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This paper studies a multi-user network model based on sparse code multiple access (SCMA), where both unicast and multicast services are considered. In the direct transmission scheme, the communication between the base station (BS) and the users is completed with one stage, in which the relay is inexistent. In the two-stage cooperative transmission scheme, any number of relays are placed to improve the reliability of wireless communication system. The BS broadcasts the requested message to users and relays in the first stage, and the successful relays forward the message to unsuccessful users in the second stage. To characterize the performance of these two schemes, we derive the exact and approximate expressions of average outage probability. Furthermore, to take full advantage of the cooperative diversity, an optimal power allocation and relay location strategy in the high signal-to-noise ratio (SNR) regime is studied. The outage probability reaches the minimum value when the first stage occupies half of the total energy consumed. Simulation and analysis results are presented to demonstrate the performance of these two schemes. The results show that the two-stage cooperative scheme effectively reduce the average outage probability in SCMA network, especially in the high SNR region.

Estimating carbon emissions and assessing their contribution are critical steps toward China’s objective of reaching a “carbon peak” in 2030 and “carbon neutrality” in 2060. This paper selects relevant statistical data on carbon emissions from 2000 to 2018, combines the emission coefficient method and the Logarithmic Mean Divisia Index model (LMDI) to calculate carbon emissions, and analyses the driving force of carbon emission growth using Henan Province as a case study. Based on the partial least squares regression analysis model (PLS), the contributions of inter-provincial factors of carbon emission are analyzed. Finally, a county-level downscaling estimation model of carbon emission is further formulated to analyze the temporal and spatial distribution of carbon emissions and their evolution. The research results show that: 1) The effect of energy intensity is responsible for 82 percent of the increase in carbon emissions, whereas the effect of industrial structure is responsible for -8 percent of the increase in carbon emissions. 2) The proportion of secondary industry and energy intensity, which are 1.64 and 0.82, respectively, have the most evident explanatory effect on total carbon emissions; 3). Carbon emissions vary widely among counties, with high emissions in the central and northern regions and low emissions in the southern. However, their carbon emissions have constantly decreased over time. 4) The number of high-emission counties, their carbon emissions, and the degree of their discrepancies are gradually reduced. The findings serve as a foundation for relevant agencies to gain a macro-level understanding of the industrial landscape and to investigate the feasibility of carbon emission reduction programs.

Alcoholic liver disease (ALD) is the major cause of chronic liver disease and a global health concern. ALD pathogenesis is initiated with liver steatosis, and ALD can progress to steatohepatitis, fibrosis, cirrhosis and even hepatocellular carcinoma. Salvianic acid A (SAA) is a phenolic acid component of Danshen, a Chinese herbal medicine with possible hepatoprotective properties. The purpose of this study was to investigate the effect of SAA on chronic alcoholic liver injury and its molecular mechanism. We found that SAA significantly inhibited alcohol‐induced liver injury and ameliorated ethanol‐induced hepatic inflammation. These protective effects of SAA were likely carried out through its suppression of the BRD4/HMGB1 signalling pathway, because SAA treatment largely diminished alcohol‐induced BRD4 expression and HMGB1 nuclear translocation and release. Importantly, BRD4 knockdown prevented ethanol‐induced HMGB1 release and inflammatory cytokine production in AML‐12 cells. Similarly, alcohol‐induced pro‐inflammatory cytokines were blocked by HMGB1 siRNA. Collectively, our results reveal that activation of the BRD4/HMGB1 pathway is involved in ALD pathogenesis. Therefore, manipulation of the BRD4/HMGB1 pathway through strategies such as SAA treatment holds great therapeutic potential for chronic alcoholic liver disease therapy.

The hierarchical edge-cloud enabled paradigm has recently been proposed to provide abundant resources for 5G wireless networks. However, the computation and communication capabilities are heterogeneous which makes the potential advantages difficult to be fully explored. Besides, previous works on mobile edge computing (MEC) focused on server caching and offloading, ignoring the computational and caching gains brought by the proximity of user equipments (UEs). In this paper, we investigate the computation offloading in a three-tier cache-assisted hierarchical edge-cloud system. In this system, UEs cache tasks and can offload their workloads to edge servers or adjoining UEs by device-to-device (D2D) for collaborative processing. A cost minimization problem is proposed by the tradeoff between service delay and energy consumption. In this problem, the offloading decision, the computational resources and the offloading ratio are jointly optimized in each offloading mode. Then, we formulate this problem as a mixed-integer nonlinear optimization problem (MINLP) which is non-convex. To solve it, we propose a joint computation offloading and resource allocation optimization (JORA) scheme. Primarily, in this scheme, we decompose the original problem into three independent subproblems and analyze their convexity. After that, we transform them into solvable forms (e.g., convex optimization problem or linear optimization problem). Then, an iteration-based algorithm with the Lagrange multiplier method and a distributed joint optimization algorithm with the adoption of game theory are proposed to solve these problems. Finally, the simulation results show the performance of our proposed scheme compared with other existing benchmark schemes.

The ubiquity of data-enabled mobile devices and wireless-enabled data applications has fostered the rapid development of wireless content caching, which is an efficient approach to mitigating cellular traffic pressure. Considering the content characteristics and real caching circumstances, a software-defined network (SDN)-based cooperative caching system is presented. First, we define a new file block library with heterogeneous content attributes [file popularity, mobile user (MU) preference, file size]. An SDN-based three-tier caching network is presented in which the base station supplies control coverage for the entire macrocell and cache helpers (CHs), MUs with cache capacities offer data coverage. Using the ‘most popular content’ and ‘largest diversity content’, a distributed cooperative caching strategy is proposed in which the caches of the MUs store the most popular contents of the file block library to mitigate the effect of MU mobility, and those of the CHs store the remaining contents in a probabilistic caching manner to enrich the content diversity and reduce the MU caching pressure. The request meet probability (RMPro) is subsequently proposed, and the optimal caching distribution of the contents in the probabilistic caching strategy is obtained via optimization. Finally, using the result of RMPro optimization, we also analyze the content retrieval delays that occur when a typical MU requests a file block or a whole file. Simulation results demonstrate that the proposed caching system can achieve quasi-optimal revenue performance compared with other contrasting schemes.

Guanylate-binding protein 2 (GBP2) is an interferon-inducible large GTPase which is crucial to the protective immunity against microorganisms. However, its biological function in cancer remains largely unknown. Glioblastoma multiforme (GBM) is the most common and deadly brain tumor in adults. Here we show that GBP2 expression is highly elevated in GBM tumor and cell lines, particularly in those of the mesenchymal subtype. High GBP2 expression is associated with poor prognosis. GBP2 overexpression significantly promotes GBM cell migration and invasion in vitro, and GBP2 silencing by RNA interference exhibits opposite effects. We further show that fibronectin (FN1) is dramatically induced by GBP2 expression at both mRNA and protein levels, and FN1 is essential for GBP2-promoted GBM invasiveness. Inhibition of Stat3 pathway prevents GBP2-promoted FN1 induction and cell invasion. Consistently, GBP2 dramatically promotes GBM tumor growth and invasion in mice and significantly reduces the survival time of the mice with tumor. Taken together, these findings establish the role of GBP2/Stat3/FN1 signaling cascade in GBM invasion and suggest GBP2 may serve as a potential therapeutic target for inhibiting GBM invasion.

Guanylate binding proteins (GBPs), a family of interferon-inducible large GTPase, play a pivotal role in cell-autonomous immunity and tumor malignant transformation. Glioblastoma (GBM) is the most prevalent and lethal primary brain tumor in adults. Here we show that GBP5 was highly expressed in GBM cell lines and in clinical samples, especially in the mesenchymal subtype. The expression levels of GBP5 were negatively correlated with the prognosis of GBM patients. Overexpression of GBP5 promoted the proliferation, migration, and invasion of GBM cells in vitro and in vivo. In contrast, silencing GBP5 by RNA interference exhibited the opposite effects. Consequently, targeting GBP5 in GBM cells resulted in impaired tumor growth and prolonged survival time of mice with GBM tumors. We further identified that the Src/ERK1/2/MMP3 axis was essential for GBP5-promoted GBM aggressiveness. These findings suggest that GBP5 may represent a novel target for GBM intervention.

Purpose: To evaluate whether the toric intra-ocular lens (IOL) power calculation based on total corneal astigmatism (TCA) in eyes with high posterior corneal astigmatism (PCA) could result in a systematic over-correction or under-correction after operation. Methods: The present study included a mono-centric retrospective study design. The data were collected from 62 consecutive eyes during uncomplicated cataract surgery by a single surgeon with a measured PCA of 0.50 diopters (D) or higher. Toric IOL calculations were made using TCA measurements. The eyes were grouped as either \"with-the-rule\" (WTR) or \"against-the-rule\" (ATR) on the basis of the steep anterior corneal meridian. The post-operative refractive astigmatic prediction error was analyzed 1 month post-operatively using the vector analysis by the Alpins method and double-angle plots method. Results: The correction indexes were 1.14 ± 0.29 in the ATR eyes and 1.25 ± 0.18 for the WTR eyes, indicating a tendency toward over-correction. The mean over-correction was 0.22 ± 0.52D in the ATR group and 0.65 ± 0.60D in the WTR group. The magnitude of error (ME) values were significantly different from the ideal value of zero in both groups (ATR: P = 0.03; WTR: P = 0.00). No significant difference in mean absolute error (MAE) in predicted residual astigmatism was found between ATR and WTR groups (0.61 ± 0.42 D versus 0.64 ± 0.39 D; P = 0.54). The ATR group yielded better results, with 48% <0.50D prediction error in the main analysis. Conclusions: The results suggested that in cases of high PCA, the toric IOL calculation, which was performed using TCA, may cause a potential over-correction in the ATR and WTR eyes. For ATR eyes, over-correction led to slight disruption of post-operative visual quality because of the \"with-the-rule\" residual astigmatism after operation. Therefore, we suggested using TCA for toric IOL calculation in ATR eyes.

Sodium-glucose co-transporter two inhibitors (SGLT2is) are widely used in clinical practice due to their proven cardiovascular and renal benefits. However, various adverse drug reactions (ADRs) have been reported. This study aims to systematically update the ADRs associated with SGLT2is and identify the differences among various SGLT2is acovigilance of various SGLT-2 inhibitors. Data from the FAERS database covering Q1 2013 to Q2 2024 were selected for disproportionality analysis. ADRs were defined using the System Organ Classes (SOC) and Preferred Terms (PT) from the MedDRA 27.0 dictionary. Four signal detection metrics-reporting odds ratio (ROR), proportional reporting ratios (PRRs), Bayesian Confidence Propagation Neural Network (BCPNN), and empirical Bayesian geometric mean (EBGM)-were utilized to infer ADRs and assess differences among specific SGLT2i drugs through intersection analysis. Except for canagliflozin, both dapagliflozin and empagliflozin showed a general increase in ADRs. Specifically, canagliflozin had 93 ADRs, dapagliflozin had 173, and empagliflozin had 214. Most of these were related to Infections and Infestations, Investigations, and Reproductive System and Breast Disorders, notably manifesting as inflammatory conditions of the urinary and reproductive systems, such as orchitis and testicular abscess, consistent with FDA labeling. Additionally, overlooked ADRs were identified, including bladder cancer, cholangiocarcinoma, and thrombotic strokes, none of which were reported for canagliflozin. While shared ADRs for SGLT2is are noted in FDA labeling, monitoring for high-risk populations, such as those with cancers or strokes, remains crucial to prevent deterioration. Medication regimens may need adjustment, including selecting canagliflozin or non-SGLT2i alternatives when necessary.

The chromosomal translocations found in acute myelogenous leukemia (AML) generate oncogenic fusion transcription factors with aberrant transcriptional regulatory properties. Although therapeutic targeting of most leukemia fusion proteins remains elusive, the posttranslational modifications that control their function could be targetable. We found that AML1-ETO, the fusion protein generated by the t(8;21) translocation, is acetylated by the transcriptional coactivator p300 in leukemia cells isolated from t(8;21) AML patients, and that this acetylation is essential for its self-renewal—promoting effects in human cord blood CD34 + cells and its leukemogenicity in mouse models. Inhibition of p300 abrogates the acetylation of AML1-ETO and impairs its ability to promote leukemic transformation. Thus, lysine acetyltransferases represent a potential therapeutic target in AML.