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Non-orthogonal multiple access (NOMA) is a relevant technology for realizing the primary goals of nextgeneration wireless networks, such as high connectivity and stability. This paper focuses on the foundational principles of Power Domain NOMA (PD-NOMA), a promising technique for meeting the needs of fifth Generation (5G) in real-world applications. PD-NOMA offers flexibility in allocating radio resources to enhance user access performance. By enabling several users to utilize the same radio resources, PD-NOMA achieves improved spectrum efficiency. This paper considers the practical aspects of PD-NOMA system design, exploring various network scenarios. This paper primarily focuses on PD-NOMA that uses the superposition coding (SC) at the transmitter side in addition to the successive interference cancellation (SIC) at the receiver side. The paper also provides a theoretical formulation and solutions for downlink PD-NOMA and addresses potential areas for future research. Finally, the paper concludes by summarizing the key findings and implications of the study. [ABSTRACT FROM AUTHOR]

Sixth generation (6G) wireless networks are envisioned to provide global coverage for the intelligent digital society of the near future, ranging from traditional terrestrial to non-terrestrial networks, where reliable communications in high-mobility scenarios at high carrier frequencies would play a vital role. In such scenarios, the conventional orthogonal frequency division multiplexing (OFDM) modulation, which has been widely used in both the fourth generation (4G) and the emerging fifth generation (5G) cellular systems, is vulnerable to severe Doppler spread. A new two-dimensional modulation technique called Orthogonal Time Frequency Space (OTFS) modulation designed in the delay-Doppler domain is introduced. Through this design, which exploits full diversity over time and frequency, OTFS coupled with equalization converts the fading, time-varying wireless channel experienced by modulated signals such as OFDM into a time-independent channel with a complex channel gain that is roughly constant for all symbols. In this paper, we evaluate and analyze the performance of the OTFS receiver using four data detection algorithms: Single-tap frequency domain equalizer, Linear minimum mean-square error detection (LMMSE), Message passing detection (MP), and Maximum-ratio combining detection (MRC). Further, we extend our study to the variants of OTFS, where the waveform is transmitted with a cyclic prefix (CP) or zero padding (ZP) added to each OTFS frame or block. The simulation results show that the MRC detector can be improved the detection of the OTFS receiver. [ABSTRACT FROM AUTHOR]

Filter bank multicarrier (FBMC) was proposed as an alternative approach to cyclic prefix - orthogonal frequency division multiplexing (CP-OFDM). FBMC is considered a promising non-orthogonal waveform due to its very low out of band radiation and high spectral efficiency. Nevertheless, the orthogonality constraint for FBMC/OQAM is relaxed being limited only to the real field which causes intrinsic interference. The presence of this interference leads to incompatibility between some well-known multiple-input and multiple-output (MIMO) schemes and FBMC/offset quadrature amplitude modulation (OQAM). From this perspective, we proposed in this paper an efficient implementation for FBMC/OQAM based on block spreading to restore the complex orthogonality to enable applying MIMO with FBMC/OQAM. The proposed scheme uses a discrete Haar transform (DHT) to enable low computational complexity. The performance of proposed approaches has been investigated and compared with CP-OFDM under three MIMO schemes, as space-time block coding (STBC) Alamuoti schemes, spatial multiplexing with zero-forcing (ZF), and maximum likelihood (ML) detection schemes. The simulation results show that the proposed schemes enable to apply of the MIMO schemes with FBMC with almost the same performance and complexity as CP-OFDM. [ABSTRACT FROM AUTHOR]

Streptococcus pneumoniae causes infection-related mortality worldwide. Immunocompromised individuals, including young children, the elderly, and those with immunodeficiency, are especially vulnerable, yet little is known regarding S. pneumoniae-related pathogenesis and protection in immunocompromised hosts. Recently, strong interest has emerged in the gut microbiota's impact on lung diseases, or the "gut-lung axis." However, the mechanisms of gut microbiota protection against gut-distal lung diseases like pneumonia remain unclear. We investigated the role of the gut commensal, segmented filamentous bacteria (SFB), against pneumococcal pneumonia in immunocompetent and immunocompromised mouse models. For the latter, we chose the Rag-/- model, with adaptive immune deficiency. Immunocompetent adaptive protection against S. pneumoniae infection is based on antibodies against pneumococcal capsular polysaccharides, prototypical T cell independent-II (TI-II) antigens. Although SFB colonization enhanced TI-II antibodies in C57BL/6 mice, our data suggest that SFB did not further protect these immunocompetent animals. Indeed, basal B cell activity in hosts without SFB is sufficient for essential protection against S. pneumoniae. However, in immunocompromised Rag-/- mice, we demonstrate a gut-lung axis of communication, as SFB influenced lung protection by regulating innate immunity. Neutrophil resolution is crucial to recovery, since an unchecked neutrophil response causes severe tissue damage. We found no early neutrophil recruitment differences between hosts with or without SFB; however, we observed a significant drop in lung neutrophils in the resolution phase of S. pneumoniae infection, which corresponded with lower CD47 expression, a molecule that inhibits phagocytosis of apoptotic cells, in SFB-colonized Rag-/- mice. SFB promoted a shift in lung neutrophil phenotype from inflammatory neutrophils expressing high levels of CD18 and low levels of CD62L, to pro-resolution neutrophils with low CD18 and high CD62L. Blocking CD47 in SFB(-) mice increased pro-resolution neutrophils, suggesting CD47 down-regulation may be one neutrophil-modulating mechanism SFB utilizes. The SFB-induced lung neutrophil phenotype remained similar with heat-inactivated S. pneumoniae treatment, indicating these SFB-induced changes in neutrophil phenotype during the resolution phase are not simply secondary to better bacterial clearance in SFB(+) than SFB(-) mice. Together, these data demonstrate that the gut commensal SFB may provide much-needed protection in immunocompromised hosts in part by promoting neutrophil resolution post lung infection. [ABSTRACT FROM AUTHOR]