Optimum Multi-hop Transmission Strategies for Energy Constrained Wireless Sensor Networks

This paper presents optimum multi-hop transmission strategies (MHTS) for energy constrained wireless sensor networks (WSNs). Nodes in a multi-hop WSN need to transmit their own information and to relay each other\u27s information to a base station (BS), and there are usually multiple available paths between a node and the BS. the optimum MHTS derived in this paper answers three questions: 1) how should a node divide its limited energy between the transmission of the self-information and the relay-information? 2) whether a single path or a combination of multiple paths should be used to route the information from a node to the BS? and 3) if multi-path routing is used, how should a single data stream be divided among the multiple paths? the answers to these questions are obtained by minimizing the energy per bit, or equivalently, by maximizing the amount of information delivered to the BS under certain energy constraints. Two different scheduling strategies are considered, the fair equal information strategy that requires all the nodes deliver the same amount of information to the BS, and the unfair maximum information strategy that maximizes the total amount of information delivered to the BS. the optimum MHTS for these two strategies are derived, with either convex optimization or analytical expressions, under a per node energy constraint and a total energy constraint, respectively. © 2012 IEEE

Prototype-guided Cross-task Knowledge Distillation for Large-scale Models

Recently, large-scale pre-trained models have shown their advantages in many tasks. However, due to the huge computational complexity and storage requirements, it is challenging to apply the large-scale model to real scenes. A common solution is knowledge distillation which regards the large-scale model as a teacher model and helps to train a small student model to obtain a competitive performance. Cross-task Knowledge distillation expands the application scenarios of the large-scale pre-trained model. Existing knowledge distillation works focus on directly mimicking the final prediction or the intermediate layers of the teacher model, which represent the global-level characteristics and are task-specific. To alleviate the constraint of different label spaces, capturing invariant intrinsic local object characteristics (such as the shape characteristics of the leg and tail of the cattle and horse) plays a key role. Considering the complexity and variability of real scene tasks, we propose a Prototype-guided Cross-task Knowledge Distillation (ProC-KD) approach to transfer the intrinsic local-level object knowledge of a large-scale teacher network to various task scenarios. First, to better transfer the generalized knowledge in the teacher model in cross-task scenarios, we propose a prototype learning module to learn from the essential feature representation of objects in the teacher model. Secondly, for diverse downstream tasks, we propose a task-adaptive feature augmentation module to enhance the features of the student model with the learned generalization prototype features and guide the training of the student model to improve its generalization ability. The experimental results on various visual tasks demonstrate the effectiveness of our approach for large-scale model cross-task knowledge distillation scenes

A JNK-Dependent Pathway Is Required for TNFα-Induced Apoptosis

AbstractTumor necrosis factor (TNFα) receptor signaling can simultaneously activate caspase 8, the transcription factor, NF-κB and the kinase, JNK. While activation of caspase 8 is required for TNFα-induced apoptosis, and induction of NF-κB inhibits cell death, the precise function of JNK activation in TNFα signaling is not clearly understood. Here, we report that TNFα-mediated caspase 8 cleavage and apoptosis require a sequential pathway involving JNK, Bid, and Smac/DIABLO. Activation of JNK induces caspase 8-independent cleavage of Bid at a distinct site to generate the Bid cleavage product jBid. Translocation of jBid to mitochondria leads to preferential release of Smac/DIABLO, but not cytochrome c. The released Smac/DIABLO then disrupts the TRAF2-cIAP1 complex. We propose that the JNK pathway described here is required to relieve the inhibition imposed by TRAF2-cIAP1 on caspase 8 activation and induction of apoptosis. Further, our findings define a mechanism for crosstalk between intrinsic and extrinsic cell death pathways

Aberrant expression of decoy receptor 3 in human breast cancer: relevance to lymphangiogenesis

AbstractBackgroundDecoy receptor 3 (DcR3), a decoy receptor against Fas ligand belonging to the tumor necrosis factor receptor superfamily, is overexpressed in some forms of cancer. It was recently reported that DcR3 could protect endothelial cells from apoptosis, implying a potential role in the development of vessels, whereas its role in the lymphangiogenesis remains unclear. In the present study, we studied the DcR3 expression and its relationship with the lymphatic microvessel density (LMVD) to investigate if it played a role in the lymph metastasis of human breast cancer.Materials and methodsReal-time polymerase chain reaction and immunohistochemistry were performed to measure the messenger RNA and protein expression of DcR3 in the breast cancer tissues, noncancerous counterparts, and axillary lymph node from 63 patients. LMVD in these specimens was assessed by counting the D2-40 labeled–microvessels. Furthermore, the correlations between DcR3 expression and LMVD and other clinicopathologic parameters were analyzed.ResultsDcR3 was overexpressed in the breast cancer tissue of 58 patients (92.1%) and was also expressed in vascular endothelial cells and tumor cells in the lymph nodes. LMVD in cancer tissue and lymph nodes were both positively correlated to the aberrant expression of DcR3.ConclusionsThe relevance between DcR3 overexpression and LMVD revealed the existence of possible links between DcR3 and lymphangiogenesis. Based on these findings, it is important to further explore the regulation of lymphangiogenesis operated by the reverse tumor necrosis factor signaling of DcR3

Unveiling the link between systemic inflammation markers and cognitive performance among older adults in the US: A population-based study using NHANES 2011–2014 data

Purpose: This study aimed to evaluate the association between systemic inflammation markers and cognitive performance among older US adults. Methods: This cross-sectional study assessed 3,632 older participants from the 2011–2014 National Health and Nutrition Examination Survey (NHANES). The main analysis included participants aged over 60 years. Systemic inflammation markers were quantified by calculating the composite inflammation indicators from the blood routine count, and cognitive performance was assessed using Consortium to Establish a Registry for Alzheimer\u27s Disease (CERAD) test, Animal Fluency test (AFT), and Digit Symbol Substitution test (DSST). Results: There were 2,743 individuals enrolled in the current analysis. The overall mean age was 64.9 years and 48.7 % were males. The levels of SIRI and PIV were significant negative associated with scores of CERAD, CERAD delayed recall, and DSST in the unadjusted models. Moreover, SII were significant negative associated with scores of CERAD and CERAD delayed recall. After adjusting the covariates of demographics, lifestyle factors, history of chronic diseases and BMI, significant negative association were observed between systematic inflammation markers and cognitive performance. Additionally, a progressive and significant decrease in the score of cognitive performance assessments with the increased levels of SIRI, SII, and PIV were respectively observed. Finally, the correlation between systemic inflammation markers and cognitive performance were evidenced in the sensitive analysis. Conclusion: Findings support a strong inverse correlation between systemic inflammation markers and cognitive performance, suggesting that addressing inflammation could be a promising avenue for enhancing cognitive health and mitigating age-related cognitive decline

Bis{2-[(4-chloro­phen­yl)imino­meth­yl]pyrrol-1-ido-κ2 N,N′}bis­(dimethyl­amido-κN)titanium(IV) toluene monosolvate

The mononuclear title compound, [Ti(C11H8ClN2)2(C2H6N)2]·C7H8, was synthesized by the reaction of N-(4-chloro­phen­yl)-2-pyrrolylcarbaldimine with Ti(C2H6N)4. The TiIV ion is situated on a twofold rotation axis and displays a distorted octa­hedral geometry defined by four N atoms from two 2-[(4-chloro­phen­yl)imino­meth­yl]pyrrol-1-ide ligands and two N atoms from two dimethyl­amine ligands. The Ti—Npyrrole bond length [2.1041 (19) Å] is longer than the Ti—Ndimethyl­amine bond length [1.9013 (19) Å]; the imine N atom exhibits the longest Ti—N bond [2.3152 (17) Å]. The toluene solvent mol­ecule is located on a twofold rotation axis running through the C atom of the methyl group. Consequently, the H atoms of the latter are rotationally disordered. The compound contains no markable hydrogen-bonding inter­actions

MAPK1 promotes the metastasis and invasion of gastric cancer as a bidirectional transcription factor

Background: The Mitogen-activated protein kinase 1 (MAPK1) has both independent functions of phosphorylating histones as a kinase and directly binding the promoter regions of genes to regulate gene expression as a transcription factor. Previous studies have identified elevated expression of MAPK1 in human gastric cancer, which is associated with its role as a kinase, facilitating the migration and invasion of gastric cancer cells. However, how MAPK1 binds to its target genes as a transcription factor and whether it modulates related gene expressions in gastric cancer remains unclear. Results: Here, we integrated biochemical assays (protein interactions and chromatin immunoprecipitation (ChIP)), cellular analysis assays (cell proliferation and migration), RNA sequencing, ChIP sequencing, and clinical analysis to investigate the potential genomic recognition patterns of MAPK1 in a human gastric adenocarcinoma cell-line (AGS) and to uncover its regulatory effect on gastric cancer progression. We confirmed that MAPK1 promotes AGS cells invasion and migration by regulating the target genes in different directions, up-regulating seven target genes (KRT13, KRT6A, KRT81, MYH15, STARD4, SYTL4, and TMEM267) and down-regulating one gene (FGG). Among them, five genes (FGG, MYH15, STARD4, SYTL4, and TMEM267) were first associated with cancer procession, while the other three (KRT81, KRT6A, and KRT13) have previously been confirmed to be related to cancer metastasis and migration. Conclusion: Our data showed that MAPK1 can bind to the promoter regions of these target genes to control their transcription as a bidirectional transcription factor, promoting AGS cell motility and invasion. Our research has expanded the understanding of the regulatory roles of MAPK1, enriched our knowledge of transcription factors, and provided novel candidates for cancer therapeutics