Case Report: Clinical Analysis of Seven Neonates With Prader-Willi Syndrome and Review of the Literature.

The clinical symptoms of neonatal Prader-Willi syndrome (PWS) are not typical and are easy to miss. The aim of the study was to investigate the clinical features and genetic characteristics of seven cases of neonatal PWS from northern China, and to improve the understanding of PWS in neonates. We retrospectively analyzed seven infants diagnosed by methylation specific multiplex ligation probe amplification technology (MS-MLPA) in the Neonatology Unit of Shengjing Hospital of China Medical University from September 2016 to July 2020.

ERK1/2 Signaling Pathway Activated by EGF Promotes Proliferation, Transdifferentiation, and Migration of Cultured Primary Newborn Rat Lung Fibroblasts.

Background: Bronchopulmonary dysplasia (BPD) is a common and serious complication in premature infants. Lung fibroblasts (LFs) are present in the extracellular matrix and participate in pulmonary development in response to BPD. The aim of this study was to investigate the effect of extracellular signal-regulated kinase (ERK) on LFs cultured from newborn rats.

Expression dynamics of caveolin-1 in fibroblasts of newborn rats with chronic lung disease and its impact on lung fibroblast proliferation.

Purpose:: To evaluate the changes of caveolin-1 in lung fibroblasts in newborn Wistar rats when exposed to hyperoxic conditions, as well as lung fibroblasts cell cycle.

Methods:: One hundred newborn Wistar rats were randomly divided (50 rats/group) into experimental and control groups, exposed to hyperoxic conditions or normal air, respectively. The fraction of inspired oxygen (FiO2) in the experimental group was 90%, whereas this value was 21% in the control group.

Vitamin D/VDR signaling attenuates lipopolysaccharide‑induced acute lung injury by maintaining the integrity of the pulmonary epithelial barrier.

Vitamin D and its receptor have a protective effect on epithelial barriers in various tissues. Low levels of vitamin D are associated with numerous pulmonary diseases, including acute lung injury (ALI) and acute respiratory distress syndrome. The present study investigated whether the vitamin D/vitamin D receptor (VDR) pathway may ameliorate lipopolysaccharide (LPS)‑induced ALI through maintaining the integrity of the alveolar epithelial barrier.

Autophagy regulates hyperoxia-induced intracellular accumulation of surfactant protein C in alveolar type II cells.

Surfactant protein C (SP-C) deficiency is a risk factor for hyperoxia-induced bronchopulmonary dysplasia in newborn infants. However, the role of SP-C deficiency in the process is unclear. Here, using neonatal rat BPD model and MLE-12, mouse alveolar epithelial type II cell, we examined the changes of SP-C levels during hyperoxia.

Association between ANKK1 (rs1800497) polymorphism of DRD2 gene and attention deficit hyperactivity disorder: a meta-analysis.

The role of dopamine neurotransmitter in attention deficit hyperactivity disorder (ADHD) remains controversial. Many molecular studies focusing on dopamine receptors have attempted to analyze the gene polymorphisms involved in dopaminergic transmission. Of these, rs1800497 (TaqIA) single nucleotide polymorphism (SNP) of the dopamine D2 receptor (DRD2) gene has been focused on by the most attention.

The role of placenta growth factor in the hyperoxia-induced acute lung injury in an animal model.

Prolonged exposure to hyperoxia leads to acute lung injury. Alveolar type II cells are main target of hyperoxia-induced lung injury. However, the cellular and molecular mechanisms remain unknown.

Expression and function of aquaporin-1 in hyperoxia-exposed alveolar epithelial type II cells.

The aim of the present study was to investigate water transport dysfunction in alveolar epithelial type II cells (AECII), which were exposed to hyperoxia, and to investigate the mechanism of pulmonary edema resulting from hyperoxic lung injury. The lung cells of newborn rats were isolated for primary cell culture and divided into control and experimental groups. The control and experimental group cells were placed into a normoxic incubator (oxygen volume fraction, 0.

[Expression of ERK1/2 protein in lung tissues of newborn rats with hyperoxia-induced chronic lung disease].

Objective: To study the expression of extracellular signal regulated protein kinase (ERK) 1/2 in lung tissues of newborn rats with chronic lung disease (CLD) caused by hyperoxia.

Methods: Forty-eight full-term newborn rats were randomly divided into two groups: hyperoxia and control. The two groups were exposed to a hyperoxic gas mixture (0.

[Effects of hyperoxia on erythropoietin receptor expression in lung development of neonatal rats].

Objective: Oxygen toxicity is thought to be a major contributing factor in the pathogenesis of bronchopulmonary dysplasia (BPD). Animal experiments reveal that erythropoietin (EPO) may have protective effects against hyperoxic lung injury, but the mechanisms remain unknown. The aim of this study was to evaluate effects of hyperoxia on erythropoietin receptor expression in lung development of neonatal rats.

[Early prediction of the injured regions in neonatal brain with hypoxic-ischemic encephalopathy by diffusion weighted imaging and measuring their apparent diffusion coefficient].

Objective: To elucidate that diffusion weighted imaging (DWI) can be used to predict the injured regions of neonatal brain with hypoxic-ischemic encephalopathy (HIE) in the early phase of injury, and to measure the apparent diffusion coefficient (ADC) values in the multiple regions of the brain.

Method: The participants in this study were twenty-six infants with HIE from neonatology ward hospitalized between July 2006 and July 2009. Nineteen patients had severe HIE, and seven had moderate HIE.

[Effects of TGF-β1 on gene expression of connective tissue growth factor in lung fibroblasts].

Objective: To study the effects of transforming growth factor-β1 (TGF-β1) on the gene expression of connective tissue growth factor (CTGF) in cultured lung fibroblasts of embryonic rats in vitro.

Methods: Wistar rats of embryonic 19 days were used for primary culture of lung fibroblasts (LFs). The cells in the experimental group were treated by different concentrations (1, 5 or 10 ng/mL) and different durations (12, 24 or 48 hrs) of TGF-β1 to stimulate the LFs.

[Anti-inflammatory effects of erythropoietin on hyperoxia-induced bronchopulmonary dysplasia in newborn rats].

Objective: Bronchopulmonary dysplasia (BPD) is a multifactorial disease resulting from the impact of injury (including oxygen toxicity, barotrauma, volutrauma, and infection) on the immature lung. Oxygen toxicity is thought to be a major contributing factor in the pathogenesis in BPD. Previous animal studies have shown that exposure to hyperoxia in the neonatal period causes lung structural changes that are similar to the histology seen in human infants with BPD.

Melatonin protects against oxidative damage in a neonatal rat model of bronchopulmonary dysplasia.

Background: Oxidative stress plays an important role in the pathogenesis of bronchopulmonary dysplasia (BPD). Melatonin (MT) has direct and indirect free radical detoxifying activity. The present study was to investigate whether treatment with MT would attenuate hyperoxia-induced lung injury and the effect of MT on imbalance of oxidants/antioxidants in the lung of neonatal rats.

[Effect of melatonin on hyperoxia-induced oxidant/antioxidant imbalance in the lung of neonatal rats with chronic lung disease].

Objective: To study the effect of melatonin, a potent antioxidant both in vitro and in vivo, on hyperoxia-induced oxidant/antioxidant imbalance in the lung of neonatal rats with chronic lung disease (CLD).

Methods: Ninety neonatal rats were randomly divided into three groups (n=30 each): air-exposed, hyperoxia-exposed, melatonin-treated (4 mg/kg melatonin was administered 30 minutes before hyperoxia exposure and once daily after exposure). CLD was induced by hyperoxia exposure (FiO2=0.

[Early diagnosis of lingual thyroglossal duct cyst in newborns: analysis of 10 cases previously misdiagnosed as laryngomalacia].

Objective: To distinguish lingual thyroglossal duct cyst (LTDC) from laryngomalacia in newborn infants.

Methods: Data of 10 newborn infants with laryngeal stridor and dyspnea, admitted to the department of neonatology in our hospital during December, 2004 to August, 2007, who were finally diagnosed with LTDC though previously diagnosed as congenital laryngeal stridor in other hospitals, were summarized and analyzed.

Results: Inspiratory stridor with chest wall retractions was cardinal symptom of newborn with LTDC.

[Early clinical presentations and MRI characteristics in newborns with cerebral infarction].

Objective: The present study aimed to characterize the clinical presentations and magnetic resonance imaging including conventional MRI and diffusion-weighted imaging (DWI) in newborns with cerebral infarction.

Methods: Clinical records of 16 newborn infants with cerebral infarction were reviewed. All cases underwent DWI examination in addition to conventional MRI examination [T1-weighted (T1W) and T2-weighted (T2W)]within 5 days after birth.

[Expression of HoxB5, SPC and AQP5 in neonatal rats with hyperoxia-induced chronic lung disease].

Objective: Alveolar epithelium impairment is one of pathological changes associated with chronic lung disease (CLD). Hoxb5 is one of the few homeobox genes strongly expressed in the developing lung. This study investigated the expression of HoxB5, SPC and AQP5 in rats with CLD in order to explore the role of Hoxb-5 in impairment and reparation of alveolar epithelium.

[Expression of HoxB5 mRNA and their effect on lung development in premature rats with hyperoxia-induced chronic lung disease].

Objective: Resolution of alveolar damage after lung injury requires finely orchestrated processes that include coordinated and effective tissue reconstruction to reestablish a functional barrier. Reconstitution of denuded type I alveolar epithelial cell that undergo apoptotic and necrotic death after lung injury is required in many pulmonary diseases. Disruption of distal airway development and type II-type I alveolar epithelial cell differentiation after lung injury and disordered repair of the alveolus after injury is one of the predominant pathological characteristics of chronic lung disease (CLD) of premature infants.

[Changes of u-PA and PAI-1 expression in the lung tissue of neonatal rats after inhaling high concentration oxygen].

Objective: Arrested lung development and lung fibrosis are characteristic pathological changes in chronic lung disease (CLD). Therefore, the role of extracellular matrix (ECM) remodeling in lung fibrosis has been emphasized recently. Plasmin system is also an important factor to modulate ECM degradation and matrix metalloproteinase (MMP) system.