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Academic literature on the topic 'LQT1'

Author: Grafiati

Published: 9 March 2023

Last updated: 10 March 2023

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Journal articles on the topic "LQT1"

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Gao, Yuanfeng, Wenling Liu, Cuilan Li, Xiaoliang Qiu, Xuguang Qin, Baojing Guo, Xueqin Liu, et al. "Common Genotypes of Long QT Syndrome in China and the Role of ECG Prediction." Cardiology 133, no. 2 (October 24, 2015): 73–78. http://dx.doi.org/10.1159/000440608.

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Objectives: Genetic testing, a gold standard for long QT syndrome (LQTS) diagnosis, is time-consuming and costly when all the 15 candidate genes are screened. Since genotype-specific ECG patterns are present in most LQT1-3 mutation carriers, we tested the utility of ECG-guided genotyping in a large cohort of Chinese LQTS patients. Methods and Results: We enrolled 230 patients (26 ± 17 years, 66% female) with a clinical diagnosis of LQTS. Genotypes were predicted as LQT1-3 based on the presence of ECG patterns typical for each genotype in 200 patients (85 LQT1, 110 LQT2 and 5 LQT3). Family-based genotype prediction was also conducted if gene-specific ECG patterns were found in other affected family members. Mutational screening identified 104 mutations (44% novel), i.e. 46 KCNQ1, 54 KCNH2 and 4 SCN5A mutations. The overall predictive accuracy of ECG-guided genotyping was 79% (157/200) and 79% (67/85), 78% (86/110) and 80% (4/5) for LQT1, LQT2 and LQT3, respectively. The predictive accuracy was 98% (42/43) when family-based ECG assessment was performed. Conclusions: From this large-scale genotyping study, we found that LQT2 is the most common genotype among the Chinese. Family-based ECG-guided genotyping is highly accurate. ECG-guided genotyping is time- and cost-effective. We therefore recommend it as an optimal approach for the genetic diagnosis of LQTS.

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Paavonen, K. J., H. Swan, K. Piippo, L. Hokkanen, P. Laitinen, M. Viitasalo, L. Toivonen, and K. Kontula. "Response of the QT interval to mental and physical stress in types LQT1 and LQT2 of the long QT syndrome." Heart 86, no. 1 (July 1, 2001): 39–44. http://dx.doi.org/10.1136/hrt.86.1.39.

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OBJECTIVETo study and compare the effects of mental and physical stress on long QT syndrome (LQTS) patients.DESIGNCase–control study.MAIN OUTCOME MEASURESQT intervals were measured from lead V3. Serum potassium and plasma catecholamine concentrations were also monitored.PATIENTS16 patients with type 1 LQTS (LQT1), 14 with type 2 LQTS (LQT2), both groups asymptomatic, and 14 healthy control subjects.INTERVENTIONSThree types of mental stress tests and a submaximal exercise stress test.RESULTSHeart rate responses to mental stress and exercise were similar in all groups. During mental stress, the mean QT interval shortened to a similar extent in controls (–29 ms), LQT1 patients (–34 ms), and LQT2 patients (–30 ms). During exercise, the corresponding QT adaptation to exercise stress was more pronounced (p < 0.01) in healthy controls (–47 ms) than in LQT1 (–38 ms) or LQT2 patients (–38 ms). During exercise changes in serum potassium concentrations were correlated to changes in QT intervals in controls, but not in LQTS patients. LQT1 and LQT2 patients did not differ in serum potassium, catecholamine or heart rate responses to mental or physical stress.CONCLUSIONSQT adaptation to mental and exercise stress in healthy people and in patients with LQTS is different. In healthy people QT adaptation is more sensitive to physical than to mental stress while no such diverging pattern was seen in asymptomatic LQTS patients.

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Harmer, S. C., and A. Tinker. "The role of abnormal trafficking of KCNE1 in long QT syndrome 5." Biochemical Society Transactions 35, no. 5 (October 25, 2007): 1074–76. http://dx.doi.org/10.1042/bst0351074.

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LQTS (long QT syndrome) is an important cause of cardiac sudden death. LQTS is characterized by a prolongation of the QT interval on an electrocardiogram. This prolongation predisposes the individual to torsade-de-pointes and subsequent sudden death by ventricular fibrillation. Mutations in a number of genes that encode ion channels have been implicated in LQTS. Hereditary mutations in the α- and β-subunits, KCNQ1 and KCNE1 respectively, of the K+ channel pore IKs are the commonest cause of LQTS and account for LQTS types 1 and 5 respectively (LQT1 and LQT5). Recently, it has been shown that disease pathogenesis in LQT1 can be influenced by the abnormal trafficking of KCNQ1. In comparison, whether defective trafficking of KCNE1 plays a role in LQT5 is less well established.

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Paci, Michelangelo, Simona Casini, Milena Bellin, Jari Hyttinen, and Stefano Severi. "Large-Scale Simulation of the Phenotypical Variability Induced by Loss-of-Function Long QT Mutations in Human Induced Pluripotent Stem Cell Cardiomyocytes." International Journal of Molecular Sciences 19, no. 11 (November 13, 2018): 3583. http://dx.doi.org/10.3390/ijms19113583.

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Loss-of-function long QT (LQT) mutations inducing LQT1 and LQT2 syndromes have been successfully translated to human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) used as disease-specific models. However, their in vitro investigation mainly relies on experiments using small numbers of cells. This is especially critical when working with cells as heterogeneous as hiPSC-CMs. We aim (i) to investigate in silico the ionic mechanisms underlying LQT1 and LQT2 hiPSC-CM phenotypic variability, and (ii) to enable massive in silico drug tests on mutant hiPSC-CMs. We combined (i) data of control and mutant slow and rapid delayed rectifying K+ currents, IKr and IKs respectively, (ii) a recent in silico hiPSC-CM model, and (iii) the population of models paradigm to generate control and mutant populations for LQT1 and LQT2 cardiomyocytes. Our four populations contain from 1008 to 3584 models. In line with the experimental in vitro data, mutant in silico hiPSC-CMs showed prolonged action potential (AP) duration (LQT1: +14%, LQT2: +39%) and large electrophysiological variability. Finally, the mutant populations were split into normal-like hiPSC-CMs (with action potential duration similar to control) and at risk hiPSC-CMs (with clearly prolonged action potential duration). At risk mutant hiPSC-CMs carried higher expression of L-type Ca2+, lower expression of IKr and increased sensitivity to quinidine as compared to mutant normal-like hiPSC-CMs, resulting in AP abnormalities. In conclusion, we were able to reproduce the two most common LQT syndromes with large-scale simulations, which enable investigating biophysical mechanisms difficult to assess in vitro, e.g., how variations of ion current expressions in a physiological range can impact on AP properties of mutant hiPSC-CMs.

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Borowiec, Karolina, Mirosław Kowalski, Magdalena Kumor, Joanna Duliban, Witold Śmigielski, Piotr Hoffman, and Elżbieta Katarzyna Biernacka. "Prolonged left ventricular contraction duration in apical segments as a marker of arrhythmic risk in patients with long QT syndrome." EP Europace 22, no. 8 (June 12, 2020): 1279–86. http://dx.doi.org/10.1093/europace/euaa107.

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Abstract Aims Long QT syndrome (LQTS) is an inherited cardiac ion channelopathy predisposing to life-threatening ventricular arrhythmias and sudden cardiac death. The aim of this study was to investigate left ventricular mechanical abnormalities in LQTS patients and establish a potential role of strain as a marker of arrhythmic risk. Methods and results We included 47 patients with genetically confirmed LQTS (22 LQT1, 20 LQT2, 3 LQT3, and 2 SCN3B) and 25 healthy controls. A history of cardiac events was present in 30 LQTS subjects. Tissue Doppler and speckle tracking echocardiography were performed and contraction duration was measured by radial and longitudinal strain. The radial strain characteristic was subdivided into two planes — the basal and the apical. Left ventricular ejection fraction and global longitudinal strain were normal in LQTS patients. Mean contraction duration was longer in LQTS patients compared with controls in regard to basal radial strain (491 ± 57 vs. 437 ± 55 ms, P < 0.001), apical radial strain (450 ± 53 vs. 407 ± 53 ms, P = 0.002), and longitudinal strain (445 ± 34 vs. 423 ± 43 ms, P = 0.02). Moreover, contraction duration obtained from apical radial strain analysis was longer in symptomatic compared with asymptomatic LQTS mutation carriers (462 ± 49 vs. 429 ± 55 ms, P = 0.024), as well as in subject with mutations other than LQT1 considered to be at higher risk (468 ± 50 vs. 429 ± 49 ms, P = 0.01). Conclusion Myocardial contraction duration is prolonged for both radial and longitudinal directions in LQTS patients. Regional left ventricular function analysis may contribute to risk stratification. Apical radial deformation seems to select subjects at higher risk of arrhythmic events.

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Odening, Katja E., Malcolm Kirk, Michael Brunner, Ohad Ziv, Peem Lorvidhaya, Gong Xin Liu, Lorraine Schofield, et al. "Electrophysiological studies of transgenic long QT type 1 and type 2 rabbits reveal genotype-specific differences in ventricular refractoriness and His conduction." American Journal of Physiology-Heart and Circulatory Physiology 299, no. 3 (September 2010): H643—H655. http://dx.doi.org/10.1152/ajpheart.00074.2010.

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We have generated transgenic rabbits lacking cardiac slow delayed-rectifier K+ current [ IKs; long QT syndrome type 1 (LQT1)] or rapidly activating delayed-rectifier K+ current [ IKr; long QT syndrome type 2 (LQT2)]. Rabbits with either genotype have prolonged action potential duration and QT intervals; however, only LQT2 rabbits develop atrioventricular (AV) blocks and polymorphic ventricular tachycardia. We therefore sought to characterize the genotype-specific differences in AV conduction and ventricular refractoriness in LQT1 and LQT2 rabbits. We carried out in vivo electrophysiological studies in LQT1, LQT2, and littermate control (LMC) rabbits at baseline, during isoproterenol infusion, and after a bolus of dofetilide and ex vivo optical mapping studies of the AV node/His-region at baseline and during dofetilide perfusion. Under isoflurane anesthesia, LQT2 rabbits developed infra-His blocks, decremental His conduction, and prolongation of the Wenckebach cycle length. In LQT1 rabbits, dofetilide altered the His morphology and slowed His conduction, resulting in intra-His block, and additionally prolonged the ventricular refractoriness, leading to pseudo-AV block . The ventricular effective refractory period (VERP) in right ventricular apex and base was significantly longer in LQT2 than LQT1 ( P < 0.05) or LMC ( P < 0.01), with a greater VERP dispersion in LQT2 than LQT1 rabbits. Isoproterenol reduced the VERP dispersion in LQT2 rabbits by shortening the VERP in the base more than in the apex but had no effect on VERP in LQT1. EPS and optical mapping experiments demonstrated genotype-specific differences in AV conduction and ventricular refractoriness. The occurrence of infra-His blocks in LQT2 rabbits under isoflurane and intra-His block in LQT1 rabbits after dofetilide suggest differential regional sensitivities of the rabbit His-Purkinje system to drugs blocking IKr and IKs.

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Joutsijoki, Henry, Kirsi Penttinen, Martti Juhola, and Katriina Aalto-Setälä. "Separation of HCM and LQT Cardiac Diseases with Machine Learning of Ca2+ Transient Profiles." Methods of Information in Medicine 58, no. 04/05 (November 2019): 167–78. http://dx.doi.org/10.1055/s-0040-1701484.

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Abstract Background Modeling human cardiac diseases with induced pluripotent stem cells not only enables to study disease pathophysiology and develop therapies but also, as we have previously showed, it can offer a tool for disease diagnostics. We previously observed that a few genetic cardiac diseases can be separated from each other and healthy controls by applying machine learning to Ca2+ transient signals measured from iPSC-derived cardiomyocytes (CMs). Objectives For the current research, 419 hypertrophic cardiomyopathy (HCM) transient signals and 228 long QT syndrome (LQTS) transient signals were measured. HCM signals included data recorded from iPSC-CMs carrying either α-tropomyosin, i.e., TPM1 (HCMT) or MYBPC3 or myosin-binding protein C (HCMM) mutation and LQTS signals included data recorded from iPSC-CMs carrying potassium voltage-gated channel subfamily Q member 1 (KCNQ1) mutation (long QT syndrome 1 [LQT1]) or KCNH2 mutation (long QT syndrome 2 [LQT2]). The main objective was to study whether and how effectively HCMM and HCMT can be separated from each other as well as LQT1 from LQT2. Methods After preprocessing those Ca2+ signals where we computed peak waveforms we then classified the two mutations of both disease pairs by using several different machine learning methods. Results We obtained excellent classification accuracies of 89% for HCM and even 100% for LQT at their best. Conclusion The results indicate that the methods applied would be efficient for the identification of these genetic cardiac diseases.

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Chakova, N. N., S. M. Komissarova, E. A. Zasim, T. V. Dolmatovich, E. S. Rebeko, S. S. Niyazova, E. V. Zaklyazminskaya, L. I. Plashchinskaya, and M. V. Dudko. "Spectrum of mutations and their phenotypic manifestations in children and adults with long QT syndrome." Russian Journal of Cardiology 26, no. 10 (November 22, 2021): 4704. http://dx.doi.org/10.15829/1560-4071-2021-4704.

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Aim. To determine the spectrum of mutations in the genes responsible for the long QT syndrome (LQTS) and study their phenotypic manifestations in patients with LQTS in different age groups.Materials and methods. The study included 35 unrelated probands with a clinical diagnosis of LQTS: 23 adults (8 men) and 12 children (9 boys). There were following clinical features: syncope — 54%, positive family history for SCD — 29%, implanted cardioverter defibrillator (ICD) — 46%. All participants underwent 12-lead electrocardiography (ECG), 24-hour Holter monitoring, genealogical analysis, echocardiography and cardiac MRI. The genetic study was performed by nextgeneration sequencing (NGS) using the MiSeq system (Illumina). The quantitative comparison of two unrelated groups was carried out using the nonparametric MannWhitney U-test. The differences were considered significant at p<0,05.Results. In the examined group of 35 probands, 23 genetic variants of pathogenicity class IV and V (hereinafter referred to as) were identified. The molecular genetic variant of the disease was verified in 66% of probands. At the same time, the detection of mutations in the group with early manifestation (children) was significantly higher: 83% (10 out of 12 children) vs 57% in adults (13 out of 23). Rare genetic variants of uncertain significance (VUS, class III pathogenicity) were detected in 4 probands (11%). In the groups of children and adults with LQT1, LQT2 and LQT3, the sex distribution deviated from the 1:1 ratio. Among children, two-thirds were boys, among adults — the same proportion was represented by women. Disease manifestation time, QTc duration and adverse events risk depended on the genetic type of LQTS, intragenic localization of mutations and sex. In children, all 4 missense mutations in the KCNQ1 gene were located in transmembrane domain, and in adults, 4 mutations were in the transmembrane domain and three — in the C-terminal domain of the protein. LQT1 in boys was characterized by early manifestation, while QTc did not exceed 500 ms and there were no adverse outcomes. Two women out of 7 adults with LQT1 with mutations in the transmembrane domain had na ICD (QTc >520 ms). All patients with LQT2 (4 children, 4 adults) had QTc >500 ms. At the same time, 2 children and 3 women had an ICD. LQT3 was diagnosed only in the children subgroup (2 boys, with QTc of 510 ms and QTc of 610 ms); one of them died suddenly despite beta-blocker therapy. Four adult patients, carriers of class III pathogenicity variants, had QTc <500 ms and delayed disease manifestation (after 30 years). Three of them had episodes of clinical death with subsequent resuscitation and implantation of cardioverter defibrillator.Conclusion. The average diagnostic efficiency of mutation identification using NGS in patients with clinically manifest LQTS was 66%. At the same time, mutations were more common in the children’s group. In genotype-positive probands, the risk of adverse outcomes correlated with sex, age and the genetic variant of disease. The greatest number of adverse outcomes was observed in carriers of mutations in both KCNH2 (LQT2) and SCN5A (LQT3) genes. Variants with unknown clinical significance were identified in 4 probands (11%), which potentially allowed to confirm the diagnosis after functional tests.

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Odening, Katja E., Omar Hyder, Leonard Chaves, Lorraine Schofield, Michael Brunner, Malcolm Kirk, Manfred Zehender, Xuwen Peng, and Gideon Koren. "Pharmacogenomics of anesthetic drugs in transgenic LQT1 and LQT2 rabbits reveal genotype-specific differential effects on cardiac repolarization." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 6 (December 2008): H2264—H2272. http://dx.doi.org/10.1152/ajpheart.00680.2008.

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Anesthetic agents prolong cardiac repolarization by blocking ion currents. However, the clinical relevance of this blockade in subjects with reduced repolarization reserve is unknown. We have generated transgenic long QT syndromes type 1 (LQT1) and type 2 (LQT2) rabbits that lack slow delayed rectifier K+ currents ( IKs) or rapidly activating K+ currents ( IKr) and used them as a model system to detect the channel-blocking properties of anesthetic agents. Therefore, LQT1, LQT2, and littermate control (LMC) rabbits were administered isoflurane, thiopental, midazolam, propofol, or ketamine, and surface ECGs were analyzed. Genotype-specific heart rate correction formulas were used to determine the expected QT interval at a given heart rate. The QT index (QTi) was calculated as percentage of the observed QT/expected QT. Isoflurane, a drug that blocks IKs, prolonged the QTi only in LQT2 and LMC but not in LQT1 rabbits. Midazolam, which blocks inward rectifier K+ current ( IK1), prolonged the QTi in both LQT1 and LQT2 but not in LMC. Thiopental, which blocks both IKs and IK1, increased the QTi in LQT2 and LMC more than in LQT1. By contrast, ketamine, which does not block IKr, IKs, or IK1, did not alter the QTi in any group. Finally, anesthesia with isoflurane or propofol resulted in lethal polymorphic ventricular tachycardia (pVT) in three out of nine LQT2 rabbits. Transgenic LQT1 and LQT2 rabbits could serve as an in vivo model in which to examine the pharmacogenomics of drug-induced QT prolongation of anesthetic agents and their proarrhythmic potential. Transgenic LQT2 rabbits developed pVT under isoflurane and propofol, underlining the proarrhythmic risk of IKs blockers in subjects with reduced IKr.

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Diamant, Ulla-Britt, Farzad Vahedi, Annika Winbo, Annika Rydberg, Eva-Lena Stattin, Steen M. Jensen, and Lennart Bergfeldt. "Electrophysiological phenotype in the LQTS mutations Y111C and R518X in the KCNQ1 gene." Journal of Applied Physiology 115, no. 10 (November 15, 2013): 1423–32. http://dx.doi.org/10.1152/japplphysiol.00665.2013.

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Long QT syndrome is the prototypical disorder of ventricular repolarization (VR), and a genotype-phenotype relation is postulated. Furthermore, although increased VR heterogeneity (dispersion) may be important in the arrhythmogenicity in long QT syndrome, this hypothesis has not been evaluated in humans and cannot be tested by conventional electrocardiography. In contrast, vectorcardiography allows assessment of VR heterogeneity and is more sensitive to VR alterations than electrocardiography. Therefore, vectorcardiography was used to compare the electrophysiological phenotypes of two mutations in the LQT1 gene with different in vitro biophysical properties, and with LQT2 mutation carriers and healthy control subjects. We included 99 LQT1 gene mutation carriers (57 Y111C, 42 R518X) and 19 LQT2 gene mutation carriers. Potassium channel function is in vitro most severely impaired in Y111C. The control group consisted of 121 healthy subjects. QRS, QT, and T-peak to T-end (Tp-e) intervals, measures of the QRS vector and T vector and their relationship, and T-loop morphology parameters were compared at rest. Apart from a longer heart rate-corrected QT interval (QT heart rate corrected according to Bazett) in Y111C mutation carriers, there were no significant differences between the two LQT1 mutations. No signs of increased VR heterogeneity were observed among the LQT1 and LQT2 mutation carriers. QT heart rate corrected according to Bazett and Tp-e were longer, and the Tp-e-to-QT ratio greater in LQT2 than in LQT1 and the control group. In conclusion, there was a marked discrepancy between in vitro potassium channel function and in vivo electrophysiological properties in these two LQT1 mutations. Together with previous observations of the relatively low risk for clinical events in Y111C mutation carriers, our results indicate need for cautiousness in predicting in vivo electrophysiological properties and the propensity for clinical events based on in vitro assessment of ion channel function alone.

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Dissertations / Theses on the topic "LQT1"

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Castiglione, Alessandro [Verfasser], and Katja Elisabeth [Akademischer Betreuer] Odening. "Genotype-specific beneficial QT-shortening effects of docosahexaenoic acid in transgenic LQT1, LQT2, LQT5 and LQT2-5 rabbit models." Freiburg : Universität, 2018. http://d-nb.info/1216417571/34.

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Takenaka, Kotoe. "Exercise stress test amplifies genotype-phenotype correlation in the LQT1 and LQT2 forms of the long-QT syndrome." Kyoto University, 2005. http://hdl.handle.net/2433/144720.

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BERNARDI, JOYCE. "Arrhythmogenic mechanisms in genetic channelopathies." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2017. http://hdl.handle.net/10281/153192.

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Introduzione: Recentemente, varianti minori di SNP del gene NOS1AP sono stati associati a prolungamento del QT e aumentata incidenza di morte improvvisa in pazienti LQT1. Il gene NOS1AP codifica per la proteina CAPON, che localizza NOS1 in prossimità del reticolo sarcoplasmico (SR). L' attività di NOS1 è importante per la modulazione mediate da NO di ICaL, dei canali RyR2 e di SERCA, interferendo così con la regolazione dell’handling del Ca2+ e la stabilità del SR. Perciò abbiamo ipotizzato che gli SNPs di NOS1AP possano alterare la localizzazione/funzione di NOS1 diminuendo la stabilità del SR. In questo contesto, il prolungamento del QT indotto da mutazione, potrebbe indurre un sovraccarico di Ca2+, il cui effetto pro-aritmico potrebbe essere smascherato da un’alterata localizzazione/funzione di NOS1. Scopo: Valutare l’effetto di cambiamenti nell’attività di NOS1 a livello della stabilità funzionale del SR, della ripolarizzazione e aritmogenesi in un contesto di perdita di IKs (LQT1). Metodi: In miociti ventricolari di cavia soggetti a blocco di IKs (per riprodurre il fenotipo LQT1) e a stimolazione adrenergica (Isoproterenolo, ISO), abbiamo misurato l’attività elettrica, le correnti di membrane e il Ca2+ intracellulare, in condizione basale e dopo inibizione selettiva di NOS1 (SMTC 3µM). Risultati: In condizioni basali, l’inibizione di NOS1 prolunga la durata del PA (APD) (152.6  11.7 ms vs 96.1  9.0 ms; 58.8%. p<0.01), aumenta la densità di ICaL (SMTC vs CTRL: -16.61.2 pA/pF vs -13.51.0 pA/pF; p<0.05) ma non altera ne IKs (SMTC vs CTRL: 2.50.4 pA/pF vs 2.60.2 pA/pF) nè IKr (SMTC vs CTRL: 0.840.04 pA/pF vs 0.910.05 pA/pF). L’isoproterenolo, agonista -adrenergico (ISO, 1nM), induce delayed afterdepolarizations (DADs), un indice di instabilità del SR, in una percentuale significativamente maggiore di cellule trattate con SMTC rispetto a quelle di controllo (93% per SMTC vs 22% per CTRL, p<0.01). Inoltre, il tempo medio di comparsa delle DADs è significativamente ridotto in miociti trattati con SMTC rispetto a quelli di CTRL (25.8 ± 3.8 s e 61.5 ± 15.3 s rispettivamente, p<0.01). In aggiunta, la durata del PA è importante per il verificarsi di questi eventi, poiché il passaggio, in AP clamp, da un PA lungo (140 ms) a uno corto (100 ms) durante applicazione di ISO, abolisce le “transient inward currents” (ITI). Conclusioni: Questi risultati indicano che la mancanza di NOS1 può contribuire al prolungamento dell’APD e aumentare l’influsso di Ca2+; questi effetti compromettono la stabilità del SR in presenza di stimolazione adrenergica. Gli effetti dell’inibizione di NOS1 sono tali da poter spiegare l’effetto aritmogenico dei polimorfismi di NOS1AP.
Background: Recently, minor SNP variants of the NOS1AP gene have been reported to be associated with QT prolongation and increased incidence of sudden death in LQT1 patients. The NOS1AP gene encodes for CAPON protein, that localizes NOS1 close to the sarcoplasmic reticulum (SR). NOS1 activity accounts for NO-mediated modulation of ICaL, RyR2 channels and SERCA, thus interfering with regulation of Ca2+ handling and SR stability. Therefore we hypothesize that NOS1AP SNPs might affect NOS1 localization/function to decrease SR stability. In this setting, mutation-induced QT prolongation would induce Ca2+ overload, whose proarrhythmic effect would be unveiled by abnormal NOS1 localization/function. Aim: To evaluate the effect of changes in NOS1 activity on SR functional stability, repolarization and arrhythmogenesis in the context of IKs deficiency (LQT1). Methods: In guinea-pig ventricular myocytes subjected to IKs blockade (to reproduce the LQT1 phenotype) and adrenergic stimulation (Isoproterenol, ISO), we measured electrical activity, membrane currents and intracellular Ca2+, in basal condition and under selective inhibition of NOS1 (SMTC 3µM). Results: Under basal conditions, NOS1 inhibition prolonged AP duration (APD) (152.6  11.7 ms vs 96.1  9.0 ms; 58.8%. p<0.01), enhanced ICaL density (peak current density at +10 mV, SMTC vs CTRL: -16.61.2 pA/pF vs -13.51.0 pA/pF; p<0.05) and did not affect IKs (SMTC vs CTRL: 2.50.4 pA/pF vs 2.60.2 pA/pF) and IKr (SMTC vs CTRL: 0.840.04 pA/pF vs 0.910.05 pA/pF). The -adrenergic agonist isoproterenol (ISO, 1nM) induced delayed afterdepolarizations (DADs), an index of SR instability, in a significantly greater percentage of SMTC treated cells, compared to control ones (93% for SMTC vs 22% for CTRL, p<0.01). Moreover, the average time of DADs appearance was significantly different between SMTC and CTRL myocytes, with a earlier rise after NOS1 inhibition (25.8 ± 3.8 s and 61.5 ± 15.3 s respectively, p<0.01). Furthermore, the duration of the AP is important for the occurrence of these events, as switching from a long AP (140 ms) to a short AP (100 ms) waveform under ISO application in AP clamp mode, transient inward currents (Iti) were abolished. Conclusions: These results indicate that NOS1 deficiency may contribute to APD prolongation and enhance Ca2+ influx; these effects compromise SR stability in the presence of adrenergic stimulation. The effects of NOS1 inhibition are such as to account for the arrhythmogenic effect of NOS1AP polymorphism.

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Zenouzi, Roman [Verfasser], and Patrick [Akademischer Betreuer] Friederich. "Bupivacain destabilisiert die Aktionspotentialdauer im zellulären und computergestützten LQT1-Modell / Roman Zenouzi. Betreuer: Patrick Friederich." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2012. http://d-nb.info/1030365504/34.

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Koppermann, Susanne [Verfasser], and Katja Elisabeth [Akademischer Betreuer] Odening. "Genotyp- und geschlechtsspezifische Unterschiede der zellulären Elektrophysiologie und Kalziumhomöostase in transgenen LQT1 und Wildtyp Kaninchen." Freiburg : Universität, 2017. http://d-nb.info/1148929495/34.

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Kobori, Atsushi. "Additional gene variants reduce effectiveness of β-blockers in the LQT1 form of the long QT syndrome." Kyoto University, 2004. http://hdl.handle.net/2433/147467.

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Claure, Oviedo Jördis [Verfasser], and Alexander [Akademischer Betreuer] Schwoerer. "Etablierung eines in vivo Meerschweinchenmodells zur Risikostratifizierung medikamenteninduzierter LQT1 anhand vonIsofluran, Sevofluran und Droperidol / Jördis Claure Oviedo ; Betreuer: Alexander Schwoerer." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2018. http://d-nb.info/1155303733/34.

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SALA, LUCA. "Long QT Syndrome modelled with human induced pluripotent stem cells (hiPSc)." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2014. http://hdl.handle.net/10281/55330.

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Cardiac arrhythmias arise when the myocardium is electrically unstable. They represent a life-threatening phenomena with more than 300,000 people dying every year for arrhythmic sudden cardiac death (SCD) only in the United States. One of the most important and well described arrhythmic condition is the Long QT Syndrome (LQTS). LQTS is an heterogeneous disorder of myocardial repolarization characterized by a prolongation of QT interval on the electrocardiogram and clinically manifested with syncopal episodes and SCD. Mutations in 13 genes regulating cardiac action potential (AP) have been found directly responsible for LQTS. In addition, genes regulating Ca2+-handling are found associated with a LQTS phenotype. Furthermore, many modifier genes were identified as responsible in shaping the phenotype of LQTS mutations. The most recent experimental model available for in vitro studies of cardiac arrhythmias is represented by human induced pluripotent stem cells (hiPSC). The subsequent differentiation generates functional cardiomyocytes (hiPSC-CMs) with the same genotype of patients. The aims of this study were: 1) to characterized the functional features underlying an asymptomatic or symptomatic phenotype derived from the same KCNQ1 mutation; 2) to assess the functional effect of a new de novo mutation in CALM1. Functional studies were performed on hiPSC-CMs with the patch clamp technique in voltage- and current-clamp configurations. In addition, an in silico IK1 conductance was injected with dynamic-clamp to provide for the low expression of native IK1, which is characteristic of immature cells. Field potential duration (FPD) was assessed by 256-electrodes MultiElectrode Array in hiPSC-CMs embryoid bodies. The first study was focused on the mutation Y111C on KCNQ1 gene, encoding for Kv7.1 responsible for the repolarizing current IKs. Two relatives with the same mutation were involved: the symptomatic (S) son, with a markedly prolonged corrected QT interval (QTc), and the asymptomatic (AS) father, with a borderline QTc. Control, AS and S hiPSC-CMs lines were generated. Results show that: 1) Y111C mutation induced a prolongation in AP duration (APD) and FPD in S but not in AS cells. 2) IKs density was diminished in S and a partial rescue was evidenced in AS. 3) A different IKs density was evidenced between AS and S hiPSC-CMs when transfected with wild type KCNQ1. These results suggest a likely trafficking defect of Kv7.1 to cell membrane; in addition, we hypothesized the presence of a rescue mechanism, likely a modifier gene, involving protein folding and degradation in AS, blunting the effect of Y111C mutation. The second study was focused on F142L mutation in CALM1 gene, which has been recently found directly related to a very severe form of LQTS. CALM1 encodes for calmodulin, an ubiquitous Ca2+-binding protein mainly involved in the regulation of the electrical activity of cardiomyocytes. Two hiPSC-CMs lines were generated from healthy donors and F142L patient. Results show that F142L mutation caused: 1) a prolongation in APD and FPD; 2) a strong reduction in Ca2+-current (ICaL) Ca2+-dependent inactivation. 3) an incomplete ICaL steady-state inactivation with an increased window current. 4) an increased rate of arrhythmogenic events under β-adrenergic stimulation. We can conclude that F142L mutation is the responsible of the severe phenotype evidenced in patients by strongly impairing ICaL biophysical properties. Overall, hiPSC-CMs totally recapitulate the clinical phenotype and allows the study of cardiac arrhythmias of genetic origin with an high-level translational relevance. Furthermore, they represent an excellent starting point for the generation of mutation-specific and patient-specific pharmacological therapies.

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Martins, João Paulo Ataíde 1980. "Desenvolvimento de softwares, algoritmos e diferentes abordagens quimiométricas em estudos de QSAR." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/248544.

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Orientador: Márcia Miguel Castro Ferreira
Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Química
Made available in DSpace on 2018-08-25T11:39:21Z (GMT). No. of bitstreams: 1 Martins_JoaoPauloAtaide_D.pdf: 3637503 bytes, checksum: 5fe52d182b4f300eb103baf168ad75ab (MD5) Previous issue date: 2013
Resumo: O planejamento de fármacos com o auxílio do computador é uma área de pesquisa de extrema importância em química e áreas correlatas. O conjunto de ferramentas disponíveis para tal fim consiste, dentre outras, em programas para geração de descritores e construção e validação de modelos matemáticos em QSAR (do inglês, Quantitative Structure-Activity Relationship). Com o objetivo de tornar esse estudo mais acessível para a comunidade científica, novas metodologias e programas para geração de descritores e construção e validação de modelos QSAR foram desenvolvidos nessa tese. Uma nova metodologia de QSAR 4D, conhecida com LQTA-QSAR, foi desenvolvida com o objetivo de gerar descritores espaciais levando em conta os perfis de amostragem conformacional das moléculas em estudo obtidos a partir de simulações de dinâmica molecular. A geração desses perfis é feita com o software livre GROMACS e os descritores são gerados a partir de um novo software desenvolvido nesse trabalho, chamado de LQTAgrid. Os resultados obtidos com essa metodologia foram validados comparando-os com resultados obtidos para conjuntos de dados disponíveis na literatura. Um outro software de fácil uso, e que engloba as principais ferramentas de construção e validação de modelos em QSAR, foi desenvolvido e chamado de QSAR modeling. Esse software implementa o método de seleção de variáveis OPS, desenvolvido em nosso laboratório, e utiliza PLS (do inglês Partial Least Squares) como método de regressão. A escolha do algoritmo PLS implementado no programa foi feita com base em um estudo sobre o desempenho e a precisão no erro de validação dos principais algoritmos PLS disponíveis na literatura. Além disso, o programa QSAR modeling foi utilizado em um estudo de QSAR 2D para um conjunto de 20 flavonóides com atividade anti-mutagênica contra 3-nitrofluoranteno (3-NFA)
Abstract: Computer aided drug design is an important research field in chemistry and related areas. The available tools used in such studies involve software to generate molecular descriptors and to build and validate mathematical models in QSAR (Quantitative Structure-Activity Relationship). A new set of methodologies and software to generate molecular descriptors and to build and validate QSAR models were developed aiming to make these kind of studies more accessible to scientific community. A new 4DQSAR methodology, known as LQTA-QSAR, was developed with the purpose to generate spatial descriptors taking into account conformational ensemble profile obtained from molecular dynamics simulations. The generation of these profiles is performed by free software GROMACS and the descriptors are generated by a new software developed in this work, called LQTAgrid. The results obtained with this methodology were validated comparing them with results available in literature. Another user friendly software, which contains some of the most important tools used to build and validate QSAR models was developed and called QSAR modeling. This software implements the OPS variable selection algorithm, developed in our laboratory, and uses PLS (Partial Least Squares) as regression method. The choice of PLS algorithm implemented in the program was performed by a study about the performance and validation precision error involving the most important PLS algorithms available in literature. Further, QSAR modeling was used in a 2D QSAR study with 20 flavonoid derivatives with antimutagenic activity against 3-nitrofluoranthene (3-NFA)
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Físico-Química
Doutor em Ciências

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Barbosa, Euzébio Guimarães. "Ferramentas para QSAR-4D dependente de receptores = aplicação em uma série de inibidores da tripanotiona redutase do T. cruzi." [s.n.], 2011. http://repositorio.unicamp.br/jspui/handle/REPOSIP/248547.

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Orientador: Márcia Miguel Castro Ferreira
Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Química
Made available in DSpace on 2018-08-18T23:41:21Z (GMT). No. of bitstreams: 1 Barbosa_EuzebioGuimaraes_D.pdf: 4420345 bytes, checksum: e9da09f02df7f4d6c0756041fc40eb36 (MD5) Previous issue date: 2011
Resumo: LQTA-QSAR é uma metodologia computacional para QSAR-4D desenvolvida pelo Laboratório de Quimiometria Teórica e Aplicada implementada em um software de acesso livre. O método permite considerar simultaneamente as vantagens da representação molecular multiconformacional e os descritores de campos de interação. Esta tese apresenta a evolução da proposta inicial da metodologia LQTA-QSAR independente de receptores para uma abordagem dependente de receptores. Sua aplicação é demonstrada na construção de modelos de QSAR-4D para a previsão da atividade inibitória de compostos fenotiazínicos da enzima tripanotiona redutase. Foi obtido um modelo com bom poder de previsão (Qprev = 0,78) e com descritores de fácil interpretação. Tal modelo pode ser usado para a proposição de compostos que poderão vir a ser usados para o tratamento da doença de chagas. Para a filtragem e seleção de descritores foi necessário o desenvolvimento de um protocolo completamente distinto daquele disponível na literatura. Foi proposto um procedimento automatizado para identificar e eliminar descritores irrelevantes quando a correlação e um algoritmo que elimina descritores com distribuição díspar em relação à atividade biológica. Foram introduzidos também testes de validação de modelos QSAR nunca antes usados para modelos que utilizam descritores de campo de interação. O protocolo completo foi testado em três conjuntos de dados e os modelos obtidos tiveram capacidade de previsão superior aos da literatura. Os modelos mostraram ser bastante simples e robustos quando submetidos aos testes leave-N-out e y-randomization
Abstract: The New Receptor-Dependent LQTA-QSAR approach is proposed as a new 4D-QSAR method. The RD-LQTA-QSAR is an evolution to the receptor independent LQTA-QSAR. This approach make use of the simulation package GROMACS to carry out molecular dynamics simulations and generate a conformational ensemble profile for each compound. Such ensemble is used to build molecular interaction field based QSAR models, as in CoMFA. To verify the usefulness of the methodology it was chosen some phenothiazine derivatives that are specific competitive T. cruzi trypanothione reductase inhibitors. Using a combination of molecular docking and molecular dynamics simulations the binding mode of 38 phenotiazine derivatives was evaluated in a simulated induced fit approach. The ligands¿ alignment, necessary to the methodology, was performed using both ligand and binding site atoms hereafter enabling unbiased alignment. The obtained models were extensively validated by Leave-N-out cross-validation and y-randomization techniques to test robustness and absence of chance correlation. The final model presented Q LOO of 0.87 and R of 0.92 and suitable external prediction = 0.78. It is possible to use the obtained adapted binding site of to perform virtual screening and ligand structures based design, as well as using models descriptors to design new inhibitors. In the process of QSAR modeling, the relevance of correlation and distribution profiles were tested in order to improve prediction power. A set of tools to filter descriptors prior to variable selection and a protocol for molecular interaction field descriptors selection and models validation are proposed. The algorithms and protocols presents are quite simple to apply and enable a different and powerful way to build LQTA-QSAR models
Doutorado
Físico-Química
Doutor em Ciências

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Books on the topic "LQT1"

1

Histoire LQT 2de Manuel 2019. NATHAN, 2019.

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Love, Aowie. Composition Notebook : Hexagon Paper: Organic Chemistry and Biochemistry Note Book, Science Notebooks-LQT6. Independently Published, 2020.

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Nuyens, Dieter. Generation & Characterization of a Mouse Model for a Sodium Channel Based Long Qt Syndrome (Lqt3), an Inherited Arrhythmogenic Disease. Leuven University Press, 2006.

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Jaslyn, Daryl. Productivity Planner: Skiing Couple I Choose You Pt Lqt Nth 110 Pages Daily Planner, Calendar and Gratitude Journal to Increase Productivity and Happiness, High Performance Organizer Planner. Independently Published, 2021.

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Day, Daryl. Productivity Planner: Ballet Not Easy Worth It Pt Lqt Dqh 110 Pages Daily Planner, Calendar and Gratitude Journal to Increase Productivity and Happiness, High Performance Organizer Planner. Independently Published, 2021.

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Haley, Mcculloch. Daily Journal: Be Cowgirl Who Loves Surfing Pt Lqt Ntv Easily Organizes Your Daily Tasks and Boosts Productivity - the Perfect Journal and Undated Office Supplies Notepad for Women, Men, Kids. Independently Published, 2021.

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Chase, Mcculloch. Daily Journal: Snowboarding Beer Murde Is Wrong Pt Lqt Nna Easily Organizes Your Daily Tasks and Boosts Productivity - the Perfect Journal and Undated Office Supplies Notepad for Women, Men, Kids. Independently Published, 2021.

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Kaiser, Mcculloch. Daily Journal: Moto Biker Race Corner Happiness Pt Lqt Ngt Easily Organizes Your Daily Tasks and Boosts Productivity - the Perfect Journal and Undated Office Supplies Notepad for Women, Men, Kids. Independently Published, 2021.

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Berry, Mcculloch. Daily Journal: Golf Golf for a Living Pt Lqt Dqh Easily Organizes Your Daily Tasks and Boosts Productivity - the Perfect Journal and Undated Office Supplies Notepad for Women, Men, Kids. Independently Published, 2021.

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Snyder, Evans. Daily Planner: Aikido Ferret Pt Lqt Pml to Do List Notebook, Hourly Schedules Undated, Boosts Productivity, Easily Organizes Daily Tasks, the Perfect Journal and Office Supplies Notepad for Women Mandala Content. Independently Published, 2021.

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Book chapters on the topic "LQT1"

1

Bari, V., T. Bassani, A. Marchi, G. Girardengo, L. Calvillo, S. Cerutti, P. A. Brink, L. Crotti, P. J. Schwartz, and A. Porta. "Symbolic Analysis of Heart Period and QT Interval Variabilities in LQT1 Patients." In IFMBE Proceedings, 531–34. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-00846-2_131.

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Domínguez, Sebastián, Joyce Reimer, Kevin R. Green, Reza Zolfaghari, and Raymond J. Spiteri. "A Simulation-Based Method to Study the LQT1 Syndrome Remotely Using the EMI Model." In Emerging Technologies in Biomedical Engineering and Sustainable TeleMedicine, 179–89. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-14647-4_12.

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Fischer, Gabriele, Annemarie Unger, W. Wolfgang Fleischhacker, Cécile Viollet, Jacques Epelbaum, Daniel Hoyer, Ina Weiner, et al. "LQTS." In Encyclopedia of Psychopharmacology, 730. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_4332.

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Leung, Alexander K. C., William Lane M. Robson, Carsten Büning, Johann Ockenga, Janine Büttner, Hartmut Schmidt, Antonio V. Delgado-Escueta, et al. "LQTS." In Encyclopedia of Molecular Mechanisms of Disease, 1212–13. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_9515.

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Leung, Alexander K. C., William Lane M. Robson, Carsten Büning, Johann Ockenga, Janine Büttner, Hartmut Schmidt, Antonio V. Delgado-Escueta, et al. "LQT Syndrome." In Encyclopedia of Molecular Mechanisms of Disease, 1212. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6927.

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Zareba, Wojciech. "Clinical Management of LQTS Patients." In Cardiac Repolarization, 165–84. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-22672-5_9.

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Mazzanti, Andrea, and Silvia G. Priori. "Inherited Arrhythmias: LQTS/SQTS/CPVT." In Cardiovascular Genetics and Genomics, 413–35. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-66114-8_13.

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Friedewald, Vincent E. "Long QT Syndrome: Acquired (LQTS)." In Clinical Guide to Cardiovascular Disease, 797–805. London: Springer London, 2016. http://dx.doi.org/10.1007/978-1-4471-7293-2_57.

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Furutani, Yoshiyuki, Emiko Hayama, Nanako Kawaguchi, Yasuhiro Katsube, Eiko Oomichi, Mitsuyo Shimada, Kei Inai, and Toshio Nakanishi. "Establishment of an In Vitro LQT3 model Using Induced Pluripotent Stem Cells from LQT3 Patient-Derived Cardiomyocytes." In Molecular Mechanism of Congenital Heart Disease and Pulmonary Hypertension, 393–94. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-1185-1_63.

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Zimmer, Thomas, and Klaus Benndorf. "Molecular Mechanisms of Voltage-Gated Na+ Channel Dysfunction in LQT3 Syndrome." In Heart Rate and Rhythm, 409–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-17575-6_22.

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Conference papers on the topic "LQT1"

1

Adolfo Sampedro-Puente, David, Fabien Raphel, Jesus Fernandez-Bes, Pablo Laguna, Damiano Lombardi, and Esther Pueyo. "In Silico Characterization of Repolarization Duration and Variability in the LQT1 Syndrome Under β-Adrenergic Stimulation." In 2020 Computing in Cardiology Conference. Computing in Cardiology, 2020. http://dx.doi.org/10.22489/cinc.2020.430.

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Borrás Pinilla, Carlos, José Luis Sarmiento, and Rubén Darío Guiza. "Modelling, System Identification and Position Control Based on LQR Formulation for an Electro-Hydraulic Servo System." In ASME 2019 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/imece2019-11505.

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Abstract This study presents the mathematical modelling, system identification using grey-box model estimation and position-tracking control for an electro-hydraulic servo system (EHSS) using four control strategies based on LQR formulation: Linear quadratic regulator (LQR) approach for servo systems, linear quadratic integral (LQI), linear quadratic tracking (LQT) and a variation of LQT named here LQTβ. First, the nonlinear model of the electro-hydraulic servo system was obtained using differential equations based on hydraulic theory and physical laws. The model was then linearized and its parameters were estimated using grey-box method when the open-loop system was excited with a chirp signal from 0 to 30 [Hz]. The estimated model was verified with experimental data of the open-loop system response for square wave and continuous step inputs of different amplitudes and frequencies. For the position-tracking four control strategies based on LQR formulation were proposed. The main difference among them is the conception of the cost function that is minimized: the LQR includes all the system’s states and the control signal, the LQI includes all system’s states, the tracking error and the control signal, the LQT includes only the tracking error and the LQTβ the tracking error and its derivative. The four control strategies were simulated in MATLAB Simulink and initially tuned using Bryson’s rule, then were implemented in the real system and finely tuned by trial and error until the best performance is achieved. They all were tested using step, square wave and sine wave inputs, and were analyzed in terms of settling time, rising time, peak time, overshoot margin, steady-state error, energy consumption and repeatability against a conventional PID controller. The experimental results showed better tracking, better repeatability and less energy consumption using the LQR based techniques than using the PID control, specifically the LQR and the LQTβ showed the fastest response and smallest steady-state error among the LQR based strategies. This study was carried out with the electro-hydraulic servo system (EHSS) of the seismic shaker table of the Dynamics and Structural Control Lab at Universidad Industrial de Santander. The seismic shaker table is composed of a Parker double rod dynamic hydraulic cylinder commanded by an MTS 252.24G-04 servo valve and powered by an MTS 505.11 hydraulic power unit. Cylinder’s position was measured using an integrated Trans-Teck LVDT. The control system was build and implemented in MATLAB Simulink using Quanser Q8-USB card.

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Alonso-Atienza, Felipe, Jesus Requena-Carrion, Jose Luis Rojo-Alvarez, Omer Berenfeld, and Jose Jalife. "Action Potential Alternans in LQT3 Syndrome: A Simulation Study." In 2007 29th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2007. http://dx.doi.org/10.1109/iembs.2007.4352371.

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Robertson, Clay J., Andrew J. Sinclair, and Emily Doucette. "Decentralized LQT in a Limited Information Environment." In AIAA Guidance, Navigation, and Control Conference. Reston, Virginia: American Institute of Aeronautics and Astronautics, 2017. http://dx.doi.org/10.2514/6.2017-1252.

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Andrzejewska, Malgorzata, Mateusz Ozimek, Karolina Rams, and Teodor Buchner. "Asymmetry of RR intervals and ECG amplitudes in LQTS patients." In 2022 12th Conference of the European Study Group on Cardiovascular Oscillations (ESGCO). IEEE, 2022. http://dx.doi.org/10.1109/esgco55423.2022.9931345.

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Pintaningrum, Yusra, and Ketut Angga Aditya Putra Pramana. "Acquired Long QT Syndrome (LQTS) Secondary to Electrolyte Imbalance: A Case Report." In 2nd Global Health and Innovation in conjunction with 6th ORL Head and Neck Oncology Conference (ORLHN 2021). Paris, France: Atlantis Press, 2021. http://dx.doi.org/10.2991/ahsr.k.220206.047.

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Bartolucci, Chiara, Cristina Moreno, Anna Oliveras, Carmen Mu�oz, Alicia de la Cruz, Diego A. Peraza, Juan R. Gimeno, et al. "IKs Computational Modeling to Enforce the Investigation of D242N, a KV7.1 LQTS Mutation." In 2017 Computing in Cardiology Conference. Computing in Cardiology, 2017. http://dx.doi.org/10.22489/cinc.2017.064-312.

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Shafiee, Pouya, and Yazdan Batmani. "Output Voltage Control of Inverters Using SDRE Tracking and LQT Controllers." In 2019 6th International Conference on Control, Instrumentation and Automation (ICCIA). IEEE, 2019. http://dx.doi.org/10.1109/iccia49288.2019.9030812.

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Zhao, "Shumo, Cunjin Luo, Ying He, and Linghua Li." "Simulation of Acquired LQT Syndrome Using Human Virtual Ventricular Cardiomyocyte Model." In 2022 Computing in Cardiology Conference. Computing in Cardiology, 2022. http://dx.doi.org/10.22489/cinc.2022.420.

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OLIVEIRA, LARA TAVARES DE, KAIQUE SILVEIRA VIANA COSTA, KENEDY MATIASSO PORTELLA, LUCAS VIZZOTTO BELLINASO, FERNANDA DE MORAIS CARNIELUTTI, and DENIEL DESCONZI MORAES. "Quadcopter Modeling and Control Using Controller Hardware-in-the-Loop." In Seminar on Power Electronics and Control (SEPOC 2021). sepoc, 2021. http://dx.doi.org/10.53316/sepoc2021.080.

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Quadcopters have many applications and an efficient controller is needed for reference tracking and to maintain vehicle stability. Quadcopter tests may require expensive laboratory setup to include certain conditions such as wind, with adequate control and monitoring. In this paper a bench markmodel of quadcopter is implemented in Hardware-In-the-Loop, in order to test the quadcopter controller considering different conditions of wind. For experimental results, an LQT controller has been implemented in a DSP, while the quadcopter was implemented in the real-time simulator Typhoon HIL.

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