Extracorporeal membrane oxygenation (ECMO) could pump the blood from human veins to the outside of the body, oxygenate the red blood cells in an artificial environment and then return them back into the body. ECMO could replace the heart and lungs to complete gas exchange and systemic blood perfusion in patients with severe cardiopulmonary insufficiency, which also plays an important role in the field of heart transplantation. Besides circulatory support treatment after heart transplantation, ECMO may also be used to prolong the waiting time for heart transplantation in patients with respiratory and circulatory failure before operation, as a bridging therapy for heart transplantation. However, at present, the application of ECMO in pediatric heart transplantation still exist challenges, such as high perioperative mortality and difficulty in determining the timing of treatment, etc. In this article, the development history of ECMO application in pediatric heart transplantation, use of ECMO before and after pediatric heart transplantation, ECMO-related complications in children, and application of ventricular assist device (VAD) in pediatric heart transplantation were briefly reviewed, aiming to provide reference for promoting the application of ECMO in pediatric heart transplantation.

Central venous stenosis is a common complication following long-term dialysis catheter placement in dialysis patients. Generally, percutaneous angioplasty is the treatment of choice, and venous stent implantation should be considered in different situations. However, the venous stent migrating into right atrium is a rare but fatal complication. We presented a patient whose superior vena cava stents migrated into right atrium, resulting in acute tamponade, and exploratory thoracotomy was proceeded.

Atrial fibrillation is a common arrhythmia associated with high mortality and morbidity, and the current treatment of atrial fibrillation is still limited. Histone deacetylase (HDAC) plays an important role in the pathophysiology of cardiovascular disease and promotes the occurrence of atrial fibrillation. Inhibition of HDAC may be a new therapeutic strategy through the regulation of atrial remodeling. Therefore, we reviewed the research progress of the HDAC and atrial fibrillation.

Objective To assess the safety of the removal of pericardial and mediastinal drain within different drainage volume after cardiac valvular replacement surgery. Methods Between July 2013 and July 2017, 201 patients with rheumatic heart disease (CHD) were treated with valve replacement in our hospital, including 57 males and 144 females, aged 15 to 72 years. They were divided into two groups according to the amount of 24-h drainage before the drain removal: a group one with 24-h drainage volume≤50 ml (n=127) and a group two with 24-h drainage volume>50 ml (n=74). The postoperative hospital stay and the incidence of severe complications between the two groups were compared. Results There was no difference between the two groups in the baseline information or the incidence of severe pericardial effusion and tamponade, while the group two tended to have a shorter length of hospital stay after surgery (8.0 dvs.7.5 d, P=0.013). Conclusion In CHD patients undergoing valvular surgery, compared with a relatively low amount of drainage before the drain removal, drawing the tube at a greater amount of drainage (24-h drainage volume>50 ml) will shorten the length of hospital stay after cardiac surgery while incidence of severe complications remains the same.

Objective: To investigate the effects of Casein kinase 2-interacting protein 1 (CKIP-1) gene silencing on the proliferation of glioma cells U87-MG. Methods: The recombinant lentiviral vectors targeting CKIP-1 gene or negative control were constructed and then used to infect glioma U87-MG cell line.The effects of knock-down on the mRNA or protein expression of CKIP-1 were evaluated by real-time qPCR and western blotting.Cell cycle was detected by the flow cytometry assay, and cell proliferation changes were evaluated by cell counting, MTT, and BrdU assay, respectively.Lastly, the colony formation was used to investigate the effect of CKIP-1 knock-down on the clone formation. Results: Compared with the group of Ctrl, CKIP-1 siRNA was observed to significantly inhibit CKIP-1 expression at the mRNA levels (Ctrl (1.01±0.13) vs CKIP-1 siRNA (0.23±0.02), P<0.01) and protein levels in the U87-MG cells.Also, CKIP-1 suppression mediated by RNAi decreased the ratio of G0/G1 phase (Ctrl (69.64±0.79) vs CKIP-1 siRNA(62.64±0.66), P<0.01), increased that of G2/M phase (Ctrl (8.36±0.52) vs CKIP-1 siRNA(13.87±2.90), P<0.05), and significantly inhibited the cell proliferation and clone formation (Colony number: Ctrl (25±2) vs CKIP-1 siRNA(2±1), P<0.05) of transfected U87-MG cells. Conclusion Knocking down the expression of CKIP-1 significantly inhibit cell proliferation in human U87-MG glioma cells, indicating that CKIP-1 is involved in the development of gliomas and could promote the cell proliferation.

Objective To explore the effects of different doses of dexmedetomidine on acute brain edema in mice with traumatic brain injury (TBI).Methods A total of 132 male C57BL/6J mice were randomly divided into six groups:control group (group C),sham-operation group (group Sham),traumatic brain injury group (group TBI),Dex 20 μg/kg (group D20),40 μg/kg (group D40),and 60 μg/kg (group D60),n=22 in each group.The TBI animal model was established by electric controlled cortical impactor (eCCI),then intraperitoneal injected by the administration of different doses of dexmedetomidine at 0,2 and 4 h after TBI.Twenty-four hours post-TBI,brain water content was measured by the dry-wet method,histological observation was performed using HE staining,and aquaporin 4 (AQP4) and NF-κB expression were detected using Western blot assay,respectively.Then,the modified neurological scale scores (mNSS) on 1,2,3,and 7 d and Morris water maze (MWM) test on 4,5,6 and 7 d post-TBI were used to evaluate the neurologic deficit of TBI mice.Results After traumatic brain injury,the mNSS scores,the escape latency,the brain water content and the expression of AQP4 and NF-κB increased significantly in group TBI (P＜0.01).Different doses of dexmedetomidine significantly reduced the mNSS scores,the escape latency,the brain water content and the expression of AQP4 and NF-κB (P ＜ 0.05 or P ＜ 0.01).And meanwhile dexrnedetomidine can lessen neuronal degeneration,and inflammation response.Additionally,the effect was remarkably in group D60 compared with group D20 (P ＜ 0.05 or P ＜ 0.01).Conclusion Dexmedetomidine can lessen brain edema and cognition impairment induced with traumatic brain injury,which is a dose-effect relationship within 20-60 μg/kg,and this effect may be related to the downregulation of AQP4 and NF-κB expression.

Objective To screen altered proteins of hippocampus in the stress-induced depression (STRID) rat model, and explore the potential molecular mechanism. Methods Twenty Sprague-Dawley rats were randomly divided into the control group and STRID group, 10 rats in each group. Chronic unpredictable mild stress (CUMS) methods including fasting for solids and liquids, electric foot-shock, reversing day and night, cold water swimming, cage tilt, scare stimulation and tail pinch were conducted on STRID rats with no repeats for 28 days to make up the depression animal model. The control group was normally fed during this period. After the stress stimulation, the hippocampus protein samples were used for two dimensional electrophoresis to screen the differentially expressed protein, and then mass spectrum identification and function analyze were conducted. Results Compared with the control group, 34 proteins were altered in STRID group. Among which, 18 were up-regulated, and 16 were down-regulated. The differentially expressed proteins mainly located in cytoplasm, mitochondrion, extracellular exosome and myelin sheath. The involved signaling pathways included metabolic pathway, oxidative phosphorylation pathway, and Alzheimer's disease, Parkinson's disease and Huntington's disease pathways. Conclusion The altered proteins and dysfunction of nerve signaling, and the excess of oxidative phosphorylation in hippocampus of STRID rats may be one of the pathogenesises.

Objective To explore the effect and mechanism of necroptosis related proteins in middle cerebral artery occlusion (MCAO) induced brain ischemia/reperfusion injury in mice.Methods C57BL/6 mice were used to establish the brain ischemia/reperfusion injury model induced by MCAO.MCAO mice were treated with z-VAD.fmk (zVAD,1.1 g/kg),GSK'872 (0.7 g/kg) and combined intervention of zVAD and GSK'872,and neurological defect was evaluated by mNSS while brain infarct volume was measured by TTC staining.Western blot and immunofluorescence assay were used to detect protein expression and location of RIP1,RIP3 and MLKL,respectively.Results Neurological defect and brain infarction were caused by MCAO.Compared with MCAO group,zVAD,GSK'872 and the combined intervention alleviated neurological defect and reduced brain infarct volume significantly (P＜0.05 or P＜0.01).The protein levels of RIP3 and RIP1 MLKL were increased in mice of MCAO group,while GSK'872 and the combined intervention obviously downregulated the aforementioned protein expression [RIP1 (GSK'872:0.64± 0.02 vs MCAO:1.28±0.02,P＜0.01);RIP3 (GSK'872:1.08±0.02 vs MCAO:1.45±0.02,P＜0.01);MLKL (GSK'872:0.54±0.01 vs MCAO:1.00±0.01,P＜0.01)].However,zVAD only slightly reduced protein expression of MLKL (P＜0.05) but didn't change the protein expression of RIP1 and RIP3 (P＞0.05).Conclusion RIP1,RIP3 and MLKL are involved in the execution of necroptosis and contribute to the pathological progress of brain ischemia/reperfusion injury.

Objective To investigate the signaling pathway and the key signal molecules of protein kinase (RIPK)3 in SH-SY5Y cells. Methods SH-SY5Y cells were transfected with RIPK3 expression plasmid vector to upregulate intracellular RIPK3, while the SH-SY5Y cells were transfected with empty vector plasmid, which was considered as control group. Western blot assay was used to check the expression of exogenous RIPK3 in cells. The proliferation rate of SH-SY5Y cells was determined by MTT assay at designated time to detect exogenous RIPK3 activity. Whole transcriptome sequencing (RNAseq) was used to detect the transcription of genes. Whole-transcriptomic gene transcription was measured by following Ingenuity Pathway Analysis (IPA) to obtain downstream signaling pathways and the key molecule, which were partly confirmed by following droplet digital PCR (ddPCR). Results Exogenous RIPK3 showed biological activity in SH-SY5Y, which inhibited the proliferation of cells. IPA showed that znic finger protein 36 (ZFP36) was significantly up-regulated as compared with that of the control group. The tran?scription levels of ZFP36 downstream genes such as tumor necrosis factor (TNF), brain derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF) and mRNA-decapping enzyme 2 (DCP2) were affected at the same time. Conclusion Within the limitations of this study, it seems that RIPK3 is notable for the development, inflammation and tumorigenesis of the nervous system as an independent regulator of ZFP36 gene and downstream effectors.

We evaluated the differential expression and function of chitinase 3‐like‐1 in macrophage stimulated by Sporothrix schenckii and Candida albicans fungicidal ability of macrophage after stimulation with Sporothrix schenckii and Candida albi‐cans separately was detected .The expression of CHI3L1 gene in macrophage stimulated by Sporothrix Schenckii and Candida albicans was evaluated with real‐time PCR .The function of CHI3L1 protein in macrophages against the reproduction of Sporo‐thrix schenckii and Candida albicans was detected in vitro .Results showed that macrophages could engulf and kill Sporothrix Schenckii and Candida albicans in vitro .The expression of CHI3L1 gene in macrophage stimulated by Candida albicans was increased obviously .At the same time ,CHI3L1 protein can damper the reproduction of Candida albicans .However ,the ex‐pression of CHI3L1 gene was not elevated when macrophage was stimulated by Sporothrix schenckii and CHI3L1 protein played little role in reproduction of Sporothrix schenckii .The expression of CHI3L1 gene in macrophage was elevated after stimulation with Candida albicans ,but was not elevated with Sporothrix Schenckii .In correspondence with differential ex‐pression ,CHI3L1 in macrophages could impair the reproduction of Candida albicans but had a weak function on Sporothrix schenckii which might contribute to the pathogenesis of spo‐rotricosis .