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Fluctuating two-ray (FTR) channel model was shown to effectively characterize millimeter wave (mmWave) communication channels. In this paper, we adopt FTR to investigate amplify-and-Forward (AF) mmWave relaying system. Two communications scenarios are considered corresponding to the presence and absence of a direct link between the transmitter and receiver. Outage probability and symbol error rate (SER) are then analytically obtained as performance metrics. The results are further compared with the corresponding metrics obtained based on conventional channel models including Nakagamim and two-wave with diffuse power (TWDP). Especially, for the high-SNR regime, our analyses indicate that performance evaluations based on the conventional models significantly deviate from that of based on the FTR model. Our results provide quantitative insights on the importance of model selection in design and performance evaluations of relay-based mmWave systems. Moreover, for the high-SNR regime, we carry out asymptotic analysis and obtain a low-complexity expression for the achieved AF relaying gain. Such an expression provides a quantitative measure on whether or not AF relaying outperforms no-relaying in a given setting. Extensive numerical and simulation results are provided to confirm the accuracy of the analysis and investigate system performance in different settings.

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Background Microglia are tissue resident macrophages with a wide range of critically important functions in central nervous system development and homeostasis. Method In this study, we aimed to characterize the transcriptional landscape of ex vivo human microglia across different developmental ages using cells derived from pre-natal, pediatric, adolescent, and adult brain samples. We further confirmed our transcriptional observations using ELISA and RNAscope. Results We showed that pre-natal microglia have a distinct transcriptional and regulatory signature relative to their post-natal counterparts that includes an upregulation of phagocytic pathways. We confirmed upregulation of CD36, a positive regulator of phagocytosis, in pre-natal samples compared to adult samples in situ. Moreover, we showed adult microglia have more pro-inflammatory signature compared to microglia from other developmental ages. We indicated that adult microglia are more immune responsive by secreting increased levels of pro-inflammatory cytokines in response to LPS treatment compared to the pre-natal microglia. We further validated in situ up-regulation of IL18 and CXCR4 in human adult brain section compared to the pre-natal brain section. Finally, trajectory analysis indicated that the transcriptional signatures adopted by microglia throughout development are in response to a changing brain microenvironment and do not reflect predetermined developmental states. Conclusion In all, this study provides unique insight into the development of human microglia and a useful reference for understanding microglial contribution to developmental and age-related human disease.

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