Search

Unlike conventional servers housed in a centralized and secured indoor environment (e.g., data centers), Internet-of-Things (IoT) devices such as sensor/actuator are geographically distributed and may be closely located to the physical systems where IoT devices are utilized. However, the resource-constrained nature of IoT devices limits their capacity to deploy sophisticated security solutions. The proposed approach assumes that a device can be compromised and hence, the need to be able to automatically isolate the compromised device(s). In order to enforce security policies even when devices are compromised, we propose using blockchain in the monitoring framework. Unlike existing centralized or distributed security solutions (which do not consider the possibility that the solutions themselves can be compromised), the proposed blockchain-based framework can enforce the security policies as long as a majority of the devices are not compromised. By employing the permissioned blockchain (Hyperledger Fabric) and add-on hardware modules, the proposed framework offers significantly lower latency and overhead compared to permissionless blockchain frameworks (e.g., Ethereum) and allows existing IoT devices to join the framework without modification.

This paper describes work in progress to analyze the cyber-physical resiliency of a microgrid when operated in islanded mode, as would be the case during an extreme event. The analysis must include each of the four components of a microgrid: sources or generation, energy storage, load, and power electronics interfaces. Two networks with disparate time constants must be accurately modeled. The electrical (and mechanical if there are generators or wind turbines) network is simulated with the power flow equations, a challenging control problem that requires accurate state estimation for its solution. In addition, there is the sensor-communication network consisting of legacy devices such as MV90 meters and SCADA hardware as well as IoT devices such as PMUs and grid management equipment.

We report that S100 proteins were reduced in patients with chronic rhinosinusitis (CRS). S100A8/9, which is important in epithelial barrier function, was particularly decreased in elderly patients with CRS. Epithelial expression of S100A8/9 is partly regulated by the IL-6 trans-signaling pathway. The goal of this study was to investigate whether or not age-related reduction of S100A8/9 in CRS is associated with blunting of IL-6 trans-signaling. The levels of IL-6, soluble IL-6 receptor (sIL-6R), soluble gp130 (sgp130), and S100A8/9 from control subjects (n = 10), and patients with CRS without nasal polyps (n = 13) and those with CRS with nasal polyps (CRSwNP) (n = 14), were measured by ELISA. Age-related differences in the level of each protein were investigated. Normal human bronchial epithelial cells were cultured in air-liquid interface and stimulated with IL-6/sIL-6R and tumor necrosis factor (TNF)-α with or without the addition of sgp130, a natural inhibitor of IL-6 trans-signaling. There was a significant age-related decline in S100A8/9 and an increase in sgp130 in nasal tissue samples from patients with CRSwNP, although there was no age-related difference in IL-6/sIL-6R production. Additionally, expression of the S100A8/9 gene and protein was increased significantly by IL-6/sIL-6R plus TNF-α in normal human bronchial epithelial cells. This increase was blocked by sgp130. These results suggest that increased sgp130 in older patients may inhibit IL-6 trans-signaling, impair barrier function, and decrease S1008/9 production in elderly patients with CRSwNP. Restoration of barrier function by targeting sgp130 may be a novel treatment strategy.

Objectives/Hypothesis Chronic Rhinosinusitis (CRS) is accompanied by evidence of a vigorous adaptive immune response, and emerging studies demonstrate that some nasal polyps manifest a polyclonal autoantibody response. We previously found that antibodies against BP180, a component of the hemidesmosome complex and the dominant epitope in autoimmune bullous pemphigoid, were found at elevated levels in nasal polyp tissue. Given the critical role of hemidesmosomes in maintaining epithelial integrity, we sought to investigate the distribution of BP180 in nasal tissue and evaluate for evidence of systemic autoimmunity against this antigen in CRS. Study Design Case-control experimental study. Methods The expression and distribution of BP180 in cultured nasal epithelial cells and normal nasal tissue were confirmed using real-time polymerase chain reaction (PCR), Western immunoblotting, immunofluorescence and immunohistochemistry. Sera were collected from three groups: control, CRSsNP, and CRSwNP. A commercially available ELISA was utilized to compare anti-BP180 autoantibody levels in sera. Results BP180 is expressed in nasal epithelium, but is not confined to the basement membrane as it is in human skin. In cultured nasal epithelial cells, confocal immunofluorescence showed a punctate distribution of BP180 along the basal surface, consistent with its distribution in epithelial keratinocytes. There are significantly higher levels of circulating nonpathologic anti-BP180 autoantibodies in CRS patients compared with normal controls (P

Glucocorticoids (GCs) are commonly prescribed to patients with a variety of inflammatory disorders, including inflammatory bowel disease (IBD). IBD is the manifestation of a dysregulated mucosal immune response, usually against commensal bacteria, involving many different immune cells. GCs mediate their immunomodulatory effects through many different mechanisms and target multiple signaling pathways. The GC dexamethasone down-modulates both innate and adaptive immune cell activation. Group 3 innate lymphocytes (ILC3s) have critical roles in mucosal inflammation. ILC3s secrete high levels of the cytokine IL-22, promoting epithelial proliferation, antimicrobial peptides and mucins. The effects of dexamethasone on T cell function are well described, however, it is not known if dexamethasone modulates the critical function of ILC3s or if dexamethasone regulates the cytokine IL-22. In this study, we examined the effects of dexamethasone on IL-22 production by ILC3s. We found that dexamethasone suppressed IL-23-mediated IL-22 production in homeostatic and activated human and mouse ILC3s. Dexamethasone did not modulate the IL-23 canonical signaling pathway of JAK2/STAT3, but did suppress phosphorylation of IkBa, an important regulator in NF-kB activation. These findings implicate NF-kB as a regulator of IL-22 production in ILC3s and have likely repercussions on GC treatment of IBD patients.

S U N D A Y 531 Elevated Expression of CC Chemokine Ligand 18 in Chronic Rhinosinusitis A. Kato, S. Peterson, J. A. Poposki, D. R. Nagarkar, R. T. Chustz, A. T. Peters, L. A. Suh, R. Carter, J. Norton, K. E. Harris, L. C. Grammer, B. Tan, R. K. Chandra, D. B. Conley, R. C. Kern, R. P. Schleimer; Division of Allergy-Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL, Department of Otolaryngology, Northwestern University Feinberg School of Medicine, Chicago, IL. RATIONALE: Chronic rhinosinusitis with nasal polyps (CRSwNP) is associated with Th2-dominant inflammation including eosinophilia, in contrast to non-polypoid CRS (CRSsNP). CCL18/PARC is a CC chemokine known to recruit na€ive T cells, B cells, and immature dendritic cells, and thought to be involved in Th2-related inflammatory diseases including asthma and atopic dermatitis. However, expression of CCL18 in CRS has not been extensively studied. METHODS:Using nasal polyp tissue (NP) and uncinate tissue (UT) from controls and patients with CRS, we examined the expression of CCL18 mRNA by real-time PCR and assayed CCL18 protein by ELISA, immunohistochemistry and western blot. RESULTS: Compared to control subjects (n59), CCL18 mRNAwas significantly increased in NP (432-fold, p