Adjusting sails for changing winds: exploring Reddit use for professional purposes in higher education.

Emerging practices of social media for professional purposes in higher education merit further attention. Reddit, a social media platform, is under-studied despite its significant presence. This study explores participation patterns on Reddit for two summer periods during 2019-2020, before and during COVID-19. We collected a total of 82,494 contributions from two subreddits, r/highereducation and r/Professors. Results show changes in contributions and interactions, with more consistent growth in r/Professors. Major topics discussed in both subreddits during summer 2020 had shifted from 2019, largely related to COVID-19. Findings are discussed with a community of practice lens, noting changes in participation and adjustment to the crisis. Additionally, we present implications for supporting and sustaining higher education professionals through Reddit during and after massive disruptions like those experienced during the COVID-19 pandemic.

Inquiring tweets want to know: #Edchat supports for #RemoteTeaching during COVID-19.

Social media use has spiked around the world during the COVID-19 global pandemic as people reach out for news, information, social connections, and support in their daily lives. Past work on professional learning networks (PLNs) has shown that teachers also use social media to find supports for their teaching and ongoing professional development. This paper offers quantitative analysis of over a half million Twitter #Edchat tweets as well as qualitative content analysis of teachers' question tweets (n = 1054) and teacher interviews (n = 4). These data and analyses provide evidence of the kinds of supports that teachers in the United States and Canada sought on social media during the rapid transition to emergency remote teaching in Spring 2020 and how these supports informed teaching practices. These results provide insights into PLN theory and teachers' social media use during times of disruption and crisis.

Balancing' privacy and open science in the context of COVID-19: a response to Ifenthaler & Schumacher (2016).

Privacy and confidentiality are core considerations in education, while at the same time, using and sharing data-and, more broadly, open science-is increasingly valued by editors, funding agencies, and the public. This manuscript responds to an empirical investigation of students' perceptions of the use of their data in learning analytics systems by Ifentahler and Schumacher (Educational Technology Research and Development, 64: 923-938, 2016). We summarize their work in the context of the COVID-19 pandemic and the resulting shift to digital modes of teaching and learning by many teachers, using the tension between privacy and open science to frame our response. We offer informed recommendations for educational technology researchers in light of Ifentahler and Schumacher's findings as well as strategies for navigating the tension between these important values. We conclude with a call for educational technology scholars to meet the challenge of studying learning (and disruptions to learning) in light of COVID-19 while protecting the privacy of students in ways that go beyond what Institutional Review Boards consider to be within their purview.

Dose and time response after intraamniotic endotoxin in preterm lambs.

Intraamniotic endotoxin causes chorioamnionitis, which is followed by improved fetal lung function after 4 d in fetal sheep. We evaluated 0.1 mg, 1 mg, 4 mg, and 10 mg endotoxin for inflammation and lung maturation effects after 7 d. Four and 10 mg endotoxin caused similar lung maturation and inflammation in the lung and chorioamnion. The number of neutrophils in cord blood and the inflammatory cells in alveolar lavage and fetal lung tissue increased in a dose-dependent manner. Lower endotoxin doses induced indicators of chorioamnionitis, lung and systemic inflammation without inducing lung maturation. Therefore, some degree of inflammation can occur without subsequent lung maturation. The inflammatory changes caused by 4 mg endotoxin were assessed after 5 h, 24 h, 72 h, and 7 d to discern local versus systemic inflammation after intraamniotic endotoxin. At 5 h active inflammatory cells were in the airways producing hydrogen peroxide, and interleukin-6 and -8 were increased in the cord blood indicating both lung and systemic responses. Cells recruited into the amniotic fluid produced proinflammatory cytokine mRNA for 7 d with no cytokine mRNA in chorioamnion, lung, or spleen after 72 h. The cells in the amniotic fluid may be a source of prolonged fetal exposure to proinflammatory cytokines.

The interactive effects of endotoxin with prenatal glucocorticoids on short-term lung function in sheep.

OBJECTIVE: Previously we have shown that neonatal lung function in sheep after preterm birth is profoundly enhanced by intra-amniotic injection of endotoxin, with a magnitude at least equal to that induced by maternal betamethasone administration. This study investigated the effects of betamethasone on lung maturation and growth in the presence of inflammation by treating sheep with both maternal intramuscular betamethasone and intra-amniotic endotoxin injections. STUDY DESIGN: Time-mated pregnant ewes at 118 days' gestation were allocated at random to receive maternal intramuscular or intra-amniotic saline solution injection (n = 10), maternal intramuscular betamethasone injection (0.5 mg/kg; n = 7), intra-amniotic endotoxin injection (20 mg Escherichia coli B055;B5; n = 11) by ultrasonographic guidance, or both betamethasone and endotoxin injections (n = 7). The lambs were delivered abdominally at 125 days' gestation (term is 150 days' gestation), and the neonates were ventilated for 40 minutes before postmortem examination. RESULTS: Combined treatment with betamethasone and endotoxin resulted in significantly greater improvements in neonatal lung function than occurred after treatment with either agent alone, and this effect was not accompanied by a further increase in surfactant levels. The reduction in birth weight that is seen after maternal betamethasone treatment was not seen when this treatment was combined with endotoxin. Endotoxin treatment resulted in inflammatory responses in cord blood and alveolar wash, and these responses were not inhibited by betamethasone treatment. There were no pregnancy losses. CONCLUSION: Both intra-amniotic endotoxin injection and maternal intramuscular betamethasone injection promoted fetal lung maturation. When these treatments were combined, there were additive effects on short-term postnatal lung function but not on surfactant levels. Endotoxin negated the growth restriction in sheep caused by maternal betamethasone treatment. These findings provide evidence that the lung maturation induced by glucocorticoids and that induced by endotoxin are mediated by different mechanisms.

Sex differences in response to steroids in preterm sheep lungs are not explained by glucocorticoid receptor number or binding affinity.

We recently reported that prenatal glucocorticoid therapy is less effective at promoting an improvement in lung function in male than in female sheep. This observation, and the higher incidence of respiratory distress syndrome in human males, suggests that the male fetal lung may be less responsive to glucocorticoids than is the female fetal lung. Since glucocorticoids are known to exert their effects via specific cytoplasmic glucocorticoid receptors (GR), we hypothesized that there may be sexual dimorphism in either the number or binding affinity of lung GR. To test the hypothesis, binding of dexamethasone (a synthetic glucocorticoid, 0.5-40 nM) by cytosolic fractions of male (n = 16) and female (n = 16) fetal sheep lung was measured at 125 days gestation (term = 148 days). Scatchard analysis of dexamethasone binding showed that the total number of GR (Bmax) did not significantly differ between male (346 +/- 42 fmol/mg protein) and female (277 +/- 23 fmol/mg protein) fetuses. The measured binding affinity (Kd) in male fetal lungs (6.85 +/- 0.43 nM) was not significantly different from that in females (8.46 +/- 1.02 nM). In conclusion, this study suggests that sex differences in fetal sheep lung responses to glucocorticoid therapy are not due to differences in the number or binding affinity of lung GR.

Lung morphometry after repetitive antenatal glucocorticoid treatment in preterm sheep.

Antenatal glucocorticoids are thought to be less effective when delivery occurs more than 7 d after initiation of treatment; therefore, repeat courses are often administered. We examined lung structure after single or repetitive antenatal glucocorticoid injections in fetal sheep. Pregnant ewes received single or repetitive doses of 0.5 mg/kg betamethasone at 7-d intervals by maternal or fetal injection, beginning at D104 or D114 with delivery at D125, D135, or D146 gestation (term = 150 d). Changes in lung structure were more pronounced after repetitive versus single injections. Repetitive fetal or maternal injections beginning at D104 (delivery at D125) resulted in comparable structural changes: alveolar volume increased by 50 to 80%, alveolar numerical density decreased by 30 to 40%, and pleural and interlobular septal volumes decreased by as much as 70%. Similar changes were seen in animals delivered at D135 after repetitive maternal injections beginning at D114. There were no structural differences between control and repetitive betamethasone animals when delivery was delayed until D146, indicating that betamethasone induced structural changes were reversible.

Effects of gestation and antenatal steroid on airway and tissue mechanics in newborn lambs.

The aim of this study was to partition airway and parenchymal mechanics in newborn lambs at different gestations and following variable exposure to antenatal maternal betamethasone using the forced oscillation technique (FOT). Pulmonary impedance data were collected in 37 sedated and intubated apneic lambs with the FOT between 0.5 and 20 Hz and fitted by a model to estimate airway resistance (Raw) and inertance (Iaw) and the coefficients of tissue resistance (GL) and elastance (HL). Total respiratory resistance (Rrs) was also determined during tidal ventilation by using the multiple linear regression technique. Advancing gestation or increasing antenatal steroid exposure had no clinically significant effect on the values of Raw and Iaw, whereas Rrs and both GL and HL decreased markedly. There was a decrease in tissue hysteresivity (GL/HL) with repeated antenatal steroid exposure. Partitioning of lung mechanics highlights the dominant contribution of the tissues to the total respiratory resistance in the immature ovine lung. Clinically relevant changes in lung mechanics associated with structural and functional maturation of the immature ovine lung are primarily confined to the tissue compartment.

Intra-amniotic endotoxin: chorioamnionitis precedes lung maturation in preterm lambs.

The inflammatory and lung maturational effects of intra-amniotic exposure to endotoxin were assessed in fetal lambs. Five hours to 25 days after intra-amniotic injection of endotoxin, preterm lambs were delivered at 119-125 days gestation. Intra-amniotic endotoxin caused an inflammatory cell infiltration in amnion/chorion at 5 h, which persisted for 25 days. At 5-15 h after endotoxin, amnion/chorion cytokine mRNAs increased [12- to 26-fold for interleukin (IL)-1beta, IL-6, and IL-8 mRNA and 3-fold for tumor necrosis factor-alpha mRNA]. At 1-2 days after endotoxin, lung cytokine mRNAs increased 6- to 49-fold. Endotoxin caused modest changes in peripheral white blood cell counts and no significant cytokine mRNA responses in fetal liver, placenta, or jejunum. Lung maturation, as characterized by increased lung volumes and alveolar saturated phosphatidylcholine, occurred at 7 days and persisted for 25 days after endotoxin. We conclude that exposure to a single dose of intra-amniotic endotoxin causes inflammation and increases in cytokine mRNA in amnion/chorion and the fetal lung before lung maturation, consistent with the hypothesis that proinflammatory cytokines signal lung maturation.

[Lung transplantation and mitochondrial function]. / Transplantation pulmonaire et fonction mitochondriale.

The mechanisms of cellular lesions induced by lung ischemia and reperfusion are not fully understood and, in particular, the consequences of pulmonary ischemia and reperfusion injury on mitochondrial function have not been previously investigated. Therefore, we studied the respiratory function of isolated pulmonary mitochondria in a swine model of lung ischemia and reperfusion. We demonstrated that prolonged hypothermic (4 degrees C) ischemia induces significant lesions of the mitochondrial respiratory chain, particularly if ischemia is followed by normothermic reperfusion. These results should be integrated in the cellular alterations induced by the ischemia-reperfusion injury. In another swine model mimicking controlled non-heart beating donors, we demonstrated that thirty minutes of cardiac arrest do not promote significant alteration of the mitochondrial respiratory function. In contrast, forty-five minutes of cardiac arrest, induced significant mitochondrial lesions. This pulmonary tolerance to normothermic cardiac arrest might be explained by the presence of air in the lung airways, allowing some aerobic metabolism after circulatory arrest. These results suggested that lung grafts might be harvested from non-heart beating donors after thirty minutes of cardiac arrest, significantly increasing the pulmonary graft pool.

Antenatal endotoxin and glucocorticoid effects on lung morphometry in preterm lambs.

In utero inflammation may accelerate fetal lung maturation but may also play a role in the pathogenesis of chronic lung disease. We examined the impact of endotoxin, a potent proinflammatory stimulus, on structural and functional maturation of preterm sheep lungs. Date bred ewes received 20 mg Escherichia coli endotoxin or saline by ultrasound guided intra-amniotic injection at 119 d gestation. A comparison group of animals received 0.5 mg/kg betamethasone, a known maturational agent, at 118 d gestation. Lambs were delivered by cesarean section at 125 d (term = 150 d) and ventilated for 40 min. Lung function data are reported elsewhere. Total and differential white cell counts were performed on amniotic fluid and fetal lung fluid samples. Morphometric analyses were performed on inflation fixed right upper lobes. Total cell count increased slightly but not significantly in both amniotic fluid and fetal lung fluid. Both endotoxin and betamethasone had similar effects on alveolarization: average alveolar volume increased by approximately 20% and total alveolar number decreased by almost 30%. Both treatments led to thinning of alveolar walls, although this was statistically significant in the betamethasone-treated group only. Although antenatal endotoxin leads to striking improvements in postnatal lung function, this may be at the expense of normal alveolar development.

Resistance of isolated pulmonary mitochondria during in vitro anoxia/reoxygenation.

The aim of the study was to investigate the effect of in vitro anoxia/reoxygenation on the oxidative phosphorylation of isolated lung mitochondria. Mitochondria were isolated after harvesting from fresh pig lungs flushed with Euro-Collins solution. Mitochondrial respiratory parameters were determined in isolated mitochondria before anoxia (control), after 5-45 min anoxia followed by 5 min reoxygenation, and after 25 or 40 min of in vitro incubation in order to follow the in vitro aging of mitochondria during respiratory assays. Respiratory parameters measured after anoxia/reoxygenation did not show any oxidative phosphorylation dysfunction, indicating a high resistance of pulmonary mitochondria to in vitro anoxia/reoxygenation (up to 45 min anoxia). These results indicate that mitochondria are not directly responsible of their oxidative phosphorylation damage observed after in vivo ischemia (K. Willet et al., Transplantation 69 (2000) 582) but are a target of others cellular injuries leading to mitochondrial dysfunction in vivo.

Endotoxin-induced lung maturation in preterm lambs is not mediated by cortisol.

Antenatal exposure to glucocorticoids, amnionitis, intraamniotic interleukin (IL)-1alpha, or endotoxin can improve postnatal lung function after preterm delivery. The relationship between early lung maturation and the dose and duration of a proinflammatory stimulus has not been evaluated. The effects of proinflammatory stimuli on fetal plasma cortisol also have not been evaluated. We hypothesized that intraamniotic endotoxin would induce early lung maturation in fetal sheep without increasing fetal cortisol. Intraamniotic injections of 1, 4, 20, or 100 mg of Escherichia coli 055:beta5 endotoxin caused 2-fold increases in compliance, 4- to 5-fold increases in lung gas volumes, and 20-fold increases in alveolar saturated phosphatidylcholine (Sat PC) when given 7 d before preterm delivery at 125 d gestation. Animals treated with 20 mg endotoxin for treatment to delivery intervals of 5 h to 15 d had no significant elevations in cord plasma cortisol levels. Increases in Sat PC in lung tissue and alveolar washes were detected 2 d after endotoxin treatment and lung function improved 4 d after endotoxin treatment. Two doses of endotoxin given 3 and 7 d or 7 and 15 d before treatment resulted in lung maturation responses equivalent to single dose comparison groups without elevations in cortisol. Early lung maturation induced by intraamniotic endotoxin in fetal sheep occurred without an increase in fetal plasma cortisol, indicating that endotoxin promoted lung maturation by a mechanism independent of cortisol.

Pulmonary interstitial emphysema 24 hours after antenatal betamethasone treatment in preterm sheep.

During a series of studies investigating the maturational response to antenatal glucocorticoids, we observed that 70% of lambs delivered at 128 d gestation (term = 150 d), 24 h after a single injection of 0.5 mg/kg betamethasone or betamethasone + L-thyroxine (15 microgram/kg), developed pulmonary interstitial emphysema (PIE), compared with less than 5% of control animals or animals delivered 48 h or 7 d after hormone treatment. This study examined whether the lungs of animals that developed PIE were functionally or structurally different from those that did not. Lambs were mechanically ventilated for 40 min after cesarean section delivery. Hormone-treated animals with PIE were ventilated at similar peak inspiratory pressure (PIP) to control animals, whereas those without PIE were able to be ventilated at significantly lower PIP. Volume-dependent elastance (E2V), which provides an index of overdistension during mechanical ventilation, was lowest in PIE animals. Alveolar architecture was distorted in almost all ventilated animals, the most severe distortion occurring in PIE animals. There was no evidence of excessive alveolar wall thinning in PIE animals, although parenchymal collagen was 30% lower, and elastin 120% higher than in control animals. PIE was associated with structural differences, but not with overventilation.

Antenatal retinoic acid does not alter alveolization or postnatal lung function in preterm sheep.

Retinoic acid exposure has been shown to promote surfactant production in foetal rats and to promote alveolization in neonatal rats. It was hypothesized that antenatal retinoic acid treatment would promote alveolization and accelerate functional maturation in the lungs of late gestation preterm sheep. Foetuses received a single i.m. injection of all-trans retinoic acid (RA, 20 mg x kg(-1)) or vehicle control at 115 days gestation (term=150 days) and were delivered at 125 days gestation. To examine the longer term effects of RA on alveolization a second group of animals received RA or vehicle at 121 days gestation and were delivered at 146 days gestation. Liver retinol levels at time of delivery were 2-3-fold higher in both preterm and near-term RA treated animals, indicating a significant impact of RA treatment on retinol metabolism. Dynamic compliance, gas exchange, lung gas volume and saturated phosphatidylcholine pool size at 125 days were unaffected by antenatal RA treatment. Alveolar volume, wall thickness and number at 125 or 146 days were also unaffected by RA treatment. Retinoic acid, as administered in this study, does not appear to accelerate structural or functional maturation of the foetal sheep lung. Response to retinoic acid may be species dependent, highlighting a need for caution when interpreting results from animal based studies.

Effects of cold and warm ischemia on the mitochondrial oxidative phosphorylation of swine lung.

BACKGROUND: The aim of the study was to investigate the consequence of warm and cold ischemia on lung mitochondria in order to define bioenergetic limits within lung could be suitable for pulmonary transplantation. METHODS: Twenty-two pigs underwent lung harvesting after lung flush with Euro-Collins solution. Mitochondria were isolated from fresh lungs, from lungs submitted to 24 or 48 hr of cold ischemia, to 30 or 45 min of warm ischemia, and to 30 min of warm ischemia followed by 24 or 48 hr of cold ischemia. Mitochondrial oxidative phosphorylation parameters were determined in isolated mitochondria by in vitro measurement of oxygen consumption. RESULTS: Relative to controls, mitochondria submitted to cold ischemia showed an alteration in the oxidoreductase activities of the respiratory chain but no membrane permeability alteration. After 48 hr of cold ischemia, there was a decrease in the yield of the oxidative phosphorylation. Thirty minutes of warm ischemia did not alter the mitochondrial respiratory parameters. However, lung submitted to 45 min of warm ischemia showed mitochondrial damage as a decrease in the oxidative phosphorylation efficiency and ADP availability but no change in the oxidoreductase activities. Relative to cold ischemia alone, 30 min of warm ischemia preceding cold ischemia promoted no significant change in the respiratory parameters. CONCLUSIONS: On bioenergetic basis, lung submitted to warm ischemia could be suitable for transplantation if the warm ischemia duration does not exceed 30 min. This could be a major concern in lung procurement from non-heart beating donors.

Effects of antenatal endotoxin and glucocorticoids on the lungs of preterm lambs.

OBJECTIVE: We hypothesized that the proinflammatory response to intra-amniotic endotoxin would induce lung maturation in preterm lambs. STUDY DESIGN: Ewes were randomly assigned to receive 20 mg Escherichia coli endotoxin by intra-amniotic injection, maternal betamethasone (0.5 mg/kg), or sodium chloride solution. Preterm lambs were delivered at 125 days' gestation and underwent ventilation to assess lung function. Lung gas volume, surfactant concentrations, and inflammation were subsequently evaluated, with data analyzed by analysis of variance. RESULTS: Fetal endotoxin exposure 6 days before delivery increased compliance by 59%, increased lung gas volume 2.3-fold, increased concentrations of surfactant lipids, increased surfactant A and B protein levels, and increased messenger ribonucleic acid expressions for surfactant proteins (all P <.01, vs control group). Betamethasone exposure resulted in less consistent effects. White blood cell counts were increased in fetal membranes and lungs after endotoxin exposure, but there was no severe inflammation. CONCLUSION: A single fetal exposure to endotoxin resulted in large improvements in postnatal lung function and increases in surfactant concentrations after preterm delivery. These effects were qualitatively larger than those achieved with betamethasone.

EGb 761 protects liver mitochondria against injury induced by in vitro anoxia/reoxygenation.

The present study investigated the protective effects of Ginkgo biloba extract (EGb 761) on rat liver mitochondrial damage induced by in vitro anoxia/reoxygenation. Anoxia/reoxygenation was known to impair respiratory activities and mitochondrial oxidative phosphorylation efficiency. ADP/O (2.57 +/- 0.11) decreased after anoxia/reoxygenation (1.75 +/- 0.09, p < .01), as well as state 3 and uncoupled respiration (-20%, p < .01), but state 4 respiration increased (p < .01). EGb 761 (50-200 microg/ml) had no effect on mitochondrial functions before anoxia, but had a specific dose-dependent protective effect after anoxia/reoxygenation. When mitochondria were incubated with 200 microg/ml EGb 761, they showed an increase in ADP/O (2.09 +/- 0.14, p < .05) and a decrease in state 4 respiration (-22%) after anoxia/reoxygenation. In EPR spin-trapping measurement, EGb 761 decreased the EPR signal of superoxide anion produced during reoxygenation. In conclusion, EGb 761 specially protects mitochondrial ATP synthesis against anoxia/reoxygenation injury by scavenging the superoxide anion generated by mitochondria.

Lung morphometry and collagen and elastin content: changes during normal development and after prenatal hormone exposure in sheep.

This study examined whether the improvement in lung function after prenatal hormone exposure coincided with changes in lung morphometry or in collagen and elastin content. Fetal lambs received a single intramuscular injection of betamethasone (0.5 mg/kg) plus L-thyroxine (T4) (15 micrograms/kg) or vehicle control 48 h before delivery at 121, 128, or 135 d gestational age (d 121, d 128, d 135, term = 150 d). T4 was administered in conjunction with betamethasone in an attempt to enhance the maturational response. The right-upper lobes were instillation fixed at 30 cm H2O by Karnovsky's fixative after a 40-min period of mechanical ventilation. A number of significant changes occurred between d 121 and d 135 in control animals: alveolar airspace volume increased by 270%; despite a 40% reduction in alveolar septal thickness, alveolar septal volume did not change appreciably, suggesting a "redistribution" of septal tissue into the formation of secondary alveolar septa, which doubled in number; and both parenchymal collagen and elastin volume increased significantly, whereas pleural collagen and elastin volume did not change. In contrast to the changes seen in control animals, exposure to betamethasone plus T4 led to alveolar septal thinning at each gestational age without an associated increase in secondary septal number, a 40% decrease in alveolar septal volume, and a proportionate reduction in parenchymal elastin at d 121. Although attenuation of alveolar septa coincides with redistribution of septal tissue into the formation of secondary septa during normal maturation, exposure to betamethasone plus T4 promotes thinning of alveolar septa in the absence of secondary septal formation, which results in a loss of alveolar septal tissue.

Fetal versus maternal and gestational age effects of repetitive antenatal glucocorticoids.

BACKGROUND: Although single courses of antenatal glucocorticoids decrease respiratory distress syndrome and mortality, repetitive courses of antenatal glucocorticoids are being given to women at risk of preterm delivery without evidence of benefit or appreciation of potential risks. OBJECTIVES: To evaluate the effects of single and repetitive antenatal glucocorticoid exposures on fetal growth and postnatal lung function in sheep. METHODS: Pregnant ewes were randomized to three protocols that included one or three doses (at 7-day intervals) of 0.5 mg/kg of betamethasone (beta) given to the ewe or fetus beginning at gestations ranging from 104 to 128 days' gestation with delivery at 125, 135, and 146 days' gestation. Postnatal assessments included measurements of gas exchange, compliance, ventilation efficiency, static lung volume, and lung tissue and alveolar wash saturated phosphatidylcholine. RESULTS: Single or repetitive maternal beta but not fetal beta caused fetal growth retardation at delivery at 125, 135, and 146 days' gestation. Single-dose fetal beta had no effect on postnatal lung function whereas single-dose maternal beta significantly increased compliance, lung volume, and tissue and alveolar surfactant after preterm delivery. Although three-dose fetal beta improved all indicators of postnatal lung function, three-dose maternal beta resulted in larger responses. The added benefits of repetitive beta relative to a single-dose beta on postnatal lung function after preterm delivery were not as great when therapy was begun later in gestation. Postnatal lung function after delivery at 146 days' gestation (term is 150 days) was improved after repetitive maternal beta at early gestational age. CONCLUSIONS: In sheep, single or repetitive maternal beta causes growth retardation from 104 to 121 days' gestation and the growth retardation persists to term. In contrast, single or repetitive fetal beta does not cause fetal growth retardation and is less potent at improving postnatal lung function and increasing surfactant pools. There are potential benefits as well as risks for the use of repetitive antenatal glucocorticoids. Randomized, controlled trials in humans are essential given the widespread use of repetitive courses of antenatal glucocorticoids in women at risk of preterm delivery. respiratory distress syndrome, maturation, prematurity, growth retardation, surfactant.