The IL-1 family consists of 11 cytokines, 7 ligands with agonist activity (IL-1α, IL-1β, IL-18, IL-33, IL-36α, IL-36β, IL-36γ) and four members with antagonistic activities [IL-1 receptor antagonist (IL-1Ra), IL-36Ra, IL-37, IL-38]. Recent articles have described that most members of IL-1 family cytokines are involved in the process of innate and adaptive immunity as well as fibrosis in systemic sclerosis (SSc). IL-1 family gene polymorphisms, abnormal expression of IL-1 and its potential role in the fibrosis process have been explored in SSc. IL-33 and IL-18 have also been discussed in the recent years. IL-33 may contribute to the fibrosis of SSc, while IL-18 remains to be researched to confirm its role in fibrosis process. There is a lack of study on the pathophysiological roles of IL-36, IL-37, and IL-38 in SSc, which might provide us new study area. Here, we aim to give a brief overview of IL-1 family cytokines and discuss their pivotal roles in the pathogenesis of SSc.
Cognitive radio improves spectrum efficiency by allowing secondary users (SU) to dynamically exploit the idle spectrum owned by primary users (PU). This paper studies optimal bandwidth allocation for SUs. Consider the following tradeoff: a SU increases its instantaneous throughput by accessing larger bands, but channel switching overhead (due to the dynamics of PU activities) and contention among multiple SUs create higher liability for larger bandwidths. So how much is too much? In this paper, we find the optimal bandwidth allocation in both the single SU and multiple SU cases, accounting for the effects of channel switching overhead. Our result is validated through both numerical simulation and real channel activity traces. We also study the impact of various factors on SU performance, namely, PU channel idle time and probability, PU channel correlation, and SU sensing and access schemes. The work sheds light on the design of spectrum sharing protocols in cognitive radio networks.
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