Effect of sampling rate and monitoring granularity on anomaly detectability

Abstract—In this paper, we quantitatively evaluate how sampling decreases the detectability of anomalous traffic. We build equations to calculate the false positive ratio (FPR) and false negative ratio (FNR) for given values of the sampling rate, statistics of normal traffic, and volume of anomalies to be detected. We show that by changing the measurement granularity, we can detect anomalies even with a low sampling rate and give the equation to derive optimal granularity by using the relationship between the mean and variance of aggregated flows. With those equations, we can answer for the practical questions that arise in actual network operations; what sampling rate to set in order to find the given volume of anomaly, or, if the sampling is too high for actual operation, then what granularity is optimal to find the anomaly for a given lower limit of sampling rate. I

Effects of HMGB1 on Tricellular Tight Junctions via TGF-β Signaling in Human Nasal Epithelial Cells

様々な組織の炎症性疾患と密接な関係があるHigh mobility group box-1（HMGB1）は，主に核内に局在して転写の制御を行うとともに，細胞死や炎症性の刺激によって細胞外に放出され細胞障害性のシグナルを誘導するとされている．アレルギー性鼻炎や慢性副鼻腔炎の病態においてHMGB1が密接な関連があり，今回われわれはHMGB1 がTGF-βシグナリングを介して3細胞間接着分子であるangulin-1/LSRの発現を低下させることでバリア機能を低下させることを明らかとした

Expression profiles of zinc transporters in rodent placental models

Abstract Zinc is a vital metal that is a structural and functional component of many proteins. The precise mechanism of zinc transport in the placenta remains unclear. In this study, we investigated the expression of zinc transporters (ZnTs) in the mouse placenta and in two rat trophoblast cell lines, TR-TBT cells, which are syncytiotrophoblast cells of the labyrinth zone, and Rcho-1 cells, which retain trophoblast cell features and differentiate into trophoblast giant cells of the junctional zone. All of the ZnTs that have been identified in mice (ZnT1-7) were detected in the mouse placenta by RT-PCR. The expression profiles of ZnTs in the placenta during pregnancy were different. The mRNA levels of ZnTs, with the exception of ZnT7, did not change during pregnancy. The ZnT7 mRNA level in placenta was elevated during pregnancy. In TR-TBT cells, ZnT1, ZnT3 and ZnT4 were detected by RT-PCR analysis. In Rcho-1 cells, all of the ZnTs that have been identified in rats (ZnT1-4) were detected by RT-PCR analysis. There were no differences between the mRNA expression levels of ZnT family members in undifferentiated Rcho-1 cells and differentiated Rcho-1 cells. This is the first report of expression profiles of ZnTs during differentiation of the placenta in the mouse placenta and rat placental cell models

UV-B Radiation Induces Epithelial Tumors in Mice Lacking DNA Polymerase η and Mesenchymal Tumors in Mice Deficient for DNA Polymerase ι

DNA polymerase η (Pol η) is the product of the Polh gene, which is responsible for the group variant of xeroderma pigmentosum, a rare inherited recessive disease which is characterized by susceptibility to sunlight-induced skin cancer. We recently reported in a study of Polh mutant mice that Pol η is involved in the somatic hypermutation of immunoglobulin genes, but the cancer predisposition of Polh(−/−) mice has not been examined until very recently. Another translesion synthesis polymerase, Pol ι, a Pol η paralog encoded by the Poli gene, is naturally deficient in the 129 mouse strain, and the function of Pol ι is enigmatic. Here, we generated Polh Poli double-deficient mice and compared the tumor susceptibility of them with Polh- or Poli-deficient animals under the same genetic background. While Pol ι deficiency does not influence the UV sensitivity of mouse fibroblasts irrespective of Polh genotype, Polh Poli double-deficient mice show slightly earlier onset of skin tumor formation. Intriguingly, histological diagnosis after chronic treatment with UV light reveals that Pol ι deficiency leads to the formation of mesenchymal tumors, such as sarcomas, that are not observed in Polh(−/−) mice. These results suggest the involvement of the Pol η and Pol ι proteins in UV-induced skin carcinogenesis