Massive MIMO NOMA: Double-Mode Model towards Green 5G Networks.

With the development of the Internet of Things (IoT), the number of devices will also increase tremendously. However, we need more wireless communication resources. It has been shown in the literature that non-orthogonal multiple access (NOMA) offers high multiplexing gains due to the simultaneous transfer of signals, and massive multiple-input-multiple-outputs (mMIMOs) offer high spectrum efficiency due to the high antenna gain and high multiplexing gains. Therefore, a downlink mMIMO NOMA cooperative system is considered in this paper. The users at the cell edge in 5G cellular system generally suffer from poor signal quality as they are far away from the BS and expend high battery power to decode the signals superimposed through NOMA. Thus, this paper uses a cooperative relay system and proposes the mMIMO NOMA double-mode model to reduce battery expenditure and increase the cell edge user's energy efficiency and sum rate. In the mMIMO NOMA double-mode model, two modes of operation are defined. Depending on the relay's battery level, these modes are chosen to utilize the system's energy efficiency. Comprehensive numerical results show the improvement in the proposed system's average sum rate and average energy efficiency compared with a conventional system. In a cooperative NOMA system, the base station (BS) transmits a signal to a relay, and the relay forwards the signal to a cluster of users. This cluster formation depends on the user positions and geographical restrictions concerning the relay equipment. Therefore, it is vital to form user clusters for efficient and simultaneous transmission. This paper also presents a novel method for efficient cluster formation.

Performance Evaluation of Cooperative OMA and NOMA Systems in 6G Deployment Scenarios.

Optimization of the energy efficiency, fairness, and rates of the system is a vital part of communication systems. Multiple access techniques have a huge potential to enhance such performance parameters. This paper studies the performance of NOMA and OMA systems in a singular cell environment, where the cellular users are distributed randomly, and cooperative relays are considered for better system reliability. The relay nodes forward the signals to the cell-edge users. This paper considers a practical scenario where all the relay equipment is distributed with non-uniform battery power levels. The performance of OMA and NOMA schemes is compared based on the key performance indicators: sum rate, fairness, and energy efficiency. The fairness factor determines fairness in the allocation of resources to all the system's users. The performance of the two schemes is assessed in three deployment scenarios: urban, suburban, and rural scenarios. Through numerical results, it is proved that the performance of the NOMA dominates the OMA scheme.

Dengue virus infection of SK Hep1 cells: inhibition of in vitro angiogenesis and altered cytomorphology by expressed viral envelope glycoprotein.

Dengue virus (DENV) infection of human endothelial cells has been implicated in the pathobiology of dengue hemorrhagic fever and dengue shock syndrome. However, the mechanisms by which DENV infections alter the functional physiology of endothelial cells remain incompletely understood. In the present study, we examined the susceptibility of a human liver sinusoidal endothelial cell line SK Hep1 to all four serotypes of DENV and studied the effect of the virus on in vitro angiogenesis. All four serotypes of DENV could infect the SK Hep1 cells, but showed variable cytopathic effects, the most pronounced being that of DENV-2. Electron microscopy of the infected cells showed significant ultrastructural changes. In vitro angiogenesis assays on DENV-2 exposed SK Hep1 cells in the matrigel system showed inhibition compared with the controls. Importantly, transfection and transient expression of the DENV-2 envelope glycoprotein (E) in these cells showed drastic alterations in cell shapes and the E protein could be localized by fluorescence microscopy in terminal knob-like structures. Therefore, SK Hep1, a human hepatic sinusoid-derived endothelial cell line, may constitute a potential model to study DENV-endothelial cell interactions in vitro, especially towards understanding the possible virus-induced changes in hepatic endothelium and its role in disease pathogenesis.

Dengue virus-induced autophagosomes and changes in endomembrane ultrastructure imaged by electron tomography and whole-mount grid-cell culture techniques.

The biogenesis events and formation of dengue virus (DENV) in the infected host cells remain incompletely understood. In the present study, we examined the ultrastructural changes associated with DENV-2 replication in three susceptible host cells, C6/36, Vero and SK Hep1, a cell line of human endothelial origin, using transmission electron microscopy, whole-mount grid-cell culture techniques and electron tomography (ET). The prominent feature in C6/36 cells was the formation of large perinuclear vacuoles with mature DENV particles, and on-grid whole-mount examination of the infected Vero cells showed different forms of DENV core structures associated with cellular membranes within 48 h after infection. Distinct multivesicular structures and prominent autophagic vesicles were seen in the infected SK Hep1 cells when compared with the other two cell lines. ET showed the three-dimensional organization of these vesicles as a continuous system. This is the first report of ET-based analysis of DENV-2 replication in a human endothelial cell line. These results further emphasizes the strong role played by intracellular host membranes-virus interactions in the biogenesis of DENV and strongly argues for the possibility of targeting compounds to block such structure formation as key anti-dengue agents.

Imaging the interaction between dengue 2 virus and human blood platelets using atomic force and electron microscopy.

Thrombocytopenia is frequently associated with dengue virus infection. Host factors such as anti-platelet immunopathogenic processes have been implicated in the origin of dengue-associated thrombocytopenia but the role of dengue virus in directly interacting with platelets and altering their hemostatic property remains incompletely understood. In the present study, we examined the effect of dengue 2 virus on the morphology and physiological activation profile of normal human platelets using atomic force microscopy, electron microscopy and flowcytometry. Platelets obtained from healthy donors were exposed to a cell culture-adapted 10(4) LD(50) dengue 2 virus isolate in vitro and the subsequent effect on morphology and activation biology studied. Our results show that dengue 2 virus exposure at doses comparable to natural viremic states in human infections can activate platelets with an increase in P-selectin expression and fibrinogen-binding property. Atomic force, scanning and transmission electron microscopy also showed typical activation-related morphological changes such as altered platelet membrane architecture, degranulation, presence of filopodia and dilatation of the open canalicular system in the dengue 2 virus-exposed platelets but not in the controls. Importantly, Japanese encephalitis virus exposure at the same dose did not activate platelets or show any morphological changes. Our findings suggest that dengue 2 virus may directly interact with and activate platelets - an event that might be important in the origin of dengue-associated thrombocytopenia. Detailed molecular characterization of this effect might provide key knowledge toward better prophylaxis of the hemostatic complications of dengue disease.

Dengue 2 virus inhibits in vitro megakaryocytic colony formation and induces apoptosis in thrombopoietin-inducible megakaryocytic differentiation from cord blood CD34+ cells.

Thrombocytopenia is frequently associated with dengue virus infection in humans. Although antiplatelet immunopathogenic processes have been implicated in the origin of dengue-associated thrombocytopenia, the effect of dengue viruses on megakaryocyte differentiation remains incompletely understood. In this study, we examined the effect of human dengue 2 virus isolates on the in vitro growth and differentiation of thrombopoietin-induced megakaryopoiesis of cord blood CD34+ cells. Dengue 2 viruses, but not Japanese encephalitis virus, showed a dose-dependent inhibition of CFU-Mk. Viral antigens could be detected by an immunohistochemical technique in 3-5% of the early megakaryocytic progenitors by the 5th postexposure day in liquid cultures with cell loss, increased annexin V binding and active caspase-3 expression. In summary, dengue 2 viruses can inhibit in vitro megakaryopoiesis, as well as infect and induce apoptotic cell death in a subpopulation of early megakaryocytic progenitors. These events might contribute towards the origin of thrombocytopenia in dengue disease.