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1,084 results for “substrate”
Extremely low frequency electromagnetic fields enhance neuronal differentiation of human mesenchymal stem cells on graphene-based substrate
GEO Series GSE64416. Homo sapiens. 3 samples. Type: Expression profiling by array.
LARP7 is a substrate of BRCA1 that regulats genome instability and tumorigenesis
GEO Series GSE124393. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
A novel functional role for the serine protease inhibitor SerpinA3N and its substrate leukocyte elastase in neuropathic pain
GEO Series GSE63442. Rattus norvegicus. 12 samples. Type: Expression profiling by array.
Global cellular metabolic rewiring adapts Corynebacterium glutamicum to efficient non-natural substrate utilization
GEO Series GSE184402. Corynebacterium glutamicum ATCC 13032. 9 samples. Type: Expression profiling by high throughput sequencing.
RNA substrate length as an indicator of exosome interactions in vivo
GEO Series GSE94889. Saccharomyces cerevisiae. 1 samples. Type: Other.
To detect the heparan sulfate proteoglycans (HSGP) core proteins that are expressed in these cell lines, so that candidates for the Sulf-2 substrate can be identified
GEO Series GSE31935. Homo sapiens. 30 samples. Type: Expression profiling by array.
A hexasome is the preferred substrate for the INO80 chromatin remodeling complex allowing versatility of function
GEO Series GSE168700. Saccharomyces cerevisiae. 4 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
Substrate specificity and protein stability drive the divergence of plant-specific DNA methyltransferases [Bisulfite-seq]
GEO Series GSE247352. Arabidopsis thaliana. 15 samples. Type: Methylation profiling by high throughput sequencing.
Global Gene Expression of Dehalococcoides Within a TCE-Dechlorinating Community Under Conditions of Periodic Substrate Supply
GEO Series GSE42635. Dehalococcoides mccartyi BAV1; Dehalococcoides; Dehalococcoides mccartyi CBDB1; Dehalococcoides mccartyi 195; Dehalococcoides mccartyi VS. 9 samples. Type: Expression profiling by array.
Deep Mutagenesis of a Transporter for Uptake of a Non-Native Substrate Identifies Conformationally Dynamic Regions
GEO Series GSE109499. Homo sapiens. 10 samples. Type: Other.
Substrate stiffness dictates unique paths towards proliferative arrest in WI-38 cells [ATAC-Seq]
GEO Series GSE276047. Homo sapiens. 36 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
CMR for Identifying the Substrate of Ventricular Arrhythmia in Patients with Q1 Normal Echocardiography
<p>OBJECTIVES This study sought to determine whether cardiac magnetic resonance (CMR) may identify structural heart<br> disease (SHD) in patients with ventricular arrhythmia who had echocardiography ruled out pathological findings.<br> BACKGROUND Approximately one-half of sudden cardiac deaths are attributable to malignant VA. Echocardiography is<br> commonly used to identify SHD that is the most frequent substrate of VA.<br> Q6 METHODS A single-center prospective study was conducted in consecutive patients with significant VA, categorized as<br> >1,000 but <10,000 ventricular ectopic beats [VEB]s/24 h; $10,000 VEBs/24 h; nonsustained ventricular tachycardia,<br> sustained ventricular tachycardia (SVT), or a history of resuscitated cardiac arrest, and no pathological findings at<br> echocardiography, requiring a clinically indicated CMR. Primary endpoint was CMR detection of SHD. Secondary endpoints<br> were a composite of CMR detection of SHD and abnormal findings not specific for a definite SHD diagnosis.<br> RESULTS A total of 946 patients were enrolled (mean 41 16 years of age; 64% men). CMR studies were used to<br> diagnose SHD in 241 patients (25.5%) and abnormal findings not specific for a definite SHD diagnosis in 187 patients<br> (19.7%). Myocarditis (n ¼ 91) was the more frequent disease, followed by arrhythmogenic cardiomyopathy (n ¼ 55),<br> dilated cardiomyopathy (n ¼ 39), ischemic heart disease (n ¼ 22), hypertrophic cardiomyopathy (n ¼ 13), congenital<br> cardiac disease (n ¼ 10), left ventricle noncompaction (n ¼ 5), and pericarditis (n ¼ 5). The strongest univariate and<br> multivariate predictors of SHD on CMR images were chest pain (odds ratios [OR]: 2.52 and 2.38, respectively) and SVT<br> (ORs: 2.67 and 2.23, respectively).<br> CONCLUSIONS SHD was able to be identified on CMR imaging in a sizable number of patients with significant VA and<br> completely normal echocardiography. Chest pain and SVT were the strongest predictors of positive CMR imaging<br> results. </p>
Data set from Ciconte G, Santinelli V, Vicedomini G, Borrelli V, Monasky MM, Micaglio E, Giannelli L, Negro G, Giordano F, Mecarocci V, Mazza BC, Locati E, Anastasia L, Calovic Z, Pappone C. Non-invasive assessment of the arrhythmogenic substrate in Brugada syndrome using signal-averaged electrocardiogram: clinical implications from a prospective clinical trial. Europace. 2019 Dec 1;21(12):1900-1910. doi: 10.1093/europace/euz295. PMID: 31647530.
<p>Data set from Ciconte G, Santinelli V, Vicedomini G, Borrelli V, Monasky MM, Micaglio E, Giannelli L, Negro G, Giordano F, Mecarocci V, Mazza BC, Locati E, Anastasia L, Calovic Z, Pappone C. Non-invasive assessment of the arrhythmogenic substrate in Brugada syndrome using signal-averaged electrocardiogram: clinical implications from a prospective clinical trial. Europace. 2019 Dec 1;21(12):1900-1910. doi: 10.1093/europace/euz295. PMID: 31647530.</p> <p> </p> <p>This is the abstract:</p> <p><strong>Aims: </strong> Brugada syndrome (BrS) represents a major cause of sudden cardiac death in young individuals. The risk stratification to forecast future life-threatening events is still controversial. Non-invasive assessment of late potentials (LPs) has been proposed as a risk stratification tool. However, their nature in BrS is still undetermined. The purpose of this study is to assess the electrophysiological determinants of non-invasive LPs.</p> <p><strong>Methods and results: </strong> Two hundred and fifty consecutive patients with (Group 1, n = 96) and without (Group 2, n = 154) BrS-related symptoms were prospectively enrolled in the registry. Signal-averaged electrocardiogram (SAECG) was performed in all subjects before undergoing epicardial mapping. Group 1 patients exhibited larger arrhythmogenic substrates (AS; 5.8 ± 2.8 vs. 2.6 ± 2.1 cm2, P < 0.001) with more delayed potentials (220.4 ± 46.0 vs. 186.7 ± 42.3 ms, P < 0.001). Late potentials were present in 82/96 (85.4%) Group 1 and in 31/154 (20.1%) Group 2 individuals (P < 0.001). Patients exhibiting LPs had more frequently a spontaneous Type 1 pattern (30.1% vs. 10.9%, P < 0.001), SCN5A mutation (34.5% vs. 21.2%, P = 0.02), and exhibited a larger AS with longer potentials (5.8 ± 2.7 vs. 2.2 ± 1.7 cm2; 231.2 ± 37.3 vs. 213.8 ± 39.0 ms; P < 0.001, respectively). Arrhythmogenic substrate dimension was the strongest predictor of the presence of LPs (odds ratio 1.9; P < 0.001). An AS area of at least 3.5 cm2 identified patients with LPs (area under the curve 0.88, 95% confidence interval 0.843-0.931; P < 0.001) with a sensitivity of 86%, specificity 88%, positive predictive value 85%, and negative predictive value 89%.</p> <p><strong>Conclusion: </strong> The results of this study support the role of the epicardial AS as an electrophysiological determinant of non-invasive LPs, which may serve as a tool in the non-invasive assessment of the BrS substrate, as SAECG-LPs could be considered an expression of the abnormal epicardial electrical activity.</p> <p>ClinicalTrials.gov number (<a href="http://clinicaltrials.gov/show/NCT02641431">NCT02641431</a>; <a href="http://clinicaltrials.gov/show/NCT03106701">NCT03106701</a>).</p> <p> </p>
Data set from Pappone C, Mecarocci V, Manguso F, Ciconte G, Vicedomini G, Sturla F, Votta E, Mazza B, Pozzi P, Borrelli V, Anastasia L, Micaglio E, Locati E, Monasky MM, Lombardi M, Calovic Z, Santinelli V. New electromechanical substrate abnormalities in high-risk patients with Brugada syndrome. Heart Rhythm. 2020 Apr;17(4):637-645. doi: 10.1016/j.hrthm.2019.11.019. Epub 2019 Nov 19. PMID: 31756528.
<p>Data set from Pappone C, Mecarocci V, Manguso F, Ciconte G, Vicedomini G, Sturla F, Votta E, Mazza B, Pozzi P, Borrelli V, Anastasia L, Micaglio E, Locati E, Monasky MM, Lombardi M, Calovic Z, Santinelli V. New electromechanical substrate abnormalities in high-risk patients with Brugada syndrome. Heart Rhythm. 2020 Apr;17(4):637-645. doi: 10.1016/j.hrthm.2019.11.019. Epub 2019 Nov 19. PMID: 31756528.</p> <p> </p> <p>This is the abstract:</p> <p><strong>Background: </strong> The relationship between the typical electrocardiographic pattern and electromechanical abnormalities has never been systematically explored in Brugada syndrome (BrS).</p> <p><strong>Objectives: </strong> The aims of this study were to characterize the electromechanical substrate in patients with BrS and to evaluate the relationship between electrical and mechanical abnormalities.</p> <p><strong>Methods: </strong> We enrolled 50 consecutive high-risk patients with BrS (mean age 42 ± 7.2 years), with implantable cardioverter-defibrillator implantation for primary or secondary prevention of ventricular tachyarrhythmias (ventricular tachycardia/ventricular fibrillation [VT/VF]), undergoing substrate mapping and ablation. Patients underwent 3-dimensional (3D) echocardiography with 3D wall motion/deformation quantification and electroanatomic mapping before and after ajmaline administration (1 mg/kg in 5 minutes); 3D mechanical changes were compared with 50 age- and sex-matched controls. The effect of substrate ablation on electromechanical abnormalities was also assessed.</p> <p><strong>Results: </strong> In all patients, ajmaline administration induced Brugada type 1 pattern, with a significant increase in the electrical substrate (P < .001), particularly in patients with previous spontaneous VT/VF (P = .007). Induction of Brugada pattern was associated with lowering of right ventricular (RV) ejection fraction (P < .001) and worsening of 3D RV mechanical function (P < .001), particularly in the anterior free wall of the RV outflow tract, without changes in controls. RV electrical and mechanical abnormalities were highly correlated (r = 0.728, P < .001). By multivariate analysis, only the area of RV dysfunction was an independent predictor of spontaneous VT/VF (odds ratio 1.480; 95% confidence interval 1.159-1.889; P = .002). Substrate ablation abolished both BrS-electrocardiographic pattern and mechanical abnormalities, despite ajmaline rechallenge.</p> <p><strong>Conclusion: </strong> BrS is an electromechanical disease affecting the RV. The typical BrS pattern reflects an extensive RV arrhythmic substrate, driving consistent RV mechanical abnormalities. Substrate ablation abolished both Brugada pattern and mechanical abnormalities.</p> <p> </p>
Neural substrates of neuropsychological profiles in dystrophynopathies: A pilot study of diffusion tractography imaging
<p>Tables and Figures sources for "Biagi L, Lenzi S, Cipriano E, Fiori S, Bosco P, Cristofani P, et al. (2021) Neural substrates of neuropsychological profiles in dystrophynopathies: A pilot study of diffusion tractography imaging. PLoS ONE 16(5): e0250420. https://doi.org/10.1371/journal.pone.0250420"</p>
ARRIVE guidelines author checklist of "Structural and functional analysis reveals the catalytic mechanism and substrate binding mode of the broad-spectrum endolysin Ply2741"
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Shadow mask assisted 193 nm Excimer laser processing of commercial Cyclo-Olefin-Copolymer (COC) substrates for low-cost micro-fluidic biosensing devices.
<p>An Abstract submitted to The 24th International Symposium on Laser Precision Microfabrication (LPM2023)</p>
Dcp1a, a novel Mek substrate, regulates the self-renewal and differentiation of mouse embryonic stem cells
GEO Series GSE269161. Mus musculus. 6 samples. Type: Other.
In Vitro Model for a Drug Assessment of Cytochrome P450 Family 3 Subfamily A Member 4 Substrates Using Human Induced Pluripotent Stem Cells and Genome Editing Technology
GEO Series GSE159159. Homo sapiens. 2 samples. Type: Expression profiling by high throughput sequencing.
Reprogramming deaminase substrate specificity for single nucleobase editing
GEO Series GSE294219. Homo sapiens. 40 samples. Type: Other.
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Annotated Behaviour and Observability Dataset (ABODe)
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