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  1. AU="Tetri, Laura H"
  2. AU="Badve, Sunil V"
  3. AU=Zhang Yinan
  4. AU="Piquero, Nicole Leeper"
  5. AU="Russo, Giorgio Ivan" AU="Russo, Giorgio Ivan"
  6. AU=Pourdowlat Guitti
  7. AU="Frisenda, Riccardo"
  8. AU=Palmucci Stefano

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  1. Artikel ; Online: ALTERED PROFILES OF EXTRACELLULAR MITOCHONDRIAL DNA IN IMMUNOPARALYZED PEDIATRIC PATIENTS AFTER THERMAL INJURY.

    Tetri, Laura H / Penatzer, Julia A / Tsegay, Kaleb B / Tawfik, Daniel S / Burk, Shelby / Lopez, Ivan / Thakkar, Rajan K / Haileselassie, Bereketeab

    Shock (Augusta, Ga.)

    2023  Band 61, Heft 2, Seite(n) 223–228

    Abstract: Abstract: Background: Thermal injury is a major cause of morbidity and mortality in the pediatric population worldwide with secondary infection being the most common acute complication. Suppression of innate and adaptive immune function is predictive of ...

    Abstract Abstract: Background: Thermal injury is a major cause of morbidity and mortality in the pediatric population worldwide with secondary infection being the most common acute complication. Suppression of innate and adaptive immune function is predictive of infection in pediatric burn patients, but little is known about the mechanisms causing these effects. Circulating mitochondrial DNA (mtDNA), which induces a proinflammatory signal, has been described in multiple disease states but has not been studied in pediatric burn injuries. This study examined the quantity of circulating mtDNA and mtDNA mutations in immunocompetent (IC) and immunoparalyzed (IP) pediatric burn patients. Methods: Circulating DNA was isolated from plasma of pediatric burn patients treated at Nationwide Children's Hospital Burn Center at early (1-3 days) and late (4-7 days) time points postinjury. These patients were categorized as IP or IC based on previously established immune function testing and secondary infection. Three mitochondrial genes, D loop, ND1, and ND4, were quantified by multiplexed qPCR to assess both mtDNA quantity and mutation load. Results: At the early time point, there were no differences in plasma mtDNA quantity; however, IC patients had a progressive increase in mtDNA over time when compared with IP patients (change in ND1 copy number over time 3,880 vs. 87 copies/day, P = 0.0004). Conversely, the IP group had an increase in mtDNA mutation burden over time. Conclusion: IC patients experienced a significant increase in circulating mtDNA quantity over time, demonstrating an association between increased mtDNA release and proinflammatory phenotype in the burn patients. IP patients had significant increases in mtDNA mutation load likely representative of degree of oxidative damage. Together, these data provide further insight into the inflammatory and immunological mechanisms after pediatric thermal injury.
    Mesh-Begriff(e) Humans ; Child ; DNA, Mitochondrial/genetics ; Coinfection ; Mitochondria ; Mutation/genetics ; Phenotype
    Chemische Substanzen DNA, Mitochondrial
    Sprache Englisch
    Erscheinungsdatum 2023-11-15
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 1185432-7
    ISSN 1540-0514 ; 1073-2322
    ISSN (online) 1540-0514
    ISSN 1073-2322
    DOI 10.1097/SHK.0000000000002253
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Association between serum prostacyclin and cerebrovascular reactivity in healthy young and older adults.

    Corkery, Adam T / Miller, Kathleen B / Loeper, Carissa A / Tetri, Laura H / Pearson, Andrew G / Loggie, Nicole A / Howery, Anna J / Eldridge, Marlowe W / Barnes, Jill N

    Experimental physiology

    2023  Band 108, Heft 8, Seite(n) 1047–1056

    Abstract: New findings: What is the central question of this study? What is the relationship between prostacyclin and cerebrovascular reactivity to hypercapnia before and after administration of a cyclooxygenase inhibitor, indomethacin, in healthy young and older ...

    Abstract New findings: What is the central question of this study? What is the relationship between prostacyclin and cerebrovascular reactivity to hypercapnia before and after administration of a cyclooxygenase inhibitor, indomethacin, in healthy young and older adults? What is the main finding and importance? Serum prostacyclin was not related to cerebrovascular reactivity to hypercapnia before or after administration of indomethacin. However, in older adults, serum prostacyclin was related to the magnitude of change in cerebrovascular reactivity from before to after indomethacin administration. This suggests that older adults with higher serum prostacyclin may rely more on cyclooxygenase products to mediate cerebrovascular reactivity.
    Abstract: Platelet activation may contribute to age-related cerebrovascular dysfunction by interacting with the endothelial cells that regulate the response to vasodilatory stimuli. This study evaluated the relationship between a platelet inhibitor, prostacyclin, and cerebrovascular reactivity (CVR) in healthy young (n = 35; 25 ± 4 years; 17 women, 18 men) and older (n = 12; 62 ± 2 years; 8 women, 4 men) adults, who were not daily aspirin users, before and after cyclooxygenase inhibition. Prostacyclin was determined by levels of 6-keto-prostaglandin F1α (6-keto PGF1α) in the blood. CVR was assessed by measuring the middle cerebral artery blood velocity response to hypercapnia using transcranial Doppler ultrasound before (CON) and 90 min after cyclooxygenase inhibition with indomethacin (INDO). In young adults, there were no associations between prostacyclin and middle cerebral artery CVR during CON (r = -0.14, P = 0.415) or INDO (r = 0.27, P = 0.118). In older adults, associations between prostacyclin and middle cerebral artery CVR during CON (r = 0.53, P = 0.075) or INDO (r = -0.45, P = 0.136) did not reach the threshold for significance. We also evaluated the relationship between prostacyclin and the change in CVR between conditions (ΔCVR). We found no association between ΔCVR and prostacyclin in young adults (r = 0.27, P = 0.110); however, in older adults, those with higher baseline prostacyclin levels demonstrated significantly greater ΔCVR (r = -0.74, P = 0.005). In conclusion, older adults with higher serum prostacyclin, a platelet inhibitor, may rely more on cyclooxygenase products for cerebrovascular reactivity to hypercapnia.
    Mesh-Begriff(e) Male ; Young Adult ; Humans ; Female ; Aged ; Hypercapnia ; Epoprostenol/pharmacology ; Platelet Aggregation Inhibitors/pharmacology ; Prostaglandin-Endoperoxide Synthases ; Endothelial Cells ; Indomethacin/pharmacology ; Prostaglandins I/pharmacology ; Cerebrovascular Circulation/physiology ; Blood Flow Velocity/physiology ; Carbon Dioxide
    Chemische Substanzen Epoprostenol (DCR9Z582X0) ; Platelet Aggregation Inhibitors ; Prostaglandin-Endoperoxide Synthases (EC 1.14.99.1) ; Indomethacin (XXE1CET956) ; Prostaglandins I ; Carbon Dioxide (142M471B3J)
    Sprache Englisch
    Erscheinungsdatum 2023-05-12
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 1016295-1
    ISSN 1469-445X ; 0958-0670
    ISSN (online) 1469-445X
    ISSN 0958-0670
    DOI 10.1113/EP090903
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Drp1/p53 interaction mediates p53 mitochondrial localization and dysfunction in septic cardiomyopathy.

    Mukherjee, Riddhita / Tetri, Laura H / Li, Sin-Jin / Fajardo, Giovanni / Ostberg, Nicolai P / Tsegay, Kaleb B / Gera, Kanika / Cornell, Timothy T / Bernstein, Daniel / Mochly-Rosen, Daria / Haileselassie, Bereketeab

    Journal of molecular and cellular cardiology

    2023  Band 177, Seite(n) 28–37

    Abstract: Background: Previous studies have implicated p53-dependent mitochondrial dysfunction in sepsis induced end organ injury, including sepsis-induced myocardial dysfunction (SIMD). However, the mechanisms behind p53 localization to the mitochondria have not ...

    Abstract Background: Previous studies have implicated p53-dependent mitochondrial dysfunction in sepsis induced end organ injury, including sepsis-induced myocardial dysfunction (SIMD). However, the mechanisms behind p53 localization to the mitochondria have not been well established. Dynamin-related protein 1 (Drp1), a mediator of mitochondrial fission, may play a role in p53 mitochondrial localization. Here we examined the role of Drp1/p53 interaction in SIMD using in vitro and murine models of sepsis.
    Methods: H9c2 cardiomyoblasts and BALB/c mice were exposed to lipopolysaccharide (LPS) to model sepsis phenotype. Pharmacologic inhibitors of Drp1 activation (ψDrp1) and of p53 mitochondrial binding (pifithrin μ, PFTμ) were utilized to assess interaction between Drp1 and p53, and the subsequent downstream impact on mitochondrial morphology and function, cardiomyocyte function, and sepsis phenotype.
    Results: Both in vitro and murine models demonstrated an increase in physical Drp1/p53 interaction following LPS treatment, which was associated with increased p53 mitochondrial localization, and mitochondrial dysfunction. This Drp1/p53 interaction was inhibited by ΨDrp1, suggesting that this interaction is dependent on Drp1 activation. Treatment of H9c2 cells with either ΨDrp1 or PFTμ inhibited the LPS mediated localization of Drp1/p53 to the mitochondria, decreased oxidative stress, improved cellular respiration and ATP production. Similarly, treatment of BALB/c mice with either ΨDrp1 or PFTμ decreased LPS-mediated mitochondrial localization of p53, mitochondrial ROS in cardiac tissue, and subsequently improved cardiomyocyte contractile function and survival.
    Conclusion: Drp1/p53 interaction and mitochondrial localization is a key prodrome to mitochondrial damage in SIMD and inhibiting this interaction may serve as a therapeutic target.
    Mesh-Begriff(e) Mice ; Animals ; Tumor Suppressor Protein p53 ; Lipopolysaccharides/adverse effects ; Cardiomyopathies/metabolism ; Dynamins/metabolism ; Sepsis/complications ; Sepsis/chemically induced ; Mitochondrial Dynamics/genetics
    Chemische Substanzen 2-phenylacetylenesulfonamide ; Tumor Suppressor Protein p53 ; Lipopolysaccharides ; Dynamins (EC 3.6.5.5)
    Sprache Englisch
    Erscheinungsdatum 2023-02-24
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 80157-4
    ISSN 1095-8584 ; 0022-2828
    ISSN (online) 1095-8584
    ISSN 0022-2828
    DOI 10.1016/j.yjmcc.2023.01.008
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Bimodal right ventricular dysfunction after postnatal hyperoxia exposure: implications for the preterm heart.

    Kumari, Santosh / Braun, Rudolf K / Tetri, Laura H / Barton, Gregory P / Hacker, Timothy A / Goss, Kara N

    American journal of physiology. Heart and circulatory physiology

    2019  Band 317, Heft 6, Seite(n) H1272–H1281

    Abstract: Rats exposed to postnatal hyperoxia develop right ventricular (RV) dysfunction, mild pulmonary hypertension, and dysregulated cardiac mitochondrial biogenesis when aged to one year, with the degree of cardiac dysfunction and pulmonary hypertension ... ...

    Abstract Rats exposed to postnatal hyperoxia develop right ventricular (RV) dysfunction, mild pulmonary hypertension, and dysregulated cardiac mitochondrial biogenesis when aged to one year, with the degree of cardiac dysfunction and pulmonary hypertension similar to that previously described in young adults born preterm. Here, we sought to understand the impact of postnatal hyperoxia exposure on RV hemodynamic and mitochondrial function across the life span. In Methods, pups from timed-pregnant Sprague-Dawley rats were randomized to normoxia or hyperoxia [fraction of inspired oxygen (
    Mesh-Begriff(e) Animals ; DNA, Mitochondrial/genetics ; Female ; Heart/growth & development ; Heart/physiopathology ; Hyperoxia/complications ; Male ; Mitochondria/metabolism ; Mutation ; Organelle Biogenesis ; Rats ; Rats, Sprague-Dawley ; Ventricular Dysfunction, Right/etiology ; Ventricular Dysfunction, Right/genetics ; Ventricular Dysfunction, Right/metabolism ; Ventricular Dysfunction, Right/physiopathology
    Chemische Substanzen DNA, Mitochondrial
    Sprache Englisch
    Erscheinungsdatum 2019-11-08
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 603838-4
    ISSN 1522-1539 ; 0363-6135
    ISSN (online) 1522-1539
    ISSN 0363-6135
    DOI 10.1152/ajpheart.00383.2019
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel: Sex-Specific Skeletal Muscle Fatigability and Decreased Mitochondrial Oxidative Capacity in Adult Rats Exposed to Postnatal Hyperoxia.

    Tetri, Laura H / Diffee, Gary M / Barton, Gregory P / Braun, Rudolf K / Yoder, Hannah E / Haraldsdottir, Kristin / Eldridge, Marlowe W / Goss, Kara N

    Frontiers in physiology

    2018  Band 9, Seite(n) 326

    Abstract: Premature birth affects more than 10% of live births, and is characterized by relative hyperoxia exposure in an immature host. Long-term consequences of preterm birth include decreased aerobic capacity, decreased muscular strength and endurance, and ... ...

    Abstract Premature birth affects more than 10% of live births, and is characterized by relative hyperoxia exposure in an immature host. Long-term consequences of preterm birth include decreased aerobic capacity, decreased muscular strength and endurance, and increased prevalence of metabolic diseases such as type 2 diabetes mellitus. Postnatal hyperoxia exposure in rodents is a well-established model of chronic lung disease of prematurity, and also recapitulates the pulmonary vascular, cardiovascular, and renal phenotype of premature birth. The objective of this study was to evaluate whether postnatal hyperoxia exposure in rats could recapitulate the skeletal and metabolic phenotype of premature birth, and to characterize the subcellular metabolic changes associated with postnatal hyperoxia exposure, with a secondary aim to evaluate sex differences in this model. Compared to control rats, male rats exposed to 14 days of postnatal hyperoxia then aged to 1 year demonstrated higher skeletal muscle fatigability, lower muscle mitochondrial oxidative capacity, more mitochondrial damage, and higher glycolytic enzyme expression. These differences were not present in female rats with the same postnatal hyperoxia exposure. This study demonstrates detrimental mitochondrial and muscular outcomes in the adult male rat exposed to postnatal hyperoxia. Given that young adults born premature also demonstrate skeletal muscle dysfunction, future studies are merited to determine whether this dysfunction as well as reduced aerobic capacity is due to reduced mitochondrial oxidative capacity and metabolic dysfunction.
    Sprache Englisch
    Erscheinungsdatum 2018-03-29
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2018.00326
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: RET receptor expression and interaction with TRK receptors in neuroblastomas.

    Tetri, Laura H / Kolla, Venkatadri / Golden, Rebecca L / Iyer, Radhika / Croucher, Jamie L / Choi, Jee-Hye / Macfarland, Suzanne P / Naraparaju, Koumudi / Guan, Peng / Nguyen, Ferro / Gaonkar, Krutika S / Raman, Pichai / Brodeur, Garrett M

    Oncology reports

    2020  Band 44, Heft 1, Seite(n) 263–272

    Abstract: Neuroblastomas (NBs) have heterogeneous clinical behavior, from spontaneous regression or differentiation to relentless progression. Evidence from our laboratory and others suggests that neurotrophin receptors contribute to these disparate behaviors. ... ...

    Abstract Neuroblastomas (NBs) have heterogeneous clinical behavior, from spontaneous regression or differentiation to relentless progression. Evidence from our laboratory and others suggests that neurotrophin receptors contribute to these disparate behaviors. Previously, the role of TRK receptors in NB pathogenesis was investigated. In the present study, the expression of RET and its co‑receptors in a panel of NB cell lines was investigated and responses to cognate ligands GDNF, NRTN, and ARTN with GFRα1‑3 co‑receptor expression, respectively were found to be correlated. RET expression was high in NBLS, moderate in SY5Y, low/absent in NBEBc1 and NLF cells. All cell lines expressed at least one of GFRα co‑receptors. In addition, NBLS, SY5Y, NBEBc1 and NLF cells showed different morphological changes in response to ligands. As expected, activation of RET/GFRα3 by ARTN resulted in RET phosphorylation. Interestingly, activation of TrkA by its cognate ligand NGF resulted in RET phosphorylation at Y905, Y1015, and Y1062, and this was inhibited in a dose‑dependent manner by the TRK inhibitor (CEP‑701). Conversely, RET activation by ARTN in NBLS cells led to phosphorylation of TrkA. This suggests a physical association between RET and TRK proteins, and cross‑talk between these two receptor pathways. Finally, RET, GFR and TRK expression in primary tumors was investigated and a significant association between RET, its co‑receptors and TRK expression was demonstrated. Thus, the present data support a complex model of interacting neurotrophin receptor pathways in the regulation of cell growth and differentiation in NBs.
    Mesh-Begriff(e) Carbazoles/pharmacology ; Cell Differentiation ; Cell Line, Tumor ; Cell Proliferation ; Gene Expression Regulation, Neoplastic ; Guanine Nucleotide Exchange Factors/pharmacology ; Humans ; Neuroblastoma/genetics ; Neuroblastoma/metabolism ; Phosphorylation/drug effects ; Proto-Oncogene Proteins c-ret/genetics ; Proto-Oncogene Proteins c-ret/metabolism ; Receptor, trkA/metabolism ; Signal Transduction ; Up-Regulation
    Chemische Substanzen Carbazoles ; Guanine Nucleotide Exchange Factors ; RAPGEF5 protein, human ; lestaurtinib (DO989GC5D1) ; Proto-Oncogene Proteins c-ret (EC 2.7.10.1) ; RET protein, human (EC 2.7.10.1) ; Receptor, trkA (EC 2.7.10.1)
    Sprache Englisch
    Erscheinungsdatum 2020-04-15
    Erscheinungsland Greece
    Dokumenttyp Journal Article
    ZDB-ID 1222484-4
    ISSN 1791-2431 ; 1021-335X
    ISSN (online) 1791-2431
    ISSN 1021-335X
    DOI 10.3892/or.2020.7583
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Blunted cardiac output response to exercise in adolescents born preterm.

    Haraldsdottir, Kristin / Watson, Andrew M / Pegelow, David F / Palta, Mari / Tetri, Laura H / Levin, Taylor / Brix, Melissa D / Centanni, Ryan M / Goss, Kara N / Eldridge, Marlowe M

    European journal of applied physiology

    2020  Band 120, Heft 11, Seite(n) 2547–2554

    Abstract: Purpose: Premature birth is associated with lasting effects, including lower exercise capacity and pulmonary function, and is acknowledged as a risk factor for cardiovascular disease. The aim was to evaluate factors affecting exercise capacity in ... ...

    Abstract Purpose: Premature birth is associated with lasting effects, including lower exercise capacity and pulmonary function, and is acknowledged as a risk factor for cardiovascular disease. The aim was to evaluate factors affecting exercise capacity in adolescents born preterm, including the cardiovascular and pulmonary responses to exercise, activity level and strength.
    Methods: 21 preterm-born and 20 term-born adolescents (age 12-14 years) underwent strength and maximal exercise testing with thoracic bioimpedance monitoring. Baseline variables were compared between groups and ANCOVA was used to compare heart rate, cardiac output (Q) and stroke volume (SV) during exercise between groups while adjusting for body surface area.
    Results: Preterm-borns had lower maximal aerobic capacity than term-borns (2.0 ± 0.5 vs. 2.5 ± 0.5 L/min, p = 0.01) and lower maximal power (124 ± 26 vs. 153 ± 33 watts, p < 0.01), despite similar physical activity scores. Pulmonary function and muscular strength did not differ significantly. Although baseline Q and SV did not differ between groups, preterm adolescents had significantly lower cardiac index (Qi) at 50, 75 and 100% of maximal time to exhaustion, driven by SV volume index (SVi, 50% max time: 53.0 ± 9.0 vs. 61.6 ± 11.4; 75%: 51.7 ± 8.4 vs. 64.3 ± 11.1; 100%: 51.2 ± 9.3 vs. 64.3 ± 11.5 ml/m
    Conclusion: Otherwise healthy and physically active adolescents born very preterm exhibit lower exercise capacity than term-born adolescents. Despite similar baseline cardiovascular values, preterm-born adolescents demonstrate significantly reduced Qi and SVi during incremental and maximal exercise.
    Mesh-Begriff(e) Adolescent ; Cardiac Output ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/etiology ; Exercise Test ; Exercise Tolerance ; Female ; Heart Rate ; Humans ; Infant, Newborn ; Infant, Premature/growth & development ; Infant, Very Low Birth Weight/growth & development ; Male ; Muscle, Skeletal/physiology ; Respiration
    Sprache Englisch
    Erscheinungsdatum 2020-08-30
    Erscheinungsland Germany
    Dokumenttyp Journal Article
    ZDB-ID 124793-1
    ISSN 1439-6327 ; 1432-1025 ; 0301-5548 ; 1439-6319
    ISSN (online) 1439-6327 ; 1432-1025
    ISSN 0301-5548 ; 1439-6319
    DOI 10.1007/s00421-020-04480-9
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: Postnatal Hyperoxia Exposure Durably Impairs Right Ventricular Function and Mitochondrial Biogenesis.

    Goss, Kara N / Kumari, Santosh / Tetri, Laura H / Barton, Greg / Braun, Rudolf K / Hacker, Timothy A / Eldridge, Marlowe W

    American journal of respiratory cell and molecular biology

    2017  Band 56, Heft 5, Seite(n) 609–619

    Abstract: Prematurity complicates 12% of births, and young adults with a history of prematurity are at risk to develop right ventricular (RV) hypertrophy and impairment. The long-term risk for pulmonary vascular disease, as well as mechanisms of RV dysfunction and ...

    Abstract Prematurity complicates 12% of births, and young adults with a history of prematurity are at risk to develop right ventricular (RV) hypertrophy and impairment. The long-term risk for pulmonary vascular disease, as well as mechanisms of RV dysfunction and ventricular-vascular uncoupling after prematurity, remain poorly defined. Using an established model of prematurity-related lung disease, pups from timed-pregnant Sprague Dawley rats were randomized to normoxia or hyperoxia (fraction of inspired oxygen, 0.85) exposure for the first 14 days of life. After aging to 1 year in standard conditions, rats underwent hemodynamic assessment followed by tissue harvest for biochemical and histological evaluation. Aged hyperoxia-exposed rats developed significantly greater RV hypertrophy, associated with a 40% increase in RV systolic pressures. Although cardiac index was similar, hyperoxia-exposed rats demonstrated a reduced RV ejection fraction and significant RV-pulmonary vascular uncoupling. Hyperoxia-exposed RV cardiomyocytes demonstrated evidence of mitochondrial dysregulation and mitochondrial DNA damage, suggesting potential mitochondrial dysfunction as a cause of RV dysfunction. Aged rats exposed to postnatal hyperoxia recapitulate many features of young adults born prematurely, including increased RV hypertrophy and decreased RV ejection fraction. Our data suggest that postnatal hyperoxia exposure results in mitochondrial dysregulation that persists into adulthood with eventual RV dysfunction. Further evaluation of long-term mitochondrial function is warranted in both animal models of premature lung disease and in human adults who were born preterm.
    Mesh-Begriff(e) Aging/pathology ; Animals ; Animals, Newborn ; Autophagy ; Body Weight ; DNA Damage ; DNA, Mitochondrial/metabolism ; Female ; Fibrosis ; Gene Expression Profiling ; Hemodynamics ; Hyperoxia/complications ; Hyperoxia/diagnostic imaging ; Hyperoxia/metabolism ; Hyperoxia/physiopathology ; Hypertrophy, Right Ventricular/diagnostic imaging ; Hypertrophy, Right Ventricular/etiology ; Hypertrophy, Right Ventricular/genetics ; Hypertrophy, Right Ventricular/physiopathology ; Male ; Myocardium/pathology ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Organ Size ; Organelle Biogenesis ; Rats, Sprague-Dawley ; Ventricular Function, Right
    Chemische Substanzen DNA, Mitochondrial
    Sprache Englisch
    Erscheinungsdatum 2017-03-23
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2016-0256OC
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: Heart rate recovery after maximal exercise is impaired in healthy young adults born preterm.

    Haraldsdottir, Kristin / Watson, Andrew M / Beshish, Arij G / Pegelow, Dave F / Palta, Mari / Tetri, Laura H / Brix, Melissa D / Centanni, Ryan M / Goss, Kara N / Eldridge, Marlowe W

    European journal of applied physiology

    2019  Band 119, Heft 4, Seite(n) 857–866

    Abstract: Purpose: The long-term implications of premature birth on autonomic nervous system (ANS) function are unclear. Heart rate recovery (HRR) following maximal exercise is a simple tool to evaluate ANS function and is a strong predictor of cardiovascular ... ...

    Abstract Purpose: The long-term implications of premature birth on autonomic nervous system (ANS) function are unclear. Heart rate recovery (HRR) following maximal exercise is a simple tool to evaluate ANS function and is a strong predictor of cardiovascular disease. Our objective was to determine whether HRR is impaired in young adults born preterm (PYA).
    Methods: Individuals born between 1989 and 1991 were recruited from the Newborn Lung Project, a prospectively followed cohort of subjects born preterm weighing < 1500 g with an average gestational age of 28 weeks. Age-matched term-born controls were recruited from the local population. HRR was measured for 2 min following maximal exercise testing on an upright cycle ergometer in normoxia and hypoxia, and maximal aerobic capacity (VO
    Results: Preterms had lower VO
    Conclusions: Autonomic dysfunction as seen in this study has been associated with increased rates of cardiovascular disease in non-preterm populations, suggesting further study of the mechanisms of autonomic dysfunction after preterm birth.
    Mesh-Begriff(e) Autonomic Nervous System/physiopathology ; Ergometry/methods ; Exercise/physiology ; Exercise Test ; Exercise Tolerance/physiology ; Female ; Heart Rate/physiology ; Humans ; Hypoxia/physiopathology ; Infant, Newborn ; Male ; Pregnancy ; Premature Birth/physiopathology ; Young Adult
    Sprache Englisch
    Erscheinungsdatum 2019-01-11
    Erscheinungsland Germany
    Dokumenttyp Journal Article
    ZDB-ID 124793-1
    ISSN 1439-6327 ; 1432-1025 ; 0301-5548 ; 1439-6319
    ISSN (online) 1439-6327 ; 1432-1025
    ISSN 0301-5548 ; 1439-6319
    DOI 10.1007/s00421-019-04075-z
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: Impaired autonomic function in adolescents born preterm.

    Haraldsdottir, Kristin / Watson, Andrew M / Goss, Kara N / Beshish, Arij G / Pegelow, David F / Palta, Mari / Tetri, Laura H / Barton, Gregory P / Brix, Melissa D / Centanni, Ryan M / Eldridge, Marlowe W

    Physiological reports

    2018  Band 6, Heft 6, Seite(n) e13620

    Abstract: Preterm birth temporarily disrupts autonomic nervous system (ANS) development, and the long-term impacts of disrupted fetal development are unclear in children. Abnormal cardiac ANS function is associated with worse health outcomes, and has been ... ...

    Abstract Preterm birth temporarily disrupts autonomic nervous system (ANS) development, and the long-term impacts of disrupted fetal development are unclear in children. Abnormal cardiac ANS function is associated with worse health outcomes, and has been identified as a risk factor for cardiovascular disease. We used heart rate variability (HRV) in the time domain (standard deviation of RR intervals, SDRR; and root means squared of successive differences, RMSSD) and frequency domain (high frequency, HF; and low frequency, LF) at rest, as well as heart rate recovery (HRR) following maximal exercise, to assess autonomic function in adolescent children born preterm. Adolescents born preterm (less than 36 weeks gestation at birth) in 2003 and 2004 and healthy age-matched full-term controls participated. Wilcoxon Rank Sum tests were used to compare variables between control and preterm groups. Twenty-one adolescents born preterm and 20 term-born controls enrolled in the study. Preterm-born subjects had lower time-domain HRV, including SDRR (69.1 ± 33.8 vs. 110.1 ± 33.0 msec, respectively, P = 0.008) and RMSSD (58.8 ± 38.2 vs. 101.5 ± 36.2 msec, respectively, P = 0.012), with higher LF variability in preterm subjects. HRR after maximal exercise was slower in preterm-born subjects at 1 min (30 ± 12 vs. 39 ± 9 bpm, respectively, P = 0.013) and 2 min (52 ± 10 vs. 60 ± 10 bpm, respectively, P = 0.016). This study is the first report of autonomic dysfunction in adolescents born premature. Given prior association of impaired HRV with adult cardiovascular disease, additional investigations into the mechanisms of autonomic dysfunction in this population are warranted.
    Mesh-Begriff(e) Adolescent ; Autonomic Nervous System Diseases/etiology ; Exercise Test ; Female ; Heart Rate/physiology ; Humans ; Infant, Newborn ; Infant, Premature/physiology ; Male ; Pregnancy ; Premature Birth/physiopathology
    Sprache Englisch
    Erscheinungsdatum 2018-03-08
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2724325-4
    ISSN 2051-817X ; 2051-817X
    ISSN (online) 2051-817X
    ISSN 2051-817X
    DOI 10.14814/phy2.13620
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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