40 results on '"Firek, B"'
Search Results
2. Baseline Nt-proBNP and peak VO2 are not predictive of positive response to cardiac resynchronization therapy in patients with chronic heart failure
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Chwyczko, T., Smolis-Bak, E., Sterlinski, M., Maciag, A., Pytkowski, M., Firek, B., Jankowska, A., and Szwed, H.
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- 2011
3. Club35 Poster Session Thursday 12 December: 12/12/2013, 08: 30–18: 00Location: Poster area
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Borowiec, A, Dabrowski, R, Kowalik, I, Firek, B, Chwyczko, T, Janas, J, and Szwed, H
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- 2013
4. Combined analysis of microbial metagenomic and metatranscriptomic sequencing data to assess in situ physiological conditions in the premature infant gut.
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Zoetendal, EG, Sher, Y, Olm, MR, Raveh-Sadka, T, Brown, CT, Sher, R, Firek, B, Baker, R, Morowitz, MJ, Banfield, JF, Zoetendal, EG, Sher, Y, Olm, MR, Raveh-Sadka, T, Brown, CT, Sher, R, Firek, B, Baker, R, Morowitz, MJ, and Banfield, JF
- Abstract
Microbes alter their transcriptomic profiles in response to the environment. The physiological conditions experienced by a microbial community can thus be inferred using meta-transcriptomic sequencing by comparing transcription levels of specifically chosen genes. However, this analysis requires accurate reference genomes to identify the specific genes from which RNA reads originate. In addition, such an analysis should avoid biases in transcript counts related to differences in organism abundance. In this study we describe an approach to address these difficulties. Sample-specific meta-genomic assembled genomes (MAGs) were used as reference genomes to accurately identify the origin of RNA reads, and transcript ratios of genes with opposite transcription responses were compared to eliminate biases related to differences in organismal abundance, an approach hereafter named the "diametric ratio" method. We used this approach to probe the environmental conditions experienced by Escherichia spp. in the gut of 4 premature infants, 2 of whom developed necrotizing enterocolitis (NEC), a severe inflammatory intestinal disease. We analyzed twenty fecal samples taken from four premature infants (4-6 time points from each infant), and found significantly higher diametric ratios of genes associated with low oxygen levels in samples of infants later diagnosed with NEC than in samples without NEC. We also show this method can be used for examining other physiological conditions, such as exposure to nitric oxide and osmotic pressure. These study results should be treated with caution, due to the presence of confounding factors that might also distinguish between NEC and control infants. Nevertheless, together with benchmarking analyses, we show here that the diametric ratio approach can be applied for evaluating the physiological conditions experienced by microbes in situ. Results from similar studies can be further applied for designing diagnostic methods to detect NEC in its ear
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- 2020
5. Advantages of exercise echocardiography in comparison to dobutamine echocardiography in the diagnosis of coronary artery disease in hypertensive subjects
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Pasierski, T, Szwed, H, Malczewska, B, Firek, B, Kośmicki, M, Rewicki, M, Kowalik, I, and Sadowski, Z
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- 2001
- Full Text
- View/download PDF
6. P429The efficacy of electrical cardioversion of long-standing persistent or permanent atrial fibrillation in cardiac resynchronization therapy recipients
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Ciszewski, J B, primary, Tajstra, M, additional, Gadula-Gacek, E, additional, Kowalik, I, additional, Maciag, A, additional, Chwyczko, T, additional, Jankowska, A, additional, Smolis-Bak, E, additional, Firek, B, additional, Kraska, A, additional, Zajac, D, additional, Szwed, H, additional, Pytkowski, M, additional, Gasior, M, additional, and Sterlinski, M, additional
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- 2020
- Full Text
- View/download PDF
7. Hospitalized Premature Infants Are Colonized by Related Bacterial Strains with Distinct Proteomic Profiles
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Gilmore, MS, Brown, CT, Xiong, W, Olm, MR, Thomas, BC, Baker, R, Firek, B, Morowitz, MJ, Hettich, RL, Banfield, JF, Gilmore, MS, Brown, CT, Xiong, W, Olm, MR, Thomas, BC, Baker, R, Firek, B, Morowitz, MJ, Hettich, RL, and Banfield, JF
- Abstract
During the first weeks of life, microbial colonization of the gut impacts human immune system maturation and other developmental processes. In premature infants, aberrant colonization has been implicated in the onset of necrotizing enterocolitis (NEC), a life-threatening intestinal disease. To study the premature infant gut colonization process, genome-resolved metagenomics was conducted on 343 fecal samples collected during the first 3 months of life from 35 premature infants housed in a neonatal intensive care unit, 14 of whom developed NEC, and metaproteomic measurements were made on 87 samples. Microbial community composition and proteomic profiles remained relatively stable on the time scale of a week, but the proteome was more variable. Although genetically similar organisms colonized many infants, most infants were colonized by distinct strains with metabolic profiles that could be distinguished using metaproteomics. Microbiome composition correlated with infant, antibiotics administration, and NEC diagnosis. Communities were found to cluster into seven primary types, and community type switched within infants, sometimes multiple times. Interestingly, some communities sampled from the same infant at subsequent time points clustered with those of other infants. In some cases, switches preceded onset of NEC; however, no species or community type could account for NEC across the majority of infants. In addition to a correlation of protein abundances with organism replication rates, we found that organism proteomes correlated with overall community composition. Thus, this genome-resolved proteomics study demonstrated that the contributions of individual organisms to microbiome development depend on microbial community context.IMPORTANCE Humans are colonized by microbes at birth, a process that is important to health and development. However, much remains to be known about the fine-scale microbial dynamics that occur during the colonization period. We conducted a
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- 2018
8. Identical bacterial populations colonize premature infant gut, skin, & oral microbiomes & exhibit different in situ growth rates
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Olm, MR, Brown, CT, Brooks, B, Firek, B, Baker, R, Burstein, D, Soenjoyo, K, Thomas, BC, Morowitz, M, and Banfield, JF
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©2017 Olm et al. The initial microbiome impacts the health and future development of premature infants. Methodological limitations have led to gaps in our understanding of the habitat range and subpopulation complexity of founding strains, as well as how different body sites support microbial growth. Here, we used metagenomics to reconstruct genomes of strains that colonized the skin, mouth, and gut of two hospitalized premature infants during the first month of life. Seven bacterial populations, considered to be identical given whole-genome average nucleotide identity of >99.9%, colonized multiple body sites, yet none were shared between infants. Gut-Associated Citrobacter koseri genomes harbored 47 polymorphic sites that we used to define 10 subpopulations, one of which appeared in the gut after 1 wk but did not spread to other body sites. Differential genome coverage was used to measure bacterial population replication rates in situ. In all cases where the same bacterial population was detected in multiple body sites, replication rates were faster in mouth and skin compared to the gut. The ability of identical strains to colonize multiple body sites underscores the habit flexibility of initial colonists, whereas differences in microbial replication rates between body sites suggest differences in host control and/or resource availability. Population genomic analyses revealed microdiversity within bacterial populations, implying initial inoculation by multiple individual cells with distinct genotypes. Overall, however, the overlap of strains across body sites implies that the premature infant microbiome can exhibit very low microbial diversity.
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- 2017
9. Disturbances of the Perioperative Microbiome Across Multiple Body Sites in Patients Undergoing Pancreaticoduodenectomy
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Rogers, MB, Aveson, V, Firek, B, Yeh, A, Brooks, B, Brower-Sinning, R, Steve, J, Banfield, JF, Zureikat, A, Hogg, M, Boone, BA, Zeh, HJ, and Morowitz, MJ
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16S ,Population Dynamics ,Clinical Sciences ,microbiome ,bile ,Pancreaticoduodenectomy ,Feces ,Pancreatic Cancer ,pancreatic fistula ,Rare Diseases ,Pancreatic Juice ,Species Specificity ,Clinical Research ,Klebsiella ,microbiota ,Genetics ,Humans ,pancreas ,Perioperative Period ,Aged ,Cancer ,Ribosomal ,Bacteria ,Gastroenterology & Hepatology ,Bacterial ,DNA ,Jejunum ,RNA ,Digestive Diseases ,Sequence Analysis - Abstract
© 2017 Wolters Kluwer Health, Inc. All rights reserved. Objective: The goals of this study were to characterize bacterial communities within fecal samples, pancreatic fluid, bile, and jejunal contents from patients undergoing pancreaticoduodenectomy (PD) and to identify associations between microbiome profiles and clinical variables. Methods: Fluid was collected from the pancreas, common bile duct, and proximal jejunum from 50 PD patients. Postoperative fecal samples were also collected. The microbial burden within samples was quantified with droplet digital polymerase chain reaction. Bacterial 16S ribosomal RNA gene sequences were amplified, sequenced, and analyzed. Data from fecal samples were compared with publicly available data obtained from volunteers. Results: Droplet digital polymerase chain reaction confirmed the presence of bacteria in all sample types, including pancreatic fluid. Relative to samples from the American Gut Project, fecal samples from PD patients were enriched with Klebsiella and Bacteroides and were depleted of anaerobic taxa (eg, Roseburia and Faecalibacterium). Similar patterns were observed within PD pancreas, bile, and jejunal samples. Postoperative fecal samples from patients with a pancreatic fistula contained increased abundance of Klebsiella and decreased abundance of commensal anaerobes, for example, Ruminococcus. Conclusions: This study confirms the presence of altered bacterial populations within samples from PD patients. Future research must validate these findings and may evaluate targeted microbiome modifications to improve outcomes in PD patients.
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- 2017
10. Concentrations and sources of airborne particles in a neonatal intensive care unit
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Licina, D, Bhangar, S, Brooks, B, Baker, R, Firek, B, Tang, X, Morowitz, MJ, Banfield, JF, Nazaroff, WW, Licina, D, Bhangar, S, Brooks, B, Baker, R, Firek, B, Tang, X, Morowitz, MJ, Banfield, JF, and Nazaroff, WW
- Abstract
Premature infants in neonatal intensive care units (NICUs) have underdeveloped immune systems, making them susceptible to adverse health consequences from air pollutant exposure. Little is known about the sources of indoor airborne particles that contribute to the exposure of premature infants in the NICU environment. In this study, we monitored the spatial and temporal variations of airborne particulate matter concentrations along with other indoor environmental parameters and human occupancy. The experiments were conducted over one year in a private-style NICU. The NICU was served by a central heating, ventilation and air-conditioning (HVAC) system equipped with an economizer and a highefficiency particle filtration system. The following parameters were measured continuously during weekdays with 1-min resolution: particles larger than 0.3 μm resolved into 6 size groups, CO2 level, dry-bulb temperature and relative humidity, and presence or absence of occupants. Altogether, over sixteen periods of a few weeks each, measurements were conducted in rooms occupied with premature infants. In parallel, a second monitoring station was operated in a nearby hallway or at the local nurses' station. The monitoring data suggest a strong link between indoor particle concentrations and human occupancy. Detected particle peaks from occupancy were clearly discernible among larger particles and imperceptible for submicron (0.3-1 μm) particles. The mean indoor particle mass concentrations averaged across the size range 0.3-10 μm during occupied periods was 1.9 μg/m3 , approximately 2.5 times the concentration during unoccupied periods (0.8 μg/m3 ). Contributions of within-room emissions to total PM10 mass in the baby rooms averaged 37-81%. Near-room indoor emissions and outdoor sources contributed 18-59% and 1-5%, respectively. Airborne particle levels in the size range 1-10 μm showed strong dependence on human activities, indicating the importance of indoor-generated particles for
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- 2016
11. Gut bacteria are rarely shared by co-hospitalized premature infants, regardless of necrotizing enterocolitis development
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Raveh-Sadka, T, Thomas, BC, Singh, A, Firek, B, Brooks, B, Castelle, CJ, Sharon, I, Baker, R, Good, M, Morowitz, MJ, Banfield, JF, Raveh-Sadka, T, Thomas, BC, Singh, A, Firek, B, Brooks, B, Castelle, CJ, Sharon, I, Baker, R, Good, M, Morowitz, MJ, and Banfield, JF
- Abstract
Premature infants are highly vulnerable to aberrant gastrointestinal tract colonization, a process that may lead to diseases like necrotizing enterocolitis. Thus, spread of potential pathogens among hospitalized infants is of great concern. Here, we reconstructed hundreds of high-quality genomes of microorganisms that colonized co-hospitalized premature infants, assessed their metabolic potential, and tracked them over time to evaluate bacterial strain dispersal among infants. We compared microbial communities in infants who did and did not develop necrotizing enterocolitis. Surprisingly, while potentially pathogenic bacteria of the same species colonized many infants, our genome-resolved analysis revealed that strains colonizing each baby were typically distinct. In particular, no strain was common to all infants who developed necrotizing enterocolitis. The paucity of shared gut colonizers suggests the existence of significant barriers to the spread of bacteria among infants. Importantly, we demonstrate that strain-resolved comprehensive community analysis can be accomplished on potentially medically relevant time scales.
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- 2015
12. Poster session 5The imaging examinationP1097Correlation between visual and quantitative assessment of left ventricle: intra- and inter-observer agreementP1099Incremental prognostic value of late gadolinium-enhanced by cardiac magnetic resonance in patients with heart failureAnatomy and physiology of the heart and great vesselsP1100Left ventricular geometry and diastolic performance in erectile dysfunction patients; a topic of differential arterial stiffness influenceAssessment of diameters, volumes and massP1101Impact of the percutaneous closure of atrial septal defect on the right heart "remodeling"P1102Left Ventricular Mass Indexation in Infants, Children and Adolescents: a Simplified Approach for the Identification of Left Ventricular Hypertrophy in Clinical PracticeP1103Impact of trabecules while quantifying cardiac magnetic resonance exams in patients with systemic right ventricleP1104Detection of subclinical atherosclerosis by carotid intima-media thickness: correlation with leukocytes telomere shorteningAssessments of haemodynamicsP1105Flow redirection towards the left ventricular outflow tract: vortex formation is not affected by variations in atrio-ventricular delayAssessment of systolic functionP1106Reproducibility and feasibility of cardiac MRI feature tracking in Fabry diseaseP1107Normal left ventricular strain values by two-dimensional strain echocardiography; result of normal (normal echocardiographic dimensions and functions in korean people) studyP1108Test-retest repeatability of global strain following st-elevation myocardial infarction - a comparison of tagging and feature trackingP1109Cardiotoxicity induced by tyrosine kinase inhibitors in patients with gastrointestinal stromal tumors (GIST)P1110Finite strain ellipses for the analysis of left ventricular principal strain directions using 3d speckle tracking echocardiographyP1111Antihypertensive therapy reduces time to peak longitudinal strainP1112Right ventricular systolic function as a marker of prognosis after inferior myocardial infarction - 5-year follow-upP1113Is artery pulmonary dilatation related with right but also early left ventricle dysfunction in pulmonary artery hypertension?P1114Right ventricular mechanics changes according to pressure overload increasing, a 2D-speckle tracking echocardiographic evaluationAssessment of diastolic functionP1115Paired comparison of left atrial strain from P-wave to P-wave and R-wave to R-waveP1116Diagnostic role of Tissue Doppler Imaging echocardiographic criteria in obese heart failure with preserved ejection fraction patientsP1117Evaluation of diastolic function of right ventricle in idiopathic pulmonary arterial hypertensionP1118Severity and predictors of diastolic dysfunction in a non-hypertensive non-ischemic cohort of Egyptian patients with documented systemic autoimmune disease; pilot reportP1119correlation between ST segment shift and cardiac diastolic function in patients with acute myocardial infarctionIschemic heart diseaseP1120Computed tomography coronary angiography verSus sTRess cArdiac magneTic rEsonance for the manaGement of sYmptomatic revascularized patients: a cost effectiveness study (STRATEGY study)P1121Utility of transmural myocardial mechanic for early infarct size prediction after primary percutaneous coronary intervention in STEMI patientsP1122Progressive Improvements of the echocardiographic deformation parameters in ST Elevation Myocardial Infarction after five years follow-upP1123Long-term prognostic value of left ventricular dyssynchrony as assessed by cardiac magnetic resonance feature-tracking imaging after a first st-segment elevation myocardial infarctionP1124Differences in mitral annulus remodeling in acute anterior ST elevation and acute inferior ST elevation myocardial infarctionP1125Reduction of microvascular injury using a novel theragnostic ultrasound strategy: a first in men feasibility and safety studyP1126Impact of focused echocardiography in clinical decision of patient presented with st elevation myocardial infarction underwent primary angioplastyHeart valve DiseasesP1127Aortic valve area calculation in aortic stenosis: a comparison among conventional and 3D-transesophageal echocardiography and computed tomographyP1128Myocardial fibrosis and microRNA-21 expression in patients with severe aortic valve stenosis and preserved ejection fraction: a 2D speckle tracking echocardiography, tissutal and plasmatic studyP1129Quantification of calcium amount in a new experimental model: a comparison between calibrated integrated backscatter of ultrasound and computed tomographyP1130Altered diffusion capacity in aortic stenosis: role of the right heartP1131Osteoprotegerin predicts all-cause mortality in calcific aortic stenosis patients with preserved left ventricle ejection fraction in long term observationP1132Mitral regurgitation as a risk factor for pulmonary hypertension in patients with aortic stenosisP1133The relationship between the level of plasma B-type natriuretic peptide and mitral stenosisP1134Aortic regurgitation, left ventricle mechanics and vascular load: a single centre 2d derived-speckle tracking studyP1135Feasibility and reproducibility issues limit the usefulness of quantitative colour Doppler parameters in the assessment of chronic aortic and mitral regurgitation severityP1136Predictors of postoperative outcome in degenerative mitral regurgitationP1137Left ventricular mechanical dyssynchrony in patients with severe mitral regurgitation of rheumatic etiology; three dimensional echocardiography studyP1138Functional mitral regurgitation and left atrial dysfunction concur in determining pulmonary hypertension and functional status in subjects with left ventricular systolic dysfunctionP11393D echocardiography allows more effective quantitative assessment of the severity of functional tricuspid regurgitation than conventional 2D/Doppler echocardiographyP1140Prosthetic valve thrombosis: still a severe disease? 10-years experience in a university hospitalP1141Validity of echocardiography in the hospital course of patients with feverP1142Do baseline 3DTEE characteristics of mitral valve apparatus predict long term result in patients undergoing percutaneous valve repair for degenerative regurgitation?P1143Influence of baseline aortic regurgitation on mitral regurgitation change after transcatheter aortic valve replacement for aortic stenosisP1144Prevalence of echocardiography detected significant valvular regurge in subclinical rheumatic carditis in assiut childrenCardiomyopathiesP1145Can we early detect left ventricular systolic dysfunction in patients with Duchenne muscular dystrophy using global longitudinal strain assessment?P1146Prevalence of isolated papillary muscle hypertrophy in young competitive athletesP1147Troponin release after exercise in patients with hypertrophic cardiomyopathy: associations with clinical and mr imaging characteristicsP1148Atrial fibrillation in hypertrophic cardiomyopathy: can we score the risk?P1149Impact of hypertrophy on multiple layer longitudinal deformation in hypertrophy cardiomyopathy and cardiac amyloidosis compared to controlsP1150Functional evaluation in hypertrophic cardiomyopathy combining cardiopulmonary exercise testing combined with exercise-echocardiographyP1151Refinement of the old diagnostic criteria of left ventricular noncompaction cardiomyopathy (LVNC) based on cardiac magnetic resonance (CMR)P1152Differences of clinical characteristics and outcomes between acute myocarditis with preserved and reduced left ventricular systolic functionP1153Value of longitudinal strain for distinguishing left ventricular non-compaction from idiopathic dilated cardiomyopathyP1154Speed of recovery of left ventricular function is not related to the prognosis of Takotsubo cardiomyopathy. A Portuguese multicentre studyP1155Predictors of in-hospital left ventricular systolic function recovery after admission with takotsubo cardiomyopathy. Portuguese multicentre studyP1156Mid-ventricular takotsubo detected by initial echocardiogram associates with recurrence of takotsubo cardiomyopathy - a portuguese multicentre studySystemic diseases and other conditionsP1157Relations between left ventricle remodelling and expression of angiotensin 2 AT2R1 geneP1158Impact of renal denervation on long-term blood pressure variability and surrogate markers of target organ damage in individuals with drug-resistant arterial hypertensionP1159Greater improvement of coronary artery function, left ventricular deformation and twisting by IL12/23 compared to TNF-a inhibition in psoriasisP1160Advanced glycation end products play a role in adverse LV remodeling following MIP1161Incidence of subclinical myocardial dysfunction in patients with systemic sclerosis and normal left ventricular systolic and diastolic functionP1162Left atrial remodeling and dysfunction occur early in patients with systemic sclerosis and normal left ventricular functionP1163Intrinsic vortex formation : a unique performance indicatorP1164P-wave morphology is unaffected by training-induced biatrial dilatation: a prospective, longitudinal study in healthy athletesP1165Usefulness of transthoracic echocardiography in diagnosis of young patients with ischemic strokeP1166Primary cardiac lymphoma: role of echocardiography in the clinical managementP1167Abnormal echocardiographic findings in cancer patients before chemotherapyMasses, tumors and sources of embolismP1168Three-dimensional transesophageal echocardiography of the left atrial appendage reduces rate of postpone electrical cardioversionP1169Detection of ventricular thrombus by cmr after reperfused st-segment elevation myocardial infarction correlated with echocardiographyP1170Clinical and transthoracic echocardiographic predictors of left atrial appendage thrombus in patients with atrial fibrillationStress echocardiographyP1171Pharmacological stress echocardiography complications: a 4-year single center experienceP1172Myocardial functional and perfusion reserve in type I diabetesP1173Feasibility of incorporating 3D Dobutamine stress echocardiography into routine clinical practiceP1174Right ventricular isovolumic acceleration at rest and during exercise in children after heart transplantP1175Right ventricular systolic and diastolic response to exercise in children after heart transplant -a bicycle exercise studyP1176Determinants of functional capacity in heart failure patients with reduced ejection fractionP1177Handgrip stress echocardiography with emotional component compared to conventional isometric exercise in coronary artery disease diagnosisP1178The relationship between resting transthoracic echocardiography and exercise capacity in patients with paroxysmal atrial fibrillationP1179Correlation between NT-proBNP and selected echocardiography parameters at rest and after exercise in patients with functional ischemic mitral regurgitation qualified for cardiosurgical treatmentReal-time three-dimensional TEEP1180Vena contracta area for severity grading in functional and degenerative mitral regurgitation: A study based on transesophageal 3D colour Doppler in 419 patientsP1181Proximal flow convergence by 3D echocardiography in the evaluation of mitral valve area in rheumatic mitral stenosisP1182Quantification of valve dimensions by transesophageal 3D echocardiography in patients with functional and degenerative mitral regurgitationTissue Doppler and speckle trackingP1183Automatic calculation of left ventricular volume changes over a cardiac cycle from echocardiography images by nonlinear dimensionality reductionP1184Effect of the mitral valve repairs on the left ventricular blood flow formationP1185Quantification of left atrial strain using cardiovascular magnetic resonance. a comparison between hypertrophic cardiomyopathy and healthy controlsP1186The role of early systolic lengthening in patients with non-ST elevation acute coronary syndrome and its relation to syntax scoreP1187Different standard two dimensional strain methods to quantity left ventricular mechanicsP1188Atrial function and electrocardiography caracteristics in sportsmen with or without paroxysmal atrial fibrillationP1189Right ventricular outflow premature contractions induce regional left ventricular dysfunctionP1190Ultrasound guided venous access for pacemaker and defibrillators. Randomized TrialP1191Atrial function analysis correlates with symptoms and quality of life of heart failure patientsP1192The use of tissue doppler echocardiography in myocardial iron overload in patients with thalassaemia majorP1193Independent association between pulse pressure and left ventricular global longitudinal strainP1194Global and regional longitudinal strain identifies the presence of coronary artery disease in patients with suspected reduction of coronary flow reserve and absence of wall motion abnormalitiesP1195Prognostic value of invasive and noninvasive parameters of right ventricular function in patients with pulmonary arterial hypertension receiving specific vasodilator therapyP1196Myocardial deformation analysis to improve arrhythmic risk stratificationP1197Quantitative assessment of regional systolic and diastolic function parameters for detecting prior transient ischemia in normokinetic segmentsP1198Left atrial function in patients with corrected tetralogy of Fallot - a three-dimensional speckle-tracking echocardiographic studyP1199Left atrial ejection force correlates with left atrial strain and volume-based functional properties as assessed by three-dimensional speckle tracking echocardiographyP1200Acute angulation of the aortic arch late after the arterial switch operation for transposition of the great arteries: impact on cardiac mechanicsP1201Circumferential deformation of the ascending thoracic aorta in hypertensive patients by three-dimensional speckle tracking echocardiographyCardiac Magnetic ResonanceP1202The incremental value of cardiac magnetic resonance on diagnosis myocardial infarction and non-obstructed coronary arteriesP1204Reference ranges of global and regional myocardial T1 values derived from MOLLI and shMOLLI at 3TComputed Tomography & Nuclear CardiologyP1205Deformation of the left atrial appendage after percutaneous closure with the Amplatzer cardiac plugP1206Prognostic impact of non-obstructive coronary artery disease on coronary computed tomographic angiography: A single-center study
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Colunga Blanco, S, primary, Gonzalez Matos, C, primary, Angelis, A, primary, Dinis, P G, primary, Chinali, M, primary, Toth, A, primary, Andreassi, M G, primary, Rodriguez Munoz, D, primary, Reid, A B, primary, Park, JH, primary, Shetye, A, primary, Novo, G, primary, De Marchi, S F, primary, Cikes, M, primary, Smarz, K, primary, Illatopa, V, primary, Peluso, D, primary, Wellnhofer, E, primary, De La Rosa Riestra, A, primary, Sattarzadeh Badkoubeh, R, primary, Mandour Ali, M, primary, Azoz, A, primary, Pontone, G, primary, Krljanac, G, primary, Acar, R, primary, Nucifora, G, primary, Sirtautas, A, primary, Roos, S T, primary, Qasem, M S, primary, Marini, C, primary, Fabiani, I, primary, Gillis, K, primary, Bandera, F, primary, Borowiec, A, primary, Lim, YJ, primary, Chalbia, T E, primary, Santos, M, primary, Gao, S A, primary, Zilberszac, R, primary, Farrag, AAM, primary, Palmiero, G, primary, Aruta, P, primary, De Diego Soler, O, primary, Fasano, D, primary, Tamborini, G, primary, Ancona, F, primary, Raafat, D M, primary, Marchel, M, primary, De Gregorio, C, primary, Gommans, D H F, primary, Godinho, A R, primary, Mielczarek, M, primary, Kubik, M, primary, Cho, J Y, primary, Tarando, F, primary, Lourenco Marmelo, B F, primary, Reis, L, primary, Domingues, K, primary, Krestjyaninov, MV, primary, Mesquita, J, primary, Ikonomidis, I, primary, Ferferieva, V, primary, King, GJ, primary, D'ascenzi, F, primary, Ferrera Duran, C, primary, Sormani, P, primary, Gonzalez Fernandez, O, primary, Tereshina, O, primary, Cambronero Cortinas, E, primary, Kupczynska, K, primary, Carvalho, J F, primary, Shivalkar, B, primary, Aghamohammadzadeh, R, primary, Cifra, B, primary, Kuznetsov, VA, primary, Van Zalen, JJ, primary, Kochanowski, J, primary, Goebel, B, primary, Ladeiras-Lopes, R, primary, Karvandi, M, primary, Alonso Salinas, G, primary, Unkun, T, primary, Ranjbar, S, primary, Hubert, A, primary, Enescu, OA, primary, Liccardo, M, primary, Cameli, M, primary, Ako, E, primary, Lembo, M, primary, Goffredo, C, primary, Enache, R, primary, Wdowiak-Okrojek, K, primary, Nemes, A, primary, Di Salvo, G, primary, Capotosto, L, primary, Caravaca, P, primary, Maceira Gonzalez, A M, primary, Iriart, X, primary, Jug, B, primary, Garcia Campos, A, additional, Capin Sampedro, E, additional, Corros Vicente, C, additional, Martin Fernandez, M, additional, Leon Arguero, V, additional, Fidalgo Arguelles, A, additional, Velasco Alonso, E, additional, Lopez Iglesias, F, additional, De La Hera Galarza, JM, additional, Chaparro-Munoz, M, additional, Recio-Mayoral, A, additional, Vlachopoulos, C, additional, Ioakeimidis, N, additional, Felekos, I, additional, Abdelrasoul, M, additional, Aznaouridis, K, additional, Chrysohoou, C, additional, Rousakis, G, additional, Aggeli, K, additional, Tousoulis, D, additional, Faustino, AC, additional, Paiva, L, additional, Fernandes, A, additional, Costa, M, additional, Cachulo, MC, additional, Goncalves, L, additional, Emma, F, additional, Rinelli, G, additional, Esposito, C, additional, Franceschini, A, additional, Doyon, A, additional, Raimondi, F, additional, Schaefer, F, additional, Pongiglione, G, additional, Mateucci, MC, additional, Vago, H, additional, Juhasz, C, additional, Janosa, C, additional, Oprea, V, additional, Balint, OH, additional, Temesvari, A, additional, Simor, T, additional, Kadar, K, additional, Merkely, B, additional, Bruno, R M, additional, Borghini, A, additional, Stea, F, additional, Gargani, L, additional, Mercuri, A, additional, Sicari, R, additional, Picano, E, additional, Lozano Granero, C, additional, Carbonell San Roman, A, additional, Moya Mur, JL, additional, Fernandez-Golfin, C, additional, Moreno Planas, J, additional, Fernandez Santos, S, additional, Casas Rojo, E, additional, Hernandez-Madrid, A, additional, Zamorano Gomez, JL, additional, Pearce, K, additional, Gamlin, W, additional, Miller, C, additional, Schmitt, M, additional, Seong, IW, additional, Kim, KH, additional, Kim, MJ, additional, Jung, HO, additional, Sohn, IS, additional, Park, SM, additional, Cho, GY, additional, Choi, JO, additional, Park, SW, additional, Nazir, SA, additional, Khan, JN, additional, Singh, A, additional, Kanagala, P, additional, Squire, I, additional, Mccann, GP, additional, Di Lisi, D, additional, Meschisi, MC, additional, Brunco, V, additional, Badalamenti, G, additional, Bronte, E, additional, Russo, A, additional, Novo, S, additional, Von Tscharner, M, additional, Urheim, S, additional, Aakhus, S, additional, Seiler, C, additional, Schmalholz, S, additional, Biering-Sorensen, T, additional, Cheng, S, additional, Oparil, S, additional, Izzo, J, additional, Pitt, B, additional, Solomon, SD, additional, Zaborska, B, additional, Jaxa-Chamiec, T, additional, Tysarowski, M, additional, Budaj, A, additional, Cordova, F, additional, Aguirre, O, additional, Sanabria, S, additional, Ortega, J, additional, Romeo, G, additional, Perazzolo Marra, M, additional, Tona, F, additional, Famoso, G, additional, Pigatto, E, additional, Cozzi, F, additional, Iliceto, S, additional, Badano, LP, additional, Kriatselis, C, additional, Gerds-Li, JH, additional, Kropf, M, additional, Pieske, B, additional, Graefe, M, additional, Martinez Santos, P, additional, Batlle Lopez, E, additional, Vilacosta, I, additional, Sanchez Sauce, B, additional, Espana Barrio, E, additional, Jimenez Valtierra, J, additional, Campuzano Ruiz, R, additional, Alonso Bello, J, additional, Martin Rios, MD, additional, Farrashi, M, additional, Abtahi, H, additional, Sadeghi, H, additional, Sadeghipour, P, additional, Tavoosi, A, additional, Abdel Rahman, TA, additional, Mohamed, LA, additional, Maghraby, HM, additional, Kora, IM, additional, Abdel Hameed, FR, additional, Ali, MN, additional, Al Shehri, A, additional, Youssef, A, additional, Gad, A, additional, Alsharqi, M, additional, Alsaikhan, L, additional, Andreini, D, additional, Rota, C, additional, Guglielmo, M, additional, Mushtaq, S, additional, Baggiano, A, additional, Beltrama, V, additional, Solbiati, A, additional, Guaricci, AI, additional, Pepi, M, additional, Trifunovic, D, additional, Sobic Saranovic, D, additional, Savic, L, additional, Grozdic Milojevic, I, additional, Asanin, M, additional, Srdic, M, additional, Petrovic, M, additional, Zlaic, N, additional, Mrdovic, I, additional, Dogan, C, additional, Izci, S, additional, Gecmen, C, additional, Unkun, T, additional, Cap, M, additional, Erdogan, E, additional, Onal, C, additional, Yilmaz, F, additional, Ozdemir, N, additional, Muser, D, additional, Tioni, C, additional, Zanuttini, D, additional, Morocutti, G, additional, Spedicato, L, additional, Bernardi, G, additional, Proclemer, A, additional, Pranevicius, R, additional, Zapustas, N, additional, Briedis, K, additional, Valuckiene, Z, additional, Jurkevicius, R, additional, Juffermans, LJM, additional, Enait, V, additional, Van Royen, N, additional, Van Rossum, AC, additional, Kamp, O, additional, Khalaf, HASSEN, additional, Hitham, SAKER, additional, Osama, AS, additional, Abazid, RAMI, additional, Guall, RAHIM, additional, Durdan, SHAFAT, additional, Mohammed, ZYAD, additional, Stella, S, additional, Rosa, I, additional, Ancona, F, additional, Spartera, M, additional, Italia, L, additional, Latib, A, additional, Colombo, A, additional, Margonato, A, additional, Agricola, E, additional, Scatena, C, additional, Mazzanti, C, additional, Conte, L, additional, Pugliese, N, additional, Barletta, V, additional, Bortolotti, U, additional, Naccarato, AG, additional, Di Bello, V, additional, Bala, G, additional, Roosens, B, additional, Hernot, S, additional, Remory, I, additional, Droogmans, S, additional, Cosyns, B, additional, Generati, G, additional, Labate, V, additional, Donghi, V, additional, Pellegrino, M, additional, Carbone, F, additional, Alfonzetti, E, additional, Guazzi, M, additional, Dabrowski, R, additional, Kowalik, I, additional, Firek, B, additional, Chwyczko, T, additional, Szwed, H, additional, Kawamura, A, additional, Kawano, S, additional, Zaroui, A, additional, Ben Said, R, additional, Ben Halima, M, additional, Kheder, N, additional, Farhati, A, additional, Mourali, S, additional, Mechmech, R, additional, Leite, L, additional, Martins, R, additional, Baptista, R, additional, Barbosa, A, additional, Ribeiro, N, additional, Oliveira, A, additional, Castro, G, additional, Pego, M, additional, Polte, C L, additional, Lagerstrand, K, additional, Johnsson, Å A, additional, Janulewicz, M, additional, Bech-Hanssen, O, additional, Gabriel, H, additional, Wisser, W, additional, Maurer, G, additional, Rosenhek, R, additional, El Aroussy, W, additional, Abdel Ghany, M, additional, Al Adeeb, K, additional, Ascione, L, additional, Carlomagno, G, additional, Sordelli, C, additional, Ferro, A, additional, Ascione, R, additional, Severino, S, additional, Caso, P, additional, Muraru, D, additional, Janei, C, additional, Haertel Miglioranza, M, additional, Cavalli, G, additional, Peluso, D, additional, Cucchini, U, additional, Badano, L, additional, Armario Bel, X, additional, Garcia-Garcia, C, additional, Ferrer Sistach, E, additional, Rueda Sobella, F, additional, Oliveras Vila, T, additional, Labata Salvador, C, additional, Serra Flores, J, additional, Lopez-Ayerbe, J, additional, Bayes-Genis, A, additional, Conte, E, additional, Gonella, A, additional, Morena, L, additional, Civelli, D, additional, Losardo, L, additional, Margaria, F, additional, Riva, L, additional, Tanga, M, additional, Carminati, C, additional, Muratori, M, additional, Gripari, P, additional, Ghulam Ali, S, additional, Fusini, L, additional, Vignati, C, additional, Bartorelli, AL, additional, Alamanni, F, additional, Marini, C, additional, Montorfano, M, additional, Ismaiel, A, additional, Ali, N, additional, Amry, S, additional, Serafin, A, additional, Kochanowski, J, additional, Filipiak, KJ, additional, Opolski, G, additional, Speranza, G, additional, Ando', G, additional, Magaudda, L, additional, Cramer, GE, additional, Bakker, J, additional, Michels, M, additional, Dieker, HJ, additional, Fouraux, MA, additional, Marcelis, CLM, additional, Timmermans, J, additional, Brouwer, MA, additional, Kofflard, MJM, additional, Vasconcelos, M, additional, Araujo, V, additional, Almeida, P, additional, Sousa, C, additional, Macedo, F, additional, Cardoso, JS, additional, Maciel, MJ, additional, Voilliot, D, additional, Huttin, O, additional, Venner, C, additional, Olivier, A, additional, Villemin, T, additional, Deballon, R, additional, Manenti, V, additional, Juilliere, Y, additional, Selton-Suty, C, additional, Dabrowska-Kugacka, A, additional, Dorniak, K, additional, Lewicka, E, additional, Szalewska, D, additional, Kutniewska-Kubik, M, additional, Raczak, G, additional, Kim, K H, additional, Yoon, H J, additional, Park, H J, additional, Ahn, Y, additional, Jeong, M H, additional, Cho, J G, additional, Park, J C, additional, Kim, J H, additional, Galli, E, additional, Habib, G, additional, Schnell, F, additional, Lederlin, M, additional, Daubert, JC, additional, Mabo, P, additional, Donal, E, additional, Faria, R, additional, Magalhaes, P, additional, Marques, N, additional, Domingues, K, additional, Lourenco, C, additional, Almeida, AR, additional, Teles, L, additional, Picarra, B, additional, Azevedo, O, additional, Oliveira, M, additional, Marmelo, B, additional, Almeida, A, additional, Bento, D, additional, Cruz, I, additional, Reis, L, additional, Gimaev, RH, additional, Melnikova, MA, additional, Olezov, NV, additional, Ruzov, VI, additional, Goncalves, P, additional, Almeida, M S, additional, Branco, P, additional, Carvalho, M S, additional, Dores, H, additional, Gaspar, M A, additional, Sousa, H, additional, Andrade, M J, additional, Mendes, M, additional, Makavos, G, additional, Varoudi, M, additional, Papadavid, E, additional, Andreadou, I, additional, Gravanis, K, additional, Liarakos, N, additional, Pavlidis, G, additional, Rigopoulos, D, additional, Lekakis, J, additional, Deluyker, D, additional, Bito, V, additional, Punzi, L, additional, Neilan, T, additional, Coen, K, additional, Gannon, S, additional, Bennet, K, additional, Clarke, JG, additional, Solari, M, additional, Cameli, M, additional, Focardi, M, additional, Corrado, D, additional, Bonifazi, M, additional, Henein, M, additional, Mondillo, S, additional, Gomez-Escalonilla, C, additional, De Agustin, A, additional, Egido, J, additional, Islas, F, additional, Simal, P, additional, Gomez De Diego, JJ, additional, Luaces, M, additional, Macaya, C, additional, Perez De Isla, L, additional, Zancanella, M, additional, Rusconi, C, additional, Musca, F, additional, Santambrogio, G, additional, De Chiara, B, additional, Vallerio, P, additional, Cairoli, R, additional, Giannattasio, G, additional, Moreo, A, additional, Alvarez Ortega, C, additional, Mori Junco, R, additional, Caro Codon, J, additional, Meras Colunga, P, additional, Ponz De Antonio, I, additional, Lopez Fernandez, T, additional, Valbuena Lopez, S, additional, Moreno Yanguela, M, additional, Lopez-Sendon, JL, additional, Surkova, E, additional, Bonanad-Lozano, C, additional, Lopez-Lereu, MP, additional, Monmeneu-Menadas, JV, additional, Gavara, J, additional, De Dios, E, additional, Paya-Chaume, A, additional, Escribano-Alarcon, D, additional, Chorro-Gasco, FJ, additional, Bodi-Peris, V, additional, Michalski, BW, additional, Miskowiec, D, additional, Kasprzak, JD, additional, Lipiec, P, additional, Morgado, G, additional, Caldeira, D, additional, Joao, I, additional, Almeida, A R, additional, Lopes, L, additional, Fazendas, P, additional, Cotrim, C, additional, Pereira, H, additional, De Block, C, additional, Buys, D, additional, Salgado, R, additional, Vrints, C, additional, Van Gaal, L, additional, Mctear, C, additional, Irwin, RB, additional, Dragulescu, A, additional, Friedberg, M, additional, Mertens, L, additional, Krinochkin, DV, additional, Yaroslavskaya, EI, additional, Zaharova, EH, additional, Pushkarev, GS, additional, Sugihara, C, additional, Patel, NR, additional, Sulke, AN, additional, Lloyd, GW, additional, Piatkowski, R, additional, Scislo, P, additional, Grabowski, M, additional, Marchel, M, additional, Roland, H, additional, Hamadanchi, A, additional, Otto, S, additional, Jung, C, additional, Lauten, A, additional, Figulla, HC, additional, Poerner, TC, additional, Sampaio, F, additional, Fonseca, P, additional, Fontes-Carvalho, R, additional, Pinho, M, additional, Campos, AS, additional, Castro, P, additional, Fonseca, C, additional, Ribeiro, J, additional, Gama, V, additional, Heck, R, additional, Hamdanchi, A, additional, Figulla, HR, additional, Ranjbar, S, additional, Ghaffaripour Jahromi, M, additional, Hinojar, R, additional, Fernandez Golfin, C, additional, Esteban, A, additional, Pascual-Izco, M, additional, Garcia-Martin, A, additional, Jimenez-Nacher, JJ, additional, Zamorano, JL, additional, Acar, R, additional, Bakal, RB, additional, Kaymaz, C, additional, Karvandi, M, additional, Galand, V, additional, Matelot, D, additional, Leclercq, C, additional, Carre, F, additional, Suran, BC, additional, Margulescu, AD, additional, Rimbas, RC, additional, Siliste, C, additional, Vinereanu, D, additional, Nocerino, P, additional, Urso, AC, additional, Borrino, A, additional, Carbone, C, additional, Follero, P, additional, Ciardiello, C, additional, Prato, L, additional, Salzano, G, additional, Marino, F, additional, Ruspetti, A, additional, Sparla, S, additional, Di Tommaso, C, additional, Loiacono, F, additional, D'ascenzi, F, additional, Porter, J, additional, Walker, M, additional, Lo Iudice, F, additional, Esposito, R, additional, Santoro, C, additional, Cocozza, S, additional, Izzo, R, additional, De Luca, N, additional, De Simone, G, additional, Trimarco, B, additional, Galderisi, M, additional, Gervasi, F, additional, Patti, G, additional, Mega, S, additional, Bono, M, additional, Di Sciascio, G, additional, Buture, A, additional, Badea, R, additional, Platon, P, additional, Ghiorghiu, I, additional, Jurcut, R, additional, Coman, IM, additional, Popescu, BA, additional, Ginghina, C, additional, Lunetta, M, additional, Spoto, MS, additional, Lo Vi, AM, additional, Pensabene, G, additional, Carita, P, additional, Coppola, G, additional, Assennato, P, additional, Shim, A, additional, Wejner-Mik, P, additional, Havasi, K, additional, Domsik, P, additional, Kalapos, A, additional, Forster, T, additional, Piros, GA, additional, Lengyel, C, additional, Orosz, A, additional, Bulbul, Z, additional, Issa, Z, additional, Al Sehly, A, additional, Pergola, V, additional, Oufi, S, additional, Conde, Y, additional, Cimino, E, additional, Rinaldi, E, additional, Ashurov, R, additional, Ricci, S, additional, Pergolini, M, additional, Vitarelli, A, additional, Lujan Valencia, JE, additional, Chaparro, M, additional, Garcia-Guerrero, A, additional, Cristo Ropero, MJ, additional, Izquierdo Bajo, A, additional, Madrona, L, additional, Monmeneu, JV, additional, Igual, B, additional, Lopez Lereu, P, additional, Garcia, MP, additional, Selmi, W, additional, Jalal, Z, additional, Thambo, JB, additional, Kosuta, D, additional, and Fras, Z, additional
- Published
- 2015
- Full Text
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13. Mucosa-associated bacterial diversity in necrotizing enterocolitis
- Author
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Brower-Sinning, R, Zhong, D, Good, M, Firek, B, Baker, R, Sodhi, CP, Hackam, DJ, Morowitz, MJ, Brower-Sinning, R, Zhong, D, Good, M, Firek, B, Baker, R, Sodhi, CP, Hackam, DJ, and Morowitz, MJ
- Abstract
Background: Previous studies of infant fecal samples have failed to clarify the role of gut bacteria in the pathogenesis of NEC. We sought to characterize bacterial communities within intestinal tissue resected from infants with and without NEC. Methods: 26 intestinal samples were resected from 19 infants, including 16 NEC samples and 10 non-NEC samples. Bacterial 16S rRNA gene sequences were amplified and sequenced. Analysis allowed for taxonomic identification, and quantitative PCR was used to quantify the bacterial load within samples. Results: NEC samples generally contained an increased total burden of bacteria. NEC and non-NEC sample sets were both marked by high inter-individual variability and an abundance of opportunistic pathogens. There was no statistically significant distinction between the composition of NEC and non-NEC microbial communities. K-means clustering enabled us to identify several stable clusters, including clusters of NEC and midgut volvulus samples enriched with Clostridium and Bacteroides. Another cluster containing both NEC and non-NEC samples was marked by an abundance of Enterobacteriaceae and decreased diversity among NEC samples. Conclusions: The results indicate that NEC is a disease without a uniform pattern of microbial colonization, but that NEC is associated with an abundance of strict anaerobes and a decrease in community diversity.
- Published
- 2014
14. Club35 Poster Session Thursday 12 December: 12/12/2013, 08:30-18:00 * Location: Poster area
- Author
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Montoro Lopez, M., primary, Iniesta Manjavacas, A., additional, Mori Junco, R., additional, Pena Conde, L., additional, Pons De Antonio, I., additional, Garcia Blas, S., additional, Lopez Fernandez, T., additional, Moreno Gomez, R., additional, Moreno Yanguela, M., additional, Lopez Sendon, J., additional, Carro, A., additional, Kiotsekoglou, A., additional, Andoh, J., additional, Brown, S., additional, Kaski, J., additional, Imamura, Y., additional, Arai, K., additional, Uematsu, S., additional, Fukushima, K., additional, Hoshi, H., additional, Ashihara, K., additional, Takagi, A., additional, Hagiwara, N., additional, Gillis, K., additional, Bala, G., additional, Roosens, B., additional, Remory, I., additional, Droogmans, S., additional, Van Camp, G., additional, Cosyns, B., additional, Van De Heyning, C., additional, Magne, J., additional, Pierard, L., additional, Bruyere, P., additional, Davin, L., additional, De Maeyer, C., additional, Paelinck, B., additional, Vrints, C., additional, Lancellotti, P., additional, Borowiec, A., additional, Dabrowski, R., additional, Kowalik, I., additional, Firek, B., additional, Chwyczko, T., additional, Janas, J., additional, Szwed, H., additional, Tufaro, V., additional, Fragasso, G., additional, Ingallina, G., additional, Marini, C., additional, Fisicaro, A., additional, Loiacono, F., additional, Margonato, A., additional, Agricola, E., additional, Ferreira, F., additional, Pereira, T., additional, Abreu, J., additional, Labandeiro, J., additional, Fiarresga, A., additional, Ferreira, A., additional, Galrinho, A., additional, Branco, L., additional, Timoteo, A., additional, Ferreira, R., additional, Marmol, R., additional, Gomez, M., additional, Garcia, K., additional, Sanmiguel, D., additional, Cabades, C., additional, Monteagudo, M., additional, Nunez, C., additional, Fernandez, C., additional, Diez, J., additional, Roldan, I., additional, Kolesnyk, M., additional, Ancona, M., additional, Oppizzi, M., additional, Krestjyaninov, M., additional, Razin, V., additional, Gimaev, R., additional, Carminati, M., additional, Piazzese, C., additional, Tsang, W., additional, Lang, R., additional, Caiani, E., additional, Goncalves, S., additional, Ramalho, A., additional, Placido, R., additional, Marta, L., additional, Cortez Dias, N., additional, Magalhaes, A., additional, Menezes, M., additional, Martins, S., additional, Almeida, A., additional, Nunes Diogo, A., additional, Stokke, T. M., additional, Ruddox, V., additional, Sarvari, S. I., additional, Otterstad, J. E., additional, Aune, E., additional, Edvardsen, T., additional, Pirone, D., additional, De Francesco, V., additional, Marino, F., additional, Gervasi, F., additional, Demartini, C., additional, Goffredo, C., additional, Bono, M., additional, Mega, S., additional, Chello, M., additional, Di Sciascio, G., additional, Martin Hidalgo, M., additional, Seoane Garcia, T., additional, Carrasco Avalos, F., additional, Mesa Rubio, M., additional, Delgado Ortega, M., additional, Ruiz Ortiz, M., additional, Mazuelos Bellido, F., additional, Suarez De Lezo Herrero De Tejada, J., additional, Pan Alvarez De Osorio, M., additional, Suarez De Lezo Cruz Conde, J., additional, Lopez Granados, A., additional, Romero Moreno, M., additional, Pan Alvarez-Ossorio, M., additional, Menichetti, F., additional, Bongiorni, M., additional, Ferro, B., additional, Segreti, L., additional, Bertini, P., additional, Mariotti, R., additional, Baldassarri, R., additional, Di Cori, A., additional, Zucchelli, G., additional, Guarracino, F., additional, Santoro, A., additional, Federco Alvino, F., additional, Giovanni Antonelli, G., additional, Raffaella De Vito, R., additional, Roberta Molle, R., additional, Sergio Mondillo, S., additional, Mahmoud, Y., additional, Abdel-Kader, M., additional, Guindy, R., additional, Elzahwy, S., additional, Dijkema, E., additional, Molenschot, M., additional, Slieker, M., additional, Oliveira Da Silva, C., additional, Sahlen, A., additional, Winter, R., additional, Back, M., additional, Ruck, A., additional, Settergren, M., additional, Manouras, A., additional, Shahgaldi, K., additional, and Ruzov, V., additional
- Published
- 2013
- Full Text
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15. Thermo-Cryo-Electron Microscopy of Macromolecular Complexes
- Author
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Cheng, N, primary, Conway, J, additional, Cardone, G, additional, Winkler, D, additional, Firek, B, additional, Hendrix, R, additional, Duda, R, additional, and Steven, A, additional
- Published
- 2011
- Full Text
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16. Poster Session 3
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Fabbri, G. M. T., primary, Baldasseroni, S., additional, Panuccio, D., additional, Zoni Berisso, M., additional, Scherillo, M., additional, Lucci, D., additional, Di Pasquale, G., additional, Mathieu, G., additional, Burazor, I., additional, Burazor, M., additional, Perisic, Z., additional, Atanaskovic, V., additional, Erakovic, V., additional, Stojkovic, A., additional, Vogtmann, T., additional, Schoebel, C., additional, Sogorski, S., additional, Sebert, M., additional, Schaarschmidt, J., additional, Fietze, I., additional, Baumann, G., additional, Penzel, T., additional, Mornos, C., additional, Ionac, A., additional, Cozma, D., additional, Dragulescu, D., additional, Mornos, A., additional, Petrescu, L., additional, Pescariu, L., additional, Brembilla-Perrot, B., additional, Khachab, H., additional, Lamberti, F., additional, Bellini, C., additional, Remoli, R., additional, Cogliandro, T., additional, Nardo, R., additional, Bellusci, F., additional, Mazzuca, V., additional, Gaspardone, A., additional, Aguinaga Arrascue, L. E., additional, Bravo, A., additional, Garcia Freire, P., additional, Gallardo, P., additional, Hasbani, E., additional, Quintana, R., additional, Dantur, J., additional, Inoue, K., additional, Ueoka, A., additional, Tsubakimoto, Y., additional, Sakatani, T., additional, Matsuo, A., additional, Fujita, H., additional, Kitamura, M., additional, Wegrzynowska, M., additional, Konduracka, E., additional, Pietrucha, A. Z., additional, Mroczek-Czernecka, D., additional, Paradowski, A., additional, Bzukala, I., additional, Nessler, J., additional, Igawa, O., additional, Adachi, M., additional, Atarashi, H., additional, Kusama, Y., additional, Kodani, E., additional, Okazaki, R., additional, Nakagomi, A., additional, Endoh, Y., additional, Baez-Escudero, J. L., additional, Dave, A. S., additional, Sasaridis, C. M., additional, Valderrabano, M., additional, Tilz, R., additional, Bai, R., additional, Di Biase, L., additional, Gallinghouse, G. J., additional, Gibson, D., additional, Pisapia, A., additional, Wazni, O., additional, Natale, A., additional, Arujuna, A., additional, Karim, R., additional, Rinaldi, A., additional, Cooklin, M., additional, Rhode, K., additional, Razavi, R., additional, O'neill, M., additional, Gill, J., additional, Kusa, S., additional, Komatsu, Y., additional, Kakita, K., additional, Takayama, K., additional, Taniguchi, H., additional, Otomo, K., additional, Iesaka, Y., additional, Ammar, S., additional, Reents, T., additional, Fichtner, S., additional, Wu, J., additional, Zhu, P., additional, Kolb, C., additional, Hessling, G., additional, Deisenhofer, I., additional, Gilbert, G., additional, Mohanty, P., additional, Cunningham, J., additional, Metz, T., additional, Horton, R., additional, Tao, S., additional, Yamauchi, Y., additional, Okada, H., additional, Maeda, S., additional, Obayashi, T., additional, Isobe, M., additional, Chan, J., additional, Johar, S., additional, Wong, T., additional, Markides, V., additional, Hussain, W., additional, Konstantinidou, M., additional, Wissner, E., additional, Fuernkranz, A., additional, Yoshiga, Y., additional, Metzner, A., additional, Kuck, K.- H., additional, Ouyang, F., additional, Kettering, K., additional, Gramley, F., additional, Mollnau, H., additional, Weiss, C., additional, Bardeleben, S., additional, Biasco, L., additional, Scaglione, M., additional, Caponi, D., additional, Di Donna, P., additional, Sergi, D., additional, Cerrato, N., additional, Blandino, A., additional, Gaita, F., additional, Fiala, M., additional, Wichterle, D., additional, Sknouril, L., additional, Bulkova, V., additional, Chovancik, J., additional, Nevralova, R., additional, Pindor, J., additional, Januska, J., additional, Choi, J. I., additional, Ban, J. E., additional, Yasutsugu, N., additional, Park, J. S., additional, Jung, J. S., additional, Lim, H. E., additional, Park, S. W., additional, Kim, Y. H., additional, Kuhne, M., additional, Reichlin, T., additional, Ammann, P., additional, Schaer, B., additional, Osswald, S., additional, Sticherling, C., additional, Ohe, M., additional, Goya, M., additional, Hiroshima, K., additional, Hayashi, K., additional, Makihara, Y., additional, Nagashima, M., additional, Fukunaga, M., additional, An, Y., additional, Dorwarth, U., additional, Schmidt, M., additional, Wankerl, M., additional, Krieg, J., additional, Straube, F., additional, Hoffmann, E., additional, Kathan, S., additional, Defaye, P., additional, Mbaye, A., additional, Cassagneau, R., additional, Gagniere, V., additional, Jacon, P., additional, Pokushalov, E., additional, Romanov, A., additional, Artemenko, S., additional, Shabanov, V., additional, Elesin, D., additional, Stenin, I., additional, Turov, A., additional, Losik, D., additional, Kondo, K., additional, Miake, J., additional, Yano, A., additional, Ogura, K., additional, Kato, M., additional, Shigemasa, C., additional, Sekiguchi, Y., additional, Tada, H., additional, Yoshida, K., additional, Naruse, Y., additional, Yamasaki, H., additional, Igarashi, M., additional, Machino, T., additional, Aonuma, K., additional, Chen, S., additional, Liu, S., additional, Chen, G., additional, Meng, W., additional, Zhang, F., additional, Yan, Y., additional, Sciarra, L., additional, Dottori, S., additional, Lanzillo, C., additional, De Ruvo, E., additional, De Luca, L., additional, Minati, M., additional, Lioy, E., additional, Calo', L., additional, Lin, J., additional, Nie, Z., additional, Zhu, M., additional, Wang, X., additional, Zhao, J., additional, Hu, W., additional, Tao, H., additional, Ge, J., additional, Johansson, B., additional, Houltz, B., additional, Edvardsson, N., additional, Schersten, H., additional, Karlsson, T., additional, Wandt, B., additional, Berglin, E., additional, Hoyt, R. 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P., additional, Louis-Simonet, M., additional, Hugli, O., additional, Yersin, B., additional, Schlaepfer, J., additional, Mischler, C., additional, Pruvot, E., additional, Occhetta, E., additional, Frascarelli, F., additional, Burali, A., additional, and Dovellini, E., additional
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- 2011
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17. Subacute cardiac perforations associated with active fixation leads
- Author
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Sterlinski, M., primary, Przybylski, A., additional, Maciag, A., additional, Syska, P., additional, Pytkowski, M., additional, Lewandowski, M., additional, Kowalik, I., additional, Firek, B., additional, Kolsut, P., additional, Religa, G., additional, Kusmierczyk, M., additional, Walczak, F., additional, and Szwed, H., additional
- Published
- 2008
- Full Text
- View/download PDF
18. Resolution of an aortic mobile mass with anticoagulation without evidence of arterial embolism
- Author
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Pasierski, T., primary, Jasek, S., additional, Firek, B., additional, Przbylski, A., additional, Szwed, H., additional, and Sadowski, Z., additional
- Published
- 1996
- Full Text
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19. Subacute cardiac perforations associated with active fixation leads.
- Author
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Sterlinski M, Przybylski A, Maciag A, Syska P, Pytkowski M, Lewandowski M, Kowalik I, Firek B, Kolsut P, Religa G, Kusmierczyk M, Walczak F, and Szwed H
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- 2009
- Full Text
- View/download PDF
20. Concentrations and Sources of Airborne Particles in a Neonatal Intensive Care Unit
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Licina, D, Bhangar, S, Brooks, B, Baker, R, Firek, B, Tang, X, Morowitz, MJ, Banfield, JF, and Nazaroff, WW
- Abstract
© 2016 Licina et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Premature infants in neonatal intensive care units (NICUs) have underdeveloped immune systems, making them susceptible to adverse health consequences from air pollutant exposure. Little is known about the sources of indoor airborne particles that contribute to the exposure of premature infants in the NICU environment. In this study, we monitored the spatial and temporal variations of airborne particulate matter concentrations along with other indoor environmental parameters and human occupancy. The experiments were conducted over one year in a private-style NICU. The NICU was served by a central heating, ventilation and air-conditioning (HVAC) system equipped with an economizer and a highefficiency particle filtration system. The following parameters were measured continuously during weekdays with 1-min resolution: particles larger than 0.3 μm resolved into 6 size groups, CO2level, dry-bulb temperature and relative humidity, and presence or absence of occupants. Altogether, over sixteen periods of a few weeks each, measurements were conducted in rooms occupied with premature infants. In parallel, a second monitoring station was operated in a nearby hallway or at the local nurses' station. The monitoring data suggest a strong link between indoor particle concentrations and human occupancy. Detected particle peaks from occupancy were clearly discernible among larger particles and imperceptible for submicron (0.3-1 μm) particles. The mean indoor particle mass concentrations averaged across the size range 0.3-10 μm during occupied periods was 1.9 μg/m3, approximately 2.5 times the concentration during unoccupied periods (0.8 μg/m3). Contributions of within-room emissions to total PM10mass in the baby rooms averaged 37-81%. Near-room indoor emissions and outdoor sources contributed 18-59% and 1-5%, respectively. Airborne particle levels in the size range 1-10 μm showed strong dependence on human activities, indicating the importance of indoor-generated particles for infant's exposure to airborne particulate matter in the NICU.
21. Empagliflozin in the treatment of heart failure with reduced ejection fraction in addition to background therapies and therapeutic combinations (EMPEROR-Reduced): a post-hoc analysis of a randomised, double-blind trial
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Subodh Verma, Nitish K Dhingra, Javed Butler, Stefan D Anker, Joao Pedro Ferreira, Gerasimos Filippatos, James L Januzzi, Carolyn S P Lam, Naveed Sattar, Barbara Peil, Matias Nordaby, Martina Brueckmann, Stuart J Pocock, Faiez Zannad, Milton Packer, M Packer, S Anker, J Butler, G Filippatos, S Pocock, F Zannad, JP Ferreira, M Brueckmann, J George, W Jamal, FK Welty, M Palmer, T Clayton, KG Parhofer, TR Pedersen, B Greenberg, MA Konstam, KR Lees, P Carson, W Doehner, A Miller, M Haas, S Pehrson, M Komajda, I Anand, J Teerlink, A Rabinstein, T Steiner, H Kamel, G Tsivgoulis, J Lewis, J Freston, N Kaplowitz, J Mann, J Petrie, S Perrone, S Nicholls, S Janssens, E Bocchi, N Giannetti, S Verma, J Zhang, J Spinar, M-F Seronde, M Boehm, B Merkely, V Chopra, M Senni, S Taddi, H Tsutsui, D-J Choi, E Chuquiure, HPB La Rocca, P Ponikowski, JRG Juanatey, I Squire, J Januzzi, I Pina, R Bernstein, A Cheung, J Green, S Kaul, C Lam, G Lip, N Marx, P McCullough, C Mehta, J Rosenstock, N Sattar, B Scirica, S Shah, C Wanner, D Aizenberg, L Cartasegna, F Colombo Berra, H Colombo, M Fernandez Moutin, J Glenny, C Alvarez Lorio, D Anauch, R Campos, A Facta, A Fernandez, R Ahuad Guerrero, L Lobo Márquez, RA Leon de la Fuente, M Mansilla, M Hominal, E Hasbani, M Najenson, G Moises Azize, H Luquez, L Guzman, H Sessa, M Amuchástegui, O Salomone, E Perna, D Piskorz, M Sicer, D Perez de Arenaza, C Zaidman, S Nani, C Poy, J Resk, R Villarreal, C Majul, T Smith Casabella, S Sassone, A Liberman, G Carnero, A Caccavo, M Berli, N Budassi, J Bono, A Alvarisqueta, J Amerena, K Kostner, A Hamilton, A Begg, J Beltrame, D Colquhoun, G Gordon, A Sverdlov, G Vaddadi, J Wong, J Coller, D Prior, A Friart, A Leone, G Vervoort, P Timmermans, P Troisfontaines, C Franssen, T Sarens, H Vandekerckhove, P Van De Borne, F Chenot, J De Sutter, E De Vuyst, P Debonnaire, M Dupont, O Pereira Dutra, LH Canani, MdC Vieira Moreira, W de Souza, LM Backes, L Maia, B De Souza Paolino, ER Manenti, W Saporito, F Villaça Guimarães Filho, T Franco Hirakawa, LA Saliba, FC Neuenschwander, CA de Freitas Zerbini, G Gonçalves, Y Gonçalves Mello, J Ascenção de Souza, L Beck da Silva Neto, EA Bocchi, J Da Silveira, JB de Moura Xavier Moraes Junior, JD de Souza Neto, M Hernandes, HC Finimundi, CR Sampaio, E Vasconcellos, FJ Neves Mancuso, MM Noya Rabelo, M Rodrigues Bacci, F Santos, M Vidotti, MV Simões, FL Gomes, C Vieira Nascimento, D Precoma, FA Helfenstein Fonseca, JA Ribas Fortes, PE Leães, D Campos de Albuquerque, JF Kerr Saraiva, S Rassi, FA Alves da Costa, G Reis, S Zieroth, D Dion, D Savard, R Bourgeois, C Constance, K Anderson, M-H Leblanc, D Yung, E Swiggum, L Pliamm, Y Pesant, B Tyrrell, T Huynh, J Spiegelman, J-P Lavoie, M Hartleib, R Bhargava, L Straatman, S Virani, A Costa-Vitali, L Hill, M Heffernan, Y Khaykin, J Ricci, M Senaratne, A Zhai, B Lubelsky, M Toma, L Yao, R McKelvie, L Noronha, M Babapulle, A Pandey, G Curnew, A Lavoie, J Berlingieri, S Kouz, E Lonn, R Chehayeb, Y Zheng, Y Sun, H Cui, Z Fan, X Han, X Jiang, Q Tang, J Zhou, Z Zheng, X Zhang, N Zhang, Y Zhang, A Shen, J Yu, J Ye, Y Yao, J Yan, X Xu, Z Wang, J Ma, Y Li, S Li, S Lu, X Kong, Y Song, G Yang, Z Yao, Y Pan, X Guo, Z Sun, Y Dong, J Zhu, D Peng, Z Yuan, J Lin, Y Yin, O Jerabek, H Burianova, T Fiala, J Hubac, O Ludka, Z Monhart, P Vodnansky, K Zeman, D Foldyna, J Krupicka, I Podpera, L Busak, M Radvan, Z Vomacka, R Prosecky, R Cifkova, V Durdil, J Vesely, J Vaclavik, P Cervinka, A Linhart, T Brabec, R Miklik, H Bourhaial, H-G Olbrich, S Genth-Zotz, E Kemala, B Lemke, M Böhm, S Schellong, W Rieker, T Heitzer, H Ince, M Faghih, A Birkenfeld, A Begemann, A Ghanem, A Ujeyl, S von Haehling, T Dorsel, J Bauersachs, M Prull, F Weidemann, H Darius, G Nickenig, A Wilke, J Sauter, U Rauch-Kroehnert, N Frey, CP Schulze, W König, L Maier, F Menzel, N Proskynitopoulos, H-H Ebert, H-E Sarnighausen, H-D Düngen, M Licka, C Stellbrink, B Winkelmann, N Menck, JL López-Sendón, L de la Fuente Galán, JF Delgado Jiménez, N Manito Lorite, M Pérez de Juan Romero, E Galve Basilio, F Cereto Castro, JR González Juanatey, JJ Gómez, M Sanmartín Fernández, X Garcia-Moll Marimon, D Pascual Figal, R Bover Freire, E Bonnefoy Cudraz, A Jobbe Duval, D Tomasevic, G Habib, R Isnard, F Picard, P Khanoyan, J-L Dubois-Rande, M Galinier, F Roubille, J Alexandre, D Babuty, N Delarche, J-B Berneau, N Girerd, M Saxena, G Rosano, Z Yousef, C Clifford, C Arden, A Bakhai, C Boos, G Jenkins, C Travill, D Price, L Koenyves, F Lakatos, A Matoltsy, E Noori, Z Zilahi, P Andrassy, S Kancz, G Simon, T Sydo, A Vorobcsuk, RG Kiss, K Toth, I Szakal, L Nagy, T Barany, A Nagy, E Szolnoki, VK Chopra, S Mandal, V Rastogi, B Shah, A Mullasari, J Shankar, V Mehta, A Oomman, U Kaul, S Komarlu, D Kahali, A Bhagwat, V Vijan, NK Ghaisas, A Mehta, J Kashyap, Y Kothari, S TaddeI, M Scherillo, V Zacà, S Genovese, A Salvioni, A Fucili, F Fedele, F Cosmi, M Volpe, C Mazzone, G Esposito, M Doi, H Yamamoto, S Sakagami, S Oishi, Y Yasaka, H Tsuboi, Y Fujino, S Matsuoka, Y Watanabe, T Himi, T Ide, M Ichikawa, Y Kijima, T Koga, S Yuda, K Fukui, T Kubota, M Manita, H Fujinaga, T Matsumura, Y Fukumoto, R Kato, Y Kawai, G Hiasa, Y Kazatani, M Mori, A Ogimoto, M Inoko, M Oguri, M Kinoshita, K Okuhara, N Watanabe, Y Ono, K Otomo, Y Sato, T Matsunaga, A Takaishi, N Miyagi, H Uehara, H Takaishi, H Urata, T Kataoka, H Matsubara, T Matsumoto, T Suzuki, N Takahashi, M Imamaki, T Yoshitama, T Saito, H Sekino, Y Furutani, M Koda, T Shinozaki, K Hirabayashi, R Tsunoda, K Yonezawa, H Hori, M Yagi, M Arikawa, T Hashizume, R Ishiki, T Koizumi, K Nakayama, S Taguchi, M Nanasato, Y Yoshida, S Tsujiyama, T Nakamura, K Oku, M Shimizu, M Suwa, Y Momiyama, H Sugiyama, K Kobayashi, S Inoue, T Kadokami, K Maeno, K Kawamitsu, Y Maruyama, A Nakata, T Shibata, A Wada, H-J Cho, JO Na, B-S Yoo, J-O Choi, SK Hong, J-H Shin, M-C Cho, SH Han, J-O Jeong, J-J Kim, SM Kang, D-S Kim, MH Kim, G Llamas Esperon, J Illescas Díaz, P Fajardo Campos, J Almeida Alvarado, A Bazzoni Ruiz, J Echeverri Rico, I Lopez Alcocer, L Valle Molina, C Hernandez Herrera, C Calvo Vargas, FG Padilla Padilla, I Rodriguez Briones, EJJR Chuquiure Valenzuela, ME Aguilera Real, J Carrillo Calvillo, M Alpizar Salazar, JL Cervantes Escárcega, R Velasco Sanchez, N Al - Windy, L van Heerebeek, L Bellersen, H-P Brunner-La Rocca, J Post, GCM Linssen, M van de Wetering, R Peters, R van Stralen, R Groutars, P Smits, A Yilmaz, WEM Kok, P Van der Meer, P Dijkmans, R Troquay, AP van Alem, R Van de Wal, L Handoko, ICD Westendorp, PFMM van Bergen, BJWM Rensing, P Hoogslag, B Kietselaer, JA Kragten, FR den Hartog, A Alings, L Danilowicz-Szymanowicz, G Raczak, W Piesiewicz, W Zmuda, W Kus, P Podolec, W Musial, G Drelich, G Kania, P Miekus, S Mazur, A Janik, J Spyra, J Peruga, P Balsam, B Krakowiak, J Szachniewicz, M Ginel, J Grzybowski, W Chrustowski, P Wojewoda, A Kalinka, A Zurakowski, R Koc, M Debinski, W Fil, M Kujawiak, J Forys, M Kasprzak, M Krol, P Michalski, E Mirek-Bryniarska, K Radwan, G Skonieczny, K Stania, G Skoczylas, A Madej, J Jurowiecki, B Firek, B Wozakowska-Kaplon, K Cymerman, J Neutel, K Adams, P Balfour, A Deswal, A Djamson, P Duncan, M Hong, C Murray, D Rinde-Hoffman, S Woodhouse, R MacNevin, B Rama, C Broome-Webster, S Kindsvater, D Abramov, M Barettella, S Pinney, J Herre, A Cohen, K Vora, K Challappa, S West, S Baum, J Cox, S Jani, A Karim, A Akhtar, O Quintana, L Paukman, R Goldberg, Z Bhatti, M Budoff, E Bush, A Potler, R Delgado, B Ellis, J Dy, J Fialkow, R Sangrigoli, K Ferdinand, C East, S Falkowski, S Donahoe, R Ebrahimi, G Kline, B Harris, R Khouzam, N Jaffrani, N Jarmukli, N Kazemi, M Koren, K Friedman, W Herzog, J Silva Enciso, D Cheung, M Grover-McKay, P Hauptman, D Mikhalkova, V Hegde, J Hodsden, S Khouri, F McGrew, R Littlefield, P Bradley, B McLaurin, S Lupovitch, I Labin, V Rao, M Leithe, M Lesko, N Lewis, D Lombardo, S Mahal, V Malhotra, I Dauber, A Banerjee, J Needell, G Miller, L Paladino, K Munuswamy, M Nanna, E McMillan, M Mumma, M Napoli, W Nelson, T O'Brien, A Adlakha, A Onwuanyi, H Serota, J Schmedtje, A Paraschos, R Potu, C Sai-Sudhakar, M Saltzberg, A Sauer, P Shah, H Skopicki, H Bui, K Carr, G Stevens, N Tahirkheli, J Tallaj, K Yousuf, B Trichon, J Welker, P Tolerico, A Vest, R Vivo, X Wang, R Abadier, S Dunlap, N Weintraub, A Malik, P Kotha, V Zaha, G Kim, N Uriel, T Greene, A Salacata, R Arora, R Gazmuri, J Kobayashi, B Iteld, R Vijayakrishnan, R Dab, Z Mirza, V Marques, M Nallasivan, D Bensimhon, B Peart, H Saint-Jacques, K Barringhaus, J Contreras, A Gupta, S Koneru, V Nguyen, Verma, S, Dhingra, N, Butler, J, Anker, S, Ferreira, J, Filippatos, G, Januzzi, J, Lam, C, Sattar, N, Peil, B, Nordaby, M, Brueckmann, M, Pocock, S, Zannad, F, Packer, M, George, J, Jamal, W, Welty, F, Palmer, M, Clayton, T, Parhofer, K, Pedersen, T, Greenberg, B, Konstam, M, Lees, K, Carson, P, Doehner, W, Miller, A, Haas, M, Pehrson, S, Komajda, M, Anand, I, Teerlink, J, Rabinstein, A, Steiner, T, Kamel, H, Tsivgoulis, G, Lewis, J, Freston, J, Kaplowitz, N, Mann, J, Petrie, J, Perrone, S, Nicholls, S, Janssens, S, Bocchi, E, Giannetti, N, Zhang, J, Spinar, J, Seronde, M, Boehm, M, Merkely, B, Chopra, V, Senni, M, Taddi, S, Tsutsui, H, Choi, D, Chuquiure, E, La Rocca, H, Ponikowski, P, Juanatey, J, Squire, I, Pina, I, Bernstein, R, Cheung, A, Green, J, Kaul, S, Lip, G, Marx, N, Mccullough, P, Mehta, C, Rosenstock, J, Scirica, B, Shah, S, Wanner, C, Aizenberg, D, Cartasegna, L, Colombo Berra, F, Colombo, H, Fernandez Moutin, M, Glenny, J, Alvarez Lorio, C, Anauch, D, Campos, R, Facta, A, Fernandez, A, Ahuad Guerrero, R, Lobo Marquez, L, Leon de la Fuente, R, Mansilla, M, Hominal, M, Hasbani, E, Najenson, M, Moises Azize, G, Luquez, H, Guzman, L, Sessa, H, Amuchastegui, M, Salomone, O, Perna, E, Piskorz, D, Sicer, M, Perez de Arenaza, D, Zaidman, C, Nani, S, Poy, C, Resk, J, Villarreal, R, Majul, C, Smith Casabella, T, Sassone, S, Liberman, A, Carnero, G, Caccavo, A, Berli, M, Budassi, N, Bono, J, Alvarisqueta, A, Amerena, J, Kostner, K, Hamilton, A, Begg, A, Beltrame, J, Colquhoun, D, Gordon, G, Sverdlov, A, Vaddadi, G, Wong, J, Coller, J, Prior, D, Friart, A, Leone, A, Vervoort, G, Timmermans, P, Troisfontaines, P, Franssen, C, Sarens, T, Vandekerckhove, H, Van De Borne, P, Chenot, F, De Sutter, J, De Vuyst, E, Debonnaire, P, Dupont, M, Pereira Dutra, O, Canani, L, Vieira Moreira, M, de Souza, W, Backes, L, Maia, L, De Souza Paolino, B, Manenti, E, Saporito, W, Villaca Guimaraes Filho, F, Franco Hirakawa, T, Saliba, L, Neuenschwander, F, de Freitas Zerbini, C, Goncalves, G, Goncalves Mello, Y, Ascencao de Souza, J, Beck da Silva Neto, L, Da Silveira, J, de Moura Xavier Moraes Junior, J, de Souza Neto, J, Hernandes, M, Finimundi, H, Sampaio, C, Vasconcellos, E, Neves Mancuso, F, Noya Rabelo, M, Rodrigues Bacci, M, Santos, F, Vidotti, M, Simoes, M, Gomes, F, Vieira Nascimento, C, Precoma, D, Helfenstein Fonseca, F, Ribas Fortes, J, Leaes, P, Campos de Albuquerque, D, Kerr Saraiva, J, Rassi, S, Alves da Costa, F, Reis, G, Zieroth, S, Dion, D, Savard, D, Bourgeois, R, Constance, C, Anderson, K, Leblanc, M, Yung, D, Swiggum, E, Pliamm, L, Pesant, Y, Tyrrell, B, Huynh, T, Spiegelman, J, Lavoie, J, Hartleib, M, Bhargava, R, Straatman, L, Virani, S, Costa-Vitali, A, Hill, L, Heffernan, M, Khaykin, Y, Ricci, J, Senaratne, M, Zhai, A, Lubelsky, B, Toma, M, Yao, L, Mckelvie, R, Noronha, L, Babapulle, M, Pandey, A, Curnew, G, Lavoie, A, Berlingieri, J, Kouz, S, Lonn, E, Chehayeb, R, Zheng, Y, Sun, Y, Cui, H, Fan, Z, Han, X, Jiang, X, Tang, Q, Zhou, J, Zheng, Z, Zhang, X, Zhang, N, Zhang, Y, Shen, A, Yu, J, Ye, J, Yao, Y, Yan, J, Xu, X, Wang, Z, Ma, J, Li, Y, Li, S, Lu, S, Kong, X, Song, Y, Yang, G, Yao, Z, Pan, Y, Guo, X, Sun, Z, Dong, Y, Zhu, J, Peng, D, Yuan, Z, Lin, J, Yin, Y, Jerabek, O, Burianova, H, Fiala, T, Hubac, J, Ludka, O, Monhart, Z, Vodnansky, P, Zeman, K, Foldyna, D, Krupicka, J, Podpera, I, Busak, L, Radvan, M, Vomacka, Z, Prosecky, R, Cifkova, R, Durdil, V, Vesely, J, Vaclavik, J, Cervinka, P, Linhart, A, Brabec, T, Miklik, R, Bourhaial, H, Olbrich, H, Genth-Zotz, S, Kemala, E, Lemke, B, Bohm, M, Schellong, S, Rieker, W, Heitzer, T, Ince, H, Faghih, M, Birkenfeld, A, Begemann, A, Ghanem, A, Ujeyl, A, von Haehling, S, Dorsel, T, Bauersachs, J, Prull, M, Weidemann, F, Darius, H, Nickenig, G, Wilke, A, Sauter, J, Rauch-Kroehnert, U, Frey, N, Schulze, C, Konig, W, Maier, L, Menzel, F, Proskynitopoulos, N, Ebert, H, Sarnighausen, H, Dungen, H, Licka, M, Stellbrink, C, Winkelmann, B, Menck, N, Lopez-Sendon, J, de la Fuente Galan, L, Delgado Jimenez, J, Manito Lorite, N, Perez de Juan Romero, M, Galve Basilio, E, Cereto Castro, F, Gonzalez Juanatey, J, Gomez, J, Sanmartin Fernandez, M, Garcia-Moll Marimon, X, Pascual Figal, D, Bover Freire, R, Bonnefoy Cudraz, E, Jobbe Duval, A, Tomasevic, D, Habib, G, Isnard, R, Picard, F, Khanoyan, P, Dubois-Rande, J, Galinier, M, Roubille, F, Alexandre, J, Babuty, D, Delarche, N, Berneau, J, Girerd, N, Saxena, M, Rosano, G, Yousef, Z, Clifford, C, Arden, C, Bakhai, A, Boos, C, Jenkins, G, Travill, C, Price, D, Koenyves, L, Lakatos, F, Matoltsy, A, Noori, E, Zilahi, Z, Andrassy, P, Kancz, S, Simon, G, Sydo, T, Vorobcsuk, A, Kiss, R, Toth, K, Szakal, I, Nagy, L, Barany, T, Nagy, A, Szolnoki, E, Mandal, S, Rastogi, V, Shah, B, Mullasari, A, Shankar, J, Mehta, V, Oomman, A, Kaul, U, Komarlu, S, Kahali, D, Bhagwat, A, Vijan, V, Ghaisas, N, Mehta, A, Kashyap, J, Kothari, Y, Taddei, S, Scherillo, M, Zaca, V, Genovese, S, Salvioni, A, Fucili, A, Fedele, F, Cosmi, F, Volpe, M, Mazzone, C, Esposito, G, Doi, M, Yamamoto, H, Sakagami, S, Oishi, S, Yasaka, Y, Tsuboi, H, Fujino, Y, Matsuoka, S, Watanabe, Y, Himi, T, Ide, T, Ichikawa, M, Kijima, Y, Koga, T, Yuda, S, Fukui, K, Kubota, T, Manita, M, Fujinaga, H, Matsumura, T, Fukumoto, Y, Kato, R, Kawai, Y, Hiasa, G, Kazatani, Y, Mori, M, Ogimoto, A, Inoko, M, Oguri, M, Kinoshita, M, Okuhara, K, Watanabe, N, Ono, Y, Otomo, K, Sato, Y, Matsunaga, T, Takaishi, A, Miyagi, N, Uehara, H, Takaishi, H, Urata, H, Kataoka, T, Matsubara, H, Matsumoto, T, Suzuki, T, Takahashi, N, Imamaki, M, Yoshitama, T, Saito, T, Sekino, H, Furutani, Y, Koda, M, Shinozaki, T, Hirabayashi, K, Tsunoda, R, Yonezawa, K, Hori, H, Yagi, M, Arikawa, M, Hashizume, T, Ishiki, R, Koizumi, T, Nakayama, K, Taguchi, S, Nanasato, M, Yoshida, Y, Tsujiyama, S, Nakamura, T, Oku, K, Shimizu, M, Suwa, M, Momiyama, Y, Sugiyama, H, Kobayashi, K, Inoue, S, Kadokami, T, Maeno, K, Kawamitsu, K, Maruyama, Y, Nakata, A, Shibata, T, Wada, A, Cho, H, Na, J, Yoo, B, Choi, J, Hong, S, Shin, J, Cho, M, Han, S, Jeong, J, Kim, J, Kang, S, Kim, D, Kim, M, Llamas Esperon, G, Illescas Diaz, J, Fajardo Campos, P, Almeida Alvarado, J, Bazzoni Ruiz, A, Echeverri Rico, J, Lopez Alcocer, I, Valle Molina, L, Hernandez Herrera, C, Calvo Vargas, C, Padilla Padilla, F, Rodriguez Briones, I, Chuquiure Valenzuela, E, Aguilera Real, M, Carrillo Calvillo, J, Alpizar Salazar, M, Cervantes Escarcega, J, Velasco Sanchez, R, Al - Windy, N, van Heerebeek, L, Bellersen, L, Brunner-La Rocca, H, Post, J, Linssen, G, van de Wetering, M, Peters, R, van Stralen, R, Groutars, R, Smits, P, Yilmaz, A, Kok, W, Van der Meer, P, Dijkmans, P, Troquay, R, van Alem, A, Van de Wal, R, Handoko, L, Westendorp, I, van Bergen, P, Rensing, B, Hoogslag, P, Kietselaer, B, Kragten, J, den Hartog, F, Alings, A, Danilowicz-Szymanowicz, L, Raczak, G, Piesiewicz, W, Zmuda, W, Kus, W, Podolec, P, Musial, W, Drelich, G, Kania, G, Miekus, P, Mazur, S, Janik, A, Spyra, J, Peruga, J, Balsam, P, Krakowiak, B, Szachniewicz, J, Ginel, M, Grzybowski, J, Chrustowski, W, Wojewoda, P, Kalinka, A, Zurakowski, A, Koc, R, Debinski, M, Fil, W, Kujawiak, M, Forys, J, Kasprzak, M, Krol, M, Michalski, P, Mirek-Bryniarska, E, Radwan, K, Skonieczny, G, Stania, K, Skoczylas, G, Madej, A, Jurowiecki, J, Firek, B, Wozakowska-Kaplon, B, Cymerman, K, Neutel, J, Adams, K, Balfour, P, Deswal, A, Djamson, A, Duncan, P, Hong, M, Murray, C, Rinde-Hoffman, D, Woodhouse, S, Macnevin, R, Rama, B, Broome-Webster, C, Kindsvater, S, Abramov, D, Barettella, M, Pinney, S, Herre, J, Cohen, A, Vora, K, Challappa, K, West, S, Baum, S, Cox, J, Jani, S, Karim, A, Akhtar, A, Quintana, O, Paukman, L, Goldberg, R, Bhatti, Z, Budoff, M, Bush, E, Potler, A, Delgado, R, Ellis, B, Dy, J, Fialkow, J, Sangrigoli, R, Ferdinand, K, East, C, Falkowski, S, Donahoe, S, Ebrahimi, R, Kline, G, Harris, B, Khouzam, R, Jaffrani, N, Jarmukli, N, Kazemi, N, Koren, M, Friedman, K, Herzog, W, Silva Enciso, J, Cheung, D, Grover-McKay, M, Hauptman, P, Mikhalkova, D, Hegde, V, Hodsden, J, Khouri, S, Mcgrew, F, Littlefield, R, Bradley, P, Mclaurin, B, Lupovitch, S, Labin, I, Rao, V, Leithe, M, Lesko, M, Lewis, N, Lombardo, D, Mahal, S, Malhotra, V, Dauber, I, Banerjee, A, Needell, J, Miller, G, Paladino, L, Munuswamy, K, Nanna, M, Mcmillan, E, Mumma, M, Napoli, M, Nelson, W, O'Brien, T, Adlakha, A, Onwuanyi, A, Serota, H, Schmedtje, J, Paraschos, A, Potu, R, Sai-Sudhakar, C, Saltzberg, M, Sauer, A, Shah, P, Skopicki, H, Bui, H, Carr, K, Stevens, G, Tahirkheli, N, Tallaj, J, Yousuf, K, Trichon, B, Welker, J, Tolerico, P, Vest, A, Vivo, R, Wang, X, Abadier, R, Dunlap, S, Weintraub, N, Malik, A, Kotha, P, Zaha, V, Kim, G, Uriel, N, Greene, T, Salacata, A, Arora, R, Gazmuri, R, Kobayashi, J, Iteld, B, Vijayakrishnan, R, Dab, R, Mirza, Z, Marques, V, Nallasivan, M, Bensimhon, D, Peart, B, Saint-Jacques, H, Barringhaus, K, Contreras, J, Gupta, A, Koneru, S, Nguyen, V, Physiologie & médecine expérimentale du Cœur et des Muscles [U 1046] (PhyMedExp), Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)
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Male ,medicine.medical_specialty ,Angiotensin receptor ,Glucoside ,Endocrinology, Diabetes and Metabolism ,[SDV]Life Sciences [q-bio] ,Vascular damage Radboud Institute for Health Sciences [Radboudumc 16] ,Adrenergic beta-Antagonists ,Angiotensin-Converting Enzyme Inhibitors ,030204 cardiovascular system & hematology ,Placebo ,03 medical and health sciences ,Angiotensin Receptor Antagonists ,0302 clinical medicine ,Endocrinology ,Mineralocorticoid receptor ,Glucosides ,Double-Blind Method ,Internal medicine ,Post-hoc analysis ,Internal Medicine ,medicine ,Empagliflozin ,Humans ,030212 general & internal medicine ,Benzhydryl Compounds ,ComputingMilieux_MISCELLANEOUS ,Aged ,Benzhydryl Compound ,Heart Failure ,Ejection fraction ,business.industry ,Angiotensin Receptor Antagonist ,Adrenergic beta-Antagonist ,Angiotensin-Converting Enzyme Inhibitor ,Stroke Volume ,medicine.disease ,3. Good health ,Heart failure ,ACE inhibitor ,Female ,Hypotension ,business ,medicine.drug ,Human - Abstract
Contains fulltext : 249977.pdf (Publisher’s version ) (Closed access) BACKGROUND: It is important to evaluate whether a new treatment for heart failure with reduced ejection fraction (HFrEF) provides additive benefit to background foundational treatments. As such, we aimed to evaluate the efficacy and safety of empagliflozin in patients with HFrEF in addition to baseline treatment with specific doses and combinations of disease-modifying therapies. METHODS: We performed a post-hoc analysis of the EMPEROR-Reduced randomised, double-blind, parallel-group trial, which took place in 520 centres (hospitals and medical clinics) in 20 countries in Asia, Australia, Europe, North America, and South America. Patients with New York Heart Association (NYHA) classification II-IV with an ejection fraction of 40% or less were randomly assigned (1:1) to receive the addition of either oral empagliflozin 10 mg per day or placebo to background therapy. The primary composite outcome was cardiovascular death and heart failure hospitalisation; the secondary outcome was total heart failure hospital admissions. An extended composite outcome consisted of inpatient and outpatient HFrEF events was also evaluated. Outcomes were analysed according to background use of angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs) or angiotensin receptor neprilysin inhibitors (ARNIs), as well as β blockers and mineralocorticoid receptor antagonists (MRAs) at less than 50% or 50% or more of target doses and in various combinations. This study is registered with ClinicalTrials.gov, NCT03057977. FINDINGS: In this post-hoc analysis of 3730 patients (mean age 66·8 years [SD 11·0], 893 [23·9%] women; 1863 [49·9%] in the empagliflozin group, 1867 [50·1%] in the placebo group) assessed between March 6, 2017, and May 28, 2020, empagliflozin reduced the risk of the primary outcome (361 in 1863 participants in the empagliflozin group and 462 of 1867 in the placebo group; HR 0·75 [95% CI 0·65-0·86]) regardless of background therapy or its target doses for ACE inhibitors or ARBs at doses of less than 50% of the target dose (HR 0·85 [0·69-1·06]) and for doses of 50% or more of the target dose (HR 0·67 [0·52-0·88]; p(interaction)=0·18). A similar result was seen for β blockers at doses of less than 50% of the target dose (HR 0·66 [0·54-0·80]) and for doses of 50% or more of the target dose (HR 0·81 [0·66-1·00]; p(interaction)=0·15). Empagliflozin also reduced the risk of the primary outcome irrespective of background use of triple therapy with an ACE inhibitor, ARB, or ARNI plus β blocker plus MRA (given combination HR 0·73 [0·61-0·88]; not given combination HR 0·76 [0·62-0·94]; p(interaction)=0·77). Similar patterns of benefit were observed for the secondary and extended composite outcomes. Empagliflozin was well tolerated and rates of hypotension, symptomatic hypotension, and hyperkalaemia were similar across all subgroups. INTERPRETATION: Empagliflozin reduced serious heart failure outcomes across doses and combinations of disease-modifying therapies for HFrEF. Clinically, these data suggest that empagliflozin might be considered as a foundational therapy in patients with HFrEF regardless of their existing background therapy. FUNDING: Boehringer Ingelheim and Eli Lilly and Company.
- Published
- 2022
22. The salivary microbiota of patients with acute lower respiratory tract infection-A multicenter cohort study.
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Rogers MB, Harner A, Buhay M, Firek B, Methé B, Morris A, Palmer OMP, Promes SB, Sherwin RL, Southerland L, Vieira AR, Yende S, Morowitz MJ, and Huang DT
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- Adult, Humans, Prospective Studies, Feces microbiology, RNA, Ribosomal, 16S genetics, Microbiota, Respiratory Tract Infections microbiology, Gastrointestinal Microbiome
- Abstract
The human microbiome contributes to health and disease, but the oral microbiota is understudied relative to the gut microbiota. The salivary microbiota is easily accessible, underexplored, and may provide insight into response to infections. We sought to determine the composition, association with clinical features, and heterogeneity of the salivary microbiota in patients with acute lower respiratory tract infection (LRTI). We conducted a multicenter prospective cohort study of 147 adults with acute LRTI presenting to the emergency department of seven hospitals in three states (Pennsylvania, Michigan, and Ohio) between May 2017 and November 2018. Salivary samples were collected in the emergency department, at days 2-5 if hospitalized, and at day 30, as well as fecal samples if patients were willing. We compared salivary microbiota profiles from patients to those of healthy adult volunteers by sequencing and analyzing bacterial 16-rRNA. Compared to healthy volunteers, the salivary microbiota of patients with LRTI was highly distinct and strongly enriched with intestinal anaerobes such as Bacteroidaceae, Ruminococcaceae, and Lachnospiraceae (e.g., mean 10% relative abundance of Bacteroides vs < 1% in healthy volunteers). Within the LRTI population, COPD exacerbation was associated with altered salivary microbiota composition compared to other LRTI conditions. The largest determinant of microbiota variation within the LRTI population was geography (city in which the hospital was located)., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2024 Rogers et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)
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- 2024
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23. Epithelial NAD + depletion drives mitochondrial dysfunction and contributes to intestinal inflammation.
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Novak EA, Crawford EC, Mentrup HL, Griffith BD, Fletcher DM, Flanagan MR, Schneider C, Firek B, Rogers MB, Morowitz MJ, Piganelli JD, Wang Q, and Mollen KP
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- Humans, Male, Animals, Mice, NAD, Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha genetics, Mice, Transgenic, Mitochondria, Inflammation, Colitis, Inflammatory Bowel Diseases
- Abstract
Introduction: We have previously demonstrated that a pathologic downregulation of peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC1α) within the intestinal epithelium contributes to the pathogenesis of inflammatory bowel disease (IBD). However, the mechanism underlying downregulation of PGC1α expression and activity during IBD is not yet clear., Methods: Mice (male; C57Bl/6, Villincre /+; Pgc1afl/fl mice, and Pgc1afl/fl ) were subjected to experimental colitis and treated with nicotinamide riboside. Western blot, high-resolution respirometry, nicotinamide adenine dinucleotide (NAD+) quantification, and immunoprecipitation were used to in this study., Results: We demonstrate a significant depletion in the NAD+ levels within the intestinal epithelium of mice undergoing experimental colitis, as well as humans with ulcerative colitis. While we found no decrease in the levels of NAD+-synthesizing enzymes within the intestinal epithelium of mice undergoing experimental colitis, we did find an increase in the mRNA level, as well as the enzymatic activity, of the NAD+-consuming enzyme poly(ADP-ribose) polymerase-1 (PARP1). Treatment of mice undergoing experimental colitis with an NAD+ precursor reduced the severity of colitis, restored mitochondrial function, and increased active PGC1α levels; however, NAD+ repletion did not benefit transgenic mice that lack PGC1α within the intestinal epithelium, suggesting that the therapeutic effects require an intact PGC1α axis., Discussion: Our results emphasize the importance of PGC1α expression to both mitochondrial health and homeostasis within the intestinal epithelium and suggest a novel therapeutic approach for disease management. These findings also provide a mechanistic basis for clinical trials of nicotinamide riboside in IBD patients., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Novak, Crawford, Mentrup, Griffith, Fletcher, Flanagan, Schneider, Firek, Rogers, Morowitz, Piganelli, Wang and Mollen.)
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- 2023
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24. Combined analysis of microbial metagenomic and metatranscriptomic sequencing data to assess in situ physiological conditions in the premature infant gut.
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Sher Y, Olm MR, Raveh-Sadka T, Brown CT, Sher R, Firek B, Baker R, Morowitz MJ, and Banfield JF
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- Case-Control Studies, Databases, Genetic, Digestive System microbiology, Digestive System Physiological Phenomena, Electron Transport Complex IV genetics, Enterocolitis, Necrotizing diagnosis, Enterocolitis, Necrotizing genetics, Enterocolitis, Necrotizing microbiology, Escherichia genetics, Escherichia isolation & purification, Female, Genes, Bacterial, Humans, Infant, Newborn, Male, Metagenome, Microbiota genetics, Transcriptome, Gastrointestinal Microbiome genetics, Gastrointestinal Microbiome physiology, Infant, Premature physiology
- Abstract
Microbes alter their transcriptomic profiles in response to the environment. The physiological conditions experienced by a microbial community can thus be inferred using meta-transcriptomic sequencing by comparing transcription levels of specifically chosen genes. However, this analysis requires accurate reference genomes to identify the specific genes from which RNA reads originate. In addition, such an analysis should avoid biases in transcript counts related to differences in organism abundance. In this study we describe an approach to address these difficulties. Sample-specific meta-genomic assembled genomes (MAGs) were used as reference genomes to accurately identify the origin of RNA reads, and transcript ratios of genes with opposite transcription responses were compared to eliminate biases related to differences in organismal abundance, an approach hereafter named the "diametric ratio" method. We used this approach to probe the environmental conditions experienced by Escherichia spp. in the gut of 4 premature infants, 2 of whom developed necrotizing enterocolitis (NEC), a severe inflammatory intestinal disease. We analyzed twenty fecal samples taken from four premature infants (4-6 time points from each infant), and found significantly higher diametric ratios of genes associated with low oxygen levels in samples of infants later diagnosed with NEC than in samples without NEC. We also show this method can be used for examining other physiological conditions, such as exposure to nitric oxide and osmotic pressure. These study results should be treated with caution, due to the presence of confounding factors that might also distinguish between NEC and control infants. Nevertheless, together with benchmarking analyses, we show here that the diametric ratio approach can be applied for evaluating the physiological conditions experienced by microbes in situ. Results from similar studies can be further applied for designing diagnostic methods to detect NEC in its early developmental stages., Competing Interests: RS affiliation to Enview, inc., does not alter our adherence to PLOS ONE policies on sharing data and materials.
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- 2020
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25. Plant-based Enteral Nutrition Modifies the Gut Microbiota and Improves Outcomes in Murine Models of Colitis.
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Yeh A, Conners EM, Ramos-Jimenez RG, Firek B, Novak EA, Rogers MB, Cheek R, Ozolek J, Mollen KP, and Morowitz MJ
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- Animals, Biodiversity, Diet, Disease Models, Animal, Mice, Treatment Outcome, Colitis microbiology, Colitis therapy, Enteral Nutrition, Gastrointestinal Microbiome, Plants
- Published
- 2019
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26. Genetic association and differential expression of PITX2 with acute appendicitis.
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Orlova E, Yeh A, Shi M, Firek B, Ranganathan S, Whitcomb DC, Finegold DN, Ferrell RE, Barmada MM, Marazita ML, Hinds DA, Shaffer JR, and Morowitz MJ
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- Acute Disease, Adolescent, Adult, Appendicitis pathology, Case-Control Studies, Child, Child, Preschool, Cohort Studies, Female, Humans, Infant, Infant, Newborn, Inflammation etiology, Inflammation pathology, Male, Meta-Analysis as Topic, Middle Aged, Prognosis, Young Adult, Homeobox Protein PITX2, Appendectomy adverse effects, Appendicitis surgery, Biomarkers analysis, Genetic Association Studies, Homeodomain Proteins genetics, Inflammation diagnosis, Polymorphism, Single Nucleotide, Transcription Factors genetics
- Abstract
Appendicitis affects 9% of Americans and is the most common diagnosis requiring hospitalization of both children and adults. We performed a genome-wide association study of self-reported appendectomy with 18,773 affected adults and 114,907 unaffected adults of European American ancestry. A significant association with appendectomy was observed at 4q25 near the gene PITX2 (rs2129979, p value = 8.82 × 10
-14 ) and was replicated in an independent sample of Caucasians (59 affected, 607 unaffected; p value = 0.005). Meta-analysis of the associated variant across our two cohorts and cohorts from Iceland and the Netherlands (in which this association had previously been reported) showed strong cumulative evidence of association (OR = 1.12; 95% CI 1.09-1.14; p value = 1.81 × 10-23 ) and some evidence for effect heterogeneity (p value = 0.03). Eight other loci were identified at suggestive significance in the discovery GWAS. Associations were followed up by measuring gene expression across resected appendices with varying levels of inflammation (N = 75). We measured expression of 27 genes based on physical proximity to the GWAS signals, evidence of being targeted by eQTLs near the signals according to RegulomeDB (score = 1), or both. Four of the 27 genes (including PITX2) showed significant evidence (p values < 0.0033) of differential expression across categories of appendix inflammation. An additional ten genes showed nominal evidence (p value < 0.05) of differential expression, which, together with the significant genes, is more than expected by chance (p value = 6.6 × 10-12 ). PITX2 impacts morphological development of intestinal tissue, promotes an anti-oxidant response, and its expression correlates with levels of intestinal bacteria and colonic inflammation. Further studies of the role of PITX2 in appendicitis are warranted.- Published
- 2019
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27. Hospitalized Premature Infants Are Colonized by Related Bacterial Strains with Distinct Proteomic Profiles.
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Brown CT, Xiong W, Olm MR, Thomas BC, Baker R, Firek B, Morowitz MJ, Hettich RL, and Banfield JF
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- Bacteria classification, Bacteria genetics, Biota, Enterocolitis, Necrotizing microbiology, Enterocolitis, Necrotizing pathology, Feces microbiology, Female, Humans, Infant, Newborn, Male, Metagenome, Metagenomics, Proteomics, Bacteria chemistry, Gastrointestinal Microbiome, Hospitalization, Infant, Premature, Microbiota, Proteome analysis
- Abstract
During the first weeks of life, microbial colonization of the gut impacts human immune system maturation and other developmental processes. In premature infants, aberrant colonization has been implicated in the onset of necrotizing enterocolitis (NEC), a life-threatening intestinal disease. To study the premature infant gut colonization process, genome-resolved metagenomics was conducted on 343 fecal samples collected during the first 3 months of life from 35 premature infants housed in a neonatal intensive care unit, 14 of whom developed NEC, and metaproteomic measurements were made on 87 samples. Microbial community composition and proteomic profiles remained relatively stable on the time scale of a week, but the proteome was more variable. Although genetically similar organisms colonized many infants, most infants were colonized by distinct strains with metabolic profiles that could be distinguished using metaproteomics. Microbiome composition correlated with infant, antibiotics administration, and NEC diagnosis. Communities were found to cluster into seven primary types, and community type switched within infants, sometimes multiple times. Interestingly, some communities sampled from the same infant at subsequent time points clustered with those of other infants. In some cases, switches preceded onset of NEC; however, no species or community type could account for NEC across the majority of infants. In addition to a correlation of protein abundances with organism replication rates, we found that organism proteomes correlated with overall community composition. Thus, this genome-resolved proteomics study demonstrated that the contributions of individual organisms to microbiome development depend on microbial community context. IMPORTANCE Humans are colonized by microbes at birth, a process that is important to health and development. However, much remains to be known about the fine-scale microbial dynamics that occur during the colonization period. We conducted a genome-resolved study of microbial community composition, replication rates, and proteomes during the first 3 months of life of both healthy and sick premature infants. Infants were found to be colonized by similar microbes, but each underwent a distinct colonization trajectory. Interestingly, related microbes colonizing different infants were found to have distinct proteomes, indicating that microbiome function is not only driven by which organisms are present, but also largely depends on microbial responses to the unique set of physiological conditions in the infant gut., (Copyright © 2018 Brown et al.)
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- 2018
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28. Identical bacterial populations colonize premature infant gut, skin, and oral microbiomes and exhibit different in situ growth rates.
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Olm MR, Brown CT, Brooks B, Firek B, Baker R, Burstein D, Soenjoyo K, Thomas BC, Morowitz M, and Banfield JF
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- Citrobacter koseri growth & development, Citrobacter koseri isolation & purification, Citrobacter koseri pathogenicity, Genome, Bacterial, Humans, Infant, Extremely Low Birth Weight, Infant, Newborn, Infant, Premature, Polymorphism, Genetic, Citrobacter koseri genetics, Gastrointestinal Microbiome, Mouth microbiology, Skin microbiology
- Abstract
The initial microbiome impacts the health and future development of premature infants. Methodological limitations have led to gaps in our understanding of the habitat range and subpopulation complexity of founding strains, as well as how different body sites support microbial growth. Here, we used metagenomics to reconstruct genomes of strains that colonized the skin, mouth, and gut of two hospitalized premature infants during the first month of life. Seven bacterial populations, considered to be identical given whole-genome average nucleotide identity of >99.9%, colonized multiple body sites, yet none were shared between infants. Gut-associated Citrobacter koseri genomes harbored 47 polymorphic sites that we used to define 10 subpopulations, one of which appeared in the gut after 1 wk but did not spread to other body sites. Differential genome coverage was used to measure bacterial population replication rates in situ. In all cases where the same bacterial population was detected in multiple body sites, replication rates were faster in mouth and skin compared to the gut. The ability of identical strains to colonize multiple body sites underscores the habit flexibility of initial colonists, whereas differences in microbial replication rates between body sites suggest differences in host control and/or resource availability. Population genomic analyses revealed microdiversity within bacterial populations, implying initial inoculation by multiple individual cells with distinct genotypes. Overall, however, the overlap of strains across body sites implies that the premature infant microbiome can exhibit very low microbial diversity., (© 2017 Olm et al.; Published by Cold Spring Harbor Laboratory Press.)
- Published
- 2017
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29. Disruption of the microbiota across multiple body sites in critically ill children.
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Rogers MB, Firek B, Shi M, Yeh A, Brower-Sinning R, Aveson V, Kohl BL, Fabio A, Carcillo JA, and Morowitz MJ
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- Adult, Alphaproteobacteria isolation & purification, Betaproteobacteria isolation & purification, Child, Child, Preschool, Critical Illness, DNA, Bacterial analysis, DNA, Ribosomal analysis, Female, Humans, Infant, Intensive Care Units, Longitudinal Studies, Male, Microbiota, Phylogeny, RNA, Ribosomal, 16S analysis, Alphaproteobacteria classification, Betaproteobacteria classification, Dysbiosis microbiology, Feces microbiology, Skin microbiology, Tongue microbiology
- Abstract
Background: Despite intense interest in the links between the microbiome and human health, little has been written about dysbiosis among ICU patients. We characterized microbial diversity in samples from 37 children in a pediatric ICU (PICU). Standard measures of alpha and beta diversity were calculated, and results were compared with data from adult and pediatric reference datasets., Results: Bacterial 16S rRNA gene sequences were analyzed from 71 total tongue swabs, 50 skin swabs, and 77 stool samples or rectal swabs. The mean age of the PICU patients was 2.9 years (range 1-9 years), and many were chronically ill children that had previously been hospitalized in the PICU. Relative to healthy adults and children, alpha diversity was decreased in PICU GI and tongue but not skin samples. Measures of beta diversity indicated differences in community membership at each body site between PICU, adult, and pediatric groups. Taxonomic alterations in the PICU included enrichment of gut pathogens such as Enterococcus and Staphylococcus at multiple body sites and depletion of commensals such as Faecalibacterium and Ruminococcus from GI samples. Alpha and beta diversity were unstable over time in patients followed longitudinally. We observed the frequent presence of "dominant" pathogens in PICU samples at relative abundance >50%. PICU samples were characterized by loss of site specificity, with individual taxa commonly present simultaneously at three sample sites on a single individual. Some pathogens identified by culture of tracheal aspirates were commonly observed in skin samples from the same patient., Conclusions: We conclude that the microbiota in critically ill children differs sharply from the microbiota of healthy children and adults. Acknowledgement of dysbiosis associated with critical illness could provide opportunities to modulate the microbiota with precision and thereby improve patient outcomes.
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- 2016
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30. Dysbiosis Across Multiple Body Sites in Critically Ill Adult Surgical Patients.
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Yeh A, Rogers MB, Firek B, Neal MD, Zuckerbraun BS, and Morowitz MJ
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- Adult, Corynebacterium genetics, Corynebacterium isolation & purification, Enterococcus genetics, Enterococcus isolation & purification, Faecalibacterium genetics, Faecalibacterium isolation & purification, Feces microbiology, Humans, Intensive Care Units statistics & numerical data, Microbiota genetics, Mycoplasma genetics, Mycoplasma isolation & purification, Polymerase Chain Reaction, RNA, Ribosomal, 16S genetics, Skin microbiology, Staphylococcus genetics, Staphylococcus isolation & purification, Tongue microbiology, Critical Illness, Dysbiosis genetics
- Abstract
The microbiota of critically ill patients likely undergoes dramatic changes but has not been rigorously studied with a culture-independent high-throughput approach. The aim of this study was to characterize spatial and temporal variation in the microbiota of critically ill patients. Trauma and acute surgery patients admitted to the intensive care unit (ICU) were sampled at five body sites (stool, tongue, skin, trachea, urine) every 3 to 4 days. A mean of 10.8 samples was collected from 32 patients with a mean sampling period of 8.8 days. Bacterial 16S rRNA sequences were amplified and sequenced for microbiota analyses. Results were compared to data from unhospitalized adult participants in the American Gut and Human Microbiome Projects. Relative to healthy adults, alpha diversity was decreased in ICU gut and skin samples at all time points. Diversity in tongue swabs decreased over time. Beta diversity measures indicated differences in community membership between critically ill and healthy adults at each body site. Taxonomic alterations in the ICU included depletion of important commensal bacteria such as Faecalibacterium in GI samples and Corynebacterium in skin swabs and enrichment with pathogens such as Enterococcus, Mycoplasma, and Staphylococcus. A high proportion of ICU sample sets contained pathogens present simultaneously at three body sites indicating widespread colonization. In several cases, clinically relevant airway infections were preceded by the appearance of the causative pathogen in tracheal microbiome profiles. These results demonstrate that the microbiome of critically ill patients undergoes a loss of diversity, loss of site specificity, and a shift toward dominant pathogens. These changes may provide opportunities to precisely modulate the microbiome and thereby improve patient outcomes.
- Published
- 2016
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31. Evidence for persistent and shared bacterial strains against a background of largely unique gut colonization in hospitalized premature infants.
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Raveh-Sadka T, Firek B, Sharon I, Baker R, Brown CT, Thomas BC, Morowitz MJ, and Banfield JF
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- Bacteria classification, Bacteria genetics, Bacteria growth & development, Cohort Studies, Feces microbiology, Female, Humans, Infant, Infant, Newborn, Infant, Premature, Male, Bacteria isolation & purification, Gastrointestinal Microbiome
- Abstract
The potentially critical stage of initial gut colonization in premature infants occurs in the hospital environment, where infants are exposed to a variety of hospital-associated bacteria. Because few studies of microbial communities are strain-resolved, we know little about the extent to which specific strains persist in the hospital environment and disperse among infants. To study this, we compared 304 near-complete genomes reconstructed from fecal samples of 21 infants hospitalized in the same intensive care unit in two cohorts, over 3 years apart. The genomes represent 159 distinct bacterial strains, only 14 of which occurred in multiple infants. Enterococcus faecalis and Staphylococcus epidermidis, common infant gut colonists, exhibit diversity comparable to that of reference strains, inline with introduction of strains from infant-specific sources rather than a hospital strain pool. Unlike other infants, a pair of sibling infants shared multiple strains, even after extensive antibiotic administration, suggesting overlapping strain-sources and/or genetic selection drive microbiota similarities. Interestingly, however, five strains were detected in infants hospitalized three years apart. Three of these were also detected in multiple infants in the same year. This finding of a few widely dispersed and persistent bacterial colonizers despite overall low potential for strain dispersal among infants has implications for understanding and directing healthy colonization.
- Published
- 2016
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32. Concentrations and Sources of Airborne Particles in a Neonatal Intensive Care Unit.
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Licina D, Bhangar S, Brooks B, Baker R, Firek B, Tang X, Morowitz MJ, Banfield JF, and Nazaroff WW
- Subjects
- Carbon Dioxide analysis, Humans, Particle Size, Statistics as Topic, Time Factors, Air Pollutants analysis, Air Pollution, Indoor analysis, Intensive Care Units, Neonatal, Particulate Matter analysis
- Abstract
Premature infants in neonatal intensive care units (NICUs) have underdeveloped immune systems, making them susceptible to adverse health consequences from air pollutant exposure. Little is known about the sources of indoor airborne particles that contribute to the exposure of premature infants in the NICU environment. In this study, we monitored the spatial and temporal variations of airborne particulate matter concentrations along with other indoor environmental parameters and human occupancy. The experiments were conducted over one year in a private-style NICU. The NICU was served by a central heating, ventilation and air-conditioning (HVAC) system equipped with an economizer and a high-efficiency particle filtration system. The following parameters were measured continuously during weekdays with 1-min resolution: particles larger than 0.3 μm resolved into 6 size groups, CO2 level, dry-bulb temperature and relative humidity, and presence or absence of occupants. Altogether, over sixteen periods of a few weeks each, measurements were conducted in rooms occupied with premature infants. In parallel, a second monitoring station was operated in a nearby hallway or at the local nurses' station. The monitoring data suggest a strong link between indoor particle concentrations and human occupancy. Detected particle peaks from occupancy were clearly discernible among larger particles and imperceptible for submicron (0.3-1 μm) particles. The mean indoor particle mass concentrations averaged across the size range 0.3-10 μm during occupied periods was 1.9 μg/m(3), approximately 2.5 times the concentration during unoccupied periods (0.8 μg/m(3)). Contributions of within-room emissions to total PM10 mass in the baby rooms averaged 37-81%. Near-room indoor emissions and outdoor sources contributed 18-59% and 1-5%, respectively. Airborne particle levels in the size range 1-10 μm showed strong dependence on human activities, indicating the importance of indoor-generated particles for infant's exposure to airborne particulate matter in the NICU.
- Published
- 2016
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33. Peroxisome Proliferator-activated Receptor-γ Coactivator 1-α (PGC1α) Protects against Experimental Murine Colitis.
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Cunningham KE, Vincent G, Sodhi CP, Novak EA, Ranganathan S, Egan CE, Stolz DB, Rogers MB, Firek B, Morowitz MJ, Gittes GK, Zuckerbraun BS, Hackam DJ, and Mollen KP
- Subjects
- Animals, Bacterial Translocation drug effects, Bacterial Translocation genetics, Colitis chemically induced, Colitis genetics, Colitis pathology, Dextran Sulfate toxicity, Disease Models, Animal, Intestinal Mucosa microbiology, Intestinal Mucosa pathology, Mice, Mice, Inbred BALB C, Mice, Knockout, Mitochondria genetics, Mitochondria pathology, Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Transcription Factors genetics, Colitis metabolism, Intestinal Mucosa metabolism, Mitochondria metabolism, Transcription Factors metabolism
- Abstract
Peroxisome proliferator-activated receptor-γ coactivator 1-α (PGC1α) is the primary regulator of mitochondrial biogenesis and was recently found to be highly expressed within the intestinal epithelium. PGC1α is decreased in the intestinal epithelium of patients with inflammatory bowel disease, but its role in pathogenesis is uncertain. We now hypothesize that PGC1α protects against the development of colitis and helps to maintain the integrity of the intestinal barrier. We selectively deleted PGC1α from the intestinal epithelium of mice by breeding a PGC1α(loxP/loxP) mouse with a villin-cre mouse. Their progeny (PGC1α(ΔIEC) mice) were subjected to 2% dextran sodium sulfate (DSS) colitis for 7 days. The SIRT1 agonist SRT1720 was used to enhance PGC1α activation in wild-type mice during DSS exposure. Mice lacking PGC1α within the intestinal epithelium were more susceptible to DSS colitis than their wild-type littermates. Pharmacologic activation of PGC1α successfully ameliorated disease and restored mitochondrial integrity. These findings suggest that a depletion of PGC1α in the intestinal epithelium contributes to inflammatory changes through a failure of mitochondrial structure and function as well as a breakdown of the intestinal barrier, which leads to increased bacterial translocation. PGC1α induction helps to maintain mitochondrial integrity, enhance intestinal barrier function, and decrease inflammation., (© 2016 by The American Society for Biochemistry and Molecular Biology, Inc.)
- Published
- 2016
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34. Utility of automated template matching for the interpretation of pace mapping in patients ablated due to outflow tract ventricular arrhythmias.
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Kuteszko R, Pytkowski M, Farkowski MM, Maciag A, Sterlinski M, Jankowska A, Kowalik I, Zajac D, Firek B, Demkow M, and Szwed H
- Subjects
- Adult, Female, Humans, Male, Middle Aged, ROC Curve, Retrospective Studies, Sensitivity and Specificity, Catheter Ablation methods, Electrocardiography methods, Heart Ventricles physiopathology, Pattern Recognition, Automated, Tachycardia, Ventricular surgery
- Abstract
Aims: One of the disadvantages of classic pace mapping (PM) is the operator's subjective interpretation. The aim of this single-centre retrospective study was to evaluate the value of automated template matching (AMT) in patients ablated due to ventricular outflow tract arrhythmias (OTAs)., Methods and Results: From an overall group of 105 patients with OTA who were scheduled for transcatheter ablation (TA), AMT was accessible in 42 patients [21 right ventricular outflow tract (RVOT), 21 left ventricular outflow tract (LVOT), 28 women, aged 51.5 ± 12.7 years]. We used AMT to compare spontaneous arrhythmia ORS (spontQRS) with paced QRS complexes during PM in sites where radiofrequency (RF) applications were successful and in sites where RF applications were unsuccessful. The concordance was presented in per cents as objective matching scores (OMS). Then, at the successful ablation sites, we examined the relationship between OMS and the visual interpretation of PM was presented as electrophysiologists matching scores (EMS). The OMS of PM at sites of successful ablation varied from 78 to 99% (mean 94.1 ± 3.8) and from 47 to 95% (mean 80.2 ± 12.6%) at sites of unsuccessful ablation. Pace mapping in unsuccessful RF sites was significantly less similar to spontQRS morphologies than in successful RF sites (P = 0.0001). There was a significant correlation between OMS and EMS (r = 0.82; P < 0.0001). The OMS that indicated optimal ablation site was 89% (sensitivity = 95%; specificity = 80%). The mean OMS for successful sites at RVOT (95.1 ± 1.8%) and LVOT (93.1 ± 4.9%) were not different (P = 0.0551)., Conclusion: This analysis revealed that AMT is a valuable technique for the interpretation of PM and for the identification of successful ablation sites in OTA., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2015. For permissions please email: journals.permissions@oup.com.)
- Published
- 2015
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35. Gut bacteria are rarely shared by co-hospitalized premature infants, regardless of necrotizing enterocolitis development.
- Author
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Raveh-Sadka T, Thomas BC, Singh A, Firek B, Brooks B, Castelle CJ, Sharon I, Baker R, Good M, Morowitz MJ, and Banfield JF
- Subjects
- Humans, Infant, Newborn, Infant, Premature, Bacteria isolation & purification, Enterocolitis, Necrotizing microbiology, Hospitalization, Intestines microbiology
- Abstract
Premature infants are highly vulnerable to aberrant gastrointestinal tract colonization, a process that may lead to diseases like necrotizing enterocolitis. Thus, spread of potential pathogens among hospitalized infants is of great concern. Here, we reconstructed hundreds of high-quality genomes of microorganisms that colonized co-hospitalized premature infants, assessed their metabolic potential, and tracked them over time to evaluate bacterial strain dispersal among infants. We compared microbial communities in infants who did and did not develop necrotizing enterocolitis. Surprisingly, while potentially pathogenic bacteria of the same species colonized many infants, our genome-resolved analysis revealed that strains colonizing each baby were typically distinct. In particular, no strain was common to all infants who developed necrotizing enterocolitis. The paucity of shared gut colonizers suggests the existence of significant barriers to the spread of bacteria among infants. Importantly, we demonstrate that strain-resolved comprehensive community analysis can be accomplished on potentially medically relevant time scales.
- Published
- 2015
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36. Mucosa-associated bacterial diversity in necrotizing enterocolitis.
- Author
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Brower-Sinning R, Zhong D, Good M, Firek B, Baker R, Sodhi CP, Hackam DJ, and Morowitz MJ
- Subjects
- Bacteria genetics, DNA, Bacterial genetics, Humans, Infant, Infant, Newborn, Sequence Analysis, DNA, Bacteria isolation & purification, Biodiversity, Enterocolitis, Necrotizing microbiology, Intestinal Mucosa microbiology
- Abstract
Background: Previous studies of infant fecal samples have failed to clarify the role of gut bacteria in the pathogenesis of NEC. We sought to characterize bacterial communities within intestinal tissue resected from infants with and without NEC., Methods: 26 intestinal samples were resected from 19 infants, including 16 NEC samples and 10 non-NEC samples. Bacterial 16S rRNA gene sequences were amplified and sequenced. Analysis allowed for taxonomic identification, and quantitative PCR was used to quantify the bacterial load within samples., Results: NEC samples generally contained an increased total burden of bacteria. NEC and non-NEC sample sets were both marked by high inter-individual variability and an abundance of opportunistic pathogens. There was no statistically significant distinction between the composition of NEC and non-NEC microbial communities. K-means clustering enabled us to identify several stable clusters, including clusters of NEC and midgut volvulus samples enriched with Clostridium and Bacteroides. Another cluster containing both NEC and non-NEC samples was marked by an abundance of Enterobacteriaceae and decreased diversity among NEC samples., Conclusions: The results indicate that NEC is a disease without a uniform pattern of microbial colonization, but that NEC is associated with an abundance of strict anaerobes and a decrease in community diversity.
- Published
- 2014
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37. Lactobacillus rhamnosus HN001 decreases the severity of necrotizing enterocolitis in neonatal mice and preterm piglets: evidence in mice for a role of TLR9.
- Author
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Good M, Sodhi CP, Ozolek JA, Buck RH, Goehring KC, Thomas DL, Vikram A, Bibby K, Morowitz MJ, Firek B, Lu P, and Hackam DJ
- Subjects
- Animals, Animals, Newborn, DNA, Bacterial pharmacology, Enterocolitis, Necrotizing metabolism, Enterocolitis, Necrotizing pathology, Mice, Premature Birth, Swine, Toll-Like Receptor 9 genetics, Enterocolitis, Necrotizing prevention & control, Lacticaseibacillus rhamnosus physiology, Probiotics pharmacology, Toll-Like Receptor 9 metabolism
- Abstract
Necrotizing enterocolitis (NEC) is the leading cause of death from gastrointestinal disease in premature infants and develops partly from an exaggerated intestinal epithelial immune response to indigenous microbes. There has been interest in administering probiotic bacteria to reduce NEC severity, yet concerns exist regarding infection risk. Mechanisms of probiotic activity in NEC are unknown although activation of the microbial DNA receptor Toll-like receptor-9 (TLR9) has been postulated. We now hypothesize that the Gram-positive bacterium Lactobacillus rhamnosus HN001 can attenuate NEC in small and large animal models, that its microbial DNA is sufficient for its protective effects, and that protection requires activation of the Toll-like receptor 9 (TLR9). We now show that oral administration of live or UV-inactivated Lactobacillus rhamnosus HN001 attenuates NEC severity in newborn mice and premature piglets, as manifest by reduced histology score, attenuation of mucosal cytokine response, and improved gross morphology. TLR9 was required for Lactobacillus rhamnosus-mediated protection against NEC in mice, as the selective decrease of TLR9 from the intestinal epithelium reversed its protective effects. Strikingly, DNA of Lactobacillus rhamnosus HN001 reduced the extent of proinflammatory signaling in cultured enterocytes and in samples of resected human ileum ex vivo, suggesting the therapeutic potential of this probiotic in clinical NEC. Taken together, these findings illustrate that Lactobacillus rhamnosus HN001 is an effective probiotic for NEC via activation of the innate immune receptor TLR9 and that Lactobacillus rhamnosus DNA is sufficient for its protective effects, potentially reducing concerns regarding the infectious risk of this novel therapeutic approach., (Copyright © 2014 the American Physiological Society.)
- Published
- 2014
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38. Novel algorithm for arrhythmogenic focus localization in patients with right ventricular outflow tract arrhythmias.
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Pytkowski M, Maciąg A, Sterliński M, Jankowska A, Kowalik I, Farkowski MM, Kuteszko R, Zając D, Firek B, Chmielak Z, and Szwed H
- Subjects
- Adult, Arrhythmias, Cardiac physiopathology, Female, Heart Conduction System surgery, Heart Ventricles diagnostic imaging, Humans, Male, Prospective Studies, Ultrasonography, Algorithms, Arrhythmias, Cardiac diagnosis, Catheter Ablation methods, Electrocardiography, Heart Conduction System physiopathology, Heart Ventricles physiopathology
- Abstract
Background: Previously presented new electrocardiography (ECG) algorithm for localization of arrhythmogenic focus (AFo) in right ventricular outflow tract (RVOT) was based on spontaneous arrhythmia QRS morphology analysis. The aim of this study was to estimate the clinical value of our RVOT algorithm in a prospective study., Methods and Results: Algorithm validation was made on 62 patients with RVOT arrhythmias (45 women), mean age 41.6 ± 14.3 years, scheduled for transcatheter ablation. Results of preablation ECG analysis with RVOT algorithm were matched with successful ablation sites and statistical indices: sensitivity (sens), specificity (spec), and positive and negative predictive values (PPV, NPV) were calculated for algorithm and for each of 9 RVOT zones (septal and free wall). An algorithm precisely localized AFo in 57 out of 62 patients (sens 91.3%, spec 99%, PPV 91%, NPV 98.8%). Sensitivity values for superior RVOT aspect (71% patients) varied from 88% to 100%, specificity from 95.9% to 100%; PPV values from 85.7% to 100%, NPV from 92.5% to 100%. Although the total number of patients was relatively small in the 2 remaining RVOT aspects (29% patients) high values (sens, spec, PPV, NPV) were gained for intermediate and inferior zones., Conclusions: On the basis of spontaneous arrhythmia QRS analysis, a novel algorithm was built for preablation localization of RVOT arrhythmia in 1 of the 9 RVOT zones. Prospective analysis of our ECG algorithm confirmed that it is a valuable tool to predict the site of successful ablation in patients with RVOT arrhythmias.
- Published
- 2014
- Full Text
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39. Intestinal epithelial Toll-like receptor 4 regulates goblet cell development and is required for necrotizing enterocolitis in mice.
- Author
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Sodhi CP, Neal MD, Siggers R, Sho S, Ma C, Branca MF, Prindle T Jr, Russo AM, Afrazi A, Good M, Brower-Sinning R, Firek B, Morowitz MJ, Ozolek JA, Gittes GK, Billiar TR, and Hackam DJ
- Subjects
- Animals, Animals, Newborn, Bile Acids and Salts metabolism, Cell Line, Disease Models, Animal, Enterocolitis, Necrotizing etiology, Enterocolitis, Necrotizing genetics, Enterocolitis, Necrotizing microbiology, Enterocolitis, Necrotizing pathology, Enterocolitis, Necrotizing prevention & control, Goblet Cells microbiology, Goblet Cells pathology, Humans, Hypoxia complications, Infant Formula, Infant, Newborn, Intestine, Small microbiology, Intestine, Small pathology, Mice, Mice, Inbred C57BL, Mice, Knockout, Organoids, RNA Interference, Rats, Receptors, Notch metabolism, Signal Transduction, Tissue Culture Techniques, Toll-Like Receptor 4 deficiency, Toll-Like Receptor 4 genetics, Transfection, Cell Differentiation, Enterocolitis, Necrotizing metabolism, Goblet Cells metabolism, Intestine, Small metabolism, Toll-Like Receptor 4 metabolism
- Abstract
Background & Aims: Little is known about factors that regulate intestinal epithelial differentiation; microbial recognition receptors such as Toll-like receptor (TLR)4 might be involved. We investigated whether intestinal TLR4 regulates epithelial differentiation and is involved in development of necrotizing enterocolitis (NEC) of the immature intestine., Methods: Mice with conditional disruption of TLR4 in the intestinal epithelium and TLR4 knockout (TLR4(-/-)) mice were generated by breeding TLR4(loxp/loxp) mice with villin-cre and Ella-cre, respectively. Enterocytes that did not express or overexpressed TLR4 were created by lentiviral or adenoviral transduction. Intestinal organoids were cultured on tissue matrices. Bile acids were measured by colorimetric assays, and microbial composition was determined by 16S pyrosequencing. NEC was induced in 7- to 10-day-old mice by induction of hypoxia twice daily for 4 days., Results: TLR4(-/-) mice and mice with enterocyte-specific deletion of TLR4 were protected from NEC; epithelial differentiation into goblet cells was increased via suppressed Notch signaling in the small intestinal epithelium. TLR4 also regulates differentiation of goblet cells in intestinal organoid and enterocyte cell cultures; differentiation was increased on deletion of TLR4 and restored when TLR4 was expressed ectopically. TLR4 signaling via Notch was increased in intestinal tissue samples from patients with NEC, and numbers of goblet cells were reduced. 16S pyrosequencing revealed that wild-type and TLR4-deficient mice had similar microbial profiles; increased numbers of goblet cells were observed in mice given antibiotics. TLR4 deficiency reduced levels of luminal bile acids in vivo, and addition of bile acids to TLR4-deficient cell cultures prevented differentiation of goblet cells., Conclusions: TLR4 signaling and Notch are increased in intestinal tissues of patients with NEC and required for induction of NEC in mice. TLR4 prevents goblet cell differentiation, independently of the microbiota. Bile acids might initiate goblet cell development., (Copyright © 2012 AGA Institute. Published by Elsevier Inc. All rights reserved.)
- Published
- 2012
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40. The Staphylococcus aureus lrgAB operon modulates murein hydrolase activity and penicillin tolerance.
- Author
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Groicher KH, Firek BA, Fujimoto DF, and Bayles KW
- Subjects
- Amino Acid Sequence, Bacterial Proteins chemistry, Bacterial Proteins genetics, Bacterial Proteins physiology, Bacteriolysis drug effects, Gene Deletion, Gene Expression Regulation, Bacterial, Genetic Complementation Test, Microbial Sensitivity Tests, Molecular Sequence Data, N-Acetylmuramoyl-L-alanine Amidase genetics, Operon genetics, Penicillins pharmacology, Phenotype, RNA, Messenger genetics, RNA, Messenger metabolism, Staphylococcus aureus drug effects, Staphylococcus aureus genetics, Staphylococcus aureus growth & development, Genes, Bacterial genetics, Genes, Regulator genetics, Membrane Proteins, N-Acetylmuramoyl-L-alanine Amidase metabolism, Operon physiology, Penicillin Resistance genetics, Staphylococcus aureus enzymology
- Abstract
Previous studies in our laboratory have shown that the Staphylococcus aureus LytSR two-component regulatory system affects murein hydrolase activity and autolysis. A LytSR-regulated dicistronic operon has also been identified and shown to encode two potential membrane-associated proteins, designated LrgA and LrgB, hypothesized to be involved in the control of murein hydrolase activity. In the present study, a lrgAB mutant strain was generated and analyzed to test this hypothesis. Zymographic and quantitative analysis of murein hydrolase activity revealed that the lrgAB mutant produced increased extracellular murein hydrolase activity compared to that of the wild-type strain. Complementation of the lrgAB defect by providing the lrgAB genes in trans restored the wild-type phenotype, indicating that these genes confer negative control on extracellular murein hydrolase activity. In addition to these effects, the influence of the lrgAB mutation on penicillin-induced lysis and killing was examined. These studies demonstrated that the lrgAB mutation enhanced penicillin-induced killing of cells approaching the stationary phase of growth, the time at which the lrgAB operon was shown to be maximally expressed. This effect of the lrgAB mutation on penicillin-induced killing was shown to be independent of cell lysis. In contrast, the lrgAB mutation did not affect penicillin-induced killing of cells growing in early-exponential phase, a time in which lrgAB expression was shown to be minimal. However, expression of the lrgAB operon in early-exponential-phase cells inhibited penicillin-induced killing, again independent of cell lysis. The data generated by this study suggest that penicillin-induced killing of S. aureus involves a novel regulator of murein hydrolase activity.
- Published
- 2000
- Full Text
- View/download PDF
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