Advances in phage-host interaction prediction: in silico method enhances the development of phage therapies.

Phages can specifically recognize and kill bacteria, which lead to important application value of bacteriophage in bacterial identification and typing, livestock aquaculture and treatment of human bacterial infection. Considering the variety of human-infected bacteria and the continuous discovery of numerous pathogenic bacteria, screening suitable therapeutic phages that are capable of infecting pathogens from massive phage databases has been a principal step in phage therapy design. Experimental methods to identify phage-host interaction (PHI) are time-consuming and expensive; high-throughput computational method to predict PHI is therefore a potential substitute. Here, we systemically review bioinformatic methods for predicting PHI, introduce reference databases and in silico models applied in these methods and highlight the strengths and challenges of current tools. Finally, we discuss the application scope and future research direction of computational prediction methods, which contribute to the performance improvement of prediction models and the development of personalized phage therapy.

Establishment of Functional PCR-Based Markers against Bacterial Leaf Blight Disease in Rice Landraces of Yunnan Province of China.

Bacterial leaf blight is a devastating disease of rice worldwide. The resistant genes are routinely transferred from landraces to cultivated varieties through backcross breeding along with marker-assisted selection. In the present study, we use the gene-specific markers to screen the rice landraces in Yunnan Province of China. We collected 404 representative samples of 24 different rice landraces from Yunnan Province of China. The initial PCR-based screening suggested that the leaf blight resistance was not evenly distributed in Yunnan Province. Our results indicate that there is a complete loss of resistance for landraces based on xa5 and xa13 genes. On the other hand, landraces harboring Xa7 and Xa21 showed a high level of resistance. Using gene-specific PCR-based data, we were able to identify the resistant, susceptible and heterozygous populations across Yunnan Province. The widely used Xa21 gene alone showed a remarkable level of resistance throughout the province, indicating its potential to develop broad-spectrum resistance in rice germplasm. The key aspects of bacterial blight spread according to local sites in Yunnan Province and the resistance conferred by different landraces due to the presence of different resistance genes are discussed.

Sensing prior constraints in deep neural networks for solving exploration geophysical problems.

One of the key objectives in geophysics is to characterize the subsurface through the process of analyzing and interpreting geophysical field data that are typically acquired at the surface. Data-driven deep learning methods have enormous potential for accelerating and simplifying the process but also face many challenges, including poor generalizability, weak interpretability, and physical inconsistency. We present three strategies for imposing domain knowledge constraints on deep neural networks (DNNs) to help address these challenges. The first strategy is to integrate constraints into data by generating synthetic training datasets through geological and geophysical forward modeling and properly encoding prior knowledge as part of the input fed into the DNNs. The second strategy is to design nontrainable custom layers of physical operators and preconditioners in the DNN architecture to modify or shape feature maps calculated within the network to make them consistent with the prior knowledge. The final strategy is to implement prior geological information and geophysical laws as regularization terms in loss functions for training the DNNs. We discuss the implementation of these strategies in detail and demonstrate their effectiveness by applying them to geophysical data processing, imaging, interpretation, and subsurface model building.

Emergence of Rice Blast AVR-Pi9 Resistance Breaking Haplotypes in Yunnan Province, China.

The rice blast disease (caused by Magnaporthe oryzae) is a devastating disease in China. Understanding the molecular mechanisms of interaction for the cognate avirulence (AVR) gene with host resistance (R) genes, as well as their genetic evolution is essential for sustainable rice production. In the present study, we conducted a high-throughput nucleotide sequence polymorphism analysis of the AVR-Pi9 gene that was amplified from the rice-growing regions of the Yunnan Province in China. We detected the presence of seven novel haplotypes from 326 rice samples. In addition, the sequences of AVR-Pi9 were also obtained from two non-rice hosts, Eleusine coracana and Eleusine indica. The sequence analysis revealed the insertions and deletions in the coding and non-coding regions of the gene. The pathogenicity experiments of these haplotypes on previously characterized monogenic lines showed that the newly identified haplotypes are virulent in nature. The breakdown of resistance was attributed to the development of new haplotypes. Our results suggest that the mutation in the AVR-Pi9 gene is an alarming situation in the Yunnan province and thus needs attention.

FTO represses NLRP3-mediated pyroptosis and alleviates myocardial ischemia-reperfusion injury via inhibiting CBL-mediated ubiquitination and degradation of ß-catenin.

Cardiac ischemia/reperfusion (I/R) injury is a complicated pathological event, which has close association with pyroptosis. This study uncovered the regulatory mechanisms of fat mass and obesity-associated protein (FTO) in NLRP3-mediated pyroptosis during cardiac I/R injury. H9c2 cells were stimulated with oxygen-glucose deprivation/reoxygenation (OGD/R). Cell viability and pyroptosis were detected by CCK-8 and flow cytometry. Western blotting or RT-qPCR was performed to analyze target molecule expression. NLRP3 and Caspase-1 expression was observed by immunofluorescence staining. IL-18 and IL-1ß production was detected by ELISA. The total m6A and m6A level of CBL was determined by dot blot assay and methylated RNA immunoprecipitation-qPCR, respectively. The interaction between IGF2BP3 and CBL mRNA was confirmed by RNA pull-down and RIP assays. The protein interaction between CBL and ß-catenin and ß-catenin ubiquitination were evaluated by Co-IP. Myocardial I/R model was established in rats. We determined infarct size by TTC staining and pathological changes by H&E staining. LDH, CK-MB, LVFS, and LVEF were also assessed. FTO and ß-catenin were down-regulated, while CBL was up-regulated by OGD/R stimulation. FTO/ß-catenin overexpression or CBL silencing restrained OGD/R-induced NLRP3 inflammasome-mediated pyroptosis. CBL repressed ß-catenin expression via ubiquitination and degradation. FTO reduced the mRNA stability of CBL by inhibiting m6A modification. CBL-mediated ubiquitination and degradation of ß-catenin were involved in FTO-induced pyroptosis inhibition during myocardial I/R injury. FTO inhibits NLRP3-mediated pyroptosis to attenuate myocardial I/R injury via repressing CBL-induced ubiquitination degradation of ß-catenin.

Genome Re-Sequencing Reveals the Host-Specific Origin of Genetic Variation in Magnaporthe Species.

Rice blast is caused by Magnaporthe oryzae (M. oryzae), which is considered one of the most serious pathogens of rice around the globe. It causes severe losses owing to its proven capability to disrupt the host resistance. Recently, its invasion of new hosts like the Musa species or banana plants has been noticed. To understand the possible level of genetic variation, we sequenced the genomes of eight different isolates of the Magnaporthe species infecting rice, Digitaria (a weed), finger millet, Elusine indica, and banana plants. Comparative genomic analysis of these eight isolates with the previously well-characterized laboratory strain M. oryzae 70-15 was made. The infectivity of the newly isolated strain from Musa species suggested that there is no resistance level in the host plants. The sequence analysis revealed that despite genome similarities, both the banana and Digitaria isolates have relatively larger genome sizes (∼38.2 and 51.1 Mb, respectively) compared to those of the laboratory reference strain M. oryzae 70-15 (∼37 Mb). The gene contraction, expansion, and InDel analysis revealed that during evolution, a higher number of gene insertions and deletions occurred in the blast fungus infecting Digitaria and banana. Furthermore, each genome shared thousands of genes, which suggest their common evolution. Overall, our analysis indicates that higher levels of genes insertion or deletions and gain in the total genome size are important factors in disrupting the host immunity and change in host selection.

Biological Control of Fusarium oxysporum f. sp. cubense Tropical Race 4 Using Natively Isolated Bacillus spp. YN0904 and YN1419.

Fusarium wilt of banana (FWB) is the main threatening factor for banana production worldwide. To explore bacterial biocontrol resources for FWB, the antagonistic effective strains were isolated from banana-producing areas in Yunnan Province, China. Two isolates (YN0904 and YN1419) displaying strong antagonism against Tropical Race 4 (TR4) were identified from a total of 813 strains of endophytic bacteria. TR4 inhibition rates of YN0904 and YN1419 were 79.6% and 81.3%, respectively. By looking at morphological, molecular, physiological and biochemical characteristics, YN0904 was identified as Bacillus amyloliquefaciens, while YN1419 was identified as B. subtillis. The control effects of YN0904 and YN1419 on TR4 in greenhouse experiments were 82.6% and 85.6%, respectively. Furthermore, YN0904 obviously promoted the growth of banana plantlets. In addition, biocontrol marker genes related to the biosynthesis of antibiotics synthesized and auxin key synthetase genes could be detected in YN0904. Surprisingly, the marker gene sboA could be exclusively detected in YN1419, while other marker genes were all absent. Molecular characterization results could provide a theoretical basis for expounding the biocontrol mechanisms of these two strains. We concluded that natively antagonistic strains derived from local banana plantations could provide new biological control resources for FWB.

Complete mitochondrial genome of banana skipper Erionota torus Evans (Lepidoptera: Hesperiidae) and phylogenetic analysis.

Erionota torus (Evans, 1941) is a banana pest and is mainly distributed in Southeast Asia and the Pacific regions. The complete mitogenome of E. torus (GenBank accession number MW586888) is 15,987 bp in size, including 13 protein-coding genes, 22 transfer RNAs, 2 ribosomal RNAs genes, and a noncoding A + T-rich region. The A + T-rich region is located between 12S rRNA and tRNAMet . The base composition of the whole E. torus mitogenome is 39.68% for A, 7.30% for G, 41.55% for T, and 11.47% for C, with a high AT content of 81.23%. The phylogeny analysis indicated that E. torus had a close relationship with Notocrypta curvifascia. The present data could contribute to the further detailed phylogeographic analysis and provide a comprehensive control strategy for this banana pest.

HLB-MCX-Based Solid-Phase Extraction Combined with Liquid Chromatography-Tandem Mass Spectrometry for the Simultaneous Determination of Four Agricultural Antibiotics (Kasugamycin, Validamycin A, Ningnanmycin, and Polyoxin B) Residues in Plant-Origin Foods.

An ultrahigh-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) method was established for the determination of four highly polar agricultural antibiotics kasugamycin, validamycin A, ningnanmycin, and polyoxin B in plant-derived foods. The samples were extracted with a 0.2% formic acid solution, purified by hydrophilic-lipophilic balance and mixed-mode cation-exchange solid-phase extraction, and then reconstituted for UPLC-MS/MS detection. The chromatographic analysis was performed on a BEH Amide column (100 mm × 2.1 mm, 1.7 µm) using gradient elution with a 0.1% formic acid solution and 0.1% formic acid acetonitrile as mobile phases. Method validation was performed on 15 matrices spiked at 0.02 (or 0.05), 0.5, and 2 mg/kg. The mean recovery rate ranged from 75 to 102% with relative standard deviations (RSD) was less than 20%. Good linearities (r > 0.99) in the range of 0.002-0.2 µg/mL were obtained. The limits of quantification (LOQs) were 0.02 and 0.05 mg/kg. Studies on the stability of the analytes in the stored kiwifruit samples showed that kasugamycin, validamycin A, and ningnanmycin were stable for at least 6 months, while polyoxin B was observed to be partially degraded (the degradation rate at 6 months was 31.3%). The method was demonstrated to be effective and reliable in real samples. In the kiwifruit samples treated after 7 days, no residues of ningnanmycin and polyoxin B were detected, while the residues of kasugamycin and validamycin A were 0.12 and 0.038 mg/kg, respectively.

LncRNA ANRIL acts as a modular scaffold of WDR5 and HDAC3 complexes and promotes alteration of the vascular smooth muscle cell phenotype.

Many studies have shown that long-noncoding RNA (lncRNA) is associated with cardiovascular disease, but its molecular mechanism is still unclear. In this study, we explored the role of lncRNA ANRIL in ox-LDL-induced phenotypic transition of human aortic smooth muscle cells (HASMC). The results of quantitative fluorescence PCR showed that the expression of ANRIL in patients with coronary atherosclerotic heart disease (CAD) was significantly higher than that in normal subjects. RNA-FISH detection showed that the ANRIL expression increased in HASMC treated by ox-LDL. Ox-LDL could upregulate the expression of ANRIL and ROS and promote the phenotypic transition of HASMC. After downregulation of ANRIL by siRNA, ROS level decreased and HASMC phenotypic transition alleviated. ANRIL could act as a molecular scaffold to promote the binding of WDR5 and HDAC3 to form WDR5 and HDAC3 complexes, they regulated target genes such as NOX1 expression by histone modification, upregulated ROS level and promote HASMC phenotype transition. Therefore, we found a new epigenetic regulatory mechanism for phenotype transition of VSMC, ANRIL was a treatment target of occlusive vascular diseases.

Effects of respiratory rate on venous-to-arterial CO2 tension difference in septic shock patients undergoing volume mechanical ventilation.

BACKGROUND: To explore the effects of the respiratory rate (RR) on the venous-to-arterial CO2 tension difference (gapCO2) in septic shock patients undergoing volume mechanical ventilation. METHODS: Adult patients with septic shock underwent volume mechanical ventilation between October 2015 and October 2016. RR was started at 10 breaths/min, and 2 breaths/min were added every 60 min until 16 breaths/min was reached. At every point, central venous and arterial blood gas measurements were obtained simultaneously. RESULTS: In this study, gapCO2 induced by hyperventilation significantly increased, while the central venous carbon dioxide pressure (PvCO2) and the partial pressure of CO2 (PaCO2) in arteries decreased. The decreasing trend of the PaCO2 was more obvious than that of the PvCO2. HCO3- and ctCO2 were markedly decreased, when the RR was increased (P < 0.05). Central venous oxygen saturation (ScvO2) had a decreasing trend between 14 (77.1 ± 8.3%) and 16 (75.2 ± 8.7%) breaths/min; however, the difference was not significant. CONCLUSIONS: In septic patients undergoing ventilation, respiratory alkalosis induced by hyperventilation caused an increase in the gapCO2. Clinicians should cautiously interpret the gapCO2 in hemodynamically stable ventilated septic shock patients and its relationship with low cardiac output and inadequate perfusion.

Complete mitochondrial genome of banana new pest Basilepta fulvipes (Coleoptera: Eumolpinae) and phylogenetic analysis.

Basilepta fulvipes (Motschulsky, 1860) is a banana new pest and mainly distributed in Eastern Asia. The complete mitogenome of B. fulvipes (GenBank accession number MT627597) is 15,762 bp in size, including 13 protein-coding genes, 22 transfer RNAs, 2 ribosomal RNAs genes and a noncoding D-loop region. The D-loop region is located between 12S rRNA and tRNAIle . The base composition of the whole B. fulvipes mitogenome is 41.66% for A, 8.89% for G, 34.32% for T and 15.12% for C, with a high AT bias of 75.98%. The present data could contribute to further detailed phylogeographic analysis and comprehensive control of this banaba new pest.

LncRNA NRON alleviates atrial fibrosis through suppression of M1 macrophages activated by atrial myocytes.

The aim of the present study was to explore the role of long non-coding RNA (lncRNA) non-coding repressor of NFAT (NRON) in the atrial fibrosis and to explore whether its underlying mechanism was associated with macrophage polarization. Enzyme-linked immunosorbent assay (ELISA) analysis of pro-inflammatory cytokines revealed that NRON overexpression suppressed, whereas NRON silencing facilitated the angiotensin II (Ang II)-induced inflammatory response in primary cultured atrial myocytes. The chromatin immunoprecipitation (ChIP) results showed that nuclear factor of activated T cell 3 (NFATc3) was recruited to the promoter region of interleukin (IL) 12 (IL-12) in atrial myocytes. Further data showed that NRON overexpression suppressed, whereas NRON silencing further promoted the Ang II-induced NFATc3 nuclear transport and IL-12 expression in atrial myocytes. Moreover, RAW264.7 macrophages were incubated with the conditioned medium from the Ang II-treated atrial myocytes transfected with NRON and IL-12 overexpression vectors. IL-12 overexpression abrogated the NRON overexpression-mediated inhibition of RAW264.7 macrophage polarization to the M1-like phenotype. Additionally, mouse atrial fibroblasts were incubated with the culture medium from RAW264.7 macrophages treated as described above. IL-12 overexpression rescued the NRON overexpression-inhibited protein levels of fibrosis markers Collagen I/III in mouse atrial fibroblasts. Collectively, our data indicate that lncRNA NRON alleviates atrial fibrosis through suppression of M1 macrophages activated by atrial myocytes.

LncRNA NRON alleviates atrial fibrosis via promoting NFATc3 phosphorylation.

The aim of this study was to explore the role of NRON in the atrial fibrosis. The expression of NRON in atrial tissue was detected using qRT-PCR. The protein levels of collagen I, collagen III, NFATc3 and p-NFATc3 were determined by western blot. Immunohistochemistry assay were performed to observe expression and distribution of collagen I in atrial tissues. The atrial fibroblasts were authenticated by vimentin/troponin immunofluorescence staining. Fibroblast proliferation was detected by CCK-8 assay. The morphological changes of cardiac tissue were observed by HE staining. Myocardial fibrosis was detected by masson staining. NRON expression was significantly downregulated in atrial tissues of AF. NRON suppressed fibroblast proliferation; expression of collagen I and collagen III; activation of NFATc3 and nucleu import. NRON promoted p-NFATc3 expression and alleviated atrial fibrosis in vivo. Our data indicated that NRON alleviates atrial fibrosis via promoting NFATc3 phosphorylation.

IFI16 regulates HTLV-1 replication through promoting HTLV-1 RTI-induced innate immune responses.

Interferon (IFN)-inducible protein 16 (IFI16) regulates human immunodeficiency virus replication by inducing innate immune responses as a DNA sensor. Human T-lymphotropic virus type 1 (HTLV-1), a delta retrovirus family member, has been linked to multiple diseases. Here, we report that IFI16 expression is induced by HTLV-1 infection or HTLV-1 reverse transcription intermediate (RTI) ssDNA90 transfection. IFI16 overexpression decreases HTLV-1 protein expression, whereas IFI16 knockdown increases it. Furthermore, the knockdown of IFI16 is followed by impaired innate immune responses upon HTLV-1 infection. In addition, IFI16 forms a complex with ssDNA90 and enhances ssDNA90-triggered innate immune responses. Collectively, our data suggest a critical role for IFI16 during HTLV-1 infection by interacting with HTLV-1 RTI ssDNA90 and restricting HTLV-1 replication.

HLA-DMB restricts human T-cell leukemia virus type-1 (HTLV-1) protein expression via regulation of ATG7 acetylation.

The roles of autophagy in viral infection are complicated. While autophagy has been shown to function in host antiviral defense by eliminating intracellular viruses and regulating adaptive immunity, several viruses have evolved molecular mechanisms to get benefits from it. The deltaretrovirus human T-cell leukemia virus type-1 (HTLV-1) has been reported to profit its replication from enhancing autophagosome accumulation. Here, we reported that HLA-DMB (generally referred to here as DMB), the beta chain of the non-classical MHC-II protein HLA-DM, had strong expression in HTLV-1-transformed T-cell lines and could be induced in Hela, PMA-differentiated THP1 (PMA-THP1) or primary human monocytes by HTLV-1 infection. Immunoblot and real-time PCR assays demonstrated that overexpression of DMB decreased HTLV-1 protein expression while the knockdown of DMB increased HTLV-1 protein expression. Immunoblot and confocal microscopy assays indicated that overexpression of DMB decreased HTLV-1 induced autophagosome accumulation while the knockdown of DMB yielded the opposite effects. Coimmunoprecipitation and immunoprecipitation experiments suggested DMB interacted with autophagy-related gene (ATG) 7 and increased the acetylation of ATG7. Taken together, these results suggested DMB modulated HTLV-1 protein expression through regulation of autophagosome accumulation and our findings suggested a new mechanism by which the host cells defended against HTLV-1 infection.

Ku70 Senses HTLV-1 DNA and Modulates HTLV-1 Replication.

Human T lymphotropic virus type 1 (HTLV-1) belongs to the deltaretrovirus family and has been linked to multiple diseases. However, the innate host defense against HTLV-1 is unclear. In this study, we report that the expression of Ku70, a known DNA sensor against DNA viruses, could be induced by HTLV-1 infection in HeLa, PMA-differentiated THP1 cells, primary human monocytes, and human monocyte-derived macrophages. In these cells, the overexpression of Ku70 inhibited the HTLV-1 protein expression, whereas the knockdown of Ku70 promoted the HTLV-1 protein expression. Furthermore, the overexpression of Ku70 enhanced the cellular response to HTLV-1 infection, whereas Ku70 knockdown yielded the opposite effect. Additionally, Ku70 was found to interact with HTLV-1 reverse transcription intermediate ssDNA90. ssDNA90 stimulation induced Ku70 expression and Ku70 promoted ssDNA90-triggered innate immune responses. Finally, HTLV-1 infection enhanced the association between Ku70 and stimulator of IFN genes, suggesting that stimulator of IFN genes was involved in Ku70-mediated host defenses against HTLV-1 infection. Taken together, our findings suggest a new sensor that detects HTLV-1 reverse transcription intermediate and controls HTLV-1 replication. These findings may provide new angles to understand host defenses against HTLV-1 infection and HTLV-1-associated diseases.

Ubiquitin specific peptidase 4 stabilizes interferon regulatory factor protein and promotes its function to facilitate interleukin-4 expression in T helper type 2 cells.

We speculated that ubiquitin specific peptidase 4 (USP4) may deubiquitinate interferon regulatory factor 4 (IRF4) and affect T helper type 2 (Th2) cell function. This study aimed to validate this hypothesis. Here, the interaction between USP4 and IRF4 were analyzed by co-immunoprecipitation assay. The deubiquitin effect of USP4 on IRF4 was analyzed by the Ni-NTA pull down assay. Luciferase reporter gene constructs were used to analyze the effects of USP4, IRF4 and nuclear factor of activated T cell-2 (NFATc2) on the activation of the interleukin-4 (IL-4) promoter. Then, the Th2 cells were infected with sh-USP4 to analyze the effects of USP4 on the expression levels of IRF4 and Th2-related cytokines. Western blotting and RT-qPCR were used to detect the protein and mRNA expression levels, respectively. To determine the levels of IL-4 and IRF4 in rheumatic heart disease (RHD) patients, peripheral blood mononuclear cells (PBMCs) were separated by density gradient centrifugation from RHD patients and healthy controls, and flow cytometric analysis was performed. Our results validated the interaction between USP4 and IRF4, and effects of USP4 on stabilization and deubiquitination of IRF4 were also found. Importantly, USP4 and IRF4 synergized with NFATc2 to specifically enhance NFAT-mediated activation of the IL-4 promoter. USP4 knockdown not only decreased the expression level of IRF4, but also affected the expression level of Th2-related cytokines. Finally, the increased level of IL-4 and IRF4 in PBMCs of RHD patients were observed. On the whole, our data indicate that USP4 interacts with and deubiquitinates IRF4, and also stabilizes IRF4 protein and promotes IRF4 function to facilitate IL-4 expression in Th2 cells, which may be related to the pathological process of RHD.

Peratrial Device Closure of Atrial Septal Defect Under Transesophageal Echocardiographic Guidance without Fluoroscopy Compared to Conventional On-Pump Surgical Closure.

Objective: This study is designed to evaluate the advantages between peratrial device closure under transesophageal echocardiographic guidance and open heart surgery in atrial septal defect. Methods: From November 2011 to September 2014, 28 patients with atrial septal defect were treated. Fourteen patients received peratrial device closure under transesophageal echocardiographic guidance (TEE group) and 14 patients received cardiopulmonary bypass (CPB group). Clinical parameters during intraoperative and postoperative periods were examined. Results: All patients recovered after surgery without serious complications. Compared with that in CPB group, clinical observations in TEE group showed significant decreases in the operation time (193.6±35.5 vs. 77.4±22.7 min, P<0.05), periods in intensive care unit (31.6±23.3 vs. 17.5±8.1 hours, P<0.05), fluid volume after operation (502.5±439.3 vs. 32.5±7.3 ml, P<0.05), postoperative length of hospital stay (8.9±2.8 vs. 6.8±2.4 days, P<0.05) and total hospitalization cost (7205.9±1617.6 vs. 5882.3±441.2 $, P<0.05). Conclusion: The peratrial device closure of atrial septal defect under transesophageal echocardiographic guidance is a mini-invasive, simple, safe and effective intervention. Its use in the clinical practice should be encouraged.

Peratrial device closure of atrial septal defect under transesophageal echocardiographic guidance without fluoroscopy compared to conventional on-pump surgical closure

Abstract Objective: This study is designed to evaluate the advantages between peratrial device closure under transesophageal echocardiographic guidance and open heart surgery in atrial septal defect. Methods: From November 2011 to September 2014, 28 patients with atrial septal defect were treated. Fourteen patients received peratrial device closure under transesophageal echocardiographic guidance (TEE group) and 14 patients received cardiopulmonary bypass (CPB group). Clinical parameters during intraoperative and postoperative periods were examined. Results: All patients recovered after surgery without serious complications. Compared with that in CPB group, clinical observations in TEE group showed significant decreases in the operation time (193.6±35.5 vs. 77.4±22.7 min, P<0.05), periods in intensive care unit (31.6±23.3 vs. 17.5±8.1 hours, P<0.05), fluid volume after operation (502.5±439.3 vs. 32.5±7.3 ml, P<0.05), postoperative length of hospital stay (8.9±2.8 vs. 6.8±2.4 days, P<0.05) and total hospitalization cost (7205.9±1617.6 vs. 5882.3±441.2 $, P<0.05). Conclusion: The peratrial device closure of atrial septal defect under transesophageal echocardiographic guidance is a mini-invasive, simple, safe and effective intervention. Its use in the clinical practice should be encouraged.