Relevant bibliographies by topics / ECS alterations

Contents

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

Academic literature on the topic 'ECS alterations'

Author: Grafiati
Published: 7 June 2025
Last updated: 17 July 2025

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Journal articles on the topic "ECS alterations"

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Smith, Evan S., Arnaud Da Cruz Paula, Karen A. Cadoo, et al. "Endometrial Cancers in BRCA1 or BRCA2 Germline Mutation Carriers: Assessment of Homologous Recombination DNA Repair Defects." JCO Precision Oncology, no. 3 (December 2019): 1–11. http://dx.doi.org/10.1200/po.19.00103.

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PURPOSE Endometrial cancer (EC) is not considered a component of the hereditary breast and ovarian cancer syndrome but can arise in patients with germline BRCA1/2 (g BRCA1/2) mutations. Biallelic BRCA1/2 alterations are associated with genomic features of homologous recombination DNA repair deficiency (HRD) in cancer. We sought to determine if ECs in g BRCA1/2 mutation carriers harbor biallelic alterations and/or features of HRD. METHODS Of 769 patients with EC who underwent germline panel testing, 10 pathogenic g BRCA1/2 mutation carriers were identified, and their tumor- and normal-derived DNA was subjected to massively parallel sequencing targeting at least 410 cancer-related genes. Three g BRCA1/2-associated ECs were identified in 232 ECs subjected to whole-exome sequencing by The Cancer Genome Atlas. Somatic mutations, copy number alterations, loss of heterozygosity, microsatellite instability (MSI), and genomic HRD features were assessed. RESULTS Of the 13 patients included who had EC, eight harbored pathogenic g BRCA1 mutations and five harbored g BRCA2 mutations. Eight (100%) and two (40%) ECs harbored biallelic BRCA1 and BRCA2 alterations through loss of heterozygosity of the wild-type allele. All ECs harbored somatic TP53 mutations. One monoallelic/sporadic g BRCA2-associated EC had MLH1 promoter methylation and was MSI high. High large-scale state transition scores, a genomic feature of HRD, were found only in ECs with bi- but not monoallelic BRCA1/2 alterations. The Signature Multivariate Analysis HRD signature Sig3 was enriched in biallelic g BRCA1/2 ECs, and the three ECs from The Cancer Genome Atlas with BRCA1 biallelic alterations subjected to whole-exome sequencing displayed a dominant HRD-related mutational signature 3. CONCLUSION A subset of g BRCA1/2-associated ECs harbor biallelic BRCA1/2 alterations and genomic features of HRD, which may benefit from homologous recombination–directed treatment regimens. ECs in BRCA2 mutation carriers might be sporadic and even MSI high, and may potentially benefit from immune-checkpoint inhibition.
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Navarro, Daniela, Ani Gasparyan, Francisco Navarrete, et al. "Molecular Alterations of the Endocannabinoid System in Psychiatric Disorders." International Journal of Molecular Sciences 23, no. 9 (2022): 4764. http://dx.doi.org/10.3390/ijms23094764.

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The therapeutic benefits of the current medications for patients with psychiatric disorders contrast with a great variety of adverse effects. The endocannabinoid system (ECS) components have gained high interest as potential new targets for treating psychiatry diseases because of their neuromodulator role, which is essential to understanding the regulation of many brain functions. This article reviewed the molecular alterations in ECS occurring in different psychiatric conditions. The methods used to identify alterations in the ECS were also described. We used a translational approach. The animal models reproducing some behavioral and/or neurochemical aspects of psychiatric disorders and the molecular alterations in clinical studies in post-mortem brain tissue or peripheral tissues were analyzed. This article reviewed the most relevant ECS changes in prevalent psychiatric diseases such as mood disorders, schizophrenia, autism, attentional deficit, eating disorders (ED), and addiction. The review concludes that clinical research studies are urgently needed for two different purposes: (1) To identify alterations of the ECS components potentially useful as new biomarkers relating to a specific disease or condition, and (2) to design new therapeutic targets based on the specific alterations found to improve the pharmacological treatment in psychiatry.
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Barchi, Marco, Elisa Innocenzi, Teresa Giannattasio, Susanna Dolci, Pellegrino Rossi, and Paola Grimaldi. "Cannabinoid Receptors Signaling in the Development, Epigenetics, and Tumours of Male Germ Cells." International Journal of Molecular Sciences 21, no. 1 (2019): 25. http://dx.doi.org/10.3390/ijms21010025.

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Endocannabinoids are natural lipid molecules whose levels are regulated by specific biosynthetic and degradative enzymes. They bind to and activate two main cannabinoid receptors type 1 (CB1) and type 2 (CB2), and together with their metabolizing enzymes form the “endocannabinoid system” (ECS). In the last years, the relevance of endocannabinoids (eCBs) as critical modulators in various aspects of male reproduction has been pointed out. Mammalian male germ cells, from mitotic to haploid stage, have a complete ECS which is modulated during spermatogenesis. Compelling evidence indicate that in the testis an appropriate “eCBs tone”, associated to a balanced CB receptors signaling, is critical for spermatogenesis and for the formation of mature and fertilizing spermatozoa. Any alteration of this system negatively affects male reproduction, from germ cell differentiation to sperm functions, and might have also an impact on testicular tumours. Indeed, most of testicular tumours develop during early germ-cell development in which a maturation arrest is thought to be the first key event leading to malignant transformation. Considering the ever-growing number and complexity of the data on ECS, this review focuses on the role of cannabinoid receptors CB1 and CB2 signaling in male germ cells development from gonocyte up to mature spermatozoa and in the induction of epigenetic alterations in these cells which might be transmitted to the progeny. Furthermore, we present new evidence on their relevance in testicular cancer.
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Wilson-Verdugo, Martí, Brandon Bustos-García, Olga Adame-Guerrero, et al. "Reversal of high-glucose–induced transcriptional and epigenetic memories through NRF2 pathway activation." Life Science Alliance 7, no. 8 (2024): e202302382. http://dx.doi.org/10.26508/lsa.202302382.

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Diabetes complications such as nephropathy, retinopathy, or cardiovascular disease arise from vascular dysfunction. In this context, it has been observed that past hyperglycemic events can induce long-lasting alterations, a phenomenon termed “metabolic memory.” In this study, we evaluated the genome-wide gene expression and chromatin accessibility alterations caused by transient high-glucose exposure in human endothelial cells (ECs) in vitro. We found that cells exposed to high glucose exhibited substantial gene expression changes in pathways known to be impaired in diabetes, many of which persist after glucose normalization. Chromatin accessibility analysis also revealed that transient hyperglycemia induces persistent alterations, mainly in non-promoter regions identified as enhancers with neighboring genes showing lasting alterations. Notably, activation of the NRF2 pathway through NRF2 overexpression or supplementation with the plant-derived compound sulforaphane, effectively reverses the glucose-induced transcriptional and chromatin accessibility memories in ECs. These findings underscore the enduring impact of transient hyperglycemia on ECs’ transcriptomic and chromatin accessibility profiles, emphasizing the potential utility of pharmacological NRF2 pathway activation in mitigating and reversing the high-glucose–induced transcriptional and epigenetic alterations.
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Shishkova, Daria, Arseniy Lobov, Egor Repkin, et al. "Calciprotein Particles Induce Cellular Compartment-Specific Proteome Alterations in Human Arterial Endothelial Cells." Journal of Cardiovascular Development and Disease 11, no. 1 (2023): 5. http://dx.doi.org/10.3390/jcdd11010005.

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Calciprotein particles (CPPs) are indispensable scavengers of excessive Ca2+ and PO43− ions in blood, being internalised and recycled by liver and spleen macrophages, monocytes, and endothelial cells (ECs). Here, we performed a pathway enrichment analysis of cellular compartment-specific proteomes in primary human coronary artery ECs (HCAEC) and human internal thoracic artery ECs (HITAEC) treated with primary (amorphous) or secondary (crystalline) CPPs (CPP-P and CPPs, respectively). Exposure to CPP-P and CPP-S induced notable upregulation of: (1) cytokine- and chemokine-mediated signaling, Ca2+-dependent events, and apoptosis in cytosolic and nuclear proteomes; (2) H+ and Ca2+ transmembrane transport, generation of reactive oxygen species, mitochondrial outer membrane permeabilisation, and intrinsic apoptosis in the mitochondrial proteome; (3) oxidative, calcium, and endoplasmic reticulum (ER) stress, unfolded protein binding, and apoptosis in the ER proteome. In contrast, transcription, post-transcriptional regulation, translation, cell cycle, and cell–cell adhesion pathways were underrepresented in cytosol and nuclear compartments, whilst biosynthesis of amino acids, mitochondrial translation, fatty acid oxidation, pyruvate dehydrogenase activity, and energy generation were downregulated in the mitochondrial proteome of CPP-treated ECs. Differentially expressed organelle-specific pathways were coherent in HCAEC and HITAEC and between ECs treated with CPP-P or CPP-S. Proteomic analysis of mitochondrial and nuclear lysates from CPP-treated ECs confirmed bioinformatic filtration findings.
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Bottiroli, Sara, Rosaria Greco, Valentina Franco, et al. "Peripheral Endocannabinoid Components and Lipid Plasma Levels in Patients with Resistant Migraine and Co-Morbid Personality and Psychological Disorders: A Cross-Sectional Study." International Journal of Molecular Sciences 25, no. 3 (2024): 1893. http://dx.doi.org/10.3390/ijms25031893.

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Resistant migraine characterizes those patients who have failed at least three classes of migraine prophylaxis. These difficult-to-treat patients are likely to be characterized by a high prevalence of psychological disturbances. A dysfunction of the endocannabinoid system (ECS), including alteration in the levels of endocannabinoid congeners, may underlie several psychiatric disorders and the pathogenesis of migraines. Here we explored whether the peripheral gene expression of major components of the ECS and the plasma levels of endocannabinoids and related lipids are associated with psychological disorders in resistant migraine. Fifty-one patients (age = 46.0 ± 11.7) with resistant migraine received a comprehensive psychological evaluation according to the DSM-5 criteria. Among the patients, 61% had personality disorders (PD) and 61% had mood disorders (MD). Several associations were found between these psychological disorders and peripheral ECS alterations. Lower plasma levels of palmitoiletanolamide (PEA) were found in the PD group compared with the non-PD group. The MD group was characterized by lower mRNA levels of diacylglycerol lipase α (DAGLα) and CB2 (cannabinoid-2) receptor. The results suggest the existence of peripheral dysfunction in some components of the ECS and an alteration in plasma levels of PEA in patients with resistant migraine and mood or personality disorders.
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Meyer, Fernando, Juliana Navarro Lizana, Luiz Felipe Dziedricki, and Luiz Fernando Bleggi-Torres. "Histologic alterations of rat kidneys perfused with a Euro-Collins diltiazem solution." Acta Cirurgica Brasileira 25, no. 6 (2010): 496–500. http://dx.doi.org/10.1590/s0102-86502010000600007.

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PURPOSE: Analyse the histologic changes of rat kidneys perfused with isotonic saline solution (ISS), Euro-Collins solution (ECS) and Euro-Collins solution with diltiazem (ECSD). METHODS: Thirty-six Wistar rats were used divided equally, as follow: group A (ISS), group B (ECS) and group C (ECSD). Through a catheter placed into the abdominal aorta, a renal perfusion was performed using a solution according to the group to which the animal belonged. After the complete perfusion, bilateral nephrectomy was performed and the organs were preserved under hypothermia for five distinct periods of time. Glomerulus and tubule were evaluated through optical microscopy. RESULTS: Renal perfusion with ECS and ECSD proved effectiveness in the preservation of the organs up to 36 hours and an increase in the percentage of injured glomeruli was noticed only in the period of 48 hours. CONCLUSIONS: The results showed that exists an association between the tubular injury and the glomeruli lesion degree; kidneys with a higher degree of tubular damage were related to severe glomerular lesion. Also, the addition of a calcium channel blocker, diltiazem, to the ECS for the renal perfusion does not decrease the percentage of glomerular lesion.
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Dorfmüller, P., D. Bazin, S. Aubert, et al. "Crystalline Ultrastructures, Inflammatory Elements, and Neoangiogenesis Are Present in Inconspicuous Aortic Valve Tissue." Cardiology Research and Practice 2010 (2010): 1–7. http://dx.doi.org/10.4061/2010/685926.

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Morbidity from calcific aortic valve disease (CAVD) is increasing. Recent studies suggest early reversible changes involving inflammation and neoangiogenesis. We hypothesized that microcalcifications, chemokines, and growth factors are present in unaffected regions of calcific aortic valves. We studied aortic valves from 4 patients with CAVD and from 1 control, using immunohistochemistry, scanning electron microscopy, and infrared spectrography. We revealed clusters of capillary neovessels in calcified (ECC), to a lesser extent in noncalcified (ECN) areas. Endothelial cells proved constant expression of SDF-1 in ECC, ECN, and endothelial cells from valvular surface (ECS). Its receptor CXCR4 was expressed in ECC. IL-6 expression correlated with CXCR4 staining and presence of lymphocytes. VEGF was expressed by ECS, its receptor by ECC and ECN. Crystalline ultrastructures were found on the surface of histologically noncalcified areas (HNCAs), spectrography revealed calcium hydroxylapatite. Our results demonstrate that crystalline ultrastructures are present in HNCAs, undergoing neoangiogenesis in an inflammatory context. These alterations could be an early witness of disease and an opening to therapy.
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Wang, Xin, Simin Li, Yihong Ma, et al. "Identification of miRNAs as the Crosstalk in the Interaction between Neural Stem/Progenitor Cells and Endothelial Cells." Disease Markers 2020 (December 11, 2020): 1–29. http://dx.doi.org/10.1155/2020/6630659.

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Aim. This study is aimed at identifying genetic and epigenetic crosstalk molecules and their target drugs involved in the interaction between neural stem/progenitor cells (NSPCs) and endothelial cells (ECs). Materials and Methods. Datasets pertaining to reciprocal mRNA and noncoding RNA changes induced by the interaction between NSPCs and ECs were obtained from the GEO database. Differential expression analysis (DEA) was applied to identify NSPC-induced EC alterations by comparing the expression profiles between monoculture of ECs and ECs grown in EC/NSPC cocultures. DEA was also utilized to identify EC-induced NSPC alterations by comparing the expression profiles between monoculture of NSPCs and NSPCs grown in EC/NSPC cocultures. The DEGs and DEmiRNAs shared by NSPC-induced EC alterations and EC-induced NSPC alterations were then identified. Furthermore, miRNA crosstalk analysis and functional enrichment analysis were performed, and the relationship between DEmiRNAs and small molecular drug targets/environment chemical compounds was investigated. Results. One dataset (GSE29759) was included and analyzed in this study. Six genes (i.e., MMP14, TIMP3, LOXL1, CCK, SMAD6, and HSPA2), three miRNAs (i.e., miR-210, miR-230a, and miR-23b), and three pathways (i.e., Akt, ERK1/2, and BMPs) were identified as crosstalk molecules. Six small molecular drugs (i.e., deptropine, fluphenazine, lycorine, quinostatin, resveratrol, and thiamazole) and seven environmental chemical compounds (i.e., folic acid, dexamethasone, choline, doxorubicin, thalidomide, bisphenol A, and titanium dioxide) were identified to be potential target drugs of the identified DEmiRNAs. Conclusion. To conclude, three miRNAs (i.e., miR-210, miR-230a, and miR-23b) were identified to be crosstalks linking the interaction between ECs and NSPCs by implicating in both angiogenesis and neurogenesis. These crosstalk molecules might provide a basis for devising novel strategies for fabricating neurovascular models in stem cell tissue engineering.
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Kra, Gitit, Jayasimha Rayalu Daddam, Uzi Moallem, et al. "Effects of Environmental Heat Load on Endocannabinoid System Components in Adipose Tissue of High Yielding Dairy Cows." Animals 12, no. 6 (2022): 795. http://dx.doi.org/10.3390/ani12060795.

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Environmental heat load (HL) adversely affects the performance of dairy cows. The endocannabinoid system (ECS) regulates metabolism and the stress response, thus we hypothesized that HL may affect the ECS of dairy cows. Our objective was to determine the levels of endocannabinoids (eCBs) and gene and protein expressions of the ECS components in adipose tissue (AT) and plasma of early postpartum (PP) and late-lactation cows. In addition, we examined eCBs in milk, and studied the interaction of eCBs with bovine cannabinoids receptors CB1 and CB2. In the first experiment, plasma and AT were sampled from cows calving during summer (S, n = 9) or winter (W, n = 9). Dry matter intake (DMI) and energy balance (EB) were lower in S vs. W, and relative gene expressions of transient-receptor-potential-cation-channel-subfamily-V-member-1 (TRPV1), the cannabinoid receptors CNR1 (CB1) and CNR2 (CB2), and monoglyceride lipase (MGLL) were decreased in AT of S compared to W. Protein abundance of peroxisome proliferator-activated-receptor-alpha (PPAR-α) was decreased, while tumor-necrosis factor-α (TNF-α) was increased in AT of S vs. W. Other components of the ECS were not different between S and W calving cows. To study whether the degree of HL may affect the ECS, we performed a second experiment with 24 late-lactation cows that were either cooled (CL) or not cooled (heat-stressed; HS) during summer. DMI was lower in HS vs. CL, AT protein abundance of PPAR-α was lower, and TRPV1 tended to be lower in HS vs. CL, but other components of the ECS were not different between groups. Milk levels of 2-arachidonoylglycerol (2-AG) tended to increase in HS vs. CL. Additionally, modeling of the bovine cannabinoid receptors demonstrated their binding to anandamide and 2-AG. Environmental HL, possibly via lower intake, is associated with limited alterations in ECS components in AT of dairy cows.
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Dissertations / Theses on the topic "ECS alterations"

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Tzong-Shi, Lu. "The effects of preconditioning heat shock treatment on vascular permeability alteration." 2004. http://www.cetd.com.tw/ec/thesisdetail.aspx?etdun=U0011-2903200614010700.

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Ruo-Chia, Tseng. "Genome-wide Allelotyping of Non-small Cell Lung Cancer:Novel Region of Allelic Loss,Refined Mapping of Novel Tumor Suppressor Genes and Their Alteration Analyses." 2004. http://www.cetd.com.tw/ec/thesisdetail.aspx?etdun=U0021-2004200712161468.

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Books on the topic "ECS alterations"

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Kelman, Melanie C. Hydrothermal alteration of a supra-subduction zone ophiolite analog, Tonga, Southwest Pacific. 1998.

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Silvestri, Rosalia. Sleep in older adults. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0050.

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Significant and progressive sleep alterations occur in elderly people, including both circadian and ultradian modifications of sleep. Among these, reduced melatonin and a diminished role of environmental zeitgebers impair sleep rhythmicity, with a tendency toward polyphasic sleep and excessive daytime sleepiness (EDS). The loss of slow-wave sleep (SWS) and EDS are significant, along with behavioral and cognitive alterations in patients with dementia. Sleep disordered breathing (SDB) and restless legs syndrome (RLS)/Willis–Ekbom disease may further aggravate the burden of insomnia and sleep fragmentation, thereby favoring multiple nocturnal arousals with sympathetic activation and cardiovascular dysfunction.
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Patisaul, Heather B., and Scott M. Belcher. Endocrine Disruptors and Neurobehavioral Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780199935734.003.0006.

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This chapter focuses on the role environmental pollutants are playing in the rapidly rising rate of neurodevelopmental disorders in children. The available EDC data are summarized and analyzed in relation to whether or not evidence supports a role for EDCs as contributing to neural disorders. The distinction between endocrine disruption and neurotoxicity is established by focusing on the differences between toxicants, toxins, and altered endocrine/neuroendocrine effects in organizational alterations of the brain. Evidence from experimental systems demonstrating effects of EDCs on the developing brain and the potential roles for EDCs as bad actors in rising rates of autism spectrum disorder (ASD), and attention deficit hyperactivity disorder (ADHD) are presented in detail. Additional impacts of EDCs on neurodegenerative disorders, including Parkinsons’s disease, are reviewed. The mechanisms of rotenone and paraquat neurodegeneration are compared and contrasted with the evidence and mechanisms of actions for organochlorine and organophosphate pesticides in Parkinsons’s disease.
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Lennon, Rachel, and Neil Turner. The molecular basis of glomerular basement membrane disorders. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0320_update_001.

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The glomerular basement membrane (GBM) is a condensed network of extracellular matrix molecules which provides a scaffold and niche to support the function of the overlying glomerular cells. Within the glomerulus, the GBM separates the fenestrated endothelial cells, which line capillary walls from the epithelial cells or podocytes, which cover the outer aspect of the capillaries. In common with basement membranes throughout the body, the GBM contains core components including collagen IV, laminins, nidogens, and heparan sulphate proteoglycans. However, specific isoforms of these proteins are required to maintain the integrity of the glomerular filtration barrier.Across the spectrum of glomerular disease there is alteration in glomerular extracellular matrix (ECM) and a number of histological patterns are recognized. The GBM can be thickened, expanded, split, and irregular; the mesangial matrix may be expanded and glomerulosclerosis represents a widespread accumulation of ECM proteins associated with loss of glomerular function. Whilst histological patterns may follow a sequence or provide diagnostic clues, there remains limited understanding about the mechanisms of ECM regulation and how this tight control is lost in glomerular disease. Monogenic disorders of the GBM including Alport and Pierson syndromes have highlighted the importance of both collagen IV and laminin isoforms and these observations provide important insights into mechanisms of glomerular disease.
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Book chapters on the topic "ECS alterations"

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Gertsch, Marc. "Alterations of Repolarization." In The ECG. Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-662-10315-9_18.

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Eberhard, Matthias. "Chest Manifestation of Cardiac Disease." In IDKD Springer Series. Springer Nature Switzerland, 2025. https://doi.org/10.1007/978-3-031-83872-9_19.

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Abstract Non-electrocardiographically (ECG)-gated chest CT is primarily used for lung evaluation but can also reveal critical cardiovascular findings. Significant incidental cardiac findings may include chamber enlargement, cardiac shunts (both intracardiac and extracardiac), valvular disease, coronary artery disease, myocardial and pericardial abnormalities, and cardiac masses. Cardiac conditions can also cause secondary effects such as vascular changes, mediastinal lymphadenopathy, and alterations in the lung parenchyma. This chapter discusses common cardiac manifestations seen on non-ECG-gated chest CT.
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Cai, Hang, and Krishna K. Venkatasubramanian. "Detecting Malicious Temporal Alterations of ECG Signals in Body Sensor Networks." In Network and System Security. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-25645-0_41.

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Mencio, Caitlin, Kuberan Balagurunathan, and Franz Goller. "Enzymatic Alteration of ECM to Explore Muscle Function and Motor Control of a Learned Behavior." In Methods in Molecular Biology. Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1398-6_39.

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Rosano, Giuseppe. "The gut and cardiovascular diseases." In ESC CardioMed. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0265.

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The physiological functioning of the gut is central for the pharmacokinetics of orally administered cardiovascular drugs and alteration of the gut homeostasis may have relevant repercussions on the effect of these drugs. The gut microbiome may affect the absorption and metabolism of nutrients favouring the development of obesity and diabetes. Furthermore, alterations in intestinal barrier permeability lead to the penetration of bacteria and bacterial wall products into the circulation and may contribute to the progression of atherosclerosis and worsening of heart failure. Despite the suggestions of the possible interaction between the gut and the cardiovascular system and of stimulating novel mechanisms for disease progression that may open to new therapeutic approaches, the available evidence must be considered preliminary.
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Ewen, Sebastian, Saarraaken Kulenthiran, and Felix Mahfoud. "Alterations in cardiovascular physiology in pathological states." In ESC CardioMed, edited by Guido Grassi. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0030_update_001.

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Increased activity of the sympathetic nervous system has been identified as a main contributor to the development and maintenance of numerous cardiovascular diseases including hypertension, chronic heart failure, supraventricular and ventricular arrhythmias, and valve disorders. This chapter aims to give an overview of the pathophysiological background of these disorders.
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Bertero, Edoardo, and Christoph Maack. "Alterations in myocardial metabolism." In The ESC Textbook of Heart Failure, edited by Petar M. Seferović, Andrew J. S. Coats, Gerasimos Filippatos, Stefan D. Anker, Johann Bauersachs, and Giuseppe Rosano. Oxford University PressOxford, 2023. http://dx.doi.org/10.1093/med/9780198891628.003.0021.

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Abstract The heart requires enormous amounts of energy in the form of adenosine triphosphate (ATP) that is mostly produced in mitochondria via oxidative phosphorylation. As an ‘omnivore’, the heart flexibly utilizes fatty acids, glucose, amino acids, lactate, and ketones. In patients with heart failure (HF), reduced phosphocreatine-to-ATP ratios predict adverse outcomes, coining the term of the failing heart as an ‘engine out of fuel’. However, metabolic dysfunction in HF goes far beyond a mere energetic deficit and involves alterations in substrate utilization, intermediary metabolism, and mitochondrial redox regulation that conspire to alter excitation–contraction (EC) coupling and dysregulate nutrient signalling pathways through epigenetic or post-translational control mechanisms. In contrast, defects in EC coupling and pathological cardiac workload in HF deteriorate energy supply-and-demand matching, to which the Krebs cycle with its key role in energy conversion, antioxidation, and production of metabolic intermediates is central. This chapter integrates cardiac metabolism with function and explains how this intricate relation is perturbed in the failing heart.
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Wei, Janet, and C. Noel Bairey Merz. "General considerations." In ESC CardioMed, edited by Vera Zagrosek-Regitz. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0685.

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Given the increased morbidity and mortality in pregnant women with cardiovascular disease, it is important for clinicians to understand how to manage cardiovascular disease during pregnancy. This chapter discusses epidemiology, haemodynamic, haemostatic, and metabolic alterations during pregnancy, genetic testing and counselling, cardiovascular diagnosis in pregnancy, and infective endocarditis.
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Díez, Javier, and Hans-Peter Brunner-La Rocca. "Ventricular remodelling." In The ESC Textbook of Heart Failure, edited by Petar M. Seferović, Andrew J. S. Coats, Gerasimos Filippatos, Stefan D. Anker, Johann Bauersachs, and Giuseppe Rosano. Oxford University PressOxford, 2023. http://dx.doi.org/10.1093/med/9780198891628.003.0022.

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Abstract The term ventricular remodelling refers to alterations in size, shape, and function due to the response of the ventricle to sustained stress. Initially, the remodelling response to pathological stress helps in compensating the cardiac performance, but over time the response becomes maladaptive and leads to ventricular dysfunction. Thus, adverse ventricular remodelling is critically involved in the development of heart failure and its poor clinical outcome. Depending on the underlying pathology, the ventricle can remodel either concentrically or eccentrically. At the myocardial level, the adverse remodelling process implies tissue alterations involving the cardiomyocyte, interstitium, and microcirculation, as well as metabolic and electrophysiological alterations. Multiple mechanisms participate in the development of these alterations, highlighting the complexity and heterogeneity of the remodelling process. Understanding these mechanisms is necessary for both preventing and effectively reversing ventricular remodelling with therapy in heart failure patients.
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Mulvagh, Sharon. "Valvular heart disease." In ESC CardioMed, edited by Noel Bairey Merz. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0681.

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Traditionally, sex differences in valvular heart disease have been described as those related to the epidemiologic predominance of rheumatic heart disease in women, particularly as exacerbated by the physiologic alterations during pregnancy. However, it has been recently recognized that valvular heart disease manifestations, and responses to interventions, demonstrate sex-specific differences in presentation, treatments, and outcomes in women when compared to men. Smaller anatomic size may contribute to some of these differences, but primarily as yet undetermined factors appear to be causative.
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Conference papers on the topic "ECS alterations"

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Jiang, Frank X., Uday Chippada, Lulu Li, et al. "The Effect of Dynamic Alterations in Stiffness of the Substrate on Cell Growth." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206291.

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Cells reside in a dynamic environment composed of extracellular matrix (ECM) and other cells, and take a variety of cues, of which mechanical stresses and strains are an important subset. ECM undergoes constant synthesis and degradation, and its mechanical stiffness can also be altered, with ageing, upon external assault or via pathological processes. Particularly in load barring tissues, the mechanical properties of the ECM can vary, by exposure to changing load conditions through, for example, collagen realignment. Tissue-implant interfaces also present medically important dynamic mechanical environment. Furthermore, recent studies revealed that the ranges of mechanical stiffness of ECM or substrates can alter specific cellular properties in distinct ways. From an engineering viewpoint, it is thus beneficial to be able to modify the physical properties of the biomaterials for the implants, providing optimal conditions for a specific desired outcome at different points during time progression. All of these reasons make it desirable to have a dynamic culture system with controlled property changes.
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Cai, Hang, and Krishna K. Venkatasubramanian. "Detecting Signal Injection Attack-Based Morphological Alterations of ECG Measurements." In 2016 International Conference on Distributed Computing in Sensor Systems (DCOSS). IEEE, 2016. http://dx.doi.org/10.1109/dcoss.2016.36.

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Ogger, P., T. Maher, C. Lloyd, and A. Byrne. "Distinct metabolic alterations in airway macrophages during pulmonary fibrosis." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.lsc-1190.

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Cottee, Alice, Leigh Seccombe, Cindy Thamrin, Gregory King, Matthew Peters, and Claude Farah. "Alterations in oxygen consumption during acute exacerbations of COPD." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa2421.

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Devilliers, Maëva A., Audrey Brisebarre, Laure Petit, et al. "Identification of molecular candidates of cilia-associated alterations in asthma." In ERS Congress 2024 abstracts. European Respiratory Society, 2024. http://dx.doi.org/10.1183/13993003.congress-2024.pa2653.

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Daniels, Ivana, Taiya Edwards, Britney Nilli, et al. "Alteration of airway pH by asthma-relevant cytokines." In ERS Congress 2024 abstracts. European Respiratory Society, 2024. http://dx.doi.org/10.1183/13993003.congress-2024.pa2667.

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Gudiel Arriaza, Paola, Amparo Sánchez Serrano, J. Luis Fernández Sánchez, and Laura Sierra. "Myocardial alterations in asymptomatic patients with obstructive sleep apnea syndrome." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa2326.

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Salgado Fernández, Fernanda, Dulce González Islas, Arturo Orea Tejeda, et al. "Body composition alterations and endothelial dysfunction in COPD and HF." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa2656.

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Gao, Jing, Petra Um-Bergström, Melvin Pourbazargan, et al. "Alterations in measures of systemic inflammation among adults born preterm." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa4349.

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Fernandez Criado, Maria Del Carmen, Antonio Javier Cruz Medina, Cristina Carrasco Carrasco, Javier Díez Sierra, and Francisco Campos Rodriguez. "Spirometric alterations in patients studied for suspected sleep-disordered breathing." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa2523.

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Reports on the topic "ECS alterations"

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Ozias-Akins, P., and R. Hovav. molecular dissection of the crop maturation trait in peanut. United States-Israel Binational Agricultural Research and Development Fund, 2020. http://dx.doi.org/10.32747/2020.8134157.bard.

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Crop maturation is one of the most recognized characteristics of peanut, and it is crucial for adaptability and yield. However, not much is known regarding its genetic and molecular control. The goals of this project were to study the molecular-genetic components that control crop maturation in peanut and identify candidate genes. Crop maturation was studied directly by phenotyping the maturity level or through other component traits such as flowering pattern and branching habit. Six different RIL populations (HH, RR, CC, FNC, TGT and FLIC) were used for the genetic analysis. In total, 14 QTLs were found for maturity level. The phenotypic explanation values ranged in 5.3%-18.6%. Common QTL were found between maturity level and harvest index (in RR and CC populations), branching habit (in HH population), flowering pattern/branching rate (in CC and TGT populations) and pod size (in CC population). Further investigations were done to define genes that control maturity level and the component traits. A map-based cloning approach was used to identify a major candidate gene for branching habit - a novel AhMADS-box gene (AhMADS). AhMADS was mainly expressed in the lateral shoot, the organ in which the difference between branching habit occurs. Sequence alignment analysis found SNPs in AhMADS that cause to exon/intron splicing alterations. Overexpression study of AhMADs-box in tobacco under 35S control revealed one line with a spreading-like lateral shoot indicating that AhMADS may be the causing effect of BH and therefore indirectly controls maturity level. In addition, several candidate genes were defined that may control flowering pattern. An RNA expression study was performed on two parental lines, Tifrunner and GT-C20, identifying four candidate genes in the flowering regulatory pathway that were down-regulated at the mainstem (non-flowering) compared to the first (flowering) shoot, indicating their influence on flowering pattern. Also, another candidate gene was identified, Terminal Flowering 1-like (AhTFL1), which was located within a small segment in chromosome B02. A 1492 bp deletion was found in AhTFL1 that completely co-segregates with the flowering pattern phenotype in the CC population and two independent EMS-mutagenized M2 families. AhTFL1 was significantly less expressed in flowering than non-flowering branches. Finally, a field trial showed that an EMS line (B78) mutagenized in AhTFL1 is ~18% days earlier than the control (Hanoch). In conclusion, our study revealed new insights into the molecular basis for the fundamentally important crop maturity trait in peanut. The results generated new information and materials that will promote informed targeting of peanut idiotypes by indirect selection and genomic breeding approaches.
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Li, Li, Joseph Burger, Nurit Katzir, Yaakov Tadmor, Ari Schaffer, and Zhangjun Fei. Characterization of the Or regulatory network in melon for carotenoid biofortification in food crops. United States Department of Agriculture, 2015. http://dx.doi.org/10.32747/2015.7594408.bard.

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The general goals of the BARD research grant US-4423-11 are to understand how Or regulates carotenoid accumulation and to reveal novel strategies for breeding agricultural crops with enhanced β-carotene level. The original objectives are: 1) to identify the genes and proteins in the Or regulatory network in melon; 2) to genetically and molecularly characterize the candidate genes; and 3) to define genetic and functional allelic variation of these genes in a representative germplasm collection of the C. melo species. Or was found by the US group to causes provitamin A accumulation in chromoplasts in cauliflower. Preliminary genetic study from the Israeli group revealed that the melon Or gene (CmOr) completely co-segregated with fruit flesh color in a segregating mapping population and in a wide melon germplasm collection, which set the stage for the funded research. Major conclusions and achievements include: 1). CmOris proved to be the gene that controls melon fruit flesh color and represents the previously described gflocus in melon. 2). Genetic and molecular analyses of CmOridentify and confirm a single SNP that is responsible for the orange and non-orange phenotypes in melon fruit. 3). Alteration of the evolutionarily conserved arginine in an OR protein to both histidine or alanine greatly enhances its ability to promote carotenoid accumulation. 4). OR promotes massive carotenoid accumulation due to its dual functions in regulating both chromoplast biogenesis and carotenoid biosynthesis. 5). A bulk segregant transcriptome (BSRseq) analysis identifies a list of genes associated with the CmOrregulatory network. 6). BSRseq is proved to be an effective approach for gene discovery. 7). Screening of an EMS mutation library identifies a low β mutant, which contains low level of carotenoids due to a mutation in CmOrto produce a truncated form of OR protein. 8). low β exhibits lower germination rate and slow growth under salt stress condition. 9). Postharvest storage of fruit enhances carotenoid accumulation, which is associated with chromoplast development. Our research uncovers the molecular mechanisms underlying the Or-regulated high level of carotenoid accumulation via regulating carotenoidbiosynthetic capacity and storage sink strength. The findings provide mechanistic insights into how carotenoid accumulation is controlled in plants. Our research also provides general and reliable molecular markers for melon-breeding programs to select orange varieties, and offers effective genetic tools for pro-vitamin A enrichment in other important crops via the rapidly developed genome editing technology. The newly discovered low β mutant could lead to a better understanding of the Or gene function and its association with stress response, which may explain the high conservation of the Or gene among various plant species.
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