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The forthcoming 6G technology aims to ensure widespread connectivity through Space-Air-Ground Integrated Networks (SAGINs), crucial for regions lacking proper terrestrial infrastructure. Utilizing High-Altitude Platform Stations (HAPSs) as aerial base stations, 6G facilitates low-latency internet access. However, the exponential growth in terrestrial wireless devices puts a strain on the available frequency bands shared by terrestrial and non-terrestrial networks. Therefore, in this research, we aim to optimize the resources between HAPS-to-satellite and HAPS-to-terrestrial uplinks. One challenge that arises is the interference caused by simultaneous uplink and downlink transmissions, especially from uplink back lobes disrupting ground user downlinks. To mitigate this interference, current methods like the Zero-Forcing (ZF) proposed a technique to steer nulls toward ground users. However, current methods randomly allocate limited nulls, potentially leaving many users outside null zones and experiencing interference. To address this issue, we propose a solution to design null directivity based on user locations. This is achieved by creating a codebook of antenna patterns that are linked to weight matrices. Selecting suitable antenna patterns from the codebook and adjusting weight matrices accordingly enables null formation at positions that maximize user communication satisfaction. Numerical analysis confirms the effectiveness of this approach, showing increased user satisfaction compared to existing methods.

Space-air-ground integrated networks (SAGINs) are attracting increasing attention for extending wireless communication coverage. Furthermore, high-altitude platform stations (HAPSs) can provide low-latency internet access to areas where terrestrial networks do not operate as unmanned flying base stations. However, as more frequency bands are used by wireless communication systems in terrestrial and non-terrestrial networks, it is necessary to make effective use of the finite frequency bands for multiple systems. Therefore, this study focuses on frequency sharing between the uplink from HAPS to satellite and the downlink from HAPS to ground users for efficient use of finite frequency bands in a SAGIN. In such frequency sharing, the back lobe toward the rear of the HAPS antenna for uplink communication causes interference when receiving the downlink signal from HAPS. Therefore, the zero-forcing (ZF) method is applied to the directivity control of the HAPS-mounted uplink antenna, which helps direct the nulls with significantly low antenna gain toward ground users. However, the coverage of the nulls due to the above control alone is extremely insignificant, which cannot sufficiently guarantee interference suppression for diverse user distributions. Therefore, this study proposes a HAPS-based null broadening approach with directivity control according to the user distribution for interference suppression in a SAGIN. The effectiveness of our proposal is evaluated by comparing it with the existing covariance matrix tapper(CMT)-based null broadening, ZF-based nulling, and no nulling for the HAPS-mounted uplink antenna using numerical analysis.

Recently, changes in the relationship between satellite communication networks and ground communication networks have led to an increase in the demands imposed on satellite communication networks. In this category of networks, the low earth orbit (LEO) satellite constellations, which cover the entire surface of Earth through cooperation among many small satellites in low orbit, are currently attracting attention. LEO satellites consume power when communicating with terrestrial terminals. However, in the absence of solar light, these satellites must operate using battery energy only. The power consumption during these periods places a heavy load on the satellite battery and can shorten their lifetimes. This entails a significant cost for satellite communication networks. In this letter, we apply Q-learning to the power allocation problem in satellite-to-ground communication using LEO satellites. Using this method, we can extend the lifetime of the LEO satellite battery by sharing the workload of overworked satellites with adjacent satellites with a lower load. The effects of the proposed method on the battery lifetime of the LEO satellites are verified.

Aceruloplasminemia is characterized by excessive neurovisceral accumulation of iron due to mutations in the ceruloplasmin gene. We report that the levels of malonaldehyde (MDA) and 4-hydroxynonenals (4-HNE) were elevated both in the frontal cortex and putamen in two patients with aceruloplasminemia compared with those in controls. Immunohistochemical analysis with an antibody raised against HNE-modified protein showed a large number of immunoreactive neurons and glias in the brain of a patient. MDA and 4-HNE are good indicators of lipid peroxidation because they are generated in the process of oxidation of polyunsaturated fatty acids. The data strongly suggest that the increase of oxygen free radicals associated with excessive iron accumulation plays an important pathogenic role in the process of neuronal cell death in the brains of patients with aceruloplasminemia.

Aceruloplasminemia is an interesting disease, the study of which helps elucidate how iron-induced oxidative stress is involved in neuronal cell death. In order to study the neuropathological characteristics associated with oxidative stress, we scrutinized the brains of 5 patients with aceruloplasminemia histopathologically and immunohistochemically. The pathological findings were essentially similar in all patients. In the frontal cortices, iron deposition and neuronal cell loss were trivial, but in the basal ganglia (especially in the caudate nucleus and putamen), severe iron overload and extensive neuronal loss were noted. Iron deposition was more prominent in the astrocytes than in the neurons in both regions. 4-hydroxynonenal (HNE), one of the most physiologically active lipid peroxides, was strongly detected on neurons and astrocytes by immunostaining. Markedly deformed astrocytes were observed in the striatum. These astrocytes were similar to Alzheimer type 1 astrocytes. Globular structures were seen in proportion to the degree of iron deposition. They clearly reacted with anti-glial fibrillary acidic protein (GFAP) and anti-S-100 antibodies and contained glial fibril-like filaments, but showed no or only faint immunoreactivity to antibodies for neuronal marker proteins, such as neurofilament and synaptophysin. Therefore, the globular structures presumably originated from astrocytes. The structures also reacted positively to anti-HNE and anti-ubiquitin antibodies. We conclude that astrocytic deformities and globular structures are characteristic neuropathological features of aceruloplasminemia and are closely linked to iron overload and subsequent oxidative stress.