Sensing as a Service in 6G Perceptive Networks: A Unified Framework for ISAC Resource Allocation

In the upcoming next-generation (5G-Advanced and 6G) wireless networks, sensing as a service will play a more important role than ever before. Recently, the concept of perceptive network is proposed as a paradigm shift that provides sensing and communication (S&C) services simultaneously. This type of technology is typically referred to as Integrated Sensing and Communications (ISAC). In this paper, we propose the concept of sensing quality of service (QoS) in terms of diverse applications. Specifically, the probability of detection, the Cramer-Rao bound (CRB) for parameter estimation and the posterior CRB for moving target indication are employed to measure the sensing QoS for detection, localization, and tracking, respectively. Then, we establish a unified framework for ISAC resource allocation, where the fairness and the comprehensiveness optimization criteria are considered for the aforementioned sensing services. The proposed schemes can flexibly allocate the limited power and bandwidth resources according to both S&C QoSs. Finally, we study the performance trade-off between S&C services in different resource allocation schemes by numerical simulations

Autophagy is involved in oligodendroglial precursor-mediated clearance of amyloid peptide

BACKGROUND: Accumulation of β-amyloid peptides is an important hallmark of Alzheimer\u27s disease (AD). Tremendous efforts have been directed to elucidate the mechanisms of β-amyloid peptides degradation and develop strategies to remove β-amyloid accumulation. In this study, we demonstrated that a subpopulation of oligodendroglial precursor cells, also called NG2 cells, were a new cell type that can clear β-amyloid peptides in the AD transgene mice and in NG2 cell line. RESULTS: NG2 cells were recruited and clustered around the amyloid plaque in the APPswe/PS1dE9 mice, which is Alzheimer\u27s disease mouse model. In vitro, NG2 cell line and primary NG2 cells engulfed β-amyloid peptides through the mechanisms of endocytosis in a time dependent manner. Endocytosis is divided into pinocytosis and phagocytosis. Aβ(42) internalization by NG2 cells was mediated by actin-dependent macropinocytosis. The presence of β-amyloid peptides stimulated the autophagic pathway in NG2 cells. Once inside the cells, the β-amyloid peptides in NG2 cells were transported to lysosomes and degraded by autophagy. CONCLUSIONS: Our findings suggest that NG2 cells are a new cell type that can clear β-amyloid peptides through endocytosis and autophagy

PACT/RAX Regulates the Migration of Cerebellar Granule Neurons in the Developing Cerebellum

PACT and its murine ortholog RAX were originally identified as a protein activator for the dsRNA-dependent, interferon-inducible protein kinase PKR. Recent studies indicated that RAX played a role in embryogenesis and neuronal development. In this study, we investigated the expression of RAX during the postnatal development of the mouse cerebellum and its role in the migration of cerebellar granule neurons (CGNs). High expression of RAX was observed in the cerebellum from postnatal day (PD) 4 to PD9, a period when the CGNs migrate from the external granule layer (EGL) to the internal granule layer (IGL). The migration of the EGL progenitor cells in vivo was inhibited by RAX knockdown on PD4. This finding was confirmed by in vitro studies showing that RAX knockdown impaired the migration of CGNs in cerebellar microexplants. PACT/RAX-regulated migration required its third motif and was independent of PKR. PACT/RAX interacted with focal adhesion kinase (FAK) and PACT/RAX knockdown disturbed the FAK phosphorylation in CGNs. These findings demonstrated a novel function of PACT/RAX in the regulation of neuronal migration

Over-the-Air Performance Testing of 5G New Radio User Equipment:Standardization and Challenges

Abstract The Third Generation Partnership Project (3GPP) is accelerating 5G new radio (NR) global standards aimed at significant enhancement of wireless system performance for higher date rate, better energy efficiency, and higher reliability than the current 4G cellular systems. The operators, manufacturers, and test equipment vendors have worked together to develop standardized over-the-air (OTA) test methodologies for the overall performance evaluation of 5G NR devices. 3GPP is taking the lead in standardizing the OTA testing of 5G NR under fading channel conditions. In 3GPP specifications, test methods have been studied to verify the multiple-input multiple-output (MIMO) performance of 5G NR user equipments (UEs) in OTA mode. This article follows the 3GPP standardization work and discusses the MIMO OTA test methodologies for 5G NR UEs working at frequency range 1 (FR1) and FR2, with a focus on its new challenges and solutions compared to 4G MIMO OTA testing methods. Then the OTA throughput testing results of real 5G NRUEs are demonstrated under the standard channel models. Finally, the challenges and limitations of standard 5G MIMO OTA test solutions are also highlighted

ADAR2-dependent RNA editing of GluR2 is involved in thiamine deficiency-induced alteration of calcium dynamics

BACKGROUND: Thiamine (vitamin B1) deficiency (TD) causes mild impairment of oxidative metabolism and region-selective neuronal loss in the central nervous system (CNS). TD in animals has been used to model aging-associated neurodegeneration in the brain. The mechanisms of TD-induced neuron death are complex, and it is likely multiple mechanisms interplay and contribute to the action of TD. In this study, we demonstrated that TD significantly increased intracellular calcium concentrations [Ca2+]i in cultured cortical neurons. RESULTS: TD drastically potentiated AMPA-triggered calcium influx and inhibited pre-mRNA editing of GluR2, a Ca2+-permeable subtype of AMPA receptors. The Ca2+ permeability of GluR2 is regulated by RNA editing at the Q/R site. Edited GluR2 (R) subunits form Ca2+-impermeable channels, whereas unedited GluR2 (Q) channels are permeable to Ca2+ flow. TD inhibited Q/R editing of GluR2 and increased the ratio of unedited GluR2. The Q/R editing of GluR2 is mediated by adenosine deaminase acting on RNA 2 (ADAR2). TD selectively decreased ADAR2 expression and its self-editing ability without affecting ADAR1 in cultured neurons and in the brain tissue. Over-expression of ADAR2 reduced AMPA-mediated rise of [Ca2+]i and protected cortical neurons against TD-induced cytotoxicity, whereas down-regulation of ADAR2 increased AMPA-elicited Ca2+ influx and exacerbated TD-induced death of cortical neurons. CONCLUSIONS: Our findings suggest that TD-induced neuronal damage may be mediated by the modulation of ADAR2-dependent RNA Editing of GluR2

Chicken IFI6 inhibits avian reovirus replication and affects related innate immune signaling pathways

Interferon-alpha inducible protein 6 (IFI6) is an important interferon-stimulated gene. To date, research on IFI6 has mainly focused on human malignant tumors, virus-related diseases and autoimmune diseases. Previous studies have shown that IFI6 plays an important role in antiviral, antiapoptotic and tumor-promoting cellular functions, but few studies have focused on the structure or function of avian IFI6. Avian reovirus (ARV) is an important virus that can exert immunosuppressive effects on poultry. Preliminary studies have shown that IFI6 expression is upregulated in various tissues and organs of specific-pathogen-free chickens infected with ARV, suggesting that IFI6 plays an important role in ARV infection. To analyze the function of avian IFI6, particularly in ARV infection, the chicken IFI6 gene was cloned, a bioinformatics analysis was conducted, and the roles of IFI6 in ARV replication and the innate immune response were investigated after the overexpression or knockdown of IFI6 in vitro. The results indicated that the molecular weight of the chicken IFI6 protein was approximately 11 kDa and that its structure was similar to that of the human IFI27L1 protein. A phylogenetic tree analysis of the IFI6 amino acid sequence revealed that the evolution of mammals and birds was clearly divided into two branches. The evolutionary history and homology of chickens are similar to those of other birds. Avian IFI6 localized to the cytoplasm and was abundantly expressed in the chicken lung, intestine, pancreas, liver, spleen, glandular stomach, thymus, bursa of Fabricius and trachea. Further studies demonstrated that IFI6 overexpression in DF-1 cells inhibited ARV replication and that the inhibition of IFI6 expression promoted ARV replication. After ARV infection, IFI6 modulated the expression of various innate immunity-related factors. Notably, the expression patterns of MAVS and IFI6 were similar, and the expression patterns of IRF1 and IFN-β were opposite to those of IFI6. The results of this study further advance the research on avian IFI6 and provide a theoretical basis for further research on the role of IFI6 in avian virus infection and innate immunity

Exact symbol error rate for variable length codes over binary symmetric channel

In this paper, we analyze the error recovery performance of variable length codes (VLCs) transmitted over binary symmetric channel (BSC). Simple expressions for the exact mean symbol error rate (MSER) and the exact variance of symbol error rate (VSER) for any crossover probability p, are presented. We also prove that the mean error propagation length (MEPL) derived for single bit inversion error case is a scaled value of MSER when p, tends to zero. Comparisons with simulations demonstrate the accuracy of the MSER and VSER expressions

Alterations of Bax/Bcl-2 ratio contribute to NaAsO2 induced thyrotoxicity in human thyroid follicular epithelial cells and SD rats

The environmental toxicant arsenic causes various human diseases and threatens millions of people worldwide. Recently, a limited number of studies have revealed that exposure to arsenic is associated with thyroid dysfunction, indicating its toxicological impact on the thyroid gland, however, its precise forms of damage and underlying mechanisms remain largely unknown. Here, we sought to observe the thyrotoxicity of sodium arsenite (NaAsO2) on human thyroid follicular epithelial cells (Nthy-ori 3–1) and SD rats, and explore the role of Bax/Bcl-2 ratio in the above process. Our results displayed that NaAsO2 exerted a dose-dependent inhibitory effect on the viability of Nthy-ori 3–1 cells. Alongside the increase doses of NaAsO2 exposure, morphological changes and elevated LDH levels were observed. Furthermore, apoptosis rates increased in a dose- and time-dependent manner, accompanied by a decrease in Bcl-2 and an opposite change in Bax expression. SD rats were treated with 0, 2.5, 5, and 10 mg/kg NaAsO2 for 36 weeks. Our findings revealed that NaAsO2 exposure resulted in arsenic accumulation in thyroid tissue, elevated ratio of Bax/Bcl-2, and histopathological changes of thyroid in rats, which accompanied by the decreased serum T3 and T4 levels and the increased serum TSH level. Furthermore, T3 and T4 levels were negatively correlated with Bax expression, whereas positively correlated with Bcl-2 expression. Collectively, our results suggest that NaAsO2 exposure induces cytotoxicity in Nthy-ori 3–1 cells, causes structural damages and dysfunction of thyroid in SD rats, in which the imbalance of Bax/Bcl-2 ratio may play a significant role