0.24) mm, respectively, in males.</p> <p>Conclusion</p> <p>These data suggest that medial mJSW values do not decrease with aging in healthy individuals but remain fairly constant throughout the lifespan with "healthy" values of 4.8 mm for females and 5.7 mm for males. Similar trends were seen for cartilage morphology. Results suggest there may be no need to differentiate a t-score and a z-score in OA diagnosis because cartilage thickness and JSW remain constant throughout life in the absence of OA.</p

Management of anterior cruciate ligament rupture in patients aged 40 years and older

The aim of anterior cruciate ligament (ACL) reconstruction is essentially to restore functional stability of the knee and to allow patients to return to their desired work and activities. While in the young and active population, surgery is often the best therapeutic option after an ACL tear, ACL reconstruction in middle-aged people is rather more controversial due to concerns about a higher complication rate. The purpose of our article is to establish, through a systematic review of the literature, useful decision-making criteria for the management of anterior cruciate ligament rupture in patients aged 40 years and older, guiding surgeons to the most appropriate therapeutic approach. Various reports have shown excellent results of ACL reconstruction in patients over the age of 40 in terms of subjective satisfaction, return to previous activity level, and reduced complication and failure rates. Some even document excellent outcomes in subjects of 50 years and older. Although there are limited high-level studies, data reported in the literature suggest that ACL reconstruction can be successful in appropriately selected, motivated older patients with symptomatic knee instability who want to return to participating in highly demanding sport and recreational activities. Deciding factors are based on occupation, sex, activity level of the subject, amount of time spent performing such highly demanding activities, and presence of associated knee lesions. Physiological age and activity level are more important than chronological age as deciding factors when considering ACL reconstruction

Quantification of Age-Dependent Somatic CAG Repeat Instability in Hdh CAG Knock-In Mice Reveals Different Expansion Dynamics in Striatum and Liver

Age at onset of Huntington's disease (HD) is largely determined by the CAG trinucleotide repeat length in the HTT gene. Importantly, the CAG repeat undergoes tissue-specific somatic instability, prevalent in brain regions that are disease targets, suggesting a potential role for somatic CAG repeat instability in modifying HD pathogenesis. Thus, understanding underlying mechanisms of somatic CAG repeat instability may lead to discoveries of novel therapeutics for HD. Investigation of the dynamics of the CAG repeat size changes over time may provide insights into the mechanisms underlying CAG repeat instability.To understand how the HTT CAG repeat length changes over time, we quantified somatic instability of the CAG repeat in Huntington's disease CAG knock-in mice from 2-16 months of age in liver, striatum, spleen and tail. The HTT CAG repeat in spleen and tail was very stable, but that in liver and striatum expanded over time at an average rate of one CAG per month. Interestingly, the patterns of repeat instability were different between liver and striatum. Unstable CAG repeats in liver repeatedly gained similar sizes of additional CAG repeats (approximately two CAGs per month), maintaining a distinct population of unstable repeats. In contrast, unstable CAG repeats in striatum gained additional repeats with different sizes resulting in broadly distributed unstable CAG repeats. Expanded CAG repeats in the liver were highly enriched in polyploid hepatocytes, suggesting that the pattern of liver instability may reflect the restriction of the unstable repeats to a unique cell type.Our results are consistent with repeat expansion occurring as a consequence of recurrent small repeat insertions that differ in different tissues. Investigation of the specific mechanisms that underlie liver and striatal instability will contribute to our understanding of the relationship between instability and disease and the means to intervene in this process