Application of a Dense Fusion Attention Network in Fault Diagnosis of Centrifugal Fan

Although the deep learning recognition model has been widely used in the condition monitoring of rotating machinery. However, it is still a challenge to understand the correspondence between the structure and function of the model and the diagnosis process. Therefore, this paper discusses embedding distributed attention modules into dense connections instead of traditional dense cascading operations. It not only decouples the influence of space and channel on fault feature adaptive recalibration feature weights, but also forms a fusion attention function. The proposed dense fusion focuses on the visualization of the network diagnosis process, which increases the interpretability of model diagnosis. How to continuously and effectively integrate different functions to enhance the ability to extract fault features and the ability to resist noise is answered. Centrifugal fan fault data is used to verify this network. Experimental results show that the network has stronger diagnostic performance than other advanced fault diagnostic models

Construction of Yeast One-hybrid Bait Reporter Vector for Screening the Binding Proteins of Cassava MeCWINV1

Cellwall invertase (CWIN) hydrolyzes sucrose into glucose and fructose irreversibly, playing key roles in carbohydrate partitioning and plant defence. MeCWINV1 is one of the CWINs in cassava, which contains several light-responsive elements and stress-responsive elements in promoter region. To analyze the regulatory function of MeCWINV1 in the cassava starch accumulation and stress defense response, a 865 bp MeCWINV1 promoter fragment was cloned and inserted into yeast one-hybrid bait vector to construct pCW1-AbAi vector, then was transformed to Y1HGold yeast strains to screen the binding proteins. It might provide a framework for further investigation on the regulation mechanism of MeCWINV1 gene in cassava

Targeting LIF-mediated paracrine interaction for pancreatic cancer therapy and monitoring.

Pancreatic ductal adenocarcinoma (PDAC) has a dismal prognosis largely owing to inefficient diagnosis and tenacious drug resistance. Activation of pancreatic stellate cells (PSCs) and consequent development of dense stroma are prominent features accounting for this aggressive biology1,2. The reciprocal interplay between PSCs and pancreatic cancer cells (PCCs) not only enhances tumour progression and metastasis but also sustains their own activation, facilitating a vicious cycle to exacerbate tumorigenesis and drug resistance3-7. Furthermore, PSC activation occurs very early during PDAC tumorigenesis8-10, and activated PSCs comprise a substantial fraction of the tumour mass, providing a rich source of readily detectable factors. Therefore, we hypothesized that the communication between PSCs and PCCs could be an exploitable target to develop effective strategies for PDAC therapy and diagnosis. Here, starting with a systematic proteomic investigation of secreted disease mediators and underlying molecular mechanisms, we reveal that leukaemia inhibitory factor (LIF) is a key paracrine factor from activated PSCs acting on cancer cells. Both pharmacologic LIF blockade and genetic Lifr deletion markedly slow tumour progression and augment the efficacy of chemotherapy to prolong survival of PDAC mouse models, mainly by modulating cancer cell differentiation and epithelial-mesenchymal transition status. Moreover, in both mouse models and human PDAC, aberrant production of LIF in the pancreas is restricted to pathological conditions and correlates with PDAC pathogenesis, and changes in the levels of circulating LIF correlate well with tumour response to therapy. Collectively, these findings reveal a function of LIF in PDAC tumorigenesis, and suggest its translational potential as an attractive therapeutic target and circulating marker. Our studies underscore how a better understanding of cell-cell communication within the tumour microenvironment can suggest novel strategies for cancer therapy

The ATLAS EventIndex: a BigData catalogue for all ATLAS experiment events

The ATLAS EventIndex system comprises the catalogue of all events collected, processed or generated by the ATLAS experiment at the CERN LHC accelerator, and all associated software tools to collect, store and query this information. ATLAS records several billion particle interactions every year of operation, processes them for analysis and generates even larger simulated data samples; a global catalogue is needed to keep track of the location of each event record and be able to search and retrieve specific events for in-depth investigations. Each EventIndex record includes summary information on the event itself and the pointers to the files containing the full event. Most components of the EventIndex system are implemented using BigData open-source tools. This paper describes the architectural choices and their evolution in time, as well as the past, current and foreseen future implementations of all EventIndex components.Comment: 21 page

The gut microbiome in atherosclerotic cardiovascular disease

The gut microbiota may play a role in cardiovascular diseases. Here, the authors perform a metagenome-wide association study on stools from individuals with atherosclerotic cardiovascular disease and healthy controls, identifying microbial strains and functions associated with the disease

Single nucleotide polymorphisms at the TRAF1/C5 locus are associated with rheumatoid arthritis in a Han Chinese population

<p>Abstract</p> <p>Background</p> <p>Genetic variants in <it>TRAF1C5 </it>and <it>PTPN22 </it>genes have been shown to be significantly associated with arthritis rheumatoid in Caucasian populations. This study investigated the association between single nucleotide polymorphisms (SNPs) in <it>TRAF1/C5 </it>and <it>PTPN22 </it>genes and rheumatoid arthritis (RA) in a Han Chinese population. We genotyped SNPs rs3761847 and rs7021206 at the <it>TRAF1/C5 </it>locus and rs2476601 SNP in the <it>PTPN22 </it>gene in a Han Chinese cohort composed of 576 patients with RA and 689 controls. The concentrations of anti-cyclic citrullinated peptide antibodies (CCP) and rheumatoid factor (RF) were determined for all affected patients. The difference between the cases and the controls was compared using <it>χ</it>²analysis.</p> <p>Results</p> <p>Significant differences in SNPs rs3761847 and rs7021206 at <it>TRAF1/C5 </it>were observed between the case and control groups in this cohort; the allelic p-value was 0.0018 with an odds ratio of 1.28 for rs3761847 and 0.005 with an odds ratio of 1.27 for rs7021206. This significant association between rs3761847 and RA was independent of the concentrations of anti-CCP and RF. No polymorphism of rs2476601 was observed in this cohort.</p> <p>Conclusions</p> <p>We first demonstrated that genetic variants at the <it>TRAF1/C5 </it>locus are significantly associated with RA in Han Chinese, suggesting that <it>TRAF1/C5 </it>may play a role in the development of RA in this population, which expands the pathogenesis role of <it>TRAF1/C5 </it>in a different ethnicity.</p

Induction of Antibodies in Rhesus Macaques That Recognize a Fusion-Intermediate Conformation of HIV-1 gp41

A component to the problem of inducing broad neutralizing HIV-1 gp41 membrane proximal external region (MPER) antibodies is the need to focus the antibody response to the transiently exposed MPER pre-hairpin intermediate neutralization epitope. Here we describe a HIV-1 envelope (Env) gp140 oligomer prime followed by MPER peptide-liposomes boost strategy for eliciting serum antibody responses in rhesus macaques that bind to a gp41 fusion intermediate protein. This Env-liposome immunization strategy induced antibodies to the 2F5 neutralizing epitope 664DKW residues, and these antibodies preferentially bound to a gp41 fusion intermediate construct as well as to MPER scaffolds stabilized in the 2F5-bound conformation. However, no serum lipid binding activity was observed nor was serum neutralizing activity for HIV-1 pseudoviruses present. Nonetheless, the Env-liposome prime-boost immunization strategy induced antibodies that recognized a gp41 fusion intermediate protein and was successful in focusing the antibody response to the desired epitope

Predicting Rural Ecological Space Boundaries in the Urban Fringe Area Based on Bayesian Network: A Case Study in Nanjing, China

Urban fringe areas are locations that compete between urban development and ecological protection; their ecological spatial boundaries face the risk of erosion and degradation. Previous studies have so far focused on the core area inside the ecological space. However, research on the ecological boundary zone has so far been insufficient. The delineation of ECR is based on large-scale administrative units, while it is less precise at the level of small-scale rural areas. This study selected Paifang village in Nanjing City as the study area and built a Bayesian network model to predict the ecological space boundary for 2030. The study also identified the driving factors and their mechanisms affecting the changes in the rural ecological space in an urban fringe area and put forward targeted suggestions for its protection. The results suggested that: (1) The ecological space of Paifang village will expand in 2030. Specifically, agricultural land has the greatest potential for restoration of ecological space, followed by shrubland and grassland, and water bodies and their surrounding areas are potentially shrinking ecological space. (2) Artificial construction activities will disturb the ecological space, with the change in agricultural land being the main factor affecting the change in the ecological space boundary. (3) The Ecological Conservation Redline has a significant effect on the protection of the rural ecological space. The results of this study can provide a reference for rural planning and the formulation of protection policies in urban fringe areas

Predicting Rural Ecological Space Boundaries in the Urban Fringe Area Based on Bayesian Network: A Case Study in Nanjing, China

Urban fringe areas are locations that compete between urban development and ecological protection; their ecological spatial boundaries face the risk of erosion and degradation. Previous studies have so far focused on the core area inside the ecological space. However, research on the ecological boundary zone has so far been insufficient. The delineation of ECR is based on large-scale administrative units, while it is less precise at the level of small-scale rural areas. This study selected Paifang village in Nanjing City as the study area and built a Bayesian network model to predict the ecological space boundary for 2030. The study also identified the driving factors and their mechanisms affecting the changes in the rural ecological space in an urban fringe area and put forward targeted suggestions for its protection. The results suggested that: (1) The ecological space of Paifang village will expand in 2030. Specifically, agricultural land has the greatest potential for restoration of ecological space, followed by shrubland and grassland, and water bodies and their surrounding areas are potentially shrinking ecological space. (2) Artificial construction activities will disturb the ecological space, with the change in agricultural land being the main factor affecting the change in the ecological space boundary. (3) The Ecological Conservation Redline has a significant effect on the protection of the rural ecological space. The results of this study can provide a reference for rural planning and the formulation of protection policies in urban fringe areas

Exposure to high-sugar diet induces transgenerational changes in sweet sensitivity and feeding behavior via H3K27me3 reprogramming

Human health is facing a host of new threats linked to unbalanced diets, including high-sugar diet (HSD), which contributes to the development of both metabolic and behavioral disorders. Studies have shown that diet-induced metabolic dysfunctions can be transmitted to multiple generations of offspring and exert long-lasting health burden. Meanwhile, whether and how diet-induced behavioral abnormalities can be transmitted to the offspring remains largely unclear. Here, we showed that ancestral HSD exposure suppressed sweet sensitivity and feeding behavior in the offspring in Drosophila. These behavioral deficits were transmitted through the maternal germline and companied by the enhancement of H3K27me3 modifications. PCL-PRC2 complex, a major driver of H3K27 trimethylation, was upregulated by ancestral HSD exposure, and disrupting its activity eliminated the transgenerational inheritance of sweet sensitivity and feeding behavior deficits. Elevated H3K27me3 inhibited the expression of a transcriptional factor Cad and suppressed sweet sensitivity of the sweet-sensing gustatory neurons, reshaping the sweet perception and feeding behavior of the offspring. Taken together, we uncovered a novel molecular mechanism underlying behavioral abnormalities spanning multiple generations of offspring upon ancestral HSD exposure, which would contribute to the further understanding of long-term health risk of unbalanced diet