Vasoactive intestinal peptide inhibits airway smooth muscle cell proliferation in a mouse model of asthma via the ERK1/2 signaling pathway.

Asthma is a heterogeneous clinical syndrome characterized by airway inflammation, hyper-responsiveness and remodeling. Airway remodeling is irreversible by current antiasthmatic drugs, and it is the main cause of severe asthma. Airway smooth muscle cells (ASMCs) act as the main effector cells for airway remodeling; the proliferation and hypertrophy of which are involved in airway remodeling.

[Alterations of SP-A, SP-D and KL-6 in serum and bronchoalveolar lavage fluid in children with Mycoplasma pneumoniae pneumonia].

Objective: To study the alterations and relationship of surfactant protein (SP)-A, SP-D and KL-6 in serum and bronchoalveolar lavage fluids (BALF) in children with Mycoplasma pneumoniae pneumonia (MPP).

Method: Self-control method was used for the study on SP-A, SP-D and KL-6 in serum, infected and non-infected BALFs in 32 MMP children with only one side of MPP.

Result: The contents of SP-A, SP-D and KL-6 in infected BALF were [mg/L;M (IQR) ]: 243 (90-468) , 187 (43-333) , 148 (47-426) ;104 (37-257) , 56 (25-131) , 35 (12-147) in non-infected BALF; 35 (25-69) , 33 (9-149) and 24 (15-62) in serum.

[Changes to surfactant proteins in the bronchoalveolar lavage fluid and serum of children with Mycoplasma pneumoniae pneumonia].

Objective: To study the changes to surfactant proteins in the serum and bronchoalveolar lavage fluids (BALF) of children with Mycoplasma pneumoniae pneumonia (MPP) and their significance.

Methods: Self-control method was used in the study. Forty-seven MPP children were divided into single lung infected (n=32) and bilateral lung infected groups (n=15) according to lung CT results.

[Expression of RANTES in the lung tissue of asthmatic rats, and the intervention effect of vitamin D on RANTES expression].

Objective: To investigate the effect of vitamin D on the expression of chemokine regulated on activation, normal T cells expressed and secreted (RANTES) in the lung tissue of asthmatic rats, and the role of vitamin D in the control of asthmatic airway inflammation and the synergistic action of hormones.

Methods: Forty female Wistar rats were randomly and equally divided into normal control, asthma, vitamin D intervention, budesonide intervention, and budesonide+vitamin D intervention groups. Hematoxylin and eosin staining was used to observe pathological changes in the lung tissue.

[Relationship between alveolar epithelial type II cells and pulmonary surfactant protein A levels in young rats with acute lung injury].

Objective: This study examined the relationship between the ultrastructural alterations of alveolar epithelial cells type II (AEC-II) and pulmonary surfactant protein A (SP-A) levels in the lung tissue of young rats with acute lung injury (ALI) in order to explore the possible mechanism of ALI.

Methods: Forty-eight young Sprague-Dawley rats were randomly divided into control and ALI groups. The rats in the ALI group were intraperitoneally injected with 4 mg/kg of lipopolysaccharide (LPS) in order to induce ALI.

[Changes of pulmonary surfactant protein A in young rats with acute lung injury induced by lipopolysaccharide].

Objective: Pulmonary surfactant protein A (SP-A) plays an important role in the maintenance of pulmonary surfactant function and innative immune defence. This study aimed to explore the changes of SP-A concentration in the lungs of young rats with acute lung injury.

Methods: Sprague-Dawley rats were randomly assigned to control and lung injury groups.

Effects of dexamethasone on the ultrastructure of alveolar type II cells in young rats with lipopolysaccharide-induced acute lung injury.

Objective: Alveolar type II (AT II) cells play a crucial role in the maintenance of pulmonary surfactant homeostasis and pulmonary immunity. The effects of dexamethasone (Dex) on the ultrastructure of AT II cells after acute lung injury remain unknown. This study focused on the ultrastructural changes caused by acute lung injury and on the effects of Dex administration on these ultrastructural changes in young rats.

Effect of dexamethasone on the content of pulmonary surfactant protein D in young rats with acute lung injury induced by lipopolysaccharide.

Objective: Pulmonary surfactant protein-D (SP-D) is regarded as a valuable biomarker in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). This study was to explore the changes of SP-D content in lung tissue following ALI and the effect of dexamethasone (Dex) on the SP-D content in young rats.

Methods: One hundred and forty-four 21-day-old Sprague-Dawley rats were randomly assigned into control, ALI and Dex-treated groups.

[Serum procalcitonin levels in children with bacterial or viral meningitis].

Objective: To investigate the ability of serum procalcitonin (PCT) to differentiate between bacterial and viral meningitis.

Methods: The serum PCT levels were measured in 41 children with acute bacterial (n=18) or viral (n=23) meningitis by immunoluminometric assay. Meanwhile serum CRP levels and erythrocyte sedimentation rate (ESR) were measured.

[Changes of platelet endothelial cell adhesion molecule-1, tissue type plasminogen activator and plasminogen activator inhibitor-1 expression in the lung tissue of neonatal rats after intraperitoneal injection with lipopolysaccharide].

Objective: To further explore the pathogenesis of neonatal acute lung injury and neonatal pulmonary hemorrhage by establishing the animal model of neonatal acute lung injury (ALI) and by investigating the changes of platelet endothelial cell adhesion molecule-1 (PECAM-1), tissue type plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) in ALI.

Methods: Totally 88 neonatal rats which were divided into 8 groups randomly including one normal saline control group and 30 min, 1 h, 2 h, 4 h, 8 h, 16 h and 24 h post injection groups. The changes of lung pathology in newborn rats were observed at different time after LPS was injected intraperitoneally.

[Effect of intrauterine acute ischemic-hypoxia on the expression of lung SP-A and SP-B in neonatal rats].

Objective: Neonatal asphyxia is one of the main causes for the acute respiratory distress syndrome (ARDS) in full-term newborns. Now it is believed that the reduced amount and abnormal function of pulmonary surfactant due to various causes is a major factor leading to acute lung injury. This study aimed at using an intrauterine acute ischemic-hypoxia rat model and investigating the effect of intrauterine acute ischemic-hypoxia on the expression of surfactant protein A (SP-A) and surfactant protein B (SP-B) in neonatal rat lungs.

[Change of neurokinin A plasma level in asthmatic children].

Objective: Chronic inflammation of airway in bronchial asthma is caused by many complicated elements. Recently, a close attention has been paid to the neurogenic inflammation in airway which is mediated by sensory neuropeptides secreted by sensory nerve in the lung. Neurokinin A (NKA) is an important sensory neuropeptide leading to neurogenic inflammation in airway.