Ob jective To research the gene expression profile of aura-absence migraine patients before and after acupuncture of Shaoyang meridian acupoints or non-acupoints. Methods Twenty aura-absence migraine patients were randomly divided into meridian acupoint group and non-acupoint group, 10 cases in each group. Gene chip technology was used to investigate the differences of two sets of gene expression profiles, and reverse transcription-polymerase chain reaction (RT-PCR) was applied for the analysis of partial genes to verify the accuracy of gene chip detection results. Results Seventy-two differentially expressed genes were obtained in meridian acupoint group, and 110 differentially expressed genes were obtained in non-acupoint group. The function genes of meridian acupoint group involved brain endorphin enzyme, adenosine triphosphate ( ATP) synthase, etc., which were closely related with the curing of aura-absence migraine. Non-acupoint group had extensive and scattered function genes involving apoptosis, DNA repair, etc., which had less correlation with the curing of aura-absence migraine. ATPAF2, PTGS2, TOR3A genes of meridian acupoint group and ACP2, AURKA, ARHGEF11, CASP8 gene of non-acupoint group presented by RT-PCR analysis had verified the reliability of microarray data. Conclusion The therapeutic effect of meridian acupoints acupuncture for aura-absence migraine has achieved through the multi-gene action at the molecular level, but the corresponding target genes for the placebo effect of non-acupoint acupuncture have not been found , which demonstrates the existence of meridian effect.

The incidence of pulmonary embolism in children is low, but the mortality rate is high.In children, pulmonary embolism(PE)is characteristically seen in combination with serious underlying medical disorders, most commonly in children with congenital heart disease, central venous catheters, and infection.The clinical manifestations of pulmonary embolism in children are atypical and difficult to distinguish from respiratory infections.Diagnostic test is necessary, especially with the lack of clinical prediction rules.In recent years, CT pulmonary angiography has replaced pulmonary angiography and become the first choice for the diagnosis of pulmonary embolism in children.Because of the lack of large sample studies in children, therapy recommendations are obtained from adult clinical trials and a few smaller pediatric studies.Treatment methods include anticoagulation, thrombolysis and surgical thrombectomy.This article reviews the high-risk factors, diagnosis and treatment of children with pulmonary embolism.

Objective:To explore the clinical characteristics and the therapeutic approach in children with pulmonary embolism(PE).Methods:The clinical data of 8 patients with PE who hospitalized at the Children′s Hospital of Chongqing Medical University from March 2001 to October 2018 were retrospectively analyzed.Results:Among the 8 cases with PE, 3 cases were male and 5 cases were female, the age of subjects ranged from 0.6 to 11.7 years old, the median age was 7.96 years old.All of them had underlying diseases, among them, congenital heart disease with infective endocarditis accounted for 37.5%(3 case). Among the 8 cases, 4 cases presented with symptoms of respiratory tract infection, 7 cases had shortness of breath, 5 cases had cough, 3 cases had chest pain, 2 cases had hemoptysis, and 1 case had typical triad of PE with chest pain, dyspnea and hemoptysis.Among the 8 cases, 7 cases did the arterial blood gas analysis and showed hypoxemia; 6 cases did the D-dimer and the value>500 μg/L; 5 cases did the electroca-rdiogram and 4 cases(80.0%) showed sinus tachycardia, and 2 cases(40.0%) had ST-T changes, all of them did echocardiography and 3 cases(37.5%) of which indicated pulmonary artery excrescence, 7 cases of which did spiral CT pulmonary angiography and 5 cases(71.4%) of them prompted pulmonary vascular filling defects, 6 cases(75.0%) of which were embolized in the lower lobe of the lung.Three cases received anticoagulant therapy, and 1 of them was treated with combined thrombectorny, 1 case of them died.Two cases received thrombectomy, 1 case of them died.Three cases were not treated with thrombectomy and anticoagulation therapy, 2 cases of them died.Conclusions:The mortality of PE in children is high.The clinical manifestations of PE in children are not typical and difficult to distinguish from respiratory infections.For children with high risk factors of PE, once clinical symptoms related to PE occur, D-dimer, echocardiography, and spiral CT pulmonary angiography should be done soon for early diagnosis and treatment.

Objective:To explore clinical features, etiology and mechanism of pulmonary bullae in children.Methods:The clinical data of children with diagnosis or suspected diagnosis of pulmonary bullae, including the general situation, etiology, pathogen composition, number and location, prognosis and so on, in the Inpatient Department of Children′s Hospital of Chongqing Medical University from March 1993 to August 2019 were retrospectively analyzed.Results:Among the 163 patients, there were 130 cases of respiratory tract infection, and 11 cases of pneumothorax alone.Totally, 22 cases were found pulmonary bullae in the chest CT examination without typical symptoms.Etiology: viruses accounted for 19.02%(31/163 cases), with mainly respiratory syncytial virus (9.20%, 15/163 cases); bacterial infection took up 28.83%(47/163 cases), mostly Haemophilus influenzae (13/163 cases, 7.98%) and Staphylococcus aureus (10/163 cases, 6.13%). Pulmonary bullae was more common in the right lung (82 cases). It took 7 days to 9 months for bullae to reduce, shrink or disappear.In some cases, there was no significant change in bullae even after 19 months. Conclusion:Pulmonary bullae can be seen in infection, tumor, auto-immune diseases and so on, most of which are bacterial infections.Bullae may exist for a long time.The mechanism of pulmonary bullae may include the narrowing of lumen, followed by the thickening of bronchial wall, ischemic necrosis and alveolar expansion due to the clogging of distal small vessels or capillaries, the degradation of connective tissue and dissociation of elastic tissue, the destruction of the bronchiolar wall, disturbing ion channels and mitochondria metabolism and destroying the connection of epithelial cells.

Objective:To investigate the clinical characteristics, long-term prognosis and changes of pulmonary function in children with idiopathic pulmonary fibrosis (IPF).Methods:The clinical data, long-term prognosis and changes of pulmonary function of children with IPF admitted to the Department of Pediatric Respiratory Center in Children′s Hospital of Chongqing Medical University from January 2008 to December 2018 were retrospectively analyzed.Results:A total of 28 cases were included, with the median age of 3.9 years (range: 0.5 to 15.7 years). Cough (28 cases, 100.0%), tachypnea (25 cases, 89.3%), cyanosis (19 cases, 67.9%), dyspnea (11 cases, 39.3%), Velcho rales (12 cases, 42.9%), inspiratory three concave sign (11 cases, 39.3%), clubbed fingers and toes (6 cases, 21.4%) and diminished breath sounds (5 cases, 17.9%) were main clinical manifestations.Chest high-resolution computed tomography (HRCT) mainly displayed grid shadow, irregular sac-like light-transparent shadow with ho-neycomb changes and dense shadow, partial (7 cases) pulmonary interstitial emphysema/emphysema/pneumomediastinum.Three cases of lung biopsy showed hyperplasia and consolidation of alveolar space and alveolar septal fibrosis, thickening of alveolar wall and coexistence of new and old lesions.In this group, 4 cases did not receive drug therapy due to other reasons (3 cases abandoned therapy, and 1case died of respiratory and circulatory failure during hospitalization). Twenty-four cases were treated with single or combination of oral Prednisone, N-acetylcysteine and Azithromycin.Eleven cases had improved symptoms when discharged, and 13 cases showed no improvement.Twenty-four cases continued to receive oral medication therapy according to the original protocol.Eight cases were followed up for chest HRCT for 3 months to 4 years, the chest HRCT lesions of 7 cases were similar to before, and those of 1 case increased than before.All cases received telephone follow-up for 2 to 7 years; the maximum duration of medication was 4 years.Twelve cases were lost to follow-up, 7 cases had motion limitation, 3 cases died, and 2 cases had no clinical symptom.Three cases were followed up for pulmonary function for 2 to 3 years, among which 2 cases had pulmonary function decreased than before; 1 case had improvements in forced vital capacity as a percentage of the predicted value and peak expiratory flow as a percentage of the predicted value, but decline in forced expiratory volume in the first se-cond as a percentage of the predicted value.Conclusions:The clinical manifestations of children with IPF are lack of specificity.Chest HRCT is of great value in the diagnosis of IPF and preliminary monitoring of the activity of lesion.In the long-term follow-up, some of cases have improvements in symptoms; pulmonary function mostly decreases, but part of indexes can be improved.

Objective: To investigate the role of neutrophil elastase inhibitor, sivelestat, in preventing and treating nonalcoholic steatohepatitis (NASH) and its underling mechanisms. Methods: A total of forty 4-week-old male C57BL/6J ApoE-/-mice were equally divided into the following four groups: standard chow (SC)+isotonic saline; SC+sivelestat; high-fat, high-cholesterol (HFHC) diet+isotonic saline; and HFHC+sivelestat. These mice were treated with above methods for 12 weeks. Blood and liver tissue samples were collected to measure biochemical parameters, hepatic steatosis and non-alcoholic fatty liver disease (NAFLD) activity score (inflammation) were evaluated by oil red O staining and HE staining, respectively. The mRNA and protein expression levels of hepatic inflammatory cytokines, CD68, and F4/80 were determined by quantitative RT-PCR and immunohistochemistry, respectively. Comparison of means between the four groups was made by one-way analysis of variance, and comparison between any two groups was made by the LSD or SNK method (for data with homogeneity of variance) or the Tamhane or Dunnett method (for data with heterogeneity of variance). Results: Mice fed with an HFHC diet for 12 weeks developed typical pathological features of NASH compared with those fed with SC. Compared with mice fed with HFHC diet without sivelestat, those treated with HFHC and sivelestat exhibited the following features: (1) significantly reduced fast blood glucose, blood cholesterol, and hepatic biochemical parameters, as well as increased insulin sensitivity; (2) significantly reduced NAFLD activity score (5.71±1.11 vs 3.16±1.16, P < 0.05); (3) reduced monocyte chemoattractant protein-1 and tumor necrosis factor -α; (4) significantly reduced mRNA levels of CD68 and F4/80; and (5) reduced expression of CD68 in the liver. Conclusion Sivelestat alleviates the hepatic steatosis and inflammation of NASH in mice by inhibiting the activation of Kupffer cells.