Co-universal algebras associated to product systems, and gauge-invariant uniqueness theorems

Let X be a product system over a quasi-lattice ordered group. Under mild hypotheses, we associate to X a C*-algebra which is co-universal for injective Nica covariant Toeplitz representations of X which preserve the gauge coaction. Under appropriate amenability criteria, this co-universal C*-algebra coincides with the Cuntz-Nica-Pimsner algebra introduced by Sims and Yeend. We prove two key uniqueness theorems, and indicate how to use our theorems to realise a number of reduced crossed products as instances of our co-universal algebras. In each case, it is an easy corollary that the Cuntz-Nica-Pimsner algebra is isomorphic to the corresponding full crossed product.Comment: 40 pages, 2 figures; v2: minor changes to the introduction, references added and update

Wireless Communication in Process Control Loop: Requirements Analysis, Industry Practices and Experimental Evaluation

Wireless communication is already used in process automation for process monitoring. The next stage of implementation of wireless technology in industrial applications is for process control. The need for wireless networked control systems has evolved because of the necessity for extensibility, mobility, modularity, fast deployment, and reduced installation and maintenance cost. These benefits are only applicable given that the wireless network of choice can meet the strict requirements of process control applications, such as latency. In this regard, this paper is an effort towards identifying current industry practices related to implementing process control over a wireless link and evaluates the suitability of ISA100.11a network for use in process control through experiments

Non-classical ProIL-1beta activation during mammary gland infection is pathogen-dependent but caspase-1 independent

Infection of the mammary gland with live bacteria elicits a pathogen-specific host inflammatory response. To study these host-pathogen interactions wild type mice, NF-kappaB reporter mice as well as caspase-1 and IL-1beta knockout mice were intramammarily challenged with Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus). The murine mastitis model allowed to compare the kinetics of the induced cytokine protein profiles and their underlying pathways. In vivo and ex vivo imaging showed that E. coli rapidly induced NF-kappaB inflammatory signaling concomitant with high mammary levels of TNF-alpha, IL-1 alpha and MCP-1 as determined by multiplex analysis. In contrast, an equal number of S. aureus bacteria induced a low NF-kappaB activity concomitant with high mammary levels of the classical IL-1beta fragment. These quantitative and qualitative differences in local inflammatory mediators resulted in an earlier neutrophil influx and in a more extensive alveolar damage post-infection with E. coli compared to S. aureus. Western blot analysis revealed that the inactive proIL-1beta precursor was processed into pathogen-specific IL-1beta fragmentation patterns as confirmed with IL-1beta knockout animals. Additionally, caspase-1 knockout animals allowed to investigate whether IL-1beta maturation depended on the conventional inflammasome pathway. The lack of caspase-1 did not prevent extensive proIL-1beta fragmentation by either of S. aureus or E. coli. These non-classical IL-1beta patterns were likely caused by different proteases and suggest a sentinel function of IL-1beta during mammary gland infection. Thus, a key signaling nodule can be defined in the differential host innate immune defense upon E. coli versus S. aureus mammary gland infection, which is independent of caspase-1

Assessment of problematic severe asthma in children

Assessment of problematic severe asthma in children should be performed in a stepwise manner to ensure an optimal approach. A four-step assessment scheme is proposed. First, a full diagnostic work-up is performed to exclude other diseases which mimic asthma. Secondly, a multi-disciplinary assessment is performed to identify issues that may need attention, including comorbidities. Thirdly, the pattern of inflammation is assessed, and finally steroid responsiveness is documented. Based upon these four steps an optimal individualised treatment plan is developed. In this article the many gaps in our current knowledge in all these steps are highlighted, and recommendations for current clinical practice and future research are made. The lack of good data and the heterogeneity of problematic severe asthma still limit our ability to optimise the management on an individual basis in this small, but challenging group of patients