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Статті в журналах з теми "ACOT8"

Автор: Grafiati

Опубліковано: 11 березня 2023

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1

St Clair, Laura A., Stephanie A. Mills, Elena Lian, Paul S. Soma, Aritra Nag, Caroline Montgomery, Gabriela Ramirez, Nunya Chotiwan, Rebekah C. Gullberg, and Rushika Perera. "Acyl-Coa Thioesterases: A Rheostat That Controls Activated Fatty Acids Modulates Dengue Virus Serotype 2 Replication." Viruses 14, no. 2 (January 25, 2022): 240. http://dx.doi.org/10.3390/v14020240.

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During infection with dengue viruses (DENVs), the lipid landscape within host cells is significantly altered to assemble membrane platforms that support viral replication and particle assembly. Fatty acyl-CoAs are key intermediates in the biosynthesis of complex lipids that form these membranes. They also function as key signaling lipids in the cell. Here, we carried out loss of function studies on acyl-CoA thioesterases (ACOTs), a family of enzymes that hydrolyze fatty acyl-CoAs to free fatty acids and coenzyme A, to understand their influence on the lifecycle of DENVs. The loss of function of the type I ACOTs 1 (cytoplasmic) and 2 (mitochondrial) together significantly increased DENV serotype 2 (DENV2) viral replication and infectious particle release. However, isolated knockdown of mitochondrial ACOT2 significantly decreased DENV2 protein translation, genome replication, and infectious virus release. Furthermore, loss of ACOT7 function, a mitochondrial type II ACOT, similarly suppressed DENV2. As ACOT1 and ACOT2 are splice variants, these data suggest that functional differences and substrate specificities due to the location (cytosol and mitochondria, respectively) of these proteins may account for the differences in DENV2 infection phenotype. Additionally, loss of mitochondrial ACOT2 and ACOT7 expression also altered the expression of several ACOTs located in multiple organelle compartments within the cell, highlighting a complex relationship between ACOTs in the DENV2 virus lifecycle.

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2

Yin, Xuewei, Chunyi Lyu, Zonghong Li, Qian Wang, Yi Ding, Yan Wang, Yan Qiu, Siyuan Cui, Dadong Guo, and Ruirong Xu. "High Expression of ACOT2 Predicts Worse Overall Survival and Abnormal Lipid Metabolism: A Potential Target for Acute Myeloid Leukemia." Journal of Healthcare Engineering 2022 (September 23, 2022): 1–15. http://dx.doi.org/10.1155/2022/2669114.

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Acyl-CoA thioesterase (ACOT) plays a considerable role in lipid metabolism, which is closely related to the occurrence and development of cancer, nevertheless, its role has not been fully elucidated in acute myeloid leukemia (AML). To explore the role of ACOT2 in AML and to provide a potential therapeutic target for AML, the expression pattern of ACOT was investigated based on the TNMplot, Gene Expression Profiling Interactive Analysis (GEPIA), and Cancer Cell Line Encyclopedia (CCLE) database, and diagnostic value, prognostic value, and clinical phenotype of ACOT were explored based on data from The Cancer Genome Atlas (TCGA). Functional annotation and enrichment analysis of the common targets between ACOT2 coexpressed and AML-related genes were further performed by Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA) analyses. The protein-protein interaction (PPI) network of ACOT2 coexpressed genes and functional ACOT2-related metabolites association network were constructed based on GeneMANIA and Human Metabolome Database. Among ACOTs, ACOT2 was highly expressed in AML compared to normal control subjects according to TNMplot, GEPIA, and CCLE database, which was significantly associated with poor overall survival (OS) in AML ( P = 0.003 ). Moreover, ACOT2 exhibited excellent diagnostic efficiency for AML (AUC: 1.000) and related to French-American-British (FAB) classification and cytogenetics. GO, KEGG, and GSEA analyses of 71 common targets between ACOT2 coexpressed and AML-related genes revealed that ACOT2 is closely related to ACOT1, ACOT4, enoyl-acyl carrier protein reductase, mitochondrial (MECR), puromycin-sensitive aminopeptidase (NPEPPS), SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily B member 1 (SMARCB1), and long-chain fatty acid-CoA ligase 1 (ACSL1) in PPI network, and plays a significant role in lipid metabolism, that is, involved in fatty acid elongation and biosynthesis of unsaturated fatty acids. Collectively, the increase of ACOT2 may be an important characteristic of worse OS and abnormal lipid metabolism, suggesting that ACOT2 may become a potential therapeutic target for AML.

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3

Gondim, Marcos Vinicius, Linda Wiltzer-Bach, Brigitte Maurer, Carina Banning, Enrique Arganaraz, and Michael Schindler. "AP-2 Is the Crucial Clathrin Adaptor Protein for CD4 Downmodulation by HIV-1 Nef in Infected Primary CD4+T Cells." Journal of Virology 89, no. 24 (September 30, 2015): 12518–24. http://dx.doi.org/10.1128/jvi.01838-15.

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HIV-1 Nef-mediated CD4 downmodulation involves various host factors. We investigated the importance of AP-1, AP-2, AP-3, V1H-ATPase, β-COP, and ACOT8 for CD4 downmodulation in HIV-1-infected short hairpin RNA (shRNA)-expressing CD4+T cells and characterized direct interaction with Nef by Förster resonance energy transfer (FRET). Binding of lentiviral Nefs to CD4 and AP-2 was conserved, and only AP-2 knockdown impaired Nef-mediated CD4 downmodulation from primary T cells. Altogether, among the factors tested, AP-2 is the most important player for Nef-mediated CD4 downmodulation.

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4

Betsha, S., D. Salilew-Wondim, V. Havlicek, U. Besenfelder, F. Rings, M. Hoelker, K. Schellander, and D. Tesfaye. "28 GLOBAL GENE EXPRESSION ANALYSIS OF ELONGATED EMBRYOS PRODUCED BY SOMATIC CELL NUCLEAR TRANSFER AND IN VITRO FERTILIZATION." Reproduction, Fertility and Development 24, no. 1 (2012): 126. http://dx.doi.org/10.1071/rdv24n1ab28.

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Despite their ability to reach to the blastocyst stage, nuclear transfer embryos showed various abnormalities with respect to pregnancy outcome. We hypothesised that once cloned embryos were transferred to a suitable recipient the conceptus and endometrial interaction during peri-implantation stage was a remarkable step that determines the pregnancy outcome. In order to elucidate the molecular mechanisms underlining this phenomenon, the present experiment was conducted to compare the transcriptome profile of Day-16 elongated embryos derived from somatic cell nuclear transfer (SCNT) and fertilized controls, namely, artificially inseminated (AI) and in vitro fertilized (IVF) using bovine genome Affymetrix array. Following total RNA isolation from 3 replicates of each group, biotin-labeled cRNA was hybridized on 9 bovine chips. Data were normalized by using guanine cytosine robust multi-array analysis (GCRMA) and analysis was performed using the LIMMA package in R software. The present findings demonstrate that the gene expression profile of SCNT elongated embryos closely resembled those of the in vitro fertilized group. Only 10 genes were found to be differentially regulated between SCNT and IVF embryos (P ≤ 0.05, fold change ≥2 and false discovery rate 20%). On the other hand 303 and 336 genes were differentially expressed in IVF vs AI and NT vs AI embryos comparisons, respectively. Majority of the transcripts were found to be down-regulated on IVF embryos, whereas only 21 transcripts were up-regulated. Moreover, 158 and 178 genes were up- and down-regulated, respectively, in NT embryos as compared with AI. The NT embryos were found to be enriched with transcripts responsible for lipid metabolism (ACOX1, ACOT4 and ACOT8) and molecular transport (B4GALT1, ERBB3, MIF and PRKAG2) compared with AI. Moreover, genes involved in cell movement (CD97, CTSL1, F2R, ITGA and ITGAV) were highly abundant in IVF embryos compared with AI. Ingenuity pathway analysis of differentially regulated genes showed that metabolic and tight junction pathways and the genes involved in these pathways were activated in NT and IVP elongated embryos, respectively, as compared with AI. In conclusion, elongated embryos from NT and IVP pregnancies show differences in expression of genes involved in various biological processes compared with their AI counterparts.

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5

Zhang, Xin, Ya Zhang, Yang Han, Zheng Tian, Xinting Hu, and Xin Wang. "Integrated Analyses of Competing Endogenous RNA Network Reveal Potential Therapeutic Targets in Chronic Lymphocytic Leukemia." Blood 138, Supplement 1 (November 5, 2021): 2624. http://dx.doi.org/10.1182/blood-2021-150218.

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Abstract Introduction Chronic lymphocytic leukemia (CLL) is a highly heterogeneous disease characterized by malignant clonal expansion of mature B lymphocytes. Competitive endogenous RNAs(ceRNAs) such as long noncoding RNAs (lncRNAs) and circular RNAs (circ RNAs) have miRNA response elements (MREs) and can bind to miRNAs to influence mRNA expression. An increasing number of studies have shown that the ceRNA network played an important role in the initiation and progression of tumors. However, the roles and functions of the ceRNA network in chronic lymphocytic leukemia (CLL) are still unclear. This study aims to explore the molecular mechanism of CLL and provide potential prognostic markers and therapeutic targets through the integrated analysis of the ceRNA network in CLL. Methods The expression profile of RNAs of CLL patients, CLL cell lines (MEC1 and EHEB) and healthy group were obtained by the illumina sequencing. R software was used for functional enrichment analysis. The data in the genome microarray map GSE22762 was used for survival analysis. The circRNA-miRNA-mRNA ceRNA networks were visualized by Cytoscape 3.7.2. The expression of the circRNA hsa_circ_0007675/hsa-miR-185-3p/TCF7L1 axis were verified by Quantitative real-time PCR and the correlation between hsa_circ_0007675 and TCF7L1 was analyzed. Results In total, we identified 57 differentially expressed mRNAs (DEmRNAs), 1391 DElncRNAs, 335 DEmiRNAs and 2413 DEcircRNAs by comparing CLL patients with healthy donors. Meanwhile, 482 mRNAs, 6085 lncRNAs, 302 miRNAs and 1847 circRNAs were explored differently expressed between CLL cell lines and healthy donors. GO analysis results showed that the functions of differentially expressed genes (DEGs) between CLL patients and control are mainly enriched in sequence−specific DNA binding, chromatin and gene expression (Figure 1A) while between CLL cell lines and control they were mainly enriched in oxidoreductase activity, ribosomal subunit and lipid metabolism (Figure 1C). KEGG pathway analysis revealed that the DEGs between CLL patients and control were mainly enriched in Notch signaling pathway, JAK-STAT signaling pathway and cGMP-PKG signaling pathway (Figure 1B). Meanwhile between CLL cell lines and control, DEGs were mainly enriched in mTOR signaling pathway, cell cycle and p53 signaling pathway (Figure 1D). The survival analyses showed that 15 DEGs (INIP, IL3RA, CHD1, NLRP12, IL20RB, HNRNPC, B3GALT4, SIT1, ACOT8, PCLAF, C19orf18, SELENOS, OR7A17, PCDH7, PHGDH) were significantly differentially expressed in the survival analyses. The overall survival of the high expression group of INIP, IL3RA, CHD1, NLRP12, IL20RB and HNRNPC were higher than that of the low expression group (Figure 2A-F) while the overall survival of the low expression group of B3GALT4, SIT1, ACOT8, PCLAF, C19orf18, SELENOS, OR7A17, PCDH7 and PHGDH were higher than that of the high expression group (Figure 2G-O). The ceRNA network were built by Cytoscape3.7.2. In total, 11 mRNA nodes, 19 miRNA nodes, 251 circRNA nodes were identified as differentially expressed profiles between CLL patients and control (Figure 3A). We verified the circRNA hsa_circ_0007675/hsa-miR-185-3p/TCF7L1 axis. Compared with normal people, the expression of TCF7L1 and hsa_circ_0007675 in patient specimens were significantly increased (p<0.05; Figure 3B, D) whereas the expression of hsa-miR-185-3p was downregulated (p<0.05; Figure 3C). TCF7L1 and hsa_circ_0007675 were positively correlated (p＜0.001, R=0.7834; Figure 3E). The correlation analysis of TCF7L1 and other genes were shown in Figure 3F. The interaction mechanism between them is that hsa_circ_0007675 can sponge hsa-miR-185-3p, thereby inhibiting the inhibitory effect of hsa-miR-185-3p on TCF7L1 and finally upregulate the expression of TCF7L1(Figure 3G). Conclusions In this study, we identified the expression profile of RNAs in CLL patients and CLL cell lines. Functional enrichment analysis and survival analysis revealed the potential functions of DEGs. The ceRNA network we established can help to further understand the pathogenesis of CLL and provide potential prognostic biomarkers and novel therapeutic targets. Keywords: Chronic lymphocytic leukemia; Competing endogenous RNA; Non-coding RNAs; Prognostic biomarkers; Therapeutic targets Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.

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6

Bowman, Caitlyn E., Ebru S. Selen Alpergin, Jessica M. Ellis, and Michael J. Wolfgang. "Loss of ACOT7 potentiates seizures and metabolic dysfunction." American Journal of Physiology-Endocrinology and Metabolism 317, no. 5 (November 1, 2019): E941—E951. http://dx.doi.org/10.1152/ajpendo.00537.2018.

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Neurons uniquely antagonize fatty acid utilization by hydrolyzing the activated form of fatty acids, long chain acyl-CoAs, via the enzyme acyl-CoA thioesterase 7, Acot7. The loss of Acot7 results in increased fatty acid utilization in neurons and exaggerated stimulus-evoked behavior such as an increased startle response. To understand the contribution of Acot7 to seizure susceptibility, we generated Acot7 knockout (KO) mice and assayed their response to kainate-induced seizures. Acot7 KO mice exhibited potentiated behavioral and molecular indices of seizure severity following kainic acid administration, suggesting that fatty acid metabolism in neurons can be a critical regulator of neuronal activity. These data are consistent with the presentation of seizures in a human with genomic deletion of ACOT7 demonstrating the conservation of function across species. To further understand the metabolic complications arising from a deletion in Acot7, we subjected Acot7 KO mice to a high-fat diet. While the loss of Acot7 did not result in metabolic complications following a normal chow diet, a high-fat diet induced greater body weight gain, adiposity, and glucose intolerance in Acot7 KO mice. These data demonstrate that Acot7, a fatty acid metabolic enzyme highly enriched in neurons, regulates both brain-specific metabolic processes related to seizure susceptibility and the whole body response to dietary lipid.

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7

Zheng, Chao, Guochao Zhang, Kai Xie, Yifei Diao, Chao Luo, Yanqing Wang, Yi Shen, and Qi Xue. "Pan-Cancer Analysis and Experimental Validation Identify ACOT7 as a Novel Oncogene and Potential Therapeutic Target in Lung Adenocarcinoma." Cancers 14, no. 18 (September 18, 2022): 4522. http://dx.doi.org/10.3390/cancers14184522.

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Background: Acyl-CoA thioesterase 7 (ACOT7) is of great significance in regulating cell cycle, cell proliferation, and glucose metabolism. The function of ACOT7 in pan-cancer and its capacity as a prognostic indicator in lung adenocarcinoma (LUAD) remains unknown. We intended to perform a comprehensive pan-cancer analysis of ACOT7 and to validate its value in LUAD. Methods: The expression levels, prognostic significance, molecular function, signaling pathways, and immune infiltration pattern of ACOT7 in 33 cancers were explored via systematic bioinformatics analysis. Multivariate Cox regression was applied to construct nomograms to predict patients’ prognoses. Moreover, we conducted in vitro experiments including CCK8, scratch, Transwell, and Matrigel assays to further explore the function of ACOT7 in LUAD. Results: Patients with high ACOT7 expression have notably poorer long-term survival in many cancer types, including LUAD. Further enrichment analyses reveal that ACOT7 is involved in immune cells’ infiltration and is substantially related to the cancer–immune microenvironment. ACOT7 could influence drug sensitivities, including afatinib, gefitinib, ibrutinib, lapatinib, osimertinib, sapitinib, taselisib, and PLX-4720 (all p < 0.01). A nomogram demonstrated a fair predictive value of ACOT7 in LUAD (C-index: 0.613, 95% CI: 0.568–0.658). The proliferation and migration of PC9 cells were significantly repressed when ACOT7 expression was downregulated. Conclusion: As an oncogene, ACOT7 is critical in the tumor microenvironment of pan-cancer and might be a novel therapeutic target for LUAD.

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8

Wei, Can, Tao Song, Hui Yuan, Xiaoxue Li, Xinying Zhang, Xiao Liang, and Ying Fan. "Transcriptomics Coupled to Proteomics Reveals Novel Targets for the Protective Role of Spermine in Diabetic Cardiomyopathy." Oxidative Medicine and Cellular Longevity 2022 (April 9, 2022): 1–14. http://dx.doi.org/10.1155/2022/5909378.

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Background. Diabetic cardiomyopathy (DbCM) is the main complication and the cause of high mortality of diabetes. Exploring the transcriptomics and proteomics of DbCM is of great significance for understanding the biology of the disease and for guiding new therapeutic targets for the potential therapeutic effect of spermine (SPM). Methods and Results. By using a mouse DbCM model, we analyzed the overall transcriptome and proteome of the myocardium, before/after treatment with SPM. The general state and cardiac structure and function changes of each group were also compared. Diabetes induced an increased blood glucose and serum triglyceride content, a decreased body weight, serum insulin level, and cardiac function-related indexes, accompanied by disrupted myocardial tissue morphology and ultrastructure damage. Using RNA sequencing (RNA-seq), we identified thousands of differentially expressed genes (DEGs) in DbCM with or without SPM treatment. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis demonstrated that the DEGs were significantly enriched in lipid metabolism and amino acid metabolism pathways. Specifically, quantitative real-time PCR (qRT-PCR) confirmed that SPM protected DbCM by reversing the expressions of lipid metabolism and amino acid metabolism-related genes, including Alox15, Gm13033, pla2g12a, Ptges, Pnpla2, and Acot1. To further reveal the pathogenesis of DbCM, we used proteome-based data-independent acquisition (DIA) and identified 139 differentially expressed proteins (DEPs) with 67 being upregulated and 72 being downregulated in DbCM. Venn intersection analysis showed 37 coexpressed genes and proteins in DbCM, including 29 upregulation and 8 downregulation in DbCM. In the protein-protein interaction (PPI) network constructed by the STRING database, the metabolism-related coexpressed genes and proteins, such as Acot2, Ephx2, Cyp1a1, Comt, Acox1, Hadhb, Hmgcs2, Acot1, Inmt, and Cat, can interact with the identified DEGs and DEPs. Conclusion. The biomarkers and canonical pathways identified in this study may hold the key to understand the mechanisms of DbCM pathobiology and provide new targets for the therapeutic effect of SPM against DbCM by targeting lipid and amino acid metabolism pathways.

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Xiong, Lin, Jie Pei, Xiaoyun Wu, Qudratullah Kalwar, Chunnian Liang, Xian Guo, Min Chu, Pengjia Bao, Xixi Yao, and Ping Yan. "The Study of the Response of Fat Metabolism to Long-Term Energy Stress Based on Serum, Fatty Acid and Transcriptome Profiles in Yaks." Animals 10, no. 7 (July 7, 2020): 1150. http://dx.doi.org/10.3390/ani10071150.

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Long-term energy stress (ES) during the cold season is a serious problem for the breeding of yaks. In this paper, the response of fat metabolism in yaks to long-term ES during the cold season was studied. Gas chromatography (GC) analysis showed that the percentage of saturated fatty acids (SFAs) in the subcutaneous fat of the yaks in the ES group was 42.7%, which was less than the 56.6% in the CO group (p < 0.01) and the percentage of polyunsaturated unsaturated fatty acids (PUFAs) in the subcutaneous fat of the yaks in the ES group was 38.3%, which was more than the 26.0% in the CO group (p < 0.01). The serum analysis showed that fatty acid oxidation in yaks was increased under long-term ES. In the subcutaneous fat of yaks under long-term ES, the gene expression levels of glycerol-3-phosphate acyltransferase 4 (GPAT4), hormone-sensitive lipase (HSL), patatin-like phospholipase domain-containing protein 2 (PNPLA2), acyl-CoA dehydrogenase (ACAD), acyl-coenzyme A thioesterase 8 (ACOT8), facilitated glucose transporter (GLUT4), 3-oxoacyl-[acyl-carrier-protein] synthase (OXSM), oestradiol 17-beta-dehydrogenase 8 (HSD17B8) and malonate-Co-A ligase ACSF3 (ACSF3) were downregulated (q < 0.05), whereas the gene expression levels of aquaporin-7 (AQP7), long-chain-fatty-acid-CoA ligase (ACSL), elongation of very long chain fatty acids protein (ELOVL) and fatty acid desaturase 1 (FADS1) were upregulated (q < 0.05), indicating the inhibition of fat catabolism, fat anabolism, fatty acid oxidation, glucose (GLU) intake and SFA synthesis and the promotion of glycerinum (GLY) transportation and PUFA synthesis. Additional findings showed that the gene expression levels of leptin (LEP), adenosine 5′-monophosphate-activated protein kinase (AMPK) and phosphatidylinositol 3-kinase (PI3K) were upregulated (q < 0.05), whereas the gene expression levels of malonyl-CoA decarboxylase (MCD), sterol regulatory element-binding protein 1 (SREBF1), mammalian target of rapamycin (mTOR) and serine/threonine-protein kinase (AKT) were downregulated (q < 0.05), indicating that fat metabolism in the subcutaneous fat of yaks under ES was mainly regulated by AMPK signaling and mTOR and PI3K-AKT signaling were also involved. Energy consumption was inhibited in the subcutaneous fat itself. This study can provide a theoretical basis for the healthy breeding and genetic breeding of yaks.

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Ellis, Jessica M., G. William Wong, and Michael J. Wolfgang. "Acyl Coenzyme A Thioesterase 7 Regulates Neuronal Fatty Acid Metabolism To Prevent Neurotoxicity." Molecular and Cellular Biology 33, no. 9 (March 4, 2013): 1869–82. http://dx.doi.org/10.1128/mcb.01548-12.

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Numerous neurological diseases are associated with dysregulated lipid metabolism; however, the basic metabolic control of fatty acid metabolism in neurons remains enigmatic. Here we have shown that neurons have abundant expression and activity of the long-chain cytoplasmic acyl coenzyme A (acyl-CoA) thioesterase 7 (ACOT7) to regulate lipid retention and metabolism. Unbiased and targeted metabolomic analysis of fasted mice with a conditional knockout of ACOT7 in the nervous system, Acot7 N−/− , revealed increased fatty acid flux into multiple long-chain acyl-CoA-dependent pathways. The alterations in brain fatty acid metabolism were concomitant with a loss of lean mass, hypermetabolism, hepatic steatosis, dyslipidemia, and behavioral hyperexcitability in Acot7 N − / − mice. These failures in adaptive energy metabolism are common in neurodegenerative diseases. In agreement, Acot7 N − / − mice exhibit neurological dysfunction and neurodegeneration. These data show that ACOT7 counterregulates fatty acid metabolism in neurons and protects against neurotoxicity.

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11

Quevedo, Katherine. "Venom In The Cloud Forest." After Dinner Conversation 3, no. 3 (2022): 108–21. http://dx.doi.org/10.5840/adc20223328.

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How important is the person who controls the stories of the past? What happens when that person changes community stories to meet his needs? In this work of philosophical fantasy short fiction, Acoti is shot with a poison dart while in the forest. With much effort, his friend takes him to Cuadelo, the community medicine man. Acoti is suspicious because he had previously spoken out to the elders that the community petroglyphs seemed to always agree with Cuadelo. Cuadelo confesses to Acoti that he is the one who poisoned him and says he will only cure Acoti if he goes before the elders to confess he was wrong in accusing Cuadelo. Acoti agrees, and is cured, but not before grabbing Cuadelo’s magic wand. Now cured, Acoti goes before the elders and shows that Cuadelo has been using his magic wand to change the petroglyphs (and their community stories) so they always agree with his opinions.

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Cotton, Bryan A., Sherry L. Sixta, Charles E. Wade, John B. Holcomb, and Nena Matijevic-Aleksic. "Mechanistic Determinants of the Acute Coagulopathy of Trauma (ACoT) in Patients Undergoing Emergency Surgery,." Blood 118, no. 21 (November 18, 2011): 3319. http://dx.doi.org/10.1182/blood.v118.21.3319.3319.

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Abstract Abstract 3319 Introduction: Acute coagulopathy of trauma (ACoT) is a highly lethal phenomenon whose mechanisms have yet to be clearly defined. While likely multi-factorial, it has been reported to only occur in the presence of blunt injury. The purpose of this study was to identify variables that might influence or contribute to the early development of ACoT. Methods: Retrospective review of all patients admitted to a Level 1 trauma center 01/2004–12/2009 who underwent emergent laparotomy. Emergent laparotomy was defined as laparotomy performed within two hours of admission. ACoT(+) was defined as arrival INR >= 1.5, while ACoT(−) was defined as arrival INR<1.5. Univariate and multivariate analyses performed. Primary outcome was the identification of those factors predicting the presence of ACoT on admission. Results: 1218 patients were included, 337 (27%) presented with ACoT(+), 881 (73%) did not. The groups had similar demographics and pre-hospital and ED fluids. Arrival base deficit (median 8.5 vs. 4.0) and ISS (25 vs. 16) were higher in ACoT(+) as were intra-operative RBC (median 4 vs. 0 U) and plasma (3 vs. 0 U); all p<0.05. 40% of ACoT(+) patients sustained penetrating injury. Six-hour (12% vs. 1%), 24-hour (15% vs. 1%), and 30-day (23% vs. 4%) mortality were significantly greater in ACoT(+); all p<0.001. Linear regression found INR values independently associated with arrival base deficit (p<0.001) but not ISS. Controlling for age, gender, mechanism of injury, and pre-hospital resuscitation, multiple logistic regression demonstrated that arrival base deficit was an independent predictor of developing ACoT. Conclusion: The current study found ACoT independently associated with metabolic (base deficit), physiologic (blood pressure) and anatomic insults (ISS). Attempts to address ACoT should focus on correcting each of these components. Moreover, contrary to prior data, 40% of ACoT(+) patients sustained penetrating mechanism. Disclosures: No relevant conflicts of interest to declare.

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Hunt, Mary C., Anna Rautanen, Maria A. K. Westin, L. Thomas Svensson, and Stefan E. H. Alexson. "Analysis of the mouse and human acyl‐CoA thioesterase (ACOT) gene clusters shows that convergent, functional evolution results in a reduced number of human peroxisomal ACOTs 1." FASEB Journal 20, no. 11 (September 2006): 1855–64. http://dx.doi.org/10.1096/fj.06-6042com.

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14

Pashaj, Anjeza, Xiaohua Yi, Mengna Xia, Stephanie Canny, Jean-Jack M. Riethoven та Régis Moreau. "Characterization of genome-wide transcriptional changes in liver and adipose tissues of ZDF (fa/fa) rats fed R-α-lipoic acid by next-generation sequencing". Physiological Genomics 45, № 23 (1 грудня 2013): 1136–43. http://dx.doi.org/10.1152/physiolgenomics.00138.2013.

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We report on the characterization of lipogenic tissue transcriptional networks that support physiological responses of obese rats to a lipid-lowering bioactive food compound, R-α-lipoic acid (LA). Nine-week-old male Zucker diabetic fatty (fa/fa) rats were fed a chow diet supplemented with 3 g LA per kg diet or pair fed for 2 wk. At the end of the trial, high-quality RNA was extracted from the liver and epididymal fat and subjected to transcriptome analysis by RNA-Seq technology. Results showed a substantially higher number of differentially expressed genes [DEG, false discovery rate adjusted P ≤ 0.05 and absolute log2 (fold change) ≥ 1] in the liver (110 genes) vs. epididymal fat (10 genes). Most epididymal fat DEG were also differentially expressed in liver and shared directionality of change. Gene Ontology (GO) analysis of these transcripts revealed significant enrichment of GO categories related to immune response, stress response, lipid metabolism, and carboxylic acid metabolic processes. Of interest, interferon-related genes involved in defense against microorganisms and innate immune response were induced by LA. Lipid metabolism-related transcript changes observed in LA-fed animals included downregulation of lipogenic genes ( Pnpla3, Pnpla5, Elovl6, Acly, Gpam, and Aacs) and concomitant upregulation of short-, medium-, and long-chain fatty acid metabolic processes ( Acot1, Acot2, Acsf2, and Crat). Transcriptional changes were accompanied by the lowering of abdominal adiposity and blood triacylglycerol levels. We conclude that LA dietary supplementation induces prominent gene expression changes in liver in support of significant improvement of whole-body lipid status.

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Castilla, Rocío, Mariana Gadaleta, Ana Fernanda Castillo, Alejandra Duarte, Isabel Neuman, Cristina Paz, Fabiana Cornejo Maciel, and Ernesto J. Podestá. "New Enzymes Involved in the Mechanism of Action of Epidermal Growth Factor in a Clonal Strain of Leydig Tumor Cells." Endocrinology 149, no. 7 (April 3, 2008): 3743–52. http://dx.doi.org/10.1210/en.2007-1580.

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The studies presented herein were designed to investigate the effect of mouse epidermal growth factor (mEGF) on arachidonic acid (AA) release in a clonal strain of cultured murine Leydig cells (designed MA-10). In MA-10 cells, mEGF promotes AA release and metabolism to lipoxygenated products to induce the steroidogenic acute regulatory (StAR) protein. However, the mechanism by which mEGF releases AA in these cells is not totally elucidated. We show that mEGF produces an increment in the mitochondrial AA content in a short-term incubation (30 min). This AA is released by the action of a mitochondrial acyl-CoA thioesterase (Acot2), as demonstrated in experiments in which Acot2 was down or overexpressed. This AA in turn regulates the StAR protein expression, indirect evidence of its metabolism to lipoxygenated products. We also show that mEGF induces the expression (mRNA and protein) of Acot2 and an acyl-CoA synthetase that provides the substrate, arachidonyl-CoA, to Acot2. This effect is also observed in another steroidogenic cell line, the adrenocortical Y1 cells. Taken together, our results show that: 1) mEGF can induce the generation of AA in a specific compartment of the cells, i.e. the mitochondria; 2) mEGF can up-regulate acyl-CoA synthetase and Acot2 mRNA and protein levels; and 3) mEGF-stimulated intramitochondrial AA release leads to StAR protein induction.

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Quan, Lin-Hu, Chuanhai Zhang, Meng Dong, Jun Jiang, Hongde Xu, Chunlong Yan, Xiaomeng Liu, et al. "Myristoleic acid produced by enterococci reduces obesity through brown adipose tissue activation." Gut 69, no. 7 (November 19, 2019): 1239–47. http://dx.doi.org/10.1136/gutjnl-2019-319114.

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ObjectiveDietary fibre has beneficial effects on energy metabolism, and the majority of studies have focused on short-chain fatty acids produced by gut microbiota. Ginseng has been reported to aid in body weight management, however, its mechanism of action is not yet clear. In this study, we focused on the potential modulating effect of ginseng on gut microbiota, aiming to identify specific strains and their metabolites, especially long-chain fatty acids (LCFA), which mediate the anti-obesity effects of ginseng.DesignDb/db mice were gavaged with ginseng extract (GE) and the effects of GE on gut microbiota were evaluated using 16S rDNA-based high throughput sequencing. To confirm the candidate fatty acids, untargeted metabolomics analyses of the serum and medium samples were performed.ResultsWe demonstrated that GE can induce Enterococcus faecalis, which can produce an unsaturated LCFA, myristoleic acid (MA). Our results indicate that E. faecalis and its metabolite MA can reduce adiposity by brown adipose tissue (BAT) activation and beige fat formation. In addition, the gene of E. faecalis encoding Acyl-CoA thioesterases (ACOTs) exhibited the biosynthetic potential to synthesise MA, as knockdown (KD) of the ACOT gene by CRISPR-dCas9 significantly reduced MA production. Furthermore, exogenous treatment with KD E. faecalis could not reproduce the beneficial effects of wild type E. faecalis, which work by augmenting the circulating MA levels.ConclusionsOur results demonstrated that the gut microbiota-LCFA-BAT axis plays an important role in host metabolism, which may provide a strategic advantage for the next generation of anti-obesity drug development.

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Cirincione, Brenda, Navin Goyal, and Rene Bruno. "The American Conference on Pharmacometrics 2017 (ACoP8)." Journal of Pharmacokinetics and Pharmacodynamics 44, S1 (September 20, 2017): 1–2. http://dx.doi.org/10.1007/s10928-017-9538-9.

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Mankamo, Tuomas. "Comment on ‘considerations in establishing ACOTs for components’." Reliability Engineering & System Safety 34, no. 2 (January 1991): 235–39. http://dx.doi.org/10.1016/0951-8320(91)90090-t.

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19

Sheahan, Michael B., David A. Collings, Ray J. Rose, and David W. McCurdy. "ACTIN7 Is Required for Perinuclear Clustering of Chloroplasts during Arabidopsis Protoplast Culture." Plants 9, no. 2 (February 10, 2020): 225. http://dx.doi.org/10.3390/plants9020225.

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In Arabidopsis, the actin gene family comprises eight expressed and two non-expressed ACTIN (ACT) genes. Of the eight expressed isoforms, ACT2, ACT7, and ACT8 are differentially expressed in vegetative tissues and may perform specific roles in development. Using tobacco mesophyll protoplasts, we previously demonstrated that actin-dependent clustering of chloroplasts around the nucleus prior to cell division ensures unbiased chloroplast inheritance. Here, we report that actin-dependent chloroplast clustering in Arabidopsis mesophyll protoplasts is defective in act7 mutants, but not act2-1 or act8-2. ACT7 expression was upregulated during protoplast culture whereas ACT2 and ACT8 expression did not substantially change. In act2-1, ACT7 expression increased in response to loss of ACT2, whereas in act7-1, neither ACT2 nor ACT8 expression changed appreciably in response to the absence of ACT7. Semi-quantitative immunoblotting revealed increased actin concentrations during culture, although total actin in act7-1 was only two-thirds that of wild-type or act2-1 after 96 h culture. Over-expression of ACT2 and ACT8 under control of ACT7 regulatory sequences restored normal levels of chloroplast clustering. These results are consistent with a requirement for ACT7 in actin-dependent chloroplast clustering due to reduced levels of actin protein and gene induction in act7 mutants, rather than strong functional specialization of the ACT7 isoform.

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Murata, Yuka, Takashi Yamashiro, Takaomi Kessoku, Israt Jahan, Haruki Usuda, Tetsuya Tanaka, Takayuki Okamoto, Atsushi Nakajima, and Koichiro Wada. "Up-Regulated MicroRNA-27b Promotes Adipocyte Differentiation via Induction of Acyl-CoA Thioesterase 2 Expression." BioMed Research International 2019 (December 17, 2019): 1–9. http://dx.doi.org/10.1155/2019/2916243.

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Nonalcoholic fatty liver disease (NAFLD) is characterized by a spectrum of liver pathologies, from simple steatosis to steatohepatitis. Recent studies have increasingly noted the aberrant expression of microRNAs closely related to NAFLD pathologies. We have previously shown the presence of increased levels of microRNA-27b (miR-27b) in patients with NAFLD. In this study, we investigated the role of miR-27b in NAFLD by examining the impact of up-regulated miR-27b on the differentiation of preadipocytes into mature adipocytes. We found that miR-27b-3p remarkably enhances the adipocyte differentiation of 3T3-L1 cells associated with lipid accumulation and intracellular triglyceride contents. Furthermore, we have demonstrated not only that miR-27b-3p induces acyl-CoA thioesterase 2 (ACOT2) expression in 3T3-L1 cells, but also that the knockdown of ACOT2 suppresses lipid accumulation and adipocyte differentiation in both the presence and absence of miR-27b-3p treatment. Our data strongly suggest that the miR-27b-ACOT2 axis is an important pathway in adipocyte differentiation and may play a role in the pathogenesis of NAFLD.

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Olson, Jane. "How Does ACOTE Help Educators Support the AOTA Vision." Occupational Therapy In Health Care 21, no. 1-2 (January 2007): 301–3. http://dx.doi.org/10.1080/j003v21n01_30.

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Olson, Jane. "How Does ACOTE Help Educators Support the AOTA Vision." Occupational Therapy In Health Care 21, no. 1 (June 18, 2007): 301–3. http://dx.doi.org/10.1300/j003v21n01_30.

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23

Mandel, Corey R., Benjamin Tweel, and Liang Tong. "Crystal structure of human mitochondrial acyl-CoA thioesterase (ACOT2)." Biochemical and Biophysical Research Communications 385, no. 4 (August 2009): 630–33. http://dx.doi.org/10.1016/j.bbrc.2009.05.122.

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24

Bar, Raphael, John L. Gainer, and Donald J. Kirwan. "Immobilization ofAcetobacter acoti on cellulose ion exchangers: Adsorption isotherms." Biotechnology and Bioengineering 28, no. 8 (August 1986): 1166–71. http://dx.doi.org/10.1002/bit.260280806.

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25

Ni, Chenming, Kailian Zheng, Yunshu Gao, Ying Chen, Keqing Shi, Canrong Ni, Gang Jin, and Guanzhen Yu. "ACOT4 accumulation via AKT-mediated phosphorylation promotes pancreatic tumourigenesis." Cancer Letters 498 (February 2021): 19–30. http://dx.doi.org/10.1016/j.canlet.2020.09.022.

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Sun, Tingting, Liming Tian, Yunyun Guo, Yu Zheng, Linglong Ouyang, Xianbin Zhang, Yingrong Lai, and Guofen Yang. "Anaplastic carcinoma showing rhabdoid features combined with ovarian mucinous borderline cystadenoma: a case report and literature review." Journal of International Medical Research 49, no. 5 (May 2021): 030006052110131. http://dx.doi.org/10.1177/03000605211013159.

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Anaplastic carcinoma in an ovarian tumor (ACOT) is rare. There have been a few controversial cases illustrating the clinical characteristics and prognostic factors of ACOT, which are not well known. A 60-year-old Chinese woman presented with a large pelvic tumor. A transvaginal ultrasound examination showed a large single ovarian cystic tumor with mural nodules and ascites. A gross ovarian mass with a size of approximately 20 × 10×15 cm3 was found. The content of the ovarian cyst was light yellow and chocolate-like, and a large grayish mural nodule of approximately 10 cm was found on the cyst wall. Histological diagnosis of ovarian mucinous borderline cystadenoma with a mural nodule of anaplastic carcinoma showing rhabdoid features and International Federation of Gynecology and Obstetrics (FIGO) stage IIIa was made. Fifteen months after surgery, the patient had received six courses of paclitaxel and carboplatin. She is still alive without any recurrence of the tumor. Findings from the present case suggest that patients with ACOT and FIGO stage IIIa would benefit from surgery and chemotherapy of paclitaxel and carboplatin. We also review the clinical features and survival rate of patients with ACOT using the Surveillance, Epidemiology, and End Result database, and summarize previously reported treatments.

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K. Sathya Sundari. "Makespan Minimization in Job Shop Scheduling." International Journal of Engineering and Management Research 11, no. 1 (February 27, 2021): 228–30. http://dx.doi.org/10.31033/ijemr.11.1.31.

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In industries, the completion time of job problems in the manufacturing unit has risen significantly. In several types of current study, the job's completion time, or makespan, is reduced by taking straight paths, which is time-consuming. In this paper, we used an Improved Ant Colony Optimization and Tabu Search (ACOTS) algorithm to solve this problem by precisely defining the fault occurrence location in order to rollback. We have used a short-term memory-based rollback recovery strategy to minimise the job's completion time by rolling back to its own short-term memory. The recent movements in Tabu quest are visited using short term memory. As compared to the ACO algorithm, our proposed ACOTS-Cmax solution is more efficient and takes less time to complete.

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Liu, Hui, Jingjing Cheng, Yongbing Zhou, Fangfang Liu, Nathan Griffin, Sam Faulkner, and Li Wang. "Interactions of perfluorooctanoic acid with acyl-CoA thioesterase 1 (Acot1)." Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology 250 (December 2021): 109159. http://dx.doi.org/10.1016/j.cbpc.2021.109159.

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Tillander, Veronika, Elisabet Arvidsson Nordstöm, Jenny Reilly, Mary C. Hunt, and Stefan E. H. Alexson. "Characterisation of ACOT9: A mitochondrial propionyl-CoA/myristoyl-CoA thioesterase." Chemistry and Physics of Lipids 164 (August 2011): S30—S31. http://dx.doi.org/10.1016/j.chemphyslip.2011.05.100.

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Wang, Fang, Jingyi Wu, Zhichao Qiu, Xiaosong Ge, Xingxiang Liu, Chun Zhang, Wenhuan Xu, et al. "ACOT1 expression is associated with poor prognosis in gastric adenocarcinoma." Human Pathology 77 (July 2018): 35–44. http://dx.doi.org/10.1016/j.humpath.2018.03.013.

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31

Ruiz, Carolina, and Max Andresen. "Treatment of Acute Coagulopathy Associated with Trauma." ISRN Critical Care 2013 (June 3, 2013): 1–7. http://dx.doi.org/10.5402/2013/783478.

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Coagulopathy is frequently present in trauma. It is indicative of the severity of trauma and contributes to increased morbidity and mortality. Uncontrolled bleeding is the most frequent preventable cause of death in trauma patients reaching hospital alive. Coagulopathy in trauma has been long thought to develop as a result of hemodilution, acidosis, and hypothermia often related to resuscitation practices. However, altered coagulation tests are already present in 25–30% of severe trauma patients upon hospital arrival before resuscitation efforts. Acute coagulopathy associated with trauma (ACoT) has been recognized in recent years as a distinct entity associated with increased mortality, morbidity, and transfusion requirements. Transfusion and nontransfusion strategies aimed at correcting ACoT, particularly in patients with massive bleeding and massive transfusion, are currently available. Early administration of tranexamic acid to bleeding trauma patients safely reduces the risk of death. It has been proposed that early aggressive blood product transfusional management of ACoT with a red blood cell : plasma : platelets ratio close to 1 : 1 : 1 could result in decreased mortality from uncontrolled bleeding.

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Pouts-Lajus, Serge, and Marielle Riché-Magnier. "Un Acot en Wallonie. Quand l’informatique pédagogique traverse l’Atlantique." Sciences et techniques éducatives 7, no. 2 (2000): 427–42. http://dx.doi.org/10.3406/stice.2000.1620.

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Vesely, W. E., and M. A. Azarm. "Reply to Mankamo's comments on ‘considerations in establishing ACOTs for components’." Reliability Engineering & System Safety 34, no. 2 (January 1991): 239–40. http://dx.doi.org/10.1016/0951-8320(91)90091-k.

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34

Fogelholm, Jesper, Samuel Inkabi, Andrey Höglund, Robin Abbey-Lee, Martin Johnsson, Per Jensen, Rie Henriksen, and Dominic Wright. "Genetical Genomics of Tonic Immobility in the Chicken." Genes 10, no. 5 (May 7, 2019): 341. http://dx.doi.org/10.3390/genes10050341.

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Identifying the molecular mechanisms of animal behaviour is an enduring goal for researchers. Gaining insight into these mechanisms enables us to gain a greater understanding of behaviour and their genetic control. In this paper, we perform Quantitative Trait Loci (QTL) mapping of tonic immobility behaviour in an advanced intercross line between wild and domestic chickens. Genes located within the QTL interval were further investigated using global expression QTL (eQTL) mapping from hypothalamus tissue, as well as causality analysis. This identified five candidate genes, with the genes PRDX4 and ACOT9 emerging as the best supported candidates. In addition, we also investigated the connection between tonic immobility, meat pH and struggling behaviour, as the two candidate genes PRDX4 and ACOT9 have previously been implicated in controlling muscle pH at slaughter. We did not find any phenotypic correlations between tonic immobility, struggling behaviour and muscle pH in a smaller additional cohort, despite these behaviours being repeatable within-test.

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Gando, Satoshi. "Hemostasis and Thrombosis in Trauma Patients." Seminars in Thrombosis and Hemostasis 41, no. 01 (January 20, 2015): 026–34. http://dx.doi.org/10.1055/s-0034-1398378.

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Hemostasis and thrombosis in trauma patients consist of physiological hemostasis for wound healing and the pathological reaction of disseminated intravascular coagulation (DIC). Whole body trauma, isolated brain injury, and fat embolism syndrome, if extremely severe, can cause DIC and affect a patient's prognosis. Shock-induced hyperfibrinolysis causes DIC with the fibrinolytic phenotype, contributing to oozing-type severe bleeding. If uncontrolled, this phenotype progresses to thrombotic phenotype at the late stage of trauma, followed by microvascular thrombosis, leading to organ dysfunction. Another type of pathological hemostatic change is acute coagulopathy of trauma shock (ACOTS), which gives rise to activated protein C–mediated systemic hypocoagulation, resulting in bleeding. ACOTS occurs only in trauma associated with shock-induced hypoperfusion and there is nothing to suggest DIC in this phenomenon. This review will provide information about the recent advances in hemostasis and thrombosis in trauma and will clarify the pathogeneses of the pathological processes observed in trauma patients.

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36

Kruschwitz, M., G. Fritzsche, R. Schwarting, K. Micklem, D. Y. Mason, B. Falini, and H. Stein. "Ber-ACT8: new monoclonal antibody to the mucosa lymphocyte antigen." Journal of Clinical Pathology 44, no. 8 (August 1, 1991): 636–45. http://dx.doi.org/10.1136/jcp.44.8.636.

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37

Zhang, Xinpei, Bo Liu, Jilei Zhang, Xinrui Yang, Gaoqi Zhang, Siyuan Yang, Jing Wang, et al. "Expression level of ACOT7 influences the prognosis in acute myeloid leukemia patients." Cancer Biomarkers 26, no. 4 (December 11, 2019): 441–49. http://dx.doi.org/10.3233/cbm-182287.

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38

Feng, Huiqin, and Xiaojian Liu. "Interaction between ACOT7 and LncRNA NMRAL2P via Methylation Regulates Gastric Cancer Progression." Yonsei Medical Journal 61, no. 6 (2020): 471. http://dx.doi.org/10.3349/ymj.2020.61.6.471.

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39

Campos Petit de Murat, Angela Isabel. "Visiones ininteligibles. El poder de la ‘no clasificación’ en las artes." Revista de Arte Ibero Nierika, no. 23 (January 5, 2023): 224–37. http://dx.doi.org/10.48102/nierika.vi23.594.

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Este comentario fue inspirado por el concepto de lo ininteligible y acota las reflexiones que la autora ha tenido en torno a sulabor como estudiosa del arte. Utilizando la obra de Memo Hojas como ejemplo y las identidades alternativas como base, el texto esboza ideas y posibles propuestas para convertir a los estudios artísticos en espacios de transformación y comunidad.

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40

Godard, Olivier. "À propos du livre de Pascal Acot,Climat, un débat dévoyé ?" Natures Sciences Sociétés 19, no. 3 (July 2011): 282–86. http://dx.doi.org/10.1051/nss/2011130.

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41

Fakhri, H. "Spectrum-Generating Symmetries for the Superpotentials Acot θ and Btanh y". International Journal of Theoretical Physics 47, № 10 (1 травня 2008): 2625–34. http://dx.doi.org/10.1007/s10773-008-9699-9.

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42

Cornwall, John. "Opening of the ACOTA Seminar “Older People At Home” Adelaide, April 17, 1986." Australian Journal on Ageing 5, no. 2 (May 1986): 32–34. http://dx.doi.org/10.1111/j.1741-6612.1986.tb00279.x.

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43

Santana-Codina, Naiara, Anna Marcé-Grau, Laia Muixí, Claudia Nieva, Mónica Marro, David Sebastián, Juan Pablo Muñoz, Antonio Zorzano, and Angels Sierra. "GRP94 Is Involved in the Lipid Phenotype of Brain Metastatic Cells." International Journal of Molecular Sciences 20, no. 16 (August 9, 2019): 3883. http://dx.doi.org/10.3390/ijms20163883.

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Metabolic adaptation may happen in response to the pressure exerted by the microenvironment and is a key step in survival of metastatic cells. Brain metastasis occurs as a consequence of the systemic dissemination of tumor cells, a fact that correlates with poor prognosis and high morbidity due to the difficulty in identifying biomarkers that allow a more targeted therapy. Previously, we performed transcriptomic analysis of human breast cancer patient samples and evaluated the differential expression of genes in brain metastasis (BrM) compared to lung, bone and liver metastasis. Our network approach identified upregulation of glucose-regulated protein 94 (GRP94) as well as proteins related to synthesis of fatty acids (FA) in BrM. Here we report that BrM cells show an increase in FA content and decreased saturation with regard to parental cells measured by Raman spectroscopy that differentiate BrM from other metastases. Moreover, BrM cells exerted a high ability to oxidize FA and compensate hypoglycemic stress due to an overexpression of proteins involved in FA synthesis and degradation (SREBP-1, LXRα, ACOT7). GRP94 ablation restored glucose dependence, down-regulated ACOT7 and SREBP-1 and decreased tumorigenicity in vivo. In conclusion, GRP94 is required for the metabolic stress survival of BrM cells, and it might act as a modulator of lipid metabolism to favor BrM progression.

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44

Baquero Escudero, Ana L. "Azorín ante los personajes del Quijote." BOLETÍN DE LA BIBLIOTECA DE MENÉNDEZ PELAYO 92, Único (December 10, 2016): 39–53. http://dx.doi.org/10.55422/bbmp.172.

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El interés por los clásicos de Martínez Ruiz queda plasmado a lo largo de su dilatada trayectoria literaria; del mismo destaca, con singular relieve, Cervantes y su obra. A partir de una previa contextualización histórica sobre el cervantismo de su época, el presente trabajo acota, pues, tan solo una pequeña parcela de la abundante producción de temática cervantina de Azorín, para analizar tanto sus interpretaciones y valoraciones críticas, como su creación literaria dedicada a los personajes del Quijote.

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45

Oktay, Kutluk H., and Loris Marin. "COMPARISON OF ORTHOTOPIC (OA) AND HETEROTOPIC (HA) AUTOLOGOUS CRYOPRESERVED OVARIAN TISSUE TRANSPLANTATION (ACOTT) OUTCOMES." Fertility and Sterility 116, no. 3 (September 2021): e68-e69. http://dx.doi.org/10.1016/j.fertnstert.2021.07.194.

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46

Arnbjörnsson, E., and M. Abdulla. "CORRELATION BETWEEN COPPER, ZINC AND CERULOPLASMIN IN PLASMA OF PATIENTS ADMITTED FOR ACOTE ABDOMEN." Acta Pharmacologica et Toxicologica 59 (March 13, 2009): 180–83. http://dx.doi.org/10.1111/j.1600-0773.1986.tb02739.x.

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47

López Quintáns, Javier. "Emilia Pardo Bazán y la vida en la calle (o como nace, y se hace, un paradigma descriptivo)." BOLETÍN DE LA BIBLIOTECA DE MENÉNDEZ PELAYO 97, no. 2 (December 10, 2021): 173–209. http://dx.doi.org/10.55422/bbmp.542.

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En la construcción del discurso periodístico y ensayístico en Pardo Bazán la autora sigue una escala de procedimientos descriptivos y de técnicas de figuración. Avanzaremos a través de distintos ejemplos en los que se ponen en valor los métodos de construcción del discurso en la presentación de grupos humanos, con un marco concreto que acota la base temática, el de ambientes lúdicos y festivos en circunstancias de concentración social o de protesta pública con el trasfondo de la calle como constante.

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48

Meledeo, Michael A., James E. Campbell, Armando C. Rodriguez, Melanie V. Valenciana, and Andrew P. Cap. "Activated Protein C Levels Found In Trauma Patients Are Insufficient To Inactivate Platelet Factor Va and Produce Coagulopathy In An In Vitro Model." Blood 122, no. 21 (November 15, 2013): 4767. http://dx.doi.org/10.1182/blood.v122.21.4767.4767.

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Background A subset of severe trauma victims suffering from uncontrolled hemorrhage present to the emergency room with an acute coagulopathy of trauma (ACoT). This condition occurs within the first 30 min following injury, is not the result of resuscitation-associated dilutional effects, and is defined by an INR > 1.2. The mechanisms behind this coagulopathy have not been completely identified, but recent studies posit that the exuberant activation of protein C is a key contributor to ACoT. Protein C is activated through the interaction of thrombin and thrombomodulin on the endothelial surface. Activated protein C (APC) has anti-inflammatory and cytoprotective functions, in addition to regulating coagulation by inactivating factor Va (FVa). Evidence that APC is implicated in ACoT includes: 1) circulating APC levels are elevated 3-5 fold in patients with high injury severity scores (>15) and base deficit (>6); 2) high APC levels (>6 ng/ml, or 105 pM) in these patients are correlated with an increase in prothrombin time (PT) and partial thromboplastin time [Cohen et al. Ann Surg 2012; 255(2): 379-85]. FVa exists in a soluble plasma fraction and in a platelet-associated fraction (in the membrane or alpha-granules). The platelet pool of FVa is more resistant to APC degradation [Camire et al. J Biol Chem 1995; 270(35): 20794-800] and is sufficient to maintain thrombin generation even in patients with severe congenital FV-deficiencies [Duckers et al. Blood 2010; 115(4): 879-86]. We hypothesize that healthy platelets in sufficient quantity will serve as an effective promoter of hemostasis in patients with ACoT, overcoming the effects of APC. Methods and Results We studied the effects of APC on coagulation in commercially obtained FV-deficient plasma (FVdp) and platelets/plasma from healthy volunteers. Tests included prothrombin time, turbidimetric assessment of fibrin cross-linking, and thromboelastography (TEG). Prothrombin time in platelet-free plasma or FVdp subjected to exogenous APC display a dose-dependent response where clotting is only significantly delayed at APC >1 nM, much higher than the systemic concentrations found in the ACoT patients (105pM) or even in subjects treated with drotrecogin alfa, a recombinant APC product intended for the treatment of sepsis (steady-state concentration was found to be ∼790pM) [Macias et al. Clin Pharmacol Ther 2002; 72(4): 391-402]. Examining fibrin crosslinking in a static 96-well turbidimetric plate assay demonstrated that concentrations of APC of 1nM or below had no effect on the initiation time, rate, or strength of clotting in FVdp or PFP from healthy volunteers. Titration of plasma FV into FVdp illustrated that clotting time and rate (as measured by TEG) were not significantly affected at 10nM FV, less than 50% of the “normal” 23nM concentration. Clot strength was unaffected by FV depletion. To examine the contributions of platelet FVa, isolated and washed platelets were introduced in increasing amounts to FVdp and PFP; the rate of clotting and clot strength aligned between the two plasmas given equivalent numbers of platelets, emphasizing the importance of platelet FVa. At lower platelet concentrations (particularly 10,000 to 100,000 / µl), there were statistically significant differences in clotting time between FVdp and normal plasma, but these differences diminished with increasing platelet concentration. To evaluate the resistance of the platelet fraction to APC effects, 200,000 platelets / µl were suspended in FVdp and treated with a titration of APC from 1pM to 100nM. The samples were unaffected by APC up to a dose of at least 10nM as measured by TEG clotting parameters, well above the amounts found in the trauma patients or drotrecogin alfa-treated subjects. Conclusions FV-deficiency affects clotting only in cases of severe depletion (<50%). In a low shear in vitro closed system, APC does not affect coagulation except at very high levels (>1nM). Healthy platelets in sufficient quantity are capable of rescuing FV-deficiency and are resistant to APC effects. APC is unlikely to be the main driver of ACoT. Disclosures: No relevant conflicts of interest to declare.

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An, Yong-Qiang, John M. McDowell, Shurong Huang, Elizabeth C. McKinney, Sharon Chambliss, and Richard B. Meagher. "Strong, constitutive expression of the Arabidopsis ACT2/ACT8 actin subclass in vegetative tissues." Plant Journal 10, no. 1 (July 1996): 107–21. http://dx.doi.org/10.1046/j.1365-313x.1996.10010107.x.

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Brocker, Chad, Christopher Carpenter, Daniel W. Nebert, and Vasilis Vasiliou. "Evolutionary divergence and functions of the human acyl-CoA thioesterase gene (ACOT) family." Human Genomics 4, no. 6 (2010): 411. http://dx.doi.org/10.1186/1479-7364-4-6-411.

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