Bernadette M. Levesque

Pulse oximetry: What's normal in the newborn nursery?

The objective of this study was to establish normal values for pulse oximetry saturation (POS) in healthy newborn infants in the nursery. POS values were obtained from the right (R) hand and R foot at admission, 24 hr, and at discharge. The following information was recorded: postnatal age, activity state, gender, gestational age (GA), birth weight (BW), mode of delivery (MOD), and Apgar scores. Charts were reviewed and follow‐up information was obtained for newborns with measurements ≤92%. The study group consisted of a convenience sample of newborn infants, excluding those on supplemental oxygen.

Dihydrotestosterone Stimulates Branching Morphogenesis, Cell Proliferation, and Programmed Cell Death in Mouse Embryonic Lung Explants

Early gestation lung development is characterized by branching morphogenesis of the airways and basic lung structure formation. Androgens delay late-gestation lung development if the androgen exposure begins in early gestation. We hypothesized that there would be effects of early gestation androgens on lung development. Embryonic mouse lungs (d 11.5) were cultured with dihydrotestosterone (DHT), DHT plus flutamide, or with nothing as controls. Branching morphogenesis was significantly increased after 24, 48, and 72 h of culture. This effect was blocked by simultaneous flutamide treatment. Fetal sex did not influence the DHT response. DHT increased cell proliferation as measured by [3H]thymidine incorporation into DNA. Autoradiography showed prominent [3H]thymidine labeling of epithelia and mesenchyme in regions of new bud formation. DHT treatment significantly increased the thymidine-labeling index of fibroblasts and airway epithelial cells. Programmed cell death, which is found in developing organs in association with cell proliferation during structure formation and tissue remodeling, was studied using terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling assay. In control lungs, programmed cell death occurred in the peripheral mesenchyme surrounding newly forming buds and underlying airway branch points. DHT treatment increased programmed cell death in association with increased branching morphogenesis. Evaluation of near-adjacent sections (control and DHT-treated lungs) showed that apoptotic mesenchymal cells were flanked by [3H]thymidine-labeled fibroblasts and epithelial cells, suggesting a coordination of these processes in the progression of branching morphogenesis. We conclude that androgen enhances the process of early lung morphogenesis by increasing cell proliferation and programmed cell death and by promoting the structural progression of branching morphogenesis.

Hypo-pharyngeal distension in an extremely low birth weight preterm infant

A preterm male infant was born at 25 weeks gestation weighing 780 g by emergency caesarean section to a multiparous woman presenting in active labour with breech presentation. The infant needed some initial resuscitation by bag and mask ventilation followed by commencement of nasal bubble continuous positive airway pressure (CPAP) in the delivery room. Orogastric tube was placed …

Implementation of a pilot program of Reach Out and Read® in the neonatal intensive care unit: a quality improvement initiative

Objective:Language exposure is important for neurodevelopment, but is sparse in the neonatal intensive care unit (NICU).Study design:We introduced Reach Out and Read (ROR) in the NICU as a quality improvement initiative to increase language exposure. Measures included availability of books, accessibility of parents, and enrollment of infants, percent infants read to by their parents, and data from parental surveys.Result:98 infants were included (40 before, 58 after). We obtained books in the mother’s language for 95% of infants, 82% eligible infants were enrolled, and 70% read to their infants (mean of 0.45 ± 0.35 times/day). Surveyed parents enjoyed reading, noted positive effect(s), and intended to read post-discharge.Conclusion:We launched a well-received pilot ROR program in the NICU and reached our goal of ≥50% infants being read to by their parents. Further study is needed to assess the impact of reading in the NICU on parents and infants.

Reply: To PMID 23711562.

VEGF is not released when blood samples are correctly processed for plasma with platelet-stabilizing anticoagulants (specifically, citrate-theophylline-adenosine-dipyridamole, CTAD) [1] , but CTAD is not always used. As some studies report serum VEGF and some report plasma VEGF (using various techniques), there is currently substantial variability in the published literature. Correcting serum VEGF for platelet count has been proposed as a means to improve the consistency of serum VEGF measurements [2] . In our study, we measured urine VEGF, not serum VEGF. Urine VEGF is thought to reflect free circulating Dear Sir, We appreciate the comments and suggestions offered by Dr. Askoy and colleagues in their letter entitled ‘Corrected VEGF levels based on platelet count should be calculated’. There is support in the literature for correcting serum VEGF for platelet count, but not for correcting urine VEGF. VEGF is stored in the α-granules of platelets, and VEGF is released by degranulation when platelets are activated. Blood samples are allowed to clot when forming serum and this activates the platelets and causes release of platelet VEGF into the sample; serum VEGF therefore reflects the sum of plasma and platelet VEGF. Platelet Received: July 3, 2013 Accepted: August 27, 2013 Published online: November 8, 2013

The Progression of Branching Morphogenesis in the Embryonic Lung Involves Apoptosis •276

Apoptosis is becoming recognized as an important mechanistic process in embryonic structural development. Branching morphogenesis of the embryonic lung involves incompletely characterized complex interactions between the developing epithelium and mesenchyme. The involvement of apoptosis in this process not known. We hypothesized that apoptosis is actively involved in the formation of new buds in the embryonic lung, and that apoptosis is altered by factors which stimulate branching morphogenesis. Day 11.5 Swiss Webster mouse lung explants were cultured for 48 hours in serum free BGJb medium with either DHT, DHT plus a 10fold excess of Flutamide (an androgen receptor blocker), or equal volumes of diluent as control. Branching morphogenesis was evaluated by counting the number of terminal buds of the left lung at 0, 24, and 48 hrs under light microscopy. At 24 and 48 hrs individual lungs were harvested, formalin fixed, embedded in OCT, and sectioned (5 microns). After treatment with Proteinase K, endogenous peroxidase activity was quenched with 2% Hydrogen Peroxide. Apoptosis was evaluated using the ApopTag Detection Kit(Oncor) by direct immunoperoxidase detection of digoxigeninlabeled DNA. DHT(106 and 107M) treatment increased the number of terminal buds after 24 and 48 hrs (DHT 106M: 127±6% of control after 48 hrs, P<0.005). This was blocked by a 10fold excess of Flutamide (DHT 106M Flutamide 105M: 109±6% of control after 48 hrs, P=NS). In control lungs apoptosis was present nearly exclusively in distal new bud structures, where intermittent clusters of mesenchymal cells in the thin septa, and occasional adjacent low cuboidal epithelial cells showed apoptosis. Rare mesenchymal cells in the more central areas were also positive. Columnar and cuboidal cells of established airways were negative. DHTtreated lungs showed a similar restriction of apoptosis to cells of new bud structures, but more new structures, and more cells per structure were positive. We speculate that apoptosis occurs in cells of newly forming terminal buds to facilitate the progressive development of new bud structures. This process is enhanced by a growth factor (DHT) that stimulates branching morphogenesis. (Supported by HL37930)

DIHYDROTESTOSTERONE (DHT) STIMULATES BRANCHING MORPHOGENESIS IN EMBRYONIC LUNG EXPLANTS. |[utrif]| 361

DHT affects late gestation lung development by increasing the proliferation of fibroblasts and Type II cells and delaying surfactant production. Based on these findings, it has been suggested that DHT prolongs late gestation (fetal) lung growth resulting in males having larger lungs than females. We postulated that DHT also affects the early gestation (embryonic) lung growth and morphogenesis. We tested this hypothesis by examining the effect of DHT on branching morphogenesis and thymidine incorporation into DNA in embryonic day 11 1/2 mouse lung explants. Lungs were cultured for 72 hours in serum free BGJb medium with either 10-8M DHT or an equal volume (10 μl/ml) of diluent as control. Branching morphogenesis was evaluated at 0, 24, 48, and 72 hours by counting the total number of terminal buds of the left lung under light microscopy. These evaluations were done without knowledge of treatment group. At 48 hours 3H-thymidine (1μCi/ml) was added to all cultures. At 72 hours lung explants were harvested and thymidine incorporation into DNA was determined. The number of terminal buds was similar in the two groups at time zero. Thereafter, the number of terminal buds in the DHT treated group was significantly increased compared to control at 24 hours (DHT: 6.3±0.7 buds; Control: 4.0±0.4 buds; mean±SEM, P=0.006), at 48 hours (DHT: 10.8±0.7; Control 6.4±0.6, P=0.0001), and at 72 hours (DHT: 16.5±1.7; Control 11.1±1.1, P=0.01). The velocity of terminal bud formation, defined as the increase in buds within a given lung over time, was significantly greater in the DHT treated group for the time intervals of zero to 24 hours (DHT: 2.6±0.5; Control: 1.1±0.3; mean±SEM, P=0.02), zero to 48 hours (DHT: 7.1±0.6; Control: 3.5±0.7, P=0.0008), and zero to 72 hours (DHT: 12.8±1.3; Control: 8.2±1.2, P=0.01). Thymidine incorporation into DNA between 48 and 72 hours was decreased in DHT treated lungs (DHT 76%±15% of control; mean±SEM). These data suggest that DHT increases the early velocity of terminal bud formation in the embryonic lung. We speculate that DHT has divergent effects on the growth of airway epithelium versus mesenchymal tissue in embryonic lung, resulting in increased terminal bud formation but decreased overall thymidine incorporation. Supported by HL37930