Relevant bibliographies by topics / CASQ1

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Academic literature on the topic 'CASQ1'

Author: Grafiati
Published: 14 March 2023

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Journal articles on the topic "CASQ1"

1

Sun, Zhipeng, Luqi Wang, Lu Han, Yue Wang, Yuan Zhou, Qiang Li, Yongquan Wu, et al. "Functional Calsequestrin-1 Is Expressed in the Heart and Its Deficiency Is Causally Related to Malignant Hyperthermia-Like Arrhythmia." Circulation 144, no. 10 (September 7, 2021): 788–804. http://dx.doi.org/10.1161/circulationaha.121.053255.

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Background: Calsequestrins (Casqs), comprising the Casq1 and Casq2 isoforms, buffer Ca 2+ and regulate its release in the sarcoplasmic reticulum of skeletal and cardiac muscle, respectively. Human inherited diseases associated with mutations in CASQ1 or CASQ2 include malignant hyperthermia/environmental heat stroke (MH/EHS) and catecholaminergic polymorphic ventricular tachycardia. However, patients with an MH/EHS event often experience arrhythmia for which the underlying mechanism remains unknown. Methods: Working hearts from conventional ( Casq1 -KO) and cardiac-specific ( Casq1 -CKO) Casq1 knockout mice were monitored in vivo and ex vivo by ECG and electric mapping, respectively. MH was induced by 2% isoflurane and treated intraperitoneally with dantrolene. Time-lapse imaging was used to monitor intracellular Ca 2+ activity in isolated mouse cardiomyocytes or neonatal rat ventricular myocytes with knockdown, overexpression, or truncation of the Casq1 gene. Conformational change in both Casqs was determined by cross-linking Western blot analysis. Results: Like patients with MH/EHS, Casq1 -KO and Casq1 -CKO mice had faster basal heart rate and ventricular tachycardia on exposure to 2% isoflurane, which could be relieved by dantrolene. Basal sinus tachycardia and ventricular ectopic electric triggering also occurred in Casq1 -KO hearts ex vivo. Accordingly, the ventricular cardiomyocytes from Casq1 -CKO mice displayed dantrolene-sensitive increased Ca 2+ waves and diastole premature Ca 2+ transients/oscillations on isoflurane. Neonatal rat ventricular myocytes with Casq1-knockdown had enhanced spontaneous Ca 2+ sparks/transients on isoflurane, whereas cells overexpressing Casq1 exhibited decreased Ca 2+ sparks/transients that were absent in cells with truncation of 9 amino acids at the C terminus of Casq1. Structural evaluation showed that most of the Casq1 protein was present as a polymer and physically interacted with ryanodine receptor-2 in the ventricular sarcoplasmic reticulum. The Casq1 isoform was also expressed in human myocardium. Mechanistically, exposure to 2% isoflurane or heating at 41 °C induced Casq1 oligomerization in mouse ventricular and skeletal muscle tissues, leading to a reduced Casq1/ryanodine receptor-2 interaction and increased ryanodine receptor-2 activity in the ventricle. Conclusions: Casq1 is expressed in the heart, where it regulates sarcoplasmic reticulum Ca 2+ release and heart rate. Casq1 deficiency independently causes MH/EHS-like ventricular arrhythmia by trigger-induced Casq1 oligomerization and a relief of its inhibitory effect on ryanodine receptor-2–mediated Ca 2+ release, thus revealing a new inherited arrhythmia and a novel mechanism for MH/EHS arrhythmogenesis.
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Paolini, Cecilia, Marco Quarta, Marco Dainese, Mirta Tomasi, Marta Canato, Alessandra Nori, Bjorn C. Knollmann, Paul D. Allen, Carlo Reggiani, and Feliciano Protasi. "Initial Characterization of CASQ1/CASQ2 Knockout (double CASQ-Null) Mice." Biophysical Journal 98, no. 3 (January 2010): 546a—547a. http://dx.doi.org/10.1016/j.bpj.2009.12.2963.

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Woo, Jin Seok, Seung Yeon Jeong, Ji Hee Park, Jun Hee Choi, and Eun Hui Lee. "Calsequestrin: a well-known but curious protein in skeletal muscle." Experimental & Molecular Medicine 52, no. 12 (December 2020): 1908–25. http://dx.doi.org/10.1038/s12276-020-00535-1.

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AbstractCalsequestrin (CASQ) was discovered in rabbit skeletal muscle tissues in 1971 and has been considered simply a passive Ca2+-buffering protein in the sarcoplasmic reticulum (SR) that provides Ca2+ ions for various Ca2+ signals. For the past three decades, physiologists, biochemists, and structural biologists have examined the roles of the skeletal muscle type of CASQ (CASQ1) in skeletal muscle and revealed that CASQ1 has various important functions as (1) a major Ca2+-buffering protein to maintain the SR with a suitable amount of Ca2+ at each moment, (2) a dynamic Ca2+ sensor in the SR that regulates Ca2+ release from the SR to the cytosol, (3) a structural regulator for the proper formation of terminal cisternae, (4) a reverse-directional regulator of extracellular Ca2+ entries, and (5) a cause of human skeletal muscle diseases. This review is focused on understanding these functions of CASQ1 in the physiological or pathophysiological status of skeletal muscle.
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Jeong, Seung Yeon, Mi Ri Oh, Jun Hee Choi, Jin Seok Woo, and Eun Hui Lee. "Calsequestrin 1 Is an Active Partner of Stromal Interaction Molecule 2 in Skeletal Muscle." Cells 10, no. 11 (October 20, 2021): 2821. http://dx.doi.org/10.3390/cells10112821.

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Calsequestrin 1 (CASQ1) in skeletal muscle buffers and senses Ca2+ in the sarcoplasmic reticulum (SR). CASQ1 also regulates store-operated Ca2+ entry (SOCE) by binding to stromal interaction molecule 1 (STIM1). Abnormal SOCE and/or abnormal expression or mutations in CASQ1, STIM1, or STIM2 are associated with human skeletal, cardiac, or smooth muscle diseases. However, the functional relevance of CASQ1 along with STIM2 has not been studied in any tissue, including skeletal muscle. First, in the present study, it was found by biochemical approaches that CASQ1 is bound to STIM2 via its 92 N-terminal amino acids (C1 region). Next, to examine the functional relevance of the CASQ1-STIM2 interaction in skeletal muscle, the full-length wild-type CASQ1 or the C1 region was expressed in mouse primary skeletal myotubes, and the myotubes were examined using single-myotube Ca2+ imaging experiments and transmission electron microscopy observations. The CASQ1-STIM2 interaction via the C1 region decreased SOCE, increased intracellular Ca2+ release for skeletal muscle contraction, and changed intracellular Ca2+ distributions (high Ca2+ in the SR and low Ca2+ in the cytosol were observed). Furthermore, the C1 region itself (which lacks Ca2+-buffering ability but has STIM2-binding ability) decreased the expression of Ca2+-related proteins (canonical-type transient receptor potential cation channel type 6 and calmodulin 1) and induced mitochondrial shape abnormalities. Therefore, in skeletal muscle, CASQ1 plays active roles in Ca2+ movement and distribution by interacting with STIM2 as well as Ca2+ sensing and buffering.
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Serano, Matteo, Laura Pietrangelo, Cecilia Paolini, Flavia A. Guarnier, and Feliciano Protasi. "Oxygen Consumption and Basal Metabolic Rate as Markers of Susceptibility to Malignant Hyperthermia and Heat Stroke." Cells 11, no. 16 (August 9, 2022): 2468. http://dx.doi.org/10.3390/cells11162468.

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Calsequestrin 1 (CASQ1) and Ryanodine receptor 1 (RYR1) are two of the main players in excitation–contraction (EC) coupling. CASQ1-knockout mice and mice carrying a mutation in RYR1 (Y522S) linked to human malignant hyperthermia susceptibility (MHS) both suffer lethal hypermetabolic episodes when exposed to halothane (MHS crises) and to environmental heat (heat stroke, HS). The phenotype of Y522S is more severe than that of CASQ1-null mice. As MHS and HS are hypermetabolic responses, we studied the metabolism of adult CASQ1-null and Y522S mice using wild-type (WT) mice as controls. We found that CASQ1-null and Y522S mice have increased food consumption and higher core temperature at rest. By indirect calorimetry, we then verified that CASQ1-null and Y522S mice show an increased oxygen consumption and a lower respiratory quotient (RQ). The accelerated metabolism of CASQ1-null and Y522S mice was also accompanied with a reduction in body fat. Moreover, both mouse models displayed increased oxygen consumption and a higher core temperature during heat stress. The results collected suggest that metabolic rate, oxygen consumption, and body temperature at rest, all more elevated in Y522S than in CASQ1-null mice, could possibly be used as predictors of the level of susceptibility to hyperthermic crises of mice (and possibly humans).
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Kraeva, Natalia, Elena Zvaritch, Wanda Frodis, Olga Sizova, Alexander Kraev, David H. MacLennan, and Sheila Riazi. "CASQ1 Gene Is an Unlikely Candidate for Malignant Hyperthermia Susceptibility in the North American Population." Anesthesiology 118, no. 2 (February 1, 2013): 344–49. http://dx.doi.org/10.1097/01.anes.0000530185.78660.da.

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Abstract Background Malignant hyperthermia (MH, MIM# 145600) is a complex pharmacogenetic disorder that is manifested in predisposed individuals as a potentially lethal reaction to volatile anesthetics and depolarizing muscle relaxants. Studies of CASQ1-null mice have shown that CASQ1, encoding calsequestrin 1, the major Ca2+ binding protein in the lumen of the sarcoplasmic reticulum, is a candidate gene for MH in mice. The aim of this study was to establish whether the CASQ1 gene is associated with MH in the North American population. Methods The entire coding region of CASQ1 in 75 unrelated patients diagnosed by caffeine-halothane contracture test as MH susceptible (MHS) was analyzed by DNA sequencing. Subsequently, three groups of unrelated individuals (130 MHS, 100 MH negative, and 192 normal controls) were genotyped for a variant that was identified by sequencing. Levels of CASQ1 expression in the muscle from unrelated MHS and MH negative individuals were estimated by Western blotting. Results Screening of the entire coding sequence of the CASQ1 gene in 75 MHS patients revealed a single variant c.260T > C (p.Met87Thr) in exon 1. This variant is unlikely to be pathogenic, because its allele frequency in the MHS group was not significantly different from that of controls. There was also no difference in calsequestrin 1 protein levels between muscle samples from MHS and controls, including those carrying the p.Met87Thr variant. Conclusions This study revealed a low level of protein coding sequence variability within the human CASQ1 gene, indicating that CASQ1 is not a major MHS locus in the North American population.
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Tomasi, Mirta, Marta Canato, Cecilia Paolini, Marco Dainese, Carlo Reggiani, Pompeo Volpe, Feliciano Protasi, and Alessandra Nori. "Calsequestrin (CASQ1) rescues function and structure of calcium release units in skeletal muscles of CASQ1-null mice." American Journal of Physiology-Cell Physiology 302, no. 3 (February 2012): C575—C586. http://dx.doi.org/10.1152/ajpcell.00119.2011.

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Amplitude of Ca2+ transients, ultrastructure of Ca2+ release units, and molecular composition of sarcoplasmic reticulum (SR) are altered in fast-twitch skeletal muscles of calsequestrin-1 (CASQ1)-null mice. To determine whether such changes are directly caused by CASQ1 ablation or are instead the result of adaptive mechanisms, here we assessed ability of CASQ1 in rescuing the null phenotype. In vivo reintroduction of CASQ1 was carried out by cDNA electro transfer in flexor digitorum brevis muscle of the mouse. Exogenous CASQ1 was found to be correctly targeted to the junctional SR (jSR), as judged by immunofluorescence and confocal microscopy; terminal cisternae (TC) lumen was filled with electron dense material and its width was significantly increased, as judged by electron microscopy; peak amplitude of Ca2+ transients was significantly increased compared with null muscle fibers transfected only with green fluorescent protein (control); and finally, transfected fibers were able to sustain cytosolic Ca2+ concentration during prolonged tetanic stimulation. Only the expression of TC proteins, such as calsequestrin 2, sarcalumenin, and triadin, was not rescued as judged by Western blot. Thus our results support the view that CASQ1 plays a key role in both Ca2+ homeostasis and TC structure.
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Semplicini, Claudio, Cinzia Bertolin, Luca Bello, Boris Pantic, Francesca Guidolin, Sara Vianello, Francesco Catapano, et al. "The clinical spectrum of CASQ1-related myopathy." Neurology 91, no. 17 (September 26, 2018): e1629-e1641. http://dx.doi.org/10.1212/wnl.0000000000006387.

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ObjectiveTo identify and characterize patients with calsequestrin 1 (CASQ1)–related myopathy.MethodsPatients selected according to histopathologic features underwent CASQ1 genetic screening. CASQ1-mutated patients were clinically evaluated and underwent muscle MRI. Vacuole morphology and vacuolated fiber type were characterized.ResultsTwenty-two CASQ1-mutated patients (12 families) were identified, 21 sharing the previously described founder mutation (p.Asp244Gly) and 1 with the p.Gly103Asp mutation. Patients usually presented in the sixth decade with exercise intolerance and myalgias and later developed mild to moderate, slowly progressive proximal weakness with quadriceps atrophy and scapular winging. Muscle MRI (n = 11) showed a recurrent fibrofatty substitution pattern. Three patients presented subclinical cardiac abnormalities. Muscle histopathology in patients with p.Asp244Gly showed vacuoles in type II fibers appearing empty in hematoxylin-eosin, Gomori, and nicotinamide adenine dinucleotide (NADH) tetrazolium reductase stains but strongly positive for sarcoplasmic reticulum proteins. The muscle histopathology of p.Gly103Asp mutation was different, showing also NADH-positive accumulation consistent with tubular aggregates.ConclusionsWe report the clinical and molecular details of the largest cohort of CASQ1-mutated patients. A possible heart involvement is presented, further expanding the phenotype of the disease. One mutation is common due to a founder effect, but other mutations are possible. Because of a paucity of symptoms, it is likely that CASQ1 mutations may remain undiagnosed if a muscle biopsy is not performed.
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Guarnier, Flávia Alessandra, Antonio Michelucci, Matteo Serano, Laura Pietrangelo, Claudia Pecorai, Simona Boncompagni, and Feliciano Protasi. "Aerobic Training Prevents Heatstrokes in Calsequestrin-1 Knockout Mice by Reducing Oxidative Stress." Oxidative Medicine and Cellular Longevity 2018 (2018): 1–14. http://dx.doi.org/10.1155/2018/4652480.

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Calsequestrin-1 knockout (CASQ1-null) mice suffer lethal episodes when exposed to strenuous exercise and environmental heat, crises known as exertional/environmental heatstroke (EHS). We previously demonstrated that administration of exogenous antioxidants (N-acetylcysteine and trolox) reduces CASQ1-null mortality during exposure to heat. As aerobic training is known to boost endogenous antioxidant protection, we subjected CASQ1-null mice to treadmill running for 2 months at 60% of their maximal speed for 1 h, 5 times/week. When exposed to heat stress protocol (41°C/1 h), the mortality rate of CASQ1-null mice was significantly reduced compared to untrained animals (86% versus 16%). Protection from heatstrokes was accompanied by a reduced increase in core temperature during the stress protocol and by an increased threshold of response to caffeine of isolated extensor digitorum longus muscles during in vitro contracture test. At cellular and molecular levels, aerobic training (i) improved mitochondrial function while reducing their damage and (ii) lowered calpain activity and lipid peroxidation in membranes isolated from sarcoplasmic reticulum and mitochondria. Based on this evidence, we hypothesize that the protective effect of aerobic training is essentially mediated by a reduction in oxidative stress during exposure of CASQ1-null mice to adverse environmental conditions.
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Michelucci, Antonio, Cecilia Paolini, Marta Canato, Lan Wei-Lapierre, Laura Pietrangelo, Alessandro De Marco, Carlo Reggiani, Robert T. Dirksen, and Feliciano Protasi. "Antioxidants Protect Calsequestrin-1 Knockout Mice from Halothane- and Heat-induced Sudden Death." Anesthesiology 123, no. 3 (September 1, 2015): 603–17. http://dx.doi.org/10.1097/aln.0000000000000748.

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Abstract Background: Mice lacking calsequestrin-1 (CASQ1-null), a Ca2+-binding protein that modulates the activity of Ca2+ release in the skeletal muscle, exhibit lethal hypermetabolic episodes that resemble malignant hyperthermia in humans when exposed to halothane or heat stress. Methods: Because oxidative species may play a critical role in malignant hyperthermia crises, we treated CASQ1-null mice with two antioxidants, N-acetylcysteine (NAC, Sigma-Aldrich, Italy; provided ad libitum in drinking water) and (±)-6-hydroxy-2,5,7,8-tetramethylchromane-2-carboxylic acid (Trolox, Sigma-Aldrich; administered by intraperitoneal injection), before exposure to halothane (2%, 1 h) or heat (41°C, 1 h). Results: NAC and Trolox significantly protected CASQ1-null mice from lethal episodes, with mortality being 79% (n = 14), 25% (n = 16), and 20% (n = 5) during halothane exposure and 86% (n = 21), 29% (n = 21), and 33% (n = 6) during heat stress in untreated, NAC-treated, and Trolox-treated mice, respectively. During heat challenge, an increase in core temperature in CASQ1-null mice (42.3° ± 0.1°C, n=10) was significantly reduced by both NAC and Trolox (40.6° ± 0.3°C, n = 6 and 40.5° ± 0.2°C, n = 6). NAC treatment of CASQ1-null muscles/mice normalized caffeine sensitivity during in vitro contracture tests, Ca2+ transients in single fibers, and significantly reduced the percentage of fibers undergoing rhabdomyolysis (37.6 ± 2.5%, 38/101 fibers in 3 mice; 11.6 ± 1.1%, 21/186 fibers in 5 mice). The protective effect of antioxidant treatment likely resulted from mitigation of oxidative stress, because NAC reduced mitochondrial superoxide production, superoxide dismutase type-1 expression, and 3-nitrotyrosine expression, and increased both reduced glutathione and reduced glutathione/oxidized glutathione ratio. Conclusion: These studies provide a deeper understanding of the mechanisms that underlie hyperthermic crises in CASQ1-deficient muscle and demonstrate that antioxidant pretreatment may prevent them.
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Dissertations / Theses on the topic "CASQ1"

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DEL, RE VALERIA. "Characterization of Calsequestrin-1 mutations in patients affected by myopathies." Doctoral thesis, Università di Siena, 2017. http://hdl.handle.net/11365/1005602.

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Calsequestrin1 (CASQ1) is the main Ca2+ buffer protein localized in the lumen of the skeletal muscle sarcoplasmic reticulum. Two isoforms of CASQ, encoded by two different genes, have been identified: the skeletal isoform (CASQ1) expressed in fast-twich skeletal fibres and the cardiac isoform (CASQ2) expressed in cardiac muscle and in slow-twich skeletal fibres. Crystallographic studies have shown that the protein is made of three thioredoxin-like domains linked by short amino acidic sequences. The main characteristic of this molecule is its ability to polymerize in presence of Ca2+, binding more and more Ca2+ ions. Mutations in CASQ2 have been reported in an autosomal-recessive form of Catecholaminergic Polymorphic Ventricular Tachycardia, whereas recently a heterozygous missense mutation has been identified in the CASQ1 gene in patients with a vacuolar aggregate myopathy. This thesis is focused on the characterization of four missense variants in the CASQ1 gene, identified in patients with different myopathies. The identified mutations affect conserved amino acids of the CASQ1 protein. Turbidity measurements in presence of increasing Ca2+ concentrations showed that two of these mutations lead to a significant reduction in Ca2+-dependent aggregation. In agreement, limited trypsin proteolysis experiments showed that these amino acid substitutions enhanced the conformational flexibility of CASQ1, which become more susceptible to trypsin cleavage in comparison to wild type. On the contrary, the CASQ1 mutation associated with the vacuolar myopathy showed an increased Ca2+-dependent aggregation. These results support the hypothesis that distinct mutations in the CASQ1 gene may cause different phenotypes.
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Semplicini, Claudio. "Investigating myopathic causes of rhabdomyolysis." Doctoral thesis, Università degli studi di Padova, 2017. http://hdl.handle.net/11577/3425727.

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Rhabdomyolysis is an acute, and frequently severe, pathological event, characterized by rapid necrosis and destruction of striated muscle tissue. It is clinically characterized by muscle pain, weakness and emission of dark urine. The mechanisms that lead to rhabdomyolysis are various and different, and share common alterations such as dysfunction of the pumps Na + / K + and Ca2 + ATPase, and rupture of the sarcolemma, which in turn determine calcium homeostasis alterations, mitochondrial dysfunction, proteases activation, reduced availability of ATP and, overall, cell apoptosis and rhabdomyolysis. Several causes can initiate this vicious circle, both acquired and genetic. When facing an episode of rhabdomyolysis, the identification of the etiological cause can be extremely complex, long, and costly. Nevertheless, the correct identification of the underlying cause is of utmost importance for the correct information regarding prognosis (risk of recurrence) and for the family genetic counselling. Despite the application of extended diagnostic work up frequently it is not easy to distinguish if the rhabdomyolysis episode is due to a genetic disorder or whether it is the result of an abnormal effort, of an infectious episode or effect of a toxic. The main objective of this study is the evaluation of the diagnostic process of rhabdomyolysis, and to propose an updated, comprehensive, rational and cost effective protocol based on the latest information and techniques. We first studied the diagnostic process currently in use for rhabdomyolysis in a large retrospective study including 208 patients (aim 1). We characterized the clinical, molecular and radiological features of a new genetic cause of rhabdomyolysis, the CASQ1-related myopathy (aim 2). We determined the clinical spectrum of limb-girdle muscular dystrophy 2E (LGMD2E), investigating the risk of rhabdomyolysis of this disease (aim 3). We demostrated the role of EMG with provocative test (Long Exercise Test) as a sensitive and specific diagnostic test in the work up of rhabdomyolysis, especially in Glycogenosis type V (aim 4). We proposed a multi gene panel that should be studied by Next Generation Sequencing (NGS) in patients presenting rhabdomyolysis (aim 5) In conclusion, the results of this study suggest a new diagnostic algorithm for rhabdomyolysis. In this algorithm, the clinical features and few first-line tests (blood tests, EMG, acylcarnitines, grip test) exclude the most frequent causes or the treatable ones. The subsequent muscle biopsy will identify certain myopathies and guide toward the use of specific genetic panels for metabolic myopathies, muscular dystrophies or mitochondrial diseases that should be studied by NGS. The diagnostic algorithm that we propose will allow cost reduction and time optimization, and hopefully will increase the rate of etiological diagnosis of rhabdomyolysis, a serious event with major impact on patients' lives that, to date, remains poorly diagnosed.
La rabdomiolisi è un evento patologico acuto e talvolta grave, caratterizzato da rapida necrosi e distruzione del tessuto muscolare striato alla quale corrisponde clinicamente dolore e debolezza muscolare ed emissione di urine scure. I meccanismi che portano alla rabdomiolisi sono vari e differenti ma condividono alterazioni comuni quali la disfunzione delle pompe Na+/K+ e Ca2+ ATPAsi, e la rottura del sarcolemma, che a loro volta determinano alterazioni dell’omeostasi del calcio, disfunzione mitocondriale, attivazione di proteasi, riduzione della disponibilità di ATP e, complessivamente, apoptosi cellulare e rabdomiolisi. La corretta identificazione della causa sottostante è di estrema importanza per una corretta informazione al paziente a fini prognostici (rischio di ricorrenza) e per il counseling genetico familiare. Nonostante l’applicazione di estesi work up diagnostici, non è sempre facile determinare se alla base di un episodio di rabdomiolisi vi sia una patologia genetica o se sia esclusivamente conseguenza di uno sforzo, di un episodio infettivo o dell’effetto di un tossico. L’obiettivo principale del presente studio è stato, pertanto, definire l’iter diagnostico ottimale in caso di rabdomiolisi, al fine di proporne uno aggiornato, completo, razionale ed economico che includa le più recenti nozioni e tecniche. Abbiamo inizialmente valutato l'iter diagnostico utilizzato ad oggi nei pazienti che presentano rabdomiolisi, in un ampio studio retrospettivo che ha incluso 208 pazienti (aim 1). Abbiamo quindi studiato le caratteristiche cliniche, radiologiche e molecolari di una causa genetica di rabdiomiolisi di recente identificazione, la miopatia da mutazoine nel gene CASQ1 (aim 2). Abbiamo in seguito valutato lo spettro clinico della distrofia dei cingoli tipo 2 E (LGMD2E), valutando il rischio di rabdomiolisi in tale patologia (aim 3). Abbiamo poi dimostrato il ruolo di EMG con test provocativi (Long Exercise Test) come test sensibile e specifico utilizzabile in pazienti affetti da rabdomiolisi, in particolare nella glicogenosi tipo 5 (aim 4). Abbiamo infine creato un pannello di geni che dovrebbe essere studiato mediante Next Generation Sequencin (NGS) in pazienti affetti da rabdomiolisi (aim 5). In conclusione, con le evidenze raccolte nel presente studio, proponiamo un nuovo algoritmo diagnostico per le rabdomiolisi. In tale algoritmo le caratteristiche cliniche e pochi test di primo livello (esami ematochimici, EMG, profilo delle acilcarnitine, “grip test”) permettono di escludere le cause più frequenti o trattabili. Tale algoritmo permetterà di contenere i costi ed ottimizzare i tempi della diagnosi, e auspicabilmente aumenterà il rate di diagnosi etiologiche della rabdomiolisi, un evento grave e con un notevole impatto sulla vita dei pazienti ma che ad oggi resta scarsamente diagnosticato.
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Wong, Shi Pey. "Analysis of the adaptation mechanism in the type II-A CRISPR-Cas system." Doctoral thesis, Humboldt-Universität zu Berlin, 2019. http://dx.doi.org/10.18452/19806.

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Das RNA-guided adaptive Immunsystem CRISPR (clustered regularly interspaced short palindromic repeats)-Cas (CRISPR-associated) immunisiert prokaryotische Zellen gegenüber mobilen genetischen Elementen (MGEs). Bei der Adaption wird eine kurze Nukleinsäurensequenz (prespacer) von den MGEs gewonnen, verarbeitet und schließlich als spacer in das CRISPR-Array integriert. Cas1 und Cas2, die Hauptbestandteile der Adaption, bilden einen Integrase-Komplex, welcher neue spacer in das CRISPR-Array integriert. Der molekulare Mechanismus für die Adaptiondes Typ II-A Systems, welches cas9, cas1, cas2, csn2 und tracrRNA codiert, ist bis heute nicht vollständig verstanden. Daher untersuchten wir die Anforderungen der verschiedenen Cas-Proteine für den Adaptionsprozess. Wir verifizierten die Adaptions-Aktivität von Typ II-A Systemen des Streptococcus thermophilus LMD-9 anhand von Adaptionsstudien nach Phagen-Infektion. Dabei beobachteten wir höhere Akquisitionsraten im CRISPR3-Lokus im Vergleich zum CRISPR1-Lokus. Unsere Plasmid-basierte Adaptionsstudie bestätigte die Notwendigkeit von Cas9, zusätzlich zu Cas1, Cas2 und Csn2 bei der Adaption. Der yeast two-hybrid und der pull-down Ansatz zeigten sowohl spezifische Interaktionen zwischen den Cas-Proteinen, als auch Interaktionen zwischen Cas-Proteinen sowie DNA-Reparatur Proteinen. Die Regionen der Cas1 und Cas9 Interaktion wurden durch SPOT peptide assay identifiziert. Zusammenfassend weist unsere Studie darauf hin, dass Cas-Proteine sowohl mit Proteinen innerhalb, als auch außerhalb des CRISPR-Cas Systems interagieren, und bietet somit eine Basis für die Erforschung der möglichen Funktionen von DNA-Reparatur Proteinen in CRISPR-Cas Systemen und vice versa.
The RNA guided adaptive immune system CRISPR (clustered regularly interspaced short palindromic repeats) Cas (CRISPR-associated) immunizes prokaryotic cells against mobile genetic elements (MGEs). During spacer acquisition stage, a short nucleic acid sequence (prespacer) is acquired from the MGEs, processed and finally integrated into the CRISPR array as a spacer, which serves as genetic memory to defend against the invasion of the cognate MGEs. The molecular mechanism for the spacer acquisition of the type II A systems, which encode cas9, cas1, cas2, csn2 and tracrRNA, is still not fully understood. Therefore, we investigated the requirement of the different Cas proteins for spacer acquisition. We verified the acquisition activity of the type II A systems of Streptococcus thermophilus LMD 9 via spacer acquisition studies by phage challenge. We observed higher acquisition rates in the CRISPR3 locus compared to the CRISPR1 locus. Our plasmid-based spacer acquisition study confirmed in addition to Cas1, Cas2 and Csn2 the requirement of Cas9 for spacer acquisition. Yeast two hybrid and pull down approaches revealed specific interactions among the Cas proteins, as well as interactions between Cas and DNA repair proteins. The interaction regions of Cas1 with Cas9 were identified by SPOT peptide assay. Altogether, our study suggests that Cas proteins interact with proteins within and beyond the CRISPR Cas systems, and it provides a basis for the investigation of the potential roles of DNA repair proteins in the CRISPR Cas systems and/or vice versa.
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4

Kalyanasundaram, Anuradha. "The Role of CASQ2D307H Mutant protein in Catecholamine Induced Polymorphic Ventricular Tachycardia (CPVT)." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1259096606.

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Ludlow, Tracy. "Measuring Explanatory Style in Children." Thesis, Griffith University, 2008. http://hdl.handle.net/10072/367383.

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Causal explanations that individuals use to explain events in their lives are referred to as explanatory style. Three dimensions: internal-external, stable-unstable, and global-specific have most frequently been measured. Internal, stable, global explanations for negative events represent a pessimistic style, whereas these same explanations for positive events are considered optimistic. Explanations for negative events that are stable and global are considered to reflect hopelessness. The psychometric properties of the most commonly used measure of explanatory style for children, the Children Attributional Style Questionnaire (CASQ; Kaslow, Tanenbaum & Seligman, 1978) are poor. This is a limitation to research and theoretical advancement. Four studies were conducted in this project to investigate the measurement of explanatory style in 9-12 year old children. In Study 1, children (N = 173) completed the CASQ in a group to investigate the psychometric properties of the composite scales and subscales and the relationship between explanatory style and depressive symptoms. Internal consistency and inter-item correlations of the composite scales and subscales were poor. Regression analyses showed explanatory style for negative events (pessimism or hopelessness) made weak but significant unique contributions to the explanations of depressive symptoms. Study 2 (N = 72) investigated the stability of the CASQ scales longitudinally. The internal consistency and inter-item correlations for the CASQ scales were poor. The stability of explanatory style was low. The predicted relationship between depressive symptoms and explanatory style was found to be inconsistent, emerging at Time 1 but not at Time 2, 12 months later. Study 3 (N = 79) examined the forced-choice response scale of the CASQ using a fuzzy set approach. A fuzzy set scale which uses a Likert-type response that ranged from completely true to completely false was used to determine how well a child’s response of choice, their natural response, matched both the selected and non-selected response from the CASQ. Items on the CASQ that measure both pessimism and hopelessness were found to be a poor match to the natural responses of children. Little separation was found between the selected and non-selected responses for all items. The internal consistency of the CASQ was poor when the forced choice scoring approach was used. When Likert-type fuzzy values were used, good internal consistency was obtained. Providing a wider range of responses, obtained using fuzzy values, produced a more sensitive measure of the components of explanatory style. When the CASQ was scored according to the forced choice protocol weak, significant relationships were found between explanatory style and depressive symptoms, and explanatory style and neuroticism. There were no significant relationships found for either pessimism or hopelessness, with either depression or neuroticism using Likert-type fuzzy values. Study 4 elicited spontaneous causal explanations following success or failure on tasks that were familiar or unfamiliar. Task familiarity was manipulated. Using an interview format, children (N = 111) responded to questions, eliciting causal explanations, following task success or failures. Likert-type scales measured the internality, stability or globality of the explanation. Results showed that, following failure on two familiar tasks, acceptable levels of internal consistency were obtained on the subscales used to produce the measure of hopelessness and for the composite measure of hopelessness. This same pattern did not emerge following failure on combinations of familiar and unfamiliar events or on two tasks that were unfamiliar. Stable and global explanations and the composite measure of hopelessness, following failure on familiar tasks, were also positively related with depressive symptoms but not neuroticism. These results show that a reliable measure of hopelessness can be obtained from spontaneous explanations for failure at familiar events. Under these conditions the theoretically predicted relationship between explanatory style and depressive symptoms emerges. Conclusions were drawn about the theoretical conceptualisation of explanatory style and measurement recommendations were made that apply to 9- to 12-year-old children. Explanations for familiar events produced a consistent measure of explanatory style. The use of a Likert-type response scale to assess agreement with internal, stable, global components were shown to improve scale reliability. The findings are discussed in relation to theory and the measurement of explanatory style in children.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Phychology
Griffith Health
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Lücking, Kerstin [Verfasser], and Uwe [Akademischer Betreuer] Kirchhefer. "Mutationen im kardialen Calsequestrin-Gen (CASQ2 ) als Ursache der katecholaminergen polymorphen ventrikulären Tachykardie (CPVT) / Kerstin Lücking. Betreuer: Uwe Kirchhefer." Münster : Universitäts- und Landesbibliothek der Westfälischen Wilhelms-Universität, 2012. http://d-nb.info/1027018726/34.

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Richards, Andrew John. "Optimism and English school children : reliability, validity and use of the Children's Attributional Style Questionnaire (CASQ) and the Youth Life Orientation Test (YLOT)." Thesis, University of Exeter, 2012. http://hdl.handle.net/10036/3624.

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This study explores the use of two tests of optimism: the Youth Life Orientation Test (YLOT) and the Children’s Attributional Style Questionnaire (CASQ) in six English primary schools with children aged between 9 years and 12 years. The study grew out of some problems I was confronted with as part of my professional practice regarding the outcomes for children in a school that was failing to meet Government Targets in attainment. In the study I worked with the staff and 9 – 11 year old children in six primary schools in rural, town, suburban and inner-city contexts. The total number of children was 305. The children were tested using the CASQ and YLOT and a range of other measures. Cronbach alpha internal consistency coefficients (coefficient alpha) and test-retest coefficients for the subscales and overall scale of the CASQ and YLOT were calculated. The validity of each measure was explored using evidence from: test content; internal structure; relations to other variables; and from the consequences of testing. Lastly the use of the YLOT as a proxy and nature of any associations between the measures used was explored looking at individual; school and community level data. The study found that the YLOT has good psychometric properties and could be used as a basis for further work both professionally and for research. The Cronbach alpha reliability coefficient for the whole scale was 0.81. The psychometric properties of the CASQ were poor in that the subscales had very low reliability coefficients and the aggregated total scale reliability coefficient was still too low at 0.53 to be able to recommend the use of the CASQ. Before the CASQ could be used there would need to be extensive work to increase its reliability and validity through lengthening the test or changing the format of the questions to reduce their specificity. The use of the YLOT as a proxy indicator of mental health and associations with school and community level data were discussed. The YLOT could provide an indication of well being particularly in relation to childhood depression. The community level data were not sensitive enough to discern hypothesised associations between communities and the children attending the schools sited in the communities.
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Michon, Jérôme. "Etude de l’oxydation biologique de l’arsenic As(III) par le consortium bactérien CAsO1 : mise au point de méthodes de détection et application à la détoxification d’effluents." Limoges, 2006. https://aurore.unilim.fr/theses/nxfile/default/6a8c8ca9-38b7-4688-89f5-1b36ed58553c/blobholder:0/2006LIMO0064.pdf.

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Ces travaux ont porté sur la mise en place et le développement d’un pilote d’oxydation bactérienne de l’As(III) en As(V), pour la potabilisation et le traitement d’effluents contaminés en arsenic. Le procédé d’oxydation biologique de l’arsenic fait appel à consortium bactérien autotrophe apparenté au genre Thiomonas, le consortiumCAsO1. Deux techniques de dosages ont été mises au point : le dosage d’As(total) par Spectrométrie d’Absorption Atomique Four Graphite (GF-AAS), et celui d’As(III), par Spectrométrie d’Absorption Atomique avec Génération d’Hydrures (HG-AAS), pour des domaines de concentration de 0,2 à 20 µg. L-1. Le pilote de traitement et le matériau support (pouzzolane) ont été caractérisés (DTS, capacité d’adsorption…). Ainsi, les performances d’oxydation de CAsO1 ont été évaluées : pour des temps de séjours supérieurs à 2 heures, 95% de la concentration en As(III) est oxydé, quel que soit le type d’alimentation étudié (ascendante ou descendante) et plus de 80%, pour un temps de séjour de 1 heure
This work concerned the evaluation and the development of an arsenic(III)-oxidizing population in reactors, for drinking water production and waste water arsenic contaminated treatment. The process of the biological oxidation of arsenite was carried out with an autotrophic bacterial population named CAsO1. This population was phylogenetically related to Thiomonas. Two easy to handle analytical methods were developed: the determination of total arsenic was carried out by Graphite Furnace Atomic Absorption Spectrometry (GF-AAS), and that concerning As(III), by Hydride Generation Atomic Absorption Spectrometry (HG-AAS), for concentration range from 0,2 to 20 µg. L-1. The treatment pilot and the support material (pozzolana) were characterized (RTD, adsorption capacity. . . ). Thus, performances of oxidation of CAsO1 were evaluated: for residence times higher than 2 hours, 95% of As(III) was oxidized, whatever the type of circulation (up- or down-flow) and more than 80%, for a residence time of 1 hour
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Khedher, Ahmed. "Utilisation de technologies d'édition du génome afin de générer des cardiomyocytes matures à partir de cellules souches pluripotentes humaines induites CtIP Fusion to Cas9 Enhances Transgene Integration by Homology-Dependent Repair." Thesis, université Paris-Saclay, 2021. http://www.theses.fr/2021UPASL002.

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Les cardiomyocytes dérivés des cellules souches pluripotentes humaines induites (hiPSC-CMs) représentent des modèles in vitro prometteurs pour plusieurs applications scientifiques et thérapeutiques allant de la modélisation de pathologies à la découverte de médicaments et de la toxicologie prédictive à la médecine régénérative. Malgré les nombreux progrès dans ce domaine, les protocoles de différenciation actuels ne permettent pas d’atteindre le stade de maturité que l’on retrouve chez le myocarde adulte de l’Homme. En effet, certaines caractéristiques majeures des hiPSC-CMs demeurent similaires à celles de cardiomyocytes fœtaux telles que l’expression de plusieurs gènes cardiaques, l’électrophysiologie ou leur fonction contractile. En effet, des analyses transcriptomiques réalisés au sein de notre laboratoire à Sanofi ont révélé que les gènes KCNJ2 et CASQ2, impliqués respectivement dans l’électrophysiologie et la gestion du calcium, étaient sous-exprimés dans les hiPSC-CMs en comparaison aux cardiomyocytes adultes. Cette thèse avait pour objectif d’améliorer la maturation des hiPSC-CMs en utilisant des technologies d’édition du génome. Ainsi, nous avons généré des lignées stables de hiPSC-CMs qui expriment de manière inductible KCNJ2 ou CASQ2 ou les deux gènes simultanément puis nous avons examiné leurs phénotypes fonctionnels et électrophysiologiques par le biais de méthodes d’analyses complémentaires. A la suite à l’induction de l’expression de KCNJ2 et CASQ2 par la doxycycline, les hiPSC-CMs montraient des bénéfices phénotypiques tels que la diminution drastique de la fréquence des battements spontanés, une hyperpolarisation du potentiel de repos membranaire, la diminution de la durée du potentiel d’action et l’amélioration du flux de calcium transitoire. En plus de ces bénéfices attendus, l’expression concomitante de ces deux gènes a amélioré la pente de la pointe du potentiel de champ extracellulaire associée au courant sodique ainsi que la gestion du calcium. Nous avons ensuite évalué le bénéfice de l’expression de ces transgènes sur la toxicologie prédictive en testant des molécules agonistes ou antagonistes de canaux ioniques utilisées classiquement dans le cadre des essais précliniques de toxicité cardiaque. Nous avons notamment observé plus d’arythmies induites par l’E4031 avec les hiPSC-CMs exprimant conjointement KCNJ2 et CASQ2 par rapport aux cardiomyocytes contrôles. Ainsi, les hiPSC-CMs exprimant simultanément KCNJ2 et CASQ2 présentent un phénotype plus mature que les hiPSC-CMs natifs et de tels cardiomyocytes édités génétiquement peuvent être utiles pour l’évaluation de la toxicité cardiaque de nouveaux médicaments candidats
Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) are a very promising model for several scientific and therapeutic applications ranging from disease modeling to drug discovery, and from predictive toxicology to regenerative medicine. Despite numerous efforts, current protocols do not yet lead to a maturation phenotype equivalent to adult human myocardium. Indeed, key features of hiPSC-CMs remaining closer to fetal stages of development, such as gene expression, electrophysiology and function. Transcriptome analysis performed at Sanofi have confirmed these findings at the genome-wide level. Indeed, KCNJ2 and CASQ2 which are implicated in the two major physiological characteristics of cardiac cells, their electrophysiological behavior and calcium handling, respectively, were expressed at very low levels in hiPSC-CMs in comparison with adult cardiomyocytes. This thesis aimed to improve the maturation of hiPSC-CMs by using genome editing technologies. We generated stable hiPSC-CMs with inducible expression of KCNJ2, or CASQ2 or both genes (KCNJ2-CASQ2 hiPSC-CMs) and studied their functional and electrophysiological phenotype by several complementary methods. Upon doxycycline induction of KCNJ2 and CASQ2, KCNJ2-CASQ2 hiPSC-CMs displayed phenotypic benefits expected from previous studies of each maturation gene, including a drastic reduction of spontaneous beating, hyperpolarized resting membrane potential, shortened action potential duration and enhanced calcium transients. In addition, co-expression of the two genes enhanced Na+ spike slope of extracellular field potential and Ca2+ handling. We tested four reference drugs and observed signatures of known cardiac effects in KCNJ2-CASQ2 hiPSC-CMs, including arrhythmias induced by QT prolonging drug (E-4031), which were more easily detected than in control hiPSC-CMs. Therefore, KCNJ2-CASQ2 hiPSC-CMs exhibited a more mature phenotype than hiPSC-CMs and such genetically engineered hiPSC-CMs could be useful for testing cardiac toxicity of novel candidate drugs
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Salama, Younes Mareï. "Validation et adaptation d'un outil de mesure (CASQ) évaluant les modes explicatifs chez les enfants sportifs et application à la prédiction des résultats sportifs et scolaires." Rennes 2, 2005. http://www.theses.fr/2005REN20050.

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Les objectifs essentiels de cette thèse portent (i) sur l'examen du cadre théorique sur lequel se fonde la théorie du " Mode explicatif " (e. G. , Abramson, Seligman, Teasdale, 1978), (ii) sur la validation d'un outil permettant une évaluation des modes explicatifs chez les enfants pratiquant des activités sportives diverses, et (iii) sur l'étude des effets des modes explicatifs sur des variables comportementales. La première partie présente les antécédents et les conséquences du mode explicatif chez des enfants âgés de 8 à 14 ans. La deuxième partie comporte une dizaine d'études ayant pour but de présenter la validation de l'outil de mesure, version française courte du CASQ (QEMEE-R), contextualisée à la fois pour les domaines scolaire et sportif. La troisième partie a pour but de présenter succinctement les bases théoriques d'un modèle inspiré des travaux d'Eccles et Wigfield (2002) incluant deux études visant à tester à la fois les effets du mode explicatif sur les résultats scolaires et sur les performances sportives. L'ensemble des études a permis de mettre en évidence son organisation hiérarchique, du plus général au plus contextualisé, et l'existence non pas de deux profils, optimiste et pessimiste, mais de quatre profils. Ces deux aspects constituent une évolution théorique dans le domaine de la recherche sur les modes explicatifs
The thesis aims to (i) valid, purify a short French version from “Children's Attributional Style Questionnaire, CASQ”, this one would be adapted in French culture and with sport children; (ii) examine the theoretical conceptual model of the attributional/explanatory style not only in sport but also in school context. It is based upon data stemming from the Attributional Reformulation of Helplessness Theory (e. G. , Abramson, Seligman, Teasdale, 1978). Despite its interest, we found a very little studies in school context for children have been realised, nothing of studies concerning the children in the sport context. The thesis consists of three parts: the first one presents the theoretical base of explanatory style theory, studies concerning the psychological effects of explanatory style for children and adolescents in many fields. In the second parts, using many methods and samples, we examine the psychometric proprieties of an experimental French version of CASQ (QEMEE), and purify a short version (QEMEE-R). Basing to this version and in order to examine many theoretical hypothesis, we contextualise a version in sport and in school context. In the third parts, we realised two studies in sport and school contexts. Basing to Eccles and Wigfield model (2002), we tested three hypotheses concerning the effect of the contextualised and/or general explanatory style to predict the result in sport and in school domains. These two studies confirm the existence of (i) hierarchical organisation of children's the explanatory style, (ii) not only two but four profiles of children's explanatory style. These result constitute an theatrical evaluation in explanatory style search
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Books on the topic "CASQ1"

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Keith Saunders Alle Einsteigen ! Selbst Tank Cass1. Hodder Arnold H&S, 1999.

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Book chapters on the topic "CASQ1"

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Pollock, Joycelyn M. "Defining Crimes." In Criminal Law, 436–55. Twelfth edition. | New York, NY; Milton Park, Abingdon, Oxon : Routledge, 2021.: Routledge, 2020. http://dx.doi.org/10.4324/9781003029984-case1.

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Werthmann (CW), Christian. "Buenos Aires – Step by Step." In Informal Urbanization in Latin America, 38–50. New York, NY : Routledge, 2021.: Routledge, 2021. http://dx.doi.org/10.4324/9781003089797-case1.

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Anderson, John. "Case grammar." In Handbook of Pragmatics, 123–29. Amsterdam: John Benjamins Publishing Company, 2022. http://dx.doi.org/10.1075/hop.m2.cas1.

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Rietjens, Mario, Mario Casales Schorr, and Visnu Lohsiriwat. "Case1 Immediate Definitive Prosthesis Technique." In Atlas of Breast Reconstruction, 7–10. Milano: Springer Milan, 2014. http://dx.doi.org/10.1007/978-88-470-5519-3_2.

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Shahid, Azmeh, Kate Wilkinson, Shai Marcu, and Colin M. Shapiro. "Cleveland Adolescent Sleepiness Questionnaire (CASQ)." In STOP, THAT and One Hundred Other Sleep Scales, 127–30. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-9893-4_23.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "Cas Scaffolding Protein Family Member 1 (CASS1)." In Encyclopedia of Signaling Molecules, 234. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100163.

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Carciofi, Ricardo. "Cooperation for the Provision of Regional Public Goods: The Iirsa Case1." In The Rise of Post-Hegemonic Regionalism, 65–79. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2694-9_4.

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Beloglazova, Natalia, Sofia Lemak, Robert Flick, and Alexander F. Yakunin. "Analysis of Nuclease Activity of Cas1 Proteins Against Complex DNA Substrates." In Methods in Molecular Biology, 251–64. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2687-9_16.

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Ożarek, Grażyna. "Quality as an Ethical Issue: Technical and Economic Aspects: A Small IT Companies Case1." In Praxiology and the Philosophy of Technology, 247–70. New York: Routledge, 2021. http://dx.doi.org/10.4324/9781315127231-16.

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"CASQ." In Encyclopedia of Metalloproteins, 569. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-1533-6_100296.

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Conference papers on the topic "CASQ1"

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Mondal, Jayanta, and Amol Deshpande. "CASQD." In DEBS '16: The 10th ACM International Conference on Distributed and Event-based Systems. New York, NY, USA: ACM, 2016. http://dx.doi.org/10.1145/2933267.2933316.

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Renbao, Z., X. Ling, and R. Zhaoyang. "The computer algebra system CAS1 for the IBM-PC." In the fifth ACM symposium. New York, New York, USA: ACM Press, 1986. http://dx.doi.org/10.1145/32439.32474.

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Ge, Keshi, Yiming Zhang, Yongquan Fu, Zhiquan Lai, Xiaoge Deng, and Dongsheng Li. "CASQ: Accelerate Distributed Deep Learning with Sketch-Based Gradient Quantization." In 2021 IEEE International Conference on Cluster Computing (CLUSTER). IEEE, 2021. http://dx.doi.org/10.1109/cluster48925.2021.00074.

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Ge, Keshi, Yiming Zhang, Yongquan Fu, Zhiquan Lai, Xiaoge Deng, and Dongsheng Li. "CASQ: Accelerate Distributed Deep Learning with Sketch-Based Gradient Quantization." In 2021 IEEE International Conference on Cluster Computing (CLUSTER). IEEE, 2021. http://dx.doi.org/10.1109/cluster48925.2021.00074.

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Liu, Zhihui, Wilson Chan, and Carol J. Thiele. "Abstract 2630: Tumor suppressor CASZ1 inhibits normal myoblast and rhabdomyosarcoma (RMS) migration." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-2630.

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Liu, Zhihui, Norris Lam, Arnulfo Mendoza, Jun S. Wei, John F. Shern, Marielle Yohe, Javed Khan, and Carol J. Thiele. "Abstract 5522: Novel myogenic differentiation transcription factor CASZ1 suppresses rhabdomyosarcoma tumor growth." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5522.

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Hu, Yifeng, Gang Chen, and Weizhe Wang. "Investigation of Stress-Strain Behavior of a Component Under Variable Frequency Non-Proportional Loading." In ASME Turbo Expo 2018: Turbomachinery Technical Conference and Exposition. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/gt2018-76768.

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With the flexibility operation demand of the plants, the load change becomes more and more often. The torsion loading due to load change becomes larger and more frequent. The influence of torsion loading frequency (the number of repeating cycles in a unit time) on the stress-strain behavior of component was numerically investigated under non-proportional loadings. A hollow cylinder specimen was chosen in this study. And three conditions of non-proportional loadings (Case1, Case2 and Case3) were chosen. The relationships between cyclic stress response and cyclic strain response were obtained for Case1, Case2 and Case3. The numerical results revealed that the distortion of stress-strain response curve was intensified with the increase of torsion loading frequency. The cyclic softening behaved in the first 2 cycles for the tension and torsion stress responses; however, the characterizations of the cyclic hardening and the cyclic softening for the material appeared after the starting 2 cycles. Furthermore, with the increase of cycle number and torsion loading frequency, there is a significant difference between the tension stress response and the torsion stress response.
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Wang, Chunxi, Chanwook Woo, Zhihui Liu, Jun Wei, Young Song, Lifeng Wang, Javed Khan, Kai Ge, and Carol J. Thiele. "Abstract 4880: CASZ1, a neuroblastoma tumor suppressor gene, is epigenetically silenced by EZH2." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4880.

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Markelić, I., L. Rumora, I. Hlapčić, F. Džubur, S. Popović Grle, M. Samaržija, and A. Vukić Dugac. "Downregulation of NLRP3, CASP1 and IL1B expression in COPD patients after lung transplantation." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.1606.

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He, Yang, Anchun Cheng, and Mingshu Wang. "Analysis of synonymous codon usage in the Cas1 gene of Riemerella anatipestifer." In 2012 5th International Conference on Biomedical Engineering and Informatics (BMEI). IEEE, 2012. http://dx.doi.org/10.1109/bmei.2012.6512980.

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