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1.
BMC Pediatr ; 24(1): 88, 2024 Feb 01.
Article in English | MEDLINE | ID: mdl-38302960

ABSTRACT

BACKGROUND AND OBJECTIVE: Evidence-based research has shown that golden hour quality improvement (QI) measures can improve the quality of care and reduce serious complications of premature infants. Herein, we sought to review golden hour QI studies to evaluate the impact on the outcome of preterm infants. METHODS: A comprehensive literature search was conducted in PubMed, Embase, Cochrane Library, and SinoMed databases from inception to April 03, 2023. Only studies describing QI interventions in the golden hour of preterm infants were included. Outcomes were summarized and qualitative synthesis was performed. RESULTS: Ten studies were eligible for inclusion. All studies were from single centers, of which nine were conducted in the USA and one in Israel. Seven were pre-post comparative studies and three were observational studies. Most included studies were of medium quality (80%). The most common primary outcome was admission temperatures and glucose. Five studies (n = 2308) reported improvements in the admission temperature and three studies (n = 2052) reported improvements in hypoglycemia after QI. Four studies (n = 907) showed that the incidence of bronchopulmonary dysplasia (BPD) was lower in preterm infants after QI: 106/408 (26.0%) vs. 122/424(29.5%) [OR = 0.68, 95% CI 0.48-0.97, p = 0.04]. CONCLUSIONS: Our study showed that the golden hour QI bundle can improve the short-term and long-term outcomes for extremely preterm infants. There was considerable heterogeneity and deficiencies in the included studies, and the variation in impact on outcomes suggests the need to use standardized and validated measures. Future studies are needed to develop locally appropriate, high-quality, and replicable QI projects.


Subject(s)
Bronchopulmonary Dysplasia , Hypoglycemia , Infant , Infant, Newborn , Humans , Quality Improvement , Infant, Extremely Premature , Bronchopulmonary Dysplasia/therapy , Glucose
2.
Biomed Rep ; 6(1): 32-38, 2017 Jan.
Article in English | MEDLINE | ID: mdl-28123704

ABSTRACT

The aim of the present study was to observe the effects of recombinant human erythropoietin (rhEPO) on the expression of epidermal growth factor-like domain 7 (EGFL7) and cell apoptosis in lung tissue following hyperoxic lung injury in newborn rats. The 96 Sprague-Dawley newborn rats were randomly divided into 4 groups (n=24) as follows: Room air-exposed control group, room air-exposed rhEPO-treated group, hyperoxia-exposed group and the hyperoxia-exposed rhEPO-treated group. Pups (n=8) from each group were sacrificed on postnatal days 3, 7 and 14. The pulmonary morphometric and microvessel density changes were observed. In addition, the mRNA and protein expression levels of EGFL7, B-cell lymphoma 2 (Bcl-2) and Bcl-2-like protein 4 (Bax) in lung tissue samples were measured. The rats in the hyperoxia-exposed group exhibited alveolar and pulmonary vascular dysplasia, as well as low mRNA and protein expression levels of EGFL7 and Bcl-2, in addition to high level of Bax in the lung tissue samples when compared with the room air-exposed control group (P<0.05). However, in the hyperoxia-exposed rhEPO-treated group the lung histopathology was improved, and the protein and mRNA expression levels of EGFL7 and Bcl-2 were increased compared with the hyperoxia-exposed group (P<0.05). Furthermore, the expression level of Bax was lower than that of the hyperoxia-exposed group (P<0.05). The present study demonstrated that rhEPO promotes alveolar development and increases pulmonary vascular density by upregulating the expression level of EGFL7 in hyperoxia-induced lung injury of newborn rats.

3.
Zhonghua Er Ke Za Zhi ; 54(1): 37-42, 2016 Jan.
Article in Chinese | MEDLINE | ID: mdl-26791922

ABSTRACT

OBJECTIVE: To explore the expression of CASZ1 and its relationship with the pulmonary microvascular development in lung tissue of newborn rats exposed to hyperoxia which induced bronchopulmonary dysplasia (BPD). METHOD: Forty-eight newborn Sprague Dawley(SD) rats (male and female unlimited) were randomly divided into two groups: experimental group and control group according to random digits table with 24 in each.The rats in experimental group were exposed to high oxygen volume fraction of 800 ml/L and the rats in control group were exposed to normal air. Eight rats were randomly selected from each group on day 3 and 7 after oxygen exposure.The sections of lung were stained with HE method in order to assess lung histological changes, the alveolar development was evaluated by the number of radial alveolar count (RAC) and septal wall thickness. CD31 was detected by immunohistochemistry (IHC) method and the capillary density was calculated. The location, distribution and expression of CASZ1 in the lung tissue were detected by the immunohistochemistry, Western blotting, and quantitative PCR (qPCR). RESULT: (1) Stained by HE, lungs of experimental group showed destroyed alveoli, alveoli fusion and increased septal wall thickness, RAC were significantly lower than those in control group(14 d: septal wall thickness (12.69 ± 0.63) µm vs. (6.53 ± 0.16) µm, RAC 5.9 ± 0.4 vs. 8.4 ± 1.0, t = 19.046, 4.760, P both = 0.000). (2) CD31 protein was expressed predominantly in cytoplasm of pulmonary microvascular endothelial cells. The experimental group CD31 average optical density (AIOD) were decreased compared with control group((16.6 ± 1.6) × 10(3) vs.(40.1 ± 2.4) × 10(3), (18.1 ± 1.4) × 10(3) vs.(83.2 ± 5.2) × 10(3), (49.2 ± 5.4) × 10(3) vs.(136.2 ± 28.1) × 10(3), t=16.185, 16.066 and 6.078, P<0.01 for all comparisons). Capillary density in experimental group was also significantly decreased compared with control group ((3.84 ± 0.15)% vs.(6.01 ± 0.22)%, (4.17 ± 0.38)% vs.(6.15 ± 0.24)%, (5.43 ± 0.44)% vs. (9.13 ± 0.25)%, t = 16.124, 8.773 and 14.076, P all < 0.01). (3)RT-qPCR and Western blotting showed that the CASZ1 mRNA significantly increased in experimental group compared with control group(0.56 ± 0.17 vs. 1.00 ± 0.26, 0.32 ± 0.29 vs. 0.58 ± 0.14, 0.14 ± 0.22 vs. 0.56 ± 0.15, t=3.890, 3.303 and 2.388, P < 0.05 for all comparisons), and the protein expression of CASZ1 also significantly increased in experimental group compared with control group (0.65 ± 0.02 vs. 0.78 ± 0.23, 0.46 ± 0.03 vs. 0.75 ± 0.05, 0.34 ± 0.22 vs. 0.75 ± 0.04, t=6.200 and 10.485 and 14.998, P < 0.05 for all comparisons). (4)The protein level of CASZ1 in experimental group was positively correlated with capillary density (r=0.519, P<0.01). CONCLUSION: CASZ1 is involved in the whole process of newborn rats BPD and may be linked to pulmonary microvascular dysplasia.


Subject(s)
Bronchopulmonary Dysplasia/pathology , Hyperoxia/pathology , Lung/blood supply , Transcription Factors/metabolism , Animals , Animals, Newborn , Female , Lung/pathology , Male , Oxygen/adverse effects , Pulmonary Alveoli , RNA, Messenger/metabolism , Random Allocation , Rats , Rats, Sprague-Dawley
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