N-acetylneuraminic acid modulates SQSTM1/p62 sialyation-mediated ubiquitination degradation contributing to vascular endothelium dysfunction in experimental atherosclerosis mice.

Sialic acid (SIA) has been reported to be a risk factor for atherosclerosis (AS) due to its high plasma levels in such patients. However, the effect of increasing SIA in circulation on endothelial function during AS progression remains unclear. In the present study, ApoE-/- mice and endothelial cells line (HUVEC cells) were applied to investigate the effect of SIA on AS progression and its potential molecular mechanism. In vivo, mice were injected intraperitoneally with Neu5Ac (main form of SIA) to keep high-level SIA in circulation. ORO, H&E, and Masson staining were applied to detect the plaque progression. In vitro, HUVECs were treated with Neu5Ac at different times, CCK-8, RT-PCR, western blot, and immunoprecipitation methods were used to analyze its effects on endothelial function and the potential involved mechanism. Results from the present study showed that high plasma levels of Neu5Ac in ApoE-/- mice could aggravate the plaque areas as well as increase necrotic core areas and collagen fiber contents. Remarkably, Neu5Ac levels in circulation displayed a positive correlation with AS plaque areas. Furthermore, results from HUVECs showed that Neu5Ac inhibited cells viability in a time/dose-dependent manner, by then induced the activation of inflammation makers such as ICAM-1 and IL-1ß. Mechanism study showed that the activation of excessive autophagy medicated by SQSTM1/p62 displayed an important role in endothelium inflammatory injury. Neu5Ac could modify SQSTM1/p62 as a sialylation protein, and then increase its level with ubiquitin binding, further inducing ubiquitination degradation and being involved in the excessive autophagy pathway. Inhibition of sialylation by P-3Fax-Neu5Ac, a sialyltransferase inhibitor, reduced the binding of SQSTM1/p62 to ubiquitin. Together, these findings indicated that Neu5Ac increased SQSTM1/p62-ubiquitin binding through sialylation modification, thereby inducing excessive autophagy and subsequent endothelial injury. Inhibition of SQSTM1/p62 sialylation might be a potential strategy for preventing such disease with high levels of Neu5Ac in circulation.

Perivascular fat tissue and vascular aging: A sword and a shield.

The understanding of the function of perivascular adipose tissue (PVAT) in vascular aging has significantly changed due to the increasing amount of information regarding its biology. Adipose tissue surrounding blood vessels is increasingly recognized as a key regulator of vascular disorders. It has significant endocrine and paracrine effects on the vasculature and is mediated by the production of a variety of bioactive chemicals. It also participates in a number of pathological regulatory processes, including oxidative stress, immunological inflammation, lipid metabolism, vasoconstriction, and dilation. Mechanisms of homeostasis and interactions between cells at the local level tightly regulate the function and secretory repertoire of PVAT, which can become dysregulated during vascular aging. The PVAT secretion group changes from being reducing inflammation and lowering cholesterol to increasing inflammation and increasing cholesterol in response to systemic or local inflammation and insulin resistance. In addition, the interaction between the PVAT and the vasculature is reciprocal, and the biological processes of PVAT are directly influenced by the pertinent indicators of vascular aging. The architectural and biological traits of PVAT, the molecular mechanism of crosstalk between PVAT and vascular aging, and the clinical correlation of vascular age-related disorders are all summarized in this review. In addition, this paper aims to elucidate and evaluate the potential benefits of therapeutically targeting PVAT in the context of mitigating vascular aging. Furthermore, it will discuss the latest advancements in technology used for targeting PVAT.

The role of prophylactic antibiotics in elective inguinal tension-free hernia repair: A systematic review and meta-analysis.

Whether to use antibiotics to prevent surgical site infection in elective inguinal tension-free hernia repair has been controversial. To systematically evaluate the effect of prophylactic antibiotic application in elective inguinal tension-free hernia repair, we identified all published randomised controlled trials of the effect of prophylactic antibiotic application on elective inguinal tension-free hernia repair were collected by computer retrieval from the China National Knowledge Infrastructure; VIP Database; Wanfang Database; China Biomedical Literature Database; and PubMed, EMBASE and Cochrane Library databases. Meta-analysis was performed by RevMan 5.3 software. The meta-analysis showed that the total incidence of surgical site infections [P = 0.003] and the incidence of superficial surgical site infections [P = 0.004] in the antibiotic group (AG) were lower than those in the non-antibiotic group (NAG). There was no significant difference in the total incidence of postoperative infections [P = 0.06], deep surgical site infections [P = 0.26] and seroma [P = 0.52] between the AG and the NAG. Based on current evidence, the application of prophylactic antibiotics in elective inguinal tension-free hernia repair can prevent the total incidence of surgical site infections and that of superficial surgical site infections but cannot prevent the total incidence of postoperative infection events, incidence of deep surgical site infections and incidence of seroma.

A Universal Detection Method for Adversarial Examples and Fake Images.

Deep-learning technologies have shown impressive performance on many tasks in recent years. However, there are multiple serious security risks when using deep-learning technologies. For examples, state-of-the-art deep-learning technologies are vulnerable to adversarial examples that make the model's predictions wrong due to some specific subtle perturbation, and these technologies can be abused for the tampering with and forgery of multimedia, i.e., deep forgery. In this paper, we propose a universal detection framework for adversarial examples and fake images. We observe some differences in the distribution of model outputs for normal and adversarial examples (fake images) and train the detector to learn the differences. We perform extensive experiments on the CIFAR10 and CIFAR100 datasets. Experimental results show that the proposed framework has good feasibility and effectiveness in detecting adversarial examples or fake images. Moreover, the proposed framework has good generalizability for the different datasets and model structures.

Phase unwrapping in ICF target interferometric measurement via deep learning.

This paper proposes an unwrapping algorithm based on deep learning for inertial confinement fusion (ICF) target interferograms. With a deep convolutional neural network (CNN), the task of phase unwrapping is transferred into a problem of semantic segmentation. A method for producing the data set for the ICF target measurement system is demonstrated. The noisy wrapped phase is preprocessed using a guided filter. Postprocessing is introduced to refine the final result, ensuring the proposed method can still accurately unwrap the phase even when the segmentation result of the CNN is not perfect. Simulations and actual interferograms show that our method has better accuracy and antinoise ability than some classical unwrapping approaches. In addition, the generalization capability of our method is verified by successfully applying it to an aspheric nonnull test system. By adjusting the data set, the proposed method may be transferred to other systems.

Low-dose aspirin use and cancer-specific mortality: a meta-analysis of cohort studies.

BACKGROUND: Considering the increased risk of bleeding caused by aspirin, and the observed benefit in all-cause mortality may be due to an improvement in cardiovascular-related mortality. We carried out this meta-analysis to estimate the association of low-dose aspirin use and risk of cancer-specific mortality. METHODS: We searched the PubMed and China National Knowledge Infrastructure (CNKI) databases for all articles within a range of published years from 1980 to 2018. RESULTS: Finally, 13 published cohort studies with 65 768 patients were available for estimating overall risk of cancer-specific mortality associating with post-diagnosis low-dose aspirin use, and 4 cohort studies were available for pre-diagnosis low-dose aspirin use with 16 654 patients. Overall, statistical evidence of significantly decreased cancer-specific mortality was found to be associated with post-diagnosis low-dose aspirin use (OR = 0.84, 95% CI = 0.75-0.93), but not with pre-diagnosis low-dose aspirin use. In terms of subgroup analyses by cancer type, post-diagnosis low-dose aspirin use was significantly with decreased cancer-specific mortality for digestive tract cancer including colorectal cancer, esophageal cancer and gastric cancer. CONCLUSION: Our meta-analysis indicated that post-diagnosis but not pre-diagnosis low-dose aspirin use may reduce cancer-specific mortality.

Ursolic Acid Inhibits Tumor Growth via Epithelial-to-Mesenchymal Transition in Colorectal Cancer Cells.

Ursolic acid (UA), a natural pentacyclic triterpenoid, is a promising compound for cancer prevention and therapy. However, its mechanisms of action have not been well elucidated in colorectal cancer cells. Here, using cultured human colon cancer cell lines SW620 and HCT116, this assay demonstrates that UA reduces cell viability, inhibits cell clone formation, and induces caspase-3 mediated apoptosis. Additional experiments show that UA inhibits cell migration and epithelial-mesenchymal transition (EMT), including E-cadherin, Vimentin, Integrin, Twist, and Zeb1 biomakers. These results suggest that UA inhibits cell proliferation, invasion, and metastasis in colorectal cancer cells by affecting mechanisms that regulate EMT. Taken together, the results suggested that the anti-proliferation and anti-metastasis activities of UA was through EMT inhibition in colorectal cancer.

[Clinical effect and safety of clopidogrel combined with aspirin in antithrombotic therapy for children with Kawasaki disease complicated by small/medium-sized coronary artery aneurysms].

OBJECTIVE: To study the clinical effect and safety of clopidogrel combined with aspirin in antithrombotic therapy for children with Kawasaki disease (KD) complicated by coronary artery aneurysm (CAA). METHODS: A total of 77 KD children who were diagnosed with multiple small/medium-sized CAAs by echocardiography between January 2013 and June 2018 were enrolled. They were randomly divided into observation group with 38 children (treated with clopidogrel and aspirin) and control group with 39 children (treated with low-molecular-weight heparin and aspirin). All children were followed up regularly, and the first 3 months of the course of the disease was the observation period. The children were observed in terms of the change of the coronary artery and the incidence of complications. RESULTS: At month 3 of follow-up, among the children in the observation group, 6 had normal coronary artery, 11 had coronary artery retraction, 19 had stable coronary artery, and 2 progressed to giant coronary aneurysm; among the children in the control group, 7 had normal coronary artery, 12 had coronary artery retraction, 19 had stable coronary artery, and 1 progressed to giant coronary aneurysm; there was no significant difference in the change of the coronary artery between the two groups (P>0.05). There were 2 cases of epistaxis and 6 cases of skin ecchymosis in the observation group, and 1 case of epistaxis and 7 cases of petechiae and ecchymosis at the injection site in the control group, and no other serious bleeding events were observed in either group. CONCLUSIONS: Clopidogrel combined with low-dose aspirin is safe and effective in antithrombotic therapy for children with KD complicated by CAA.

Polymorphism of ABCG2 Gene in Hyperuricemia Patients of Han And Uygur Ethnicity with Phlegm/Non-Phlegm Block in Xinjiang, China.

BACKGROUND This study investigated the relationship between hyperuricemia (with phlegm/non-phlegm block) and ABCG2 gene polymorphism in Han and Uygur people from Xinjiang, China. MATERIAL AND METHODS We recruited 600 hyperuricemia patients with phlegm/non-phlegm block. Genomic DNA was extracted from the whole blood. Gene polymorphism was classified by SnaPshot method. RESULTS The SNP loci rs2725220 and rs2231137 of the ABCG2 gene, but not rs2231142, were significantly different between patients with non-phlegm block and phlegm block (P<0.05). The rs2231142 allele G was the protective factor in Uygur hyperuricemia patients. In both Han and hyperuricemia patients, the rs2725220 allele G was a protective factor and the rs2231137 allele C was a risk factor. For non-phlegm-block hyperuricemia, the rs2231142 and rs2231137 genotypes were significantly different between Uygur and Han patients (P<0.05). The rs2231142 allele G was 1.563 times higher in the Uygur patients compared with Han, and rs2231137 allele C was 1.673 times higher in the Uygur patients compared with the Han. For phlegm-block hyperuricemia, rs2231142 allele G was 1.397 times higher in the Uygur patients compared with the Han. CONCLUSIONS ABCG2 gene rs2231137 with more allele C tends to be phlegm-block type and rs2725220 with more allele G tends to be non-phlegm-block type. In the Uygur hyperuricemia patients, ABCG2 gene rs2231142 with more allele G tends to be non-phlegm-block type. Allele C of rs2231137 and allele G of rs2231142 in ABCG2 gene are more likely to be found in the Uygur people.

The relationship between Interleukin-27 gene polymorphisms and Kawasaki disease in a population of Chinese children.

BACKGROUND: Kawasaki disease is the leading cause of acquired heart disease in children from developed countries. The Interleukin-6/ Interleukin-12 cytokine family has many members, including the paradoxical anti- and pro-inflammatory Interleukin-27. Recent studies have demonstrated that Interleukin-27 plays a role in immune diseases. Given this, we sought to evaluate the association between Interleukin-27 genetic polymorphisms and Kawasaki disease in Chinese children.Methods and resultsInterleukin-27 was genotyped in 100 Kawasaki disease children and 98 healthy children (controls), resulting in the direct sequencing of eight Single-nucleotide Polymorphisms: rs17855750, rs40837, rs26528, rs428253, rs4740, rs4905, rs153109, and rs181206). There were no significant differences in Interleukin-27 genotypes between Kawasaki disease and control groups. Of the eight Single-nucleotide Polymorphisms, there was a significant increase in the risk of Kawasaki disease with coronary arterial lesions in children with the rs17855750 (T>G), rs40837 (A>G), rs4740 (G>A), rs4905 (A>G), rs153109 (T>C), and rs26528 (A>G) Single-nucleotide Polymorphisms. This was particularly true for rs17855750 (T>G), which had a greater frequency in Kawasaki disease children with coronary arterial aneurysm. CONCLUSION: These findings may be used as risk factors when assessing a child's likelihood of developing Kawasaki disease, as well as for the development of future therapeutic treatments for Kawasaki disease.

An Identity-Based Anti-Quantum Privacy-Preserving Blind Authentication in Wireless Sensor Networks.

With the development of wireless sensor networks, IoT devices are crucial for the Smart City; these devices change people's lives such as e-payment and e-voting systems. However, in these two systems, the state-of-art authentication protocols based on traditional number theory cannot defeat a quantum computer attack. In order to protect user privacy and guarantee trustworthy of big data, we propose a new identity-based blind signature scheme based on number theorem research unit lattice, this scheme mainly uses a rejection sampling theorem instead of constructing a trapdoor. Meanwhile, this scheme does not depend on complex public key infrastructure and can resist quantum computer attack. Then we design an e-payment protocol using the proposed scheme. Furthermore, we prove our scheme is secure in the random oracle, and satisfies confidentiality, integrity, and non-repudiation. Finally, we demonstrate that the proposed scheme outperforms the other traditional existing identity-based blind signature schemes in signing speed and verification speed, outperforms the other lattice-based blind signature in signing speed, verification speed, and signing secret key size.

Association of apolipoprotein E (ApoE) polymorphisms with risk of primary hyperuricemia in Uygur men, Xinjiang, China.

BACKGROUND: Apolipoprotein E (ApoE) participates in lipoprotein metabolism and immune regulation. This study assessed association between ApoE polymorphisms with hyperuricemia and uric acid metabolism in Uygur men, Xinjiang, China. METHODS: A total of 474 hyperuricemia patients and 518 healthy male controls were recruited from the Health Screening Center, Uygur region of Xinjiang, China and subjected to ApoE genotyping using a multiplex amplification refractory mutation system PCR. RESULTS: Apolipoprotein E3/3 genotype was the predominant type with a frequency of 67.7%, while E2/2 was lower than E4/4 in Uygur males. The frequencies of ApoE2, E3, and E4 alleles were 8.5%, 80.1% and 11.4%, respectively. Distribution of ApoE genotypes was significantly different in hyperuricemia patients from the healthy controls (p<0.001). Particularly, the frequency of ApoE E3/3 was 71.7%, E2/3 9.3%, E3/4 9.3%, E4/4 3.2%, E2/4 2.3%, and E2/2 0.2% in patients vs. 68.1%, 4.6%, 2.9%, 12%, 0.6%, and 4.6% in controls, respectively. Moreover, frequency of ApoE E2 allele was greater in the healthy controls than in patients (p<0.001) and the highest level of uric acid occurred in those with ApoE2/4 and E3/4 genotypes, whereas the lowest uric acid level occurred in those with ApoE E2/2 genotype. In addition, the subjects with the ApoE2 allele had a lower uric acid and LDL-C level than those with the ApoE3 allele and ApoE4 allele (p<0.05). The risk of developing hyperuricemia in subjects without the ApoE2 allele was 1.7 fold higher than those subjects with the ApoE2 allele. CONCLUSIONS: This study revealed frequencies and distributions of ApoE alleles and genotypes in Uygur males, which are different from Han Chinese. ApoE E4 was associated with a slightly higher risk of primary hyperuricemia, whereas ApoE E2 was associated with reduced risk of primary hyperuricemia and LDL-C level.

[Relationship between heart rate variability and coronary artery lesion in children with Kawasaki disease].

OBJECTIVE: To explore the correlation of heart rate variability (HRV) indices with cardiac troponin I (cTnI) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) in children with Kawasaki disease (KD) and their prognostic value. METHODS: A total of 130 children with KD were assigned into coronary artery lesion (CAL) group (n=47) and non-coronary artery lesion (NCAL) group (n=83). Meanwhile, 110 healthy children and 29 children in the recovery stage of non-cardiovascular diseases were selected as control and non-KD groups, respectively. Patients in the four groups received 24-hour HRV monitoring. Levels of serum cTnI and NT-proBNP were measured in the KD and the non-KD group. RESULTS: Compared with the controls of the same sex and age, the KD patients had significantly reduced standard deviation of all normal sinus RR intervals (SDNN), mean of SDNN (SDNN index), percentage of successive normal sinus RR intervals>50 ms (pNN50), very low frequency (VLF), low frequency (LF), and high frequency (HF) but a significantly increased LF/HF ratio (P<0.05). The HRV indices including SDNN, standard deviation of all mean 5-minute RR intervals (SDANN), SDNN index, root mean squared successive difference, pNN50, VLF, LF, and HF in the CAL group all significantly decreased compared with those in the control and non-KD groups, while the LF/HF ratio was higher in the CAL group than in the control group (P<0.05). The serum levels of cTnI and NT-proBNP in the CAL and NCAL groups were significantly higher than those in the non-KD group (P<0.05). In children with KD, serum cTnI level was negatively correlated with SDNN and HF but positively correlated with the LF/HF ratio (P<0.05); serum NT-proBNP level was negatively correlated with SDNN, SDANN, and HF (P<0.05). CONCLUSIONS: HRV indices have certain clinical significance in assessing CAL of children with KD.

Influence of dredging on sedimentary arsenic release for a tide-influenced waterfront body.

We evaluated the influence of sediment dredging on sedimentary As release for the Inner Lake, a typical tide-influenced waterfront body in the middle to lower reaches of the Yangtze River in Zhengjiang, China. By field investigation and laboratory experiment, the As content in the deposited sediment before dredging was analyzed and the relationship between dynamic disturbance and sedimentary As release intensity was established. Using a numerical model in which the factors of water current, suspended sediment, and As were coupled, the processes of As migration were simulated for typical years and tidal cycles before and after dredging. The results show that: (i) the amounts of sedimentary As release during the tidal cycles in the flood season and the dry season after dredging were reduced by 14.6 and 28.1%, respectively, compared with before dredging; (ii) after removal of the surface polluted sediment, the annual volumes of internal released As in the high-water year, common-water year, and low-water year were decreased to 11.89, 4.94, and 4.89 Mg, respectively; and (iii) the highest reduction rate could reach 27.5% in the common-water year, while the lowest was 10.92% in the high-water year because the massive water exchange with the Yangtze River in the high-water year resulted in an enhanced dynamic disturbance that played a more dominating role in the internal As release than the surface sediment removal. The results of this study may be useful for other researchers of water environment protection for waterfront bodies.

Screening miRNA and their target genes related to tetralogy of Fallot with microarray.

Our aim is to screen miRNAs and genes related to tetralogy of Fallot and construct a co-expression network based on integrating miRNA and gene microarrays. We downloaded the gene expression profile GSE35490 (miRNA) and GSE35776 (mRNA) of tetralogy of Fallot from the Gene Expression Omnibus database, which includes eight normal and 15 disease samples from infants, and screened differentially expressed miRNAs and genes between normal and disease samples (cut-off: p < 0.05; FDR < 0.05; and log FC > 2 or log FC < -2); in addition, we downloaded human miRNA and their targets, which were collected in the miRNA targets prediction database TargetScan, and selected ones that also appeared in our differentially expressed miRNAs and their predicted targets (score >0.9) and then made a relationship of diff_miRNAs and diff_genes of our results. Finally, we uploaded all the diff_target genes into String, constructed a co-expression network regulated by diff_miRNAs, and performed functional analysis with the software DAVID. Comparing normal and disease lesion tissue, we got 32 and 875 differentially expressed miRNAs and genes, respectively, and found hsa-miR-124 with 34 diff_target genes and hsa-miR-138 with two diff_target genes. Then we constructed a co-expression network that contains 231 pairs of genes. Genes in the network were enriched into 14 function clusters, and the most significant one is protein localisation. We screened the tetralogy of Fallot-related hsa-miR-124 and hsa-miR-138 with their direct and indirect differentially expressed target genes, and found that protein localisation is the significant cause affecting tetralogy of Fallot. Our approach may provide the groundwork for a new therapy approach to treating tetralogy of Fallot.

[The role of endogenous vascular elastase in coronary artery reconstruction in Kawasaki disease].

OBJECTIVE: To investigate the role of endogenous vascular elastase (EVE) in coronary artery between reconstruction among pediatric patients with Kawasaki disease (KD). METHODS: Sixty children who were diagnosed with KD between January 2012 and April 2013 were selected as the case group, and peripheral venous blood samples were collected on days 0-11 (pathological stage I) and days 12-25 (pathological stage II) after the onset of disease; another 60 children without KD who visited the hospital due to acute fever during the same period were selected as the control group, and fasting peripheral venous blood samples were collected in the acute stage of fever. For both groups, serum levels of EVE and interleukin-6 (IL-6) and plasma vascular endothelial growth factor (VEGF) level were measured by enzyme-linked immunosorbent assay. For the case group, ultrasonic cardiography was used to detect coronary artery lesions (CALs) at the first, second and fourth weekends. The correlations of EVE level with IL-6 and VEGF levels were evaluated by Pearson correlation analysis. RESULTS: Serum levels of EVE and IL-6 in the case group in pathological stages I and II were significantly higher than in the control group (P<0.05), but plasma VEGF levels in stages I and II were significantly lower than in the control group (P<0.05); in the case group, EVE and IL-6 levels were significantly higher in stage II than in stage I (P<0.05). In pathological stage II, KD patients with CALs had significantly higher serum levels of EVE and IL-6 but significantly lower plasma VEGF levels compared with those without CALs (P<0.05); KD patients with coronary artery aneurysms (CAAs) had significantly higher serum levels of EVE and IL-6 but significantly lower plasma VEGF level compared with those without CAAs (P<0.05 for all). EVE level was positively correlated with IL-6 level (r=0.915, P<0.05), yet negatively correlated with VEGF level (r=-0.769, P<0.05). CONCLUSIONS: EVE may participate in coronary artery reconstruction in children with KD. To interfere EVE activity may reduce and prevent CALs.

REDD1 knockdown ameliorates endothelial cell senescence through repressing TXNIP-mediated oxidative stress.

Endothelial cell senescence characterized by reactive oxygen species (ROS) accumulation and chronic inflammation is widely recognized as a key contributor to atherosclerosis (AS). Regulated in development and DNA damage response 1 (REDD1), a conserved stress-response protein that regulates ROS production, is involved in the pathogenesis of various age-related diseases. However, the role of REDD1 in endothelial cell senescence is still unclear. Here, we screened REDD1 as a differentially expressed senescence-related gene in the AS progression using bioinformatics methods, and validated the upregulation of REDD1 expression in AS plaques, senescent endothelial cells, and aging aorta by constructing AS mice, D-galactose (DG)-induced senescent endothelial cells and DG-induced accelerated aging mice, respectively. siRNA against REDD1 could improve DG-induced premature senescence of endothelial cells and inhibit ROS accumulation, similar to antioxidant N-Acetylcysteine (NAC) treatment. Meanwhile, NAC reduced the upregulation of REDD1 induced by DG, supporting the positive feedback loop between REDD1 and ROS contributes to endothelial cell senescence. Mechanistically, the regulatory effect of REDD1 on ROS might be related to the TXNIP-REDD1 interaction in DG-induced endothelial cell senescence. Collectively, experiments above provide evidence that REDD1 participates in endothelial cell senescence through repressing TXNIP-mediated oxidative stress, which may be involved in the progression of atherosclerosis.

[Plasma concentration of growth-differentiation factor-15 in children with congenital heart disease: relation ship to heart function and diagnostic value in heart failure].

OBJECTIVE: To study the correlation between growth differentiation factor-15(GDF-15) and cardiac function in pediatric patients with congenital heart disease, and the diagnostic value of GDF-15 in heart failure(HF). METHODS: From March 2011 to May 2012, 97 pediatric patients with congenital heart disease(CHD) who consecutively attended Chengdu Women's & Children's Central Hospital were enrolled in the study and assigned to HF (patients with heart failure, n=71) and Non-HF(patients without heart failure, n=26) groups. HF was defined as patients presenting with modified Ross score≥3. Plasma concentrations of GDF-15 and NT-proBNP were determined using ELISA. Left ventricular ejection fraction(LVEF) was tested by echocardiography. The correlation between GDF-15 and modified Ross score, LVEF and NT-proBNP was evaluated with Spearman's analysis. The area under the receiver-operating characteristic(ROC) curve for GDF-15 was examined, and the cut-off concentration of GDF-15 for diagnosing HF was detected. RESULTS: The HF group demonstrated higher levels of GDF-15 and NT-proBNP, and a lower LVEF level (P<0.01) than the Non-HF group. Plasma GDF-15 level was positively correlated with modified Ross score and plasma NT-proBNP concentration (r=0.705, r=0.810 respectively; P<0.01), and negatively correlated with LVEF(r=-0.391, P<0.01). According to ROC analysis, the AUC of GDF-15 for detection of HF was 0.757. Sensitivity and specificity was 68.8% and 71.2% respectively for the cut-off value of 1306 ng/mL. CONCLUSIONS: Plasma GDF-15 levels are significantly elevated in children with HF induced by CHD. Plasma GDF-15 levels are related to cardiac function, LVEF and plasma concentration of NT-proBNP. GDF-15 may potentially indicate HF in pediatric patients with CHD.

Blind identification of active landslides in urban areas: a new set of comprehensive criteria.

More than 70% of catastrophic landslides were previously unknown and brought tremendous losses to human life and property in urban regions; therefore, there is an urgent need for early identification of active landslides to eliminate landslide risk at the early stage. However, early identification of landslides has always been a worldwide challenge due to high concealment, steep topography, inaccessible location, and sudden onset. This work suggests a new set of comprehensive criteria for the early identification of landslides by integrating surface deformation, geological, topographic, geomorphological, and disaster-failure features. This set of criteria is universally applicable with no use of the prior knowledge of landslide locations (blind identification) and is successfully validated by a field survey. This work selects the Xuecheng region, a hard-hit area of landslides, as the study area and employs multisource data (seismic, geological, topographic, meteorological, SAR, and optical remote sensing data) and time-series InSAR technology to identify active landslides and reveal their deformation rules. Some new viewpoints are suggested. (1) The new comprehensive criteria synthesize the surface deformation, disaster-controlling, and disaster-inducing characteristics and achieve relatively high accuracy by field validation. (2) Forty-seven active landslides are identified in Xuecheng with no use of the prior knowledge of landslides. The soft rocks or soft-hard interbeddings, tectonic movement, fluvial undercutting and eroding, precipitation, earthquakes, and human engineering activity control or induce the development of these active landslides. (3) Two giant landslides that significantly threaten human lives and properties and exhibit different movement modes are selected to highlight the deformation rules of active landslides under the coupled action of poor lithologic condition, tectonic movement, river erosion, precipitation, and human engineering activity. The suggested new criteria can be applied to other landslide hard-hit urban regions and contribute to the timely and effective prevention and control of catastrophic landslides, reduction of enormous disaster losses, and rational management of the environment.

Infant Alstrom syndrome diagnosed by a new gene mutation: a case report.

Alstrom syndrome is a rare autosomal recessive disorder resulting from an ALMS1 gene mutation. Here, we present the clinical data of a case of an infant diagnosed with Alstrom syndrome through whole-exome sequencing. A 2-month-old male infant was admitted to Sichuan Provincial Maternity and Child Health Care Hospital on 30 May 2019 after "coughing for half a day and dyspnea for 2 hours". He was diagnosed with severe pneumonia, acute congestive heart failure, Grade III cardiac function, acute respiratory failure, and myocarditis. After treatment, he was discharged with a prescription for oral medication. After a 4-month follow-up, the patient's left ventricle exhibited spherical enlargement and a decrease in left ventricular function. The infant's whole-exome sequencing results revealed compound heterozygous mutations in the ALMS1 gene: c.2179dup (p. Y727Lfs*12), a frameshift mutation, that was heterozygous and originated from the mother, while c.11140C>T (p. Q3714*) was a heterozygous nonsense mutation that originated from the father. Both mutations are classified as "category 1-pathogenic mutations" according to the American College of Medical Genetics and Genomics (ACMG) assessment. A novel ALMS1 mutation was identified in this case report, highlighting the importance of genetic testing for the early diagnosis of Alstrom syndrome.