Publications by authors named "Nan Yang"

666 Publications

Feature Pyramid Non-local Network with Transform Modal Ensemble Learning For Breast Tumor Segmentation in Ultrasound Images.

IEEE Trans Ultrason Ferroelectr Freq Control 2021 Jul 19;PP. Epub 2021 Jul 19.

Automated breast ultrasound image segmentation is essential in a Computer-Aided Diagnosis (CAD) system for breast tumors. In this paper, we present a Feature Pyramid Non-local Network (FPNN) with Transform Modal Ensemble Learning (TMEL) for accurate breast tumor segmentation in ultrasound images. Specifically, the FPNN fuses multi-level features under special consideration of long-range dependencies by combining the non-local module and feature pyramid network. Additionally, the TMEL is introduced to guide two FPNNs to extract different tumor details. Two publicly available datasets, i.e., the Dataset-Cairo University and Dataset-Merge, were used for evaluation. The proposed FPNN-TMEL achieves a Dice score of 84.70%± 0.53%, Jaccard Index (Jac) of 78.10%± 0.48% and Hausdorff Distance (HD) of 2.815± 0.016 mm on the Dataset-Cairo University, and Dice of 87.00%±0.41%, Jac of 79.16% ±0.56% and HD of 2.781±0.035 mm on Dataset-Merge. Qualitative and quantitative experiments show that our method outperforms other state-of-the-art methods for breast tumor segmentation in ultrasound images. Our code is available at https://github.com/pixixiaonaogou/FPNNTMEL.
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http://dx.doi.org/10.1109/TUFFC.2021.3098308DOI Listing
July 2021

Colorectal cancer risk variant rs7017386 modulates two oncogenic lncRNAs expression via ATF1-mediated long-range chromatin loop.

Cancer Lett 2021 Jul 15;518:140-151. Epub 2021 Jul 15.

Department of Epidemiology and Biostatistics, And the Ministry of Education Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Electronic address:

The activating transcription factor 1 (ATF1) has been identified as a vital pathogenic factor in the progression of colorectal cancer (CRC), whiles, the precise regulatory mechanisms remain elusive. Here, we comprehensively characterized the ATF1 cistrome by RNA-seq and ChIP-seq assays in CRC cell lines. As the results, we identified 358 genes differentially regulated and 15,029 ATF1 binding sites and demonstrated that ATF1 was widely involved in major signaling pathways in CRC, such as Wnt, TNF, Jak-STAT. Subsequently, by the expression quantitative trait loci (eQTL) analyses, we found that rs7017386 was associated with the expression of CCAT1 and PVT1 in the Wnt pathway. By a two-stage population study with 6,131 CRC cases and 10,022 healthy controls, we identified the variant was associated with CRC risk. Mechanistically, we found rs7017386 allele-specifically enhanced the binding affinity of ATF1 and promoted the expressions of PVT1 and CCAT1, via forming a long-range chromatin loop. Moreover, those two lncRNAs could synergistically facilitate c-Myc expression to activate the Wnt pathway in CRC progression. Our findings not only demonstrated the transcriptomic profiling of ATF1 in CRC, but also provided important clues for the etiology of CRC.
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http://dx.doi.org/10.1016/j.canlet.2021.07.021DOI Listing
July 2021

Production of Margarines Rich in Unsaturated Fatty Acids Using Oxidative-stable Vitamin C-Loaded Oleogel.

J Oleo Sci 2021 Jul 9. Epub 2021 Jul 9.

College of Food Science and Technology, South China University of Technology.

Vitamin C (VC)-loaded oleogel (VCOG) with corn oil and monoglyceride stearate was used to replace lipid phase of margarine completely. The oxidative stability of VCOG was evaluated at 60±1°C in a lightproof oven for 18 days and the result showed that VCOG peroxide (> 6 days) and p-anisidine value (> 4 days) was significantly lower than that of bulk oil and VC-free oleogel (p < 0.05). Then, the margarine containing 79.70% VCOG (VCOGM) was in comparison with four commercial butter in sensory and physical characteristic. Results showed that firmness, solid fat content and trans fatty acid of VCOGM were in the lowest values while unsaturated fatty acid and adhesiveness of VCOGM was in the highest values. Furthermore, VCOGM presented the similar springiness, cohesiveness, gumminess, score appearance, texture, taste and overall impression to some/all commercial butters selected in this research (p > 0.05). These results implied that VC-loaded oleogel was an excellent alternative of lipid phase in margarine which confirmed by 55% "definitely buy" and 25% "try once-then decide".
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http://dx.doi.org/10.5650/jos.ess20264DOI Listing
July 2021

Development of a Clinically Relevant Reporter for Chimeric Antigen Receptor T-Cell Expansion, Trafficking, and Toxicity.

Cancer Immunol Res 2021 Jul 8. Epub 2021 Jul 8.

Hematology, Mayo Clinic

Although chimeric antigen receptor T (CART)-cell therapy has been successful in treating certain hematological malignancies, wider adoption of CART-cell therapy is limited due to minimal activity in solid tumors and development of life-threatening toxicities, including cytokine release syndrome (CRS). There is a lack of a robust, clinically relevant imaging platform to monitor in vivo expansion and trafficking to tumor sites. To address this, we utilized the sodium iodide symporter (NIS) as a platform to image and track CART-cells. We engineered CD19-directed and BCMA-directed CART-cells to express NIS (NIS+CART19 and NIS+BCMA-CART, respectively) and tested the sensitivity of 18F-TFB-PET to detect trafficking and expansion in systemic and localized tumor models and in a CART-cell toxicity model. NIS+CART19 and NIS+BCMA-CART-cells were generated through dual transduction with two vectors and demonstrated exclusive 125I uptake in vitro. 18F-TFB-PET detected NIS+CART-cells in vivo to a sensitivity level of 40,000 cells. 18F-TFB-PET confirmed NIS+BCMA-CART-cell trafficking to the tumor sites in localized and systemic tumor models. In a xenograft model for CART-cell toxicity, 18F-TFB-PET revealed significant systemic uptake, correlating with CART-cell in vivo expansion, cytokine production, and development of CRS-associated clinical symptoms. NIS provides a sensitive, clinically applicable platform for CART-cell imaging with PET scan.
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http://dx.doi.org/10.1158/2326-6066.CIR-20-0901DOI Listing
July 2021

Improvement of skin lesions in corticosteroid withdrawal-associated severe eczema by multicomponent traditional Chinese medicine therapy.

Allergy Asthma Clin Immunol 2021 Jul 9;17(1):68. Epub 2021 Jul 9.

Department of Microbiology and Immunology, Department of Otolaryngology, School of Medicine, New York Medicine College, 40 Sunshine Cottage Rd, Valhalla, NY, 10595, USA.

Rationale: We recently showed that multicomponent traditional Chinese medicine (TCM) therapy had steroid-sparing effects in moderate-to-severe eczema. We sought to evaluate TCM effects in severe eczema in a 7-year-old male with refractory disease and corticosteroid withdrawal syndrome.

Methods: Prior to referral, the patient had been treated since infancy with increasingly intensive standard of care, including high-dose topical and systemic corticosteroid and antibiotic therapy and was unable to tolerate further steroid treatment. The patient was administered a combination of oral and topical TCM for 17 months following discontinuation of his steroid regimen. His overall medical condition was assessed by SCORAD criteria and laboratory evaluations of serum IgE, absolute eosinophil count, and liver and kidney function tests.

Results: The patient showed rapid improvement of clinical measures of disease after starting TCM therapy, with marked improvement of sleep quality within the first week, complete resolution of itching, oozing, and erythema at 2 weeks, and a 79% and 99% decrease in his SCORAD values after one month and 3-6 months of TCM, respectively. Serum total IgE decreased by 75% (from 19,000 to 4630 (kIU/L), and absolute eosinophil counts decreased by 60% (from 1000 to 427 cells/μL) after 12 months of treatment. The patient did not require oral or topical steroids during the 17-month trial of TCM. TCM was tapered without complications. His dermatologic manifestations continued to be well-controlled 3 months after discontinuation.

Conclusion: This case study suggests TCM should be further evaluated in controlled clinical studies of patients with severe, refractory eczema and steroid withdrawal syndrome.
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http://dx.doi.org/10.1186/s13223-021-00555-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8268267PMC
July 2021

Novel Targeted Biological Agents for the Treatment of Atopic Dermatitis.

BioDrugs 2021 Jul 2;35(4):401-415. Epub 2021 Jul 2.

Department of Dermatology, Shanghai Skin Disease Hospital, School of Medicine, Tongji University, Shanghai, 200443, China.

Atopic dermatitis (AD) is a common inflammatory dermatologic disease clinically characterized by intense itch, recurrent eczematous lesions, and a chronic or relapsing disease course. Mild-to-moderate AD can be controlled by using moisturizers and topical immunomodulators such as topical corticosteroids and calcineurin inhibitors. If topical therapies fail, phototherapy and systemic immunosuppressant therapies, such as ciclosporin, methotrexate, and azathioprine, can be considered. However, relapse and side effects could still occur. The pathogenesis of AD involves epidermal barrier dysfunction, skin microbiome abnormalities, and cutaneous inflammation. Inflammatory mediators, such as interleukin (IL)-4, IL-13, IL-31, IL-33, IL-17, IL-23, and thymic stromal lymphopoietin, are involved in AD development. Therefore, a series of biological agents targeting these cytokines are promising approaches for treating AD. Dupilumab is the first biological agent approved for the treatment of AD in patients aged 6 years and older in the United States. Tralokinumab, lebrikizumab, and nemolizumab have also been confirmed to have significant efficacy against AD in phase III or IIb clinical trials. Also, fezakinumab was effective in severe AD patients in a phase IIa trial. However, phase II trials of ustekinumab, tezepelumab, etokimab, secukinumab, and omalizumab have failed to meet their primary endpoints. Phase II trials of GBR 830 and KHK 4083 are ongoing. In general, further studies are needed to explore new therapeutic targets and improve the efficacy of biological agents.
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http://dx.doi.org/10.1007/s40259-021-00490-xDOI Listing
July 2021

Efficient generation of dopaminergic induced neuronal cells with midbrain characteristics.

Stem Cell Reports 2021 Jul 24;16(7):1763-1776. Epub 2021 Jun 24.

Institute for Stem Cell Biology and Regenerative Medicine and Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address:

The differentiation of pluripotent stem cells can be accomplished by sequential activation of signaling pathways or through transcription factor programming. Multistep differentiation imitates embryonic development to obtain authentic cell types, but it suffers from asynchronous differentiation with variable efficiency. Transcription factor programming induces synchronous and efficient differentiation with higher reproducibility but may not always yield authentic cell types. We systematically explored the generation of dopaminergic induced neuronal cells from mouse and human pluripotent stem cells. We found that the proneural factor Ascl1 in combination with mesencephalic factors Lmx1a and Nurr1 induce peripheral dopaminergic neurons. Co-delivery of additional midbrain transcription factors En1, FoxA2, and Pitx3 resulted in facile and robust generation of functional dopaminergic neurons of midbrain character. Our results suggest that more complex combinations of transcription factors may be needed for proper regional specification of induced neuronal cells generated by direct lineage induction.
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http://dx.doi.org/10.1016/j.stemcr.2021.05.017DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8282497PMC
July 2021

A Domain-Guided Noise-Optimization-Based Inversion Method for Facial Image Manipulation.

IEEE Trans Image Process 2021 9;30:6198-6211. Epub 2021 Jul 9.

A style-based architecture (StyleGAN2) yields outstanding results in data-driven unconditional generative image modeling. This work proposes a Domain-guided Noise-optimization-based Inversion (DNI) method to perform facial image manipulation. It works based on an inverse code that includes: 1) a novel domain-guided encoder called Image2latent to project the image to StyleGAN2 latent space, which can reconstruct an input image with high-quality and maintain its semantic meaning well; 2) a noise optimization mechanism in which a set of noise vectors are used to capture the high-frequency details such as image edges, further improving image reconstruction quality; and 3) a mask for seamless image fusion and local style migration. We further propose a novel semantic alignment evaluation pipeline. It evaluates the semantic alignment with an inverse code by using different attribute boundaries. Extensive qualitative and quantitative comparisons show that DNI can capture rich semantic information and achieve a satisfactory image reconstruction. It can realize a variety of facial image manipulation tasks and outperform state of the art.
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http://dx.doi.org/10.1109/TIP.2021.3089905DOI Listing
July 2021

M1 macrophage-derived exosomes impair beta cell insulin secretion via miR-212-5p by targeting SIRT2 and inhibiting Akt/GSK-3β/β-catenin pathway in mice.

Diabetologia 2021 Jun 11. Epub 2021 Jun 11.

Key Laboratory of Human Functional Genomics of Jiangsu Province, Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, China.

Aims/hypothesis: Macrophage levels are elevated in pancreatic islets, and the resulting inflammatory response is a major contributor to beta cell failure during obesity and type 2 diabetes mellitus. Previous studies by us and others have reported that exosomes released by macrophages play important roles in mediating cell-to-cell communication, and represent a class of inflammatory factors involved in the inflammatory process associated with type 2 diabetes mellitus. However, to date, no reports have demonstrated the effect of macrophage-derived exosomes on beta cells, and little is known regarding their underlying mechanisms in beta cell injury. Thus, we aimed to study the impact of macrophage-derived exosomes on islet beta cell injury in vitro and in vivo.

Methods: The phenotypic profiles of islet-resident macrophages were analysed in C57BL/6J mice fed a high-fat diet (HFD). Exosomes were collected from the medium of cultured bone marrow-derived macrophages (BMDMs) and from isolated islet-resident macrophages of HFD-fed mice (HFD-Exos). The role of exosomes secreted by inflammatory M1 phenotype BMDMs (M1-Exos) and HFD-Exos on beta cell function was assessed. An miRNA microarray and quantitative real-time PCR (qPCR) were conducted to test the level of M1-Exos-derived miR-212-5p in beta cells. Then, miR-212-5p was overexpressed or inhibited in M1-Exos or beta cells to determine its molecular and functional impact.

Results: M1-polarised macrophages were enriched in the islets of obese mice. M1 macrophages and islet-resident macrophages of HFD-fed mice impaired beta cell insulin secretion in an exosome-dependent manner. miR-212-5p was notably upregulated in M1-Exos and HFD-Exos. Enhancing the expression of miR-212-5p impaired beta cell insulin secretion. Blocking miR-212-5p elicited a significant improvement in M1-Exos-mediated beta cell insulin secretion during injury. Mechanistically, M1-Exos mediated an intercellular transfer of the miR-212-5p, targeting the sirtuin 2 gene and regulating the Akt/GSK-3β/β-catenin pathway in recipient beta cells to restrict insulin secretion.

Conclusions/interpretation: A novel exosome-modulated mechanism was delineated for macrophage-beta cell crosstalk that drove beta cell dysfunction and should be explored for its therapeutic utility.
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http://dx.doi.org/10.1007/s00125-021-05489-1DOI Listing
June 2021

Collagen VI as a driver and disease biomarker in human fibrosis.

FEBS J 2021 Jun 9. Epub 2021 Jun 9.

Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics Rheumatology and Musculoskeletal Science, University of Oxford, UK.

Fibrosis of visceral organs such as the lungs, heart, kidneys and liver remains a major cause of morbidity and mortality and is also associated with many other disorders, including cancer and metabolic disease. In this review, we focus upon the microfibrillar collagen VI, which is present in the extracellular matrix (ECM) of most tissues. However, expression is elevated in numerous fibrotic conditions, such as idiopathic pulmonary disease (IPF), and chronic liver and kidney diseases. Collagen VI is composed of three subunits α1, α2 and α3, which can be replaced with alternate chains of α4, α5 or α6. The C-terminal globular domain (C5) of collagen VI α3 can be proteolytically cleaved to form a biologically active fragment termed endotrophin, which has been shown to actively drive fibrosis, inflammation and insulin resistance. Tissue biopsies have long been considered the gold standard for diagnosis and monitoring of progression of fibrotic disease. The identification of neoantigens from enzymatically processed collagen chains have revolutionised the biomarker field, allowing rapid diagnosis and evaluation of prognosis of numerous fibrotic conditions, as well as providing valuable clinical trial endpoint determinants. Collagen VI chain fragments such as endotrophin (PRO-C6), C6M and C6Mα3 are emerging as important biomarkers for fibrotic conditions.
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http://dx.doi.org/10.1111/febs.16039DOI Listing
June 2021

LncRNA HAS2-AS1 Promotes Glioblastoma Proliferation by Sponging miR-137.

Front Oncol 2021 20;11:634893. Epub 2021 May 20.

Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, China.

GBM (Glioblastoma multiform) is the most malignant tumor type of the central nervous system and has poor diagnostic and clinical outcomes. LncRNAs (Long non-coding RNAs) have been reported to participate in multiple biological and pathological processes, but their underlying mechanism remains poorly understood. Here, we aimed to explore the role of the lncRNA HAS2-AS1 (HAS2 antisense RNA 1) in GBM. GSE103227 was analyzed, and qRT-PCR was performed to measure the expression of HAS2-AS1 in GBM. FISH (Fluorescence hybridization) was performed to verify the localization of HAS2-AS1. The interaction between HAS2-AS1 and miR-137 (microRNA-137) was predicted by LncBook and miRcode followed by dual-luciferase reporter assays, and the relationships among HAS2-AS1, miR-137 and LSD1 (lysine-specific demethylase 1) were assessed by WB (western blot) and qRT-PCR. Colony formation and CCK-8 (cell counting kit-8) assays were performed as functional tests. In vivo, nude mice were used to confirm the function of HAS2-AS1. HAS2-AS1 expression was upregulated in GBM cell lines, and HAS2-AS1 was localized mainly in the cytoplasm. , high HAS2-AS1 expression promoted proliferation, and knockdown of HAS2-AS1 significantly inhibited proliferation. Furthermore, HAS2-AS1 functioned as a ceRNA (competing endogenous RNA) of miR-137, leading to the disinhibition of its downstream target LSD1. The miR-137 level was downregulated by HAS2-AS1 overexpression and upregulated by HAS2-AS1 knockdown. In a subsequent study, LSD1 expression was negatively regulated by miR-137, while miR-137 reversed the LSD1 expression levels caused by HAS2-AS1. These results were further supported by the nude mouse tumorigenesis experiment; compared with xenografts with high HAS2-AS1 expression, the group with low levels of HAS2-AS1 exhibited suppressed proliferation and better survival. We conclude that lncRNA HAS2-AS1 promotes proliferation by functioning as a miR-137 decoy to increase LSD1 levels and thus might be a possible biomarker for GBM.
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http://dx.doi.org/10.3389/fonc.2021.634893DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8173206PMC
May 2021

A putative PKA phosphorylation site S227 in MoSom1 is essential for infection-related morphogenesis and pathogenicity in Magnaporthe oryzae.

Cell Microbiol 2021 Jun 5:e13370. Epub 2021 Jun 5.

State Key Laboratory of Rice Biology & Ministry of Agriculture Key Lab of Molecular Biology of Crop Pathogens and Insects, Institute of Biotechnology, Zhejiang University, Hangzhou, China.

In the rice blast fungus Magnaporthe oryzae, the cAMP signalling pathway plays a critical role in regulating leaf surface recognition and the initiation of appressorium development. Direct downstream targets of the cAMP signalling pathway are, however, not well-characterised. The MoSom1 protein functions downstream of the cAMP dependent protein kinase A (cAMP-PKA) and is essential for infection-related morphogenesis and pathogenicity. In this study, we show that mutation of a putative PKA phosphorylation site in MoSom1 is essential for its role in appressorium differentiation and pathogenicity in M. oryzae. Mutation of serine 227 in MoSom1 by deletion or serine (S) substitution to alanine (A), valine (V) or tyrosine (Y), resulted in defects of conidiation, appressorium-like structure formation and fungal pathogenicity. Western blot analysis confirmed that S227 in MoSom1 is a putative PKA phosphorylation site. Furthermore, a ΔMosom1 mutant showed reduced expression of PMK1 and was defective in Pmk1 phosphorylation, indicating that the Pmk1 mitogen-activated protein kinase (MAPK) acts downstream of MoSom1 in M. oryzae. We conclude that the cAMP-PKA pathway may regulate the Pmk1 MAPK pathway through MoSom1 during rice infection by the blast fungus. TAKE AWAYS: S227 is crucial for MoSom1 function in M. oryzae. S227 in MoSom1 was identified as a putative PKA phosphorylation site in M. oryzae. S227 is essential for infection-related morphogenesis and pathogenicity in M. oryzae.
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http://dx.doi.org/10.1111/cmi.13370DOI Listing
June 2021

Comparison of a new predictive model with other critical scores for predicting in-hospital mortality among children with pneumonia-related bacteremia.

J Investig Med 2021 Jun 3. Epub 2021 Jun 3.

Department of Respiratory Disease, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders. Chongqing Key Laboratory of Pediatrics, Chongqing, China

Prediction of mortality in children with pneumonia-related bacteremia is necessary for providing timely care and treatment. This study aims to develop and validate a nomogram and compare it with Pediatric Risk of Mortality III (PRISM III), Brighton Pediatric Early Warning Score (Brighton PEWS) and Pediatric Critical Illness Score (PCIS), which are widely used in predicting in-hospital mortality in children with pneumonia-related bacteremia. This retrospective study collected clinical data of hospitalized children with pneumonia-related bacteremia in Chongqing, China (January 2013-May 2019). The nomogram was built using multivariate logistic regression analysis. The nomogram was compared with PRISM III, PEWS and PCIS in accuracy and clinical benefits in predicting in-hospital mortality in children with pneumonia-related bacteremia. A total of 242 children were included. The nomogram including time to first positivity of blood cultures (TTFP), serum albumin (ALB) and lactate dehydrogenase (LDH) was established. The area under the receiver operating characteristic curve of the nomogram was 0.84 (95% CI 0.77 to 0.91) in the training set and 0.82 (95% CI 0.71 to 0.93) in the validating set. Good consistency was observed between the predictions and the actual observations, and the decision curve analysis showed that the nomogram was clinically useful. The results showed that the nomogram significantly performed better than the three critical scores. In conclusion, a nomogram-illustrated model incorporating TTFP, ALB and LDH for predicting in-hospital mortality in children with pneumonia-related bacteremia at the early stage was established and validated. It performed better than PRISM III, PEWS and PCIS.
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http://dx.doi.org/10.1136/jim-2020-001688DOI Listing
June 2021

Infection microenvironment-activated nanoparticles for NIR-II photoacoustic imaging-guided photothermal/chemodynamic synergistic anti-infective therapy.

Biomaterials 2021 May 25;275:120918. Epub 2021 May 25.

Key Laboratory of Flexible Electronics (KLOFE) and Institute of Advanced Materials (IAM), School of Physical and Mathematical Sciences, Nanjing Tech University (NanjingTech), Nanjing, 211800, China. Electronic address:

Subcutaneous abscesses caused by drug-resistant bacteria pose huge challenges to human health. The design of infection microenvironment-activated biomaterials has an advantage for the diagnosis and treatment of infective diseases due to its high specificity and efficiency. Herein, a novel theranostic platform based on CuO nanoparticles (NPs) is successfully constructed via a simple, fast and low-cost approach. The CuO NPs exhibit high sensitivity to overexpressed HS and HO in the bacterial infection microenvironment. After in situ injection, the CuO NPs will rapidly react with the endogenous HS to generate CuS NPs, which exhibits high absorbance in the second near-infrared (NIR-II) biowindow. The CuS NPs serving as NIR-II photoacoustic contrast agents can exactly distinguish between inflammatory and normal tissues. With the guidance of NIR-II photoacoustic imaging (PAI), HS-activated photothermal antibacterial therapy (PTAT) can realize excellent antibacterial performance under 1060 nm laser irradiation. Meanwhile, the CuO NPs can effectively catalyze HO at the site of inflammation to produce hydroxyl radicals with strong antibacterial property via Fenton-like reaction, resulting in the damage of bacterial cell membrane. Furthermore, the application of CuO NPs can enhance epidermic migration and facilitate the re-epithelialization of the infected skin. In vivo experiment shows that 97.9% methicillin-resistant Staphylococcus aureus are eliminated by the synergistic PTAT and chemodynamic antibacterial therapy.
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http://dx.doi.org/10.1016/j.biomaterials.2021.120918DOI Listing
May 2021

miR-451 suppresses EMT and metastasis in glioma cells.

Cell Cycle 2021 May 28:1-9. Epub 2021 May 28.

Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, China.

The metastasis of tumor cells is a challenge for the clinical treatment of glioma. Epithelial-mesenchymal transition (EMT) contributes to glioma cell invasiveness. Our previous study confirmed that the expression of miRNA-451, which inhibits the PI3K/Akt signaling pathway by directly targeting CAB39 and plays a repressive role in glioma, is downregulated in glioma. However, the specific mechanism of miRNA-451 regulation in glioma is unclear. In this study, we investigated whether miRNA-451 blocks the processes of EMT and metastasis in glioma cells in vivo and in vitro. By targeting CAB39, miRNA-451 likely triggers the PI3K/Akt/Snail signaling pathway to reduce glioma proliferation, invasion, migration and EMT. We used Western blotting experiments to demonstrate that overexpression of miRNA-451 significantly reduced p-AKT(Ser473), N-cadherin, Vimentin, Twist, Snail and Cyclin D1 expression and increased E-cadherin expression. We demonstrated that overexpression of miR-451 suppressed glioma cell proliferation, invasion, migration and EMT by MTT and colony formation assays, Transwell assays, wound healing assays and animal experiments. Taken together, these results suggest that miRNA-451 can reduce EMT and metastasis in glioma cells through the suppression of the PI3K/Akt/Snail signaling pathway by targeting CAB39 in vitro and in vivo. miR-451 may be a new target for glioma treatment.
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http://dx.doi.org/10.1080/15384101.2021.1933303DOI Listing
May 2021

MiR-21-5p in Macrophage-Derived Exosomes Targets Smad7 to Promote Epithelial Mesenchymal Transition of Airway Epithelial Cells.

J Asthma Allergy 2021 18;14:513-524. Epub 2021 May 18.

Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning, 110004, People's Republic of China.

Background: Asthma is usually associated with airway inflammation and airway remodeling. Epithelial mesenchymal transition (EMT) often occurs in airway remodeling. The purpose of this study is to identify the effect of miR-21-5p and Smad7 signaling pathway in macrophage-derived exosomes on EMT of airway epithelial cells.

Methods: HE staining and Masson staining were used to verify the successful establishment of the asthma model. The levels of epithelial cell adhesion factor and stromal cell markers were detected by Western blot. The levels of miR-21-5p were detected by qRT-PCR. The expression of miR-21-5p in lung tissue was further verified by fluorescence in situ hybridization (FISH). Exosome morphology was observed by transmission electron microscopy (TEM) and nanoparticle tracking analysis (NTA). Luciferase reporter assay was applied to analyze the interaction of miR-21-5p with Smad7.

Results: The expression of miR-21-5p was upregulated in macrophages of rats in vivo with OVA-induced asthma. In vitro cultured alveolar macrophages stimulated by LPS could secrete exosomes with high levels of miR-21-5p. The exosome-derived miR-21-5p promotes EMT in rat tracheal epithelial cells through TGFβ1/Smad signaling pathway by downregulating Smad7. This process can be blocked by miR-21-5p inhibitor.

Conclusion: Rat alveolar macrophages produced high levels of miR-21-5p-containing exosomes, which transported miR-21-5p to tracheal epithelial cells, thus promoting EMT through TGF-β1/Smad signaling pathway by targeting Smad7.
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http://dx.doi.org/10.2147/JAA.S307165DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8140948PMC
May 2021

AMOTL2‑knockdown promotes the proliferation, migration and invasion of glioma by regulating β‑catenin nuclear localization.

Oncol Rep 2021 07 26;46(1). Epub 2021 May 26.

Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.

Glioblastoma multiforme (GBM) is the most prevalent type of malignant cancer in the adult central nervous system; however, its mechanism remains unclear. Angiomotin‑like 2 (AMOTL2) is a member of the motin family of angiostatin‑binding proteins. It has been reported as an oncogene in cervical and breast cancer, but its association with glioma remains unknown. The aim of the present study was to investigate AMOTL2‑regulated processes in glioma cell lines using extensive assays and certain bioinformatics tools. These results revealed that AMOTL2 was downregulated in high‑grade glioma cells and tissues, with patients with glioma exhibiting a high AMOTL2 expression having a higher survival rate. The results of the glioma cell phenotype experiment showed that AMOTL2 suppressed GBM proliferation, migration and invasion. In addition, immunoblotting, co‑immunoprecipitation and immunofluorescence assays demonstrated that AMOTL2 could directly bind to β‑catenin protein, the key molecule of the Wnt signaling pathway, and regulate its downstream genes by regulating β‑catenin nuclear translocation. In conclusion, the present study demonstrated that AMOTL2 inhibited glioma proliferation, migration and invasion by regulating β‑catenin nuclear localization. Thus, AMOTL2 may serve as a therapeutic target to further improve the prognosis and prolong survival time of patients with glioma.
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http://dx.doi.org/10.3892/or.2021.8090DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8165599PMC
July 2021

Cysteine inducing formation and reshuffling of disulfide bonds in cold-extruded whey protein molecules: From structural and functional characteristics to cytotoxicity.

Food Chem 2021 Oct 15;360:130121. Epub 2021 May 15.

Key Laboratory of Dairy Science (Northeast Agricultural University), Ministry of Education, College of Food Science and Technology, Harbin, Heilongjiang Province 150030, PR China. Electronic address:

Polymer chemistry, rheology and cytotoxicity of cysteine initiated S-S redistribution in cold-extruded whey protein (TWPI) molecules were investigated. The locations of disulfide bonds in whey protein isolate (WPI), WPI dried without being extruded (OWPI) and cold-extruded WPI (TWPI), Cysteine (Cys)-treated WPI (WPI-Cys), OWPI (OWPI-Cys) and TWPI (TWPI-Cys) were precisely analyzed using liquid chromatography electrospray ionization tandem mass spectrometry (LC/MS/MS) combined with pLink software approaches. The numbers of intermolecular disulfide cross-linked peptides identified in Cys-treated samples increased by 4, 6 and 1, respectively, in the order of TWPI-Cys, OWPI-Cys and WPI-Cys. Fourier Transform infrared spectroscopy (FTIR) showed cysteine treatment loosed secondary structure of protein samples. Meanwhile, size exclusion chromatography (SEC) assay demonstrated the extensive polymerization in TWPI-Cys. Furthermore, Cys-treatment decreased the gelling temperature of TWPI to 57 °C sharply. Cys-treated TWPI has 19.11 times storage modulus (G') and 25.86 times loss modulus (G") of Cys-untreated TWPI at 85 °C. Additionally, cell viability with Cys addition indicate modified whey proteins are not toxic to human umbilical vein endothelial cells (HUVECs).
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http://dx.doi.org/10.1016/j.foodchem.2021.130121DOI Listing
October 2021

Current Status and Trends in Peptide Receptor Radionuclide Therapy in the Past 20 Years (2000-2019): A Bibliometric Study.

Front Pharmacol 2021 27;12:624534. Epub 2021 Apr 27.

Department of Pharmacy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

Peptide receptor radionuclide therapy (PRRT) is an emerging therapeutic option for the treatment of neuroendocrine tumors (NETs), and the number of publications in this field has been increasing in recent years. The aim of the present study was to present the research status and summarize the key topics through bibliometric analysis of published PRRT literature. A literature search for PRRT research from 2000 to 2019 was conducted using the Science Citation Index Expanded of Web of Science Core Collection (limited to SCIE) on August 4, 2020. The VOSviewer, R-bibliometrix, and CiteSpace software were used to conduct the bibliometric analysis. From 2000 to 2019, a total of 681 publications (523 articles and 158 reviews) were retrieved. Annual publication outputs grew from three to 111 records. Germany had the largest number of publications, making the largest contribution to the field ( = 151, 22.17%). Active cooperation between countries/regions was observed. Kwekkeboom from the Erasmus Medical Center is perhaps a key researcher in the field of PRRT. The and ranked first for productive ( = 84, 12.33%) and co-cited ( = 3,438) journals, respectively. Important topics mainly included matters related to the efficacy of PRRT (e.g., Y-dotatoc and Lu-dotatate), the long-term adverse effects of PRRT (e.g., hematologic and renal toxicities), standardization of NETs and PRRT in practice, the development of medical imaging techniques, and the individual dose optimization of PRRT. Using bibliometric analysis, we gained deep insight into the global status and trends of studies investigating PRRT for the first time. The PRRT field is undergoing a period of rapid development, and our study provides a valuable reference for clinical researchers and practitioners.
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http://dx.doi.org/10.3389/fphar.2021.624534DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8111084PMC
April 2021

Porcine circovirus type 2 infection attenuates the K63-linked ubiquitination of STING to inhibit IFN-β induction via p38-MAPK pathway.

Vet Microbiol 2021 Jul 4;258:109098. Epub 2021 May 4.

College of Veterinary Medicine, Northwest A&F University, Yangling, 712100, China. Electronic address:

Porcine circovirus 2 (PCV2) has been proved to increase the risk of other pathogens infection via immunosuppression. Although the co-infection of PCV2 and porcine parvovirus (PPV) is commonly observed in worldwide, the relative immune mechanisms promoting PPV infection in PCV2-infected piglets are currently unknown. Herein, we found that PCV2 infection suppressed IFN-β expression and promoted PPV infection in the piglets. Consistent with this finding, we confirmed that PCV2 infection significantly inhibited the induction of IFN-β to promote PPV replication in cell level. Furthermore, PCV2 infection attenuated the K63-linked ubiquitination of STING induced by PPV, blocked the formation of complex of STING, TBK1 and IRF3, and further prevented the phosphorylation of TBK1 and IRF3, resulting in a decreased IFN-β transcription response to PPV infection. Consistently, using cGAMP to direct stimulate STING also appeared a reduced STING-K63 ubiquitination and IFN-β induction in PCV2-infected cells. However, we noted that knockdown of p38-MAPK signaling could markedly attenuate the inhibitory effect of PCV2 on STING-K63 ubiquitination, and improve the induction of IFN-β in PCV2-infected whenever theses cells were challenged with PPV infection or cGAMP stimulation. Meanwhile, we found that PCV2 infection promoted the phosphorylation of USP21 to inhibit the K63 ubiquitination of STING and the transcription of IFN-β via activation of p38-MAPK signaling. Taken together, our results demonstrate that PCV2 infection activates the p38-MAPK signaling pathway-mediated USP21 phosphorylation to inhibit the K63 ubiquitination of STING, which prevents the phosphorylation and transportation to the nucleus of IRF3, leading to an increase risk for PPV infection.
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http://dx.doi.org/10.1016/j.vetmic.2021.109098DOI Listing
July 2021

Lesion synthesis to improve intracranial hemorrhage detection and classification for CT images.

Comput Med Imaging Graph 2021 Jun 6;90:101929. Epub 2021 May 6.

Ping An Technology (Shenzhen) Co., Ltd., Shanghai 200000, China. Electronic address:

Computer-aided diagnosis (CAD) for intracranial hemorrhage (ICH) is needed due to its high mortality rate and time sensitivity. Training a stable and robust deep learning-based model usually requires enough training examples, which may be impractical in many real-world scenarios. Lesion synthesis offers a possible solution to solve this problem, especially for the issue of the lack of micro bleedings. In this paper, we propose a novel strategy to generate artificial lesions on non-lesion CT images so as to produce additional labeled training examples. Artificial masks in any location, size, or shape can be generated through Artificial Mask Generator (AMG) and then be converted into hemorrhage lesions through Lesion Synthesis Network (LSN). Images with and without artificial lesions are combined for training an ICH detection with a novel Residual Score. We evaluate our method by the auxiliary diagnosis task of ICH. Our experiments demonstrate that the proposed approach can improve the AUC value from 84% to 91% in the ICH detection task and from 89% to 96% in the classification task. Moreover, by adding artificial lesions of small size, the sensitivity of micro bleeding is remarkably improved from 49% to 70%. Besides, the proposed method overcomes the other three synthetic approaches by a large margin.
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http://dx.doi.org/10.1016/j.compmedimag.2021.101929DOI Listing
June 2021

A genetic variant conferred high expression of CAV2 promotes pancreatic cancer progression and associates with poor prognosis.

Eur J Cancer 2021 Jul 8;151:94-105. Epub 2021 May 8.

Department of Epidemiology and Biostatistics, Key Laboratory for Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Sciences and Technology, Wuhan, China. Electronic address:

Aim: This study aimed to identify the functional genes and genetic variants associated with the prognosis of pancreatic ductal adenocarcinoma (PDAC) and reveal the mechanism underlying their prognostic roles.

Methods: First, we implement a two-stage exome-wide association study in a total of 1070 patients to identify the genetic variant correlated with PDAC prognosis. Then we performed fine mapping through bioinformatics analysis and dual-luciferase reporter assays to reveal the causal functional variant and prognostic gene. Next, we established the gene knockdown, knockout, and overexpression cell lines with small interfering RNA, CRISPR/Cas9, and lentivirus, respectively, and investigated the gene function on cell proliferation and migration in vivo and in vitro. Finally, we performed the RNA-seq to elucidate downstream genes and mechanisms altering PDAC prognosis.

Results: We identified the CAV1-CAV2 locus tagged by rs8940 was significantly associated with PDAC prognosis, and rs10249656 in the 3'untranslated region of CAV2 was the real functional variant, which upregulated CAV2 expression through abolishing miR-548s binding. We observed upregulated CAV2 in PDAC and the higher expression correlated with worse prognosis. Transient knockdown of CAV2 inhibited PDAC migration without affecting proliferation rate. Knockout of CAV2 suppressed PDAC progression and metastasis, whereas stable overexpression of CAV2 promoted. Overexpressed CAV2 promoted the PDAC progression and metastasis via perturbing genes in the focal adhesion (CCND1, IGTA1, and ZYX) and extracellular matrix organisation (PLOD2, CAST, and ITGA1) pathways mechanically.

Conclusion: These findings shed light on an important role of CAV2 on PDAC progression and the prognostic impact of its genetic variation.
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http://dx.doi.org/10.1016/j.ejca.2021.04.008DOI Listing
July 2021

Recent advances in Extracellular Vesicles and their involvements in vasculitis.

Free Radic Biol Med 2021 08 2;171:203-218. Epub 2021 May 2.

Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA; Corporal Michael J. Crescenz VA Medical Center (Philadelphia), Philadelphia, PA, 19104, USA. Electronic address:

Systemic vasculitis is a heterogeneous group of multisystem autoimmune disorders characterized by inflammation of blood vessels. Although many progresses in diagnosis and immunotherapies have been achieved over the past decades, there are still many unanswered questions about vasculitis from pathological understanding to more advanced therapies. Extracellular vesicles (EVs) are double-layer phospholipid membrane vesicles harboring various cargoes. EVs can be classified into exosomes, microvesicles (MVs), and apoptotic bodies depending on their size and origin of cellular compartment. EVs can be released by almost all cell types and may be involved in physical and pathological processes including inflammation and autoimmune responses. In systemic vasculitis, EVs may have pathogenic involvement in inflammation, autoimmune responses, thrombosis, endothelium injury, angiogenesis and intimal hyperplasia. EV-associated redox reaction may also be involved in vasculitis pathogenesis by inducing inflammation, endothelial injury and thrombosis. Additionally, EVs may serve as specific biomarkers for diagnosis or monitoring of disease activity and therapeutic efficacy, i.e. AAV-associated renal involvement. In this review, we have discussed the recent advances of EVs, especially their roles in pathogenesis and clinical involvements in vasculitis.
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http://dx.doi.org/10.1016/j.freeradbiomed.2021.04.033DOI Listing
August 2021

Cirsilineol attenuates LPS-induced inflammation in both in vivo and in vitro models via inhibiting TLR-4/NF kB/IKK signaling pathway.

J Biochem Mol Toxicol 2021 May 5:e22799. Epub 2021 May 5.

Department of Emergency, Dongzhimen Hospital, Beijing University of Traditional Chinese Medicine, Beijing, China.

The anti-inflammatory activity of cirsilineol in in vivo condition was assessed by measuring the relative organ weight, lung dry/wet weight ratio, protein concentration, and infiltration of inflammatory cells in bronchoalveolar lavage fluid. We estimated the myeloperoxidase activity and levels of cytokines, chemokines, and inflammatory markers to analyze the efficacy of cirsilineol against lipopolysaccharide (LPS)-induced lung inflammation. Furthermore, we quantified the gene expression of NF kB/IKK signaling molecules in cirsilineol-treated and untreated acute lung injury mice to confirm the anti-inflammatory property of cirsilineol. The lung histology was assessed with hematoxylin and eosin staining. Apart from in vivo experiments, in vitro tests with LPS-stimulated RAW 264.7 macrophages were also performed. Cell viability assay was performed in the presence and absence of LPS in RAW 264.7 macrophages to determine the cytotoxic effect of cirsilineol against macrophages. Reverse-transcription polymerase chain reaction (RT-PCR) analysis was done to analyze the gene expression of inflammatory markers in LPS-treated RAW 264.7 macrophages to prove that cirsilineol effectively inhibits inflammation in vitro. The results of our study prove that cirsilineol effectively inhibits inflammation in both in vivo and in vitro conditions. RT-PCR analysis results of NF kB/IKK signaling molecules clearly illustrate that cirsilineol inhibited the expression of NF kB/IKK signaling protein and thereby prevented inflammation in in vivo condition, and it is further confirmed with the results of inflammatory protein expression in vitro model. The lung histopathological studies authentically confirm that cirsilineol potentially prevented the mice from LPS-induced lung inflammation.
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http://dx.doi.org/10.1002/jbt.22799DOI Listing
May 2021

RAB1A regulates glioma cellular proliferation and invasion via the mTOR signaling pathway and epithelial-mesenchymal transition.

Future Oncol 2021 Aug 5;17(24):3203-3216. Epub 2021 May 5.

Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.

We aimed at investigating the mechanism of RAB1A proliferation and invasion in gliomas. Genome-wide expression profile data and immunohistochemistry were analyzed to assess expression in gliomas. The Transwell assay, wound healing assay, brain slice coculture model, cellular fluorescence and intracranial xenograft model of nude mice were used to determine the proliferation and invasion of glioma cells. was highly expressed in gliomas compared with normal brain tissue. The overall survival time of glioma patients with high expression was significantly shortened. RAB1A regulated the activity of RAC1 by inhibiting the mTOR signaling pathway, affecting actin polymerization, cell morphology and cell polarity. downregulation inhibited the epithelial-mesenchymal transition, proliferation and invasion of glioma cells.
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http://dx.doi.org/10.2217/fon-2021-0116DOI Listing
August 2021

Dietary nutrition for neurological disease therapy: Current status and future directions.

Pharmacol Ther 2021 Oct 23;226:107861. Epub 2021 Apr 23.

Institute of Cancer Neuroscience, Medical Frontier Innovation Research Center, The First Hospital of Lanzhou University, The First Clinical Medical College of Lanzhou University, Lanzhou 730000, PR China. Electronic address:

Adequate food intake and relative abundance of dietary nutrients have undisputed effects on the brain function. There is now substantial evidence that dietary nutrition aids in the prevention and remediation of neurologic symptoms in diverse pathological conditions. The newly described influences of dietary factors on the alterations of mitochondrial dysfunction, epigenetic modification and neuroinflammation are important mechanisms that are responsible for the action of nutrients on the brain health. In this review, we discuss the state of evidence supporting that distinct dietary interventions including dietary supplement and dietary restriction have the ability to tackle neurological disorders using Alzheimer's disease, Parkinson's disease, stroke, epilepsy, traumatic brain injury, amyotrophic lateral sclerosis, Huntington's disease and multiple sclerosis as examples. Additionally, it is also highlighting that diverse potential mechanisms such as metabolic control, epigenetic modification, neuroinflammation and gut-brain axis are of utmost importance for nutrient supply to the risk of neurologic condition and therapeutic response. Finally, we also highlight the novel concept that dietary nutrient intervention reshapes metabolism-epigenetics-immunity cycle to remediate brain dysfunction. Targeting metabolism-epigenetics-immunity network will delineate a new blueprint for combating neurological weaknesses.
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http://dx.doi.org/10.1016/j.pharmthera.2021.107861DOI Listing
October 2021

Efficacy of Antiviral Treatment in Liver Biopsy-Proven Immune-Tolerant Chronic Hepatitis B Patients: A Retrospective Cohort Study.

Front Med (Lausanne) 2021 8;8:655530. Epub 2021 Apr 8.

Department of Infectious Diseases, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.

The optimal timing of initiating antiviral treatment for immune-tolerant (IT) patients remains unknown. We conducted this study in liver biopsy-proven IT patients to compare the long-term outcomes of untreated and treated patients suffering non-cirrhotic chronic hepatitis B (CHB). This retrospective cohort study recruited 171 consecutive treatment-naïve CHB patients who completed liver biopsy test. Patients were stratified into IT ( = 60), mildly-active (MA; = 31), immune-active (IA; = 80), according to alanine aminotransferase (ALT) and liver biopsy data. One hundred and nine patients receiving antiviral treatment constituted the treated set, and 62 patients under close follow-up comprised the untreated set. Primary outcomes were virological response, HBeAg seroconversion, HBsAg loss, ALT normalization, and liver stiffness measurement normalization (NCT03740789). The study population was predominantly male (62.6%) with a mean age of 31 years. The proportion of virological response in treated patients in the MA phase was 57.1%, and the proportion of HBeAg seroconversion was 28.6%, which showed no difference with the 43.8% virological response and 31.5% HBeAg seroconversion in IA patients. The proportions of virological response and seroconversion were 18.2 and 9.1%, respectively, in the IT phase, which were lower than the rates in the MA and IA phases. However, 95.5% of IT patients persisted normal ALT, and 100% of IT patients persisted normal liver stiffness measurement in the treated group. Therefore, antiviral treatment should be considered for CHB patients with high viral load regardless of phase to minimize further damage to hepatocytes.
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http://dx.doi.org/10.3389/fmed.2021.655530DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8060436PMC
April 2021

Associations of hand washing frequency with the incidence of illness: a systematic review and meta-analysis.

Ann Transl Med 2021 Mar;9(5):395

Evidence-Based Medicine Center, School of Basic Medical Sciences, Lanzhou University, Lanzhou, China.

Background: Hand hygiene is one of the ways to prevent the spread of diseases. Our aim was to explore the relationship between hand washing frequency and the impact on disease, and give recommendations on the number of times to wash hands.

Methods: We searched seven electronic databases from their inception to April 11, 2020, and reference lists of related reviews for all studies on hand washing frequency and disease prevention. The Review Manager 5.3. software was used to conduct a meta-analysis. We assessed the risk of bias of included studies, and quality of evidence of the main findings.

Results: A total of eight studies were included. The results of the meta-analysis showed that there was no statistical significance between the effect of disease prevention and washing more than 4 times/day compared to not [odds ratio (OR) =0.61, 95% confidence interval (CI): 0.37 to 1.01]. The results of a case-control study showed that compared with hand washing ≤4 times/day, hand washing 5-10 times/day (OR =0.75, 95% CI: 0.63 to 0.91) and hand washing >10 times/day (OR =0.65, 95% CI 0.53 to 0.80) could reduce the risk of disease infection. There was no statistical significance advantage to hand washing more than 10 times/day compared to 5-10 times/day (OR =0.86, 95% CI: 0.70 to 1.06). Comparing hand washing ≤10 times/day with hand washing >10 times/day, increased hand washing was a protective factor against infection (OR =0.59, 95% CI: 0.36 to 0.97).

Conclusions: The more frequently hands were washed, the lower risk of disease. So far however, there is no high-quality evidence indicating the best range of hand washing frequency for disease prevention.
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http://dx.doi.org/10.21037/atm-20-6005DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8033386PMC
March 2021

Sudden death of COVID-19 patients in Wuhan, China: A retrospective cohort study.

J Glob Health 2021 Mar 27;11:05006. Epub 2021 Mar 27.

Department of Epidemiology and Biostatistics, Key Laboratory for Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Sciences and Technology, Wuhan, China.

Background: In December 2019, coronavirus disease 2019 (COVID-19) emerged in Wuhan city and rapidly spread throughout China. So far, it has caused ~ 4000 deaths in this country. We aimed to systematically characterize clinical features and determine risk factors of sudden death for COVID-19 patients.

Methods: Deceased patients with COVID-19 in Tongji hospital from January 22 to March 23, 2020 were extracted. Patients who died within 24 hours after admission were identified as sudden deaths, and the others formed non-sudden deaths. The differences in clinical characteristics between the two groups were estimated. Risk factors associated with sudden deaths were explored by logistic regression.

Results: 281 deceased patients were enrolled in this study. Sudden death occurred in 28 (10.0%) patients, including 4 (14.3%) admitted to the intensive care unit. Fatigue was more common in sudden deaths (11, 47.8%) than in non-sudden deaths (40, 17.2%). Both the count and percentage of eosinophils were lower in sudden deaths than that in non-sudden deaths ( = 0.006 and  = 0.004). Compared with non-sudden deaths, sudden deaths had higher plasma levels of procalcitonin, C-reactive protein, D-dimer, alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase, lactate dehydrogenase, alkaline phosphatase and N-terminal pro-brain natriuretic peptide. There were not significant differences in gender, age, chest CT image features and comorbidities observed.

Conclusions: The differences between the two groups suggested more severe systemic inflammation, multi-organ dysfunction, especially impaired liver and heart function in COVID-19 patients who died suddenly after admission. More researches are needed to verify these points.
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http://dx.doi.org/10.7189/jogh.11.05006DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8005311PMC
March 2021

Sex Differences of Clinical Presentation and Outcomes in Propensity-Matched Patients with Acute Type A Aortic Dissection.

Heart Surg Forum 2021 03 30;24(2):E311-E316. Epub 2021 Mar 30.

Department of Cardiovascular Surgery, Xijing Hospital, Air Force Medical University, Xi'an, China.

Objectives: To assess sex differences of clinical presentation and outcomes in propensity-matched patients with acute type A aortic dissection (AAAD).

Methods: We collected the clinical data of patients with AAAD from a single heart center between January 2009 and July 2014. After propensity score matching, we compared differences in clinical presentation and outcomes of patients with AAAD between men and women.

Results: There were 590 patients (295 men and 295 women) with AAAD through propensity matching on demographics and patients' history. We found that the presentation and diagnosis of AAAD often were more delayed in women. Severe signs of congestive heart failure (9.8% vs. 5.1%, P = 0.017), cardiac tamponade/shock (9.1% vs. 4.1%, P < 0.001), and periaortic hematoma (26.4% vs. 21.7%, P < 0.001) were more commonly presented in women. Surgery was more commonly performed in men than in women (95.4% (281/295) vs. 91.5% (270/295), P = 0.045), indicating the association of sex with surgical decision. To investigate the association of sex with outcomes after surgery, patients who underwent surgical treatment were re-matched (262 men and 262 women) by propensity score. Women suffered from greater in-hospital mortality than men (8.4% vs. 3.4%, P < 0.001). Postoperative complications of congestive heart failure (9.1% vs. 3.8%, P < 0.001), visceral ischemia (6.8% vs. 1.1%, P < 0.001), and limb ischemia (7.6% vs. 1.5%, P < 0.001) were more frequent in women. For women, prolonged operative time may increase in-hospital mortality, especially after 12 hours from the start of surgery (30.0% vs. 14.3%, P < 0.001). Kaplan-Meier survival analysis indicated worse late outcomes in women in the matched surgery group (log-rank P = 0.012).

Conclusions: Our analysis provides new insights into sex differences in clinical presentation and outcomes of AAAD.
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http://dx.doi.org/10.1532/hsf.3615DOI Listing
March 2021