Bank market structure and firm innovation-evidence from China.

This study explores the impact of bank market structure on firm innovation in China using a two-way fixed effects model. Our analysis is based on a dataset comprising 2,412,316 firm-city level observations. Our findings suggest that there exists a U-shaped relationship between bank market structure and firm innovation in China. Specifically, we identify that the financing channel is a crucial pathway through which bank market structure influences firm innovation. Moreover, our results indicate that this relationship is mainly driven by small firms and innovative firms, and is more pronounced in regions with stronger intellectual property rights protection or greater openness to foreign markets. In sum, this study contributes to the existing literature by advancing our understanding of the impact of bank market structure on innovation in Chinese firms.

The Complementary Relationship Between Echocardiography and Multi-Slice Spiral CT Coronary Angiography in the Diagnosis of Coronary Artery Thrombosis in Children With Kawasaki Disease.

Aim: To compare the diagnostic values by using transthoracic echocardiography (ECHO) and multi-slice spiral CT coronary angiography (CTCA) for identifying coronary artery thrombosis in children with Kawasaki disease (KD). Methods: Total 97 KD children with coronary artery dilation complications in our hospital from June 2012 to December 2020 were included in the study. CTCA and ECHO were performed after over 1 month of illness. Results: Coronary artery thrombosis was found in 14 out of 97 patients. Among them, 10 were identified as positive by CTCA, 9 were identified as positive by ECHO, and 5 were identified as positive by both CTCA and ECHO. Conclusion: Both CTCA and ECHO can be used to diagnose coronary artery thrombosis. ECHO has advantage in identifying low-density thrombus, and CTCA is better for the clot in distal coronary artery. They can complement each other.

Correlation Between Arrhythmia and the Prognosis in Children With EFE/LVNC/DCM.

Aim: To explore the correlation between different phenotypes of arrhythmia and the prognosis in children with EFE/LVNC/DCM. Methods: A total of 167 children with cardiomyopathy diagnosed and treated in Shengjing Hospital between January 2010 and May 2019 were evaluated. After patient screening, 31 patients with endomyocardial fibroelastosis (EFE), left ventricular non-compaction, or dilated cardiomyopathy with significant arrhythmias were selected. In addition, 42 children with primary EFE were selected to evaluate the prognosis with or without arrhythmia. Follow-up was undertaken 0, 1, 3, 6, 9, and 12 months after treatment. Results: We revealed the outcomes for five types of cardiomyopathy: EFE patients with Wolff-Parkinson-White syndrome B and supraventricular tachycardia, intraventricular block and complete left bundle branch block recovered slower than EFE patients with atrial flutter and atrial fibrillation, even slower than EFE with ventricular tachycardia. The average recovering time for LVEF and LVED in EFE patients without arrythmia was 10 months after diagnosis, while 76.9% (3/13 cases) of those with significant arrythmia hadn't recovered until 24 months after diagnosis. Three of patients died at 6, 7, and 6 and half years after diagnosis. Conclusion: The long-term prognosis in children with cardiomyopathy is associated with the type of arrhythmia and time of intervention. The prognosis of EFE patients with arrhythmia is worse than EFE patients without arrhythmia. Patients with Wolff-Parkinson-White syndrome B, especially a significantly widen QRS complex, carry a poor prognosis if radiofrequency ablation is not undertaken. CLBBB patients have similar poor prognosis if proper pacemaker is not implanted timely.

[Comparison analysis of muscle enzymes in children with myocarditis and Duchene/Becker muscular dystrophy].

OBJECTIVE: To compare the changes in muscle enzyme between children with myocarditis and Duchene/Becker muscular dystrophy (DMD/BMD), and to seek the explanations for variation.
 METHODS: The retrospective analysis for 83 myocarditis children (myocarditis group) and 69 DMD/BMD children (DMD/BMD group), who were collected from Department of Pediatric of Shengjing Hospital affiliated to China Medical University since January 2008 to May 2015, was carried out. At the same time, 24 healthy children from the Department of Pediatric Development served as a control group. The examination indexes included creatine kinase (CK), creatine kinase-isoenzyme MB (CK-MB), creatine kinase isoenzyme MB mass (CK-MB mass), cardiac troponin I (cTnI) and high-sensitive-cTnT (hs-cTnT).
 RESULTS: 1) In the myocarditis group, the CK increased from 100 to 1 000 U/L, reached a peak after 5 days, which lasted for a week and then dropped to the normal; the CK-MB reached a peak after 5 to 7 days and dropped to the normal a month later; the CK-MB mass reached a peak on the first day and dropped to the normal after 3 weeks; the cTn reached to a peak after 5 days and dropped to the normal after about 17 days; hs-cTnT reached to a peak on the first day and dropped to the normal after about 19 days. 2) In the DMD/BMD group, the CK increased significantly and 27 cases had a CK value of more than 10 000 U/L. After the treatment for 1 to 2 weeks, their enzyme rose again after a slight drop. In terms of cTnI, 6 cases showed a moderate increase, 5 of them couldn't drop to the normal level until more than 3 weeks later; the hs-cTnT increased in the 45 cases, which lasted for more than 3 weeks in the 31 cases of them and showed a tendency of persisting increase.
 CONCLUSION: The cTnI and hs-cTnT rise significantly and possess wider observation window than CK and CK-MB mass in myocarditis children, with more sensitive and specific changes. The myocardial damage can occur before myasthenia and keep this trend for a long time in the DMD/BMD children. The trend of cTnI change in myocarditis children is similar to hs-cTnT, while hs-cTnT in DMD/BMD children is more sensitive than cTnI.

Exploring the genes associated with the response to intravenous immunoglobulin in patients with Kawasaki disease using DNA microarray analysis.

In this study we aimed to screen genes associated with intravenous immunoglobulin (IVIG) responding in patients with Kawasaki disease (KD) and thus explore the underlying molecular mechanism of IVIG resistance. The differentially expressed genes (DEGs) were identified by samr package in R. Then, protein-protein interaction (PPI) networks were constructed by STRING software. We further collected the regulatory data from TRANSFAC database, followed by regulatory interaction network construction. A total 194 of DEGs, including 185 up- and 9 down-regulated DEGs, were identified between IVIG-responding and non-responding patients with KD at acute stage. In contrast, no DEGs were found at convalescent stage. PPI networks and regulatory networks were constructed based on the 185 up-regulated genes at acute stage. The degrees of TFRC (transferrin receptor protein 1) and GADD45A (growth arrest and DNA-damage-inducible alpha) were higher than other genes, and meanwhile MYC (V-Myc Myelocytomatosis Viral Oncogene Homolog) and E2F1 (E2F Transcription Factor 1) were found to be two TFs (transcription factors) with the highest degrees. In conclusions, the response to IVIG in Kawasaki disease patients may be involved in the expression of TFRC, GADD45A, MYC and E2F1.

Maternal protein restriction induces alterations in hepatic tumor necrosis factor-α/CYP7A1 signaling and disorders regulation of cholesterol metabolism in the adult rat offspring.

It is well recognized that adverse events in utero impair fetal development and lead to the development of obesity and metabolic syndrome in adulthood. To investigate the mechanisms linking impaired fetal growth to increased cholesterol, an important clinical risk factor characterizing the metabolic syndrome and cardiovascular disease, we examined the impact of maternal undernutrition on tumor necrosis factor-α (TNF-α)/c-jun N-terminal kinase (JNK) signaling pathway and the cholesterol 7α-hydroxylase (CYP7A1) expression in the livers of the offspring with a protein restriction model. The male offspring with intrauterine growth restriction (IUGR) caused by the isocaloric low-protein diet showed decreased liver weight at birth and augmented circulation and hepatic cholesterol levels at 40 weeks of age. Maternal undernutrition significantly upregulated cytokine TNF-α expression and JNK phospholytion levels in the livers from fetal age to adulthood. Elevated JNK phospholytion could be linked to downregulated hepatocyte nuclear factor-4α and CYP7A1 expression, subsequently led to higher hepatic cholesterol. This work demonstrated that intrauterine malnutrition-induced IUGR might result in intrinsic disorder in hepatic TNF-α/CYP7A1 signaling, and contribute to the development of hypercholesterolemia in later life.

Meta-analysis of the relationship between single nucleotide polymorphism rs72689236 of caspase-3 and Kawasaki disease.

Kawasaki disease is a pediatric systemic vasculitis of unknown etiology, for which a genetic influence is suspected. But whether single nucleotide polymorphism (SNP) of caspase-3 rs72689236 is associated with Kawasaki disease is controversial. The aim of our study is to assess the association between the SNP of caspase-3 and risk for Kawasaki disease. We searched PubMed, MEDLINE, EMBASE, Springer, Elsevier Science Direct, Cochrane Library Google scholar, CNKI (China National Knowledge Infrastructure, in Chinese) and Wanfang database (in Chinese) to identify studies investigating the association between rs72689236 polymorphism and Kawasaki disease occurrence. There were five eligible studies, which included 4,241 (case group 1,560; control group 2,681) participants in this meta-analysis. Pooled odds ratios (ORs) and 95 % confidence intervals (95 % CIs) were calculated in a fixed-effects model (the Mantel-Haenszel method) or a random-effects model (the DerSimonian and Laird method) when appropriate. Significant associations were found under the overall ORs for A-allele comparison (A vs. G, pooled OR 1.33, 95 % CI 1.21-1.46), AA versus GG comparison (pooled OR 1.64, 95 % CI 1.35-2.00), GA versus GG comparison (pooled OR 1.42, 95 % CI 1.24-1.63), recessive model (AA vs. GG + GA, pooled OR 1.37, 95 % CI 1.15-1.64) and dominant model (AA + GA vs. GG, pooled OR 1.47, 95 % CI 1.29-1.67). This meta-analysis suggested that SNP rs72689236 of caspase-3 might be associated with susceptibility of Kawasaki disease and the allele A might increase the risk of Kawasaki disease in Asian samples such as Japanese and Chinese. In addition, individual studies with large sample size are needed to further evaluate the associations in various ethnic populations.

[The limitation of MB isoenzyme of creatine kinase mass in assess myocardial injury with muscular disease].

OBJECTIVE: To examine the changes in serum MB isoenzyme of creatine kinase mass (CK-MB mass), cardiac troponin I (cTnI), and myoglobulin (Mb) in children with myocarditis and muscular disease in order to evaluate the significance of index CK-MB mass for the diagnosis of myocardium injury in these diseases. METHODS: Blood samples were collected from 40 children with myocarditis, 38 children with muscular diseases, and 10 healthy children, for the measurement of creatine kinase (CK), CK-MB activity, CK-MB mass, cTnI, and Mb. Myocarditis patients also received electrocardiogram and pulse Doppler electrocardiogram examination while muscular diseases patients were subjected to electro-myographic examination, inherit-metabolic diseases screening and related gene analysis. The data were analyzed for differences between groups, and differences between values before and after the treatment. RESULTS: In comparison with healthy controls [CK (U/L): 95.0 ± 27.0, CK-MB activity (U/L): 22.6 ± 1.3, CK-MB mass (µg/L): 2.4 ± 0.3, cTnI (µg/L): 0.012 ± 0.001], the patients with myocarditis had significantly (all P < 0.01) higher mean values in CK (1033.0 ± 408.0), CK-MB activity (101.2 ± 31.5), CK-MB mass (38.2 ± 13.2) and cTnI (5.544 ± 1.554) before the treatment. After 2 weeks of treatment these indexes returned to the level of controls, with cTnI responded the last (CK: 59.3 ± 25.1, CK-MB activity: 24.6 ± 13.2, CK-MB mass: 3.3 ± 2.9, cTnI: 0.125 ± 0.128). One week after treatment, the incidences of CK and CK-MB mass elevation were significantly lower than the values before the treatment [CK: 5.9% (1/17) vs. 56.4% (22/39); CK-MB mass: 8.3% (1/12) vs. 61.1% (22/36), both P < 0.01], with the change in CK-MB mass appeared significantly earlier than cTnI [8.3% (1/12) vs. 73.7% (14/19), P < 0.05]. The patients with muscular disease also had significantly elevated mean value in CK (10193.0 ± 1447.0), CK-MB activity (311.7 ± 44.4), and CK-MB mass (229.2 ± 47.9) in comparison with healthy controls before the treatment (all P < 0.01). But their cTnI (0.021 ± 0.002) was not significantly different from the control at this time. Two weeks after treatment, the elevated indexes were still significantly higher than the control (CK: 5735.6 ± 6187.8, CK-MB activity: 170.7 ± 143.0, CK-MB mass: 207.4 ± 136.6), while the level of cTnI (0.230 ± 0.150) remained at the level of the control group. The incidence of index elevation was not significantly different from the values before the treatment for all the indexes tested [CK: 85.7% (6/7) vs. 97.4% (37/38); CK-MB activity: 85.7% (6/7) vs. 97.4% (37/38); CK-MB mass: 100.0% (2/2) vs. 94.1% (32/34); cTnI: 0(0/1) vs. 6.4% (2/31), all P > 0.05]. CONCLUSIONS: In patients with myocarditis, CK-MB mass and cTnI both follow a consistent pattern of change: elevated in the acute stage of the disease but return to normal after recovery. In patients with muscular diseases, these 2 indexes have different pattern of change. CK-MB mass is significantly higher than control even after the treatment, while cTnI value remain unchanged. Therefore, CK-MB mass has very limited value as an index for myocardial injury in these patients.

Gonadal mosaicism of a TAZ (G4.5) mutation in a Japanese family with Barth syndrome and left ventricular noncompaction.

TAZ (G4.5) was initially identified as the gene associated with Barth syndrome and left ventricular noncompaction (LVNC). The purpose of this study was to investigate patients with LVNC for disease-causing mutations in TAZ. In 124 Japanese patients, including 50 families, mutation analysis of TAZ was performed using DNA sequencing. A splice donor mutation was identified in two brothers with Barth syndrome and LVNC, and a sister who was asymptomatic. However, the variant was not identified in either parent or the maternal grandparents, all of whom were asymptomatic. Due to the recurrent inheritance of this variant by each of the children we concluded that this was evidence of gonadal mosaicism in the obligate carrier mother, the first reported occurrence of this in Barth syndrome.

Assessment of coronary artery lesions in children with Kawasaki disease: evaluation of MSCT in comparison with 2-D echocardiography.

BACKGROUND: Transthoracic two-dimensional echocardiography is an effective method for detecting coronary arterial injury in Kawasaki disease. However, its accuracy in the diagnosis of coronary arterial lesions is limited. OBJECTIVE: To investigate the value of multislice spiral CT for coronary angiography for observing the coronary arterial injury caused by infantile Kawasaki disease. MATERIALS AND METHODS: Coronary angiography, using a 64-slice spiral CT scanner, and 2-D echocardiography were performed in 48 children with Kawasaki disease in whom the position, internal diameter, and length of each coronary artery were measured. RESULTS: MSCT showed coronary artery injury in 15 of the 48 children. Among these 15 children, 20 coronary artery branches showed complications, including the left coronary artery branches in 15 (31.2%) and the right coronary artery branches in 5 (10.4%). Complications in the left coronary artery branches included dilation in 12 (25.0%) and stenosis, calcification and the combination of the two in one each, and the right coronary artery branches showed dilation; two branches also showed beaded changes. MSCT also showed dilation in the left anterior descending arteries in two children. These children showed no abnormality on 2-D echocardiography. CONCLUSION: MSCT is a valuable examination method for detecting coronary artery injury in Kawasaki disease.

SCN5A variants in Japanese patients with left ventricular noncompaction and arrhythmia.

Left ventricular noncompaction (LVNC) is a genetically heterogenous disorder. Mutations in the human cardiac sodium channel alpha-subunit gene (SCN5A) are involved in the pathophysiology of cardiac arrhythmias and cardiomyopathies. This study was performed to compare the frequency of SCN5A variants in LVNC patients with or without arrhythmias, and to investigate the relationship between variants and disease severity. DNA was isolated from the peripheral blood of 62 Japanese probands with LVNC, comprising 17 familial cases and 45 sporadic cases. Blood samples were screened for variants in SCN5A using single-strand conformational polymorphism analysis (SSCP) and DNA sequencing. Seven variants, rs6599230:G > A, c.453C > T, c.1141-3C > A, rs1805124:A > G (p.H558R), rs1805125:C > T (p.P1090L), c.3996C > T, and rs1805126:T > C were identified in 7 familial and 12 sporadic cases. The frequency of SCN5A variants was significantly higher in the patients with arrhythmias than those without (50% vs 7%: P = 0.0003), suggesting these variants represent a risk factor for arrhythmia and supporting the hypothesis that genes encoding ion channels are involved in LVNC pathophysiology. The LVNC patients with heart failure also had high occurrence of SCN5A variants, suggesting the presence of SCN5A variants and/or arrhythmias increase the severity of LVNC.

Expression of myeloid-related protein-8 and -14 in patients with acute Kawasaki disease.

OBJECTIVES: This study investigated patients with acute Kawasaki disease (KD) to validate myeloid-related protein (MRP)-8/MRP-14 as a marker of disease activity and severity of coronary artery lesion development. BACKGROUND: Both MRP-8 and -14, which are S100-proteins secreted by activated neutrophils and monocytes, bind specifically to endothelial cells and induce thrombogenic and inflammatory responses in a variety of disease conditions. METHODS: We investigated 61 patients with acute KD and examined sequential changes in serum levels of MRP-8/MRP-14, messenger ribonucleic acid (mRNA) expression of MRP-8 and -14 in circulating granulocytes and monocytes, and amounts of MRP-8/MRP-14 bound to circulating endothelial cells. RESULTS: The serum MRP-8/MRP-14 levels as well as mRNA expressions of MRP-8 and -14 in granulocytes were strongly upregulated during the early stage of acute KD, and decreased dramatically within 24 h of intravenous immune globulin therapy (p < 0.05) in 45 responders. In contrast, in 16 nonresponders both of these increased after the initial treatment. The number of MRP-8/MRP-14-positive circulating endothelial cells was higher in patients with acute KD than in control patients and increased significantly by 2 weeks after the onset of KD, especially in patients in whom coronary artery lesions developed. CONCLUSIONS: We show for the first time that MRP-8/MRP-14 are exclusively secreted by granulocytes in patients with acute KD, and intravenous immune globulin treatment suppresses their gene expression. Serum levels of MRP-8/MRP-14 may be useful markers of disease activity, and the levels of MRP-8/MRP-14-positive circulating endothelial cell may predict the severity of vasculitis, confirming an important role for distinct inflammatory reactions in endothelium.

Interstitial 1q43-q43 deletion with left ventricular noncompaction myocardium.

We describe a newborn infant with del(1)(q) syndrome, presenting with rare congenital cardiomyopathy and left ventricular noncompaction myocardium (LVNC), as well as typical clinical features such as facial dysmorphism and psychomotor retardation. Although conventional chromosome banding at 850 bands per haploid set indicated a karyotype of 46,XX,add(1)(q42.3), FISH analysis confirmed that the deleted portion was limited to within q43, and q44 was preserved. Therefore, the chromosome constitution is 46,XX,del(1)(q43q43), which has not previously been reported in the literature. Screening for the mutations in the candidate genes for LVNC, i.e. G4.5, CSX, Dystrobrevin, FKBP12, and Desmin, produced negative results. Interestingly, the deleted portion includes the locus for the cardiac ryanodine receptor type 2 gene (RyR2), that selectively binds to the FKBP12 homolog, FKBP12.6. The relationship between this rare myocardial abnormality and deletion of q43 is currently unknown and awaits further accumulation of cases with the same chromosomal aberration.

Genetic analysis in patients with left ventricular noncompaction and evidence for genetic heterogeneity.

Left ventricular noncompaction (LVNC) is a cardiomyopathy characterized by numerous excessively trabeculations and deep intertrabecular recesses. This study was performed to investigate Japanese LVNC patients for disease-causing mutations in a series of selected candidate genes. DNA was isolated from the peripheral blood of 79 cases including 20 familial cases and 59 sporadic cases. DNA samples were screened for mutations in the genes encoding G4.5 (TAZ), alpha-dystrobrevin (DTNA), alpha1-syntrophin (SNTA1), FK506 Binding protein 1A (FKBP1A or FKPB12: FKBP1A), and LIM Domain Binding protein 3 (Cypher/ZASP: LDB3), using single-strand conformational polymorphism analysis and DNA sequencing. DNA variants were identified in 6 of the 79 cases, including four familial cases and two sporadic cases. A splice acceptor mutation of intron 8 in TAZ (IVS8-1G>C) was identified in one family with isolated LVNC, resulting in deletion of exon 9 from mRNA. In a sporadic case of isolated LVNC and Barth syndrome (BTHS), a 158insC in exon 2 of TAZ resulting in a frame-shift mutation was identified. A 1876G>A substitution changing an aspartic acid to asparagine (D626N) was identified in LDB3 in four members of two families with LVNC. A 163G>A polymorphism was identified in LDB3, which changed a valine to isoleucine (V55I) in one patient with isolated LVNC. In addition, in a family with nonisolated LVNC, a 362C>T mutation was identified in DTNA. LVNC, like other forms of inherited cardiomyopathy, is a genetically heterogeneous disease, associated with variable clinical symptoms and can be inherited as an autosomal or X-linked recessive disorder.

[Value of multislice spiral computed tomography in finding coronary artery lesion in children with Kawasaki disease].

OBJECTIVE: Kawasaki disease is an acute systemic vasculitis syndrome primarily affecting small and medium-sized arteries, with development of severe coronary artery lesion (CAL). CAL may induce myocardial infarction and sudden death. So it is very important to find CAL early. In this study the value of multislice spirral computed tomography (MSCT) was investigated to find CAL in patients with Kawasaki disease. METHODS: Thirty-four patients with Kawasaki disease were examined respectively by using MSCT and two dimensional echocardiography (TDE), then the findings were analyzed. RESULTS: MSCT showed CAL in 12 of 34 patients involving 16 coronary arteries, including 9 (26%) dilated left coronary arteries (LCA), 1 constricted, 1 calcified and 1 LCA which had both stenosis and 4 (12%) dilated right coronary artery. TDE showed that 10 patients had 13 dilated coronary arteries, including 7 (21%) left coronary arteries and 6 (18%) right coronary arteries. TDE failed to show the abnormalities in 3 patients with coronary artery stenosis or calcification and in 2 patients with left descending artery dilation demonstrated by MSCT. However, no significant difference was found between the two methods (P > 0.05) in the rates of positive findings. The correlation between TDE and MSCT, in left as well as right coronary artery, was significantly positive (r = 0.90, r = 0.82, respectively, P < 0.01). However, compared with TDE, MSCT was significantly better in finding coronary artery stenosis and calcification (chi(2) = 24.3, P < 0.01). CONCLUSIONS: Use of MSCT may help better find the lesions of coronary artery, especially those in middle and distant sections as compared to TDE. MSCT is better than TDE in exploring coronary wall calcification and coronary artery stenosis. MSCT could be a helpful new addition to the current CAL monitoring method in long-term follow-up of patients with Kawasaki disease.