OBJECTIVE: To explore the effect of unidirectional valved patch (UVP) for congenital heart disease (CHD) with severe pulmonary hypertension (PH). METHODS: We retrospectively analyzed the treatment of 37 CHD patients with severe PH by UVP in the operation, and summarized its short-term to mid-term effect to find an optimum therapeutic regimen. RESULTS: Before the operation, the ECG showed that the mean pulmonary artery pressure (MPAP) ranged 65-72 mmHg, and the cardiac catheterization showed the pulmonary artery pressure ranged 80-120 mmHg, P(P)/P(A) ranged 0.8-1.05,PVR ranged 8.5-19.2 (under oxygen inhalation 6.8-14.6) wood unit.After the operation, P(P)/P(A) ranged 0.4-0.72 on weaning-off CPB. Postoperative ECG showed the MPAP ranged 32-48 mmHg. No pulmonary hypertension crisis occurred and no patient died. Mechanical ventilation time ranged from 32 h to 8 d and the SaO₂ ranged 93%-96% at rest after the extubation.The right-to-left shunt situations by ECG were as follows:22 cases had shunt 5 d after the operation, 11 cases had shunt 1 month after the operation,4 cases 3 months after the operation, and none 1 year after the operation but one patient lost follow-up.However,there were no long-term follow-up data: 12 patients had a 1-year follow-up, 5 patients had a 3-year follow-up, and most patients had just 3-month follow-up. CONCLUSION UVP can decrease the operative risk in CHD with severe PH at perioperative period. The short-term to mid-term effect is satisfactory, while long-term effect remains uncertain.
Adolescent ; Cardiac Surgical Procedures ; methods ; Child ; Female ; Heart Defects, Congenital ; complications ; surgery ; Heart Septal Defects, Ventricular ; complications ; surgery ; Humans ; Hypertension, Pulmonary ; etiology ; surgery ; Male ; Pericardium ; transplantation ; Prosthesis Implantation ; Retrospective Studies ; Young Adult

Objective Based on the network pharmacology and animal experiments,to investigate the protective effect and possible molecular mechanism of ethanol extract from Atractylodes lancea on liver function in mice with liver fibrosis induced by bile duct ligation.Methods The main active ingredients atractylodin,atractylenolide Ⅰ,Ⅱ and Ⅱ from Atractylodes lancea were selected,which had been verified by literature and experiments,and the targets of these active ingredients were obtained through the SwissTargetPrediction database.The liver fibrosis disease targets were obtained through On-line Mendelian Inheritance in Man (OMIM),DisGeNET and GeneCards databases.The targets were added to the Wei Sheng Xin platform to find the intersection target for Atractylodes lancea in treating liver fibrosis.Cytoscape 3.10.1 was used to construct the "drug-component-target-disease" network diagram and protein-protein interaction core target network diagram.GO functional enrichment analysis and KEGG pathway analysis were performed,and molecular docking was performed between active components and core targets.Liver fibrosis was induced in mice by bile duct ligation,and liver function markers were measured.Results A total of 91 corresponding targets of atractylodin,atractylenolide Ⅰ,Ⅱ and Ⅲ and 9296 liver fibrosis disease targets were obtained,including 74 intersecting targets and 31 core targets.KEGG enrichment analysis showed that the main signaling pathways involved included inflammatory pathways such as epidermal growth factor receptor (EGFR) and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt).Molecular docking results showed that the active ingredients had strong binding activity with the core target protein.The results of animal experiments showed that,compared with the sham surgery group,the model group displayed notable,the liver index,spleen index,activity of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST),degree of liver fibrosis,mRNA and protein expression of α-smooth muscle actin (α-SMA) and recombinant collagen type Ⅰ alpha 1 (COL1A1),and mRNA of recombinant collagen type Ⅳ alpha 2 (COL4A2) were significantly increased,and the thymus index was sigficantly decreased (P<0.05);compared with the model group,the liver injury of mice in the Atractylodes lancea administration group reduced liver injury,its liver index,spleen index,activity of serum ALT and AST,degree of liver fibrosis,mRNA and protein expression of α-SMA and COL1A1,and mRNA of COL4A2 were significantly decreased,and the thymus index was sigficantly increased (P<0.05).Conclusion Atractylodes lancea can improve liver function and alleviate tissue pathological damage in mice with liver fibrosis,which may be related to activating pathways such as PI3K/Akt,inhibiting oxidative stress and inflammatory reactions,and intervening in liver fibrosis.

ObjectiveTo investigate the efficacy and mechanism of berberine hydrochloride （BBH） against lung cancer cells through the mevalonate （MVA） pathway. MethodHuman lung cancer A549 cells and mouse Lewis lung carcinoma （LLC） cells were used as research subjects. Cell proliferation and cell counting kit-8 （CCK-8） assay were performed to detect the inhibitory effect of BBH （10， 20， 30， 40， 50 μmol·L^-1） on the proliferation of the two kinds of cells （48 h）. Then cell scratch assay was used to explore the influence of BBH （40 μmol·L^-1） on the migration of A549 and LLC cells （24， 48 h）， and colony formation assay was conducted to compare the colony formation ability of the cells under different concentrations of BBH （10， 20， 40 μmol·L^-1）. Moreover， the effects of BBH （40 μmol·L^-1） on the content of acetyl-coenzyme A （A-CoA） and total cholesterol （TC） in A549 and LLC cells were determined by kit assay. AutoDock Vina was used for the dock of BBH and MVA pathway regulatory protein， sterol regulatory element-binding protein 2 （SREBP2）. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to observe the effects of BBH （40 μmol·L^-1） on the mRNA expression of nine genes related to the MVA pathway in A549 and LLC cells： hydroxymethylglutaryl-CoA synthase 1 （HMGCS1）， hydroxymethylglutaryl-CoA Reductase （HMGCR）， mevalonate kinase （MVK）， phosphomevalonate kinase （PMVK）， mevalonate 5-pyrophosphate decarboxylase （MVD）， farnesyl diphosphate synthase （FDPS）， squalene epoxidase （SQLE）， farnesyl-diphosphate farnesyltransferase 1 （FDFT1）， and geranylgeranyl diphosphate synthase 1 （GGPS1）. Western blot was performed to clarify the effects of BBH （40 μmol·L^-1） on the expression of three key proteins of the MVA pathway： HMGCS1， HMGCR， and FDFT1. The Cancer Genome Atlas （TCGA） database was searched to analyze the relationship between HMGCS1， HMGCR， FDFT1 and transcription gene SREBF2 in non-small cell lung cancer （NSCLC）. ResultCompared with the conditions in the control group， the proliferation， migration， and colony formation of A549 and LLC cells in the BBH group were decreased （P<0.01）， while the cell apoptosis rate was increased （P<0.01）. Molecular docking showed that BBH had good binding activity with SREBP2. In addition， the content of A-CoA and TC of the MVA pathway was reduced （P<0.01）. BBH down-regulated the mRNA expression of HMGCS1， HMGCR， MVK， PMVK， MVD， FDPS， SQLE， FDFT1， and GGPS1 in A549 and LLC cells （P<0.01）， and lowered the levels of HMGCS1， HMGCR， and FDFT1 proteins （P<0.05， P<0.01）. In NSCLC patients， HMGCS1， HMGCR， and FDFT1 were highly correlated with SREBF2 （R=0.54， R=0.57， and R=0.48）. ConclusionBBH can inhibit the proliferation， migration， and colony formation of A549 and LLC cells and promote cell apoptosis， which may be related to the regulation of MVA pathway by BBH binding to SREBP2.

According to the pathological characteristics of symptomatic chronic thoracic and lumbar osteoporotic vertebral fracture (SCOVF), the different clinical treatment methods are selected, including vertebral augmentation, anterior-posterior fixation and fusion, posterior decompression fixation and fusion, and posterior correction osteotomy. However, there is still a lack of a unified understanding on how to choose appropriate treatment method for SCOVF. In order to reflect the new treatment concept and the evidence-based medicine progress of SCOVF in a timely manner and standardize its treatment, the clinical guideline for surgical treatment of SCOVF is formulated in compliance with the principle of scientificity, practicability and advancement and based on the level of evidence-based medicine.