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Article ; Online: Pulmonary hypertension in premature infants. Sharpening the tools of detection.

Farrow, Kathryn N / Steinhorn, Robin H

American journal of respiratory and critical care medicine

2015 Volume 191, Issue 1, Page(s) 12–14

MeSH term(s)	Bronchopulmonary Dysplasia/prevention & control ; Female ; Humans ; Hypertension, Pulmonary/complications ; Infant, Premature ; Lung/physiopathology ; Male ; Oxygen Inhalation Therapy/adverse effects ; Respiration, Artificial/adverse effects ; Vascular Diseases/complications
Language	English
Publishing date	2015-01-01
Publishing country	United States
Document type	Comment ; Editorial
ZDB-ID	1180953-x
ISSN	1535-4970 ; 0003-0805 ; 1073-449X
ISSN (online)	1535-4970
ISSN	0003-0805 ; 1073-449X
DOI	10.1164/rccm.201411-2112ED
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Uh II Zs.80: Show issues

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Article ; Online: Early low-dose hydrocortisone: is the neurodevelopment affected?

Ofman, Gaston / Perez, Marta / Farrow, Kathryn N

Journal of perinatology : official journal of the California Perinatal Association

2018 Volume 38, Issue 6, Page(s) 636–638

Abstract: Type of investigation: Prognosis; exploratory secondary analysis of an interventional randomized controlled trial.: Question: In extremely preterm infant (<28 weeks), is early low-dose hydrocortisone compared to placebo associated with ... ...

Abstract	Type of investigation: Prognosis; exploratory secondary analysis of an interventional randomized controlled trial. Question: In extremely preterm infant (<28 weeks), is early low-dose hydrocortisone compared to placebo associated with neurodevelopmental impairment at 2 years of age? Methods: Patients: Surviving infants enrolled in the PREMILOC trial conducted in France between 2008 and 2014. Intervention: Double-blind, multicenter, randomized, placebo-controlled trial of infants born between 24 0/7 weeks and 27 6/7 weeks of gestation and before 24 h of postnatal age, assigned to receive either placebo or low-dose hydrocortisone (0.5 mg/kg twice per day for 7 days, followed by 0.5 mg/kg per day for 3 days). Main results: For the pre-specified exploratory outcome, the distribution of patients without neurodevelopmental impairment (73% in the hydrocortisone group vs. 70% in the placebo group), with mild neurodevelopmental impairment (20% in the hydrocortisone group vs. 18% in the placebo group), or with moderate to severe neurodevelopmental impairment (7% in the hydrocortisone group vs. 11% in the placebo group) was not found to be statistically significantly different between the two groups (p = 0.33). Qualitative assessment of patients using standardized neurological examination also was not statistically significantly different between groups (p = 0.87). Study conclusion: In this follow-up study of premature infants who were randomly assigned at birth to receive low-dose hydrocortisone or placebo for 10 days, hydrocortisone treatment was not associated with any adverse effects on neurodevelopmental outcome at 22 months of corrected age.
MeSH term(s)	Bronchopulmonary Dysplasia/drug therapy ; Bronchopulmonary Dysplasia/mortality ; Bronchopulmonary Dysplasia/prevention & control ; Critical Care/methods ; Dexamethasone/therapeutic use ; Dose-Response Relationship, Drug ; Double-Blind Method ; Drug Administration Schedule ; Female ; France ; Humans ; Hydrocortisone/therapeutic use ; Infant ; Infant Mortality/trends ; Infant, Extremely Premature ; Infant, Newborn ; Intensive Care Units, Neonatal ; Logistic Models ; Male ; Neurodevelopmental Disorders/diagnosis ; Neurodevelopmental Disorders/drug therapy ; Neurologic Examination/methods ; Pregnancy
Chemical Substances	Dexamethasone (7S5I7G3JQL) ; Hydrocortisone (WI4X0X7BPJ)
Language	English
Publishing date	2018-02-21
Publishing country	United States
Document type	Journal Article ; Multicenter Study ; Randomized Controlled Trial
ZDB-ID	645021-0
ISSN	1476-5543 ; 0743-8346
ISSN (online)	1476-5543
ISSN	0743-8346
DOI	10.1038/s41372-018-0086-y
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Zs.A 2412: Show issues

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Article ; Online: Neonatal lung function and therapeutics.

Auten, Richard L / Farrow, Kathryn N

Antioxidants & redox signaling

2014 Volume 21, Issue 13, Page(s) 1819–1822

Abstract: Respiratory diseases are increasingly recognized as having their origins during perinatal and early postnatal lung development, a time of significant adaptation to large changes in redox conditions as well as to mechanical forces. This Forum of the ... ...

Abstract	Respiratory diseases are increasingly recognized as having their origins during perinatal and early postnatal lung development, a time of significant adaptation to large changes in redox conditions as well as to mechanical forces. This Forum of the journal presents a Forum highlighting studies of the interplay between reactive oxygen/nitrogen species and the systems that have evolved to degrade them or exploit them, as well as the cellular repair processes which respond to early life redox stress in the lung. This group of authors suggests new understandings of these events that may point the way to improved therapeutic approaches.
MeSH term(s)	Animals ; Animals, Newborn ; Humans ; Infant, Newborn ; Lung/metabolism ; Lung/pathology ; Oxidation-Reduction ; Oxidative Stress/physiology ; Reactive Nitrogen Species/metabolism ; Reactive Oxygen Species/metabolism ; Respiratory Tract Diseases/metabolism ; Respiratory Tract Diseases/pathology
Chemical Substances	Reactive Nitrogen Species ; Reactive Oxygen Species
Language	English
Publishing date	2014-09-16
Publishing country	United States
Document type	Editorial
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2014.5959
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Zs.A 5488: Show issues

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Article ; Online: Developmental regulation of antioxidant enzymes and their impact on neonatal lung disease.

Berkelhamer, Sara K / Farrow, Kathryn N

Antioxidants & redox signaling

2014 Volume 21, Issue 13, Page(s) 1837–1848

Abstract: Significance: Deficient antioxidant defenses and compromised ability to respond to oxidative stress burden the immature lung. Routine neonatal therapies can cause increased oxidative stress with subsequent injury to the premature lung. Novel therapeutic ...

Abstract	Significance: Deficient antioxidant defenses and compromised ability to respond to oxidative stress burden the immature lung. Routine neonatal therapies can cause increased oxidative stress with subsequent injury to the premature lung. Novel therapeutic approaches to protect the premature lung are greatly needed. Recent advances: Live cell imaging with targeted redox probes allows for the measurement of subcellular oxidative stress and for comparisons of oxidative stress across development. Comprehension of subcellular and cell-type-specific responses to oxidative stress may influence the targeting of future antioxidant therapies. Critical issues: Challenges remain in identifying the optimal cellular targets, degree of enzyme activity, and appropriate antioxidant therapy. Further, the efficacy of delivering exogenous antioxidants to specific cell types or subcellular compartments remains under investigation. Treatment with a nonselective antioxidant could unintentionally compromise cellular function or impact cellular defense mechanisms and homeostasis. Future directions: Genetic and/or biomarker screening may identify infants at the greatest risk for oxidative lung injury and guide the use of more selective antioxidant therapies. Novel approaches to the delivery of antioxidant enzymes may allow cell type- or cellular organelle-specific therapy. Improved comprehension of the antioxidant enzyme regulation across cell type, cell compartment, gender, and developmental stage is critical to the design and optimization of therapy.
MeSH term(s)	Animals ; Animals, Newborn ; Antioxidants/metabolism ; Humans ; Infant, Newborn ; Lung/metabolism ; Lung Diseases/metabolism ; Oxidation-Reduction ; Oxidative Stress/physiology
Chemical Substances	Antioxidants
Language	English
Publishing date	2014-02-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2013.5515
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Article: Phosphodiesterases: emerging therapeutic targets for neonatal pulmonary hypertension.

Farrow, Kathryn N / Steinhorn, Robin H

Handbook of experimental pharmacology

2011 , Issue 204, Page(s) 251–277

Abstract: Pulmonary hypertension in the neonate is associated with multiple underlying problems such as respiratory distress syndrome, meconium aspiration syndrome, congenital diaphragmatic hernia, bronchopulmonary dysplasia, sepsis, or congenital heart disease. ... ...

Abstract	Pulmonary hypertension in the neonate is associated with multiple underlying problems such as respiratory distress syndrome, meconium aspiration syndrome, congenital diaphragmatic hernia, bronchopulmonary dysplasia, sepsis, or congenital heart disease. Because of the heterogeneous group of disorders, the therapeutic approach and response often depends on the underlying disease. In many of these conditions, there is evidence that cyclic nucleotide signaling and specifically phosphodiesterases (PDEs) are disrupted. PDE inhibitors represent an emerging class of pulmonary vasodilators in adults. Studies are now under way to evaluate the utility, efficacy, and safety of such therapies in infants with pulmonary hypertension.
MeSH term(s)	Humans ; Infant ; Infant, Newborn ; Persistent Fetal Circulation Syndrome/drug therapy ; Persistent Fetal Circulation Syndrome/etiology ; Phosphodiesterase Inhibitors/therapeutic use ; Phosphoric Diester Hydrolases/physiology
Chemical Substances	Phosphodiesterase Inhibitors ; Phosphoric Diester Hydrolases (EC 3.1.4.-)
Language	English
Publishing date	2011-06-22
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ISSN	0171-2004
ISSN	0171-2004
DOI	10.1007/978-3-642-17969-3_11
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Article: Peripherally Inserted Central Catheters Complicated by Vascular Erosion in Neonates.

Blackwood, Brian P / Farrow, Kathryn N / Kim, Stan / Hunter, Catherine J

JPEN. Journal of parenteral and enteral nutrition

2016 Volume 40, Issue 6, Page(s) 890–895

Abstract: Peripherally inserted central catheters (PICCs) are widely used in the pediatric population, and their use continues to grow in popularity. These catheters provide a reliable source of venous access to neonatal patients but can also be the cause of life- ... ...

Abstract	Peripherally inserted central catheters (PICCs) are widely used in the pediatric population, and their use continues to grow in popularity. These catheters provide a reliable source of venous access to neonatal patients but can also be the cause of life-threatening complications. There are several well-documented complications such as infections, catheter thrombosis, vascular extravasations, and fractured catheters. However, the complication of vascular erosion into the pleural space using both small and silicone-based catheters is rarely described. After obtaining institutional review board approval, we identified 4 cases to review of PICCs complicated by vascular erosions in the past 2 years. Herein, we also review the current literature of PICC complications. Getting the catheter tip as close to the atrial-caval junction as possible and confirmation of this placement are of the utmost importance. The thick wall of the vena cava near the atrium seems to be less likely to perforate; in addition, this position provides increased volume and turbulence to help dilute the hyperosmolar fluid, which seems to also be a factor in this complication. A daily screening chest x-ray in patients with upper extremity PICCs and ongoing parenteral nutrition (PN) are not necessary at this time given the overall low rate of vascular erosion and concerns regarding excessive radiation exposure in pediatric populations. However, a low threshold for chest x-ray imaging in patients with even mild respiratory symptoms in the setting of upper extremity PN is recommended.
Language	English
Publishing date	2016-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	800861-9
ISSN	0148-6071
ISSN	0148-6071
DOI	10.1177/0148607115574000
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Zs.A 1524: Show issues

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Article ; Online: Photoreceptor oxidative stress in hyperoxia-induced proliferative retinopathy accelerates rd8 degeneration.

Lajko, Michelle / Cardona, Herminio J / Taylor, Joann M / Farrow, Kathryn N / Fawzi, Amani A

PloS one

2017 Volume 12, Issue 7, Page(s) e0180384

Abstract: To investigate the impact of photoreceptor oxidative stress on photoreceptor degeneration in mice carrying the rd8 mutation (C57BL/6N). We compared the hyperoxia-induced proliferative retinopathy (HIPR) model in two mouse strains (C57BL/6J and C57BL/6N). ...

Abstract	To investigate the impact of photoreceptor oxidative stress on photoreceptor degeneration in mice carrying the rd8 mutation (C57BL/6N). We compared the hyperoxia-induced proliferative retinopathy (HIPR) model in two mouse strains (C57BL/6J and C57BL/6N). Pups were exposed to 75% oxygen, starting at birth and continuing for 14 days (P14). Mice were euthanized at P14, or allowed to recover in room air for one day (P15), seven days (P21), or 14 days (P28). We quantified retinal thickness and the length of residual photoreceptors not affected by rosette formation. In addition we explored differences in retinal immunostaining for NADPH oxidase 4 (NOX4), Rac1, vascular endothelium, and activated Mϋller cells. We analyzed photoreceptor oxidative stress using DCF staining in cross sections and quantified NOX4 protein levels using western blotting. C57BL/6N mice in HIPR showed increased oxidative stress, NOX4, and Rac1 in the photoreceptors at P14 and P15 compared to C57BL/6J. In addition, we observed significant progression of photoreceptor degeneration, with significantly accelerated rosette formation in C57BL/6N under HIPR, compared to their room air counterparts. Furthermore, C57BL/6N under HIPR had significantly thinner central retinas than C57BL/6J in HIPR. We did not find a difference in vascular disruption or Mϋller cell activation comparing the two strains in hyperoxia. In HIPR, the C57BL/6N strain carrying the rd8 mutation showed significantly accelerated photoreceptor degeneration, mediated via exacerbated photoreceptor oxidative stress, which we believe relates to Rac1-NOX dysregulation in the setting of Crb1 loss-of-function.
MeSH term(s)	Animals ; Hyperoxia/metabolism ; Immunohistochemistry ; Mice ; Mice, Inbred C57BL ; Mutation ; Neovascularization, Pathologic ; Oxidative Stress ; Photoreceptor Cells/metabolism ; Reactive Oxygen Species/metabolism ; Retinal Diseases/metabolism
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2017-07-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0180384
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Article ; Online: Photoreceptor oxidative stress in hyperoxia-induced proliferative retinopathy accelerates rd8 degeneration.

Michelle Lajko / Herminio J Cardona / Joann M Taylor / Kathryn N Farrow / Amani A Fawzi

PLoS ONE, Vol 12, Iss 7, p e

2017 Volume 0180384

Abstract	To investigate the impact of photoreceptor oxidative stress on photoreceptor degeneration in mice carrying the rd8 mutation (C57BL/6N). We compared the hyperoxia-induced proliferative retinopathy (HIPR) model in two mouse strains (C57BL/6J and C57BL/6N). Pups were exposed to 75% oxygen, starting at birth and continuing for 14 days (P14). Mice were euthanized at P14, or allowed to recover in room air for one day (P15), seven days (P21), or 14 days (P28). We quantified retinal thickness and the length of residual photoreceptors not affected by rosette formation. In addition we explored differences in retinal immunostaining for NADPH oxidase 4 (NOX4), Rac1, vascular endothelium, and activated Mϋller cells. We analyzed photoreceptor oxidative stress using DCF staining in cross sections and quantified NOX4 protein levels using western blotting. C57BL/6N mice in HIPR showed increased oxidative stress, NOX4, and Rac1 in the photoreceptors at P14 and P15 compared to C57BL/6J. In addition, we observed significant progression of photoreceptor degeneration, with significantly accelerated rosette formation in C57BL/6N under HIPR, compared to their room air counterparts. Furthermore, C57BL/6N under HIPR had significantly thinner central retinas than C57BL/6J in HIPR. We did not find a difference in vascular disruption or Mϋller cell activation comparing the two strains in hyperoxia. In HIPR, the C57BL/6N strain carrying the rd8 mutation showed significantly accelerated photoreceptor degeneration, mediated via exacerbated photoreceptor oxidative stress, which we believe relates to Rac1-NOX dysregulation in the setting of Crb1 loss-of-function.
Keywords	Medicine ; R ; Science ; Q
Subject code	571
Language	English
Publishing date	2017-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
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Article ; Online: Dose-dependent effects of glucocorticoids on pulmonary vascular development in a murine model of hyperoxic lung injury.

Perez, Marta / Wisniewska, Kamila / Lee, Keng Jin / Cardona, Herminio J / Taylor, Joann M / Farrow, Kathryn N

Pediatric research

2016 Volume 79, Issue 5, Page(s) 759–765

Abstract: Background: Exposure of neonatal mice to hyperoxia results in pulmonary vascular remodeling and aberrant phosphodiesterase type 5 (PDE5) signaling. Although glucocorticoids are frequently utilized in the NICU, little is known about their effects on the ... ...

Abstract	Background: Exposure of neonatal mice to hyperoxia results in pulmonary vascular remodeling and aberrant phosphodiesterase type 5 (PDE5) signaling. Although glucocorticoids are frequently utilized in the NICU, little is known about their effects on the developing pulmonary vasculature and on PDE5. We sought to determine the effects of hydrocortisone (HC) on pulmonary vascular development and on PDE5 in a neonatal mouse model of hyperoxic lung injury. Methods: C57BL/6 mice were placed in 21% O2 or 75% O2 within 24 h of birth and received HC (1, 5, or 10 mg/kg subcutaneously every other day) or vehicle. At 14 d, right ventricular hypertrophy (RVH), medial wall thickness (MWT), lung morphometry, and pulmonary artery (PA) PDE5 activity were assessed. PDE5 activity was measured in isolated pulmonary artery smooth muscle cells exposed to 21 or 95% O2 ± 100 nmol/l HC for 24 h. Results: Hyperoxia resulted in alveolar simplification, RVH, increased MWT, and increased PA PDE5 activity. HC decreased hyperoxia-induced RVH and attenuated MWT. HC had dose-dependent effects on alveolar simplification. HC decreased hyperoxia-induced PDE5 activity both in vivo and in vitro. Conclusions: HC decreases hyperoxia-induced pulmonary vascular remodeling and attenuates PDE5 activity. These findings suggest that HC may protect against hyperoxic injury in the developing pulmonary vasculature.
MeSH term(s)	Animals ; Cyclic Nucleotide Phosphodiesterases, Type 5/metabolism ; Dose-Response Relationship, Drug ; Elastin/metabolism ; Glucocorticoids/pharmacology ; Humans ; Hydrocortisone/pharmacology ; Hyperoxia/metabolism ; Hyperoxia/pathology ; Hypertension, Pulmonary/physiopathology ; Hypertrophy, Right Ventricular/physiopathology ; Lung/growth & development ; Lung/pathology ; Lung Injury/pathology ; Mice ; Mice, Inbred C57BL ; Pulmonary Alveoli/metabolism ; Pulmonary Artery/pathology ; Signal Transduction
Chemical Substances	Glucocorticoids ; Elastin (9007-58-3) ; Cyclic Nucleotide Phosphodiesterases, Type 5 (EC 3.1.4.35) ; Hydrocortisone (WI4X0X7BPJ)
Language	English
Publishing date	2016-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	4411-8
ISSN	1530-0447 ; 0031-3998
ISSN (online)	1530-0447
ISSN	0031-3998
DOI	10.1038/pr.2016.1
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Zs.A 564: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Isolation of pulmonary artery smooth muscle cells from neonatal mice.

Lee, Keng Jin / Czech, Lyubov / Waypa, Gregory B / Farrow, Kathryn N

Journal of visualized experiments : JoVE

2013 , Issue 80, Page(s) e50889

Abstract: Pulmonary hypertension is a significant cause of morbidity and mortality in infants. Historically, there has been significant study of the signaling pathways involved in vascular smooth muscle contraction in PASMC from fetal sheep. While sheep make an ... ...

Abstract	Pulmonary hypertension is a significant cause of morbidity and mortality in infants. Historically, there has been significant study of the signaling pathways involved in vascular smooth muscle contraction in PASMC from fetal sheep. While sheep make an excellent model of term pulmonary hypertension, they are very expensive and lack the advantage of genetic manipulation found in mice. Conversely, the inability to isolate PASMC from mice was a significant limitation of that system. Here we described the isolation of primary cultures of mouse PASMC from P7, P14, and P21 mice using a variation of the previously described technique of Marshall et al. that was previously used to isolate rat PASMC. These murine PASMC represent a novel tool for the study of signaling pathways in the neonatal period. Briefly, a slurry of 0.5% (w/v) agarose + 0.5% iron particles in M199 media is infused into the pulmonary vascular bed via the right ventricle (RV). The iron particles are 0.2 μM in diameter and cannot pass through the pulmonary capillary bed. Thus, the iron lodges in the small pulmonary arteries (PA). The lungs are inflated with agarose, removed and dissociated. The iron-containing vessels are pulled down with a magnet. After collagenase (80 U/ml) treatment and further dissociation, the vessels are put into a tissue culture dish in M199 media containing 20% fetal bovine serum (FBS), and antibiotics (M199 complete media) to allow cell migration onto the culture dish. This initial plate of cells is a 50-50 mixture of fibroblasts and PASMC. Thus, the pull down procedure is repeated multiple times to achieve a more pure PASMC population and remove any residual iron. Smooth muscle cell identity is confirmed by immunostaining for smooth muscle myosin and desmin.
MeSH term(s)	Animals ; Animals, Newborn ; Cattle ; Culture Media ; Cytological Techniques/methods ; Desmin/analysis ; Mice ; Muscle Contraction ; Muscle Relaxation ; Muscle, Smooth, Vascular/chemistry ; Muscle, Smooth, Vascular/cytology ; Myosins/analysis ; Pulmonary Artery/chemistry ; Pulmonary Artery/cytology
Chemical Substances	Culture Media ; Desmin ; Myosins (EC 3.6.4.1)
Language	English
Publishing date	2013-10-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Video-Audio Media
ZDB-ID	2259946-0
ISSN	1940-087X ; 1940-087X
ISSN (online)	1940-087X
ISSN	1940-087X
DOI	10.3791/50889
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