Relevant bibliographies by topics / ACSL4

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'ACSL4'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'ACSL4.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "ACSL4"

1

Durgan, David J., Justin K. Smith, Margaret A. Hotze, Oluwaseun Egbejimi, Karalyn D. Cuthbert, Vlad G. Zaha, Jason R. B. Dyck, E. Dale Abel, and Martin E. Young. "Distinct transcriptional regulation of long-chain acyl-CoA synthetase isoforms and cytosolic thioesterase 1 in the rodent heart by fatty acids and insulin." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 6 (June 2006): H2480—H2497. http://dx.doi.org/10.1152/ajpheart.01344.2005.

Full text
Abstract:
The molecular mechanism(s) responsible for channeling long-chain fatty acids (LCFAs) into oxidative versus nonoxidative pathways is (are) poorly understood in the heart. Intracellular LCFAs are converted to long-chain fatty acyl-CoAs (LCFA-CoAs) by a family of long-chain acyl-CoA synthetases (ACSLs). Cytosolic thioesterase 1 (CTE1) hydrolyzes cytosolic LCFA-CoAs to LCFAs, generating a potential futile cycle at the expense of ATP utilization. We hypothesized that ACSL isoforms and CTE1 are differentially regulated in the heart during physiological and pathophysiological conditions. Using quantitative RT-PCR, we report that the five known acsl isoforms ( acsl1, acsl3, acsl4, acsl5, and acsl6) and cte1 are expressed in whole rat and mouse hearts, as well as adult rat cardiomyocytes (ARCs). Streptozotocin-induced insulin-dependent diabetes (4 wk) and fasting (≤24 h) both dramatically induced cte1 and repressed acsl6 mRNA, with no significant effects on the other acsl isoforms. In contrast, high-fat feeding (4 wk) induced cte1 without affecting expression of the acsl isoforms in the heart. Investigation into the mechanism(s) responsible for these transcriptional changes uncovered roles for peroxisome proliferator-activated receptor-α (PPARα) and insulin as regulators of specific acsl isoforms and cte1 in the heart. Culturing ARCs with oleate (0.1–0.4 mM) or the PPARα agonists WY-14643 (1 μM) and fenofibrate (10 μM) consistently induced acsl1 and cte1. Conversely, PPARα null mouse hearts exhibited decreased acsl1 and cte1 expression. Culturing ARCs with insulin (10 nM) induced acsl6, whereas specific loss of insulin signaling within the heart (cardiac-specific insulin receptor knockout mice) caused decreased acsl6 expression. Our data expose differential regulation of acsl isoforms and cte1 in the heart, where acsl1 and cte1 are PPARα-regulated genes, whereas acsl6 is an insulin-regulated gene.
APA, Harvard, Vancouver, ISO, and other styles
2

Wang, Wei, Xiao Hao, Lina Han, Zhe Yan, Wen-Jun Shen, Dachuan Dong, Kathrin Hasbargen, et al. "Tissue-Specific Ablation of ACSL4 Results in Disturbed Steroidogenesis." Endocrinology 160, no. 11 (August 27, 2019): 2517–28. http://dx.doi.org/10.1210/en.2019-00464.

Full text
Abstract:
Abstract ACSL4 is a member of the ACSL family that catalyzes the conversion of long-chain fatty acids to acyl-coenzyme As, which are essential for fatty-acid incorporation and utilization in diverse metabolic pathways, including cholesteryl ester synthesis. Steroidogenic tissues such as the adrenal gland are particularly enriched in cholesteryl esters of long-chain polyunsaturated fatty acids, which constitute an important pool supplying cholesterol for steroid synthesis. The current studies addressed whether ACSL4 is required for normal steroidogenesis. CYP11A1 promoter‒mediated Cre was used to generate steroid tissue‒specific ACSL4 knockout (KO) mice. Results demonstrated that ACSL4 plays an important role in adrenal cholesteryl ester formation, as well as in determining the fatty acyl composition of adrenal cholesteryl esters, with ACSL4 deficiency leading to reductions in cholesteryl ester storage and alterations in cholesteryl ester composition. Statistically significant reductions in corticosterone and testosterone production, but not progesterone production, were observed in vivo, and these deficits were accentuated in ex vivo and in vitro studies of isolated steroid tissues and cells from ACSL4-deficient mice. However, these effects on steroid production appear to be due to reductions in cholesteryl ester stores rather than disturbances in signaling pathways. We conclude that ACSL4 is dispensable for normal steroidogenesis.
APA, Harvard, Vancouver, ISO, and other styles
3

Wu, Jinchun, Zhengxi He, Xianyu Liu, Yanhua Mou, Jingchen Lu, Chaojun Duan, and Bin Li. "High expression of ferroptosis-sensitizer ACSL4 as an indicator of good response to immune checkpoint inhibitors and preferable survival with increased TIICs in skin cutaneous melanoma." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): e21594-e21594. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e21594.

Full text
Abstract:
e21594 Background: Skin cutaneous melanoma (SKCM) has a high incidence and mortality. Immune checkpoint inhibitors (ICIs) are promising but show heterogeneous efficacy in the SKCM treatment. T cell-promoted tumor ferroptosis is a vital anti-tumor mechanism of ICIs. Acyl-CoA synthetase long chain family member 4 (ACSL4) can sensitize ferroptosis by facilitating lipid peroxidation. So we proposed that ACSL4 is a positive predictor for ICIs efficacy and correlated with tumor-infiltrating immune cells (TIICs) in SKCM. Methods: The responses of SKCM patients to ICIs were evaluated from Tumor Immune Dysfunction and Exclusion (TIDE) using the gene expression data of The Cancer Genome Atlas (TCGA)-SKCM downloaded from UCSC Xena browser and datasets within TIDE. The correlation between ACLS4 expression and survival was obtained from the Online consensus Survival webserver for Skin Cutaneous Melanoma (OSskcm) and TIDE databases. The relationships between ACSL4 and TIICs were evaluated using the database of Tumor Immune Estimation Resource 2.0 (TIMER2.0). Results: ACSL4 expression was positively correlated with the predicted responder of ICIs in TCGA dataset (R = 0.12, p = 0.0093) and therapy outcomes of ICIs in Gide2019_PD1+CTLA4 (Progression-free survival(PFS), contimuous z = -2.39, p = 0.0169) and Lauss2017_ACT (PFS, contimuous z = -2.08, p = 0.0371; overall survival(OS), contimuous z = -2.96, p = 0.00309). Favorable OS was observed in the patients with high ACSL4 expression in the TCGA (HR = 0.6567, 95% CI = 0.5015̃0.8599, p = 0.0022) and GSE19234 (HR = 0.4135, 95% CI = 0.1748̃0.9784, p = 0.0445) from OSskcm and the GSE8401 (contimuous z = -2,24, p = 0.025) and GSE54467 (contimuous z = -2.26, p = 0.0239) from TIDE database. TIICs including CD8+ T cells, CD4+ T cells (memory, Th2), B cells, neutrophils, monocytes, M1 macrophages, and cancer-associated fibroblasts (CAFs) were positively associated with the expression level of ACSL4. Conclusions: High ACSL4 expression maybe indicates a good response to ICIs and long survival in SKCM. The increased T cells within the tumor microenvironment correlated with high ACSL4 expression possibly implied the synergism effects of ferroptosis and ICIs, deserving further investigation. Keywords: ACSL4, ICIs, TIICs, SKCM.
APA, Harvard, Vancouver, ISO, and other styles
4

Singh, Amar B., Chin Fung K. Kan, Fredric B. Kraemer, Raymond A. Sobel, and Jingwen Liu. "Liver-specific knockdown of long-chain acyl-CoA synthetase 4 reveals its key role in VLDL-TG metabolism and phospholipid synthesis in mice fed a high-fat diet." American Journal of Physiology-Endocrinology and Metabolism 316, no. 5 (May 1, 2019): E880—E894. http://dx.doi.org/10.1152/ajpendo.00503.2018.

Full text
Abstract:
Long-chain acyl-CoA synthetase 4 (ACSL4) has a unique substrate specificity for arachidonic acid. Hepatic ACSL4 is coregulated with the phospholipid (PL)-remodeling enzyme lysophosphatidylcholine (LPC) acyltransferase 3 by peroxisome proliferator-activated receptor δ to modulate the plasma triglyceride (TG) metabolism. In this study, we investigated the acute effects of hepatic ACSL4 deficiency on lipid metabolism in adult mice fed a high-fat diet (HFD). Adenovirus-mediated expression of a mouse ACSL4 shRNA (Ad-shAcsl4) in the liver of HFD-fed mice led to a 43% reduction of hepatic arachidonoyl-CoA synthetase activity and a 53% decrease in ACSL4 protein levels compared with mice receiving control adenovirus (Ad-shLacZ). Attenuated ACSL4 expression resulted in a substantial decrease in circulating VLDL-TG levels without affecting plasma cholesterol. Lipidomics profiling revealed that knocking down ACSL4 altered liver PL compositions, with the greatest impact on accumulation of abundant LPC species (LPC 16:0 and LPC 18:0) and lysophosphatidylethanolamine (LPE) species (LPE 16:0 and LPE 18:0). In addition, fasting glucose and insulin levels were higher in Ad-shAcsl4-transduced mice versus control (Ad-shLacZ). Glucose tolerance testing further indicated an insulin-resistant phenotype upon knockdown of ACSL4. These results provide the first in vivo evidence that ACSL4 plays a role in plasma TG and glucose metabolism and hepatic PL synthesis of hyperlipidemic mice.
APA, Harvard, Vancouver, ISO, and other styles
5

Wu, Hongxia, and Aiwen Liu. "Long non-coding RNA NEAT1 regulates ferroptosis sensitivity in non-small-cell lung cancer." Journal of International Medical Research 49, no. 3 (March 2021): 030006052199618. http://dx.doi.org/10.1177/0300060521996183.

Full text
Abstract:
Objectives Ferroptosis is caused by iron-dependent lipid peroxide accumulation, the sensitivity of which might be regulated by acyl-CoA synthetase long chain family member 4 (ACSL4). Non-small-cell lung cancer (NSCLC) can resist oxidative stress and reduce the sensitivity of tumor cells to ferroptosis by changing the expression of some proteins. Mechanisms involving ferroptosis sensitivity in NSCLC are not fully understood. Methods A dual-luciferase reporter assay was used to confirm a targeting relationship between long non-coding (lnc)RNA NEAT1 and ACSL4. Overexpression and silencing assays of NEAT1 function were used to determine its roles in cell death (by TUNEL staining) and lipid peroxidation (by malondialdehyde levels). Expression of ferroptosis-related proteins (SLCA11, GPX4, and TFR4) was evaluated by western blot in NSCLC cells treated or not with the ferroptosis inducer erastin. Results Erastin-induced cell death was positively correlated with ACSL4 level. NEAT1 regulated levels of ACSL4 and proteins related to the ferroptosis and classical apoptosis pathways. Levels of ACSL4, SLC7A11, and GPX4 were decreased more by NEAT1 silencing plus erastin than by erastin alone. Conclusion NEAT1 regulates ferroptosis and ferroptosis sensitivity, with the latter depending on ACSL4, suggesting that targeting NEAT1 or ACSL4 may be a viable therapeutic approach to the treatment of NSCLC.
APA, Harvard, Vancouver, ISO, and other styles
6

Fan, Yongliang, Ziyin Han, Xubin Lu, Huimin Zhang, Abdelaziz Adam Idriss Arbab, Juan J. Loor, Yi Yang, and Zhangping Yang. "Identification of Milk Fat Metabolism-Related Pathways of the Bovine Mammary Gland during Mid and Late Lactation and Functional Verification of the ACSL4 Gene." Genes 11, no. 11 (November 16, 2020): 1357. http://dx.doi.org/10.3390/genes11111357.

Full text
Abstract:
The concentration of bovine milk fat changes regularly with lactation stages. In particular, milk fat percentage is higher in late lactation than mid lactation. Furthermore, milk fat composition is highly subject to a few genes. Thus, transcriptome sequencing was performed to explore the expression patterns of differentially-expressed genes (DEGs) in the parenchymal mammary gland of Holstein dairy cows between mid and late lactation. The 725 DEGs were screened (fold change > 2 and p-value < 0.05), and the peroxisome proliferator-activated receptor (PPAR) signaling pathway associated with lipid synthesis had a significant variation between the two periods (p-value < 0.05). The activation of the PPAR signal pathway may a key factor in the increasing of milk fat content in late lactation compared to mid lactation. Acyl-CoA synthetase long-chain family member 4 (ACSL4), a member of the PPAR signaling pathway, was upregulated in late lactation compared to mid lactation (p < 0.05). ACSL4 catalyzes the activation of long-chain fatty acids for cellular lipid synthesis. However, it remains uncertain that the molecular mechanism of milk fat synthesis is regulated by ACSL4 in dairy cows. Subsequently, the function verification of ACSL4 was performed in bovine mammary epithelial cells (BMECs). The upregulated expression of ACSL4 was accompanied by the increase of the concentration of intracellular triglycerides, whereas knockdown of ACSL4 decreased the concentration of intracellular triglycerides, which demonstrated that ACSL4 plays an important role in modulating milk fat synthesis. In conclusion, the results displayed that ACSL4 expression regulates triglyceride metabolism in ruminant mammary cells.
APA, Harvard, Vancouver, ISO, and other styles
7

Jin, Zheng-Long, Wen-Ying Gao, Shao-Jun Liao, Tao Yu, Qing Shi, Shang-Zhen Yu, and Ye-Feng Cai. "Paeonol inhibits the progression of intracerebral haemorrhage by mediating the HOTAIR/UPF1/ACSL4 axis." ASN Neuro 13 (January 2021): 175909142110106. http://dx.doi.org/10.1177/17590914211010647.

Full text
Abstract:
Intracerebral haemorrhage (ICH) is a devastating subtype of stroke with high morbidity and mortality. It has been reported that paeonol (PAN) inhibits the progression of ICH. However, the mechanism by which paeonol mediates the progression of ICH remains unclear. To mimic ICH in vitro, neuronal cells were treated with hemin. An in vivo model of ICH was established to detect the effect of paeonol on ferroptosis in neurons during ICH. Cell viability was tested by MTT assay. Furthermore, cell injury was detected by GSH, MDA and ROS assays. Ferroptosis was examined by iron assay. RT-qPCR and western blotting were used to detect gene and protein expression, respectively. The correlation among HOTAIR, UPF1 and ACSL4 was explored by FISH, RNA pull-down and RIP assays. Paeonol significantly inhibited the ferroptosis of neurons in ICH mice. In addition, paeonol significantly reversed hemin-induced injury and ferroptosis in neurons, while this phenomenon was notably reversed by HOTAIR overexpression. Moreover, paeonol notably inhibited ferroptosis in hemin-treated neuronal cells via inhibition of ACSL4. Additionally, HOTAIR bound to UPF1, and UPF1 promoted the degradation of ACSL4 by binding to ACSL4. Furthermore, HOTAIR overexpression reversed paeonol-induced inhibition of ferroptosis by mediating the UPF1/ACSL4 axis. Paeonol inhibits the progression of ICH by mediating the HOTAIR/UPF1/ACSL4 axis. Therefore, paeonol might serve as a new agent for the treatment of ICH.
APA, Harvard, Vancouver, ISO, and other styles
8

Sen, Progga, Chin Fung Kelvin Kan, Amar B. Singh, Monica Rius, Fredric B. Kraemer, Elizabeth Sztul, and Jingwen Liu. "Identification of p115 as a novel ACSL4 interacting protein and its role in regulating ACSL4 degradation." Journal of Proteomics 229 (October 2020): 103926. http://dx.doi.org/10.1016/j.jprot.2020.103926.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Soupene, Eric, and Frans A. Kuypers. "Multiple Erythroid Isoforms of Human Long-Chain acyl-CoA Synthetases Are Produced by a Switch of the Fatty Acid Gate-Domains." Blood 106, no. 11 (November 16, 2005): 1672. http://dx.doi.org/10.1182/blood.v106.11.1672.1672.

Full text
Abstract:
Abstract In mammals, long-chain acyl-CoA synthetases (ACSL) are necessary for fatty acid degradation, phospholipid remodeling, and production of long acyl-CoA esters that regulate various physiological processes. These enzymes play a crucial role in plasma membrane phospholipid turnover in erythrocytes, maintaining the complex phospholipid molecular species composition essential for proper membrane function. The mechanism by which this highly dynamic turnover together with an ever-changing plasma fatty acid pool maintains phospholipid composition is poorly understood. We have previously cloned Acyl-CoA Synthetase Long-chain member 6 (ACSL6), the isoform responsible for activation of long-chain fatty acids in erythrocytes. Two additional transcript variants of this protein were subsequently isolated from brain and testis. We report the expression of four different variants of ACLS6 in reticulocytes, one as we originally reported, two of which are novel, one as was identified in brain cells. PCR amplifications using primers for the predicted variable regions were performed from cDNAs of CD34 positive erythroid progenitors, K562 cells, fetal blood cells, reticulocytes and placenta. ACSL variants were expressed in E. coli host BL21DE3 cells using the pET28a vector, and detected by His tag immuno detection. Sequence alignments were generated using sequences retrieved from RefSeq and GenBank databases on the NCBI site. Exon and intron definition for ACSL members were obtained using evidence viewer and model maker available at the map viewer page of each gene. We identified four different spliced variants of ACSL6 in erythroid cells based on a mutually exclusive exon pair. Each exon of this pair encodes a slightly different short motif that contains the fatty acid Gate domain, a conserved structural domain found in all vertebrate and invertebrate ACSL homologs. The motif differs in the presence of either the aromatic residue phenylalanine (Phe) or tyrosine (Tyr), and seems to play a role in substrate specificity. One of the new forms contained an exon not found in any other ACSL isoforms. Erythroid precursors also express the closely related ACSL1, and we characterized two additional isoforms of this protein, similar to ACSL6. When analyzed on denaturing SDS polyacrylamide gel both ACSL1 and 6 appeared to exist as a dimer. Based on our results, we propose the generation of two different Gate-domains by alternative splicing of the two exons in these proteins. One represents a switch of the Phe to the Tyr Gate-domain motif, the other resulted of the exclusion of both. Swapping of this motif appears to be common to all mammalian homologs of ACSL1 and 6. We conclude that the Phe to a Tyr substitution in the Gate-domain, or its removal, together with the formation of homo or heterodimers will allow ACSL6 the structural diversity to define substrate specificity that maintains the complex plasma membrane phospholipid molecular species composition in erythrocytes.
APA, Harvard, Vancouver, ISO, and other styles
10

Yu, Xiang, Xibi Fang, Hang Xiao, Zhihui Zhao, Steffen Maak, Mengyan Wang, and Runjun Yang. "The effect of acyl-CoA synthetase long-chain family member 5 on triglyceride synthesis in bovine preadipocytes." Archives Animal Breeding 62, no. 1 (May 6, 2019): 257–64. http://dx.doi.org/10.5194/aab-62-257-2019.

Full text
Abstract:
Abstract. Acyl-CoA synthetase long-chain family member 5 (ACSL5) is a member of the acyl coenzyme A (CoA) long-chain synthase families (ACSLs), and it plays a key role in fatty acid metabolism. In this study, we proved an association between the ACSL5 gene and triglyceride metabolism at the cellular level in cattle. pBI-CMV3-ACSL5 and pGPU6/GFP/Neo-ACSL5 plasmids were constructed and transfected into bovine preadipocytes by electroporation. The expression level of ACSL5 was detected by real-time quantitative PCR and western blot. The triglyceride content was detected by a triglyceride kit. The results indicated that the expression level of ACSL5 mRNA and protein in the pBI-CMV3-ACSL5-transfected group was significantly increased compared with those in the control group. Furthermore, the pGPU6/GFP/Neo-ACSL5-transfected group was significantly decreased compared with those in the control group. A cell triglyceride test showed that overexpression or silencing of the ACSL5 gene could affect synthesis of cellular triglycerides. This study investigated the mechanism of ACSL on bovine fat deposition, and also provides a new candidate gene for meat quality traits in beef cattle.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "ACSL4"

1

Reis, Sarita Badiglian Ascenço. "Mutação no gene ACSL4 (acyl-CoA synthetase long-chain family member 4) como causa de deficiência mental de herança ligada ao X." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/41/41131/tde-25112009-101653/.

Full text
Abstract:
Estudamos uma família com cinco homens (dois falecidos) afetados por deficiência mental (DM) não-sindrômica em duas gerações, num padrão de herança ligada ao cromossomo X. A análise do padrão de inativação do cromossomo X, com base na metilação do gene AR, evidenciou que a mulher portadora obrigatória tinha desvio completo de inativação nos leucócitos, uma característica freqüente em portadoras de mutações do cromossomo X relacionadas com DM. Para o mapeamento da DM, genotipamos 28 locos de microssatélites ao longo do cromossomo X e delimitamos um segmento de cerca de 32 Mb, entre os marcadores DXS986 e DXS8067, compartilhado pelos afetados e pela portadora obrigatória, mas não pelo homem normal ou pelas possíveis portadoras que não tinham desvio do padrão de inativação do cromossomo X. Na busca do gene mutado, analisamos, por seqüenciamento direto, genes mapeados no intervalo compartilhado e já relacionados a DM ou que tivessem expressão em cérebro e leucócitos. Nos afetados e na portadora obrigatória, encontramos a mutação c.845C→T no gene ACSL4, que resulta na substituição do aminoácido histidina, conservado na família de sintetases de acil-CoA humanas e em diversos outros organismos, por tirosina (p.H323Y da isoforma cérebro-específica). Tratando-se de mutação que altera um aminoácido evolutivamente conservado em gene já relacionado com DM, que segregava com a DM na família, não tendo sido encontrada em amostra controle de 160 indivíduos do sexo masculino, concluímos que era a causa da DM na família. Mutações de ponto no gene ACSL4 foram relacionadas com a DM não sindrômica em três famílias descritas na literatura. O gene ACSL4 codifica a acil-coA sintetase 4 da família das sintetases de cadeia longa, que catalisa a formação de ésteres acil-coA a partir de ácidos graxos de cadeia longa. Sua expressão já foi documentada em vários tecidos, incluindo o cérebro e dados recentes mostraram que a proteína é essencial para a formação normal de espinhos dendríticos. A nova mutação do gene ACSL4 que descrevemos como causa de DM vem reforçar a relação alterações desse gene e a DM de herança ligada ao X. O padrão de inativação do X totalmente desviado foi mais uma vez observado em mulher portadora da mutação, indicando a importância da expressão desse gene em leucócitos. A presença de dificuldades de aprendizado na portadora da mutação concorda com o observado nas três famílias da literatura em que o estudo das portadoras foi relatado, indicando o efeito de mutações do gene ACSL4 sobre a função intelectual mesmo em heterozigose. A ausência de correlação entre o padrão de inativação do cromossomo X em células do sangue periférico e o comprometimento intelectual foi confirmada. Na família estudada, a identificação da mutação permitiu o aconselhamento genético.
We studied a family with five men (two of them deceased) affected by nonsyndromic mental retardation in two generations, in a pattern of X-linked inheritance (MRX). The study aimed at identifying the causative mutation. The obligate female carrier showed completely skewed inactivation of the X chromosome, based on the methylation status of the AR gene in peripheral blood in leukocytes, a common feature in carriers of X-linked mutations that cause mental retardation. We genotyped 28 microsatellite loci mapped throughout the X chromosome and delimited a 32 Mb segment, between markers DXS986 and DXS8067, that was shared by the affected males and obligate carrier, but was not present in a normal man or in two women who did not show skewed X-inactivation. We searched for the causative mutation by sequencing genes mapped to this candidate interval that had been associated with MR and/or were expressed in brain and leukocytes. In the affected men and obligate carrier, we found a c.845C→T mutation in the ACSL4 gene, resulting in the amino acid tyrosine substituting for a histidine (p.H323Y in brain isoform), which is conserved in the acyl-CoA synthetase family in humans and others organisms. This mutation was not found in a control sample of 160 men. Previously, point mutations in the ACSL4 gene had been identified as the cause of MRX in three families. ACSL4 encodes the acyl-CoA synthetase long-chain family member 4, which catalyzes the formation of acyl-CoA esters from long-chain fatty acids. It is expressed in several tissues, and in brain it is essential for the normal formation of dendritic spines. The novel mutation here described confirmed the causal association of ACSL4 mutations with non-syndromic mental retardation. The completely skewed Xinactivation, also observed in the previously described carriers, supported a functional role for this gene in peripheral blood leukocytes. The intellectual impairment present in the carrier in the family here reported is in accordance with previous findings pointing to the effect on intellectual abilities of ACSL4 mutations in heterozygosis. The absence of correlation between the pattern of X-inactivation in leukocytes and mental status was confirmed.
APA, Harvard, Vancouver, ISO, and other styles
2

Quigley, Caitlin M. "The Drosophila Homolog of the Intellectual Disability Gene ACSL4 Acts in Glia to Regulate Morphology and Neuronal Activity: A Dissertation." eScholarship@UMMS, 2007. http://escholarship.umassmed.edu/gsbs_diss/839.

Full text
Abstract:
Recent developments in neurobiology make it clear that glia play fundamental and active roles, in the adult and in development. Many hereditary cognitive disorders have been linked to developmental defects, and in at least two cases, Rett Syndrome and Fragile X Mental Retardation, glia are important in pathogenesis. However, most studies of developmental disorders, in particular intellectual disability, focus on neuronal defects. An example is intellectual disability caused by mutations in ACSL4, a metabolic enzyme that conjugates long-chain fatty acids to Coenzyme A (CoA). Depleting ACSL4 in neurons is associated with defects in dendritic spines, a finding replicated in patient tissue, but the etiology of this disorder remains unclear. In a genetic screen to discover genes necessary for visual function, I identified the Drosophila homolog of ACSL4, Acsl, as a gene important for the magnitude of neuronal transmission, and found that it is required in glia. I determined that Acsl is required in a specific subtype of glia in the Drosophila optic lobe, and that depletion of Acsl from this population causes morphological defects. I demonstrated that Acsl is required in development, and that the phenotype can be rescued by human ACSL4. Finally, I discovered that ACSL4 is expressed in astrocytes in the mouse hippocampus. This study is highly significant for understanding glial biology and neurodevelopment. It provides information on the role of glia in development, substantiates a novel role for Acsl in glia, and advances our understanding of the potential role that glia play in the pathogenesis of intellectual disability.
APA, Harvard, Vancouver, ISO, and other styles
3

Quigley, Caitlin M. "The Drosophila Homolog of the Intellectual Disability Gene ACSL4 Acts in Glia to Regulate Morphology and Neuronal Activity: A Dissertation." eScholarship@UMMS, 2016. https://escholarship.umassmed.edu/gsbs_diss/839.

Full text
Abstract:
Recent developments in neurobiology make it clear that glia play fundamental and active roles, in the adult and in development. Many hereditary cognitive disorders have been linked to developmental defects, and in at least two cases, Rett Syndrome and Fragile X Mental Retardation, glia are important in pathogenesis. However, most studies of developmental disorders, in particular intellectual disability, focus on neuronal defects. An example is intellectual disability caused by mutations in ACSL4, a metabolic enzyme that conjugates long-chain fatty acids to Coenzyme A (CoA). Depleting ACSL4 in neurons is associated with defects in dendritic spines, a finding replicated in patient tissue, but the etiology of this disorder remains unclear. In a genetic screen to discover genes necessary for visual function, I identified the Drosophila homolog of ACSL4, Acsl, as a gene important for the magnitude of neuronal transmission, and found that it is required in glia. I determined that Acsl is required in a specific subtype of glia in the Drosophila optic lobe, and that depletion of Acsl from this population causes morphological defects. I demonstrated that Acsl is required in development, and that the phenotype can be rescued by human ACSL4. Finally, I discovered that ACSL4 is expressed in astrocytes in the mouse hippocampus. This study is highly significant for understanding glial biology and neurodevelopment. It provides information on the role of glia in development, substantiates a novel role for Acsl in glia, and advances our understanding of the potential role that glia play in the pathogenesis of intellectual disability.
APA, Harvard, Vancouver, ISO, and other styles
4

Idnani, Sunil Charan 1964. "An ACSL interface for DYMOLA." Thesis, The University of Arizona, 1991. http://hdl.handle.net/10150/291863.

Full text
Abstract:
This MS thesis proposes the use of DYMOLA, an object-oriented language for modeling hierarchically structured systems, to generate ACSL simulation programs for continuous system analysis. An ACSL model described in terms of time dependent non-linear differential equations or transfer functions can be generated from a hierarchical model description of the system using DYMOLA. The model description in DYMOLA can be an equation description or a non-linear hierarchical bond graph abstraction to describe the system under investigation. The interface provides an automated method to generate ACSL simulation programs, hence eliminating the need for manual coding. The provision to specify an experiment description for run-time analysis and additional model statements is implemented. The implementation of the compiler's code generator includes parsing, error checking and system dependent file handling routines. Implementation techniques, model and control file specifications, and validation with examples in several application areas are described.
APA, Harvard, Vancouver, ISO, and other styles
5

Sander, Simone [Verfasser], and Britta [Akademischer Betreuer] Brügger. "Relevance of ACSL3-mediated ACS activity and ACSL3 localization in anabolic and catabolic lipid droplet metabolism / Simone Sander ; Betreuer: Britta Brügger." Heidelberg : Universitätsbibliothek Heidelberg, 2019. http://d-nb.info/1177695626/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Costa, Bruna Vieira de Lima. "Consumo de carnes e derivados e fatores associados ao estado nutricional de idosos em instiruição de longa permanência de Belo Horizonte - MG." Universidade Federal de Minas Gerais, 2009. http://hdl.handle.net/1843/ACSL-7YAQLW.

Full text
Abstract:
Sectional study, to identify the consumption of meat and meat products of elderly residents in geriatric institution of Belo Horizonte. Random sample (n = 52). Nutritional assessment was made by anthropometry, dietary and MAN. The process of acquisition, receipt, storage, handling of meat and meat products was observed. Was also carried out a cohort study to determine the anthropometric development. The results showed the need to reassess the process of buying, receiving and preparation of foodstuffs since there was a delivery of meat inappropriate amount and form of receipt, which contributed to a correction factor and per capita inadequate. The sample studied, 82.7% were women. The prevalence of overweight (BMI) was 46.1% and 23.1% underweight. According to MAN the prevalence of risk for malnutrition was 67.3%. According to the dietary analysis, the consumption of fat, polyunsaturated fatty acid and potassium had been insufficient in 100% of the elderly. The intake of B12 and zinc was inadequate in 44.2% and 82.7%, respectively, suggesting a low consumption of meat products. There was a prevalence of overweight and older people at high risk of diseases associated with obesity. However, from the MAN, there was a high rate of elderly people at risk for malnutrition
Estudo seccional, objetivo de identificar o consumo de carnes e derivados de idosos residentes em Instituição Geriátrica de Belo Horizonte. Amostra aleatória simples (n=52). A avaliação nutricional foi composta pela antropometria, MAN e dietética. O processo de aquisição, recepção, armazenamento, manipulação da carne e derivados foi observado. Realizou-se também estudo de coorte para verificar a evolução antropométrica. Os resultados mostraram a necessidade de reavaliar o processo de compra, recebimento e preparo dos gêneros alimentícios já que se observou uma entrega inapropriada das carnes em quantidade e forma de recebimento, o que contribuía para um fator de correção e per capita inadequados. Da amostra estudada, 82,7% eram mulheres. A prevalência de sobrepeso (IMC) foi de 46,1% e de baixo peso 23,1%. Segundo a MAN a prevalência de risco para desnutrição foi 67,3%. Segundo a análise dietética, o consumo de lipídeo, ácido graxo poliinsaturado e potássio apresentaram-se insuficiente em 100% dos idosos. A ingestão de B12 e zinco foi insuficiente em 44,2% e 82,7%, respectivamente, o que sugere um baixo consumo de produtos cárneos. Observou-se uma prevalência de idosos com sobrepeso e com risco elevado de doenças associadas à obesidade. Em contrapartida, a partir da MAN, observou-se um alto índice de idosos com risco para desnutrição
APA, Harvard, Vancouver, ISO, and other styles
7

Hose, Josephine [Verfasser], Nikolaus [Akademischer Betreuer] Gaßler, and Christian [Akademischer Betreuer] Liedtke. "Modulation der intestinalen Apoptose durch ACSL5-abhängige Palmitoylierung / Josephine Hose ; Nikolaus Gaßler, Christian Liedtke." Aachen : Universitätsbibliothek der RWTH Aachen, 2019. http://d-nb.info/1216201781/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Fochler, Franziska. "Das Schwefelwasserstoff-freisetzende Aspirinderivat ACS14 zeigt starke antithrombotische Effekte in vitro und in vivo." Diss., Ludwig-Maximilians-Universität München, 2015. http://nbn-resolving.de/urn:nbn:de:bvb:19-182925.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Playl, Lauren A. "Sry Transcript Expression in Five Adult Male Rat Tissues and Correlation with Acsl3 Transcript Expression." University of Akron / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=akron1290632541.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Teng, Allen C. T. "Transcriptional Control of Metabolism and the Response to Ischemia in Muscle." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20479.

Full text
Abstract:
Skeletal muscle is one of the largest tissues in humans and provides many pivotal functions to support life. Abnormality in skeletal muscle functions can lead to disease. For example, insulin resistance in skeletal muscle leads to type II diabetes. The underlying mechanisms that control energy balance in skeletal muscle remain largely elusive, especially at the genetic level. Here in the second chapter, I showed that MyoD mediated the transcriptional regulation of ACSL5, a mitochondrial protein, in C2C12 myoblasts via two E-box elements. A SNP rs2419621 (T) created a de novo E-box that together with the two pre-existing proximal E-boxes strongly enhances ACSL5 expression in both CV1 and C2C12 cells. In the third chapter, I identified a novel VGLL4-interacting protein IRF2BP2 and verified the interaction with co-immunoprecipitation and mammalian two-hybrid assays. Functionally, overexpression of IRF2BP2 and transcription factor TEAD1 activates mouse VEGF-A promoter in CV1 cells and enhances the biosynthesis of VEGF-A in C2C12 myoblasts. In vivo studies showed that ischemia induced the expression of IRF2BP2 by more than three fold, suggesting that IRF2BP2 could play a pivotal role during tissue ischemia. IRF2BP2 is a nuclear protein in both mouse cardiac myocytes and C2C12 myoblasts as demonstrated by immunohistochemistry and immunocytochemistry, respectively. Therefore, I sought to delineate the mechanism for the nuclear shuttling of IRF2BP2 in the fourth chapter. With various DNA alternations, I mapped the NLS to an evolutionarily conserved sequence 354ARKRKPSP361 in IRF2BP2. Deletion of the positively charged amino acids resulted in the abolishment of the NLS signal. Next, I showed that phosphorylation of serine 360 (S360) mediates the nuclear import of the protein. Whereas an alanine substitution (S360A) at the site resulted in perinuclear accumulation of the protein, an aspartic acid substitution (S360D) forced the nuclear accumulation. Nevertheless, the forced accumulation of the S360D mutant did not enhance the activation of VEGF-A promoter in CV1 cells as did the wild-type protein. My studies revealed two novel mechanisms by which skeletal muscle could harvest energy, thus providing new insight into the energy metabolism in skeletal muscle
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "ACSL4"

1

Breitenecker, Felix, Horst Ecker, and Ingrid Bausch-Gall. Simulation mit ACSL. Wiesbaden: Vieweg+Teubner Verlag, 1993. http://dx.doi.org/10.1007/978-3-322-96175-4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Holmes, K. P. ACSL simulation for aircraft control design THESIS. Manchester: UMIST, 1988.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Mitchell and Gauthier Assoc. Advanced Continuous Simulation Language (Acsl Reference Manual). Mitchell & Gauthier Assoc, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Advanced Continuous Simulation Language (ACSL): Reference manual. Concord, Mass: Mitchell and Gauthier, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Associates, Mitchell and Gauthier. Advanced Continuous Simulation Language (Acsl Reference Manual). Mitchell & Gauthier Associates, Incorporated, 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Advanced Continuous Simulation Language (ACSL): Reference manual. 4th ed. Concord, Mass: Mitchell and Gauthier, 1986.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Associates, Mitchell and Gauthier. Acsl for Windows: Installation and How to Use. Mitchell & Gauthier Assoc, 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Breitenecker, Felix, Horst Ecker, and Ingrid Bausch-Gall. Simulation mit ACSL: Eine Einführung in die Modellbildung, numerischen Methoden und Simulation. Vieweg+Teubner Verlag, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "ACSL4"

1

Maloberti, Paula M., Ana F. Castillo, Ulises Orlando, and Ernesto J. Podesta. "ACSL4." In Encyclopedia of Signaling Molecules, 109–16. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101897.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Maloberti, Paula M., Ana F. Castillo, Ulises Orlando, and Ernesto J. Podesta. "ACSL4." In Encyclopedia of Signaling Molecules, 1–8. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101897-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Moerke, Caroline, Franziska Theilig, Ulrich Kunzendorf, and Stefan Krautwald. "ACSL4 as the First Reliable Biomarker of Ferroptosis Under Pathophysiological Conditions." In Ferroptosis in Health and Disease, 111–23. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-26780-3_7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Breitenecker, Felix, Horst Ecker, and Ingrid Bausch-Gall. "Einleitung." In Simulation mit ACSL, 1–5. Wiesbaden: Vieweg+Teubner Verlag, 1993. http://dx.doi.org/10.1007/978-3-322-96175-4_1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Breitenecker, Felix, Horst Ecker, and Ingrid Bausch-Gall. "Optimierung in ACSL." In Simulation mit ACSL, 381–96. Wiesbaden: Vieweg+Teubner Verlag, 1993. http://dx.doi.org/10.1007/978-3-322-96175-4_10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Breitenecker, Felix, Horst Ecker, and Ingrid Bausch-Gall. "Einführende Beispiele mit ACSL." In Simulation mit ACSL, 7–88. Wiesbaden: Vieweg+Teubner Verlag, 1993. http://dx.doi.org/10.1007/978-3-322-96175-4_2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Breitenecker, Felix, Horst Ecker, and Ingrid Bausch-Gall. "Sprachdefinition." In Simulation mit ACSL, 89–134. Wiesbaden: Vieweg+Teubner Verlag, 1993. http://dx.doi.org/10.1007/978-3-322-96175-4_3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Breitenecker, Felix, Horst Ecker, and Ingrid Bausch-Gall. "Numerische Verfahren." In Simulation mit ACSL, 135–218. Wiesbaden: Vieweg+Teubner Verlag, 1993. http://dx.doi.org/10.1007/978-3-322-96175-4_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Breitenecker, Felix, Horst Ecker, and Ingrid Bausch-Gall. "Diskrete Modellteile — Ereignisse." In Simulation mit ACSL, 219–48. Wiesbaden: Vieweg+Teubner Verlag, 1993. http://dx.doi.org/10.1007/978-3-322-96175-4_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Breitenecker, Felix, Horst Ecker, and Ingrid Bausch-Gall. "Modellbildung mit Macros." In Simulation mit ACSL, 249–82. Wiesbaden: Vieweg+Teubner Verlag, 1993. http://dx.doi.org/10.1007/978-3-322-96175-4_6.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "ACSL4"

1

Piche, J., T. Otto, A. Mohs, MM Woitok, and C. Trautwein. "ACSL4 and its tumor protective role in chronic liver disease." In 37. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0040-1722045.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Zhou, Xiang, Weiming Wang, Baofu Zhang, Zixia Lin, Yi Wang, and Gang Chen. "Abstract 6330: DPP4 modulates ACSL4 to promote lipid peroxidation and regulate ferroptosis in pancreatic cancer." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-6330.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Mbarik, Maroua, Anissa Belkaid, and Marc E. Surette. "Abstract 4419: HER2 expression and 17β-estradiol induce ACSL4 expression in estrogen receptor positive mammary carcinoma cells." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4419.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Son, Ji Woong, Seul-Gi Kim, In Beom Jeong, and Sun Jung Kwon. "Abstract 4417: MicroRNA 181a-5p reprogrammed glucose and lipid metabolism in lung cancer though regulating SIRT1 and ACSL4." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4417.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Belkaid, Anissa, Rodney J. Ouellette, and Marc E. Surette. "Abstract A09: ACSL4 is a target of the 17beta-estradiol/estrogen-receptor alpha pathway in mammary carcinoma cell lines." In Abstracts: Fourth AACR International Conference on Frontiers in Basic Cancer Research; October 23-26, 2015; Philadelphia, PA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.fbcr15-a09.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Al-Qeraiwi, Maha, Manar Al-Rashid, Nasser Rizk, Abdelrahman El Gamal, and Amena Fadl. "Hepatic Gene Expression Profile of Lipid Metabolism of Obese Mice after treatment with Anti-obesity Drug." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0214.

Full text
Abstract:
Obesity is a global disorder with multifactorial causes. The liver plays a vital role in fat metabolism. Disorder of hepatic fat metabolism is associated with obesity and causes fatty liver. High fat diet intake (HFD) to mice causes the development of dietinduced obesity (DIO). The study aimed to detect the effects of anti-obesity drugs (sulforaphane; SFN and leptin) on hepatic gene expression of fat metabolism in mice that were fed HFD during an early time of DIO. Twenty wild types (WT) CD1 male mice aged ten weeks were fed a high fat diet. The mice were treated with vehicle; Veh (control group), and SFN, then each group is treated with leptin or saline. Four groups of treatment were: control group (vehicle + saline), Group 2 (vehicle + leptin), group 3 (SFN + saline), and group 4 (SFN + leptin). Body weight and food intake were monitored during the treatment period. Following the treatments of leptin 24 hour, fasting blood samples and liver tissue was collected, and Total RNA was extracted then used to assess the gene expression of 84 genes involved in hepatic fat metabolism using RT-PCR profiler array technique. Leptin treatment upregulated fatty acid betaoxidation (Acsbg2, Acsm4) and fatty acyl-CoA biosynthesis (Acot6, Acsl6), and downregulated is fatty acid transport (Slc27a2). SFN upregulated acylCoA hydrolase (Acot3) and long chain fatty acid activation for lipids synthesis and beta oxidation (Acsl1). Leptin + SFN upregulated fatty acid beta oxidation (Acad11, Acam) and acyl-CoA hydrolase (Acot3, Acot7), and downregulated fatty acid elongation (Acot2). As a result, treatment of both SFN and leptin has more profound effects on ameliorating pathways involved in hepatic lipogenesis and TG accumulation and lipid profile of TG and TC than other types of intervention. We conclude that early intervention of obesity pa could ameliorate the metabolic changes of fat metabolism in liver as observed in WT mice on HFD in response to anti-obesity treatment.
APA, Harvard, Vancouver, ISO, and other styles
7

Signoles, Julien. "The e-ACSL perspective on runtime assertion checking." In ISSTA '21: 30th ACM SIGSOFT International Symposium on Software Testing and Analysis. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3464974.3468451.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Watts, J. W., T. E. Dwan, and R. W. Garman. "A Model and State-Space Controllers for an Intercooled, Regenerated (ICR) Gas Turbine Engine." In ASME 1992 International Gas Turbine and Aeroengine Congress and Exposition. American Society of Mechanical Engineers, 1992. http://dx.doi.org/10.1115/92-gt-043.

Full text
Abstract:
A two-and-one-half spool gas turbine engine was modeled using the Advanced Computer Simulation Language (ACSL), a high level simulation environment based on FORTRAN. A possible future high efficiency engine for powering naval ships is an intercooled, regenerated (ICR) gas turbine engine and these features were incorporated into the model. Utilizing sophisticated instructions available in ACSL linear state-space models for this engine were obtained. A high level engineering computational language, MATLAB, was employed to exercise these models to obtain optimal feedback controllers characterized by the following methods: (1) state feedback; (2) linear quadratic regulator (LQR) theory; and (3) polygonal search. The methods were compared by examining the transient curves for a fixed off-load, and on-load profile.
APA, Harvard, Vancouver, ISO, and other styles
9

Gauthier, Joseph, and Christine Kovach. "A missile system simulation benchmark using the ACSL graphic modeller." In AIAA Modeling and Simulation Technologies Conference and Exhibit. Reston, Virigina: American Institute of Aeronautics and Astronautics, 2001. http://dx.doi.org/10.2514/6.2001-4122.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Watts, J. W., T. E. Dwan, and C. G. Brockus. "Optimal State Space Control of a Gas Turbine Engine." In ASME 1991 International Gas Turbine and Aeroengine Congress and Exposition. American Society of Mechanical Engineers, 1991. http://dx.doi.org/10.1115/91-gt-219.

Full text
Abstract:
An analog fuel control for a gas turbine engine was compared with several state space derived fuel controls. A single spool, simple cycle gas turbine engine was modeled using ACSL (high level simulation language based on FORTRAN). The model included an analog fuel control representative of existing commercial fuel controls. The ACSL model was stripped of non-essential states to produce an 8 state linear state space model of the engine. The A, B, and C matrices, derived from rated operating conditions, were used to obtain feedback control gains by the following methods: (1) state feedback; (2) LQR theory; (3) Bellman method; and (4) polygonal search. An off-load transient followed by an on-load transient was run for each of these fuel controls. The transient curves obtained were used to compare the state space fuel controls with the analog fuel control. The state space fuel controls did better than the analog control.
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "ACSL4"

1

Collins, Thomas R. ACSL as a Parallel Simulation Language. Fort Belvoir, VA: Defense Technical Information Center, January 1990. http://dx.doi.org/10.21236/ada395503.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Damiano, B. Summary of ACSL Simulations of the MSRE Auxiliary Charcoal Bed Vacuum System. Office of Scientific and Technical Information (OSTI), October 2000. http://dx.doi.org/10.2172/885543.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'ACSL4' for particular source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography