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2.
IEEE Trans Cybern ; 50(1): 374-385, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31107670

RESUMO

In this paper, a robust online multilabel learning method dealing with dynamically changing multilabel data streams is proposed. The proposed method has three advantages: 1) higher accuracy due to a newly defined objective function based on labels ranking; 2) fast training and update based on a newly derived closed-form (rather than gradient descent based) solution for the new objective function; and 3) high robustness to a newly identified concept drift in multilabel data streams, namely, changes in data distribution with labels (CDDL). The high robustness benefits from two novel works: 1) a new sequential update rule that preserves the labels ranking information learned from all old (but discarded) samples while updating the model only based on new incoming samples and 2) a fixed threshold for label bipartition that is insensitive to any kind of changes in data distribution including CDDL. The proposed method has been evaluated over 13 benchmark datasets from various domains. As shown in the experimental results, the proposed work is highly robust to CDDL in both the sequential model update and multilabel thresholding. Furthermore, the proposed method improves the performance in different evaluation measures, including Hamming loss, F1-measure, Precision, and Recall while taking short training time on most evaluated datasets.

3.
Arch Pharm Res ; 2019 Dec 03.
Artigo em Inglês | MEDLINE | ID: mdl-31797253

RESUMO

Gestational diabetes mellitus (GDM) is a disease characterized by insufficient insulin secretion and glucose metabolic disorder during pregnancy. Tetramethylpyrazine has been reported to inhibit endoplasmic reticulum (ER) stress and high glucose-induced inflammation, which are closely associated with GDM. This study aimed to investigate the effects of tetramethylpyrazine on inflammatory responses, ER stress and oxidative stress of the placenta in a mouse model of GDM. Our results showed that tetramethylpyrazine treatment significantly alleviated the GDM symptoms characterized by low body weight and serum insulin levels, high blood glucose, and decreased ß-cell function in pregnant C57BL/KsJdb/+ mice. In addition, tetramethylpyrazine reduced the level of malondialdehyde, and increased the levels of superoxide dismutase, glutathione peroxidase and glutathione. Moreover, tetramethylpyrazine decreased the total serum cholesterol, serum triglyceride, and serum low-density lipoprotein levels and increased the high-density lipoprotein level. Further, tetramethylpyrazine regulated the levels of serum and placental inflammatory factors and the expression of ER stress related proteins. Taken together, the present study demonstrated that tetramethylpyrazine attenuated placental oxidative stress, inflammatory responses and ER stress in GDM mice.

4.
J Pathol ; 2019 Nov 22.
Artigo em Inglês | MEDLINE | ID: mdl-31758542

RESUMO

The immunoproteasome contains three catalytic subunits (ß1i, ß2i and ß5i) that are important modulators of immune cell homeostasis. A previous study showed a correlation between ß5i and human atherosclerotic plaque instability; however, the causative role of ß5i in atherosclerosis and the underlying mechanisms remain unknown. Here we explored this issue in apolipoprotein E (Apoe) knockout (KO) mice with genetic deletion or pharmacological inhibition of ß5i. We found that ß5i expression was upregulated in lesional macrophages after atherogenic diet (ATD) feeding. ß5i/Apoe double KO (dKO) mice fed on ATD had a significant decrease in both lesion area and necrotic core area, compared with Apoe KO (eKO) controls. Moreover, dKO mice had less caspase-3+ apoptotic cell accumulation but enhanced efferocytosis of apoptotic cells and increased expression of Mer receptor tyrosine kinase (MERTK). Consistently, similar phenotypes were observed in eKO mice transplanted with dKO bone marrow (BM) or treated with ß5i-specific inhibitor PR-957. Mechanistic studies in vitro revealed that ß5i deletion reduced IκBα degradation and inhibited NF-κB activation, promoting Mertk transcription and efferocytosis, thereby attenuated apoptotic cell accumulation. In conclusion, we demonstrate that ß5i plays an important role in diet-induced atherosclerosis by altering MERTK-mediated efferocytosis. ß5i might be a potential pharmaceutical target against atherosclerosis. This article is protected by copyright. All rights reserved.

5.
Sci Rep ; 9(1): 14083, 2019 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-31575993

RESUMO

Low-density lipoprotein cholesterol (LDL-C) has been associated with the occurrence of abdominal aortic aneurysm. However, whether LDL-C elevation associated with aneurysms in large vessel vasculitis is unknown. The aim of this study is to investigate the clinical and laboratory features of Takayasu arteritis (TAK) and explore the risk factors that associated with aneurysm in these patients. This retrospective study compared the clinical manifestations, laboratory parameters, and imaging results of 103 TAK patients with or without aneurysms and analyzed the risk factors of aneurysm formation. 20.4% of TAK patients were found to have aneurysms. The LDL-C levels was higher in the aneurysm group than in the non-aneurysm group (2.9 ± 0.9 mmol/l vs. 2.4 ± 0.9 mmol/l, p = 0.032). Elevated serum LDL-C levels increased the risk of aneurysm by 5.8-fold (p = 0.021, odds ratio [OR] = 5.767, 95% confidence interval [CI]: 1.302-25.543), and the cutoff value of level of serum LDL-C was 3.08 mmol/l. The risk of aneurysm was 4.2-fold higher in patients with disease duration >5 years (p = 0.042, OR = 4.237, 95% CI: 1.055-17.023), and 2.9-fold higher when an elevated erythrocyte sedimentation rate was present (p = 0.077, OR = 2.851, 95% CI: 0.891-9.115). In this study, elevated LDL-C levels increased the risk of developing aneurysms in patients with TAK.

6.
Fish Shellfish Immunol ; 94: 861-870, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31585246

RESUMO

The main advantage of antimicrobial peptides (AMPs) used as the effectors in the innate immunity system of invertebrates is that the high specificity is not indispensable. And they play important roles in the systemic defenses against microbial invasion. In this study, a new full-length cDNA of the crustins molecule was identified in red swamp crayfish, P. clarkii (named Pc-crustin 4). The ORF of Pc-crustin 4 contained 369 bp which encoded a protein of 122 amino acids, with a 20-amino-acid signal peptide sequence. On the base of the classification method established by Smith et al., Pc-crustin 4 belonged to Type Ⅰ crustin molecule. The Pc-crustin 4 transcripts were expressed in hemocytes at relatively high level, and relatively low level in hepatopancreas, gills, and intestine in normal crayfish. After respectively challenged with S. aureus or E. ictaluri, the expression levels of Pc-crustin 4 showed up-regulation trends at different degrees in the hemocytes, hepatopancreas, gills, and intestine tissues. Besides, the results of liquid antibacterial assay showed that rPc-crustin 4 inhibited obviously the growth of S. aureus and E. ictaluri. The results of bacteria binding assay showed that rPc-crustin 4 could bind strongly to S. aureus and E. ictaluri. Finally, RNAi assay was performed to study the immunity roles of Pc-crustin 4 in crayfish in vivo. Taken together, Pc-crustin 4 is an important immunity effector molecule, which plays crucial roles in defending against bacterial infection in crayfish.

7.
Diabetes Ther ; 2019 Oct 26.
Artigo em Inglês | MEDLINE | ID: mdl-31654346

RESUMO

INTRODUCTION: Gestational diabetes mellitus (GDM) is a gestational complication that affects maternal and child health. The placenta provides the fetus with the necessary nutrition and oxygen and takes away the metabolic waste. Patients with GDM are diagnosed and treated merely on the basis of the blood glucose level; this approach does nothing to help evaluate the status of the placenta, which is worth noting in GDM. The purpose of this research was to clarify the relation between thioredoxin-interacting protein (TXNIP) and reactive oxygen species (ROS) in the placenta of patients with GDM, which has thus far remained unclear. METHODS: The expression of TXNIP in the placentas of 10 patients with GDM and 10 healthy puerperae (control group) was investigated via immunofluorescence. The relation among TXNIP, ROS, and the function of mitochondria was explored in HTR-8/SVneo cells stimulated by high glucose (HG). RESULTS: The results showed the expression of TXNIP in the placentas of patients with GDM was higher than that in the control group, and the expression of TXNIP in HTR-8/SVneo cells treated with HG was higher than that in the control group, causing the accumulation of ROS and changes of mitochondria, promoting apoptosis and inhibition of migration. CONCLUSIONS: High expression of TXNIP caused by HG mediates the increasing ROS and the mitochondria dysfunction in GDM; this impairs the function of the placenta and is the basis for the prediction of perinatal outcome.

8.
Int J Mol Sci ; 20(20)2019 Oct 11.
Artigo em Inglês | MEDLINE | ID: mdl-31614494

RESUMO

We investigated the effects of a fibrin-hyaluronic acid hydrogel (FBG-HA) and fibroblast growth factor 18 (FGF-18) for nucleus pulposus (NP) regeneration. Healthy bovine (n = 4) and human degenerated NP cells (n = 4) were cultured for 14 days in FBG-HA hydrogel with FGF-18 (∆51-mutant or wild-type) in the culture medium. Gene expression, DNA content, and glycosaminoglycan (GAG) synthesis were evaluated on day 7 and 14. Additionally, histology was performed. Human NP cells cultured in FBG-HA hydrogel showed an increase in collagen type II (COL2) and carbonic anhydrase XII (CA12) gene expression after 14 or 7 days of culture, respectively. GAG release into the conditioned medium increased over 14 days. Healthy bovine NP cells showed increased gene expression of ACAN from day 7 to day 14. Wild type FGF-18 up-regulated CA12 gene expression of human NP cells. Histology revealed an increase of proteoglycan deposition upon FGF-18 stimulation in bovine but not in human NP cells. The FBG-HA hydrogel had a positive modulatory effect on human degenerated NP cells. Under the tested conditions, no significant effect of FGF-18 was observed on cell proliferation or GAG synthesis in human NP cells.

9.
Cardiovasc Res ; 2019 Oct 12.
Artigo em Inglês | MEDLINE | ID: mdl-31605122

RESUMO

AIMS: Genetic contribution to coronary artery disease (CAD) remains largely unillustrated. Although transcriptomic profiles have identified dozens of genes that are differentially expressed in normal and atherosclerotic vessels, whether those genes are genetically associated with CAD remains to be determined. Here, we combined genetic association studies, transcriptome profiles and in vitro and in vivo functional experiments to identify novel susceptibility genes for CAD. METHODS AND RESULTS: Through an integrative analysis of transcriptome profiles with genome-wide association studies for CAD, we obtained 18 candidate genes and selected one representative SNP for each gene for multi-centered validations. We identified an intragenic SNP, rs1056515 in RGS5 gene (OR = 1.17, 95%CI =1.10-1.24, P = 3.72 × 10-8) associated with CAD at genome-wide significance. Rare genetic variants in linkage disequilibrium with rs1056515 were identified in CAD patients leading to a decreased expression of RGS5. The decreased expression was also observed in atherosclerotic vessels and endothelial cells treated by various cardiovascular risk factors. Through siRNA knockdown and adenoviral overexpression, we further showed that RGS5 regulated endothelial inflammation, vascular remodeling, as well as canonical NF-κB signaling activation. Moreover, CXCL12, a specific downstream target of the noncanonical NF-κB pathway, was strongly affected by RGS5. However, the p100 processing, a well-documented marker for noncanonical NF-κB pathway activation, was not altered, suggesting an existence of a novel mechanism by which RGS5 regulates CXCL12. CONCLUSIONS: We identified RGS5 as a novel susceptibility gene for CAD and showed that the decreased expression of RGS5 impaired endothelial cell function and functionally contributed to atherosclerosis through a variety of molecular mechanisms. How RGS5 regulates the expression of CXCL12 needs further studies. TRANSLATIONAL PERSPECTIVE: Current knowledge of the genetic contribution to CAD and mechanism underlying CAD associated loci identified in GWAS are both limited. Our study identifies a common variant rs1056515 as a genetic marker for CAD and rare variants in LD with rs1056515 leading to decreased expression of RGS5, which contributes to atherosclerosis by impairing endothelial cell function. Our study provides novel means for (i) Identification of patients at risk of CAD, (ii) Understanding the basis for disease pathogenesis, and (iii) development of new therapeutic strategies for the treatment of the disease.

10.
Med Image Anal ; 58: 101548, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31525671

RESUMO

It is essential to measure anatomical parameters in prenatal ultrasound images for the growth and development of the fetus, which is highly relied on obtaining a standard plane. However, the acquisition of a standard plane is, in turn, highly subjective and depends on the clinical experience of sonographers. In order to deal with this challenge, we propose a new multi-task learning framework using a faster regional convolutional neural network (MF R-CNN) architecture for standard plane detection and quality assessment. MF R-CNN can identify the critical anatomical structure of the fetal head and analyze whether the magnification of the ultrasound image is appropriate, and then performs quality assessment of ultrasound images based on clinical protocols. Specifically, the first five convolution blocks of the MF R-CNN learn the features shared within the input data, which can be associated with the detection and classification tasks, and then extend to the task-specific output streams. In training, in order to speed up the different convergence of different tasks, we devise a section train method based on transfer learning. In addition, our proposed method also uses prior clinical and statistical knowledge to reduce the false detection rate. By identifying the key anatomical structure and magnification of the ultrasound image, we score the ultrasonic plane of fetal head to judge whether it is a standard image or not. Experimental results on our own-collected dataset show that our method can accurately make a quality assessment of an ultrasound plane within half a second. Our method achieves promising performance compared with state-of-the-art methods, which can improve the examination effectiveness and alleviate the measurement error caused by improper ultrasound scanning.

11.
Cancer Gene Ther ; 2019 Sep 23.
Artigo em Inglês | MEDLINE | ID: mdl-31543512

RESUMO

The present study discusses the expression and effect of the SOX17 gene in endometrioid adenocarcinoma. MTT assay is performed to determine the growth inhibition ratio of the DNA methyltransferase inhibitor 5-AZA for endometrial carcinoma cells, and the real-time fluorescence quantification PCR (qRT-PCR) was used to detect the mRNA expression of SOX17, ß-catenin, and CyclinD1 in endometrial carcinoma tissues before and after using 5-AZA to treat the endometrial carcinoma cell line. There were 30 cases on endometrioid adenocarcinoma tissues and 10 cases on normal endometrial tissues. The results revealed that the expression of SOX17 in endometrioid adenocarcinoma tissues was downregulated (P < 0.05), the expression of ß-catenin and CyclinD1 was upregulated (P < 0.05), and the expression of SOX17, CyclinD1, and ß-catenin was negatively correlated (r = -0.353, P > 0.05; R = -0.463, P < 0.05). The higher the histological grade and FIGO staging were, the lower the expression level of SOX17 was (P < 0.05). After HEC1A cells were treated by 5-AZA, the cell growth inhibition was most obvious (IC50 = 12.033) at 72 h, as determined by MTT assay. After cell treatment by 5-AZA, the genetic expression of SOX17 significantly increased, when compared with that before treatment (P < 0.05), while the genetic expression of ß-catenin and CyclinD1 significantly declined (P < 0.05). These results indicate that the expression level of SOX17 in endometrioid adenocarcinoma declined, and the upregulated expression level of SOX17 in cells inhibited the growth of tumor cells.

14.
Cardiovasc Res ; 2019 Aug 28.
Artigo em Inglês | MEDLINE | ID: mdl-31504241

RESUMO

Aims Aberrant activation of cardiac fibroblasts leads to cardiac fibrosis, and evolving evidences suggest that endogenous bioactive substances derived from cardiac fibroblasts regulate cardiac fibroblasts activation in an autocrine/paracrine manner. Here we firstly presented evidence that cardiac fibroblasts can synthesize and secrete calcitonin gene-related peptide (CGRP), therefore, this study aimed to investigate the role of cardiac fibroblasts-derived CGRP in cardiac fibroblasts activation and its regulative mechanism. Methods and results The abundantly expression of CGRP in rat, mouse and human myocardium allowed us to explore the cellular origin of CGRP, and found that the cardiac CGRP was mainly derived from cardiac fibroblasts. Activating TRPA1 with a specific agonist AITC promoted the synthesis and secretion of CGRP, as well as intracellular Ca2+. These effects were reversed by TRPA1 specific antagonist HC030031 and Ca2+ chelator BAPTA-AM. TGF-ß1 was applied to induce the activation of cardiac fibroblasts, and found that TGF-ß1 can increase the mRNA expression and secretion levels of CGRP in cardiac fibroblasts. Either CGRP8-37 (CGRP receptor antagonist) or α-CGRP siRNA aggravated TGF-ß1-induced proliferation, differentiation, collagen production, and instigated inflammation in cardiac fibroblasts. Moreover, TGF-ß1-induced NF-κB activation including IκBα phosphorylation and p65 nuclear translocation were also promoted by CGRP8-37 and α-CGRP siRNA. NF-κB inhibitor PDTC reversed the effects of CGRP8-37 on NF-κB activation. The promotive effects of CGRP8-37 on TGF-ß1-induced activation of cardiac fibroblasts were all reversed by PDTC. Monocrotaline (MCT) induces pulmonary arterial hypertension, progressively leading to right ventricular fibrosis. This model of cardiac fibrosis was developed here to test the potentially beneficial effects of TRPA1 activation in vivo. The non-toxic TRPA1 agonist Cinnamaldehyde (CA) inhibited MCT-induced elevation in RVSP, RV/LV+S and right ventricular collagen accumulation, as well as down-regulation of CGRP. CA increased the synthesis and secretion of CGRP, and inhibited TGF-ß1-induced activation in cardiac fibroblasts. Conclusion Our data suggested an autocrine role for cardiac fibroblasts-derived CGRP in suppressing activation of cardiac fibroblasts through inhibiting NF-κB activation. Increasing autocrine CGRP by activating TRPA1 can ameliorate cardiac fibrosis. These findings support the notion that CGRP derived from cardiac fibroblasts is an endogenous suppressor of cardiac fibrosis.

15.
J Biol Chem ; 294(43): 15672-15685, 2019 Oct 25.
Artigo em Inglês | MEDLINE | ID: mdl-31462534

RESUMO

Macrophages play an essential role in skeletal muscle regeneration. The phagocytosis of muscle cell debris induces a switch of pro-inflammatory macrophages into an anti-inflammatory phenotype, but the cellular receptors mediating this phagocytosis are still unclear. In this paper, we report novel roles for SRB1 (scavenger receptor class BI) in regulating macrophage phagocytosis and macrophage phenotypic transitions for skeletal muscle regeneration. In a mouse model of cardiotoxin-induced muscle injury/regeneration, infiltrated macrophages expressed a high level of SRB1. Using SRB1 knockout mice, we observed the impairment of muscle regeneration along with decreased myogenin expression and increased matrix deposit. Bone marrow transplantation experiments indicated that SRB1 deficiency in bone marrow cells was responsible for impaired muscle regeneration. Compared with WT mice, SRB1 deficiency increased pro-inflammatory macrophage number and pro-inflammatory gene expression and decreased anti-inflammatory macrophage number and anti-inflammatory gene expression in injured muscle. In vitro, SRB1 deficiency led to a strong decrease in macrophage phagocytic activity on myoblast debris. SRB1-deficient macrophages easily acquired an M1 phenotype and failed to acquire an M2 phenotype in lipopolysaccharide/myoblast debris activation. Furthermore, SRB1 deficiency promoted activation of ERK1/2 MAPK signaling in macrophages stimulated with lipopolysaccharide/myoblast debris. Taken together, SRB1 in macrophages regulates phagocytosis and promotes M1 switch into M2 macrophages, contributing to muscle regeneration.

16.
Cardiovasc Toxicol ; 2019 Aug 06.
Artigo em Inglês | MEDLINE | ID: mdl-31385242

RESUMO

Normotensive patients with acute pulmonary embolism (APE) are accompanied by heterogeneously adverse events. Responding to tissue injury, lipocalin-2 (LCN-2) is elevated in experimental APE model and associated with short-term prognosis. However, the prognostic value of LCN-2 in normotensive patients with APE for long-term major adverse events (MAEs) remains unknown. We evaluated the association of plasma LCN-2 levels with the median 467-day outcome in 170 normotensive patients with APE. We also assessed whether LCN-2 could improve risk stratification. MAEs consisted of mortality or recurrence of venous thromboembolism. During follow-up, 17 (10%) patients suffered from MAEs. These patients had higher LCN-2 levels compared with patients without MAEs (median: 13.97 vs. 8.55 ng/ml, P = 0.01). The proportion of MAEs in the intermediate-low-risk group (14.0%) was higher than that in the intermediate-high-risk group (5.3%). LCN-2 levels independently had prognostic value for MAEs in overall (HR = 3.40, 95% CI 1.46-7.90) and intermediate-risk group (HR = 3.88, 95% CI 1.63-9.23). LCN-2 also showed incremental value in overall (ΔC-index: 0.13, 95% CI 0.02-0.24; category-based NRI = 0.25, 95% CI 0.07-0.42) and intermediate-risk patients (ΔC-index: 0.13, 95% CI 0.05-0.31; category-based NRI = 0.44, 95% CI 0.24-0.65). Adding LCN-2 (cut-off value = 11 ng/ml) to the current risk algorithm improved MAEs of intermediate-risk reclassification (intermediate-high vs. intermediate-low = 25.6% vs. 6.0%, P = 0.002). Elevated plasma LCN-2 levels predict long-term MAEs among normotensive patients with APE. LCN-2 might be a useful biomarker for risk stratification in the intermediate-risk group.

17.
Appl Radiat Isot ; 154: 108873, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31470193

RESUMO

To develop PET tracers for imaging of Alzheimer's disease, new carbon-11 labeled potent and selective PDE5 inhibitors have been synthesized. The reference standards (5) and (12), and their corresponding desmethylated precursors (6) and (13) were synthesized from methyl 2-amino-5-bromobenzoate and (4-methoxyphenyl)methanamine in multiple steps with 2%, 1%, 1% and 0.2% overall chemical yield, respectively. The radiotracers ([11C]5) and ([11C]12) were prepared from their corresponding precursors 6 and 13 with [11C]CH3OTf through O-11C-methylation and isolated by HPLC combined with SPE in 40-50% radiochemical yield, based on [11C]CO2 and decay corrected to EOB. The radiochemical purity was >99%, and the molar activity (Am) at EOB was in a range of 370-740 GBq/µmol.

18.
Am J Physiol Gastrointest Liver Physiol ; 317(4): G453-G462, 2019 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-31411504

RESUMO

Diets high in animal fats are associated with increased risks of inflammatory bowel disease, but the mechanism remains unclear. In this study, we investigated the effect of high-fat diet (HFD) on the development of experimental colitis in mice. Relative to mice fed low-fat diet (LFD), HFD feeding for 4 wk increased the levels of triglyceride, cholesterol, and free fatty acids in the plasma as well as within the colonic mucosa. In an experimental colitis model induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS), mice on 4-wk HFD exhibited more severe colonic inflammation and developed more severe colitis compared with the LFD counterparts. HFD feeding resulted in higher production of mucosal pro-inflammatory cytokines, greater activation of the myosin light chain kinase (MLCK) tight junction regulatory pathway, and greater increases in mucosal barrier permeability in mice following TNBS induction. HFD feeding also induced gp91, an NADPH oxidase subunit, and promoted reactive oxygen species (ROS) production in both colonic epithelial cells and lamina propria cells. In HCT116 cell culture, palmitic acid or palmitic acid and TNF-α combination markedly increased ROS production and induced the MLCK pathway, and these effects were markedly diminished in the presence of a ROS scavenger. Taken together, these data suggest that HFD promotes colitis by aggravating mucosal oxidative stress, which rapidly drives mucosal inflammation and increases intestinal mucosal barrier permeability.NEW & NOTEWORTHY This study demonstrates high-fat diet feeding promotes colitis in a 2,4,6-trinitrobenzenesulfonic acid-induced experimental colitis model in mice. The underlying mechanism is that high-fat diet induces oxidative stress in the colonic mucosa, which increases colonic epithelial barrier permeability and drives colonic mucosal inflammation. These observations provide molecular evidence that diets high in saturated fats are detrimental to patients with inflammatory bowel diseases.

19.
Sci Adv ; 5(8): eaav9801, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31457079

RESUMO

A parasite-infected host may promote performance of associated insect vectors; but possible parasite effects on nonvector insects have been largely unexplored. Here, we show that Begomovirus, the largest genus of plant viruses and transmitted exclusively by whitefly, reprogram plant immunity to promote the fitness of the vector and suppress performance of nonvector insects (i.e., cotton bollworm and aphid). Infected plants accumulated begomoviral ßC1 proteins in the phloem where they were bound to the plant transcription factor WRKY20. This viral hijacking of WRKY20 spatiotemporally redeployed plant chemical immunity within the leaf and had the asymmetrical benefiting effects on the begomoviruses and its whitefly vectors while negatively affecting two nonvector competitors. This type of interaction between a parasite and two types of herbivores, i.e., vectors and nonvectors, occurs widely in various natural and agricultural ecosystems; thus, our results have broad implications for the ecological significance of parasite-vector-host tripartite interactions.

20.
Nat Commun ; 10(1): 3184, 2019 07 18.
Artigo em Inglês | MEDLINE | ID: mdl-31320641

RESUMO

Thoracic aortic dissection (TAD) is an aggressive vascular disease that requires early diagnosis and effective treatment. However, due to the particular vascular structure and narrowness of lesion location, there are no effective drug delivery systems for the therapy of TAD. Here, we report a multifunctional delivery nanosystem (TP-Gd/miRNA-ColIV) composed of gadolinium-chelated tannic acid (TA), low-toxic cationic PGEA (ethanolamine-aminated poly(glycidyl methacrylate)) and type IV collagen targeted peptide (ColIV) for targeted nucleic acid therapy, early diagnosis and noninvasive monitoring of TAD. Such targeted therapy with miR-145 exhibits impressive performances in stabilizing the vascular structures and preventing the deterioration of TAD. After the treatment with TP-Gd/miR-145-ColIV, nearly no dissection occurs in the thoracic aortic arches of the mice with TAD model. Moreover, TP-Gd/miRNA-ColIV also demonstrates good magnetic resonance imaging (MRI) ability and can be used to noninvasively monitor the development conditions of TAD.

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