Exploration of anatomical distribution of brain metastasis from breast cancer at first diagnosis assisted by artificial intelligence.

Objectives: This study aimed to explore the spatial distribution of brain metastases (BMs) from breast cancer (BC) and to identify the high-risk sub-structures in BMs that are involved at first diagnosis. Methods: Magnetic resonance imaging (MRI) scans were retrospectively reviewed at our centre. The brain was divided into eight regions according to its anatomy and function, and the volume of each region was calculated. The identification and volume calculation of metastatic brain lesions were accomplished using an automatically segmented 3D BUC-Net model. The observed and expected rates of BMs were compared using 2-tailed proportional hypothesis testing. Results: A total of 250 patients with BC who presented with 1694 BMs were retrospectively identified. The overall observed incidences of the substructures were as follows: cerebellum, 42.1 %; frontal lobe, 20.1 %; occipital lobe, 9.7 %; temporal lobe, 8.0 %; parietal lobe, 13.1 %; thalamus, 4.7 %; brainstem, 0.9 %; and hippocampus, 1.3 %. Compared with the expected rate based on the volume of different brain regions, the cerebellum, occipital lobe, and thalamus were identified as higher risk regions for BMs (P value ≤ 5.6*10-3). Sub-group analysis according to the type of BC indicated that patients with triple-negative BC had a high risk of involvement of the hippocampus and brainstem. Conclusions: Among patients with BC, the cerebellum, occipital lobe and thalamus were identified as higher-risk regions than expected for BMs. The brainstem and hippocampus were high-risk areas of the BMs in triple negative breast cancer. However, further validation of this conclusion requires a larger sample size.

Complete mitochondrial genome of Brachionus rubens from wuhu, China (Rotifera, Brachionidae).

The complete mitochondrial genome of Brachionus rubens was sequenced using primers design, clone culture, DNA extraction, LONG-PCR amplification, purification and clone sequencing. We found that it is composed of two circular chromosomes, designated mtDNA I (11,398 bp) and mtDNA II (12,820 bp). The gene content of the B. rubens mitochondrial genome was similar to that of the previously reported mitochondrial genome of B. plicatilis. It contained 22 tRNA genes, 2 rRNA genes and 12 protein-coding genes (PCGs). Four of the 12 PCGs had an incomplete stop codons, TA（cob, atp6, nd3）or T(cox3). The A + T content of B. rubens mitochondrial genome was apparently higher (mtDNA-I 70.2% and mtDNA II 70.4%) than that of the mitochondrial genome of B. plicatilis (mtDNA-I 63.9% and mtDNA-II 62.9%).

Sirtuin 1 Mediates Hydrogen Sulfide-induced Cytoprotection Effects in Neonatal Mouse Cardiomyocytes.

BACKGROUND: Current knowledge indicates that oxidative damage and the following inflammation is pivotal pathway for myocardial cell death. In recent decades, hydrogen sulfide (H2S) has been identified as a novel endogenous vasodilator and neuromodulator due to its antioxidation capacity. However, whether H2S pretreatment in neonatal mouse cardiomyocytes is a protection effect against oxidative stress remains elusive. METHODS: Primary neonatal mouse cardiomyocytes were isolated and cultured, subsequently, pretreated with the H2S donor, sodium hydrosulfide (NaHS). Cell viability, lactate dehydrogenase (LDH) release, and reactive oxygen species (ROS) production are evaluated. The levels of superoxide dismutase (Sod2) and Sirtuin 1 (Sirt1), a deacetylation enzyme, were detected by Western blotting. The statistics was performed using independent-sample t-test. RESULTS: NaHS (100 µmol/L) had no toxicity to primary neonatal mouse cardiomyocytes. Furthermore, NaHS pretreatment significantly improved neonatal mouse cardiomyocytes survival after H2O2-induced cell death, indicated by the decrease in LDH release (40.00 ± 2.65% vs. 65.33 ± 4.33%, P < 0.01) and ROS production (1.90 ± 0.33 vs. 4.56 ± 0.56, P < 0.05), and that the salubrious effect was accompanied by the upregulation of Sod2 expression. In addition, the study showed that NaHS pretreatment improved mitochondrial DNA number in neonatal mouse cardiomyocyte. Furthermore, the result demonstrated NaHS increased the expression of Sirt1 in neonatal mouse cardiomyocyte. Ex 527, an inhibitor of Sirt1, could attenuate these effects of NaHS-induced Sod2 expression and mtDNA number increase, furthermore, abrogate the cytoprotective effects of NaHS for neonatal mouse cardiomyocytes. CONCLUSION: Sirt1 mediated H2S-induced cytoprotection effects in neonatal mouse cardiomyocytes.

Correlation between GATA4 gene polymorphism and congenital heart disease.

OBJECTIVE: The correlation between GATA4 gene polymorphism and congenital heart disease (CHD) was analyzed. METHOD: Clinical data and blood samples were collected from 350 CHD patients who were treated at the Department of Cardiology in Beijing Anzhen Hospital. The control group consisted of 350 healthy subjects receiving physical examination at our hospital during the same period. Polymorphism was detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis for locus rs11392441 of GATA4 gene. RESULTS: Polymorphism of locus rs1139244 of GATA4 gene was detected in CHD patients. The distribution frequencies of GG genotype and G allele were significantly higher than those of the control group. CONCLUSION: Polymorphism of locus rs1139244 of GATA4 gene was correlated with CHD.

Serum UCH-L1 as a Novel Biomarker to Predict Neuronal Apoptosis Following Deep Hypothermic Circulatory Arrest.

BACKGROUND: Deep hypothermic circulatory arrest (DHCA) has been used in cardiac surgery involving infant complex congenital heart disease and aortic dissection. DHCA carries a risk of neuronal apoptotic death in brain. Serum ubiquitin C-terminal hydrolase L1 (UCH-L1) level is elevated in a number of neurological diseases involving neuron injury and death. We studied the hypothesis that UCH-L1 may be a potential biomarker for DHCA-induced ischemic neuronal apoptosis. METHODS: Anesthetized piglets were used to perform cardiopulmonary bypass (CPB). DHCA was induced for 1 hour followed by CPB rewarming. Blood samples were collected and serum UCH-L1 levels were measured. Neuron apoptosis and Bax and Bcl-2 proteins in hippocampus were examined. The relationship between neuron apoptosis and UCH-L1 level was determined by receiver operating characteristics (ROC) curves and correlation analysis. RESULTS: DHCA resulted in marked neuronal apoptosis, significant increase in Bax:Bcl-2 ratio in hippocampus and UCH-L1 level elevations in serum (all P<0.05). Positive correlation was obtained between serum UCH-L1 level and the severity of neuron apoptosis (r= 0.78, P<0.01). By ROC, the area under the curve were 0.88 (95% CI: 0.74-0.99; P<0.01), 0.81 (95% CI: 0.81-0.96; P<0.05), 0.71 (95% CI: 0.47-0.92; P=0.11) for UCH-L1, Bax/Bcl-2 ratio and Bax, respectively. Using a cut-off point of 0.25, the UCH-L1 predicted neuronal apoptosis with a sensitivity of 85% and specificity of 57%. CONCLUSION: Serum UCH-L1, as an easy and quick measurable biomarker, can predict neural apoptosis induced by DHCA. The elevation in UCH-L1 concentration is consistent with the severity of neural apoptosis following DHCA.

Association between high-density lipoprotein cholesterol and renal function in elderly hypertension: a cross-sectional study in Chinese population.

Few studies have yet investigated the possible association between high-density lipoprotein cholesterol (HDL-C) and kidney function in elderly patients with primary hypertension. Accordingly, the aim of the present study was to evaluate the relationship between HDL-C and kidney function in elderly hypertension. A total of 14,644 elderly hypertensive subjects were enrolled in our cross-sectional study. The patients were categorized based on serum HDL-C level and glomerular filtration rate (GFR) value, respectively. One-way analysis of variance was used to compare the parameters among different groups. Bonferroni correction was performed for multiple comparisons. Analysis of covariance was used to control for confounding factors. The significance of difference between 3 groups and more was determined by chi-square test for categorical variables. Serum creatinine and uric acid were negatively related to HDL-C level, whereas GFR was positively related to HDL-C level in elderly hypertensive patients according to tertiles of HDL-C and tertiles of HDL-C/total cholesterol ratio (all P for trends <0.05). The male elderly hypertensive patients showed stronger relationship between HDL-C and renal function than the female elderly hypertensive subjects. Low HDL-C was associated with renal insufficiency and proteinuria in the hypertensive elderly (P < 0.05). The elderly "renal-hyperfiltrator" appeared to have lower HDL-C level, compared with the "normal renal-filtrator" (P < 0.05). There was an inverse "V" shape between HDL-C and GFR by GFR strata. Our results point out that there is an association of low HDL-C level with impaired kidney function in elderly hypertensive patients. Glomerular hyperfiltration may also affect HDL-C level and sex might be an influential factor for the association of HDL-C with kidney function in elderly hypertension.

Inhibitory effects of C-type natriuretic peptide on the differentiation of cardiac fibroblasts, and secretion of monocyte chemoattractant protein-1 and plasminogen activator inhibitor-1.

The present study aimed to investigate the effect of C-type natriuretic peptide (CNP) on the function of cardiac fibroblasts (CFs). Western blotting was used to investigate the expression of myofibroblast marker proteins: α-smooth muscle actin (α-SMA), extra domain-A fibronectin, collagen I and collagen III, and the activity of extracellular signal-regulated kinase 1/2 (ERK1/2). Immunofluorescence was used to examine the morphological changes; a transwell assay was used to analyze migration, and reverse transcription-quantitative polymerase chain reaction and ELISA were employed to determine the mRNA expression and protein secretion of monocyte chemoattractant protein-1 (MCP-1) and plasminogen activator inhibitor-1 (PAI-1). The results demonstrated that CNP significantly reduced the protein expression of α-SMA, fibronectin, collagen I and collagen III, and suppressed the migratory ability of CFs. Additionally, the mRNA and protein expression of MCP-1 and PAI-1 was inhibited under the CNP treatment; and this effect was mediated by the inhibition of the ERK1/2 activity. In conclusion, CNP inhibited cardiac fibroblast differentiation and migration, and reduced the secretion of MCP-1 and PAI-1, which demonstrates novel mechanisms to explain the antifibrotic effect of CNP.

The complete mitochondrial genome of the Zacco platypus, Huangshan, China (Cypriniformes: Cyprinidae, subfamily Daninninae).

The mitochondrial genome of Zacco platypus (Cypriniformes: Cyprinidae, subfamily Daninninae) is a circular molecule of 16,611 bp in length, containing 37 typical animal mitochondrial genes: 13 protein-coding genes (PCGs), 2 ribosomal RNAs, 22 transfer RNAs and a D-loop region. Its gene order and arrangement are identical to the common type found in most fish mitogenomes. All PCGs start with a typical ATG codon except for COI which use GTG as start codon; all PCGs terminate in the common stop codon TAA or TAG, except for the COII which use single T as stop codon. The D-loop region is 928 bp long, located between tRNAPro and tRNAPhe genes. It contains some structures of repeated motifs and microsatellite-like elements characteristic of the Cyprinidae.

The complete mitochondrial genome of the Acrossocheilus fasciatus (Cyprinidae, Barbinae).

The mitochondrial genome of Acrossocheilus fasciatus (Cyprinidae, Barbinae) is a circular molecule of 16,589 bp in length, containing 37 typical animal mitochondrial genes: 13 protein-coding genes (PCGs), 2 r RNAs, 22 t RNAs and a non-coding D-loop region. Its gene order and arrangement are identical to the common type found in most fish mitogenomes. All PCGs start with a typical ATG codon except for COI which use GTG as a start codon; all PCGs terminate in the common stop codon TAA or TAG, except for the ND2, ND3, ND4, COII, Cytb and COIII which use single T or TA as a stop codon. The non-coding D-loop region is 938 bp long, located between tRNAPro and tRNAPhe genes. It contains some structures of repeated motifs and microsatellite-like elements characteristic of the Cyprinidae.

The follow-up surgical results of coarctation of the aorta procedures in a cohort of Chinese children from a single institution.

OBJECTIVES: The aim of this study was to evaluate the results following surgeries for the treatment of coarctation of the aorta in Chinese paediatric patients and to compare the surgery outcomes between simple and complex coarctation procedures. METHODS: Between January 2006 and December 2011, 107 consecutive paediatric patients with coarctation of the aorta underwent surgery. Forty-four patients (41.12%) were classified as having simple coarctations (group A), and 54 patients (50.47%) were classified as having complex coarctations (group B). Echocardiography and the resting systolic blood pressure were evaluated prior to the operation, at one month following the operation, and then once annually. RESULTS: Follow-up was 93.5% complete (100 patients), without significant differences between the two groups. Arch hypoplasias and bicuspid aortic valves were initially present in 10 (9.35%) and 11 (10.28%) of 107 patients, respectively. There were no deaths among the group A patients and three (5.56%) early deaths among the group B patients. There was a significant difference in the restenosis incidence rate between the two groups during the most recent follow-up consultations (p<0.05). Additionally, only 10 of 43 group A and 10 of 51 group B patients had persistently abnormal blood pressures during the annual follow-up consultations. CONCLUSIONS: The postoperative restenosis ratio was increased in the complex coarctation group compared with the simple coarctation group. Additionally, the complex coarctation patients who did not have restenosis at follow-up had a lower proportion of hypertension.

Stented elephant trunk technique for retrograde type A aortic dissection after endovascular stent graft repair.

BACKGROUND: Retrograde type A aortic dissection is a rare but deadly complication after thoracic endovascular aortic repair of type B aortic dissection. Total arch replacement combined with a modified stented elephant trunk technique (SET), was performed for these complicated dissections. We reviewed our results of the procedure for this serious complication, aiming to evaluate the feasibility of the technique. METHODS: Between April 2005 and September 2012, 24 patients with retrograde type A aortic dissection after thoracic endovascular aortic repair underwent the SET procedure in our center. The mean age at operation was 44.1±8.8 years old. Postoperative mortality and morbidity were analyzed to evaluate the immediate and mid-term results. RESULTS: Death at 30 days was 4.2% (1 of 24 patients). No patient suffered paraplegia or stroke after operation. Follow-up was completed with 23 survivors. The mean follow-up period was 32.2±13.1 months (range, 12 to 49 months). No late deaths occurred during follow-up. One patient underwent reoperation for replacement of the thoracoabdominal aorta and enjoyed an uneventful survival. CONCLUSIONS: The stented elephant trunk technique could be an alternative for treatment of retrograde type A aortic dissection with acceptable surgical risks and satisfactory results.

The effects of neuromuscular blockade on operating conditions during general anesthesia for spinal surgery.

BACKGROUND: Muscle relaxants are prescribed routinely for patients undergoing general anesthesia, but the requirement for paralysis in spinal surgery is unclear. This study compared the operating conditions of general anesthesia with and without a muscle relaxant on spinal surgery patients. METHODS: Eighty-six adults who underwent elective spinal surgery were randomly assigned to a relaxant group (group R) or a no-relaxant group (group NR). All patients were induced with intravenous midazolam (0.05 mg/kg), fentanyl (4 µg/kg), propofol (1.0 mg/kg), and succinylcholine (2 mg/kg) and then atracurium was used in group R but not in group NR. The operating conditions, including muscle tone, body movements, airway pressure, anesthetics consumption, eye-opening time, extubation time, and the Observer's Assessment of the Alertness/Sedation (OAA/S) score 20 minutes after the extubation were compared between the 2 groups. RESULTS: The operating conditions including muscle tone scales, body movements, and airway pressure did not differ between the 2 groups. Eye-opening time (9.35±2.34 vs. 11.02±2.50 min; P=0.002) and extubation time (13.95±3.41 vs. 16.72±3.67 min; P=0.001) were shorter in group NR than in group R. The BIS score at extubation (87.2±5.0 vs. 83.3±5.7; P=0.001) and the OAA/S score 20 minutes after extubation (5 [3 to 5] vs. 4 [3 to 5]; P=0.005) were significantly higher in group NR than in group R. Propofol consumption was higher in group NR than in group R (4206.10±415.80 vs. 3900.60±365.40 µg/kg, respectively; P=0.001). CONCLUSIONS: General anesthesia without muscle relaxant provides similar working conditions to those observed with muscle relaxant, and it is associated with earlier eye opening and extubation and higher level of consciousness on emergence from spinal surgery.

Total liquid ventilation reduces oleic acid-induced lung injury in piglets.

BACKGROUND: Pediatric patients are susceptible to lung injury that does not respond to traditional therapies. Total liquid ventilation has been developed as an alternative ventilatory strategy for severe lung injury. The aim of this study is to investigate the effect of total liquid ventilation on oleic acid (OA)-induced lung injury in piglets. METHODS: Twelve Chinese immature piglets were induced acute lung injury by OA. Twelve piglets were randomly treated with conventional gas ventilation (control group) or total liquid ventilation (study group) for 240 minutes. Samples for blood gas analysis were collected before, and at 60-minute intervals after OA-induced lung injury. The degree of lung injury was quantified by histologic examination. The inflammatory cells and the levels of IL-1ß, IL-6, IL-10 and TNF-α in plasma, tissue and bronchoalveolar lavage were analyzed. RESULTS: Neutrophil and macrophage counts in bronchoalveolar lavage were significantly decreased in the study group (P < 0.05). The total lung injury score was also reduced in the study group (P < 0.05). The concentrations of IL-1ß, IL-6, IL-10 and TNF-α in plasma, tissue and bronchoalveolar lavage were significantly reduced in the study group (P < 0.05). CONCLUSIONS: Total liquid ventilation reduces biochemical and histologic OA-induced lung injury in piglets.

Progression of aortic regurgitation in Asian patients with congenital sinus of valsalva aneurysm.

BACKGROUND: We reviewed the experience of An Zhen and Fu Wai Hospital for congenital sinus of Valsalva aneurysm (SVA) to determine risk factors for aortic valve replacement (AVR) and postoperative progression of aortic regurgitation (AR). METHODS: Over a 7-year period, 255 patients underwent surgical repair of an SVA. Aneurysms originated from the right sinus and the noncoronary sinus in 212 patients (83.1%) and 38 patients (14.9%), respectively, and protruded into the right ventricle and right atrium in 171 patients (67.1%) and 80 patients (31.4%), respectively. AR presented in 142 patients (55.7%), 60 patients underwent AVR, and 13 patients underwent aortic valvuloplasty (3 patients eventually received AVR for valvuloplasty failure). RESULTS: All patients survived the operation. Late death occurred in 2 patients (0.8%), and 2 patients (0.8%) experienced anticoagulation-related complications. Logistic regression analysis revealed that infective endocarditis, the cardiothoracic ratio, and a nonruptured SVA were risk factors for AVR. Late follow-up of 150 patients by echocardiographic assessment revealed that AR improved in 17 patients and worsened in 20 patients. Cox regression analysis revealed AR at discharge to be an independent risk factor for AR aggravation at late follow-up. CONCLUSIONS: SVA can be repaired with low mortality and excellent long-term results. AR at discharge is an important factor in determining AR aggravation at late follow-up after the operation. We recommend early diagnosis and aggressive treatment for SVA.

Surgical closure of apical multiple muscular septal defects via right ventriculotomy using a single patch with intermediate fixings.

BACKGROUND: Multiple apical muscular ventricular septal defects (VSDs) remain a challenge for surgeons because of their anatomical features. We used single patch with intermediate fixations to repair multiple apical muscular VSDs through right ventriculotomy. METHODS: We analysed the data of 16 children (median age 8 months, range 2 months to 144 months) with multiple apical muscular VSDs who underwent a single patch technique via apical right ventriculotomy. Perioperative data were collected and analysed, and the patients were followed up for three months to 66 months (median, 46 months) to investigate the outcomes. RESULTS: All patients recovered from cardiopulmonary bypass easily with median of cardiopulmonary bypass time 87 minutes and of aortic crossclamp time 53 minutes. No surgically related death occurred and no patient required reoperation. One patient died of pseudomonas pyocyanea infection on day 11 postoperatively. Residual shunt happened in one patient with a diameter of 2 mm and spontaneously closed in 12 months after operation. Two patients presented slightly reduced right ventricular volume and apical hypokinesia postoperatively and recovered 24 and 36 months later respectively. No other complication was found during the three months to 66 months follow-up. CONCLUSION: Our experiences using a single patch technique with intermediate fixations via right ventriculotomy in the management of multiple muscular VSDs had favourable outcomes.

Effect of oleic acid-induced acute lung injury and conventional mechanical ventilation on renal function in piglets.

BACKGROUND: Animal models that demonstrate changes of renal function in response to acute lung injury (ALI) and mechanical ventilation (MV) are few. The present study was performed to examine the effect of ALI induced by oleic acid (OA) in combination with conventional MV strategy on renal function in piglets. METHODS: Twelve Chinese mini-piglets were randomly divided into two groups: the OA group (n = 6), animals were ventilated with a conventional MV strategy of 12 ml/kg and suffered an ALI induced by administration of OA, and the control group (n = 6), animals were ventilated with a protective MV strategy of 6 ml/kg and received the same amount of sterile saline. RESULTS: Six hours after OA injection a severe lung injury and a mild-moderate degree of renal histopathological injury were seen, while no apparent histological abnormalities were observed in the control group. Although we observed an increase in the plasma concentrations of creatinine and urea after ALI, there was no significant difference compared with the control group. Plasma concentrations of neutrophil gelatinase-associated lipocalin (NGAL) and cystatin C increased (5.6 ± 1.3) and (7.4 ± 1.5) times in the OA group compared to baseline values, and were significantly higher than the values in the control group. OA injection in combination with conventional MV strategy resulted in a dramatic aggravation of hemodynamic and blood gas exchange parameters, while these parameters remained stable during the experiment in the control group. The plasma expression of TNF-α and IL-6 in the OA group were significantly higher than that in the control group. Compared with high expression in the lung and renal tissue in the OA group, TNF-α and IL-6 were too low to be detected in the lung and renal tissue in the control group. CONCLUSIONS: OA injection in combination with conventional MV strategy not only resulted in a severe lung injury but also an apparent renal injury. The potential mechanisms involved a cytokine response of TNF-α and IL-6 in plasma, lung and renal tissues.

Comparative analysis of early and middle outcomes of the arterial switch operation in children with complete transposition of the great arteries with ventricular septal defect and severe pulmonary artery hypertension.

BACKGROUND: The best age for the arterial switch operation (ASO) in complete transposition of great arteries with ventricular septal defect is usually considered to be within six months. This is because of severe pulmonary arterial hypertension and pulmonary arterial obstructive pathological changes. There are few reports on ASO surgery in children older than three years old. METHODS: We studied 41 children, including 24 males and 17 females, from January 2010 to December 2011. They were divided into three groups by operation age; 15 patients were < 1 year old, 13 were 1 - 3 years old, and 13 were > 3 years old. Associated cardiac abnormalities included patent ductus arteriosus in six cases, atrial septal defect in five cases, and mitral regurgitation in two cases. All the patients had echocardiography before the operation. Seventeen patients underwent a coronary computed tomography examination and five patients underwent right heart catheterization. All ASO surgeries were performed under inhalation anesthesia and hypothermic cardiopulmonary bypass. RESULTS: Three operative deaths occurred. Two were in the < 1 year old group, who died from severe postoperative low cardiac output. The other was two years old and died of postoperative multiple organ failure. There was no significant difference in postoperative mortality and the recent mid-term survival rate among the three groups. Thirty-eight cases were followed up for an average of 11.2 months, ranging 6 - 20 months. One seven years old patient died of acute diarrhea and electrolyte disturbance arrhythmia caused by food poisoning. Three patients more than three years old still had residual pulmonary arterial hypertension. CONCLUSION: Children older than three years old can still undergo the ASO procedure, but residual pulmonary hypertension is present.

Lung microRNA profile in chronic cyanotic piglets with decreased pulmonary blood flow.

BACKGROUND: Cyanotic congenital heart defects with decreased pulmonary blood flow due to lung ischemia, hypoxia, and others lead to infant morbidity and mortality more than acyanotic heart disease does. Despite the great effort of medical research, their genetic link and underlying microRNAs molecular mechanisms remain obscure. In this study, we aimed to investigate microRNAs regulation during cyanotic defects in lung of immature piglets. METHODS: Cyanotic piglet model was induced by main pulmonary artery-left atrium shunt with distal pulmonary artery banding. Four weeks later, hemodynamic parameters confirmed the development of cyanotic defects and pulmonary lobe RNA was extracted from all animals. We studied the repertoire of porcine lung microRNAs by Solexa deep sequencing technology and quantified highly expressed microRNAs by microarray hybridization. Furthermore, we quantitated selected microRNAs from cyanotic and control piglets by quantitative RT-PCR. RESULTS: After surgical procedure 4 weeks later, the cyanotic model produced lower arterial oxygen tension, arterial oxygen saturation, and higher arterial carbon dioxide tension, hematocrit and hemoglobin concentration than controls (all P < 0.05). In 1273 miRNAs expressed in the immature piglets lungs, 2 most abundant microRNAs (miR-370 and miR-320) demonstrated significant difference between cyanotic and control group (all P < 0.05). CONCLUSION: Our results extended lung microRNA profile in immature piglets and suggested that miR-370 and miR-320 are significantly up-regulated in cyanotic lung tissues.

Clinical results of combined palliative procedures for cyanotic congenital heart defects with intractable hypoplasia of pulmonary arteries.

BACKGROUND: Congenital heart defects with intractable hypoplasia of the pulmonary arteries without intercourse or with intercourse stenosis is unsuitable for surgical correction or regular palliative procedures. We reported our experience with combined palliative procedures for congenital heart defects with intractable hypoplasia pulmonary arteries. METHODS: From 2001 to 2012, a total of 41 patients with cyanotic congenital heart defects and intractable hypoplasia of the pulmonary arteries underwent surgical procedures. From among them, 31 patients had pulmonary atresia with ventricular septal defect (VSD) and the other 10 cases had complicated congenital heart defects with pulmonary stenosis. Different kinds of palliative procedures were performed according to the morphology of the right and left pulmonary arteries in every patient. If the pulmonary artery was well developed, a Glenn procedure was performed. A modified Blalock-Taussig shunt or modified Waterston shunt was performed if pulmonary arteries were hypoplastic. If the pulmonary arteries were severely hypoplastic, a Melbourne shunt was performed. Systemic pulmonary artery shunts were performed bilaterally in 25 cases. A systemic-pulmonary shunt was performed on one side and a Glenn procedure was performed contralaterally in 16 cases. Major aortopulmonary collateral arteries were unifocalized in six cases, ligated in two cases and interventionally embolized in two cases. There was one early death because of cardiac arrest and the hospital mortality was 2.4%. RESULTS: Five patients suffered from postoperative low cardiac output syndrome, three had perfusion of the lungs, and two pulmonary infections. Systemic pulmonary shunts were repeated after the original operation in three cases due to the occlusion of conduits. The mean follow-up time was 25 months. The pre- and the post-operation left pulmonary indices were (8.13 ± 3.68) vs. (14.9 ± 6.21) mm(2)/m(2). The pre- and post-operation right pulmonary indices were (12.7 ± 8.13) vs. (17.7 ± 7.78) mm(2)/m(2). The pre- and post-operational pulmonary indices were (20.87 ± 9.43) vs. (32.6 ± 11.7) mm(2)/m(2). They were all significantly increased (P < 0.001). The diameter of the pulmonary artery increased after the modified Blalock-Taussig shunt ((5.51 ± 0.94) mm(2)/m(2) pre-operation vs. (7.01 ± 1.97) mm(2)/m(2) post-operation), the modified Waterston shunt ((5.70 ± 3.96) mm(2)/m(2) pre-operation vs. (9.17 ± 3.62) mm(2)/m(2) post-operation) and the Melbourne shunt ((2.17 ± 0.41) mm(2)/m(2) pre-operation vs. (7.35 ± 2.49) mm(2)/m(2) post-operation) (all P < 0.05). Bilateral pulmonary arteries developed well as compared to their pre-operation development. Hemoglobin decreased from (194 ± 27) to (174 ± 24) g/L (P < 0.05) and peripheral oxygen saturation increased from (65 ± 11)% to (84 ± 6)% (P < 0.001). During the follow-up of 27 to 49 months, ultimate complete repair was performed in four cases and one patient underwent a Glenn procedure. CONCLUSIONS: The procedures should be considered on a case to case basis in patients having hypoplasia of the pulmonary arteries with cyanotic congenital heart defects. Combined palliative operations could be an adequate strategic treatment.