Cellular Communication Networks Research Articles

Cellular communication network factor 1 promotes retinal leakage in diabetic retinopathy via inducing neutrophil stasis and neutrophil extracellular traps extrusion

BackgroundDiabetic retinopathy (DR) is a major cause of blindness and is characterized by dysfunction of the retinal microvasculature. Neutrophil stasis, resulting in retinal inflammation and the occlusion of retinal microvessels, is a key mechanism driving DR. These plugging neutrophils subsequently release neutrophil extracellular traps (NETs), which further disrupts the retinal vasculature. Nevertheless, the primary catalyst for NETs extrusion in the retinal microenvironment under diabetic conditions remains unidentified. In recent studies, cellular communication network factor 1 (CCN1) has emerged as a central molecule modulating inflammation in pathological settings. Additionally, our previous research has shed light on the pathogenic role of CCN1 in maintaining endothelial integrity. However, the precise role of CCN1 in microvascular occlusion and its potential interaction with neutrophils in diabetic retinopathy have not yet been investigated.MethodsWe first examined the circulating level of CCN1 and NETs in our study cohort and analyzed related clinical parameters. To further evaluate the effects of CCN1 in vivo, we used recombinant CCN1 protein and CCN1 overexpression for gain-of-function, and CCN1 knockdown for loss-of-function by intravitreal injection in diabetic mice. The underlying mechanisms were further validated on human and mouse primary neutrophils and dHL60 cells.ResultsWe detected increases in CCN1 and neutrophil elastase in the plasma of DR patients and the retinas of diabetic mice. CCN1 gain-of-function in the retina resulted in neutrophil stasis, NETs extrusion, capillary degeneration, and retinal leakage. Pre-treatment with DNase I to reduce NETs effectively eliminated CCN1-induced retinal leakage. Notably, both CCN1 knockdown and DNase I treatment rescued the retinal leakage in the context of diabetes. In vitro, CCN1 promoted adherence, migration, and NETs extrusion of neutrophils.ConclusionIn this study, we uncover that CCN1 contributed to retinal inflammation, vessel occlusion and leakage by recruiting neutrophils and triggering NETs extrusion under diabetic conditions. Notably, manipulating CCN1 was able to hold therapeutic promise for the treatment of diabetic retinopathy.

An optimized cooperative data transmission scheme in relay‐enabled cellular communication networks

SummaryCooperative transmission is of great significance in data transmission and resource schedule in mobile cellular communication networks. To attain the desired network transmission performance objectives over the whole cellular network system, we propose an appropriate cooperative data transmission scheme to optimize the data delivery efficiency in terms of the transmission time consumption for each and every transmission group. The proposed transmission optimization scheme includes the tasks of determining the transmission group, allocating the channel rate resource, specifying the cooperative transmission mechanism, and performing resource allocation and schedule as well. Firstly, we propose a utility function based rate allocation scheme to optimize the channel rate resource utilization for all those transmission groups over the cellular communication network. Based on it, we further present a cooperative data transmission scheme to deal with the data delivery and reception for all those subgroups with high efficiency over the whole network system. Particularly, we propose a resource efficiency function‐based coordination scheduling (EFCS) scheme to conduct the cooperative data transmission and resource schedule as well for each transmission group within the network. The EFCS scheme facilitates to determine the subgroups for schedule over each scheduling cycle, which can produce the best data transmission efficiency across both the direct and cooperative transmission hop. Both the theoretical analysis and the simulation evaluation results verify the superior performance of our proposed cooperative data transmission scheme.

LPA-induced expression of CCN2 in muscular fibro/adipogenic progenitors (FAPs): Unraveling cellular communication networks

Cellular Communication Network Factor 2, CCN2, is a profibrotic cytokine implicated in physiological and pathological processes in mammals. The expression of CCN2 is markedly increased in dystrophic muscles. Interestingly, diminishing CCN2 genetically or inhibiting its function improves the phenotypes of chronic muscular fibrosis in rodent models. Elucidating the cell-specific mechanisms behind the induction of CCN2 is a fundamental step in understanding its relevance in muscular dystrophies. Here, we show that the small lipids LPA and 2S-OMPT induce CCN2 expression in fibro/adipogenic progenitors (FAPs) through the activation of the LPA1 receptor and, to a lower extent, by also the LPA6 receptor. These cells show a stronger induction than myoblasts or myotubes. We show that the LPA/LPARs axis requires ROCK kinase activity and organized actin cytoskeleton upstream of YAP/TAZ signaling effectors to upregulate CCN2 levels, suggesting that mechanical signals are part of the mechanism behind this process. In conclusion, we explored the role of the LPA/LPAR axis on CCN2 expression, showing a strong cytoskeletal-dependent response in muscular FAPs.

An Efficient Vector-Based CRISPR/Cas9 System in Zebrafish Cell Line.

The clustered regularly interspaced short palindromic repeats/CRISPR-associated protein 9 (CRISPR/Cas9) system has been widely applied in animals as an efficient genome editing tool. However, the technique is difficult to implement in fish cell lines partially due to the lack of efficient promoters to drive the expression of both sgRNA and the Cas9 protein within a single vector. In this study, it was indicated that the zebrafish U6 RNA polymerase III (ZFU6) promoter could efficiently induce tyrosinase (tyr) gene editing and lead to loss of retinal pigments when co-injection with Cas9 mRNA in zebrafish embryo. Furthermore, an optimized all-in-one vector for expression of the CRISPR/Cas9 system in the zebrafish fibroblast cell line (PAC2) was constructed by replacing the human U6 promoter with ZFU6 promoter, basing on the lentiCRISPRV2 system that widely applied in mammal cells. This new vector could successfully target the cellular communication network factor 2a (ctgfa) gene and demonstrated its function in the PAC2 cell. Notably, the vector could also be used to edit the endogenous EMX1 gene in the mammal 293T cell line, implying its wide application potential. In conclusion, we established a new gene editing tool for zebrafish cell line, which could be a useful in vitro platform for high-throughput analyzing gene function in fish.

Spatiotemporal Evolution of Developing Palate in Mice

The intricate formation of the palate involves a series of complex events, yet its mechanistic basis remains uncertain. To explore major cell populations in the palate and their roles during development, we constructed a spatiotemporal transcription landscape of palatal cells. Palate samples from C57BL/6 J mice at embryonic days 12.5 (E12.5), 14.5 (E14.5), and 16.5 (E16.5) underwent single-cell RNA sequencing (scRNA-seq) to identify distinct cell subsets. In addition, spatial enhanced resolution omics-sequencing (stereo-seq) was used to characterize the spatial distribution of these subsets. Integrating scRNA-seq and stereo-seq with CellTrek annotated mesenchymal and epithelial cellular components of the palate during development. Furthermore, cellular communication networks between these cell subpopulations were analyzed to discover intercellular signaling during palate development. From the analysis of the middle palate, both mesenchymal and epithelial populations were spatially segregated into 3 domains. The middle palate mesenchymal subpopulations were associated with tooth formation, ossification, and tissue remodeling, with initial state cell populations located proximal to the dental lamina. The nasal epithelium of the palatal shelf exhibited richer humoral immune responses than the oral side. Specific enrichment of Tgfβ3 and Pthlh signals in the midline epithelial seam at E14.5 suggested a role in epithelial–mesenchymal transition. In summary, this study provides high-resolution transcriptomic information, contributing to a deeper mechanistic understanding of palate biology and pathophysiology.

CCN2/CTGF expression does not correlate with fibrosis in myeloproliferative neoplasms, consistent with noncanonical TGF-β signaling driving myelofibrosis

The classical BCR::ABL1-negative myeloproliferative neoplasms (MPN) form a group of bone marrow (BM) diseases with the potential to progress to acute myeloid leukemia or develop marrow fibrosis and subsequent BM failure. The mechanism by which BM fibrosis develops and the factors that drive stromal activation and fibrosis are not well understood. Cellular Communication Network 2 (CCN2), also known as CTGF (Connective Tissue Growth Factor), is a profibrotic matricellular protein functioning as an important driver and biomarker of fibrosis in a wide range of diseases outside the marrow. CCN2 can promote fibrosis directly or by acting as a factor downstream of TGF-β, the latter already known to contribute to myelofibrosis in MPN.To study the possible involvement of CCN2 in BM fibrosis in MPN, we assessed CCN2 protein expression by immunohistochemistry in 75 BM biopsies (55 × MPN and 20 × normal controls). We found variable expression of CCN2 in megakaryocytes with significant overexpression in a subgroup of 7 (13%) MPN cases; 4 of them (3 × essential thrombocytemia and 1 × prefibrotic primary myelofibrosis) showed no fibrosis (MF-0), 2 (1 × post-polycythemic myelofibrosis and 1 × primary myelofibrosis) showed moderate fibrosis (MF-2), and 1 (primary myelofibrosis) severe fibrosis (MF-3). Remarkably, CCN2 expression did not correlate with fibrosis or other disease parameters such as platelet count or thrombovascular events, neither in this subgroup nor in the whole study group. This suggests that in BM of MPN patients other, CCN2-independent pathways (such as noncanonical TGF-β signaling) may be more important for the development of fibrosis.

Abstract 560: IGF1 induces the expression of CYR61 in metastatic prostate cancer

Abstract The cysteine-rich angiogenic inducer 61 (CYR61) is a member of the cellular communication network (CCN) protein family that can be induced by growth factors. CYR61-specific functions are dependent on cellular context. In prostate cancer (PCa), CYR61 contributes to cell growth and survival through its interactions with extracellular ligands, such as integrins avb3 and a6b4, in the extracellular matrix space. Interestingly, CYR61 contains an insulin-like growth factor-binding protein domain suggesting that it may interact with insulin-like growth factor-I (IGF1). High serum levels of IGF1 are directly linked to PCa development and recently have been studied as a predictor of metastatic disease. Given the important roles that IGF1 and CYR61 play in PCa and their potential interaction, it is critical to investigate their molecular interplay. The correlation between PCa aggressiveness and circulating levels of CYR61 and IGF1 is poorly studied. Our goal was to assess the contribution of CYR61-IGF1 interaction to PCa cell proliferation. Their combined role may explain a proportion of aggressive PCa. This study was designed to characterize the role of IGF1-induced expression of CYR61 in metastatic PCa cellular models and to determine if this interaction contributes to aggressive tumor properties (e.g., proliferation, migration, tumorsphere formation). Using immunoblotting, we demonstrated that CYR61 is upregulated in the metastatic cell line PC3. Furthermore, optimized knockdown of CYR61 using siRNA significantly reduced PC3 cell proliferation, viability, and prostasphere formation. To examine the underlying mechanisms associated with IGF1 signaling, we assessed the activation of either the PI3/Akt and MAPK pathways in PC3 cells with CYR61 silencing. CYR61 siRNA-mediated knockdown decreased activation of the PI3/Akt pathway but did not affect the MAPK pathway. In addition, we found that IGF1 induces protein expression of CYR61 in a time-dependent manner, validated by both immunoblotting and confocal microscopy. In conclusion, these data provided evidence that CYR61 expression is induced by IGF1, and its inhibition decreased the capacity of metastatic PCa cells to proliferate, indicating a potential utilization of CYR61 inhibition in the therapy of metastatic PCa. Citation Format: Greisha L. Ortiz Hernandez, Mya Walker, Leanne Woods-Burnham, Rick A. Kittles, Carlos A. Casiano, Susan Neuhausen. IGF1 induces the expression of CYR61 in metastatic prostate cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 560.

Abstract 4316: Investigation the role of DDI2 in autophagy

Abstract Background: The ubiquitin-proteasome system (UPS) and autophagy-lysosomal pathway (ALP) are critical intracellular protein degradation pathways. In response to proteasome dysfunction, cells initiate compensatory autophagy to manage proteotoxic stress, which impacts cancer therapy efficacy. Despite current insights, the exact molecular mechanisms underlying the induction of autophagy due to impaired proteasome function remain unclear. The transcription factor nuclear factor erythroid-2-related factor 1 (NRF1) is the master regulator of proteasome subunit genes, which is activated by the protease DNA damage inducible 1 homolog 2 (DDI2) upon proteasome inhibition. DDI2 also acts as an ubiquitin shuttling factor, and its depletion causes the accumulation of highly ubiquitinated proteins, resulting in increased sensitivity to proteasome inhibition in cancer cells. However, cancer cells might trigger compensatory autophagy in response to DDI2 depletion to degrade ubiquitinated protein aggregates. Here, we demonstrated that DDI2 depletion plays a role in autophagy induction. Methods: A panel of cell lines of different origins (EW16 and ES1 human Ewing sarcoma, MIA PaCa-2 human pancreatic cancer, and NIH-3T3 murine fibroblasts) either control or DDI2-deficient were examined for autophagy activity following treatment with the autophagy inhibitor chloroquine (CQ). Through total proteome analysis, we identified an increase in cellular communication network factor 1 (CCN1) protein levels in DDI2-depleted cells, which plays a role in autophagy induction. To determine whether CCN1 is required and sufficient to induce autophagy, we applied small interfering RNA (siRNA), and viral constructs to knockdown and overexpress CCN1. Results: The autophagic flux measurements in four different DDI2-deficient cell lines revealed elevated LC3B-II protein levels, a known autophagy marker, following CQ treatment compared to their control. Western blotting analysis confirmed increased CCN1 protein levels in the same cell lines. The autophagy induction observed in DDI2-deficient cells was diminished by CCN1-siRNA, demonstrating that CCN1 may be required for autophagy induction. Furthermore, overexpressing CCN1 in wild-type cells resulted in increased LC3B-II protein levels, indicating that CCN1 alone is sufficient to induce autophagy. Conclusion: Targeting autophagy is a promising therapeutic strategy to improve the effects of anti-cancer therapies. We demonstrated that upon depletion of ubiquitin shuttle factor DDI2, secretory protein CCN1 accumulates leading to the subsequent induction of autophagy. These findings improve our understanding of the molecular basis governing DDI2’s role in crosstalk between protein degradation pathways. Targeting DDI2 in combination with autophagy inhibition could further potentiate these drugs as anti-cancer therapies. Citation Format: Nayyerehalsadat Hosseini, Holly A. Byers, Senthil K. Radhakrishnan. Investigation the role of DDI2 in autophagy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 4316.

Genetic Algorithm for Mode Selection in Device-to-Device (D2D) Communication for 5G Cellular Networks

The widespread use of smart devices and mobile applications is leading to a massive growth of wireless data traffic. With the rapidly growing of the customers’ data traffic demand, improving the system capacity and increasing the user throughput have become essential concerns for the future fifth-generation (5G) wireless communication network. In a conventional cellular system, devices are not allowed to directly communicate with each other in the licensed cellular spectrum and all communications take place through the base stations (BS) and core network. Device-to-Device (D2D) communication refers to a technology that enables devices to communicate directly with each other, without sending data to the base station and the core network. This technology has the potential to improve system performance, enhance the user experience, increase spectral efficiency, reduce the terminal transmitting power, reduce the burden of the cellular network, and reduce end to end latency. In D2D communication user equipment’s (UEs) are enabled to select among different modes of communication which are defined based on the frequency resource sharing. Dedicated mode where D2D devices directly transmit by using dedicated resources. Reuse mode where D2D devices reuse some resources of the cellular network. Outband mode where D2D communication uses unlicensed spectrum (e.g. the free 2.4 GHz Industrial Scientific and Medical (ISM) band or the 38 GHz millimetre wave band) where cellular communication does not take place. Cellular mode where the D2D communication is relayed via gNode B (gNB) and it is treated as cellular users. In this work, the target was to reach the optimal mode selection policy and genetic algorithm method was used with the objective of maximizing the total fitness function. Optimal mode selection policy was presented and analysed amongst cellular, dedicated, reused and outband mode. In the present study of mode selection issues in D2D enabled networks, genetic algorithm was proposed for the case when the cellular user equipment (UE) moves in the network. Quality of service (QoS) parameters, mobility parameters and Analytic Hierarchy Process (AHP) method were used to define the mode selection algorithm. To evaluate the performance of the proposed genetic algorithm, a study of the convergence of the algorithm and the signal-to-interference plus noise ratio (SINR) was done.

D2D Communication in a 5G mm-Wave Cellular Network for Wireless Sensor Networks

D2D Communication in a 5G mm-Wave Cellular Network for Wireless Sensor Networks

Optimal resource allocation strategy for integrated sensing and communication cellular network with multiple user demands

AbstractFuture communication networks are widely considered to be able to provide both high‐speed communication service and reliable sensing service. Integrated sensing and communication (ISAC) is considered to be the key technology to realize this vision. Appropriate resource allocation strategy is essential for ensuring the quality of both communication and sensing services in terms of ISAC. Existing ISAC‐based resource allocation schemes mainly focus on the coexistence of sensing and communication. However, in multi‐user ISAC networks, the services required by users are diverse, including sensing‐only, communication‐only and dual‐function cases. To this end, a resource allocation strategy is proposed based on user quality of service (QoS). Specifically, the sum rate of cellular network is maximized via optimizing spectrum resource selection and transmit power, while satisfying the sensing QoS. The optimal solution to the entire problem is achieved by first demonstrating that the communication rate in this paper is a monotonically increasing function of sensing power, which allows to obtain the optimal power allocation scheme. Subsequently, a matching method is employed to obtain the optimal spectrum sharing scheme. Numerical results validate the effectiveness of the proposed algorithm and also unveil a flexible trade‐off in ISAC systems over the benchmark scheme.

Transient analysis of energy-saving strategy for cognitive radio networks using G-queue with heterogeneity

Energy efficiency, high data speeds, and effective spectrum utilization stand as the primary factors governing 5G and beyond networks. A base station (BS) in a cognitive radio network (CRN) that conserves energy during sleep periods is a promising contender for achieving more effective spectrum allocation. An efficient energy-saving strategy is offered in this study to achieve greener communication in wireless cellular networks. This study aims to propose and analyze an energy-saving scheme for the BS, taking into account the heterogeneity and reliability of networks. The entire system is modeled as a three-dimensional Markov chain by establishing a discrete-time preemptive priority queueing model with single vacation, heterogeneous packets, and negative packets such as viruses. Then, the transient analysis of the Markov chain is performed using the recursive method. Utilizing the transient probability distribution, we present numerical results derived from reliability analysis and queueing analysis to substantiate the validity of the proposed model. Furthermore, results based on the energy-saving degree are showcased to affirm the effectiveness of the proposed scheme. Finally, a reward cost function is obtained depending on the successful transmission of secondary packets, and the Quasi-Newton method is used to determine the optimal reward cost.

Single-Cell RNA Sequencing Reveals the Cellular Landscape of Longissimus Dorsi in a Newborn Suhuai Pig.

The introduction of single-cell RNA sequencing (scRNA-seq) technology has spurred additional advancements in analyzing the cellular composition of tissues. The longissimus dorsi (LD) in pigs serves as the primary skeletal muscle for studying meat quality in the pig industry. However, the single-cell profile of porcine LD is still in its infancy stage. In this study, we profiled the transcriptomes of 16,018 cells in the LD of a newborn Suhuai pig at single-cell resolution. Subsequently, we constructed a cellular atlas of the LD, identifying 11 distinct cell populations, including endothelial cells (24.39%), myotubes (18.82%), fibro-adipogenic progenitors (FAPs, 18.11%), satellite cells (16.74%), myoblasts (3.99%), myocytes (5.74%), Schwann cells (3.81%), smooth muscle cells (3.22%), dendritic cells (2.99%), pericytes (1.86%), and neutrophils (0.33%). CellChat was employed to deduce the cell-cell interactions by evaluating the gene expression of receptor-ligand pairs across different cell types. The results show that FAPs and pericytes are the primary signal contributors in LD. In addition, we delineated the developmental trajectory of myogenic cells and examined alterations in the expression of various marker genes and molecular events throughout various stages of differentiation. Moreover, we found that FAPs can be divided into three subclusters (NR2F2-FAPs, LPL-FAPs, and TNMD-FAPs) according to their biological functions, suggesting that the FAPs could be associated with the differentiation of tendon cell. Taken together, we constructed the cellular atlas and cell communication network in LD of a newborn Suhuai pig, and analyzed the developmental trajectory of myogenic cells and the heterogeneity of FAPs subpopulation cells. This enhances our comprehension of the molecular features involved in skeletal muscle development and the meat quality control in pigs.

Examining the function of macrophage oxidative stress response and immune system in glioblastoma multiforme through analysis of single-cell transcriptomics.

Glioblastoma (GBM), a prevalent malignant neoplasm within the neuro-oncological domain, has been a subject of considerable scrutiny. Macrophages, serving as the principal immunological constituents, profoundly infiltrate the microenvironment of GBM. However, investigations elucidating the intricate immunological mechanisms governing macrophage involvement in GBM at the single-cell level remain notably limited. We conducted a comprehensive investigation employing single-cell analysis, aiming to redefine the intricate cellular landscape within both the core and peripheral regions of GBM tumors. Our analytical focus extended to the profound study of macrophages, elucidating their roles within the context of oxidative stress, intercellular information exchange, and cellular trajectories concerning GBM and its assorted subpopulations. We pursued the identification of GBM prognostic genes intricately associated with macrophages. Utilizing experimental research to investigate the relevance of MANBA in the context of GBM. Our investigations have illuminated the central role of macrophages in the intricate interplay among various subpopulations within the GBM microenvironment. Notably, we observed a pronounced intensity of oxidative stress responses within macrophages when compared to their GBM counterparts in other subpopulations. Moreover, macrophages orchestrated intricate cellular communication networks, facilitated by the SPP1-CD44 axis, both internally and with neighboring subpopulations. These findings collectively suggest the potential for macrophage polarization from an M1 to an M2 phenotype, contributing to immune suppression within the tumor microenvironment. Furthermore, our exploration unearthed GBM prognostic genes closely associated with macrophages, most notably MANBA and TCF12. Remarkably, MANBA appears to participate in the modulation of neuroimmune functionality by exerting inhibitory effects on M1-polarized macrophages, thereby fostering tumor progression. To bolster these assertions, experimental validations unequivocally affirmed the promotional impact of MANBA on GBM, elucidated through its capacity to curb cell proliferation, invasiveness, and metastatic potential. These revelations represent a pivotal step towards unraveling the intricate immunological mechanisms governing the interactions between macrophages and diverse subpopulations within the GBM milieu. Furthermore, they lay the foundation for the development of an innovative GBM prognostic model, with MANBA at its epicenter, and underscore the potential for novel immunotherapeutic targets in the ongoing pursuit of enhanced treatment modalities for this formidable malignancy.

CCN3/NOV inhibition attenuates oxidative stress-induced apoptosis of mouse neural stem/progenitor cells by blocking the activation of p38 MAPK: An in vitro study

Neural stem/progenitor cells (NSPCs) hold immense promise in clinical applications, yet the harsh conditions resulting from central nervous system (CNS) injuries, particularly oxidative stress, lead to the demise of both native and transplanted NSPCs. Cellular communication network factor 3 (CCN3) exhibits a protective effect against oxidative stress in various cell types. This study investigates the impact of CCN3 on NSPCs apoptosis induced by oxidative stress. To establish models of primary cultured mouse NSPCs under oxidative stress, we exposed them to 50 μM H2O2 for 4 h. Remarkably, pre-exposing CCN3 exacerbated the H2O2-induced decline in cell viability in a concentration-dependent manner. However, employing gene-targeted siRNA to inhibit CCN3 protected NSPCs against H2O2-induced cell death. Conversely, CCN3 replenishment reversed this protective effect, as evidenced by TUNEL staining, the ratio of Cleaved-caspase-3 to Pro-caspase-3, and Bcl-2/Bax. Further investigations revealed that CCN3 pretreatment increased the phosphorylation level of p38 MAPK, while silencing CCN3 diminished p38 MAPK activation. Ultimately, the impact of changes in CCN3 protein expression on H2O2-induced apoptosis was nullified using anisomycin (a p38 activator) and SB 203580 (a p38 inhibitor). Our findings suggest that CCN3 inhibition prevents H2O2-induced cell death in cultured mouse NSPCs via the p38 pathway. These discoveries may contribute to the development of strategies aimed at enhancing the survival of both endogenous and transplanted NSPCs following CNS oxidative stress insults.

Blockchain based mobile communication data privacy protection algorithm for cellular networks

The rapid development of mobile communication technology not only brings great convenience to users, but also brings the risk of user data privacy leakage. Due to the broadcasting nature of mobile communication transmission, open wireless interfaces have become a security vulnerability for mobile devices such as mobile phones, which can be easily eavesdropped. This article studied a data privacy protection algorithm suitable for mobile communication in cellular networks based on the anonymous mechanism of blockchain. This article first analyzes the overall framework and anonymity technology of blockchain data from the perspective of privacy and queryability. Then, based on blockchain technology, consistency mechanisms, privacy control, and access rights management are designed. Finally, mobile communication data privacy protection algorithms are designed and implemented through data encryption and verification. The latency of transactions under different task volumes and throughput at different nodes were analyzed to verify the reliability of several anonymous mechanisms in cellular network mobile communication data privacy protection in blockchain. Based on the experimental results, it was concluded that the reliability range of CryptoNote and the zero coin and zero currency protocol mechanism in the specified nodes was between 92 and 99%. This article utilized blockchain technology to distribute mobile communication data in nodes and achieve decentralized data transmission, thus protecting the privacy of wireless network communication data. By analyzing the reliability of anonymous mechanisms based on blockchain in mobile communication nodes, it was concluded that this method had certain research value.

Renewable energy electric sources as a support for multilevel cellular communication networks in various environment conditions – case study

Renewable energy electric sources as a support for multilevel cellular communication networks in various environment conditions – case study

A Novel Resource Sharing Scheme for Vehicular Communication in 5G Cellular Networks for Smart Cities

A Novel Resource Sharing Scheme for Vehicular Communication in 5G Cellular Networks for Smart Cities

Energy Efficiency-Oriented Joint Communication and Computation Resource Management in NOMA-Enabled V2X Underlaid Cellular Networks

Energy Efficiency-Oriented Joint Communication and Computation Resource Management in NOMA-Enabled V2X Underlaid Cellular Networks

Interference Management Using Distance-based Clustering Method for D2D Communication Underlaying Multicell Cellular Network

Device-to-Device (D2D) communication is a technology candidate to support the next generation of cellular communication networks. D2D has the potential to boost the efficiency of frequency resources and system capacity. Generally, D2D performs in-band underlaying or shares frequency channels with traditional cellular users, which can cause co-channel interference problems between these two types of users. This paper offers a solution through a clustering technique for D2D users (DUEs) to reduce interference among DUEs. Clustering technique is performed on DUEs by allocating different frequency channels in a group, in order to reduce the interference effects experienced. Thus, it is expected that through this proposed method, both D2D and cellular users can experience better signal quality with minimal interference effects. Two systems have been considered i.e., the conventional/baseline system and the system with the proposed clustering method. The simulation results show that the SINR (Signal to Interference plus Noise Ratio) values and throughput for the proposed system compared to the baseline system has increased. The SINR result obtained is 16.8 dB for the baseline system and 17.68 dB for the proposed system, and resulting an improvement of 5.4%. Therefore, applying the proposed clustering method is able to increase acceptability of the desired signals for the observed DUEs. Then, the throughput value also increases by 5%, i.e., from 56.17 to 59 Mbps, which the system with the proposed clustering method provides a better increase in data transmission speed compared to the baseline system.