Risk-prediction models for intravenous immunoglobulin resistance in Kawasaki disease: Risk-of-Bias Assessment using PROBAST.

BACKGROUND: The prediction model of intravenous immunoglobulin (IVIG) resistance in Kawasaki disease can calculate the probability of IVIG resistance and provide a basis for clinical decision-making. We aim to assess the quality of these models developed in the children with Kawasaki disease. METHODS: Studies of prediction models for IVIG-resistant Kawasaki disease were identified through searches in the PubMed, Web of Science, and Embase databases. Two investigators independently performed literature screening, data extraction, quality evaluation, and discrepancies were settled by a statistician. The checklist for critical appraisal and data extraction for systematic reviews of prediction modeling studies (CHARMS) was used for data extraction, and the prediction models were evaluated using the Prediction Model Risk of Bias Assessment Tool (PROBAST). RESULTS: Seventeen studies meeting the selection criteria were included in the qualitative analysis. The top three predictors were neutrophil measurements (peripheral neutrophil count and neutrophil %), serum albumin level, and C-reactive protein (CRP) level. The reported area under the curve (AUC) values for the developed models ranged from 0.672 (95% confidence interval [CI]: 0.631-0.712) to 0.891 (95% CI: 0.837-0.945); The studies showed a high risk of bias (ROB) for modeling techniques, yielding a high overall ROB. CONCLUSION: IVIG resistance models for Kawasaki disease showed high ROB. An emphasis on improving their quality can provide high-quality evidence for clinical practice. IMPACT STATEMENT: This study systematically evaluated the risk of bias (ROB) of existing prediction models for intravenous immunoglobulin (IVIG) resistance in Kawasaki disease to provide guidance for future model development meeting clinical expectations. This is the first study to systematically evaluate the ROB of IVIG resistance in Kawasaki disease by using PROBAST. ROB may reduce model performance in different populations. Future prediction models should account for this problem, and PROBAST can help improve the methodological quality and applicability of prediction model development.

c-Jun N-terminal kinase activation contributes to improving low temperature tolerance via regulating apoptosis in the Pacific white shrimp Penaeus vannamei.

Temperature is an essential environmental factor for the survival of aquatic animals. Low temperature stress can induce mitochondria to produce excessive ROS and free radicals, and destroy homeostasis. c-Jun N-terminal kinase (JNK) is involved in regulating various physiological processes, including inflammatory responses, cell cycle, reproduction, and apoptosis. Here, we investigated the mechanism of ROS/JNK pathway under low temperature stress both in vitro and in vivo. In this study, transcriptome analysis revealed that apoptosis, autophagy, calcium channel, and antioxidant were involved in the mediation of low temperature tolerance in Pacific white shrimp (penaeus vannamei). PvJNK was activated in response to low temperature stress. Treatments with different temperature caused oxidative stress as demonstrated by increased intensity of the ROS indicator H2DCF-DA, and induced apoptosis as confirmed by indicator FITC. Pretreatment with N-acetylcysteine, an ROS scavenger, attenuated low temperature induced apoptosis, and inhibited the expression of PvJNK. In addition, we demonstrate that mediator PvJNK translocated to nuclear through interacting with PvRheb. By using flow cytometry, inhibiting PvJNK can increase the expression of apoptosis related genes, accelerate tissue damage, and induce ROS and cell apoptosis. The ultimate inhibition of PvJNK accelerates the mortality of shrimp under low temperature stress. Overall, these findings suggest that during low temperature stress, PvJNK was activated by ROS to regulates apoptosis via interacting with PvRheb to promote PvJNK into the nucleus and to improve low temperature tolerance of shrimp.

Breastfeeding has no protective effects on the development of coronary artery lesions in Kawasaki disease: a retrospective cohort study.

BACKGROUND: Kawasaki disease (KD) is a self-limiting vasculitis with an unknown etiology. It has been reported that breastfeeding has a potential protective effect on KD development. However, whether breastfeeding has an effect on the development of coronary artery lesions (CALs) remains unclear. METHODS: We retrospectively reviewed the medical records of patients with the main diagnosis of KD hospitalized in our hospital from May 2017 to November 2018. Standardized telephone interviews were carried out to obtain feeding practices before KD was onset. RESULTS: Two hundred and ninety-three (51.6%) were exclusively breastfed, 223 (39.3%) were partially breastfed and 52 (9.2%) were formula fed. There were no significant differences in the characteristics regarding age, gender, incomplete KD, intravenous immunoglobulin (IVIG) resistance, and the laboratory variables among the three groups. With formula feeding as a reference, patients exclusively breastfed and partially breastfed seemed to have a higher incidence of CALs, even after adjusting confounders, but were not statistically significant. After grouping patients who were older than six months into formula feeding, partial breastfeeding for < 2 months, partial breastfeeding for ≥ 2 and < 4 months, partial breastfeeding for ≥ 4 and < 6 months and exclusively breastfeeding based on the length of breastfeeding, the results remained the same (P > 0.05). CONCLUSIONS: Breastfeeding has no protective effect on the development of CALs in KD.

First report of Colletotrichum chlorophyti causing peanut anthracnose in China.

Peanut (Arachis hypogaea L.) is an important oil crop - mainly in Shandong and Henan Provinces, in China. In 2018-2019, the occurrence of a black spot disease on the leaves and stems were found in two fields (a total of 10 ha) in Niulingguanzhuang village of Yishui county in Linyi, Shandong Province, China, and 20% to 40% of plants were infected, thereby reducing the amount of marketable product. Natural symptoms were circular, dark brown-to-black lesions (2-6 mm in diameter) and coalescent necrosis on leaves and black necrosis in stems. Six symptomatic leaves and stems collected from six plants of two fields, were used for isolation. Portions of infected tissue were surfaced-sterilized with 0.5% NaClO for two minutes, 70% alcohol for 30 seconds and washed twice with sterile water. The tissues were placed on potato dextrose agar (PDA) at 28℃ for 5 days. Felt or fleece forming colonies about 4 cm in diameter that were circular, flat, and with dark center and white narrow margins were formed. Three isolates (LSJF-4, HSGF, HSJF) were purified and one culture (LSJF-4) was deposited in the China General Microbiological Culture Collection Center (CGMCC, NO. 3.19617). The chlamydospore were dark brown, verruculose, organized in chains and clusters, yellow-brown to black-brown color, and mostly spherical, 10.3 - 18.4 µm × 8.3-11.4 µm (n = 50, av. 12.6 ± 2.1× 10.1 ± 1.1 µm). The conidia were colorless, crescent or sickle-shaped, with one acute end and one blunt end. They were 16.7 - 24.3 µm × 3.6 - 5.5 µm (n= 50, av. 21.2 ± 1.7× 4.5 ± 0.36 µm), with dark brown, straight, septate setae, 40.3 - 86.9 µm × 3.6-5.5 µm (n=50, av. 70.0 ± 19.1 × 4.5 ± 0.7 µm) in size. Setae were straight, dark brown. These morphological characteristics of our isolates were identical to Colletotrichum chlorophyti (Damm et al. 2009). The internal transcribed spacer (ITS, ITS1/ITS4) rDNA of three fungus (LSJF-4, HSGF, HSJF) were amplified using PCR and sequenced, as described by Damm et al (2009). The sequencing results (GenBank Accession No. MK796409, MN756650, MN756651) were submitted to the GenBankand blast analysis showed that it had 99.0% identity with those of Colletotrichum chlorophyti (No. GU227894). Actin (ACT, ACT-512F/ACT-783R), beta-tubulin (Tub2, T1/T2 ), Glyceraldehyde-3-phosphate dehydrogenase (GAPDH, GDF1/GDR1), chitin synthase (CHS1, CHS-79f/CHS-345R), histone (H3, Cy1H3F/ Cy1H3R) of LSJF-4 (Nos. MN688800, MN688797, MN097811, MN688799 and MN688798, respectively) (Damm et al. 2009) were also sequenced and BLAST. The results showed high identity of all the five sequences to the CGMCC 3.19617 (Nos. GU228286/GU228287 in GAPDH = 99.6%, GU228384/GU22385 in CHS1 = 96.8%, GU228090/GU228091 in H3 = 99.0%, GU227992/GU227993 in ACT = 98.7%, and GU228188/GU228189 in Tub2 = 98.8%). Therefore, isolate CGMCC 3.19617 was identified as C. chlorophyti based on morphological and molecular characteristics. To determine pathogenicity, a conidial suspension containing 106 conidia/mL was sprayed on leaves and stems of six 40-day old peanut seedlings. Three control plants were similarly sprayed with sterile water. All treated plants were kept moist (>85% relative humidity) at 30℃ for 48 h in darkness, and then kept in 60% relative humidity and 28℃ conditions. Two weeks post-inoculation, small, dark, near elliptical lesions appeared on inoculated leaves and stems, which were similar to those naturally infected plants. While controls remained symptomless. C. chlorophyti was reisolated from infected tissues and identified based on the previous methods, fulfilling Koch's postulates. The test was repeated twice. C. chlorophyti has been reported as a pathogen associated with soybean anthracnose isolated from the Netherlands (Damm et al. 2009). C. chlorophyti was first detected on soybean plants imported from Uruguay (Li et al. 2017) in China. To our knowledge, this is the first report of C. chlorophyti causing peanut anthracnose in China. C. chlorophyti may be a new threat to Leguminous plant species, especially peanuts plants. We proposed paying close attention to taking necessary control meatures.

Kawasaki disease OX40-OX40L axis acts as an upstream regulator of NFAT signaling pathway.

BACKGROUND: We investigated a costimulatory molecule OX40-OX40L acting as an upstream regulator to regulate the nuclear factor of activated T cell (NFAT) in the acute phase of Kawasaki disease (KD). METHODS: One hundred and one samples were collected and divided into six groups: coronary artery lesion (KD-CAL) before intravenous immunoglobulin (IVIG), KD-CAL after IVIG, KD without CAL (KD-nCAL) before IVIG, KD-nCAL after IVIG, fever of unknown (Fou), and Healthy. In vitro OX40-stimulating and OX40L-inhibiting tests were conducted in Healthy and KD groups, respectively. Both the messenger RNA (mRNA) and protein expression levels of OX40, OX40L, NFAT1, and NFAT2 were investigated using quantitative reverse transcription PCR and immunoblotting assay, respectively. RESULTS: The mRNA and protein expression levels of NFAT1, NFAT2, OX40, and OX40L were significantly increased in KD-CAL and KD-nCAL groups before IVIG compared with Fou and Healthy groups and decreased after IVIG. A positive correlation was found between them in KD. In vitro OX40-stimulating test demonstrated the significantly increased mRNA and protein expression levels of NFAT1 and NFAT2 in the peripheral blood mononuclear cells of the Healthy group. Meanwhile, OX40L-inhibiting test showed significantly decreased expression levels of NFAT1 and NFAT2 in the KD group. CONCLUSION: OX40-OX40L acts as an upstream regulator in the NFAT signaling pathway involved in KD.

Predictors of intravenous immunoglobulin-resistant Kawasaki disease in children: a meta-analysis of 4442 cases.

The purpose of this study was to identify the clinical features and laboratory factors that are predictive of intravenous immunoglobulin (IVIG)-resistant Kawasaki disease. Multiple databases were searched for relevant studies on IVIG-resistant Kawasaki disease published from January 2002 to April 2017. Eligible studies were retrieved by manual review of the references. Stata 12 was used for the meta-analysis. Weighted mean differences and odds ratios with 95% confidence intervals were calculated for several indices. Twenty-eight studies involving 26,260 patients comprising 4442 IVIG-resistant Kawasaki disease patients and 21,818 IVIG-sensitive Kawasaki disease patients were included. The meta-analysis showed that the erythrocyte sedimentation rate (ESR) in the IVIG-resistant group was significantly higher than that in the IVIG-sensitive group, and that platelet count and hemoglobin levels were significantly lower in the IVIG-resistant group. The patients with oral mucosa alterations, cervical lymphadenopathy, swelling of the extremities, polymorphous rash, and initial administration of IVIG ≤ 4.0 days after the onset of symptoms were more likely to be IVIG resistant. CONCLUSION: The initial administration of IVIG ≤ 4.0 days after the onset of symptoms increased ESR and decreased hemoglobin and platelet counts, oral mucosa alterations, cervical lymphadenopathy, swelling of the extremities, and polymorphous rash and are the risk factors for IVIG-resistant Kawasaki disease. What is Known: • Recent reports on this topic are about aspartate aminotransferase (AST), alanine aminotransferase (ALT), gammaglutamyl transferase, total bilirubin, white blood cells, platelets, erythrocyte sedimentation rate (ESR), polymorphonuclear leukocytes (PMN), C-reactive protein (CRP), pro-brain natriuretic peptide (BNP), albumin, and sodium as the risk factors in the IVIG-resistant Kawasaki disease; however, no studies have been published on clinical features as predictors of IVIG resistance. What is New: • This meta-analysis identified the clinical features, the initial administration of IVIG ≤ 4.0 days after the onset of symptoms, and much more comprehensive laboratory indicators, such as hemoglobin, as predictors of IVIG-resistant Kawasaki disease.

Bioinformatics analysis and identification of hub genes of neutrophils in Kawasaki disease: a pivotal study.

BACKGROUND: Kawasaki disease (KD) is considered the main contributor to acquired heart diseases in developed countries. However, the precise pathogenesis of KD remains unclear. Neutrophils play roles in KD. This study aimed to select hub genes in neutrophils in acute KD. METHODS: mRNA microarray of neutrophils from four acute KD patients and three healthy controls was performed to screen differentially expressed mRNAs (DE-mRNAs). DE-mRNAs were analyzed and predicted by Gene Ontology (GO), Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathways, and protein-protein interaction networks. Real time-PCR was finally conducted to confirm the reliability and validity of the expression level of DE-mRNAs from blood samples of healthy controls and KD patients in both acute and convalescent stage. RESULTS: A total of 1950 DE-mRNAs including 1287 upregulated and 663 downregulated mRNAs were identified. GO and KEGG analyses revealed the DE-mRNAs were mainly enriched in the regulation of transcription from RNA polymerase II promoter, apoptotic process, intracellular signal transduction, protein phosphorylation, protein transport, metabolic pathways, carbon metabolism, lysosome, apoptosis, pyrimidine metabolism, alzheimer disease, prion disease, sphingolipid metabolism, huntington disease, glucagon signaling pathway, non-alcoholic fatty liver disease, pyruvate metabolism, sphingolipid signaling pathway, and peroxisome. Twenty hub DE-mRNAs were selected including GAPDH, GNB2L1, PTPRC, GART, HIST2H2AC, ACTG1, H2AFX, CREB1, ATP5A1, ENO1, RAC2, PKM, BCL2L1, ATP5B, MRPL13, SDHA, TLR4, RUVBL2, TXNRD1, and ITGAM. The real-time PCR results showed that BCL2L1 and ITGAM mRNA were upregulated in acute KD and were normalized in the convalescent stage. CONCLUSIONS: These findings may improve our understanding of neutrophils in KD. Key Points • Neutrophilic BCL2L1 and ITGAM mRNA were first reported to be correlated with the pathogenic mechanism of KD.

Dynamic process and mechanism of crude oil release from silty intertidal sediment under different influencing factors.

Under tidal scouring, residual petroleum in the intertidal sediment after oil spills could release again, causing secondary pollution in the marine ecosystem. The current study aimed to investigate the dynamic process and principles of crude oil release from silty intertidal sediment under different influencing factors and screened for the key factors. In this paper, the fitting equations and correlation between the release amount and various factors were explored through the single-factor and orthogonal experiments. Then, the key influencing factors were selected for multi-factor fitting of the release amount. The results showed that the oil release amount rose with the increase in oil concentration, oscillation frequency, and release time, but decreased with an increase in salinity. As the pH decreased, the oil release amount increased. The relationship between release amount and concentration/oscillation frequency can be equipped by the polynomial equation, and the average R2 was 0.95 and 0.84, respectively. The release amount can be fitted by the Lagergren pseudo-second-order kinetic equation with time, with the average R2 0.89. The pH was negatively correlated with the release amount in the fresh contaminated sediment but positively correlated with the weathered one. The correlation between each factor and oil release amount was ranked (from large to small) as oil concentration, oscillation frequency, salinity, time, and pH. At last, a polynomial equation can be fitted between the key influencing factors (oil concentration and oscillation frequency) and the release amount. The results can provide a theoretical basis for predicting the secondary pollution owing to the oil re-release from intertidal sediment.

The role of FOXO4/NFAT2 signaling pathway in dysfunction of human coronary endothelial cells and inflammatory infiltration of vasculitis in Kawasaki disease.

Aims: The Ca+/NFAT (Nuclear factor of activated T cells) signaling pathway activation is implicated in the pathogenesis of Kawasaki disease (KD); however, we lack detailed information regarding the regulatory network involved in the human coronary endothelial cell dysfunction and cardiovascular lesion development. Herein, we aimed to use mouse and endothelial cell models of KD vasculitis in vivo and in vitro to characterize the regulatory network of NFAT pathway in KD. Methods and Results: Among the NFAT gene family, NFAT2 showed the strongest transcriptional activity in peripheral blood mononuclear cells (PBMCs) from patients with KD. Then, NFAT2 overexpression and knockdown experiments in Human coronary artery endothelial cells (HCAECs) indicated that NFAT2 overexpression disrupted endothelial cell homeostasis by regulation of adherens junctions, whereas its knockdown protected HCAECs from such dysfunction. Combined analysis using RNA-sequencing and transcription factor (TF) binding site analysis in the NFAT2 promoter region predicted regulation by Forkhead box O4 (FOXO4). Western blotting, chromatin immunoprecipitation, and luciferase assays validated that FOXO4 binds to the promoter and transcriptionally represses NFAT2. Moreover, Foxo4 knockout increased the extent of inflamed vascular tissues in a mouse model of KD vasculitis. Functional experiments showed that inhibition NFAT2 relieved Foxo4 knockout exaggerated vasculitis in vivo. Conclusions: Our findings revealed the FOXO4/NFAT2 axis as a vital pathway in the progression of KD that is associated with endothelial cell homeostasis and cardiovascular inflammation development.

Neutropenia Is Not Associated With the Outcomes in Patients With Kawasaki Disease.

Objective: To investigate the outcomes of coronary artery lesions (CALs) and intravenous immunoglobulin (IVIG) resistance in patients with and without neutropenia during the disease course and to explore the relationships between Δ absolute neutrophils count (ΔANC) and the outcomes. Methods: We retrospectively reviewed the medical records of patients hospitalized in Children's Hospital of Soochow University with a main diagnosis of KD during January 2019 and December 2019. 1:4 propensity score matching was carried out to adjust the baseline characteristics. Smoothed plots and threshold effect analyses were performed to reveal the relationships between ΔANC and the outcomes. Results: Of the 438 patients enrolled, 75 (17.1%) were neutropenia cases and 363 (82.9%) were non-neutropenia cases. Patients with neutropenia were younger, had lower levels of initial ANC, white blood cell (WBC) count and C-reactive protein (CRP). Propensity score matching included 75 neutropenia and 247 non-neutropenia patients. No significant difference was found between neutropenia and non-neutropenia groups regarding CALs, coronary artery aneurysms, irregular coronary lumen, IVIG resistance and days of fever duration. There was a non-linear relationship between ΔANC and IVIG resistance. However, threshold effect analysis showed the incidence of IVIG resistance decreased with increasing ΔANC before the turning point (ΔANC = 1.6) (OR = 0.65, 95% CI = 0.50-0.8.4 P = 0.001). On the other hand, there was a linear relationship between ΔANC and CALs, even after adjusting the confounders (OR = 1.06, 95% CI = 1.02-1.11, P = 0.008). Conclusions: Neutropenia after IVIG was not exactly associated with the outcomes. However, ΔANC was in relation to CALs and IVIG resistance.

AST-to-ALT ratio and coronary artery lesions among patients with Kawasaki disease.

BACKGROUND: The aim of this study was to explore the associations between the aspartate aminotransferase-to-alanine aminotransferase ratio (AST/ALT) and coronary artery lesions (CALs) among patients with Kawasaki disease (KD). METHODS: Medical records of KD patients presenting to a single center between January 2019 and December 2020 were retrospectively collected and analyzed. Univariate, multivariable-adjusted analyses, subgroup analyses, restricted cubic spline test, and fitted curves were used to evaluate the associations between AST/ALT and CALs. RESULTS: A total of 831 patients were enrolled, of which 201 (24.2%) had CALs on admission and 21 (2.5%) developed CALs de novo after intravenous immunoglobulin (IVIG). Multivariable-adjusted analyses models revealed that a lower AST/ALT was associated with an increased risk of CALs on admission when AST/ALT was a continuous variable (P = 0.007) and when it was a categorical variable (P for trend = 0.004). Each unit increase in AST/ALT was associated with a 22% lower risk of CALs on admission (odds ratio = 0.78, 95% confidence interval 0.65-0.94). A negative linear relationship was noted between AST/ALT and the risk of CALs on admission in both observed and fitted models. However, such associations were not observed in AST/ALT and CALs de novo after IVIG. None of the variables significantly modified the association between AST/ALT and CALs on admission and CALs de novo after IVIG (P > 0.05). CONCLUSION: Our findings suggested that AST/ALT was a risk factor of CALs, but was not associated with progressive CALs.

Fatty acid comparison of four sympatric loliginid squids in the northern South China Sea: Indication for their similar feeding strategy.

Feeding strategies of sympatric squid species help to understand their role in marine ecosystems. Four loliginid squids, Uroteuthis duvaucelii, Uroteuthis edulis, Uroteuthis chinensis, and Loliolus uyii are the major cephalopod species in the coastal waters of the northern South China Sea, where they occur together. We investigated their feeding strategies in terms of foraging behavior and habitat use by comparing fatty acid profiles and spatial distributions. There were no significant differences in the proportions of saturated or polyunsaturated fatty acids among species. Similar findings were obtained for most individual fatty acids that made up of an average of more than 84% of total fatty acid content for each species. Substantial overlap and high similarity in the fatty acid composition were observed. However, there were no significant effects of individual size or sampling station on the fatty acid compositions. The spatial overlap analysis demonstrated that there was clear spatial segregation and habitat use among the species. Cumulatively, our results suggest that the four squids are opportunistic carnivores, unselectively foraging on similar prey items, while spatial segregation is likely a major mechanism leading to their coexistence in the northern South China Sea.

Salt stress induced differential metabolic responses in the sprouting tubers of Jerusalem artichoke (Helianthus tuberosus L.).

To better understand the mechanism of inherent salt resistance in Jerusalem artichoke (Helianthus tuberosus L.), physiological and metabolic responses of tubers at the initiation stage of sprouting under different salt stress levels were evaluated in the present study. As a result, 28 metabolites were identified using proton nuclear magnetic resonance (1H-NMR) spectroscopy. Jerusalem artichoke tubers showed minor changes in metabolic response under moderate salt stress when they had not yet sprouted, where metabolism was downregulated at the start of sprouting and then upregulated significantly after plants became autotrophic. However, mild and severe salt stress levels caused different metabolic response patterns. In addition, the accumulation of fructose and sucrose was enhanced by moderate salt stress, while glucose was highly consumed. Aspartate and asparagine showed accelerated accumulation in sprouting Jerusalem artichoke tubers that became autotrophic, suggesting the enhancement of photosynthesis by moderate salt stress.

Ubiquitin specific protease 5 negatively regulates the IFNs-mediated antiviral activity via targeting SMURF1.

Type I interferons are broadly used for antiviral therapy in clinical. However, the IFNs-mediated antiviral efficacy is commonly restricted by negative regulators. Here, we show that the ubiquitin-specific protease 5 (USP5) inhibits the IFNs-induced p-STAT1 activation (phosphorylation at tyrosine site of STAT1) and its downstream antiviral genes expression. We clarify that USP5 physically interacts with SMURF1 (Smad ubiquitination regulating factor 1) and IFNs signaling regulates the interaction and turnover of both proteins. USP5 enhances the stability and turnover of SMURF1 via decreasing its polyubiquitin expression level, which caused STAT1 to decrease. Importantly, USP5 is also involved in the SMURF1-mediated antiviral response, and its small-molecule inhibitor PYR41 remarkably enhances the IFNs antiviral efficacy. These findings reveal a previously unrecognized function of the USP5 and USP5-SMURF1 axis in regulating the IFNs-mediated antiviral activity.

Genome-wide characterization and expression analysis of aquaporins in salt cress (Eutrema salsugineum).

Aquaporins (AQPs) serve as water channel proteins and belong to major intrinsic proteins (MIPs) family, functioning in rapidly and selectively transporting water and other small solutes across biological membranes. Importantly, AQPs have been shown to play a critical role in abiotic stress response pathways of plants. As a species closely related to Arabidopsis thaliana, Eutrema salsugineum has been proposed as a model for studying salt resistance in plants. Here we surveyed 35 full-length AQP genes in E. salsugineum, which could be grouped into four subfamilies including 12 plasma membrane intrinsic proteins (PIPs), 11 tonoplast intrinsic proteins (TIPs), nine NOD-like intrinsic proteins (NIPs), and three small basic intrinsic proteins (SIPs) by phylogenetic analysis. EsAQPs were comprised of 237-323 amino acids, with a theoretical molecular weight (MW) of 24.31-31.80 kDa and an isoelectric point (pI) value of 4.73-10.49. Functional prediction based on the NPA motif, aromatic/arginine (ar/R) selectivity filter, Froger's position and specificity-determining position suggested quite differences in substrate specificities of EsAQPs. EsAQPs exhibited global expressions in all organs as shown by gene expression profiles and should be play important roles in response to salt, cold and drought stresses. This study provides comprehensive bioinformation on AQPs in E. salsugineum, which would be helpful for gene function analysis for further studies.

Characterization of the complete chloroplast genome of Sargassum fusiforme and its phylogenomic position within phaeophyceae.

Sargassum fusiforme is an important economic seaweed in East Asia. In this study, we characterized the complete chloroplast genome sequence of S. fusiforme using PacBio long-read sequencing technology. It had a circular mapping molecular with the length of 124,286 bp, with a large single-copy region (LSC, 73,437 bp) and a small single copy region (SSC, 40,131 bp) separated by a pair of inverted repeats (IRs, 5,359 bp). The cp genome contained 173 genes including 139 protein-coding, 6 rRNA, and 28 tRNA genes. The phylogenomic analysis indicated that S. fusiforme is closely related to S. thunbergii.

Echocardiographic Prediction of Left Ventricular Dysfunction After Transcatheter Patent Ductus Arteriosus Closure in Children.

Objectives: To evaluate the change of left ventricular (LV) systolic function after transcatheter patent ductus arteriosus (PDA) closure in children, and to identify whether echocardiography parameters could be the predictors of LV dysfunction post-PDA closure if present. Methods: This study enrolled 191 pediatric PDA patients, and all of them underwent successful transcatheter PDA closure between January 2016 and December 2018. The patent ductus arteriosus diameter (PDAd), aortic root diameter (AOd), left atrial diameter (LAd), right ventricular outflow tract dimension (RVOT), LV end-diastolic dimension (LVEDD), and LV end-systolic dimension (LVESD) were all measured by echocardiography at pre-closure, post-closure (within 24 h after the procedure), and follow-up (3 months after the procedure). The ratio of PDAd to AOd (PDAd/AOd), the ratio of LAd to AOd (LAd/AOd), the left ventricular ejection fraction (LVEF), and the fractional shortening (FS) were calculated. Results: The LAd, LVESD, LVEDD, FS, and LVEF decreased significantly in the 24 h after closure, compared to pre-closure levels. However, all echocardiography parameters recovered to pre-closure levels at 3 months after PDA closure in all patients. Moreover, the pre-closure LAd, LVEF, PDAd/AOd, and LAd/AOd were higher in the patients with post-closure LV systolic dysfunction than in those without post-closure LV systolic dysfunction. Furthermore, the pre-closure LVEF, PDAd/AOd, and LAd/AOd were correlated with the post-closure LVEF, and pre-closure LVEF ≤ 66.5%, PDAd/AOd ≥ 0.28, and LAd/AOd ≥ 1.54 predict the post-closure LV systolic dysfunction. Conclusion: Transcatheter closure of PDA causes a significant deterioration in LV systolic function early after PDA closure, which recovered completely within 3 months of post-closure in children. Pre-closure LVEF, PDAd/AOd, and LAd/AOd can be the predictors of post-closure left ventricular systolic dysfunction.

A comparison of efficacy of six prediction models for intravenous immunoglobulin resistance in Kawasaki disease.

BACKGROUND: Kawasaki disease (KD) is the most common pediatric vasculitis. Several models have been established to predict intravenous immunoglobulin (IVIG) resistance. The present study was aimed to evaluate the efficacy of prediction models using the medical data of KD patients. METHODS: We collected the medical records of patients hospitalized in the Department of Cardiology in Children's Hospital of Soochow University with a diagnosis of KD from Jan 2015 to Dec 2016. IVIG resistance was defined as recrudescent or persistent fever ≥36 h after the end of their IVIG infusion. RESULTS: Patients with IVIG resistance tended to be younger, have higher occurrence of rash and changes of extremities. They had higher levels of c-reactive protein, aspartate aminotransferase, neutrophils proportion (N%), total bilirubin and lower level of albumin. Our prediction model had a sensitivity of 0.72 and a specificity of 0.75. Sensitivity of Kobayashi, Egami, Kawamura, Sano and Formosa were 0.72, 0.44, 0.48, 0.20, and 0.68, respectively. Specificity of these models were 0.62, 0.82, 0.66, 0.91, and 0.48, respectively. CONCLUSIONS: Our prediction model had a powerful predictive value in this area, followed by Kobayashi model while all the other prediction models had less excellent performances than ours.

Kawasaki disease associated with Mycoplasma pneumoniae.

BACKGROUND: Kawasaki disease (KD) is an illness of unknown etiology that mostly occurs in children under 5 years of age and is the leading cause of acquired heart disease all over the world. Mycoplasma pneumoniae (MP) was one of the likely causative agents of KD. However, the etiologic effect of MP in KD has not been fully recognized. METHODS: We prospectively analyzed the clinical records of 450 patients with KD hospitalized in Children's Hospital of Soochow University from 2012 to 2014. Using medical records, we retrospectively identified patients with low respiratory tract infection (non-KD group). RESULTS: Of the 450 KD patients, MP was positive in 62 (13.8 %). The median age of the MP + KD+ group was significantly older than the MP-KD+ group (25 vs 14.5 months, P < 0.01). MP + KD+ group had higher levels of ESR, N% and CRP than the MP-KD+ group. MP + KD+ group were more frequent in respiratory disorders than MP-KD+ group with a P < 0.05. No statistical difference of non-responders or coronary artery lesion was found between the groups. CONCLUSIONS: MP infections are found in an important proportion of the KD patients (13.8 % in our series). MP infection tended to occur in older populations and with a higher rate of respiratory tract involvement in patients with KD. No statistical difference of non-responders or coronary artery lesion was found between the MP+ and MP- KD patients.

Prediction of intravenous immunoglobulin resistance in Kawasaki disease in an East China population.

The objectives of the study were to find the risk factors associated with intravenous immunoglobulin (IVIG) resistance and generate a prediction scoring system of IVIG resistance in patients with Kawasaki disease (KD). We retrospectively reviewed the clinical records of KD patients between January 2006 and December 2014. Multivariate logistic regression was performed to identify the risk factors of IVIG non-responders. The independent risk factors were used to construct a new scoring system and compared with Kobayashi and Egami scoring systems. Multivariate logistic regression analysis identified age <6 months, rash, edema of extremities, % neutrophils, and serum albumin as independent risk factors for IVIG non-responders. We assigned one point for rash, edema of extremities, and % neutrophils ≥80 %. Two points were assigned for age <6 months and serum albumin <35 g/L. Using a cutoff point of three or more, we identified the IVIG non-responders with 71.4 % sensitivity and 76.0 % specificity. The new scoring system had a relatively better performance than Kobayashi and Egami scoring systems in the KD patients in East China. Clinical pediatricians must pay more attention to these high-risk patients, and use of additional therapies early in the course of their illness is necessary.