Identification of GPD1L as a Potential Prognosis Biomarker and Associated with Immune Infiltrates in Lung Adenocarcinoma.

Lung adenocarcinoma (LUAD) is one of the most prevalent pathological kinds of lung cancer, which is a common form of cancer that has a high death rate. Over the past several years, growing studies have indicated that GPD1L was involved in the advancement of a number of different cancers. However, its clinical significance in LUAD has not been investigated. In this study, following an examination of the TGCA datasets, we found that GPD1L displayed a dysregulated state in a wide variety of cancers; this led us to believe that GPD1L is an essential regulator in the progression of malignancies. In addition, we found that the expression of GPD1L was much lower in LUAD tissues when compared with nontumor specimens. According to the findings of ROC tests, GPD1L was able to effectively identify LUAD specimens from nontumor samples with an AUC value of 0.828 (95% confidence interval: 0.793 to 0.863). On the basis of the clinical study, a low expression of GPD1L was clearly related with both the N stage and the clinical stage. Moreover, based on the findings of a Kaplan-Meier survival study, elevated GPD1L expression was a strong indicator of considerably improved overall survival (OS) and disease-specific survival (DSS). GPD1L expression and clinical stages were found to be independent prognostic indicators for overall survival and disease-free survival in LUAD patients, according to multivariate analyses. Based on multivariate analysis, the C-indexes and calibration plots of the nomogram demonstrated an effective prediction performance for LUAD patients. Besides, the expression of GPD1L was positively related to mast cells, eosinophils, Tcm, TFH, iDC, DC, and macrophages, while negatively associated with Th2 cells, NK CD56dim cells, Tgd, Treg, and neutrophils. Finally, qRT-PCR was able to demonstrate that GPD1L had a significant amount of expression in LUAD. Additionally, according to the results of functional tests, overexpression of GPD1L had a significant inhibiting effect on the proliferation of LUAD cells. In general, the results of our study suggested that GPD1L had the potential to serve as a diagnostic and prognostic marker for LUAD.

[Combined use of prefabricated rib-locking titanium plate with ultrasound-guided thoracic paravertebral nerve blockade in the treatment of multiple rib fractures among the elderly].

OBJECTIVE: This paper is aimed at investigating the efficacy of combining internal fixation using prefabricated rib-locking titanium plate with ultrasound-guided thoracic paravertebral nerve blockade in treating multiple rib fractures among the elderly. METHODS: Retrospective analysis of 221 elderly patients with multiple rib fractures treated from February 2016 to November 2020. According to whether surgery was performed, they were divided into the plate-blockage combination group (surgical group, 102 cases) and conservative treatment group (non-surgical group, 119 cases). The surgical group consisted of 58 males and 44 females aged from 60 to 85 years old, with an average of (67.2±3.6 ) years old, who suffered from 3 to 12 rib fractures with an average of (5.3±2.1) fractures. The non-surgical group consisted of 66 males and 53 females aged from 60 to 84 years old with an average of (66.8±3.2) years old, who suffered from 2 to 11 rib fractures with an average of(6.1±2.3) fractures. The clinical data, efficacies observed, and complications associated with both groups were compared and analyzed. RESULTS: There was no significant difference in preoperative clinical data between two groups (P>0.05), and all patients were discharged smoothly. Pulmonary infection (P=0.028), atelectasis (P=0.032), respiratory failure (P=0.026), time to get out of bed (P=0.040), time to fracture healing (P=0.035), length of hospital stay in the operation group (P=0.043), visual analogue scale (VAS) at 3 days (P=0.028), 5 days(P=0.032), and 7 days(P=0.019), maximal voluntary ventilation (MVV) at 3 months after surgery (P=0.042), forced expiratory volume in one second (FEV1)(P=0.035), and maximal voluntary ventilation at 6 months, the maximal voluntary ventilation(MVV)(P=0.021) and forced FEV1(P=0.026) were all significantly better than those in non-surgical treatment group. CONCLUSION: For elderly patients with severe multiple rib fractures, the proposed plate-blockade combination can timely and effectively relieve pain, restore thoracic stability, shorten hospital stay, and reduce the incidence of complications such as pulmonary infections and acute respiratory distress syndrome(ARDS) compared with non-surgical treatments. Prefabricated rib-locking titanium plates have proved to demonstrate high clinical efficacy in treating multiple rib fractures among the elderly.

UBE4B promotes the development of lung adenocarcinoma by enhancing proliferation, migration and glycolysis via PP2A/AKT signaling.

This study was designed to explore the function of UBE4B in the development of lung adenocarcinoma (LUAD) and the role of PP2A/AKT in this process. Bioinformatics analysis, qRT-PCR, western blot, and immunohistochemistry were used to assess the gene expression in clinical samples, human LUAD database, human LUAD tissue microarrays, LUAD cells, and tumor xenograft model, respectively. The UBE4B overexpression and shRNA vector was constructed and transfected into LUAD cells, and the cell viability, migration, lactate production, and glycolysis were detected. The interaction between UBE4B and PP2A was assessed by CoIP and ubiquitination assay. The enhanced UBE4B expression is confirmed in LUAD datasets, clinical samples, human LUAD tissue microarrays and LUAD cells. UBE4B is positively associated with the proliferation, migration, lactate production, and glycolysis in LUAD cells, and UBE4B elevated proliferation, migration, lactate production, and glycolysis are abolished by PP2A overexpression. Mechanistically, UBE4B ubiquitinates PP2A and induces the activation of AKT. In conclusion, UBE4B act as an oncogene in the development of LUAD through PP2A/AKT signaling. UBE4B could be a new target for diagnosis and treatment of lung adenocarcinoma.

SKA3, negatively regulated by miR-128-3p, promotes the progression of non-small-cell lung cancer.

Aim: To investigate the effects of SKA3 on cell proliferation and metastasis in non-small-cell lung cancer (NSCLC) and its underlying mechanism. Methods: Immunohistochemistry was employed to analyze the expression of SKA3 in NSCLC. CCK-8 assay, EdU assay, Transwell assay and flow cytometry analysis were employed to assess cell proliferation, metastatic potential and apoptosis in vitro, respectively. A lung metastasis model was used to evaluate metastasis of NSCLC cells in vivo. A luciferase reporter gene assay was conducted to verify the targeting relationship. Results: SKA3 exhibited high expression in NSCLC tissues and cells. Overexpression of SKA3 remarkably accelerated cell proliferation and metastasis and suppressed apoptosis of NSCLC cells and promoted lung metastasis in a mouse model. miR-128-3p repressed SKA3 expression by targeting it. Conclusion:miR-128-3p inhibited the progression of NSCLC through targeting SKA3.

It is reported that the protein SKA3 can promote the growth and spread of cancer cells in multiple tumors. However, the biological role and action of SKA3 in the progression of non-small-cell lung cancer remain unknown. This study showed that a high level of SKA3 was linked with poor outcomes in non-small-cell lung cancer patients. SKA3 overexpression facilitated cell growth and spread, but inhibited cell death. miR-128-3p directly targeted SKA3 and reversed its effects. Our work suggests that SKA3 and miR-128-3p are promising therapy targets and diagnostic markers for non-small-cell lung cancer.

Sevoflurane suppresses glioma tumorigenesis via regulating circ_0079593/miR-633/ROCK1 axis.

BACKGROUND: Sevoflurane is a common inhalational anesthetic, which has been revealed to have anticancer effect in glioma. However, the mechanisms of sevoflurane in glioma progression remain largely unclear. METHODS: Cell proliferation, cell cycle, apoptosis and metastasis were monitored by cell counting kit-8 (CCK-8), flow cytometry, Transwell and Western blot assays. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot assays were used to examine the expression levels of circ_0079593, microRNA (miR)-633 and ROCK1 (Rho Associated Coiled-Coil Containing Protein Kinase 1). The dual-luciferase reporter assay was employed to confirm the targeting relationship between miR-633 and circ_0079593 or ROCK1. Animal experiment was conducted to explore the effect of sevoflurane in vivo. RESULTS: Sevoflurane inhibited glioma cell proliferation, metastasis and induced apoptosis in vitro as well as impeded tumor growth in vivo. The expression of circ_0079593 was higher in glioma tissues and cells, and was decreased by sevoflurane treatment in glioma cells. Functional experiments showed that circ_0079593 overexpression in glioma cells reversed the inhibitory effects of sevoflurane on cell growth and metastasis. In a mechanism analysis, circ_0079593 acted as a sponge for miR-633 to elevate ROCK1 expression in glioma cells, and sevoflurane could regulate ROCK1 expression via circ_0079593/miR-633 axis. Besides that, circ_0079593/miR-633/ROCK1 axis mediated the protective effects of sevoflurane on glioma cell tumorigenesis. CONCLUSION: Sevoflurane repressed glioma tumorigenesis via regulating circ_0079593/miR-633/ROCK1 axis, suggesting a new insight into the application of sevoflurane in glioma therapy.

Airway reconstruction using decellularized aortic xenografts in a dog model.

Tracheal reconstruction after extensive resection remains a challenge in thoracic surgery. Aortic allograft has been proposed to be a potential tracheal substitute. However, clinically, its application is limited for the shortage of autologous aortic segment. Whether xenogeneic aortic biosheets can be used as tracheal substitutes remains unknown. In the present study, we investigated the possibility in dog model. The results show that all dogs were survived without airway symptoms at 6 months after tracheal reconstruction with gently decellularized bovine carotid arteries. In the interior of engrafted areas, grafted patch integrated tightly with the residual native tracheal tissues and tracheal defects in the lumen were repaired smoothly without obvious inflammation, granulation, anastomotic leakage, or stenosis. In addition, histological and scanning electron microscopy examination showed that grafted patches were covered with ciliated columnar epithelium similar to epithelium in native trachea, which indicated successfully re-epithelialization of decellularized bovine carotid arteries in dogs. These findings provide preclinical investigation of xenogeneic aortic biosheets in serving as tracheal substitute in a dog model, which proposes that decellularized biosheets of bovine carotid may be a potential material for bioartificial tracheal graft.

Circ_ZNF124 promotes non-small cell lung cancer progression by abolishing miR-337-3p mediated downregulation of JAK2/STAT3 signaling pathway.

BACKGROUND: Previous genome-wide transcriptome profiling found circ_ZNF124 was highly expressed in lung adenocarcinoma, however, the role of circ_ZNF124 in non-small cell lung cancer (NSCLC) is still unknown. The purpose of this study was to investigate the role and molecular mechanism of circ_ZNF124 in NSCLC development. METHODS: The expression of circ_ZNF124, miR-337-3p and JAK2 (Janus Kinase 2) in lung cancer cell lines and normal epithelial cells were detected by qRT-PCR (quantitative real-time PCR). siRNA was used to knockdown circ_ZNF124 expression in cells. The effects of circ_ZNF124 in NSCLC cells were determined by cell growth, cell migration, cell cycle analysis and colony formation. Bioinformatics analysis, RNA immunoprecipitation, luciferase assay and western blots were used to study the molecular mechanism of circ_ZNF124 in NSCLC. RESULTS: The results showed that circ_ZNF124 expression was highly upregulated in NSCLC cells than in normal epithelial cells. Knockdown of circ_ZNF124 by using siRNA significantly decreased cell growth, promoted cell cycle arrested in sub-G1 phase, impaired cell migration and colony formation. Bioinformatic analysis discovered that miR-337-3p was a direct target of circ_ZNF124. In contrast to circ_ZNF124, miR-337-3p expression was significantly downregulated in NSCLC cells. Biotin labeled circ_ZNF124 immunoprecipitation and luciferase assay showed that miR-337-3p could directly bind to and affect circ_ZNF124 activity. The regulation of circ_ZNF124 on miR-337-3p was also investigated. Further analysis showed that despite STAT3 (signal transducer and activator of transcription 3), JAK2 was also a target of miR-337-3p, overexpression of miR-337-3p greatly downregulated JAK2, STAT3 and JAK2/STAT3 downstream regulated oncogenes HIF1a (Hypoxia-inducible factor 1-alpha), BCL2 (B cell lymphoma 2) and c-FOS expression, however, the roles of miR-337-3p in JAK2/STAT3 signaling pathway were greatly inhibited in the presence of circ_ZNF124. CONCLUSION: In NSCLC, highly expressed circ_ZNF124 promoted the activation of JAK2/STAT3 signaling pathway by acting as a sponge of miR-337-3p, thus promoting the occurrence and development of NSCLC. Circ_ZNF124 could be a potential biomarker or target for the treatment of NSCLC patients in the future.

FAM46B suppresses proliferation, migration and invasion of non-small cell lung cancer via ß-catenin/MMP7 signaling.

BACKGROUND: This study investigated the functions of FAM46B in non-small cell lung cancer (NSCLC) cells and determined the role of ß-catenin/matrix metalloproteinase 7 (MMP7) signaling in mediating these functions. METHODS: Human paracancerous and cancer tissues were collected from lung cancer patients. Cell proliferation was assessed by cell counting kit-8 (CCK-8) assay while migration and invasion were examined by transwell chamber assays. Relative mRNA expression and protein levels were determined by quantitative reverse transcription (q-RT) polymerase chain reaction (PCR) and western blot, respectively. RESULTS: FAM46B displayed reduced expression in lung cancer tissues compared with paired paracancerous tissues. In contrast, ß-catenin protein levels were elevated in lung cancer tissues compared with paired paracancerous tissues. FAM46B over-expression reduced proliferation, migration and invasion of A549 and H292 cells, as well as decreased the protein levels of ß-catenin, MMP7 and vascular endothelial growth factor (VEGF). On the other hand, FAM46B knockdown by shRNA in H1975 cells enhanced proliferation, migration and invasion, as well as increased the protein levels of ß-catenin and MMP7. These enhanced effects were ameliorated by treatment with the Wnt/ß-catenin inhibitor XAV939, suggesting a role for Wnt signaling in mediating the functions of FAM46B in NSCLC. CONCLUSIONS: FAM46B functions as a tumor suppressor by inhibiting ß-catenin/MMP7 signaling.

Anticancer effects of α-Bisabolol in human non-small cell lung carcinoma cells are mediated via apoptosis induction, cell cycle arrest, inhibition of cell migration and invasion and upregulation of P13K/AKT signalling pathway.

PURPOSE: Non-small lung cancer (NSLC) is one of the leading causes of cancer-related deaths world over. Excempting operable cases the treatments for NSCLC mainly include chemotherapy and radiotherapy. However, the survival rate for NSCLC is still far from satsifactory. Moreover, chemotherapy has lot of associated side effects. Therefore, there is an urgent need to look for novel and more viable treatment options. Against this background, the present study was designed to evaluate the anticancer activity of α-Bisabolol against NSCLC. METHODS: Cell viability was assessed by MTT assay. Apoptosis was determined by DAPI and annexin V/propidium iodide (PI) staining. Mitochondrial membrane potential (MMP) and cell cycle analysis were determined by flow cytometry. Cell migration was investigated by wound healing assay and protein expression was evaluated by western blotting. RESULTS: α-Bisabolol exerted significant anticancer activity on A549 NSCLC cells with IC50 of 15 µM. The anticancer effects of α-Bisabolol were found to be due to G2/M cell cycle arrest and mitochondrial apoptosis. α-Bisabolol also inhibited cell migration of A549 cells dose-dependently. Moreover, the results showed that α-Bisabolol could inhibit the PI3K/AKT signalling pathway in a dose-dependent manner. The results of the present study indicate that α-Bisabolol exerted selective anticancer effects on A549 cells via induction of cell cycle arrest, mitochondrial apoptosis and inhibition of PI3K/Akt signalling pathways. CONCLUSIONS: This molecule showed promising anticancer features and could be developed as a potent lead candidate for the management and treatment of NSCLC.

HOXA4, down-regulated in lung cancer, inhibits the growth, motility and invasion of lung cancer cells.

The involvement of HOXA4 in colorectal cancer and epithelial ovarian cancer has been reported. Although it has been reported that the Hoxa4 gene is involved in the patterning of the mouse lung during embryonic development, little is known about the biological functions of HOXA4 in lung cancer. In the current study, HOXA4 expression was down-regulated in lung cancer tissues when compared with non-cancerous tissues. HOXA4 expression was associated with tumor size, TNM stage, lymph node metastasis and prognosis. Bioinformatics analysis revealed that HOXA4 expression was negatively correlated with cell cycle, metastasis, and the Wnt signaling pathway. Moreover, HOXA4 overexpression in lung cancer cell lines suppressed cell proliferation, migration, and invasion. HOXA4 decreased the protein expression levels of ß-catenin, Cyclin D1, c-Myc and Survivin, indicating the inhibition of Wnt signaling. HOXA4 significantly increased the protein and mRNA levels of glycogen synthase kinase-3ß (GSK3ß) by promoting its transcription. Furthermore, inhibition of GSK3ß by LiCl abolished the suppression of cell growth, migration, and invasion mediated by HOXA4. Overexpression of HOXA4 in xenograft tumors also decreased tumor growth and Wnt signaling. Collectively, these data suggest that HOXA4 is a potential diagnostic and prognostic marker in lung cancer, and its overexpression could inhibit lung cancer progression in part by promoting GSK3ß transcription.

Detection of G-Quadruplex Structures Formed by G-Rich Sequences from Rice Genome and Transcriptome Using Combined Probes.

Putative G-quadruplex (G4) forming sequences (PQS) are highly prevalent in the genome and transcriptome of various organisms and are considered as potential regulation elements in many biological processes by forming G4 structures. The formation of G4 structures highly depends on the sequences and the environment. In most cases, it is difficult to predict G4 formation by PQS, especially PQS containing G2 tracts. Therefore, the experimental identification of G4 formation is essential in the study of G4-related biological functions. Herein, we report a rapid and simple method for the detection of G4 structures by using a pair of complementary reporters, hemin and BMSP. This method was applied to detect G4 structures formed by PQS (DNA and RNA) searched in the genome and transcriptome of Oryza sativa. Unlike most of the reported G4 probes that only recognize part of G4 structures, the proposed method based on combined probes positively responded to almost all G4 conformations, including parallel, antiparallel, and mixed/hybrid G4, but did not respond to non-G4 sequences. This method shows potential for high-throughput identification of G4 structures in genome and transcriptome. Furthermore, BMSP was observed to drive some PQS to form more stable G4 structures or induce the G4 formation of some PQS that cannot form G4 in normal physiological conditions, which may provide a powerful molecular tool for gene regulation.

Tunnel-type open reduction and internal fixation of rib fractures with / 中国胸心血管外科临床杂志

@#Objective    To investigate the tunnel-type open reduction and internal fixation of rib fractures (ORIF) with titanium locking plate in traumatic rib fractures. Methods    Clinical data of 10 patients with multiple rib fractures from June 2016 to January 2017 in the Sixth People’s Hospital Affiliated to Shanghai Jiaotong University were analyzed. There were 6 males and 4 males with an average age of 38.5±9.0 years (range, 30–63 years). All patients underwent emergency treatment, chest CT and ultrasound examination before they admitted to the hospital. According to rib fractures and injuries, patients were given the tunnel-type ORIF of rib fractures with titanium locking plates, the chest tube and negative suction drainage. The patients were followed up over three months. Results    All patients were cured. There was no complication during follow-up. No wound infection and death occurred. Postoperative three-month follow-up showed that chest pain was significantly relieved without pulmonary atelectasis and pleural effusion or other complications. Conclusion    Tunnel-type internal fixation of rib fractures with titanium locking plates is effective, which can quickly restore the stability and integrity of the thorax. Surgical procedure is simple and can get fast postoperative recovery to improve the patient's quality of life.

The oncogenetic role of stanniocalcin 1 in lung adenocarcinoma: a promising serum candidate biomarker for tracking lung adenocarcinoma progression.

Stanniocalcin 1 (STC1) is reported to functionally participate in the development of several cancers. However, the role of STC1 in the tumorigenesis and progression of lung adenocarcinoma remains to be fully elucidated. Here, we found that the average levels of serum STC1 were 5.47, 5.53, and 6.94 ng/mL (P = 0.0045) in the healthy subjects and patients with lung adenocarcinoma at tumor stages I-II and III-IV according to Union for International Cancer Control (UICC), respectively. Subsequently, the positive correlation between the STC1 expression level in lung adenocarcinoma tissues and tumor stages was confirmed by immunohistochemical staining assay. Additionally, studies in the STC1-overexpressing or STC1-silenced stable cell lines showed that STC1 increased cell proliferation by promoting G1/S transition in cell cycle progression via up-regulating cyclin B1 and cyclin E. Moreover, studies in the STC1-overexpressing or STC1-silenced stable cell lines also showed that STC1 inhibited cell apoptosis by up-regulating the expression of anti-apoptosis proteins Bcl-2 and Bcl-xl and down-regulating the expression of pro-apoptosis proteins Bax, Bak, and Bid via the activation of the ERK and JNK signaling pathway. In addition, neutralization of STC1 with monoclonal antibody significantly increased the apoptosis of A549 cells. Taken together, our findings strongly suggest that elevated expression of STC1 protein at the III-IV stage of lung adenocarcinoma promotes tumorigenesis of lung adenocarcinoma and positively associates with the cancer progression, which may be of potential value as tumor marker in clinical tracking lung adenocarcinoma progression.

Percutaneous cardiopulmonary support for catastrophic pulmonary fat embolism in pigs.

OBJECTIVE: The purpose of this study was to evaluate the effect of percutaneous cardiopulmonary support (PCPS) for fatal fat embolism. METHODS: Twelve piglets were randomly assigned into either a conventional treatment group (CT group, n = 6) or a PCPS group (n = 6) after receiving 0.3 mL/kg of fat intravenously. The piglets in the CT group received conventional treatments including mechanical ventilation with 100% oxygen, steroid, fluids, anticoagulant, and positive inotropic agents. In addition to conventional treatments, the piglets in the PCPS group received PCPS after fat injection. Mean arterial pressure, central venous pressure, pressure of end tidal carbon dioxide, oxygen saturation, partial pressure of oxygen in arterial blood, arterial carbon dioxide pressure or tension, plasmic lactic acid, and free fatty acid were monitored. The survival rate and the consumption of positive inotropic agents were also recorded. RESULTS: The survival rate of piglets 10 hours after fat injection was much higher in the PCPS group than that in the CT group (100% vs. 0%, p < 0.01). The dosages of positive inotropic agents in the PCPS group were much lower than that in the CT group (p < 0.01). Oxygen saturation, partial pressure of oxygen in arterial blood, and arterial carbon dioxide pressure or tension were significantly improved in the PCPS group in the first 3 hours after fat injection when compared with those in the CT group (p < 0.05 or 0.01), but there were no statistical differences between the two groups in mean arterial pressure, central venous pressure, free fatty acid, and lactic acid at the period. CONCLUSION: PCPS can increase the survival rate of piglets with fatal fat embolism by providing effective cardiopulmonary support. This study suggests that PCPS might be an effective treatment for a patient with severe fat embolism if conventional treatments have not worked.

Preseeding of human vascular cells in decellularized bovine pericardium scaffold for tissue-engineered heart valve: an in vitro and in vivo feasibility study.

Human vascular cells from saphenous veins have been used for cell seeding on the synthetic scaffolds for constructing tissue-engineered heart valve (TEHV). However, little is known about the seeding of human vascular cells on bovine pericardium, a potential natural scaffold for TEHV. This study was aimed to assess the basic in vitro and in vivo characteristics of the human vascular cells seeded on decellularized bovine pericardium. In vitro, bovine pericardium samples with cell seeding were inspected on day 7, 14, and 21 by histology, scanning electron microscopy, and immunohistochemistry. In vivo, experiments were performed in nude mice by bilateral dorsal incision for the implantation of decellularized bovine pericardium with and without cell seeding. Results demonstrated that a total of 8-10 × 10(6) cells were obtained within 4-5 wk by the primary co-culture, which were detected positive for von Willebrand factor, α-smooth muscle actin antibodies, and fibronectin, indicating the presence of endothelial cells, smooth muscle cells, and fibroblasts, respectively. In vitro, the seeded cells showed a steady increase of endothelial activity from day 1 to day 7 and remained stable until day 21. After 30 days of implantation in vivo, the cells on the decellularized bovine pericardium could differentiate directionally and show all the identities of human endothelial cells, smooth muscle cells, and fibroblasts. These results indicate that the human vascular cells from the saphenous vein are an optional cell source for seeding on decellularized bovine pericardium scaffold for constructing TEHV.

Off-pump occlusion of trans-thoracic minimal invasive surgery (OPOTTMIS) on simple congenital heart diseases (ASD, VSD and PDA) attached consecutive 210 cases report: a single institute experience.

OBJECTIVE: This paper intends to report our experiences by using an operation of off-pump occlusion of trans-thoracic minimal invasive surgery (OPOTTMIS) on the treatment of consecutive 210 patients with simple congenital heart diseases (CHD) including atrial septal defect (ASD), ventricular septal defect (VSD) and patent ductus arteriosus (PDA). METHODS: The retrospective clinical data of OPOTTMIS in our institute were collected and compared to other therapeutic measures adopted in the relevant literatures. After operation, all the patients received electrocardiography (ECG) and echocardiography (echo) once a month within the initial 3 months, and no less than once every 3 ~ 6 months later. RESULTS: The successful rate of the performed OPOTTMIS operation was 99.5%, the mortality and complication incidence within 72 hours were 0.5% and 4.8%, respectively. There were no major complications during peri-operation such as cardiac rupture, infective endocarditis, strokes, haemolysis and thrombosis. The post-operation follow-up outcomes by ECG and echo checks of 3 months to 5 years showed that there were no III° AVB, no obvious Occluder migration and device broken and no moderate cardiac valve regurgitation, except 1 VSD and 1 PDA with mild residual shunts, and 2 PDA with heart expansion after operation. However, all the patients' heart functions were in class I~II according to NYH standard. CONCLUSION: The OPOTTMIS is a safe, less complex, feasible and effective choice to selected simple CHD patients with some good advantages and favorable short-term efficacies.

Hemodynamic support with the pulsatile catheter pump in a sheep model of acute heart failure.

This study was aimed to mimic clinical heart failure (HF) conditions and to assess the effect of pulsatile catheter (PUCA) pump support on hemodynamics and tissue perfusion in a sheep model of acute HF. In 14 sheep, HF was induced by partial occluding the middle left circumflex coronary artery combined with pacemaker-induced tachycardia. PUCA pump was then activated to support the HF for 3 h. Hemodynamic parameters were recorded at baseline, HF, and then every 30 min during experiments. Blood samples were taken in carotid artery (CA), pulmonary artery (PA), and coronary sinus (CS) for the determination of oxygen saturation (SO2) and lactate concentration as markers of tissue perfusion. Results showed that HF model was induced successfully in 10 sheep and failed in four sheep due to refractory ventricular fibrillation. PUCA pump support was successful in seven out of 10 sheep for 3 h. Three cases failed due to technical problems. After HF (n = 10), cardiac output (CO) was decreased from 3.7 +/- 0.5 to 2.0 +/- 0.5 L/min (P < 0.001). Mean arterial pressure (MAP) was lowered from 116.1 +/- 14.2 to 68.1 +/- 14.7 mm Hg (P < 0.001). In seven sheep supported with PUCA pump, MAP rose from 68.9 +/- 15.2 to 94.7 +/- 14.7 mm Hg (P = 0.005), systolic blood pressure increased from 86.6 +/- 17.0 to 112.6 +/- 17.1 mm Hg (P = 0.009), and diastolic blood pressure increased from 57.7 +/- 12.6 to 79.9 +/- 13.9 mm Hg (P = 0.011). CO remained at about 2.0 L/min. SO2 in CA, PA, and CS decreased significantly after HF (P < 0.001), with an increase after support (compared with HF, P < 0.001, 0.066 and 0.114, respectively). Lactate concentrations increased gradually in CA, PA, and CS toward the end of experiments without difference among different sampling sites. This HF model in sheep is simple, easy to manipulate, reproducible and reflecting clinical HF conditions. PUCA pump can maintain the hemodynamic status for 3 h in this acute HF model.

A new approach to completely autologous cardiovascular tissue in humans.

In cardiovascular tissue engineering, synthetic or biologic scaffolds serve as templates for tissue development. Currently used scaffolds showing toxic degradation and immunogenic reactions are still far from ideal. We present a new alternative method to develop completely autologous human tissue without using any scaffold materials. Human vascular cells of arterial and venous origin were cultured to form cell sheets over a 4 week period under standard conditions. Thereafter, cell sheets of each origin were folded and cultured in a newly developed frame device for an additional 4 weeks. Controls remained under standard culture conditions. Tissue development was evaluated by morphology and biochemical assays. The formation of multilayered cell sheets and production of extracellular matrix were observed in all groups. Folded and framed neo-tissue showed a solid structure, with increased matrix formation and tissue organization when compared with the control groups. DNA content indicated significantly lower cell proliferation, and hydroxyproline assay indicated significantly higher collagen content in the framed cell sheets. We present a new approach to the engineering of cardiovascular tissue without the use of biodegradable scaffold material. Three-dimensional, completely autologous human tissue may be developed on the basis of this structure, thus avoiding scaffold induced toxic degradation or inflammatory reaction.