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Owing to its potential to satisfy all outstanding requests for the same data item with a single response, on-demand data broadcast becomes a widely accepted approach to dynamic and scalable wireless information dissemination. In the existing works, clients must wait until the deadline of their requests in the case the requests cannot be satisfied. In this paper, broadcast admission control is introduced to data broadcast systems such that the clients can be informed in advance on the result of admission control for the requests. Furthermore, a matching based allocation scheme is proposed for batch scheduling to maximize data sharing among requests. Simulation results show that our proposed algorithms have better comprehensive performance than traditional algorithms in terms of scheduling, admission control and QoS.

Background：Among HlV-infected patients initiating antiretroviral therapy （ART）,early changes in CD4＋ T-cell subsets are well described.However,HIV-infected late presenters initiating treatment present with a suboptimal CD4＋ T-cell reconstitution and remain at a higher risk for AIDS and non-AIDS events.Therefore,factors associated with CD4＋ T-cell reconstitution need to be determined in this population,which will allow designing effective immunotherapeutic strategies.Methods：Thirty-one adult patients with baseline CD4＋ T-cell count 〈350 cells/mm^3 exhibiting viral suppression after ART initiation were followed in the HIV/AIDS research center of Peking Union Medical College Hospital in Beijing,China,from October 2002 to September 2013.Changes in T-cell subsets and associated determinants were measured.Results：Median baseline CD4＋ T-cell count was 70 cells/mm3.We found a biphasic reconstitution ofT-cell subsets and immune activation：a rapid change during the first 6 months followed by a more gradual change over the subsequent 8 years.Baseline CD4＋ T-cell count 〉200 cells/ mm3 in comparison to CD4＋ T-cell count ≤200 cells/mm3 was associated with more complete immune Reconstitution （77.8% vs.27.3% respectively;P =0.017） and normalized CD4/CD8 ratio.We showed that the baseline percentage of naive CD4＋ T-cell was a predictive marker for complete immune reconstitution （area under receiver operating characteristic curve 0.907）,and 12.4% as cutoffvalue had a sensitivity of 84.6% and a specificity of 88.2%.Conclusions：Baseline naive CD4＋ T-cell percentage may serve as a predictive marker for optimal immune reconstitution during long-term therapy.Such study findings suggest that increasing thymic output should represent an avenue to improve patients who are diagnosed late in the course of infection.

The research and development of organometallic supramolecular complexes as anticancer supramolecular drugs, which are aggregates mainly formed by one or more inorganic metal compounds with one or more either inorganic or organic molecules in general via coordination bonds, has been a quite rapidly developing, increasingly active and newly rising highlight interdisciplinary field. Numerous efforts have been directed toward organometallic supramolecular complexes as potential anticancer agents and the unprecedented progress has been made. This has opened up a wholly new and infinite space to create novel metal-based bioactive supermolecules. More importantly, metal-based complex supermolecules as potential anticancer agents with wide potential applications have become highlight topics in recent years, and are becoming increasingly useful and important in preventing and treating cancer diseases. In view of the rapid progress in organometallic complex anticancer supermolecules with rich variation of structural types, this work systematically reviewed the recent research and development of the whole range of metal-based supramolecular complexes as anticancer agents mainly since 2009. The perspectives of the foreseeable future and potential application of organometallic supramolecular complexes in cancer therapy were also presented. It is hoped that this review will serve as a stimulant for new thoughts in the quest for rational designs of more active and less toxic organometallic supramolecular complex anticancer drugs.

Amorphous carbon holds great promise as anode material for sodium‐ion batteries due to its cost‐effectiveness and good performance. However, its sodium storage mechanism, particularly the insertion process and origin of plateau capacity, remains controversial. Here, an extended adsorption/insertion‐filling sodium storage mechanism is proposed using petroleum coke‐derived amorphous carbon as a multi‐microcrystalline model. Combining in situ X‐ray diffraction, in situ Raman, theoretical calculations, and neutron scattering, the effective storage form and location of sodium ions in amorphous carbon are revealed. The sodium adsorption at defect sites leads to a high‐potential sloping capacity. The sodium insertion process occurs in both the pseudo‐graphite phase (d002 > 0.370 nm) and graphite‐like phase (0.345 ≤ d002 < 0.370 nm) rather than the graphite phase, contributing to low‐potential sloping capacity. The sodium filling into accessible closed pores forms quasi‐metallic sodium clusters, contributing to plateau capacity. The threshold of the effective interlayer spacing for sodium insertion is extended to 0.345 nm, breaking the consensus of insertion interlayer threshold and enhancing understanding of closed pore filling. The extended adsorption/insertion‐filling mechanism explains the sodium storage behavior of amorphous carbon with different microstructures, providing theoretical guidance for the rational design of high‐performance amorphous carbon anodes. The threshold of the effective interlayer spacing for sodium insertion is extended from 0.370 to 0.345 nm in petroleum coke‐derived amorphous carbon. In conjunction with the optimized structural model of amorphous carbon, an extended adsorption/insertion‐filling sodium storage mechanism is proposed, which can accurately explain the sodium storage behavior of amorphous carbon with different microstructures.

Nonalcoholic fatty liver disease (NAFLD) is the most prevalent form of chronic liver disease, and the mechanisms underpinning its pathogenesis have not been completely established. Transmembrane member 16A (TMEM16A), a component of the Ca2+‐activated chloride channel (CaCC), has recently been implicated in metabolic events. Herein, TMEM16A is shown to be responsible for CaCC activation in hepatocytes and is increased in liver tissues of mice and patients with NAFLD. Hepatocyte‐specific ablation of TMEM16A in mice ameliorates high‐fat diet‐induced obesity, hepatic glucose metabolic disorder, steatosis, insulin resistance, and inflammation. In contrast, hepatocyte‐specific TMEM16A transgenic mice exhibit the opposite phenotype. Mechanistically, hepatocyte TMEM16A interacts with vesicle‐associated membrane protein 3 (VAMP3) to induce its degradation, suppressing the formation of the VAMP3/syntaxin 4 and VAMP3/synaptosome‐associated protein 23 complexes. This leads to the impairment of hepatic glucose transporter 2 (GLUT2) translocation and glucose uptake. Notably, VAMP3 overexpression restrains the functions of hepatocyte TMEM16A in blocking GLUT2 translocation and promoting lipid deposition, insulin resistance, and inflammation. In contrast, VAMP3 knockdown reverses the beneficial effects of TMEM16A downregulation. This study demonstrates a role for TMEM16A in NAFLD and suggests that inhibition of hepatic TMEM16A or disruption of TMEM16A/VAMP3 interaction may provide a new potential therapeutic strategy for NAFLD. Transmembrane member 16A (TMEM16A) is an essential component of the hepatocyte calcium‐activated chloride channel and is increased in livers with hepatic steatosis. It interacts with vesicle‐associated membrane protein 3 to disrupt soluble Nethylmaleimide‐sensitive factor attachment protein receptors formation, thereby limiting glucose transporter 2 translocation and hepatic glucose uptake. Liver‐specific deficiency of TMEM16A ameliorates glucose metabolic disorder and nonalcoholic fatty liver disease.

Background Identify genes probably associated with chronic heart failure and predict potential target genes for dilated cardiomyopathy using bioinformatics analyses. Methods Gene expression profiles (series number GSE3585 and GSE42955) of cardiomyopathy patients and healthy controls were downloaded from the Expression Omnibus Gene (GEO) database. Differential expression of genes (DEGS) between the two groups of total 14 cardiomyopathy patients and 10 healthy controls were subsequently identified by limma package of R. Database for Annotation, Visualization, and Integrated Discovery (DAVID Tool), which is an analysis of enriched biological processes. Search Tool for the Retrieval Interacting Genes (STRING) was used as well for the analysis of protein-protein interaction network (PPI). Prediction of the potential drugs was suggested based on the preliminarily identified genes using Connectivity Map (CMap). Results Eighty-nine DEGs were identified (57 up-regulated and 32 down-regulated). The most enrichment Gene Ontology (GO) terms ( P  < 0.05) contain genes involved in extracellular matrix (ECM) and biological adhesion signal pathways ( P  < 0.05, ES > 1.5) such as ECM-receptors, focal adhesion and transforming growth factor beta (TGF-β), etc. Fifty-one differentially expressed genes were found to encode interacting proteins. Eleven key genes along with related transcription factors were identified including CTGF, POSTN, CORIN, FIGF, etc. Conclusion Bioinformatics-based analyses reveal the targeted genes probably associated with cardiomyopathy, which provide clues for pharmacological therapies aiming at the targets.

The transition from acute kidney injury (AKI) to chronic kidney disease (CKD) is a critical clinical issue. Although previous studies have suggested macrophages as a key player in promoting inflammation and fibrosis during this transition, the heterogeneity and dynamic characterization of macrophages are still poorly understood. Here, we used integrated single‐cell RNA sequencing and spatial transcriptomic to characterize the spatiotemporal heterogeneity of macrophages in murine AKI‐to‐CKD model of unilateral ischemia‐reperfusion injury. A marked increase in macrophage infiltration at day 1 was followed by a second peak at day 14 post AKI. Spatiotemporal profiling revealed that injured tubules and macrophages co‐localized early after AKI, whereas in late chronic stages had spatial proximity to fibroblasts. Further pseudotime analysis revealed two distinct lineages of macrophages in this transition: renal resident macrophages differentiated into the pro‐repair subsets, whereas infiltrating monocyte‐derived macrophages contributed to chronic inflammation and fibrosis. A novel macrophage subset, extracellular matrix remodeling‐associated macrophages (EAMs) originating from monocytes, linked to renal fibrogenesis and communicated with fibroblasts via insulin‐like growth factors (IGF) signalling. In sum, our study identified the spatiotemporal dynamics of macrophage heterogeneity with a unique subset of EAMs in AKI‐to‐CKD transition, which could be a potential therapeutic target for preventing CKD development. This study sheds new light on the heterogeneous roles of macrophages in the complex and cumbersome pathological process of AKI to CKD. Integrating high‐throughput spatial and single‐cell transcriptomic data, the study identifies distinct macrophage lineages, with renal resident macrophages promoting repair and monocyte‐derived ECM remodeling macrophages (EAMs) contributing to renal fibrogenesis. These findings pave the way for the development of innovative therapeutic strategies to halt disease progression.

Background: Disanthus cercidifolius var. longipes is an ancient relic plant unique to China. However, the typical shade-loving plant is largely exposed to the sun, which poses a major challenge to its conservation. Methods: This study explored dynamic changes in primary and secondary metabolites in D. cercidifolius leaves at different stages of development, combining metabolomics and transcriptome analysis to discuss the differentially accumulated metabolites (DAMs) and differentially expressed genes (DEGs). Results: The DAMs and DEGs were enriched in pathways related to photosynthesis, carbon (C) metabolism, anthocyanin synthesis, plant hormone signal transduction, and flavonoid synthesis. At the initial stage of leaf development, many primary metabolites were synthesized in the leaves. Before leaf maturity, many primary metabolites were converted into secondary metabolites. Combined transcriptome and metabolome analysis showed that the metabolites and genes related to anthocyanin synthesis and flavonoid metabolism were upregulated. In contrast, the genes related to C metabolism and C fixation were downregulated. After leaf maturity, photosynthetic capacity increased, total flavonoid content peaked (implying the strongest photoprotection capacity), and the transformation of anthocyanins and flavonoids was weakened. Conclusions: Light intensity indirectly affects the accumulation of the primary and secondary metabolism of D. cercidifolius. With the enhancement of photoprotection, the photosynthetic energy capacity decreases. It is, therefore, inferable that D. cercidifolius has shading properties and achieves a stable nutrient supply during growth and development through these strategies. Thus, D. cercidifolius protection requires a shaded environment.

Treating bone cancer pain continues to be a clinical challenge and underlying mechanisms of bone cancer pain remain elusive. Here, we reported that sonic hedgehog signaling plays a critical role in the development of bone cancer pain. Tibia bone cavity tumor cell implantation produces bone cancer-related mechanical allodynia, thermal hyperalgesia, and spontaneous and movement-evoked pain behaviors. Production and persistence of these pain behaviors are well correlated with tumor cell implantation-induced up-regulation and activation of sonic hedgehog signaling in primary sensory neurons and spinal cord. Spinal administration of sonic hedgehog signaling inhibitor cyclopamine prevents and reverses the induction and persistence of bone cancer pain without affecting normal pain sensitivity. Inhibiting sonic hedgehog signaling activation with cyclopamine, in vivo or in vitro, greatly suppresses tumor cell implantation-induced increase of intracellular Ca2+ and hyperexcitability of the sensory neurons and also the activation of GluN2B receptor and the subsequent Ca2+-dependent signals CaMKII and CREB in dorsal root ganglion and the spinal cord. These findings show a critical mechanism underlying the pathogenesis of bone cancer pain and suggest that targeting sonic hedgehog signaling may be an effective approach for treating bone cancer pain.

The potential for aerobic NO2− removal by Alcaligenes faecalis strain NR was investigated. 35 mg/L of NO2−-N was removed by strain NR under aerobic conditions in the presence of NH4+. 15N-labeling experiment demonstrated that N2O and N2 were possible products during the aerobic nitrite removal process by strain NR. The key enzyme genes of nirK, norB and nosZ, which regulate the aerobic nitrite denitrification process, were successfully amplified from strain NR. The gene sequence analysis indicates that copper-containing nitrite reductase (NIRK) and periplasmic nitrous oxide reductase (NOSZ) were both hydrophilic protein and the transmembrane structures were absent, while nitric oxide reductase large subunit (NORB) was a hydrophobic and transmembrane protein. According to the three-dimensional structure and binding site analysis, the bulky and hydrophobic methionine residue proximity to the nitrite binding sites of NIRK was speculated to be related to the oxygen tolerance of NIRK from strain NR.