RISK ASSESSMENT IN GAS DISTRIBUTION NETWORK LEAKS USING THE PRELIMINARY RISK ANALYSIS AND EISENBERG VULNERABILITY METHOD

The natural gas distribution system is made up of an extensive network of pipelines and some equipment such as regulators, valves, filters, meters and converters that require maintenance to maintain operation and identify any gas leaks in advance. The risk analysis process is widely used in the gas industries to locate faults in operations and processes that could cause accidental release of chemicals, fire or explosion and to provide decisions to improve operational risk safety. It was concluded that for risk analysis (PRA) accidents occur due to lack of maintenance in the facilities and equipment set and the Eisenberg Vulnerability Method provided an assessment of the probability of damage to infrastructure and damage to the environment for 1%, 50% and 99% lethality

Efficient Multi-Scale Attention Module with Cross-Spatial Learning

Remarkable effectiveness of the channel or spatial attention mechanisms for producing more discernible feature representation are illustrated in various computer vision tasks. However, modeling the cross-channel relationships with channel dimensionality reduction may bring side effect in extracting deep visual representations. In this paper, a novel efficient multi-scale attention (EMA) module is proposed. Focusing on retaining the information on per channel and decreasing the computational overhead, we reshape the partly channels into the batch dimensions and group the channel dimensions into multiple sub-features which make the spatial semantic features well-distributed inside each feature group. Specifically, apart from encoding the global information to re-calibrate the channel-wise weight in each parallel branch, the output features of the two parallel branches are further aggregated by a cross-dimension interaction for capturing pixel-level pairwise relationship. We conduct extensive ablation studies and experiments on image classification and object detection tasks with popular benchmarks (e.g., CIFAR-100, ImageNet-1k, MS COCO and VisDrone2019) for evaluating its performance.Comment: Accepted to ICASSP202

Influence of early post-burn enteral nutrition on clinical outcomes of patients with extensive burns

Sepsis commonly occurs in severe post-burn patients, often resulting in death. We aimed to evaluate the influence of early enteral feeding on outcomes in patients with extensive burns, including infection incidence, healing and mortality. We retrospectively reviewed 60 patients with extensive burns, 35 who had received early enteral nutrition and 25 who had received parenteral nutrition. Average healing time, infection incidence and mortality were clinically observed. Hemoglobin and serum albumin were monitored weekly in both groups during treatment. Causative organisms were identified in patients with sepsis. Infection incidence was significantly less in the enteral nutrition group than the parenteral nutrition group (17.1% vs 44.0%; p = 0.023); and latency duration was longer in the enteral nutrition group than in the parenteral nutrition group (30.5 ± 4.7 days vs 14.5 ± 2.3 days; p<0.001). Duration of antibiotic therapy of the enteral nutrition group was significantly shorter than that of the parenteral nutrition group (12.5 ± 3.0 days vs 19.8 ± 3.6 days; p<0.001). Mean hemoglobin results (10.1 ± 1.3 g/L vs 8.3 ± 1.5 g/L; p<0.001) and serum albumin results (44.7 ± 5.7 g/L vs 36.2 ± 6.9 g/L; p<0.001) of enteral nutrition and parenteral nutrition groups, respectively, provided an overview of systemic nutrition and protein metabolism, suggesting higher systemic nutrition and protein synthesis in enteral nutrition group than in parenteral nutrition group. Risk of post-burn infection is reduced in burn patients who are supported by earliest possible enteral nutrition

A Root-Knot Nematode Secretory Peptide Functions as a Ligand for a Plant Transcription Factor

Parasitism genes expressed in the esophageal gland cells of root-knot nematodes encode proteins that are secreted into host root cells to transform the recipient cells into enlarged multinucleate feeding cells called giant-cells. Expression of a root-knot nematode parasitism gene which encodes a novel 13-amino-acid secretory peptide in plant tissues stimulated root growth. Two SCARECROW-like transcription factors of the GRAS protein family were identified as the putative targets for this bioactive nematode peptide in yeast two-hybrid analyses and confirmed by in vitro and in vivo coimmunoprecipitations. This discovery is the first demonstration of a direct interaction of a nematode-secreted parasitism peptide with a plant-regulatory protein, which may represent an early signaling event in the root-knot nematode-host interaction

The 8D05 Parasitism Gene of Meloidogyne incognita Is Required for Successful Infection of Host Roots

Parasitism genes encode effector proteins that are secreted through the stylet of root-knot nematodes to dramatically modify selected plant cells into giant-cells for feeding. The Mi8D05 parasitism gene previously identified was confirmed to encode a novel protein of 382 amino acids that had only one database homolog identified on contig 2374 within the Meloidogyne apla genome. Mi8D05 expression peaked in M. incognita parasitic second-stage juveniles within host roots and its encoded protein was limited to the subventral esophageal gland cells that produce proteins secreted from the stylet. Constitutive expression of Mi8D05 in transformed Arabidopsis thaliana plants induced accelerated shoot growth and early flowering but had no visible effects on root growth. Independent lines of transgenic Arabidopsis that expressed a double-stranded RNA complementary to Mi8D05 in host-derived RNA interference (RNAi) tests had up to 90% reduction in infection by M. incognita compared with wild-type control plants, suggesting that Mi8D05 plays a critical role in parasitism by the root-knot nematode. Yeast two-hybrid experiments confirmed the specific interaction of the Mi8D05 protein with plant aquaporin tonoplast intrinsic protein 2 (TIP2) and provided evidence that the Mi8D05 effector may help regulate solute and water transport within giant-cells to promote the parasitic interaction

A Profile of Putative Parasitism Genes Expressed in the Esophageal Gland Cells of the Root-knot Nematode Meloidogyne incognita

Identifying parasitism genes encoding proteins secreted from a nematode\u27s esophageal gland cells and injected through its stylet into plant tissue is the key to understanding the molecular basis of nematode parasitism of plants. Meloidogyne incognita parasitism genes were cloned by microaspirating the cytoplasm from the esophageal gland cells of different parasitic stages to provide mRNA to create a gland cell-specific cDNA library by long-distance reverse-transcriptase polymerase chain reaction. Of 2,452 cDNA clones sequenced, deduced protein sequences of 185 cDNAs had a signal peptide for secretion and, thus, could have a role in root-knot nematode parasitism of plants. High-throughput in situ hybridization with cDNA clones encoding signal peptides resulted in probes of 37 unique clones specifically hybridizing to transcripts accumulating within the subventral (13 clones) or dorsal (24 clones) esophageal gland cells of M. incognita. In BLASTP analyses, 73% of the predicted proteins were novel proteins. Those with similarities to known proteins included a pectate lyase, acid phosphatase, and hypothetical proteins from other organisms. Our cell-specific analysis of genes encoding secretory proteins provided, for the first time, a profile of putative parasitism genes expressed in the M. incognita esophageal gland cells throughout the parasitic cycle

609 Combining bintrafusp alfa with abituzumab enhances suppression of the TGF-β signaling pathway

BackgroundBintrafusp alfa is a first-in-class bifunctional fusion protein composed of the extracellular domain of the TGF-βRII receptor fused to a human IgG1 antibody blocking PD-L1. The TGF-βRII moiety of bintrafusp alfa functions as a "trap" to sequester active TGF-β but does not block TGF-β release from its latent form. Multiple mechanisms lead to the release of active TGF-β. Integrins control local activation of latent TGF-β stored in the extracellular matrix and cell-surface reservoirs in the tumor microenvironment (TME). Alpha v integrin mRNA expression is correlated with multiple TGF-β gene signatures. It has been shown that αvβ8 integrin mediates TGF-β activation without releasing it from the latent TGF-β complex, suggesting that the TGF-βRII moiety of bintrafusp alfa may be unable to sequester TGF-β activated by αvβ8 integrin. Therefore, we hypothesize that combining abituzumab, a pan–αv integrin antibody, with bintrafusp alfa may lead to enhanced suppression of TGF-β signaling.MethodsThe expression of αv and β6 integrin mRNA was determined by RNA sequencing of triple-negative breast cancer (TNBC) tumor samples from a phase 1 clinical trial of bintrafusp alfa and correlated with patient response to bintrafusp alfa. The combination of bintrafusp alfa and abituzumab was investigated in vitro and in vivo in a TGF-β–dependent human tumor model, Detroit 562. In this study, CellTiter-Glo 2.0 Assay measured cell proliferation in vitro and enzyme-linked immunosorbent assay measured the level of latency-associated protein (LAP). A TGF-β reporter cell line MDA-MB-231 measured the level of active TGF-β. Antitumor activity in vivo was evaluated via tumor growth of Detroit 562 xenograft model in SCID mice.ResultsIn TNBC, increased expression of αv and β6 integrin mRNA was associated with poor response to bintrafusp alfa, suggesting that TGF-β activated by αv integrin may not be blocked by bintrafusp alfa. In Detroit 562 cells, abituzumab increased LAP levels in the cell culture medium, confirming modulation of the TGF-β pathway. As a result, the amount of active TGF-β released into culture medium was reduced by abituzumab. In vitro, both abituzumab and bintrafusp alfa suppressed Detroit 562 cell proliferation, and the combination suppressed cell proliferation further. In vivo, the combination led to increased tumor growth inhibition of Detroit 562 xenograft tumors relative to either monotherapy, further supporting the potential of this combination.ConclusionsCollectively, these preclinical findings support clinical development of bintrafusp alfa and abituzumab combination therapy to maximally suppress TGF-β signaling in the TME.AcknowledgementsWe thank George Locke for his analysis of the RNAseq data.Ethics ApprovalThis study was approved by the Institutional Animal Care and Use Committee at EMD Serono, Inc.; approval number [17–008]