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Background: By changing the paradigm of neonatal intensive care and integrating parents into the care team, the 'family integrated care' (FICare) model developed in Canada ensures that infants receive more consistent care and parents are better able to care for their infants within the neonatal intensive care unit (NICU) and at home. However, Chinese health policy dictates that parents are not allowed into the NICU during their infant's stay, which inhibits this type of parent-infant interaction and may affect infant outcomes. This project aims to demonstrate that allowing parents to care for their newborn infants in the NICU improves the medical outcomes of infants.Methods/design: This cluster randomized controlled trial will evaluate the feasibility and efficacy of FICare in six Chinese tertiary-level NICUs in China - three 'intervention' and three 'control' NICUs. The study steps are: (1) planning and preparation; (2) staff recruitment and training; (3) pilot study in two centers; (4) interim analysis and confirmation of sample size for main study; (5) implementation of main study; (6) data analysis and preparation and publication of study reports. The primary outcome measure is duration of hospital stay from admission to discharge. Secondary outcome measures are: (1) clinical outcomes, such as nosocomial infection, (2) weight gain, (3) breastfeeding, (4) time to full feed, and (5) maternal stress.Discussion: This study will assess the feasibility and cost-effectiveness of FICare in China. By establishing that FICare is a practical model of NICU care for stable preterm infants in China, this project will have a significant impact on health outcomes, medical practice and policy, and the cost of medical care. The approach used in this project could be transferable to many other areas of medical care, such as pediatrics, chronic care, and geriatrics. Data in this project can be used to inform health policy in NICUs across China so that parents are allowed to enter the NICU and be at their infant's bedside during the baby's hospitalization, and modifying the design of NICUs in China to facilitate the participation of parents in caring for their newborns.Trial Registration: Chinese Clinical Trial Registry ChiCTR-TRC-14004736. [ABSTRACT FROM AUTHOR]

Objective This study aimed to compare the outcomes for symmetrical (sSGA) versus asymmetrical (aSGA) small for gestational age (SGA) < 32 weeks preterm infants. Study Design A total of 12,179 eligible infants admitted to the Canadian tertiary neonatal intensive care units (NICUs) over a 7-year-period in the Canadian Neonatal Network database were subcategorized as aSGA (n = 536), sSGA (n = 732), or appropriate for GA (AGA, n = 10,911). Baseline demographics, mortality, and major morbidities were compared using multivariable analysis to calculate adjusted odds ratios (AOR) and 95% confidence interval (CI). Results sSGA had higher GA (p < 0.01) and more antenatal tobacco exposure (p ¼ 0.03). Although both the SGA groups had worse outcomes than AGA controls, aSGA versus sSGA comparison revealed lower odds (AOR [CI]) for mortality and chronic lung disease (CLD) for aSGA in the entire cohort (0.45 [0.27, 0.75] and 0.61 [0.44, 0.84], respectively) as well as for infants < 28 weeks GA (0.50 [0.27, 0.92] and 0.47 [0.29, 0.77], respectively). aSGA infants < 28 weeks GA had comparable outcomes to AGA except higher odds for CLD (1.61 [1.13, 2.27]). sSGA infants needed longer hospital stay and had higher use of oxygen and continuous positive airway pressure than aSGA. Conclusion Among SGA infants < 32 weeks GA, significant intragroup differences exist in the neonatal outcomes and hospital resource utilization depending upon the presence or absence of relative “head sparing.” [ABSTRACT FROM AUTHOR]

Hydrogen peroxide (H2O2) causes cell damage via oxidative stress. Heme oxygenase-1 (HO-1) is an antioxidant enzyme that can protect cardiomyocytes against oxidative stress. In this study, we investigated whether the heme precursor 5-aminolevulinic acid (5-ALA) with sodium ferrous citrate (SFC) could protect cardiomyocytes from H2O2-induced hypertrophy via modulation of HO-1 expression. HL-1 cells pretreated with/without 5-ALA and SFC were exposed to H2O2 to induce a cardiomyocyte hypertrophy model. Hypertrophy was evaluated by planar morphometry, ³H-leucine incorporation, and RT-PCR analysis of hypertrophy-related gene expressions. Reactive oxygen species (ROS) production was assessed by 5/6-chloromethyl- 2=,7=-ichlorodihydrofluorescein diacetate acetylester. HO-1 and nuclear factor erythroid 2-related factor 2 (Nrf2) protein expressions were analyzed by Western blot. In our experiments, HL-1 cells were transfected with Nrf2 siRNA or treated with a signal pathway inhibitor. We found several results. 1) ROS production, cell surface area, protein synthesis, and expressions of hypertrophic marker genes, including atrial natriuretic peptide, brain natriuretic peptide, atrial natriuretic factor, and β-myosin heavy chain, were decreased in HL-1 cells pretreated with 5-ALA and SFC. 2) 5-ALA and SFC increased HO-1 expression in a dose- and time-dependent manner, associated with upregulation of Nrf2. Notably, Nrf2 siRNA dramatically reduced HO-1 expression in HL-1 cells. 3) ERK1/2, p38, and SAPK/JNK signaling pathways were activated and modulate 5-ALA- and SFCenhanced HO-1 expression. SB203580 (p38 kinase), PD98059 (ERK), or SP600125 (JNK) inhibitors significantly reduced this effect. In conclusion, our data suggest that 5-ALA and SFC protect HL-1 cells from H2O2-induced cardiac hypertrophy via activation of the MAPK/ Nrf2/HO-1 signaling pathway. [ABSTRACT FROM AUTHOR]