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Gated Blood-Pool Imaging

Gated Blood-Pool Imaging: Unlocking the Potential of Cardiac Imaging.
This non-invasive technique captures dynamic images of the heart's blood flow, allowing for detailed assessment of cardiac function and structure.
By synchronizing image acquisition with the patient's heartbeat, Gated Blood-Pool Imaging provides valuable insights into ventricular ejection fraction, wall motion, and other hemodynamic parameters.
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Most cited protocols related to «Gated Blood-Pool Imaging»

Genomic DNA was extracted from each DO mouse (n = 192 total samples) and genotyped at 57,973 single nucleotide polymorphisms (SNPs) on the Mega-MUGA platform (Geneseek)44 (link). A total of 177 out of 192 samples passed SNP quality control metrics. For these samples, founder haplotypes were inferred from SNP probe intensities using a hidden Markov model implemented in the DOQTL R package27 (link),45 (link), and then used to interpolate a grid of 64,000 evenly-spaced genetic intervals. In addition, founder haplotypes were independently inferred from the RNA-seq data by genotyping by RNA-seq (GBRS) protocol (see next section) and interpolated to the same 64,000 interval grid.
For each sample, we verified that the haplotype reconstructions agreed between the DNA Mega-MUGA and GBRS reconstructions by calculating the Pearson correlation between each pair of samples. When a Mega-MUGA sample had a correlation below 0.4 with the same sample ID in the RNA-seq data, we assumed that this sample was mismatched. We searched the RNA-seq data for the correct match to the Mega-MUGA sample by looking for another sample that was more highly correlated. If we found an RNA-seq sample with a correlation >0.4 that was not assigned to another sample, we matched it with the Mega-MUGA sample. When a sample was removed from the Mega-MUGA data for technical reasons, we used the GBRS haplotype reconstructions (samples F326, F328, F362, F363, F368, M377, M388, M392, M393, M394, M404, M408, M411, M419 and M425).
Publication 2016
Gated Blood-Pool Imaging Genome Haplotypes Mice, House Reconstructive Surgical Procedures RNA-Seq
High-confidence SNPs and indels of <100 bases from the DO founder strains were obtained from the Sanger Mouse Genomes website [(Keane et al. 2011 (link)) Release 20111102, ftp://ftp-mouse.sanger.ac.uk]. “High-confidence” SNPs were defined by Sanger’s criterion and denoted in the variant file by an above-threshold genotype (ATG) value = 1. There are additional variants in these genomes that will not be captured but the individualized genomes represent a good approximation to the actual genomes of these strains. SNPs and indels were incorporated into the reference mouse genome sequence (NCBIM37) to construct a strain-specific genome in fasta format. Genome coordinates in the gene annotation file (Ensembl version 67) were adjusted to reflect indels in each strain. The individualized genome and gene annotation files were used to construct strain-specific transcriptomes containing all annotated gene isoforms with SNPs and indels incorporated.
Genomic DNA was extracted from each DO mouse and genotyped at 7664 SNPs on the Mouse Universal Genotyping Array (“MUGA”, GeneSeek) (Welsh and McMillan 2012 ). Founder haplotypes were inferred from SNP probe intensities, using a hidden Markov model in the DOQTL R package (Broman et al. 2012 ; Gatti et al. 2014 ). At each SNP, the genotype with the highest posterior probability was recorded, and genotype state transitions were inferred at the physical midpoint between adjacent markers with differing genotypes. Individual chromosomes were phased to construct haplotypes by minimizing the number of recombination events consistent with the observed genotypes. Accurate long-range phasing is not critical for our purposes. For each DO sample, this process yields two genotype transition files [designated left (“L”) and right (“R”)] from which a pair of homologs is reconstructed. Chromosomal coordinates are mapped back to the reference genome (NCBIM37) to obtain annotation specific to each homolog. A diploid transcriptome is constructed with two copies of each transcript, one for each homolog.
Seqnature uses the genotype transition files and founder strain variant call data to construct individualized genomes and gene annotation files. Seqnature scans through the variant call format (VCF) files, and at each position with a known SNP or indel, if the sample haplotype matches the founder strains with the variant, the variant is added to the individualized genome. For each sample two haploid genomes are produced and merged into one diploid genome file with chromosomes designated as L or R [e.g., chromosome (Chr) 1L, Chr 1R]. Offset tracking data are used to update the coordinates of features in the gene annotation file (Ensembl v67), and the two annotation files are merged. The pair of records for each feature in the merged file is annotated to the L or R chromosomes and an additional annotation indicates the founder strain origin (A–H) of each feature. Features that span inferred recombination boundaries are labeled with both founders. One copy of the reference mitochondrial genome and any unassigned contig sequences are added to the merged genome sequence. One copy of the reference Y chromosome sequence is added to male samples.
Publication 2014
Chromosomes Diploidy Gated Blood-Pool Imaging Gene Annotation Genes Genome Genome, Mitochondrial Genotype Haplotypes INDEL Mutation Males Mice, House Physical Examination Protein Isoforms Radionuclide Imaging Recombination, Genetic Reproduction Transcriptome Y Chromosome
A wide range of complementary data resources were used to analyze the CC genomes. Second generation MegaMUGA genotypes (∼70,000 markers) are available for the MRCAs of each CC strain. From these genotypes, we inferred all possible founder origin combinations at each marker genotype (8 inbred and 28 heterozygous combinations for autosomes and 8 founder for hemizygous chromosomes and mitochondria), which, hereafter we refer to as “36-state probabilities” founder probabilities at each marker of each individual MRCA. The founder probabilities from the MRCA set of a CC strain were conservatively merged into a composite MRCA 36-state probability to estimate residual heterozygosity (evidence of multiple alleles at any marker between different MRCA samples was declared heterozygous). The founder probabilities of MRCA samples and their composites are summarized by selecting the maximum-likelihood genotype at each locus and allocating its alleles across two pseudophased haplotypes such that the number of founder transitions were minimized, resulting in a “hapfile.” All hapfiles were tested to be consistent with the original genotypes. Statistics on the number of recombinations, the fraction of founder contribution to each CC strain, and chromosome ideograms are derived from these hapfiles.
A similar inference pipeline was applied to the 69 sequenced samples, which were also genotyped using the third generation GigaMUGA (∼140,000 markers). The hapfiles and 36-state founder probabilities of different genotyping platforms can be directly compared. We also chose to infer the founder probabilities from the sequenced data using the msBWTs so that the results (36-state probabilities and hapfiles) were compatible, but at much higher resolution, with the genotyped samples.
A set of three samples from CC018/Unc were later genotyped using the first generation MUGA platform (∼7,000 markers), to assess how representative the sequenced sample is of its CC line. Once more, we generated 36-state founder inferences and hapfiles to allow us to compare results ascertained by different platforms and technologies.
The genomic founder mosaics, as represented by the hapfiles, were used to partition the CC strain genomes according to their origin for calling new and private mutations. The resulting browser extensible data (BED) and VCF files are provided.
All of the founder inference-related data resources: genotypes, the 36-state probabilities of samples and MRCA composites, hapfiles, chromosome ideograms, and msBWTs for each sequenced CC line, are available online (http://csbio.unc.edu/CCstatus/CCGenomes).
The ENA accession PRJEB14673 provides access to the following files:
Zenodo accession no. 377036 provides access to the following files:
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Publication 2017
Alleles Chromosomes Chromosomes, Human, Pair 8 Gated Blood-Pool Imaging Genetic Markers Genome Genotype Haplotypes Hemizygote Heterozygote Mitochondria Mutation Recombination, Genetic Strains
gQTL was implemented using the R Shiny framework (Chang et al. 2016 ), which provides necessary tools for rapid prototyping of interactive web applications. gQTL relies on functions from the DOQTL R package to perform QTL mapping (Gatti et al. 2014 (link)). Since the CC population has a fixed genetic architecture, associated genotypes and haplotype probabilities for each CC line are stored and loaded into memory in the backend when gQTL is launched. The genotype probabilities for each CC and founder strain were obtained from UNC Systems Genetics data repository (http://csbio.unc.edu/CCstatus/index.py), while the MegaMUGA and GigaMUGA marker set from which the genotypes are determined in the CC was obtained from The Jackson Laboratory data repository (ftp://ftp.jax.org/MUGA/). The user has the ability to choose between either of these marker sets during the submission of the analysis.
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Publication 2018
Gated Blood-Pool Imaging Genitalia Genotype Haplotypes Memory Reproduction Strains
The study sample consisted of consecutive patients with cancer who had both MUGA and CMR within 30 days between January 2007 and September 2016 at the University of Minnesota Medical Center, Minneapolis, Minnesota, USA. The institutional MUGA database was cross-matched with the University of Minnesota Cardiovascular Magnetic Resonance Registry, an ongoing observational registry including all patients that undergo CMR at the University of Minnesota, to identify the study patients. Patients were excluded if their records indicated any of these intervening clinical events that could potentially impact cardiac function: acute myocardial infarction, heart failure hospitalization, administration of potentially cardiotoxic cancer treatment, or acute systemic illness such as sepsis. An electronic database was created to include demographic information, medical history including reasons for the studies, co-morbidities and medications, and MUGA and CMR findings for each patient. This retrospective cross-sectional study was approved by University of Minnesota’s Institutional Review Board with a waiver of informed consent.
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Publication 2017
Cardiotoxicity Cardiovascular System Congestive Heart Failure Ethics Committees, Research Gated Blood-Pool Imaging Heart Hospitalization Magnetic Resonance Imaging Malignant Neoplasms Myocardial Infarction Patient Care Management Patients Pharmaceutical Preparations Septicemia

Most recents protocols related to «Gated Blood-Pool Imaging»

Proteins from the defatted pupae powder of both silkworms were isolated using the alkaline extraction method, as described by Jia et al. [11 (link)] with modifications. Briefly, 5% (w/v) defatted powder in water was calibrated to pH 9.5, using 1 M NaOH. The solution was then stirred for 2 h at room temperature and then centrifuged at 4 °C for 30 min at 8000× g (F-35-6-30 rotor, Eppendorf 5430R, Eppendorf AG, Hamburg, Germany). The collected pellet was re-extracted twice using the same procedure. Supernatants obtained from the total four extractions were adjusted to pH 4.0–5.8, using 1 M HCl to screen the isoelectric point. The pellet, having precipitated proteins at pH 4.7, was isolated from the supernatant after centrifugation for 30 min and 8000× g at 4 °C. The pellets labeled as MPPC (Muga pupae protein concentrate) and EPPC (Eri pupae protein concentrate) were neutralized with 0.2 M NaOH before lyophilization and stored at −20 °C.
MPPC and EPPC were hydrolyzed with Alcalase (50 °C, pH 8.0), Flavourzyme (50 °C, pH 7.0), Thermolysin (70 °C, pH 8.0), Papain (60 °C, pH 6.0), Pepsin (37 °C, pH 1.7) and Trypsin (37 °C, pH 7.5) at 0.5% enzymes: substrate (E/S) ratio. The protein concentration was adjusted to 5.0% in each reaction mixture and the solutions were set to their appropriate temperature and pH point. During the reaction, pH was kept constant using either 1 M NaOH or HCl. Finally, the digestions were performed in a shaking water bath for a total of 6 h. Five hundred µL samples were taken out after 15, 30, 60, 120, 180, 240, 300 and 360 min to measure their degree of hydrolysis (DH) and ACE inhibition. At the reaction end, to inactivate the enzymes, each hydrolysate was boiled for 10 min, cooled and centrifuged at 10,000 × g for 10 min at 20 °C. Finally, the supernatants containing the peptide mix were collected and labeled accordingly. The pupae proteins treated at the same conditions for each protease with no protease addition were used as controls. The degree of hydrolysis (DH) % was calculated using the trinitro benzene sulfonic acid (TNBS) method given by Hall et al. [12 (link)].
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Publication 2023
1-myristoyl-2-palmitoyl-sn-glycero-3-phosphocholine Bath Bombyx Centrifugation Digestion Enzymes flavourzyme Freeze Drying Gated Blood-Pool Imaging Hydrolysis Papain Pellets, Drug Pepsin A Peptide Hydrolases Peptides Powder Proteins Psychological Inhibition Pupa Subtilisin Carlsberg Thermolysin Trinitrobenzenesulfonic Acid Trypsin
Muga and Eri pupae protein hydrolysates with the highest potential of in vitro ACE inhibition and antioxidant activities were fractionated using Amicon® Ultra 15 mL centrifugal filters with molecular weight (MW) cutoff membranes of 3 kDa and 10 kDa (EMD Millipore; Billerica, MA, USA). The resultant filtrates of MW < 3 kDa, 3 < MW < 10 KDa and MW > 10 KDa were later freeze-dried to determine their biological activities.
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Publication 2023
Antioxidant Activity Biopharmaceuticals Freezing Gated Blood-Pool Imaging Protein Hydrolysates Psychological Inhibition Pupa Tissue, Membrane
A retrospective cohort analysis was used for this study. Ninety-seven patients diagnosed with CAD at the Department of Cardiovascular Medicine in the Affiliated Hospital of Xuzhou Medical University from September 2021 and January 2022 were selected. LVEDP ≥ 16 mmHg (1 mmHg = 0.133 kPa) was defined as increased LV filling pressure [7 (link), 8 (link)]. Based on LVEDP, patients were divided into the HFpEF group (LVEDP ≥ 16 mmHg, 47 cases) and the normal LV diastolic function group (LVEDP < 16 mmHg, 50 cases). The Medical Ethics Committee approved the study of the Affiliated Hospital of Xuzhou Medical University (Number: XYFY2021-KL164-01).
Inclusion criteria: (1) All patients with suspected or known coronary artery disease who have completed echocardiography, planar MUGA and cardiac catheterization 1–3 days after admission and whose diagnosis of CAD was confirmed by coronary arteriography with a subepicardial coronary artery diameter stenosis more than 50% [9 (link)]; (2) sinus rhythm; (3) hemodynamic stability; (4) LVEF ≥ 50% (based on left ventriculography findings) .
Exclusion criteria: pulmonary heart disease (10), congenital heart disease (1), rheumatic heart disease (0), cardiomyopathy and pericardial disease (2), hyperthyroidism (2), arrhythmias (5), severe anemia (0), severe hepatic and renal dysfunction (1), LVESV′ < 20 mL measured by planar MUGA (3) (because assessment of LV volume and function is less accurate in very small volume patients [6 (link), 10 (link)]).
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Publication 2023
Anemia Cardiac Arrhythmia Cardiomyopathies Cardiovascular Agents Catheterizations, Cardiac Cerebral Ventriculography Congenital Heart Defects Coronary Angiography Coronary Artery Disease Coronary Stenosis Cor Pulmonale Diagnosis Diastole Echocardiography Ethics Committees Gated Blood-Pool Imaging Hemodynamics Hyperthyroidism Kidney Failure Patients Pericardium Pressure Rheumatic Heart Disease Sinuses, Nasal
This was a prospective, open-label, multicentre regional single-arm Phase II study, involving eight centres in five countries and regions. Eligible patients each received Osimertinib 80 mg daily until progression (determined by RECIST v1.1), lack of clinical benefit or unacceptable toxicity. Patients underwent clinical assessments at baseline and monthly and cardiac assessments with electrocardiograms and a 2D echocardiogram or multigated acquisition scan at baseline and every 3 months. Tumour assessment by computed tomography scan was performed every 8 weeks; tumour response was assessed by investigators according to RECIST v1.1. Safety was assessed by documentation of adverse events, patient reporting, physical examination and laboratory tests. History, physical examination and blood tests for haematology and biochemistry analysis were conducted at baseline and at the start of each monthly cycle of treatment. Information on adverse events was collected from the time of consent, throughout the treatment period and until the end of the safety follow-up period, defined as 28 days after study treatment was discontinued. Adverse events were graded with the use of the Common Terminology Criteria for Adverse Events of the National Cancer Institute version 4 (NCI CTCAE v4). Plasma was taken for exploratory biomarker analysis at baseline, cycle 3 and at the end of the trial visit.
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Publication 2023
Biological Markers BLOOD Disease Progression Echocardiography Electrocardiogram Gated Blood-Pool Imaging Heart Hematologic Tests Neoplasms osimertinib Patients Physical Examination Plasma Radionuclide Imaging Safety X-Ray Computed Tomography
The design of the multicenter, open-label, phase III JAVELIN Ovarian 200 trial (NCT02580058) has been described previously.5 (link) Briefly, eligible women had advanced ­platinum-resistant or platinum-refractory epithelial ovarian, fallopian tube, or peritoneal cancer and had received 1-3 prior treatment lines for platinum-sensitive disease and none for ­platinum-resistant disease. Exclusion criteria included baseline LVEF <50% (by echocardiography or MUGA scans) and prior ­anthracycline-related cardiotoxicity or ­anthracycline exposure approaching the lifetime limit (450-550 mg/m2). Full eligibility criteria have been reported previously.5 (link) Patients were randomized 1:1:1 to receive avelumab 10 mg/kg intravenously every 2 weeks, PLD 40 mg/m2 intravenously every 4 weeks, or avelumab plus PLD. Cardiac monitoring was performed throughout the trial, and comprised electrocardiogram at baseline and every 4 weeks and LVEF assessment by MUGA scans or echocardiography at baseline and every 8 weeks until discontinuation or end of treatment. Electrocardiogram and LVEF results were read locally. Decrease in LVEF to below institutional lower limit of normal (LLN) or by ≥15% from baseline required treatment interruption, and LVEF was reassessed within 45 days and every 3 months. Upon recovery (LVEF increase to within 5% of baseline within 45 days from nadir), treatment could be resumed at investigator’s discretion, and an additional LVEF evaluation was performed within 2 weeks. AEs were investigator reported, analyzed descriptively, and graded using National Cancer Institute Common Terminology Criteria for Adverse Events, version 4.03.
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Publication 2023
Anthracyclines avelumab Cardiotoxicity Echocardiography Electrocardiography Eligibility Determination Fallopian Tubes Gated Blood-Pool Imaging Heart LINE-1 Elements Malignant Neoplasms Ovary Patients Peritoneum Platinum Radionuclide Imaging Woman

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