Background Data regarding the safety and efficacy of balloon expandable valves (BEVs) for transcatheter aortic valve replacement (TAVR) in patients with Sievers type 0 bicuspid aortic valve (BAV) stenosis remain limited. Aims This study aims to evaluate the clinical outcomes of BEVs implantation in patients with Sievers type 0 BAV. Methods We conducted a multicenter, retrospective study across 28 centers in China between October 2020 and March 2023. Consecutive patients with Sievers type 0 BAV anatomy undergoing TAVR with the Edwards Sapien 3 BEV were enrolled. Results The study included 131 patients with Sievers type 0 BAV (mean age 69.8 ± 7.5 years; 52.7 % male). The lateral-lateral type predominated (86.3 %). Calcification distribution analysis identified the superior leaflet margin as the most primary site (62.6 %). All procedures utilized femoral artery access. High implantation depth (The ratio of the aortic side of the prosthetic valve to the outflow tract side is > 8:2) was achieved in 80.2 % of cases. Prosthetic valves smaller than 26 mm were implanted in nearly half of the patients (49.6 %). The 30-day all-cause mortality rate was 0.8 %, with no incidence of disabling stroke. The overall technical success rate was 98.5 %. Conclusion The findings of this study demonstrate that BEVs implantation in patients with Sievers type 0 BAV is associated with favorable safety and efficacy outcomes. These results provide valuable insights for current TAVR practice in this specific patient population.

Objective:Long noncoding RNAs (lncRNAs), including some members of small nucleolar RNA host gene (SNHG), are important regulators in myocardial injury, while the role of SNHG4 in myocardial infarction (MI) is rarely known. This study is aimed at exploring the regulatory role and mechanisms of SNHG4 on MI.Methods:Cellular and rat models of MI were established. The expression of relating genes was measured by qRT-PCR and/or western blot. In vitro, cell viability was detected by MTT assay, and cell apoptosis was assessed by caspase-3 level, Bax/Bcl-2 expression, and/or flow cytometry. The inflammation was evaluated by TNF-α, IL-1β, and IL-6 levels. The myocardial injury in MI rats was evaluated by echocardiography, TTC/HE/MASSON/TUNEL staining, and immunohistochemistry (Ki67). DLR assay was performed to confirm the target relationships.Results:SNHG4 was downregulated in hypoxia-induced H9c2 cells and MI rats, and its overexpression enhanced cell viability and inhibited cell apoptosis and inflammation both in vitro and in vivo. SNHG4 overexpression also decreased infarct and fibrosis areas, relieved pathological changes, and improved heart function in MI rats. In addition, miR-148b-3p was an action target of SNHG4, and its silencing exhibited consistent results with SNHG4 overexpression in vitro. DUSP1 was a target of miR-148b-3p, which inhibited the apoptosis of hypoxia-induced H9c2 cells. Both miR-148b-3p overexpression and DUSP1 silencing weakened the effects of SNHG4 overexpression on protecting H9c2 cells against hypoxia.Conclusions:Overexpression of SNHG4 relieved MI through regulating miR-148b-3p/DUSP1, providing potential therapeutic targets.

[This retracts the article doi: 10.1590/1414-431X20186555].

ABSTRACT:Cyanotic congenital heart disease (CCHD) is the main cause of death in infants worldwide. Long noncoding RNAs (lncRNAs) have been pointed to exert crucial roles in development of CHD. The current research is designed to illuminate the impact and potential mechanism of lncRNA SNHG14 in CCHD in vitro. The embryonic rat ventricular myocardial cells (H9c2 cells) were exposed to hypoxia to establish the model of CCHD in vitro. Quantitative real-time polymerase chain reaction was conducted to examine relative expressions of SNHG14, miR-25-3p, and KLF4. Cell viability was determined by the MTT assay. Lactate dehydrogenase (LDH) was measured by an LDH assay kit. Apoptosis-related proteins (Bax and Bcl-2) and KLF4 were detected by Western Blot. The targets of SNHG14 and miR-25-3p were verified by the dual-luciferase reporter assay. SNHG14 and KLF4 were upregulated, whereas miR-25-3p was downregulated in hypoxia-induced H9c2 cells and cardiac tissues of patients with CCHD compared with their controls. Knockdown of SNHG14 or overexpression of miR-25-3p facilitated cell viability, while depressing cell apoptosis and release of LDH in hypoxia-induced H9c2 cells. MiR-25-3p was a target of SNHG14 and inversely modulated by SNHG14. MiR-25-3p could directly target KLF4 and negatively regulate expression of KLF4. Repression of miR-25-3p or overexpression of KLF4 reversed the suppression impacts of sh-SNHG14 on cell apoptosis and release of LDH as well as the promotion impact of sh-SNHG14 on cell viability in hypoxia-induced H9c2 cells. Sh-SNHG14 protected H9c2 cells against hypoxia-induced injury by modulating miR-25-3p/KLF4 axis in vitro.

BACKGROUND:Hypoxia/reoxygenation (H/R)-mediated apoptosis and inflammation are major causes of tissue injury in acute myocardial infarction (AMI). Exploring the underlying mechanisms of cardiomyocyte injury induced by H/R is important for AMI treatment. Circular RNAs have been demonstrated to paly vital roles in the pathogenesis of AMI. Our study aimed to explore the function of circular RNA UBXN7 (circUBXN7) in regulating H/R-induced cardiomyocyte injury.METHODS:H/R-treated H9c2 cells and a mouse model of AMI were used to investigate the function of circUBXN7 in H/R damage and AMI. The expressions of circUNXN7, miR-622 and MCL1 were analyzed by RT-qPCR. CCK-8 was used for examining cell viability. Cell apoptosis was evaluated with caspase 3 activity and Annexin V/PI staining. MCL1, Bax, Bcl-2 and cleaved-caspase 3 were examined with western blot. ELISA was used to examine the secretion of IL-6, TNF-α and IL-1β.RESULTS:CircUBXN7 was downregulated in patients and mice with AMI, as well as in H/R-treated cells. Overexpression of circUBXN7 mitigated H/R-mediated apoptosis and secretion of inflammatory factors including IL-6, TNF-α and IL-1β. CircUBXN7 suppressed cell apoptosis and inflammatory reaction induced by H/R via targeting miR-622. MiR-622 targeted MCL1 to restrain its expression in H9c2 cells. Knockdown of MCL1 abrogated circUBXN7-mediated alleviation of apoptosis and inflammation after H/R treatment.CONCLUSION:CircUBXN7 mitigates cardiomyocyte apoptosis and inflammatory reaction in H/R injury by targeting miR-622 and maintaining MCL1 expression. Our study provides novel potential therapeutic targets for AMI treatment.

Oxidized low-density lipoprotein (ox-LDL)- induced endothelial insults plays an important role in the pathogenesis of atherosclerosis. Donepezil is a well-known acetylcholinesterase inhibitor, with its primary application being the treatment of Alzheimer's disease. More recently, there has been increased interest in donepezil as an anti-atherosclerosis treatment as it possesses a host of relevant and potentially beneficial properties. In the present study, we found that donepezil could reduce the expression of lectin-type oxidized low-density lipoprotein receptor-1 (LOX-1)in human aortic endothelial cells (HAECs). We found that donepezil could suppress the expression of intercellular adhesion molecule-1 (ICAM-1), which recruits monocytes to adhere to the endothelium, by more than half. Another key finding of our study is that donepezil could reduce the expression of tumor necrosis factor receptor-α (TNF-α) and interleukin-6 (IL-6) by more than half at both the mRNA and protein transcriptional levels. Donepezil also reduced the expression of tissue factor (TF), which is considerably upregulated in atherosclerotic lesions, by more than half. Finally, we turned our attention to the early growth response protein-1 (Egr-1) for its potential role in mediating the effects of donepezil. Through our Egr-1 overexpression experiment, we found that overexpression of Egr-1 almost completely abolished the effects of donepezil described above. Thus, the effects of donepezil are likely mediated through downregulation of Egr-1. These findings provide evidence that donepezil may exert protective effects against atherosclerosis.

Previous studies have shown that phosphatase and tensin homolog (PTEN) are key regulators of the development of many malignant tumors and other diseases. However, its regulatory effect on coronary heart disease (CHD) has rarely been reported. Therefore, the regulatory effect of PTEN on the survival and cell death of vascular smooth muscle cells (VSMCs) in CHD mice was elucidated in this study. It was found that the protein and messenger RNA expressions of PTEN in VSMCs of 10 CHD mice were lower than those of normal mice. Then PTEN was overexpressed in VSMCs. It was suggested that the upregulation of PTEN was not conducive to the proliferation and survival of VSMCs in the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and colony formation assay. The flow cytometry (Annexin V-Fluorescein isothiocyanate (FITC)/propidium iodide) and the terminal deoxynucleotidyl transferase dUTP nick end labeling assay were used to detect the apoptotic rate of overexpressing PTEN cells. Some data showed that the expression of PTEN could lead to increased apoptotic rate. It was shown that antiapoptotic Bcl-2 levels were decreased, but cleaved caspase-3 and proapoptotic Bax levels were promoted by SIRT6 overexpression in Western blot analysis. Moreover, PI3K/Akt expression and phosphorylation were significantly decreased in cells expressing PTEN. Recovery of PI3K expression inhibited the suppressive influence of PTEN on VSMC survival, as evidenced by the activated PI3K/Akt pathway, increased cell proliferative rate, reduced the apoptotic level, and reversed expression patterns of Bcl-2 and Bax. Therefore, the findings in this study provide a new idea on the occurrence and development mechanism of CHD and may promote the discovery of innovative therapies.

microRNAs are an emerging class of molecules that regulate pathogenesis of cardiovascular diseases. Here we aim to elucidate the effects and mechanism of miR-135a, a previously reported regulator of ischemia-reperfusion (I/R) injury, in myocardial I/R injury. Quantitative real-time polymerase chain reaction analysis revealed that the expression level of miR-135a was significantly decreased both in the rat I/R group and H9c2 cells subjected to hypoxia/reoxygenation. Overexpression of miR-135a in vivo markedly decreased the infarct size and inhibited the I/R-induced cardiomyocyte apoptosis. Overexpression of miR-135a in H9c2 also exerted antiapoptosis effects. Furthermore, bioinformatics analysis, luciferase activity, and the Western blot assay indicated that protein tyrosine phosphatase 1B (PTP1B) is a direct target of miR-135a. In addition, the expression of proapoptotic-related genes, such as p53, Bax, and cleaved caspase3, were decreased in association with the downregulation of PTP1B. In summary, this study demonstrates that miR-135a exerts protective effects against myocardial I/R injury by targeting PTP1B.

Objective To investigate the protective mechanism of overexpression of ilent information regulator 1 (SIRT1) on myocardium in mice undergoing cardiac transplantation.Methods Thirty BALB/c mice were randomly divided into control group and experimental group.The experimental group mice were injected with SIRT1-Flag adeno-associated virus specifically expressed in myocardium via tail vein,while the control group mice were injected with SIRT1-Flag adeno-associated virus via tail vein.After 4 weeks of expression,heterotopic heart transplantation was performed with Cuff vascular anastomosis using mouse hearts as donors and C57BL/6 as receptors.The survival rate of transplanted heart was observed.The levels of inflammatory factors in peripheral blood of recipient mice were analyzed by enzyme linked immunosorbent assay (ELISA).The levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in peripheral blood were measured by biochemical reaction.The apoptotic level of cardiomyocyte was analyzed by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL).The expression of apoptotic protein in cardiomyocyte was analyzed by Western blotting.Results Compared with the control group,the heart survival time of the experimental group was significantly increased (12.46 ± 3.14) days (P ＜0.05).Compared with the control group,interleukin (IL)-1β,IL-6 and tumor necrosis factor-α (TNF-α) in peripheral blood [(189.10 ± 15.39),(209.44 ± 10.98),(59.21 ± 9.90) mmol/L],IL-1β,IL-6 and TNF-α [(55.12± 11.32),(41.32 ±9.21),(29.44± 7.80) mmo]/L] in the experimental group were significantly down-regulated (P ＜ 0.05).Compared with the control group,SOD and MDA levels in peripheral blood [(6.19 ± 1.20) (3.44 ±0.76) mmol/L],SOD (3.09 ± 0.89) U/m1 in peripheral blood of mice in the experimental group significantly increased and MDA (2.01 ± 0.45) μmol/L in peripheral blood of mice in the experimental group significantly decreased (P ＜ 0.05).Compared with the control group,the myocardial apoptotic index of the experimental group was significantly decreased (P ＜ 0.05).Compared with the expression levels of cysteinyl aspartate-specific protease-3 (Caspase-3) and B cell lymphoma/leukemia-2 (bcl-2) in the control group,the expression of Caspase-3 in the myocardium of the experimental group was significantly down-regulated,while the expression of bcl-2 was significantly up-regulated (P ＜ 0.05).Conclusion Overexpression of SIRT1 in myocardial tissue can significantly reduce the levels of inflammation,oxidative stress and apoptosis of transplanted heart,and prolong the survival time of transplanted heart.

BackgroundMyocardial infarction (MI) is a common cardiovascular disease caused by myocardial ischemia. Also, microRNA (miRNA) participates in the pathophysiology of many cardiovascular diseases, which can affect stem cell transplantation in the treatment of MI. In this study, our aim is to explore effect of miR-26b on inflammatory response and myocardial remodeling through the MAPK pathway by targeting PTGS2 in mice with MI.MethodsMicroarray data analysis was conducted to screen MI-related differentially expressed gens (DEGs). Relationship between miR-26b and PTGS2 was testified. Cardiac function, inflammatory reaction, infarct size, and myocardial fibrosis were observed. The miR-26b expression and mRNA and protein levels of, PTGS2, ERK, JNK and p38 and Bcl-2/Bax were examined. The effect of miR-26b on cell apoptosis was also analyzed.ResultsMiR-26b was predicted to target PTGS2 further to mediate the MAPK pathway, thus affecting MI. MiR-26b negatively targeted PTGS2. MI mice showed decreased cardiac function, as well as increased inflammatory reaction, myocardial injury, area of fibrosis and myocardial cell apoptosis. After injection of miR-26b agomir or NS-398 (PTGS2 inhibitor), inflammatory response of MI mice was attenuated and myocardial remodeling induced by MI was alleviated.ConclusionThese findings indicate that miR-26b inhibits PTGS2 to activate the MAPK pathway, so as to reduce inflammatory response and improve myocardial remodeling in mice with MI.

OBJECTIVES Recent reports indicated that percutaneous coronary intervention (PCI) may be correlated with increased mortality in patients undergoing transcatheter aortic valve implantation (TAVI). Therefore, we performed a meta-analysis to determine the feasibility and safety of combined PCI in high-risk patients with severe aortic stenosis undergoing TAVI. METHODS A comprehensive literature search was performed using PubMed, Embase and the Cochrane Central Register of Controlled trials through June 2016. RESULTS Five clinical trials including 1634 patients were identified. The pooled analysis revealed no significant differences in 30-day all-cause mortality [odds ratio (OR) 1.25, 95% confidence interval (CI) 0.52-3.05; P = 0.62], 30-day cardiovascular mortality rate (OR 1.59, 95% CI 0.52-4.88; P = 0.41) and 1-year mortality rate (OR 1.16, 95% CI 0.85-1.59; P = 0.34) among the patients assigned to TAVI and those undergoing TAVI+PCI. The incidence of myocardial infarction (OR 2.96, 95% CI 1.03-8.45; P = 0.04) was slightly higher in the TAVI+PCI group. Other complications, such as stroke, kidney injury, bleeding and vascular complications, were not significantly increased in the TAVI+PCI group. Patients treated with a staged procedure of TAVI and PCI but not simultaneous TAVI+PCI showed higher 30-day all-cause mortality as compared to those undergoing isolated TAVI. CONCLUSIONS Combined TAVI+PCI showed similar rates of death from any cause at 30 days and 1 year as compared to isolated TAVI. Except for myocardial infarction, the rate of operative complications in the TAVI+PCI group was not detrimental as compared to the isolated TAVI group. The simultaneous treatment of significant coronary artery lesions may be preferred in selected patients undergoing TAVI.

Objective To investigate the change of autophagy level after cardiac ransplantation in mice and its relationship with immune exclusion.Methods BALB/c was used as donor,C57BL/6 as receptor and Cuff vascular anastomosis to carry out heterotopic heart transplantation in the neck of mice.At 4 and 8 days after transplantation,autophagy related gene p62 was analyzed by Western blot to detect the changes of autophagy in the heart of transplanted mice;enzyme linked immunosorbent assay (ELISA) was used to analyze the expression level of interferon (IFN)-γ and interleukin (IL)-17.After the treatment of rapamycin,the autophagy level,the survival time and the cytokine level were analyzed in the control group and the experimental group.Results Compared with the normal donor heart (1.23 ± 0.31),the level of autophagic protein p62 (0.43 ± 0.18) of donor heart after fourth days in transplantation significantly reduced (t =2.198,P =0.010),and the p62 level of autophagic protein (1.19 ±0.29) after fourth days in transplantation was not statistically significant (t =0.194,P =0.291).Compared with IFN-γ and IL-17 in normal mice,IFN-γ and IL-17 in the recipient mice significantly reduced in fourth days after transplantation (t =3.127,P =0.000;t =4.015,P =0.000).The level of IFN-γ and IL-17 in the sera of the recipient mice eighth days after transplantation significantly enhanced than that of IFN-γ and IL-17 in normal mice (t =4.192,P =0.000;t =5.091,P =0.000).The p62 level of donor heart was significantly lower than that of the control group after treatment (t =5.921,P =0.000,t =6.994,P =0.000).The survival time of the heart in the experimental group after treatment (11.5 days) was significantly longer than that of the control group (LogRank =3.129,P =0.010).The level of IFN-γ and IL-17 in the serum of the experimental group fourth and eighth days after transplantation was significantly lower than that of the control group (t =5.109,P =0.000;t =5.409,P =0.000 and t =7.098,P =0.000;t =6.153,P =0.000).Conclusion Autophagy can reduce immune rejection in cardiac allograft mice and improve the survival of transplanted heart.

Cardiac rupture and ventricular remodeling are recognized as the severe complications and major risk factors of acute myocardial infarction (AMI). This study aims to evaluate the regulatory roles of interleukin-1 receptor-associated kinase 3 (IRAK3) and nuclear factor-κB (NF-κB) signaling pathway in cardiac rupture and ventricular remodeling. Microarray analysis was performed to screen AMI-related differentially expressed genes and IRAK3 was identified. The models of AMI were established in male C57BL/6 mice to investigate the functional role of IRAK3. Afterwards, lentivirus recombinant plasmid si-IRAK3 was constructed for IRAK3 silencing. Next, cardiac function parameters were measured in response to IRAK3 silencing. The regulatory effects that IRAK3 had on myocardial infarct size and the content of myocardial interstitial collagen were analyzed. The regulation of IRAK3 silencing on the NF-κB signaling pathway was further assayed. The obtained results indicated that highly expressed IRAK3 and activated NF-κB signaling pathway were observed in myocardial tissues of mouse models of AMI, accompanied by increased expression of matrix metalloproteinase (MMP)-2/9 and tissue inhibitor of metalloproteinase 2 (TIMP-2). Notably, IRAK3 gene silencing inhibited the activation of NF-κB signaling pathway. Furthermore, IRAK3 gene silencing led to the decreased thickness of infarct area and collagen content of myocardial interstitium, alleviated diastolic, and systolic dysfunctions, as well as, facilitated cardiac functions in mice with AMI, corresponding to decreased expression of MMP-2/9 expression and increased expression of TIMP-2. Taken together, silencing of IRAK3 inactivates the NF-κB signaling pathway, and thereby impeding the cardiac rupture and ventricular remodeling, which eventually prevents AMI progression.

This study aims to evaluate the effectiveness and tolerability of esomeprazole and omeprazole in patients with gastroesophageal reflux disease (GERD). Electronic searches on PubMed, EMBASE, the Cochrane Library, and ClinicalTrials.gov databases were carried out for reports up to February 28, 2015. Ten eligible studies from 8 articles were found that enrolled a total of 10,286 patients for meta-analysis. These results revealed a significant difference between esomeprazole vs. omeprazole (RR=1.06, 95% CI [1.01, 1.10], I2=72%, p=0.01) by subgroup according to dosage by random effects model, and a significant difference between esomeprazole 40 mg vs. omeprazole 20 mg (RR=1.07, 95% CI [1.004, 1.14], I2=78%, p=0.04) based on healing rate as determined by endoscopy, using a random effects model. A significant difference between esomeprazole 20 mg and omeprazole 40 mg (RR=0.68, 95% CI [0.47, 0.97], I2=not applicable, p=0.03) was also found in comparing relief of symptoms by random effects model. There were no significant differences in outcomes between other subgroups, including tolerability. Based on these results, a high dose of esomeprazole is recommended for GERD treatment and control in adults.

Objective To detect the effect of glutahione S-transferases (GSTP1) expression on the migration,proliferation and apoptosis of cardiac microvascular endothelial cells (CMECs).Methods After obtaining CMECs from SD rats by enzymatic digestion method,the special plasmid of GSTP was transfected.The ability of migration,proliferation and apoptosis of CMECs were examined by using Transwell assay,methyl thiazol tetrazolium (MTT) assay and flow cytometry,respectively.Results The ability of migration of CMECs was significantly reduced in GSTP1 over-expression group as compared with control group (9.0 ±2.7 vs.12.8 ±2.5,P ＜0.05),and the ability of proliferation of CMECs was also obviously reduced in comparison with control group (0.26 ± 0.02 vs.0.05 ± 0.01,P ＜ 0.05).But the apoptotic index was increased significantly (P ＜ 0.05).Conclusion GSTP1 expression can effectively inhibit migration and proliferation,and promote apoptosis of CMECs.

Background The radial artery (RA) is becoming a popular conduit for coronary artery bypass grafting (CABG), yet data reporting the long-term results are rare. We reported our clinical, angiographic and intravascular ultrasound findings on 93 patients who had the RA used as part of the conduit for the CABG procedures during a 12-year period from June 2001 to June 2013.Methods A total of 118 radial artery conduits were harvested in 87 males and 6 females, age from 28 to 66 (mean 49.9) years. An "intra-operative Allen's test" was developed to safeguard blood supply to the arm and hand. A "double-clip & scissors-cut" technique was carried out to minimize the thermal injury to the radial artery from the diathermy. The left radial artery was used in 67 patients, the right in one, and bilateral radial arteries in 25 patients. One hundred and twenty-two out of 272 distal anastomoses (44.9%) were constructed with radial arteries, with an average of 2.9 grafts per patient (range 2-6).Results Follow-up angiography and intravascular ultrasound study at 3-139 postoperative months (mean 59 months) revealed a 93.1% RA patency. String sign occurred in one patient in whom the RA was directed to a big right coronary artery with a stenosis of around 50%. The patency for the internal mammary artery was 96.4%.Conclusions The RA is an excellent conduit that broadens the options for total arterial CABG surgery. Good graft patency could be achieved through careful harvesting techniques and choice of proper target coronary vessels.

Mitral valve-related operations are easy to perform and show good results, but to prevent severe thromboembolism or a high ratio of prosthetic valve destruction by tissue, lifetime anticoagulant therapy is essential after the operation. Thus, identifying a new type of surgical procedure and prosthetic valve to cure mitral valve diseases is necessary. Pulmonary valve autograft transplantation (Ross II) with the "top hat" transplantation technique was first reported by Ross DN to cure mitral disease. Because the "top hat" procedure has some shortcomings, we designed the scaffold-pulmonary autograft transplantation procedure and performed animal experiments to confirm the feasibility and effectiveness of the procedure. A total of 13 minipigs, weighing 20-25 kg, were employed as experimental animals to undergo scaffold-pulmonary autograft valve transplantation in our surgical animal lab. The surgical procedure was performed under hypothermic general anaesthesia and extracorporeal circulation (or cardiopulmonary bypass, CPB). Briefly, the chest cave was opened through the left intercostal, the pulmonary valve autograft was harvested during on-pump beating heart, and the pulmonary valve autograft was mounted in a self-made pulmonary valve scaffold and transferred to the mitral valve annulus without removing the mitral instruments. Finally, the outflow tract of the right ventricle was re-established with a pig pulmonary homograft. After finishing data collection, all animals were executed 1 hour after removal from the CPB. For the 13 minipigs that underwent the operation, the CPB time was 182.4 ± 23.4 min. Two of the thirteen cases died of bleeding during the operation and of a post-operative pulmonary embolism, and the remaining eleven survived for one hour. The pressure of the left atrium did not increase significantly (P = 1.00), and the ultrasonic cardiograph (UCG) showed good function of the new mitral valves, with mean ejection fraction (EF) values of 63.6%. The mitral valve orifice areas were 1.10 ± 0.13 cm(2) (pre-operation) and 1.01 ± 0.08 cm(2) (post-operation) (P = 0.013). The function and structure of the new mitral valves were normal. We preliminarily consider scaffold-pulmonary autograft valve transplantation to be a new alternative to cure mitral valve disease, but advanced chronic animal experiments will be needed to confirm the long-term results of the operation. The results showed it could be a new alternative to cure mitral valve disease.

Objective Clinical understanding of female nursing staff during the demand and status of reproductive health,As the pregnancy health care to provide reference.Methods A survey research methods.the 2 local general hospital clinical female nursing stcff survey questionnaire,on female reproductive health and maternal demand issues relating to the anonymous survey.Questionnaires were sent to438,recycles 438,the recovery rate is 100%,which effectively answer406answer92.7%,effective rate.Results Clinical nursing personnel of female reproductive health decline.During adverse reactions increase,mainly for infertility and spontaneous abortion.Conclusion Work pressure,night shift female nursing staff frequently is influenced by the clinical pregnancy health factors.The hospital should pay attention to the nursing staff during pregnancy needs,to ensure physical and mental health.

Parasitic ventricle hypothesis: a normal human heart is composed of four chambers that include two atria and two ventricles; the left ventricle is juxtaposed to the right ventricle. The left ventricle receives arterial blood from the left atrium and then ejects it into the general circulation, while the right ventricle receives venous blood from the right atrium and ejects it into the pulmonary circulation. So this structure restricts the arterial blood from mixing with the venous blood. But the heart of the patients suffering from single ventricle is composed of only one ventricle, and the patients can survive for several years, but eventually they die of hypoxemia induced by mixing up of arterial and venous blood in single ventricle. Based on these observations, we hypothesized that if an artificial akinesic ventricle device made of a biomaterial (such as pericardium autograft) (named as parasitic ventricle) is put into the single ventricle chamber of such patients, it would function as the right ventricle, and the single ventricle chamber is rendered to function as the left ventricle. Unlike the normal heart, this parasitic relationship enables to form a new type of heart structure. It has been found that the parasitic ventricle works relying on the function of the single ventricle, and the relationship of parasitism can be established between the two ventricles, "left ventricle" containing "right ventricle". This kind of heart structure can prevent the venous blood from mixing with the arterial blood; therefore, the patient in the absence of hypoxemia may survive longer. The theory is a completely new heart structure and work mode theory. We hope that this theory can open a new way to design a new operative procedure for effectively anatomically treating a patient with single ventricle. In addition, it may supply a new theory for designing a new total artificial heart with many advantages.