A Control Plane Enabling Automated and Fully Adaptive Network Traffic Monitoring With eBPF

The extended Berkeley Packet Filter (eBPF) enables the dynamic injection of user-defined processing logic at run-time in the Linux networking stack without disrupting any active monitoring process. This enables the selective extraction of only the traffic features that are needed in a given instant of time, which is what we define fully adaptive network traffic monitoring. However, eBPF programs require ad-hoc control plane routines for each specific scenario in order to orchestrate the underlying data plane and export the required metrics, resulting in potentially duplicated source codes to maintain, and creating the risk of deploying, at runtime, unverified user-defined code that controls the devices running the monitoring process. This paper presents a control plane that automatically adapts both its management tasks and data extraction methodologies based on the underlying data plane provided by the user, who can merely focus on the monitoring logic definition. The paper evaluates the performance of the control plane's modules and demonstrates the advantages, in terms of processing speed and memory consumption, of a fully-adaptive monitoring approach with respect to nProbe (a state-of-the-art solution), an adaptive and a non-adaptive methodology in eBPF. Experiments prove that the control plane monitoring options do not significantly affect the underlying data plane (0.15% degraded throughput) and leverage the most efficient extraction primitives (20x faster execution time). Moreover, the fully-adaptive monitoring leads to a higher number of processed packets (10x) and significantly lower memory occupancy (10x) when extracting the smallest set of features

Collagen Content in Skin and Internal Organs of the Tight Skin Mouse: An Animal Model of Scleroderma.

The Tight Skin mouse is a genetically induced animal model of tissue fibrosis caused by a large in-frame mutation in the gene encoding fibrillin-1 (Fbn-1). We examined the influence of gender on the collagen content of tissues in C57BL/6J wild type (+/+) and mutant Tight Skin (Tsk/+) mice employing hydroxyproline assays. Tissue sections were stained with Masson\u27s trichrome to identify collagen in situ. Adult Tsk/+ mice skin contains ~15% more collagen, on average, than skin from +/+ mice of the same gender. The heart of Tsk/+ males had significantly more collagen than that of +/+ males. No significant gender differences were found in lungs and kidney collagen content. Overall, the collagen content of Tsk/+ males and +/+ males was higher than that of their Tsk/+ and +/+ female counterparts, respectively. Our data confirm increased deposition of collagen in skin and hearts of Tsk/+ mice; however, the effects of the Tsk mutation on collagen content are both tissue specific and gender specific. These results indicate that comparative studies of collagen content between normal and Tsk/+ mice skin and internal organs must take into account gender differences caused by expression of the androgen receptor

A tandem duplication within the fibrillin 1 gene is associated with the mouse tight skin mutation.

Mice carrying the Tight skin (Tsk) mutation have thickened skin and visceral fibrosis resulting from an accumulation of extracellular matrix molecules. These and other connective tissue abnormalities have made Tskl + mice models for scleroderma, hereditary emphysema, and myocardial hypertrophy. Previously we localized Tsk to mouse chromosome 2 in a region syntenic with human chromosome 15. The microfibrillar glycoprotein gene, fibrillin 1 (FBN1), on human chromosome 15q, provided a candidate for the Tsk mutation. We now demonstrate that the Tsk chromosome harbors a 30- to 40-kb genomic duplication within the Fbn1 gene that results in a larger than normal in-frame Fbn1 transcript. These findings provide hypotheses to explain some of the phenotypic characteristics of Tskl + mice and the lethality of Tsk/Tsk embryos

Optical Backplane Based on Ring-Resonators: Scalability and Performance Analysis for 10Gb/s OOK-NRZ

The use of architectures that implement optical switching without any need of optoelectronic conversion allows us to overcome the limits imposed by today’s electronic backplane, such as power consumption and dissipation, as well as power supply and footprint requirements. We propose a ring-resonator based optical backplane for router line-card interconnection. In particular we investigate how the scalability of the architecture is affected by the following parameters: number of line cards, switching-element round-trip losses, frequency drifting due to thermal variations, and waveguide-crossing effects. Moreover, to quantify the signal distortions introduced by filtering operations, the bit error rate for the different parameter conditions are shown in case of an on-off keying non-return-to-zero (OOK-NRZ) input signal at 10 Gb/s

The tight skin mouse: demonstration of mutant fibrillin-1 production and assembly into abnormal microfibrils

Mice carrying the Tight skin (Tsk) mutation harbor a genomic duplication within the fibrillin-1 (Fbn 1) gene that results in a larger than normal in-frame Fbn 1 transcript. In this study, the consequences of the Tsk mutation for fibrillin-containing microfibrils have been examined. Dermal fibroblasts from Tsk/+ mice synthesized and secreted both normal fibrillin (approximately 330 kD) and the mutant oversized Tsk fibrillin-1 (approximately 450 kD) in comparable amounts, and Tsk fibrillin-1 was stably incorporated into cell layers. Immunohistochemical and ultrastructural analyses of normal and Tsk/+ mouse skin highlighted differences in the gross organization and distribution of microfibrillar arrays. Rotary shadowing of high Mr preparations from Tsk/+ skin demonstrated the presence of abundant beaded microfibrils. Some of these had normal morphology and periodicity, but others were distinguished by diffuse interbeads, longer periodicity, and tendency to aggregate. The presence of a structurally abnormal population of microfibrils in Tsk/+ skin was unequivocally demonstrated after calcium chelation and in denaturating conditions. Scanning transmission electron microscopy highlighted the presence of more mass in Tsk/+ skin microfibrils than in normal mice skin microfibrils. These data indicate that Tsk fibrillin-1 polymerizes and becomes incorporated into a discrete population of beaded microfibrils with altered molecular organization