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Objective:: To evaluate the effect of duration of caffeine use on long-term neurodevelopmental (ND) outcomes at 3 years corrected age (CA) in preterm infants with birthweights (BW) ≤ 1250 g. Design/Methods:: All surviving infants with BW ≤ 1250 g admitted to the Foothills Medical Center neonatal intensive care unit (NICU) from January 2002 to December 2009 who received the first dose of caffeine in the first week of life and were followed up at three years CA were included in the study. Demographics and follow-up outcomes were compared based on early cessation of caffeine ≤ 14 days (ECC), intermediate cessation of caffeine 15–30 days (ICC), and late cessation of caffeine >30 days (LCC). The primary outcome of ND impairment was present if a child had any one of the following: cerebral palsy, cognitive delay, visual impairment, or hearing impairment or deafness. Univariate and logistic regression analyses were performed. Results:: Of the 508 eligible infants, 448 (88%) were seen at 3 years CA at follow-up. ECC (n= 139), ICC (n= 122) and LCC (n= 187) groups had a median (range) BW of 979 (560–1250), 1010 (530–1250), and 980 (520–1250) g (p= 0.524) and median (range) gestational age (GA) of 27 (23–33), 28 (24–33), and 27 (24–32) weeks, respectively (p= 0.034). In logistic regression models adjusting for GA, maternal smoking, and each neonatal risk factor separately (IVH, NEC, sepsis, blood transfusions, BPD, postnatal dexamethasone, SNAP-II, and ventilator days), none of the models showed a statistically significant association between caffeine duration and ND impairment. Conclusion:: The duration of caffeine use in premature infants in the NICU does not impact on long-term ND outcomes at 3 years CA.

Objective:To compare the neurodevelopmental outcomes at 18 to 21 months corrected age (CA) of infants born at <29 weeks that received room air, an intermediate oxygen concentration or 100% oxygen at the initiation of resuscitation.Study design:In this retrospective cohort study, we compared neonatal and neurodevelopmental outcomes at 18 to 21 months CA among inborn infants born before 29 weeks’ gestation that received room air, intermediate oxygen concentration or 100% oxygen at the initiation of resuscitation.Results:Of 1509 infants, 445 received room air, 483 received intermediate oxygen concentrations and 581 received 100% oxygen. Compared to infants that received room air, the primary outcome of death or neurodevelopmental impairment (NDI) was not different in intermediate oxygen (adjusted odds ratio (aOR) 1.01; 95% confidence interval (CI) 0.77, 1.34) or 100% oxygen (aOR 1.03; 95% CI 0.78, 1.35). Compared to room air, there was no difference in odds of death or severe NDI in intermediate oxygen (aOR 1.14; 95% CI 0.82, 1.58) or 100% oxygen group (aOR 1.22; 95% CI 0.90, 1.67). The odds of severe NDI among survivors were significantly higher in infants that received 100% oxygen as compared to room air (aOR 1.57, 95% CI 1.05, 2.35).Conclusions:We observed no significant difference in the primary composite outcomes of death or NDI and death or severe NDI at 18 to 21 months CA between infants that received room air, intermediate oxygen concentration or 100% oxygen at the initiation of resuscitation. However, use of 100% oxygen was associated with increased odds of severe NDI among survivors as compared to room air.

TASTE avoidances were conditioned in male rats by pairing ingestion of a novel sucrose (0.3 M solution) taste with injections of 17β oestradiol (100 μg kg−1, s.c.). Following conditioning and prior to a two-bottle choice test (sucrose vswater), taste reactivity responses to three 30 s intraoral sucrose infusions were quantified. A robust conditioned shift in palatability, consisting of reduced ingestive and increased aversive taste reactivity responses, was obtained in the oestradiol group but not the vehicle control group. This conditioned palatability shift was also reflected in subsequent strong avoidance of the sucrose solution in the two-bottle choice test. The findings that oestradiol can condition taste aversions and shift food preferences support a role for oestrogens in the production of anorexia.