Automatic feature extraction and fusion recognition of motor imagery EEG using multilevel multiscale CNN.

A motor imagery EEG (MI-EEG) signal is often selected as the driving signal in an active brain computer interface (BCI) system, and it has been a popular field to recognize MI-EEG images via convolutional neural network (CNN), which poses a potential problem for maintaining the integrity of the time-frequency-space information in MI-EEG images and exploring the feature fusion mechanism in the CNN. However, information is excessively compressed in the present MI-EEG image, and the sequential CNN is unfavorable for the comprehensive utilization of local features. In this paper, a multidimensional MI-EEG imaging method is proposed, which is based on time-frequency analysis and the Clough-Tocher (CT) interpolation algorithm. The time-frequency matrix of each electrode is generated via continuous wavelet transform (WT), and the relevant section of frequency is extracted and divided into nine submatrices, the longitudinal sums and lengths of which are calculated along the directions of frequency and time successively to produce a 3 × 3 feature matrix for each electrode. Then, feature matrix of each electrode is interpolated to coincide with their corresponding coordinates, thereby yielding a WT-based multidimensional image, called WTMI. Meanwhile, a multilevel and multiscale feature fusion convolutional neural network (MLMSFFCNN) is designed for WTMI, which has dense information, low signal-to-noise ratio, and strong spatial distribution. Extensive experiments are conducted on the BCI Competition IV 2a and 2b datasets, and accuracies of 92.95% and 97.03% are yielded based on 10-fold cross-validation, respectively, which exceed those of the state-of-the-art imaging methods. The kappa values and p values demonstrate that our method has lower class skew and error costs. The experimental results demonstrate that WTMI can fully represent the time-frequency-space features of MI-EEG and that MLMSFFCNN is beneficial for improving the collection of multiscale features and the fusion recognition of general and abstract features for WTMI.

Coordination between NADPH oxidase and vascular peroxidase 1 promotes dysfunctions of endothelial progenitor cells in hypoxia-induced pulmonary hypertensive rats.

Previous studies have demonstrated that NADPH oxidase (NOX)/vascular peroxidase (VPO1) pathway - mediated oxidative stress plays an important role in the pathogenesis of multiple cardiovascular diseases. This study aims to evaluate the correlation between NOX/VPO1 pathway and endothelial progenitor cells (EPCs) dysfunctions in hypoxia-induced pulmonary hypertension (PH). The rats were exposed to 10% hypoxia for 3 weeks to establish a PH model, which showed increases in right ventricle systolic pressure, right ventricular and pulmonary vascular remodeling, acceleration in apoptosis and impairment in functions of the peripheral blood derived - EPCs (the reduced abilities in adhesion, migration and tube formation), accompanied by up-regulation of NOX (NOX2 and NOX4) and VPO1. Next, normal EPCs were cultured under hypoxia to induce apoptosis in vitro. Consistent with the in vivo findings, hypoxia enhanced the apoptosis and dysfunctions of EPCs concomitant with an increase in NOX and VPO1 expression, hydrogen peroxide (H2O2) and hypochlorous acid (HOCl) production; these phenomena were attenuated by NOX2 or NOX4 siRNA. Knockdown of VPO1 showed similar results to that of NOX siRNA except no effect on NOX expression and H2O2 production. Based on these observations, we conclude that NOX/VPO1 pathway-derived reactive oxygen species promote the oxidative injury and dysfunctions of EPCs in PH, which may contribute to endothelial dysfunctions in PH.

Magnesium Lithospermate B Derived from Salvia miltiorrhiza Ameliorates Right Ventricle Remodeling in Pulmonary Hypertensive Rats via Inhibition of NOX/VPO1 Pathway.

Right ventricle (RV) remodeling is a major pathological feature in pulmonary arterial hypertension (PAH). Magnesium lithospermate B (MLB) is a compound isolated from the roots of Salvia miltiorrhiza and it possesses multiple pharmacological activities such as anti-inflammation and antioxidation. This study aims to investigate whether MLB is able to prevent RV remodeling in PAH and the underlying mechanisms. In vivo, SD rats were exposed to 10% O2 for 21 d to induce RV remodeling, which showed hypertrophic features (increases in the ratio of RV weight to tibia length, cellular size, and hypertrophic marker expression), accompanied by upregulation in expression of NADPH oxidases (NOX2 and NOX4) and vascular peroxidase 1 (VPO1), increases in hydrogen peroxide (H2O2) and hypochlorous acid (HOCl) production and elevation in phosphorylation levels of ERK; these changes were attenuated by treating rats with MLB. In vitro, the cultured H9c2 cells were exposed to 3% O2 for 24 h to induce hypertrophy, which showed hypertrophic features (increases in cellular size and hypertrophic marker expression). Administration of MLB or VAS2870 (a positive control for NOX inhibitor) could prevent cardiomyocyte hypertrophy concomitant with decreases in NOX (NOX2 and NOX4) and VPO1 expression, H2O2 and HOCl production, and ERK phosphorylation. Based on these observations, we conclude that MLB is able to prevent RV remodeling in hypoxic PAH rats through a mechanism involving a suppression of NOX/VPO1 pathway as well as ERK signaling pathway. MLB may possess the potential clinical value for PAH therapy.

Magnesium lithospermate B prevents phenotypic transformation of pulmonary arteries in rats with hypoxic pulmonary hypertension through suppression of NADPH oxidase.

Magnesium lithospermate B (MLB) shows multiple biological activities including anti-oxidation and anti-proliferation in various diseases. However, the function of MLB in pulmonary arterial hypertension (PAH) is still unknown. This study aims to investigate the effect of MLB on hypoxia-induced phenotypic transformation of pulmonary arterial smooth muscle cells (PASMCs) and the underlying mechanisms. SD rats (or PASMCs) were exposed to 10% O2 for 3 weeks (or 3% O2 for 48 h) along with MLB or NADPH oxidase （NOX） inhibitor intervention. The effects of MLB on hemodynamics, pulmonary vascular remodeling and phenotypic transformation of PASMCs were observed first. Then, its effects on the protein levels of NOX (NOX2 and NOX4), ERK and p-ERK were examined. The results showed that MLB prevented the elevation in right ventricular systolic pressure and the increase in ratio of wall thickness to vessel external diameter of pulmonary arteries in PAH rats, and attenuated phenotypic transformation of PASMCs (decrease in α-smooth muscle actin while increase in osteopontin), accompanied by downregulation of NOX (NOX2 and NOX4) protein levels, decrease of ROS and H2O2 production, and suppression of the phosphorylation of ERK. NOX inhibitor (VAS2870) achieved similar results to that of MLB did in the hypoxia-treated PASMCs. Based on the observations, we conclude that MLB is able to prevent phenotypic transformation of pulmonary arteries in hypoxic PAH rats through suppression of NOX/ROS/ERK pathway, and MLB might have the potentials in PAH therapy.

The time-dependent effects of St John's wort on cytochrome P450, uridine diphosphate-glucuronosyltransferase, glutathione S-transferase, and NAD(P)H-quinone oxidoreductase in mice.

Hypericum perforatum [St. John's wort (SJW)] is known to cause a drug interaction with the substrates of cytochrome P450 (P450, CYP) isoforms, mainly CYP3A. This study aims to determine the dose response and time course of the effects of SJW extract on P450s, UDP-glucuronosyltransferase (UGT), glutathione S-transferase (GST), and NAD(P)H-quinone oxidoreductase (NQO) in mice. The oral administration of SJW extract to male mice at 0.6 g/kg/d for 21 days increased hepatic oxidation activity toward a Cyp3a substrate nifedipine. By extending the SJW treatment to 28 days, hepatic nifedipine oxidation (NFO) and warfarin 7-hydroxylation (WOH) (Cyp2c) activities were increased by 95% and 34%, respectively. Immunoblot analysis of liver microsomal proteins revealed that the Cyp2c protein level was elevated by the 28-day treatment. However, the liver microsomal activities of the oxidation of the respective substrates of Cyp1a, Cyp2a, Cyp2b, Cyp2d, and Cyp2e1 remained unchanged. In the kidney, SJW increased the NFO, but not the WOH activity. The extended 28-day treatment did not alter mouse hepatic and renal UGT, GST, and NQO activities. These findings demonstrate that SJW stimulates hepatic and renal Cyp3a activity and hepatic Cyp2c activity and expression. The induction of hepatic Cyp2c requires repeated treatment for a period longer than the initial induction of Cyp3a.

Suppression of NADPH oxidase attenuates hypoxia-induced dysfunctions of endothelial progenitor cells.

NADPH oxidases (NOX) - derived reactive oxygen species (ROS) contribute to oxidative injury in hypoxia-induced pulmonary arterial hypertension. This study aims to evaluate the status of NOX in endothelial progenitor cells (EPCs) under hypoxic condition and to determine whether NOX inhibitors could attenuate hypoxia-induced dysfunctions of EPCs. EPCs were isolated from peripheral blood of SD rats and subjected to hypoxia (O2/N2/CO2, 1/94/5) for 24 h. The cells were collected for ß-galactosidase or Hoechst staining, or for functional analysis (migration, adhesion and tube formation). The NOX expression, activity and H2O2 content in EPCs were measured. The results showed that hypoxia treatment promoted EPC senescence and apoptosis, accompanied by the deteriorated functions of EPCs (the reduced abilities in adhesion, migration and tube formation), as well as an increase in NOX2 and NOX4 expression, NOX activity and H2O2 production, these phenomena were attenuated by NOX inhibitors. Furthermore, administration of catalase could also improve the functions of hypoxia-treated EPCs. Based on these observations, we conclude that NOX-derived ROS contributes to the dysfunctions of EPCs under hypoxic condition. Thus, suppression of NOX may provide a novel strategy to improve endothelial functions in hypoxia-relevant diseases.

Duplication of 10q22.3-q23.3 encompassing BMPR1A and NGR3 associated with congenital heart disease, microcephaly, and mild intellectual disability.

Chromosome region 10q22.3-q23.3 contains several low copy repeats (LCRs) and is prone to recombination. Deletions with breakpoints within LCR3 and LCR4 have been described to be associated with intellectual disability and dysmorphic features, while the reciprocal duplications are rarely reported. We present an additional case with multiple congenital anomalies that include microcephaly, cardiac defect, and mild intellectual disability, in which a de novo interstitial 8.2-Mb duplication of 10q22.3-q23.3, including BMPR1A and NGR3, was identified by Illumina SNP array platform. Our study is consistent with the hypothesis that the BMPR1A is a plausible candidate gene for congenital heart disease (CHD) and should contribute to the diagnosis and treatment of these genomic diseases.

Anomalous origin of the right pulmonary artery from the ascending aorta: results of direct implantation surgical repair in 6 infants.

BACKGROUND: Anomalous origin of the right pulmonary artery from the ascending aorta (AORPA) is a rare and potential fatal kind of congenital heart disease. This study summarizes the techniques and outcomes of 6 infants with AORPA who underwent the surgical repair. METHODS: Between November 2012 and November 2014, 6 infants with AORPA received surgical repair in the Second Xiangya Hospital and were included in the present study. RESULTS: Six infants (4 male, 66.7 %) with a median age of 101.5 ± 70.0 days, and a median body weight of 4.13 ± 0.62 kg underwent the surgical repair at our institute. There were no operative, in-hospital or follow-up deaths. Clinical symptoms of all 6 patients relieved at time of discharge, and mean pulmonary artery pressure (MPAP) decreased significantly after surgery. During follow-up, there were no further operations or interventions, mild stenosis at the anastomotic site presented in one patient, and all patients were asymptomatic and in stable clinical condition. CONCLUSIONS: The short and mid-term surgical outcomes of AORPA are excellent in this group of operations. Moreover, we believe the direct implantation to be the optimal surgical strategy for the patients with the proximal form of AORPA.

Whole-exome sequencing identifies Y1495X of SCN5A to be associated with familial conduction disease and sudden death.

SCN5A mutations have been reported to underlie a variety of inherited arrhythmias, while the complex overlapping phenotype, especially with congenital heart disease (CHD), is rarely reported. The 48-year-old proband underwent a recent syncope during rest. A CHD (tetralogy of Fallot) and conduction disease was revealed by echocardiogram and ultrasonic cardiogram examination. We combined whole-exome sequencing (WES) and bioinformatics strategies to identify the pathogenic gene for this autosomal-dominant cardiac conduction disease (CCD) in a multi-generation pedigree. We examined four members of this family, including three affected and one unaffected. A novel nonsense mutation (Y1495X) in SCN5A was identified in the affected family members. This mutation is predicted to generate a truncated SCN5A protein, which could result in the loss of sodium current, a defined mechanism of SCN5A related arrhythmias. Our study provides evidence that WES is a highly effective approach for genetic analyses of rare clinical phenotypes. Our study also offers accurate genetic testing information for those yet clinically negative relatives.

Rare de novo copy number variants in patients with congenital pulmonary atresia.

BACKGROUND: Ongoing studies using genomic microarrays and next-generation sequencing have demonstrated that the genetic contributions to cardiovascular diseases have been significantly ignored in the past. The aim of this study was to identify rare copy number variants in individuals with congenital pulmonary atresia (PA). METHODS AND RESULTS: Based on the hypothesis that rare structural variants encompassing key genes play an important role in heart development in PA patients, we performed high-resolution genome-wide microarrays for copy number variations (CNVs) in 82 PA patient-parent trios and 189 controls with an Illumina SNP array platform. CNVs were identified in 17/82 patients (20.7%), and eight of these CNVs (9.8%) are considered potentially pathogenic. Five de novo CNVs occurred at two known congenital heart disease (CHD) loci (16p13.1 and 22q11.2). Two de novo CNVs that may affect folate and vitamin B12 metabolism were identified for the first time. A de novo 1-Mb deletion at 17p13.2 may represent a rare genomic disorder that involves mild intellectual disability and associated facial features. CONCLUSIONS: Rare CNVs contribute to the pathogenesis of PA (9.8%), suggesting that the causes of PA are heterogeneous and pleiotropic. Together with previous data from animal models, our results might help identify a link between CHD and folate-mediated one-carbon metabolism (FOCM). With the accumulation of high-resolution SNP array data, these previously undescribed rare CNVs may help reveal critical gene(s) in CHD and may provide novel insights about CHD pathogenesis.

576 kb deletion in 1p36.33-p36.32 containing SKI is associated with limb malformation, congenital heart disease and epilepsy.

1p36 deletion (monosomy 1p36) is one of the most common terminal deletions observed in humans, characterized by special facial features, mental retardation, heart defects, development delay and epilepsy. Previously, we reported molecular findings in patients with limb, congenital heart disease (CHD) and other malformations with SNP-array. In a syndromic patient of the same cohort, we detected a small deletion of 1p36.33-p36.32 containing SKI (Sloan-Kettering Institute protooncoprotein). Recently, dominant mutations in SKI were identified to be correlated with Shprintzen-Goldberg syndrome. Retrospective examination revealed this patient with limb malformations, CHD, epilepsy and mild development delay. Together with previous reports, our study suggests that the 1p36.33-1p36.32 deletion encompassing SKI may represents a previous undescribed microdeletion disorder.

A 1.1Mb deletion in distal 13q deletion syndrome region with congenital heart defect and postaxial polydactyly: additional support for a CHD locus at distal 13q34 region.

13q deletion syndrome is a rare genetic disorder, especially for group 3 deletion (13q33-q34 deletion). Previously we described a patient with congenital heart defect and mental retardation and proposed that a distal 6Mb region might contain the causative gene of congenital heart defect. Here we present a new patient with congenital heart defects (CHD), hand and foot anomalies and mild mental retardation. We identified a 1.1Mb deletion at chromosome 13q34 with high resolution SNP-array BeadChips (HumanOmni1-Quad, Illumina, USA). This chromosome region contains ten annotated genes, including GRK1, TFDP1, RASA3 and GAS6. To our knowledge, this represents the smallest 13q34 deletion identified to date. Our study provides additional support that distal 13q34 deletion region might contain key gene(s) responsible for cardiac development.

Duplication of 8q12 encompassing CHD7 is associated with a distinct phenotype but without duane anomaly.

Interstitial duplications of 8q12 encompassing CHD7 have recently been described as a new microduplication syndrome. Three 8q12 duplications have been reported with shared recognizable phenotype: Duane anomaly, developmental delay and dysmorphic facial features. We identified a 2.7 Mb duplication on chromosome 8q12 with SNP-array in a patient with growth delay, congenital heart defects, ear anomalies and torticollis. To our knowledge, this is the smallest duplication reported to date. Our findings support the notion that increased copy number of CHD7 may underlie the phenotype of the 8q12 duplication. Our study together with previous studies suggest that the 8q12 duplication could be defined as a novel syndrome.

Microduplication of 3p25.2 encompassing RAF1 associated with congenital heart disease suggestive of Noonan syndrome.

Noonan syndrome (NS) is a clinically variable and genetically heterogeneous disorder with congenital heart defects (CHD), short stature, and craniofacial dysmorphisms. Gain-of-function mutations in RAF1 can cause NS and the highly related NS with multiple lentigines (previously known as LEOPARD syndrome). Here we report on a 15-year-old male with NS phenotype: short stature, heart defects, low posterior hairline, facial malformations, malformed left ear with sensorineural hearing loss, widely spaced nipples, and unilateral upper limb anomaly. Using high-resolution SNP array technology, we identified in this patient a 0.25 Mb microduplication at 3p25.2 in which RAF1 is located. Sequence analysis did not identify mutations in genes associated with Holt-Oram syndrome. These findings suggest that duplications of genomic regions encompassing RAF1 could cause NS and are consistent with the notion that rare copy number variations encompassing causative genes may underlie a small percentage of patients with syndromic CHD like NS.

[Experimental study of rat mesenchymal stem cells transfected with Sonic Hedgehog gene].

OBJECTIVE: To evaluate the feasibility of genetic modification of mesenchymal stem cells (MSC) with Sonic Hedgehog (Shh) gene. METHODS: The pcDNA3.1-Shh eukaryotic expression plasmid was constructed and its correctness evaluated by the restriction enzyme analysis and sequencing. MSC were isolated from Wistar rats by density gradient centrifugation and purified, transfected with pcDNA3.1-Shh, blank plasmid pcDNA3.1(-) or pmaxGFP respectively by Nucleofector(TM). The protein expression of Shh in MSC was detected by Western blot after 48 hours. RESULTS: Correct construction of pcDNA3.1-Shh was identified by the methods of restriction enzyme analysis and nucleotide sequence determination. The expression of green fluorescent protein (GFP) could be observed by fluorescence microscopy after 48 hours. The expression of Shh gene was detected by Western blot. But the MSC transfected with empty plasmid expression was not detected. CONCLUSIONS: Recombinant Eukaryotic expression plasmid pcDNA3.1-Shh is successfully detected in rat MSC. It may provide experimental rationales for the future gene therapy.

[Efficacy comparison between micro invasive occlusion procedure and extracorporeal circulation procedure for treating patients with simple ventricular septal defect].

OBJECTIVE: To compare the efficacy between micro invasive occlusion procedure and extracorporeal circulation procedure for treating patients with simple ventricular septal defect. METHODS: Two hundred and twenty patients with simple ventricular septal defect (except subarterial ventricular septal defect) were randomly divided into micro invasive group (n = 116) and traditional cardiopulmonary bypass surgery group (n = 104). Clinical data were collected and compared at baseline and at 3, 30 and 180 days after surgery. RESULTS: Age, gender, body weight and ventricular septal defect type were similar between the two groups (all P > 0.05). Operation time and hospitalization duration were significantly shorter in the micro invasive group than the traditional cardiopulmonary bypass surgery group (all P < 0.05). The proportion of blood transfusion was less in micro invasive group than the traditional cardiopulmonary bypass surgery group [2.59% (3/116) vs. 72.12% (75/104), P < 0.01]. Three days after surgery, incidence of mild and above tricuspid insufficiency was less in micro invasive group than the traditional cardiopulmonary bypass surgery group [0.86% (1/116) vs. 2.88% (3/104), P < 0.05]. There was one patient developed mild pericardial effusion at 30 days post surgery in micro invasive group. There was no intracardiac infection in the two groups during follow-up. At 30 and 180 days post surgery, incidence of residual shunt was also less in micro invasive group than the traditional cardiopulmonary bypass surgery group [1.72% (2/116) vs. 7.69 (8/104) and 0(0/116) vs. 7.69(8/104), all P < 0.05]. After surgery for 3, 30 and 180 days, transthoracic echocardiography derived chamber size, left ventricular end-diastolic volume index and left ventricular ejection fraction were similar between the two groups (all P > 0.05). CONCLUSIONS: The efficacy is similar for patients with simple ventricular septal defect (except subarterial ventricular septal defect) using micro invasive occlusion therapy or extracorporeal circulation surgery. Micro invasive occlusion procedure can shorten operation and hospitalization time, and reduce the need for blood transfusion and risk of developing procedural-related tricuspid insufficiency and post-procedural residual shunt.

[1,25(OH)(2)D(3) influences endothelial cell proliferation, apoptosis and endothelial nitric oxide synthase expression of aorta in apolipoprotein E-deficient mice].

OBJECTIVE: To study possible influences of 1,25(OH)(2)D(3) on endothelial cell proliferation, apoptosis and endothelial nitric oxide synthase (eNOS) expression of aorta in apolipoprotein E-deficient (apoE(-/-)) mice and to explore the relationship between vitamin D and atherosclerosis. METHOD: Endothelial cell of aorta in apoE(-/-) mice were isolated and cultured, and the influence of 1,25(OH)(2)D(3) on endothelial cell proliferation were observed by MTT, apoptosis of cells were quantitated by terminal deoxynucleotidyl transferase mediated dUTP nick end labelling, Bcl-2 mRNA, fas mRNA and eNOS mRNA was detected by reverse transcription-polymerase chain reaction. RESULT: Endothelial cell proliferation rate of aorta did not significantly change in the two control groups (0.162 ± 0.031 vs. 0.158 ± 0.006, P > 0.05). Compared with control groups, 1,25(OH)(2)D(3) stimulated endothelial cell proliferation of aorta (P < 0.05), but endothelial cell proliferation rate did not significantly change in different 1,25(OH)(2)D(3) concentration groups [1,25(OH)(2)D(3) concentration: 10(-4)mol/L, 10(-5) mol/L, 10(-6) mol/L, 10(-7) mol/L, 10(-8) mol/L, endothelial cell proliferation rate: 0.189 ± 0.013 vs. 0.285 ± 0.011 vs. 0.296 ± 0.026 vs. 0.284 ± 0.017 vs. 0.233 ± 0.010, P > 0.05]. 1,25(OH)(2)D(3) research concentration as chosen as 10(-6) mol/L. In 1,25(OH)(2)D(3) 10(-6) mol/L group, the expression of Bcl-2, eNOS mRNA was significantly increased (0.78 ± 0.16 vs. 0.46 ± 0.21 vs. 0.42 ± 0.17, 0.56 ± 0.16 vs. 0.39 ± 0.13 vs. 0.35 ± 0.11, 0.46 ± 0.2 vs. 10.42 ± 0.17 vs. 0.78 ± 0.16, 0.79 ± 0.21 vs. 0.81 ± 0.20 vs. 0.43 ± 0.12), apoptotic index, Fas mRNA was significantly decreased (15.14 ± 3.19 vs. 18.94 ± 4.22 vs. 19.27 ± 4.58, 0.43 ± 0.12 vs.0.79 ± 0.21 vs. 0.81 ± 0.20)(P < 0.05). The quantity of eNOS gene expression was inversely associated with apoptosis index and Fas mRNA, was positively associated with Bcl-2 mRNA (r = -0.676, -0.758, 0.762, P < 0.01). CONCLUSION: 1,25(OH)(2)D(3) stimulated endothelial cell proliferation, inhibited apoptosis and increased eNOS expression of aorta in apoE(-/-) mice. These results may deepen understanding of the pathogenesis of atherosclerosis.

[CT angiography-based simulation of the surgical approach in early operation for ruptured aneurysm].

OBJECTIVE: To simulate the surgical approaches for intracranial aneurysms using three-dimensional CT angiography (3D-CTA) and assess the value of 3D-CTA in early microneurosurgery for ruptured intracranial aneurysms. METHODS: Forty-eight patients with spontaneous subarachnoid hemorrhage due to ruptured intracranial aneurysm were confirmed by early operation. All the patients were classified according to Hunt-Hess, including 11 of grade I, 29 of grade II, and 8 of grade III. CTA was performed before the operation and surgical simulation was conducted. The preoperative findings on CTA and the intraoperative findings were compared and the clinical value of cerebral 3D-CTA was analyzed. RESULTS: Pre-operative 3D-CTA clearly displayed the location, size and shape of the aneurysms, the axis direction of the aneurysm apex and the width of aneurysm neck. The spatial relation between the parent aneutysm artery, the aneurysm, the peripheral vessels and the bony structures were also demonstrated. These findings were basically consistent with the intraoperative findings. The Glasgow outcome score was 5 in 41 patients, 4 in 4 patients, 3 in 2 patients, and 2 in 1 patient upon discharge from the hospital. CONCLUSIONS: Preoperative 3D-CTA examination can simulate the surgery for ruptured aneurysms to help improve the surgical success rate.

[Relationship between the expression of heat shock protein 25 and selenium binding protein 1 with ischemia/reperfusion lung injury in vivo: experiment with rats].

OBJECTIVE: To analyze the differential expression proteins of rat ischemia/reperfusion (I/R) lung tissues in vivo and normal lung tissues by comparative proteome analysis, and to study the mechanism of donor lung I/R injury. METHODS: Forty male SD rats were randomly divided into 2 equal groups: I/R group undergoing mimic orthotopic left lung auto-grafting and harvesting of the left lung five hours after the operation, and control group undergoing isolation of the left hilus of lung and then harvesting of the left lung. The differential proteins in the left ventricle of transplanted heart were separated by means of immobilized pH gradient-based two-dimensional gel electrophoresis (2-DE), identified by matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF-MS), and searched through Matrix Science software system. Western blotting was used to verify part of the differentially expressed proteins. RESULTS: Well-resolved and reproducible 2-DE profile of rat I/R lung tissues and normal lung tissues were obtained. In the I/R lung tissue profile, the average spot number from 3 gels was 489 +/- 52 spots (P > 0.05) with an average matching rate of 89.28% (P > 0.05), and in the control group, the average spot number from 3 gels was 511 +/- 83 spots (P > 0.05) with an average matching rate of 91.22% (P > 0.05). Fourteen differential proteins were identified by peptide mass fingerprinting (PMF) searched in Matrix Science (P < 0.05). Western blotting confirmed that the protein expression of selenium binding protein 1 (SBP-1) and heat shock protein 25 (HSP25) increased at the early stage of I/R group. CONCLUSION: The protein expression of HSP25 and SBP-1 with stress protection function is upregulated in the early stage of lung I/R injury. Other differentially expressed proteins identified may have important functions in energy metabolism, tissue stress, cell apoptosis, and signal transduction.