Development of an Aeroelastic Modeling Capability for Transient Nozzle Side Load Analysis

Lateral nozzle forces are known to cause severe structural damage to any new rocket engine in development. Currently there is no fully coupled computational tool to analyze this fluid/structure interaction process. The objective of this study was to develop a fully coupled aeroelastic modeling capability to describe the fluid/structure interaction process during the transient nozzle operations. The aeroelastic model composes of three components: the computational fluid dynamics component based on an unstructured-grid, pressure-based computational fluid dynamics formulation, the computational structural dynamics component developed in the framework of modal analysis, and the fluid-structural interface component. The developed aeroelastic model was applied to the transient nozzle startup process of the Space Shuttle Main Engine at sea level. The computed nozzle side loads and the axial nozzle wall pressure profiles from the aeroelastic nozzle are compared with those of the published rigid nozzle results, and the impact of the fluid/structure interaction on nozzle side loads is interrogated and presented

Aeroelastic Modeling of a Nozzle Startup Transient

Lateral nozzle forces are known to cause severe structural damage to any new rocket engine in development during test. While three-dimensional, transient, turbulent, chemically reacting computational fluid dynamics methodology has been demonstrated to capture major side load physics with rigid nozzles, hot-fire tests often show nozzle structure deformation during major side load events, leading to structural damages if structural strengthening measures were not taken. The modeling picture is incomplete without the capability to address the two-way responses between the structure and fluid. The objective of this study is to develop a tightly coupled aeroelastic modeling algorithm by implementing the necessary structural dynamics component into an anchored computational fluid dynamics methodology. The computational fluid dynamics component is based on an unstructured-grid, pressure-based computational fluid dynamics formulation, while the computational structural dynamics component is developed under the framework of modal analysis. Transient aeroelastic nozzle startup analyses at sea level were performed, and the computed transient nozzle fluid-structure interaction physics presented

An Improved LMI Approach for Static Output Feedback Fault-tolerant Control With Application to Flight Tracking Control

Abstract-This paper proposes an improved Linear Matrix Inequality (LMI) approach for the synthesis of Static Output Feedback (SOF) Fault-Tolerant Control (FTC). A novel slack variable is introduced into the matrix inequalities, which provides an additional degree of freedom to compute the numerical solution. Subsequently, an improved iterative algorithm is developed to obtain an optimal SOF gain with less conservativeness. In this paper, designs of the SOF gain are shown in the framework of tracking control. The nonlinear simulations of the ADMIRE aircraft are included to demonstrate the effectiveness of the proposed method

An Improved LMI Approach for Static Output Feedback Fault-tolerant Control With Application to Flight Tracking Control

Abstract-This paper proposes an improved Linear Matrix Inequality (LMI) approach for the synthesis of Static Output Feedback (SOF) Fault-Tolerant Control (FTC). A novel slack variable is introduced into the matrix inequalities, which provides an additional degree of freedom to compute the numerical solution. Subsequently, an improved iterative algorithm is developed to obtain an optimal SOF gain with less conservativeness. In this paper, designs of the SOF gain are shown in the framework of tracking control. The nonlinear simulations of the ADMIRE aircraft are included to demonstrate the effectiveness of the proposed method

Comparative transcriptome analysis reveals resistance-related genes and pathways in Musa acuminata banana 'Guijiao 9' in response to Fusarium wilt.

Fusarium wilt caused by Fusarium oxysporum f. sp. cubense (Foc), is one of the most devastating diseases in bananas resulting in significant loss of Cavendish bananas production worldwide. Here we show the agronomic traits and the resistance of 'Guijiao 9' in the field trials from 2012 to 2017. And then we dissect and compare the transcriptome response from these two cultivars (cv. 'Guijiao 9' and cv. Williams) in an attempt to understand the molecular basis that contribute to the enhanced Foc tropical race 4 (Foc-TR4) resistance. 'Guijiao 9' is a Cavendish cultivar with strong resistance to Foc-TR4, which was reflected in a lower disease severity and incidence in glasshouse and field trails, when compared to the susceptible cultivar Williams. Gene expression profiles of 'Guijiao 9' and Williams were captured by performing RNA-Seq analysis on 16 biological samples collected over a six day period post inoculation with Foc-TR4. Transcriptional reprogramming in response to Foc-TR4 was detected in both genotypes but the response was more drastic in 'Guijiao 9' than in Williams. Specific genes involved in plant-pathogen interaction and defense signaling including MAPK, calcium, salicylic acid, jasmonic acid and ethylene pathways were analyzed and compared between 'Guijiao 9' and Williams. Genes associated with defense-related metabolites synthesis such as NB-LRR proteins, calmodulin-binding protein and phenylpropanoids biosynthesis genes were significantly up-regulated in 'Guijiao 9' resistant to Foc-TR4 infection. Taken together, this study highlights the important roles of plant hormone regulation and defense gene activation in mediating resistance in 'Guijiao 9'

Cadmium suppresses the proliferation of piglet Sertoli cells and causes their DNA damage, cell apoptosis and aberrant ultrastructure

<p>Abstract</p> <p>Objective</p> <p>Very little information is known about the toxic effects of cadmium on somatic cells in mammalian testis. The objective of this study is to explore the toxicity of cadmium on piglet Sertoli cells.</p> <p>Methods</p> <p>Sertoli cells were isolated from piglet testes using a two-step enzyme digestion and followed by differential plating. Piglet Sertoli cells were identified by oil red O staining and Fas ligand (FasL) expression as assayed by immunocytochemistry and expression of transferrin and androgen binding protein by RT-PCR. Sertoli cells were cultured in DMEM/F12 supplemented with 10% fetal calf serum in the absence or presence of various concentrations of cadmium chloride, or treatment with p38 MAPK inhibitor SB202190 and with cadmium chloride exposure. Apoptotic cells in seminiferous tubules of piglets were also performed using TUNEL assay in vivo.</p> <p>Results</p> <p>Cadmium chloride inhibited the proliferation of Piglet Sertoli cells as shown by MTT assay, and it increased malondialdehyde (MDA) but reduced superoxide dismutase (SOD) and Glutathione peroxidase (GSH-Px) activity. Inhibitor SB202190 alleviated the proliferation inhibition of cadmium on piglet Sertoli cells. Comet assay revealed that cadmium chloride caused DNA damage of Piglet Sertoli cells and resulted in cell apoptosis as assayed by flow cytometry. The in vivo study confirmed that cadmium induced cell apoptosis in seminiferous tubules of piglets. Transmission electronic microscopy showed abnormal and apoptotic ultrastructure in Piglet Sertoli cells treated with cadmium chloride compared to the control.</p> <p>Conclusion</p> <p>cadmium has obvious adverse effects on the proliferation of piglet Sertoli cells and causes their DNA damage, cell apoptosis, and aberrant morphology. This study thus offers novel insights into the toxicology of cadmium on male reproduction.</p

Deletions in CWH43 cause idiopathic normal pressure hydrocephalus

Idiopathic normal pressure hydrocephalus (iNPH) is a neurological disorder that occurs in about 1% of individuals over age 60 and is characterized by enlarged cerebral ventricles, gait difficulty, incontinence, and cognitive decline. The cause and pathophysiology of iNPH are largely unknown. We performed whole exome sequencing of DNA obtained from 53 unrelated iNPH patients. Two recurrent heterozygous loss of function deletions in CWH43 were observed in 15% of iNPH patients and were significantly enriched 6.6-fold and 2.7-fold, respectively, when compared to the general population. Cwh43 modifies the lipid anchor of glycosylphosphatidylinositol-anchored proteins. Mice heterozygous for CWH43 deletion appeared grossly normal but displayed hydrocephalus, gait and balance abnormalities, decreased numbers of ependymal cilia, and decreased localization of glycosylphosphatidylinositol-anchored proteins to the apical surfaces of choroid plexus and ependymal cells. Our findings provide novel mechanistic insights into the origins of iNPH and demonstrate that it represents a distinct disease entity

DNA damage and decrease of cellular oxidase activity in piglet sertoli cells exposed to gossypol

The study was designated to explore the toxic effects of gossypol on piglet sertoli cells. Sertoli cells were isolated from piglet testes using a two-step enzyme digestion and followed by differential plating. Piglet sertoli cells were cultured and classified into five groups, that is, group A, the control without gossypol, group B with 2.5 μg/ml gossypol, group C with 5 μg/ml gossypol, group D with 10 μg/ml gossypol and group E with 20 μg/ml gossypol. We found that sertoli cells’ growth was inhibited by gossypol at dose 2.5 μg/ml when compared with the control group. The oxidase activity of sertoli cell also decreased at 2.5 μg/m gossypol. Moreover, DNA damage of sertoli cells was observed at 5 μg/ml gossypol. Putting this into consideration, our study suggests that exposure of gossypol to sertoli cells leads to an inhibition of sertoli cell growth and oxidase activity of sertoli cells at a low concentration, whereas gossypol results in DNA damage of sertoli cells at a higher concentration.Keywords: Gossypol, sertoli cells, oxidase, DNA damag

Single-cell analysis reveals the COL11A1+ fibroblasts are cancer-specific fibroblasts that promote tumor progression

Background: Cancer-associated fibroblasts (CAFs) promote tumor progression through extracellular matrix (ECM) remodeling and extensive communication with other cells in tumor microenvironment. However, most CAF-targeting strategies failed in clinical trials due to the heterogeneity of CAFs. Hence, we aimed to identify the cluster of tumor-promoting CAFs, elucidate their function and determine their specific membrane markers to ensure precise targeting.Methods: We integrated multiple single-cell RNA sequencing (scRNA-seq) datasets across different tumors and adjacent normal tissues to identify the tumor-promoting CAF cluster. We analyzed the origin of these CAFs by pseudotime analysis, and tried to elucidate the function of these CAFs by gene regulatory network analysis and cell-cell communication analysis. We also performed cell-type deconvolution analysis to examine the association between the proportion of these CAFs and patients’ prognosis in TCGA cancer cohorts, and validated that through IHC staining in clinical tumor tissues. In addition, we analyzed the membrane molecules in different fibroblast clusters, trying to identify the membrane molecules that were specifically expressed on these CAFs.Results: We found that COL11A1+ fibroblasts specifically exist in tumor tissues but not in normal tissues and named them cancer-specific fibroblasts (CSFs). We revealed that these CSFs were transformed from normal fibroblasts. CSFs represented a more activated CAF cluster and may promote tumor progression through the regulation on ECM remodeling and antitumor immune responses. High CSF proportion was associated with poor prognosis in bladder cancer (BCa) and lung adenocarcinoma (LUAD), and IHC staining of COL11A1 confirmed their specific expression in tumor stroma in clinical BCa samples. We also identified that CSFs specifically express the membrane molecules LRRC15, ITGA11, SPHK1 and FAP, which could distinguish CSFs from other fibroblasts.Conclusion: We identified that CSFs is a tumor specific cluster of fibroblasts, which are in active state, may promote tumor progression through the regulation on ECM remodeling and antitumor immune responses. Membrane molecules LRRC15, ITGA11, SPHK1 and FAP could be used as therapeutic targets for CSF-targeting cancer treatment