- Dr. Zanelli: Neonatal Hypoxic-Ischemic Injury, Basic Mechanisms of cellular injury, role or nitric oxide, mitochondrial function, and electrophysiology
- Dr. Fairchild: Hypothermia and white blood cell function, Neonatal sepsis.
- Dr. Kattwinkel: Laryngeal Mask Delivery of Surfactant with CPAP in term and preterm infants with Respiratory Distress Syndrome; Heart Rate Variability and Infection
- Dr. Kaufman: Fluconazole in preventing invasive yeast infection in ELBW babies; Bacterial infection prevention, Capillary leak on ECMO, pathogenesis of fungal infections
- Dr. Boyle: Ethics and Neonatology; Prevention of infection in preterm infants
- Dr. Attridge: B-type Natriuretic Peptide (BNP ) and PDA closure-with Dr. Scott Lim (Pediatric Cardiology)
Fellow Research
- Neonatal Pulmonary Research in the area of airway pH and S-Nitroothiol metabolism and Bronchopulmonary Dysplasia is being done with Alix Paget-Brown and Dr. Ben Gaston, Pediatric Pulmonologist
- Neonatal Hypoxic-Ischemic Injury, Basic Mechanisms of cellular injury, with Drs. Santina Zanelli and Jaideep Kapur (Neurology)
- Corrine Stewart is working with Dr. Fairchild with white blood cell function and hypothermia
- John Swanson is working with Dr. Gordon with intestinal development and diseases (NEC and focal bowel perforations)
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Dr. Karen Fairchild has been active in studying the effects of hypothermia on the immunue system. Despite enthusiasm and neurologic efficacy in clinical applications of hypothermia, little is known about its cellular and molecular effects. Some of Dr. Fairchild's recent work has demonstrated that enhanced NF kappa B may contribute to immunological effects such as delaying the onset as well as prolonging cytokine responses (e.g. TNF-alpha, IL-1) which may be detrimental and clinically important in conditions such as sepsis. Appropriate regulation of inflammatory cytokine production is critical to successful host defense in patients with infection or injury. 
Hypothermia enhances phosphorylation of IkB kinase. THP-1 cells differentiated with vitamin D3 and stimulated with 100 ng/ml LPS were cultured at 28°C, 32°C, or 37°C for up to 4 h. At the indicated time points, cells were lysed and analyzed for activated IKK-alpha and IKK-B using Western blot analysis with a phosphospecific antibody. Blots were stripped and reprobed for total IKK-alpha as a control for equal protein loading. Densitometry was performed on Western blots from 3 independent experiments and normalized to baseline levels at 37°C (no LPS), which were set at 1. Data are means SE relative band density for phospho-IKK-alpha and IKK-B. *P < 0.05 vs. 37°C. Am J Physiol Cell Physiol 289: C1114-C1121, 2005.
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Dr. Santina Zanelli has been active in research since her residency when she started working with Dr. Maria Delivoria-Papadopoulos. Her interest has emerged in investigating Ca++-mediated, free radical-mediated and nitric oxide pathways of neuronal injury during hypoxia in the immature brain. More recently she has expanded her models to include mitochondrial dynamics and electrophysiologic changes. 
Effect of hypoxia/re-oxygenation on mitochondrial movement and morphology. (a) A bar graph demonstrating the effect of 6 h of hypoxia followed by 0, 1, 2, 6 and 24 h re-oxygenation on mean mitochondrial velocity is shown. Neurons exposed to hypoxia/re-oxygenation demonstrated a significant decrease in mean mitochondrial velocity for up to 3 h of re-oxygenation with recovery at 6 h and 24 h of re-oxygenation. Data is expressed as mean ± SEM. *p < 0.001 vs. control, 6 and 24 h of re-oxygenation; **p < 0.001 vs. 6 h re-oxygenation and not significant vs. control; #p < 0.001 vs. control and 0, 1, 2 and 24 h of re-oxygenation; ##p < 0.001 vs. 0 and 1 h of re-oxygenation and not significant vs. control. (b)-(d) Representative micrographs of mitochondria labeled with Mitotracker Red CMX-Ros are shown. Compared with mitochondria in normoxic control neurons (b), mitochondria exposed to hypoxia with no re-oxygenation were significantly shorter and more punctate (c). Mitochondrial morphology, however, returned to pre-hypoxia morphology by 24 h of re-oxygenation (d). Original magnification ¼ 60·; scale bars ¼ 5 lm. J. Neurochem. (2006) 97, 724-736.
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Initial neonatal heart rate variability findings suggests that this technique may be able to predict neonatal sepsis up to 12 hours before a clinician will suspect it. An NIH multicenter trial began in September 2005 and HRV is now available commercially.
