Tracking Cyber Adversaries with Adaptive Indicators of Compromise

A forensics investigation after a breach often uncovers network and host indicators of compromise (IOCs) that can be deployed to sensors to allow early detection of the adversary in the future. Over time, the adversary will change tactics, techniques, and procedures (TTPs), which will also change the data generated. If the IOCs are not kept up-to-date with the adversary's new TTPs, the adversary will no longer be detected once all of the IOCs become invalid. Tracking the Known (TTK) is the problem of keeping IOCs, in this case regular expressions (regexes), up-to-date with a dynamic adversary. Our framework solves the TTK problem in an automated, cyclic fashion to bracket a previously discovered adversary. This tracking is accomplished through a data-driven approach of self-adapting a given model based on its own detection capabilities. In our initial experiments, we found that the true positive rate (TPR) of the adaptive solution degrades much less significantly over time than the naive solution, suggesting that self-updating the model allows the continued detection of positives (i.e., adversaries). The cost for this performance is in the false positive rate (FPR), which increases over time for the adaptive solution, but remains constant for the naive solution. However, the difference in overall detection performance, as measured by the area under the curve (AUC), between the two methods is negligible. This result suggests that self-updating the model over time should be done in practice to continue to detect known, evolving adversaries.Comment: This was presented at the 4th Annual Conf. on Computational Science & Computational Intelligence (CSCI'17) held Dec 14-16, 2017 in Las Vegas, Nevada, US

A Riemann solver at a junction compatible with a homogenization limit

We consider a junction regulated by a traffic lights, with n incoming roads and only one outgoing road. On each road the Phase Transition traffic model, proposed in [6], describes the evolution of car traffic. Such model is an extension of the classic Lighthill-Whitham-Richards one, obtained by assuming that different drivers may have different maximal speed. By sending to infinity the number of cycles of the traffic lights, we obtain a justification of the Riemann solver introduced in [9] and in particular of the rule for determining the maximal speed in the outgoing road.Comment: 19 page

コウホ イデンシ アプローチ ニ ヨル SKT KIAA1217 ト ヨウツイ ツイカンバン ヘルニア ト ノ ソウカン カイセキ

SktのヒトホモログであるKIAA1217(SKT)をLDH の疾患感受性遺伝子の候補遺伝子と考え、ケース・コントロール相関解析を行うことにより、SKT がLDH の疾患感受性遺伝子である可能性を明らかにする事を目的とした

The remaining teres minor and subscapularis may contribute to preventing superior migration of the humeral head and progression of osteoarthritic change in rotator cuff tears

Background: Superior migration of the humeral head is common in large and massive rotator cuff tears (RCTs). Humeral heads migrate superiorly according to an increase in the RCT size; however, the relevance of the remaining cuff has not been elucidated. This study investigated the relation between superior migration of the humeral head and the remaining rotator cuff, especially the teres minor (TM) and subscapularis (SSC), in RCTs involving tears and atrophy of the infraspinatus (ISP). Methods: Plain anteroposterior radiographic and magnetic resonance imaging examinations were performed on 1345 patients between January 2013 and March 2018. A total of 188 shoulders with tears of the supraspinatus and ISP with atrophic ISP were evaluated. Gradings of superior migration of the humeral head and osteoarthritic change were evaluated using the acromiohumeral interval, Oizumi classification, and Hamada classification on plain anteroposterior radiographs. The cross-sectional area of the remaining rotator cuff muscles was evaluated using oblique sagittal magnetic resonance imaging. The TM was classified as hypertrophic (H) and normal and atrophic (NA). The SSC was classified as nonatrophic (N) and atrophic (A). All shoulders were classified as groups A (H-N), B (NA-N), C (H-A), and D (NA-A). Age- and sex-matched patients with no cuff tears were also enrolled (control). Results: The acromiohumeral intervals of the control group and groups A-D were 11.4 ± 2.4, 9.5 ± 3.8, 7.8 ± 4.1, 7.2 ± 4.0, and 5.4 ± 3.5 mm (84, 74, 64, 21, and 29 shoulders, respectively), with significant differences between groups A and D (P < .001) and groups B and D (P = .016). Grade 3 of the Oizumi classification and grades 3, 4, and 5 of the Hamada classification were significantly higher in group D than in others (P < .001). Conclusion: The group showing hypertrophic TM and nonatrophic SSC prevented significantly migration of the humeral head and cuff tear osteoarthritis compared to the group showing atrophic TM and SSC in posterosuperior RCTs. The findings indicate that the remaining TM and SSC may prevent superior migration of the humeral head and progression of osteoarthritic change in RCTs. In treating patients with large and massive posterosuperior RCTs, the status of the remaining TM and SSC muscles should be assessed

Role of Scx+/Sox9+ cells as potential progenitor cells for postnatal supraspinatus enthesis formation and healing after injury in mice.

A multipotent cell population co-expressing a basic-helix-loop-helix transcription factor scleraxis (Scx) and SRY-box 9 (Sox9) has been shown to contribute to the establishment of entheses (tendon attachment sites) during mouse embryonic development. The present study aimed to investigate the involvement of Scx+/Sox9+ cells in the postnatal formation of fibrocartilaginous entheses and in the healing process after injury, using ScxGFP transgenic mice. We demonstrate that Scx+/Sox9+ cells are localized in layers at the insertion site during the postnatal formation of fibrocartilaginous entheses of supraspinatus tendon until postnatal 3 weeks. Further, these cells were rarely seen at postnatal 6 weeks, when mature fibrocartilaginous entheses were formed. Furthermore, we investigated the involvement of Scx+/Sox9+ cells in the healing process after supraspinatus tendon enthesis injury, comparing the responses of 20- and 3-week-old mice. In the healing process of 20-week-old mice with disorganized fibrovascular tissue in response to injury, a small number of Scx+/Sox9+ cells transiently appeared from 1 week after injury, but they were rarely seen at 4 weeks after injury. Meanwhile, in 3-week-old mice, a thin layer of fibrocartilaginous tissue with calcification was formed at healing enthesis at 4 weeks after injury. From 1 to 2 weeks after injury, more Scx+/Sox9+ cells, widely distributed at the injured site, were seen compared with the 20-week-old mice. At 4 weeks after injury, these cells were located near the surface of the recreated fibrocartilaginous layer. This spatiotemporal localization pattern of Scx+/Sox9+ cells at the injured enthesis in our 3-week-old mouse model was similar to that in postnatal fibrocartilaginous enthesis formation. These findings indicate that Scx+/Sox9+ cells may have a role as entheseal progenitor-like cells during postnatal maturation of fibrocartilaginous entheses and healing after injury in a manner similar to that seen in embryonic development

TGF-β1 ワ ケン サイボウ ケイフ ノ ゾウフク オ トモナワズ ニ サイボウ ガイ キシツ ノ チクセキ オ カイシテ ラット ケンバン シュウフク モデル ノ リキガク キョウド オ ジョウショウ サセル

熊本大

Association of the Tag SNPs in the Human SKT Gene (KIAA1217) With Lumbar Disc Herniation

Lumbar disc herniation (LDH) is one of the most common musculo-skeletal diseases. Recent studies have indicated that LDH has strong genetic determinants, and several susceptibility genes have been reported to associate with LDH; however, its etiology and pathogenesis still remain unclear. KIAA1217 (alias SKT, the human homolog of murine Skt [Sickle tail]) is a good candidate for an LDH susceptibility gene because SKT is specifically expressed in nucleus pulposa of intervertebral discs (IVDs) in humans and mice, and SktGt mice, which are established through a large-scale gene-trap mutagenesis, exhibit progressive, postnatal onset abnormality of the IVDs. Here, we report the association of SKT with LDH. Using tag SNPs, we examined the association in two independent Japanese case-control populations and found a significant association with SKT rs16924573 in the allele frequency model (p = 0.0015). The association was replicated in a Finnish case-control population (p = 0.026). The combined p value of the two population by meta-analysis is 0.00040 (OR, 1.34; 95% CI, 1.14–1.58). Our data indicate that SKT is involved in the etiology of LDH