No abstract

LoRa is a low-power long-range IoT standard that uses the chirp spread spectrum technique, and we have strived to further extend its coverage by utilizing the direct device-to-device (D2D) links to construct a multi-hop relay network. In LoRa, the spreading factor (SF) is an important parameter, which not only provides great flexibility between the data rate and sensitivity but also presents a new dimension for multiple accesses. Our approach to improving the capacity of a multihop LoRa network is to attempt to off-load the data traffic into several subnets by utilizing this multiple-access dimension. Each subnet rooted at a sink node is allocated a specific SF on the basis of network clustering. This enables packet transmission in parallel with multiple SFs to become feasible. To allow such parallel transmissions, our considerations are: 1) ensuring the connectivity of all subnets; 2) off-loading the traffic according to the number of nodes, data rates, and network topologies of each subnet; and 3) shortening the airtime of each subnet by reducing the hop count. Toward these objectives, we present a tree-based SF clustering algorithm (TSCA) to conduct SF allocation in a multihop LoRa network. The TSCA focuses on balancing the airtime between the subnets while ensuring connectivity. Furthermore, we use simulations to show that our approach can significantly increase the network performance compared with other approaches. We additionally deploy a real-chip experiment to evaluate the feasibility of parallel transmission in practice. INDEX TERMS Low-power wide area network (LPWAN), LoRa, spreading factor (SF) allocation algorithm, tree-based spreading factor clustering algorithm (TSCA), multi-hop network.

Microglia are the major inflammatory cells in the brain. Recent studies have highlighted the reciprocal roles of other brain cells in modulating the microglial inflammatory responses. Urocortin (UCN) is a member of the corticotropin-releasing hormone (CRH) family of neuropeptides that function to regulate stress responses. In the present study, we demonstrated that expression of UCN in rat substantia nigra was found to be localized principally to dopaminergic neurons. In cell culture models, the CRH receptors were expressed in microglia, and CRHR expression was up-regulated by treatment with LPS. Thus, it might be proposed that UCN regulates cellular communication between dopaminergic neurons and microglia. We show that femtomolar concentrations of UCN could inhibit LPS-induced TNF-α production in cultured microglia. Investigation of the underlying signaling pathway that mediated the anti-inflammatory effect of UCN the involved PI3K/Akt and glycogen synthase kinase-3β pathway, but not cAMP pathway. Furthermore, UCN protected dopaminergic neurons against LPS-induced neurotoxicity by inhibiting microglial activation in LPS-treated mesencephalic neuron-glia cultures. These results suggest that endogenous UCN and its receptors might be involved in a complex network of paracrine interaction between dopaminergic neurons and glia.