USP29 activation mediated by FUBP1 promotes AURKB stability and oncogenic functions in gastric cancer.

BACKGROUND: Gastric cancer is a highly prevalent cancer type and the underlying molecular mechanisms are not fully understood. Ubiquitin-specific peptidase (USP) 29 has been suggested to regulate cell fate in several types of cancer, but its potential role in gastric carcinogenesis remains unclear. METHODS: The expression of USP29 in normal and gastric cancer tissues was analyzed by bioinformatics analysis, immunohistochemistry and immunoblot. Gene overexpression, CRISPR-Cas9 technology, RNAi, and Usp29 knockout mice were used to investigate the roles of USP29 in cell culture, xenograft, and benzo[a]pyrene (BaP)-induced gastric carcinogenesis models. We then delineated the underlying mechanisms using mass spectrometry, co-immunoprecipitation (Co-IP), immunoblot, ubiquitination assay, chromatin immunoprecipitation (ChIP), quantitative real-time PCR (qRT-PCR), and luciferase assays. RESULTS: In this study, we found that USP29 expression was significantly upregulated in gastric cancers and associated with poor patient survival. Ectopic expression of USP29 promoted, while depletion suppressed the tumor growth in vitro and in vivo mouse model. Mechanistically, transcription factor far upstream element binding protein 1 (FUBP1) directly activates USP29 gene transcription, which then interacts with and stabilizes aurora kinase B (AURKB) by suppressing K48-linked polyubiquitination, constituting a FUBP1-USP29-AURKB regulatory axis that medicates the oncogenic role of USP29. Importantly, systemic knockout of Usp29 in mice not only significantly decreased the BaP-induced carcinogenesis but also suppressed the Aurkb level in forestomach tissues. CONCLUSIONS: These findings uncovered a novel FUBP1-USP29-AURKB regulatory axis that may play important roles in gastric carcinogenesis and tumor progression, and suggested that USP29 may become a promising drug target for cancer therapy.

A prognostic signature of fatty acid metabolism-related genes for predicting survival of gastric cancer patients.

To analyze the expression profile of fatty acid metabolism (FAM)-related genes, identify a prognostic signature, and evaluate its clinical value for gastric cancer (GC) patients. The mRNA expression profiles of 493 FAM-related genes were obtained from TCGA database. Differentially expressed genes (DEGs) between cancer and non-cancer samples were identified, and their relationships with overall survival (OS) of GC patients were evaluated. A prognostic signature of FAM-related genes was identified by the LASSO regression model, and its predictive performance was tested by an independent external cohort. Ninety-three DEGs were identified, of which 44 were downregulated and 49 were upregulated. After optimizing risk characteristics, a prognostic signature of four FAM-related genes (ACBD5, AVPR1A, ELOVL4, and FAAH) were developed. All patients were divided into high-risk (>1.020) and low-risk groups (≤1.020) on the basis of the median risk score. Survival analysis indicated that high-risk patients had a shorter OS than low-risk patients (5-year OS rate, 26.3% vs. 45.0%, p < 0.001). The AUC values for the prediction of 3-year and 5-year OS were 0.664 and 0.624, respectively. In the GSE62254 data set, the 5-year OS rate of high-risk and low-risk patients were 44.7% versus 61.5%, respectively (p = 0.003). The AUC values were 0.632 and 0.627 at 3-year and 5-year prediction. The prognostic signature of FAM-related genes was an independent predictor of OS (hanzard ratio [HR] for TCGA cohort: 1.851, 95% confidence interval [CI]: 1.394-2.458, p < 0.001; HR for GSE62254: 1.549, 95% CI: 1.098-2.185, p = 0.013). The risk signature of four FAM-related genes was a valuable prognostic tool, and it might be helpful for clinical management and therapeutic decision of gastric cancer patients.

Research on Computing Resource Measurement and Routing Methods in Software Defined Computing First Network.

Computing resource measurement and computing routing are essential technologies in the computing first network (CFN), serving as its foundational elements. This paper introduces a Software Defined Computing First Network (SD-CFN) architecture. Building upon this framework, a Dynamic-Static Integrated Computing Resource Measurement Mechanism (DCRMM) is proposed, incorporating methods such as the entropy weight method and K-Means clustering. The DCRMM algorithm outperforms the Maximum-closest Static Algorithm (MSA) and Maximum Closest Dynamic Algorithm (MDA) in terms of node stability, node utilization, and node matching accuracy. Additionally, a Reinforcement Learning and Software Defined Computing First Networking Routing (RSCR) algorithm is presented as a software-defined computing routing solution within the SD-CFN. RSCR introduces a knowledge plane responsible for computing routing calculations. It comprehensively considers factors such as link latency, available bandwidth, and packet loss rate. Simulation experiments conducted on the GÉANT topology demonstrate that RSCR outperforms the OSPF algorithm in terms of link latency, packet loss rate, and throughput. DCRMM and RSCR offer innovative solutions for computing resource measurement and computing routing in computing first networks.

Mixed adenoneuroendocrine carcinoma originating from the appendix and colorectum: a comparative analysis of a large population-based database.

PURPOSE: As a rare gastrointestinal neoplasm, the demographic, clinicopathological, and prognostic characteristics of mixed adenoneuroendocrine carcinoma (MANEC) remain unclear. The purpose of this study was to evaluate its biological features, survival outcome, and prognostic factors. METHODS: From the Surveillance, Epidemiology, and End Results (SEER) database, we retrospectively reviewed clinicopathological and survival data of 513 patients who were histopathologically diagnosed with MANEC of the appendix and colorectum bettween 2004 and 2015. The clinicopathological features and survival outcomes of MANEC located at different anatomical locations were compared, and predictive factors for cancer-specific survival (CSS) and overall survival (OS) were assessed. RESULTS: In terms of anatomical distribution of MANEC, the appendix (64.5%, 331/513) was more frequently involved, followed by colon (28.1%, 144/513) and rectum (7.4%, 38/513). The MANEC at different anatomical locations had a distinct clinicopathological characteristic, and colorectal MANEC was significantly associated with more aggressive biological features. The survival outcomes of appendiceal MANEC were significantly better than that of colorectal MANEC (3-year CSS rate 73.8% vs 59.4%, P = 0.010; 3-year OS 69.2% vs 48.3%, P < 0.001). In addition, hemicolectomy had a better survival benefit than appendicectomy for patients with appendiceal MANEC, regardless of lymph node metastasis (P < 0.05). Tumor location, histology grade III, tumor size > 2 cm, T3-T4 stage, lymph node metastasis, and distant metastasis were independent prognostic factors for patients with MANEC. CONCLUSIONS: Tumor location had an important prognostic significance for MANEC. As an uncommon clinical entity, colorectal MANEC had more aggressive biological features and worse prognosis than its appendiceal counterpart. The standard surgical procedure and clinical management strategy for MANEC need to be established.

Reducing Flow Table Update Costs in Software-Defined Networking.

In software-defined networking (SDN), the traffic forwarding delay highly depends on the latency associated with updating the forwarding rules in flow tables. With the increase in fine-grained flow control requirements, due to the flexible control capabilities of SDN, more rules are being inserted and removed from flow tables. Moreover, the matching fields of these rules might overlap since multiple control domains might generate different rules for similar flows. This overlap implies dependency relationships among the rules, imposing various restrictions on forwarding entries during updates, e.g., by following update orders or storing entries at specified locations, especially in flow tables implemented using ternary content addressable memory (TCAM); otherwise, mismatching or packet dropping will occur. It usually takes a while to resolve and maintain dependencies during updates, which hinders high forwarding efficiency. To reduce the delay associated with updating dependent rules, in this paper, we propose an updating algorithm for TCAM-based flow tables. We formulate the TCAM maintenance process as an NP-hard problem and analyze the inefficiency of existing moving approaches. To solve the problem, we propose an optimal moving chain for single rule updates and provide theoretical proof for its minimum moving steps. For multiple rules arriving at a switch simultaneously, we designed a dynamic approach to update concurrent entries; it is able to update multiple rules heuristically within a restricted TCAM region. As the update efficiency concerns dependencies among rules, we evaluate our flow table by updating algorithms with different dependency complexities. The results show that our approach achieves about 6% fewer moving steps than existing approaches. The advantage is more pronounced when the flow table is heavily utilized and rules have longer dependency chains.

Synergistic targeting of CHK1 and mTOR in MYC-driven tumors.

Deregulation of v-myc avian myelocytomatosis viral oncogene homolog (MYC) occurs in a broad range of human cancers and often predicts poor prognosis and resistance to therapy. However, directly targeting oncogenic MYC remains unsuccessful, and indirectly inhibiting MYC emerges as a promising approach. Checkpoint kinase 1 (CHK1) is a protein kinase that coordinates the G2/M cell cycle checkpoint and protects cancer cells from excessive replicative stress. Using c-MYC-mediated T-cell acute lymphoblastic leukemia (T-acute lymphoblastic leukemia) and N-MYC-driven neuroblastoma as model systems, we reveal that both c-MYC and N-MYC directly bind to the CHK1 locus and activate its transcription. CHIR-124, a selective CHK1 inhibitor, impairs cell viability and induces remarkable synergistic lethality with mTOR inhibitor rapamycin in MYC-overexpressing cells. Mechanistically, rapamycin inactivates carbamoyl-phosphate synthetase 2, aspartate transcarbamoylase, and dihydroorotase (CAD), the essential enzyme for the first three steps of de novo pyrimidine synthesis, and deteriorates CHIR-124-induced replicative stress. We further demonstrate that dual treatments impede T-acute lymphoblastic leukemia and neuroblastoma progression in vivo. These results suggest simultaneous targeting of CHK1 and mTOR as a novel and powerful co-treatment modality for MYC-mediated tumors.

WEE1 inhibition induces glutamine addiction in T-cell acute lymphoblastic leukemia.

T-cell acute lymphoblastic leukemias (T-ALLs) are aggressive and heterogeneous hematologic tumors resulting from the malignant transformation of T-cell progenitors. The major challenges in the treatments of T-ALL are dose-limiting toxicities of chemotherapeutics and drug resistance. Despite important progress in deciphering the genomic landscape of T-ALL, translation of these findings into effective targeted therapies remains largely unsuccessful. New targeted agents with significant antileukemic efficacy and less toxicity are in urgent need. We herein report that the expression of WEE1, a nuclear tyrosine kinase involved in cell cycle G2-M checkpoint signaling, is significantly elevated in T-ALL. Mechanistically, oncogenic MYC directly binds to the WEE1 promoter and activates its transcription. T-ALL cells particularly rely on the elevated WEE1 for cell viability. Pharmacological inhibition of WEE1 elicits global metabolic reprogramming which results in a marked suppression of aerobic glycolysis in T-ALL cells, leading to an increased dependency on glutaminolysis for cell survival. As such, dual targeting of WEE1 and glutaminase (GLS1) induces synergistic lethality in multiple T-ALL cell lines and shows great efficacy in T-ALL patient-derived xenografts. These findings provide mechanistic insights in the regulation of WEE1 kinase in T-ALL and suggest an additional vulnerability during WEE1 inhibitor treatments. In aggregate, we highlight a promising combination strategy of dual inhibition of cell cycle kinase and metabolic enzymes for T-ALL therapeutics.

Controllable chiral behavior of type-II core/shell quantum dots adjusted by shell thickness and coordinated ligands.

Chiral semiconductor nanomaterials induced by capped chiral ligands are of great interest for both theoretical studies and advanced applications. In this study, CdTe/CdSe quantum dots (QDs), defined as type-II core/shell nanostructure, with the advantage of a good separation of holes and electrons are imparted chirality with L/D-cysteine and L/D-penicillamine molecules. Circular dichroism (CD) at exciton transitions from cysteine- and penicillamine-capped QDs is different in shape and intensity. CD intensities decrease with increasing shell thickness from three monolayers to six monolayers, indicating a decreased hybridization degree between the holes in CdTe core and the electrons in chiral ligands. Elevated cysteine concentration leads to decreased g-factor, probably due to an altered binding mode from tridentate to bidentate. Our observations provide further insights into the understanding of chiral phenomenon as well as optimized design and applications of chiral nanostructures.

Cloning, expression profile of the complement component C9 gene and influence of the recombinant C9 protein on peripheral mononuclear leukocytes transcriptome in half-smooth tongue sole (Cynoglossus semilaevis).

The ninth complement component (C9) is a terminal complement component (TCC) that is involved in creating the membrane attack complex (MAC) on the target cell surface. In this study, the CsC9 (C9 of Cynoglossus semilaevis) cDNA sequence was cloned and characterized. The full-length CsC9 cDNA measured 2,150 bp, containing an open reading frame (ORF) of 1,803 bp, a 5'-untranslated region (UTR) of 24 bp and a 3'-UTR of 323 bp. A domain search revealed that the CsC9 protein contains five domains, including two TSP1s, an LDLRA, an EGF, and a MACPF. Quantitative real-time PCR analysis showed that CsC9 at the mRNA level was expressed in all the tested tissues, with the highest expression being observed in the liver. CsC9 expression is significantly upregulated in the tested tissues after challenge with Vibrio anguillarum. To further characterize the role of CsC9, peripheral blood mononuclear cells of C. semilaevis were used for transcriptome analysis after incubation with recombinant CsC9 (rCsC9) protein. A total of 3,775 significant differentially expressed genes (DEGs) were identified between the control and the rCsC9-treated group, including 2,063 upregulated genes and 1,712 downregulated genes. KEGG analyses revealed that the DEGs were enriched in cell adhesion molecules, cytokine-cytokine receptor interactions, T cell receptor signaling pathways, B cell receptor signaling pathways and Toll-like receptor signaling pathways. The results of this study indicate that in addition to participating in MAC formation, CsC9 might play multiple roles in the innate and adaptive immunity of C. semilaevis.

Autophagy regulates apoptosis by targeting NOXA for degradation.

Apoptosis and autophagy mutually regulate various cellular physiological and pathological processes. The crosstalk between autophagy and apoptosis is multifaceted and complicated. Elucidating the molecular mechanism of their crosstalk will advance the therapeutic applications of autophagy for treating cancer and other diseases. NOXA, a BH3-only member of the BCL-2 family, was reported to induce apoptosis and promote autophagy. Here, we report that autophagy regulates apoptosis by targeting NOXA for degradation. Inhibiting autophagy increases NOXA protein levels by extending the protein half-life. NOXA accumulation effectively suppresses tumor cell growth by inducing apoptosis, which is further enhanced when p53 is present. Mechanistically, NOXA is hijacked by p62 as autophagic cargo, and its three lysine residues at the C-terminus are necessary for NOXA degradation in lysosomes. Taken together, our study demonstrates that NOXA serves as a bridge in the crosstalk between autophagy and apoptosis and implies that autophagy inhibitors could be an effective therapy for cancer, especially wild-type p53-containing cancer.

Chiroptical Activity of Type II Core/Shell Cu2S/CdSe Nanocrystals.

Ligand-induced chirality in core/shell nanocrystals (NCs) has attracted extensive attention because of many valuable potential applications. However, the cause of chirality especially in semiconductor nanomaterials is still under debate despite the creation of chiral type I core/shell structures. Herein, we synthesized a kind of new Cu2S/CdSe core/shell nanostructure to study the underlying reason. Four samples of Cu2S/CdSe were synthesized utilizing successive ion layer adsorption and reaction to vary the thickness of the CdSe shell upon a Cu2S core with 5 nm diameter. The chirality of type II Cu2S/CdSe NCs is imparted by l-/d-cysteine and penicillamine, which could be modulated with an increasing thickness of the CdSe shell. To the best of our knowledge, this is the first report of chiral type II core/shell semiconductor NCs. The hybridization theory can explain the variation trend of g factors with every increase in shell thickness from four monolayers (4 ML) to 7 ML. The results indicate that the chiroptical activity of semiconductor NCs is mainly due to hybridization between the holes in the valence band of NCs and the highest occupied molecular orbitals of the chiral ligands. In addition, Cu2S/CdSe NCs show a better chiroptical intensity in comparison with the type I structure according to previous work. The first design of chiral type II Cu2S/CdSe core/shell NCs and a detailed investigation of chiral variation trend help to give a better understanding of the chiral interaction between ligands and core/shell semiconductor nanostructures.

FoxG1 facilitates proliferation and inhibits differentiation by downregulating FoxO/Smad signaling in glioblastoma.

BACKGROUND: To investigate the effects and underlying molecular mechanisms of FoxG1 expression on glioblastoma multiforme (GBM) models. METHODS: Expression levels of FoxG1 and other cancer-related biomarkers were evaluated by qRT-PCR, immunoblotting and immunohistochemistry. Crystal violet staining and MTT assay and were applied in this study to verify cell proliferation ability and viability of GBM cell models with/without drug treatment. RESULTS: Immunohistochemical and qRT-PCR assays showed that endogenous FoxG1 expression levels were positively correlated to the GBM disease progression. Overexpression of FoxG1 protein resulted in increased cell viability, G2/M cell cycle arrest, as well as the downregulation of p21 and cyclin B1. In addition, western blot assays reported that enforced expression of FoxG1 suppressed GAPF and facilitated the expression of Sox2 and Sox5. Meanwhile the downstream targets of FoxG1, such as FoxO1 and pSmad1/5/8 were activated. Overexpression of FoxG1 under TMZ treatment restored the cell viability as well as the expression levels of Sox2 and Sox5, yet downregulated expression levels of p21 and cyclin B1. The downstream FoxG1-induced FoxO/Smad signaling was re-inhibited under TMZ treatments. CONCLUSIONS: Our findings suggest that FoxG1 functions as an onco-factor by promoting proliferation, as well as inhibiting differential responses in glioblastoma by downregulating FoxO/Smad signaling.

Expression analysis of genes encoding double B-box zinc finger proteins in maize.

The B-box proteins play key roles in plant development. The double B-box (DBB) family is one of the subfamily of the B-box family, with two B-box domains and without a CCT domain. In this study, 12 maize double B-box genes (ZmDBBs) were identified through a genome-wide survey. Phylogenetic analysis of DBB proteins from maize, rice, Sorghum bicolor, Arabidopsis, and poplar classified them into five major clades. Gene duplication analysis indicated that segmental duplications made a large contribution to the expansion of ZmDBBs. Furthermore, a large number of cis-acting regulatory elements related to plant development, response to light and phytohormone were identified in the promoter regions of the ZmDBB genes. The expression patterns of the ZmDBB genes in various tissues and different developmental stages demonstrated that ZmDBBs might play essential roles in plant development, and some ZmDBB genes might have unique function in specific developmental stages. In addition, several ZmDBB genes showed diurnal expression pattern. The expression levels of some ZmDBB genes changed significantly under light/dark treatment conditions and phytohormone treatments, implying that they might participate in light signaling pathway and hormone signaling. Our results will provide new information to better understand the complexity of the DBB gene family in maize.

A nematicidal tannin from Punica granatum L. rind and its physiological effect on pine wood nematode (Bursaphelenchus xylophilus).

The ethanol extract of Punica granatum L. rind was tested to show significant nematicidal activity against pine wood nematode. Three nematicidal compounds were obtained from the ethanol extract by bioassay-guided fractionation and identified as punicalagin 1, punicalin 2, and corilagin 3 by mass and nuclear magnetic resonance spectral data analysis. Punicalagin 1 was most active against PWN among the purified compounds with the LC50 value of 307.08µM in 72h. According to the enzyme assays in vitro, punicalagin 1 could inhibit the activity of acetylcholinesterase, amylase and cellulase from PWN with IC50 value of 0.60mM, 0.96mM and 1.24mM, respectively. The morphological structures of PWNs treated by punicalagin 1 were greatly changed. These physiological effects of punicalagin 1 on PWN may helpful to elucidate its nematicidal mechanism.

Arsenic Uptake and Translocation in Plants.

Arsenic (As) is a highly toxic metalloid that is classified as a non-threshold class-1 carcinogen. Millions of people worldwide suffer from As toxicity due to the intake of As-contaminated drinking water and food. Reducing the As concentration in drinking water and food is thus of critical importance. Phytoremediation of soil contaminated with As and the reduction of As contamination in food depend on a detailed understanding of As uptake and transport in plants. As transporters play essential roles in As uptake, translocation and accumulation in plant cells. In this review, we summarize the current understanding of As transport in plants, with an emphasis on As uptake, mechanisms of As resistance and the long-distance translocation of As, especially the accumulation of As in grains through phloem-mediated transport.

Triptolide inhibits transcription of hTERT through down-regulation of transcription factor specificity protein 1 in primary effusion lymphoma cells.

Primary effusion lymphoma (PEL) is a rare and aggressive non-Hodgkin's lymphoma. Human telomerase reverse transcriptase (hTERT), a key component responsible for the regulation of telomerase activity, plays important roles in cellular immortalization and cancer development. Triptolide purified from Tripterygium extracts displays a broad-spectrum bioactivity profile, including immunosuppressive, anti-inflammatory, and anti-tumor. In this study, it is investigated whether triptolide reduces hTERT expression and suppresses its activity in PEL cells. The mRNA and protein levels of hTERT were examined by real time-PCR and Western blotting, respectively. The activity of hTERT promoter was determined by Dual luciferase reporter assay. Our results demonstrated that triptolide decreased expression of hTERT at both mRNA and protein levels. Further gene sequence analysis indicated that the activity of hTERT promoter was suppressed by triptolide. Triptolide also reduced the half-time of hTERT. Additionally, triptolide inhibited the expression of transcription factor specificity protein 1(Sp1) in PEL cells. Furthermore, knock-down of Sp1 by using specific shRNAs resulted in down-regulation of hTERT transcription and protein expression levels. Inhibition of Sp1 by specific shRNAs enhanced triptolide-induced cell growth inhibition and apoptosis. Collectively, our results demonstrate that the inhibitory effect of triptolide on hTERT transcription is possibly mediated by inhibition of transcription factor Sp1 in PEL cells.

Bioinformatics analysis of proteomics profiles in senescent human primary proximal tubule epithelial cells.

BACKGROUND: Dysfunction of renal tubule epithelial cells is associated with renal tubulointerstitial fibrosis. Exploration of the proteomic profiles of senesced tubule epithelial cells is essential to elucidate the mechanism of tubulointerstitium development. METHODS: Primary human proximal tubule epithelial cells from passage 3 (P3) and passage 6 (P6) were selected for evaluation. EdU and SA-ß-galactosidase staining were used to detect cell senescence. p53, p21, and p16 were detected by Western blot analysis. Liquid chromatography mass spectrometry (LC-MS) was used to examine differentially expressed proteins (DEPs) between P6 and P3 cells. The expression of DEPs was examined by Western blot analysis. Bioinformatics analysis was performed by protein-protein interaction and gene ontology analyses. RESULTS: The majority of tubule cells from passage 6 (P6) stained positive for SA-ß-galactosidase, whereas passage 3 (P3) cells were negative. Senescence biomarkers, including p53, p21, and p16, were upregulated in P6 cells relative to P3 cells. EdU staining results showed a lower rate of EdU positive cells in P6 cells than in P3 cells. LC-MS was used to examine DEPs between P6 and P3 cells. These DEPs are involved in glycolysis, response to stress, cytoskeleton regulation, oxidative reduction, ATP binding, and oxidative stress. Using Western blot analysis, we validated the down-regulation of AKR1B1, EEF2, EEF1A1, and HSP90 and the up-regulation of VIM in P6 cells seen in the LC-MS data. More importantly, we built the molecular network based on biological functions and protein-protein interactions and found that the DEPs are involved in translation elongation, stress, and glycolysis, and that they are all associated with cytoskeleton regulation, which regulates senescent cell activities such as apoptosis and EMT in tubule epithelial cells. CONCLUSIONS: We explored proteomic profile changes in cell culture-induced senescent cells and built senescence-associated molecular networks, which will help to elucidate the mechanisms of senescence in human proximal tubule epithelial cells.

Performance Analysis of Integrated Wireless Sensor and Multibeam Satellite Networks Under Terrestrial Interference.

This paper investigates the performance of integrated wireless sensor and multibeam satellite networks (IWSMSNs) under terrestrial interference. The IWSMSNs constitute sensor nodes (SNs), satellite sinks (SSs), multibeam satellite and remote monitoring hosts (RMHs). The multibeam satellite covers multiple beams and multiple SSs in each beam. The SSs can be directly used as SNs to transmit sensing data to RMHs via the satellite, and they can also be used to collect the sensing data from other SNs to transmit to the RMHs. We propose the hybrid one-dimensional (1D) and 2D beam models including the equivalent intra-beam interference factor ß from terrestrial communication networks (TCNs) and the equivalent inter-beam interference factor α from adjacent beams. The terrestrial interference is possibly due to the signals from the TCNs or the signals of sinks being transmitted to other satellite networks. The closed-form approximations of capacity per beam are derived for the return link of IWSMSNs under terrestrial interference by using the Haar approximations where the IWSMSNs experience the Rician fading channel. The optimal joint decoding capacity can be considered as the upper bound where all of the SSs' signals can be jointly decoded by a super-receiver on board the multibeam satellite or a gateway station that knows all of the code books. While the linear minimum mean square error (MMSE) capacity is where all of the signals of SSs are decoded singularly by a multibeam satellite or a gateway station. The simulations show that the optimal capacities are obviously higher than the MMSE capacities under the same conditions, while the capacities are lowered by Rician fading and converge as the Rician factor increases. α and ß jointly affect the performance of hybrid 1D and 2D beam models, and the number of SSs also contributes different effects on the optimal capacity and MMSE capacity of the IWSMSNs.

Triptolide inhibits proliferation of Epstein-Barr virus-positive B lymphocytes by down-regulating expression of a viral protein LMP1.

Epstein-Barr virus (EBV) infects various types of cells and mainly establishes latent infection in B lymphocytes. The viral latent membrane protein 1 (LMP1) plays important roles in transformation and proliferation of B lymphocytes infected with EBV. Triptolide is a compound of Tripterygium extracts, showing anti-inflammatory, immunosuppressive, and anti-cancer activities. In this study, it is determined whether triptolide inhibits proliferation of Epstein-Barr virus-positive B lymphocytes. The CCK-8 assays were performed to examine cell viabilities of EBV-positive B95-8 and P3HR-1 cells treated by triptolide. The mRNA and protein levels of LMP1 were examined by real time-PCR and Western blotting, respectively. The activities of two LMP1 promoters (ED-L1 and TR-L1) were determined by Dual luciferase reportor assay. The results showed that triptolide inhibited the cell viability of EBV-positive B lymphocytes, and the over-expression of LMP1 attenuated this inhibitory effect. Triptolide decreased the LMP1 expression and transcriptional levels in EBV-positive B cells. The activity of LMP1 promoter ED-L1 in type III latent infection was strongly suppressed by triptolide treatment. In addition, triptolide strongly reduced growth of B95-8 induced B lymphoma in BALB/c nude mice. These results suggest that triptolide decreases proliferation of EBV-induced B lymphocytes possibly by a mechanism related to down-regulation of the LMP1 expression.

Energy-Efficient Transmissions for Remote Wireless Sensor Networks: An Integrated HAP/Satellite Architecture for Emergency Scenarios.

A typical application scenario of remote wireless sensor networks (WSNs) is identified as an emergency scenario. One of the greatest design challenges for communications in emergency scenarios is energy-efficient transmission, due to scarce electrical energy in large-scale natural and man-made disasters. Integrated high altitude platform (HAP)/satellite networks are expected to optimally meet emergency communication requirements. In this paper, a novel integrated HAP/satellite (IHS) architecture is proposed, and three segments of the architecture are investigated in detail. The concept of link-state advertisement (LSA) is designed in a slow flat Rician fading channel. The LSA is received and processed by the terminal to estimate the link state information, which can significantly reduce the energy consumption at the terminal end. Furthermore, the transmission power requirements of the HAPs and terminals are derived using the gradient descent and differential equation methods. The energy consumption is modeled at both the source and system level. An innovative and adaptive algorithm is given for the energy-efficient path selection. The simulation results validate the effectiveness of the proposed adaptive algorithm. It is shown that the proposed adaptive algorithm can significantly improve energy efficiency when combined with the LSA and the energy consumption estimation.