Publications by authors named "Yao Wu"

533 Publications

Integrative analysis of the metabolome and transcriptome reveal the phosphate deficiency response pathways of alfalfa.

Plant Physiol Biochem 2021 Nov 25;170:49-63. Epub 2021 Nov 25.

Grassland Agri-Husbandry Research Center, College of Grassland Science, Qingdao Agricultural University, Qingdao, China. Electronic address:

Understanding the mechanisms underlying the responses to inorganic phosphate (Pi) deficiency in alfalfa will help enhance Pi acquisition efficiency and the sustainable use of phosphorous resources. Integrated global metabolomic and transcriptomic analyses of mid-vegetative alfalfa seedlings under 12-day Pi deficiency were conducted. Limited seedling growth were found, including 13.24%, 16.85% and 33.36% decreases in height, root length and photosynthesis, and a 24.10% increase in root-to-shoot ratio on day 12. A total of 322 and 448 differentially abundant metabolites and 1199 and 1061 differentially expressed genes were identified in roots and shoots. Increased (>3.68-fold) inorganic phosphate transporter 1;4 and SPX proteins levels in the roots (>2.15-fold) and shoots (>2.50-fold) were related to Pi absorption and translocation. The levels of phospholipids and Pi-binding carbohydrates and nucleosides were decreased, while those of phosphatases and pyrophosphatases in whole seedlings were induced under reduced Pi. In addition, nitrogen assimilation was affected by inhibiting high-affinity nitrate transporters (NRT2.1 and NRT3.1), and nitrate reductase. Increased delphinidin-3-glucoside might contribute to the gray-green leaves induced by Pi limitation. Stress-induced MYB, WRKY and ERF transcription factors were identified. The responses of alfalfa to Pi deficiency were summarized as local systemic signaling pathways, including root growth, stress-related responses consisting of enzymatic and nonenzymatic systems, and hormone signaling and systemic signaling pathways including Pi recycling and Pi sensing in the whole plant, as well as Pi recovery, and nitrate and metal absorption in the roots. This study provides important information on the molecular mechanism of the response to Pi deficiency in alfalfa.
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http://dx.doi.org/10.1016/j.plaphy.2021.11.039DOI Listing
November 2021

M2 macrophage microvesicle-inspired nanovehicles improve accessibility to cancer cells and cancer stem cells in tumors.

J Nanobiotechnology 2021 Nov 27;19(1):397. Epub 2021 Nov 27.

State Key Laboratory of Drug Research & Center of Pharmaceutics, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.

Cancer cells and cancer stem cells (CSCs) are the major players of cancer malignancy and metastasis, but they are extremely difficult to access. Inspired by the vital role of macrophages and microvesicle-mediated cell-cell communication in tumors, we herein designed M2 macrophage microvesicle-inspired nanovehicle of cabazitaxel (M-CFN) to promote accessibility to cancer cells and CSCs in tumors. In the 4T1 tumor model, M-CFN flexibly permeated the tumor mass, accessed cancer cells and CD90-positive cells, and significantly promoted their entry into CSC fractions in tumors. Moreover, M-CFN treatment profoundly eliminated aldehyde dehydrogenase (ALDH)-expressing CSCs in 4T1 and MCF-7 tumors, produced notable depression of tumor growth and caused 93.86% suppression of lung metastasis in 4T1 models. Therefore, the M2 macrophage microvesicle-inspired nanovehicle provides an encouraging strategy to penetrate the tumor tissues and access these insult cells in tumors for effective cancer therapy.
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http://dx.doi.org/10.1186/s12951-021-01143-5DOI Listing
November 2021

Effect of pH on lipid oxidation mediated by hemoglobin in washed chicken muscle.

Food Chem 2022 Mar 28;372:131253. Epub 2021 Sep 28.

The College of Food Science, Shenyang Agricultural University, Shenyang 110866, Dongling Street No.120, Shenyang, China.

To investigate the effect of pH on lipid oxidation of chicken muscle, chicken hemolysates were added to washed chicken muscles to analyze lipid oxidation at pH 5.7, 6.3, and 7.2. The results showed that with a blue shift of the Soret peak, oxyhemoglobin gradually transformed to methemoglobin during storage, the shape of porphyrin rings of heme in fluorescence electron microscopy changed from round to trail-like structure. These changes were more significant at low pH. Comparing hemoglobin (Hb) structure, the distance ofamino acids between the E10 of lysine and metHb-7-propionate groups is longer at pH 5.7 than other pHs, which makes solvent easily enter the heme cavity, leading tothe severe destruction of Hb. The linear correlation between color and lipid oxidation also further confirmed that the increased oxidation of chicken Hb causes more rapid lipid oxidation in pH 5.7 than the other 2 pHs (p < 0.05).
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http://dx.doi.org/10.1016/j.foodchem.2021.131253DOI Listing
March 2022

Research progress on the mechanism of ferroptosis and its clinical application.

Exp Cell Res 2021 Nov 17;409(2):112932. Epub 2021 Nov 17.

Department of Occupational and Environment Health, School of Public Health, Zhengzhou University, No.100 Science Avenue, Zhengzhou, 450001, Henan Province, PR China. Electronic address:

Ferroptosis is a mode of cell death dependent on iron ions, which is mainly induced by the decrease of the biological activity of glutathione peroxidase or the accumulation of lipid peroxidation and reactive oxygen species (ROS). It is significantly different from autophagy and other forms of cell death in terms of cell morphology and biochemistry. The exact mechanisms of ferroptosis are not clear. More and more studies have shown that various tumor diseases and nervous system diseases are closely related to ferroptosis. The occurrence and development of related diseases can be tolerated by stimulating or inhibiting the occurrence of ferroptosis. Therefore, ferroptosis has occupied a very important position in recent years. This article reviews the discovery process, characteristics, mechanisms, inducers, inhibitors of ferroptosis and its related clinical applications to lay a foundation for follow-up researchers to study ferroptosis and provide some reference value.
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http://dx.doi.org/10.1016/j.yexcr.2021.112932DOI Listing
November 2021

The expression of STEAP4 in peripheral blood predicts the outcome of septic patients.

Ann Transl Med 2021 Oct;9(20):1519

Department of Emergency Medicine, Affiliated Hospital of Nantong University, Nantong, China.

Background: Sepsis is a systemic disease characterized by extensive inflammatory responses and impaired organ function, which are characteristics that make it easily missed and complex to treat. A large number of laboratory and clinical studies on the diagnosis and treatment of sepsis have been continuously carried out, confirming the importance of mitochondrial function during the development of sepsis. STEAP4 is an important metalloreductase in mitochondria, which is involved in the biogenesis and respiratory chain of mitochondria. The role of STEAP4 in inflammation remains controversial. Research in this field may contribute to the development of new diagnostic and treatment options for sepsis.

Methods: The expression of STEAP4 was measured in the peripheral blood of patients with severe sepsis and compared with healthy controls. Cell and mouse inflammatory models were established to detect the expression of STEAP4 and other inflammatory cytokines.

Results: (I) The expression of STEAP4 in the peripheral blood of patients with severe sepsis is higher than that of healthy volunteers (P<0.01), which is related to the SOFA score and transaminase. (II) STEAP4 has a certain predictive effect on the outcome of patients [area under curve (AUC) =0.696, P<0.05, 95% CI: 0.528 to 0.833]. (III) Inflammation led to increased expression of gene in RAW264.7 cells and mouse liver tissue.

Conclusions: The expression of STEAP4 is elevated in the early stage of sepsis and the degree of its elevation can be used to predict the clinical outcome of sepsis patients.
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http://dx.doi.org/10.21037/atm-21-2794DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8576732PMC
October 2021

Relationship between Polymorphism and Telomere Length in Workers Exposed to Omethoate.

Biomed Environ Sci 2021 Oct;34(10):838-841

Department of Occupational Health and Occupational Diseases, College of Public Health, Zhengzhou University, Zhengzhou 450001, Henan, China;The Key Laboratory of Nano medicine and Health Inspection of Zhengzhou, Zhengzhou 450001, Henan, China.

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http://dx.doi.org/10.3967/bes2021.115DOI Listing
October 2021

Notch pathway inhibitor DAPT accelerates proliferation and adipogenesis in infantile hemangioma stem cells.

Oncol Lett 2021 Dec 26;22(6):854. Epub 2021 Oct 26.

Department of Anatomy, Anhui Medical University, Hefei, Anhui 230000, P.R. China.

The Notch signaling pathway is crucial in both adipogenesis and tumor development. It serves a vital role in the development and stability of blood vessels and may be involved in the proliferative phase of infantile hemangiomas, which express various related receptors. Therefore, it was hypothesized that the Notch signaling pathway inhibitor N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT), a γ-secretase inhibitor, might help accelerate the regression of infantile hemangiomas. The present study evaluated whether inhibition of the Notch signaling pathway using DAPT could alter adipogenesis in hemangioma stem cells (HemSCs) derived from infantile hemangioma (IH) specimens. A total of 20 infants (age, ≤6 months) with hemangiomas who had not yet received any treatment were selected, and their discarded hemangioma tissues were obtained. HemSCs were isolated from the fresh, sterile IH specimens and treated with DAPT. Reverse transcription-quantitative PCR and western blotting were used to demonstrate the inhibition of the Notch signaling pathway by DAPT. A proliferation assay (Cell Counting Kit-8), oil red O staining, flow cytometry and a transwell assay were used to detect proliferation, adipogenesis, apoptosis and migration of HemSCs. Treatment with DAPT upregulated the expression levels of CCAAT/enhancer-binding protein (C/EBP) α, C/EBPβ, peroxisome proliferator-activated receptor-γ, adiponectin and insulin-like growth factor 1, and promoted the proliferation, apoptosis, migration and lipid accumulation in HemSCs . Targeting the Notch signaling pathway using DAPT may potentially accelerate the regression of infantile hemangiomas.
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http://dx.doi.org/10.3892/ol.2021.13115DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8581475PMC
December 2021

In Situ Controllable Fabrication of Two-Dimensional Magnetic FeO/[email protected] Composites for Highly Efficient Phosphopeptides Enrichment.

ACS Appl Mater Interfaces 2021 Nov 11;13(46):54665-54676. Epub 2021 Nov 11.

National Engineering Research Center for Biomaterials, College of Biomedical Engineering, Sichuan University, Chengdu610064, P. R. China.

Highly efficient enrichment of phosphopeptides is of great significance for phosphoproteomics-related biological and pathological processes research, but it remains challenging due to the lack of affinity materials which hold high enrichment efficiency and capacity. TiCT MXene, a novel two-dimensional material with outstanding physicochemical properties, has attracted wide research interests for application in various fields. However, there are few reports on the use of MXene-derived materials for phosphopeptides separation in the biomedical field. In this work, we proposed a facile one-pot method that in situ oxidation and modification of TiCT MXene, to prepare two-dimensional (2D) magnetic FeO/[email protected] composites for potential application in phosphopeptides enrichment. Benefiting from the outstanding magnetic responsiveness and multiaffinity sites (Ti-O, Fe-O, and NH groups), the FeO/[email protected] composites possessed excellent enrichment performance with high sensitivity (0.1 fmol μL), excellent selectivity (β-casein: bovine serum albumin = 1:5000, molar ratio), good repeatability (5 times), and high enrichment capacity (200 mg g). Moreover, the results of selective enrichment of phosphopeptides from nonfat milk, human saliva, human serum, and rat brain lysates indicated the great potential of FeO/[email protected] composites in low-abundance phosphopeptides enrichment from complex biological samples. This work has put forward a versatile method to prepare magnetic MXene composites and promoted the use of MXene composites in phosphoproteome in biomedicine.
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http://dx.doi.org/10.1021/acsami.1c13936DOI Listing
November 2021

Hesperetin inhibits KSHV reactivation and is reversed by HIF1α overexpression.

J Gen Virol 2021 11;102(11)

Central Laboratory, The Fourth Affiliated Hospital, Zhejiang University School of Medicine, Yiwu, 322000, Zhejiang, PR China.

Kaposi's sarcoma-associated herpesvirus (KSHV), an oncogenic virus, has two life cycle modes: the latent and lytic phases. KSHV lytic reactivation is important for both viral propagation and KSHV-induced tumorigenesis. The KSHV replication and transcription activator (RTA) protein is essential for lytic reactivation. Hesperetin, a citrus polyphenolic flavonoid, has antioxidant, anti-inflammatory, hypolipidemic, cardiovascular and anti-tumour effects. However, the effects of hesperetin on KSHV replication and KSHV-induced tumorigenesis have not yet been reported. Here, we report that hesperetin induces apoptotic cell death in BCBL-1 cells in a dose-dependent manner. Hesperetin inhibits KSHV reactivation and reduces the production of progeny virus from KSHV-harbouring cells. We also confirmed that HIF1α promotes the RTA transcriptional activities and lytic cycle-refractory state of KSHV-infected cells. Hesperetin suppresses HIF1α expression to inhibit KSHV lytic reactivation. These results suggest that hesperetin may represent a novel strategy for the treatment of KSHV infection and KSHV-associated lymphomas.
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http://dx.doi.org/10.1099/jgv.0.001686DOI Listing
November 2021

Sestrin2 protects against lethal sepsis by suppressing the pyroptosis of dendritic cells.

Cell Mol Life Sci 2021 Dec 6;78(24):8209-8227. Epub 2021 Nov 6.

Chinese PLA General Hospital and Medical School of Chinese PLA, Beijing, 100853, People's Republic of China.

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. Sestrin2 (SESN2), a highly evolutionarily conserved protein, is critically involved in the cellular response to various stresses and has been confirmed to maintain the homeostasis of the internal environment. However, the potential effects of SESN2 in regulating dendritic cells (DCs) pyroptosis in the context of sepsis and the related mechanisms are poorly characterized. In this study, we found that SESN2 was capable of decreasing gasdermin D (GSDMD)-dependent pyroptosis of splenic DCs by inhibiting endoplasmic reticulum (ER) stress (ERS)-related nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3)-mediated ASC pyroptosome formation and caspase-1 (CASP-1) activation. Furthermore, SESN2 deficiency induced NLRP3/ASC/CASP-1-dependent pyroptosis and the production of proinflammatory cytokines by exacerbating the PERK-ATF4-CHOP signaling pathway, resulting in an increase in the mortality of septic mice, which was reversed by inhibiting ERS. These findings suggest that SESN2 appears to be essential for inhibiting NLRP3 inflammasome hyperactivation, reducing CASP-1-dependent pyroptosis, and improving sepsis outcomes through stabilization of the ER. The present study might have important implications for exploration of novel potential therapeutic targets for the treatment of sepsis complications.
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http://dx.doi.org/10.1007/s00018-021-03970-zDOI Listing
December 2021

TNF-α-induced protein 8-like 2 negatively regulates the immune function of dendritic cells by suppressing autophagy via the TAK1/JNK pathway in septic mice.

Cell Death Dis 2021 10 30;12(11):1032. Epub 2021 Oct 30.

Translational Medicine Research Center, Medical Innovation Research Division and Fourth Medical Center of the Chinese PLA General Hospital, 100048, Beijing, People's Republic of China.

Tumor necrosis factor (TNF)-α-induced protein 8-like 2 (TIPE2) is a newly discovered negative immunoregulatory protein that is involved in various cellular immune responses to infections. However, the underlying mechanism by which TIPE2 affects the immune function of dendritic cells (DCs) is not yet understood. This study aimed to determine the correlations among DCs TIPE2 expression, autophagic activity and immune function in the context of sepsis. In addition, the signaling pathway by which TIPE2 regulates autophagy in DCs was investigated. We reported for the first time that TIPE2 overexpression (knock-in, KI) exerted an inhibitory effect on autophagy in DCs and markedly suppressed the immune function of DCs upon septic challenge both in vitro and in vivo. In addition, TIPE2 knockout (KO) in DCs significantly enhanced autophagy and improved the immune response of DCs in sepsis. Of note, we found that the transforming growth factor-β (TGF-β)-activated kinase-1 (TAK1)/c-Jun N-terminal kinase (JNK) pathway was inhibited by TIPE2 in DCs, resulting in downregulated autophagic activity. Collectively, these results suggest that TIPE2 can suppress the autophagic activity of DCs by inhibiting the TAK1/JNK signaling pathway and further negatively regulate the immune function of DCs in the development of septic complications.
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http://dx.doi.org/10.1038/s41419-021-04327-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8557212PMC
October 2021

PPARγ/LXRα axis mediated phenotypic plasticity of lung fibroblasts in silica-induced experimental silicosis.

Environ Pollut 2022 Jan 28;292(Pt A):118272. Epub 2021 Oct 28.

School of Public Health, Zhengzhou University, Henan, China. Electronic address:

Silicosis is a disease mainly caused by pulmonary interstitial fibrosis caused by long-term inhalation of dust with excessively high content of free SiO. Transdifferentiation of lung fibroblasts into myofibroblasts is an important cellular basis for silicosis, but the key transcription factors (TFs) involved in this process are still unclear. In order to explore the biological regulation of transcription factor PPARγ/LXRα in silica-induced pulmonary fibrosis, this study explored the molecular mechanism of PPARγ/LXRα involved in regulating transcription factors related to SiO-induced lung injury at the cellular level and in animal models. ChIP-qPCR detected that PPARγ directly regulated the transcriptional activity of the LXRα gene promoter, while the PPARγ agonist RSG increased the expression of LXRα. In addition, we demonstrated in the cell model that upregulation of LXRα can inhibit silica-mediated fibroblast transdifferentiation, accompanied by an increase in the expression of SREBF1, PLTP and ABCA1. The results of LXRα silencing experiment matched those of overexpression experiment. These studies explored the role of LXRα in plasticity and phenotypic transformation between lung fibroblasts and myofibroblasts. Therefore, inhibiting or reversing the transdifferentiation of lung fibroblasts to myofibroblasts by intervening PPARγ/LXRα may provide a new therapeutic target for the treatment of silicosis.
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http://dx.doi.org/10.1016/j.envpol.2021.118272DOI Listing
January 2022

Sirt6 protects cardiomyocytes against doxorubicin-induced cardiotoxicity by inhibiting P53/Fas-dependent cell death and augmenting endogenous antioxidant defense mechanisms.

Cell Biol Toxicol 2021 Oct 28. Epub 2021 Oct 28.

Molecular Medicine Research Center, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, Sichuan, 610041, People's Republic of China.

Sirt6, a class III NAD-dependent deacetylase of the sirtuin family, is a highly specific H3 deacetylase and plays important roles in regulating cellular growth and death. The induction of oxidative stress and death is the critical mechanism involved in cardiomyocyte injury and cardiac dysfunction in doxorubicin-induced cardiotoxicity, but the regulatory role of Sirt6 in the fate of DOX-impaired cardiomyocytes is poorly understood. In the present study, we exposed Sirt6 heterozygous (Sirt6) mice and their littermates as well as cultured neonatal rat cardiomyocytes to DOX, then investigated the role of Sirt6 in mitigating oxidative stress and cardiac injury in the DOX-treated myocardium. Sirt6 partial knockout or silencing worsened cardiac damage, remodeling, and oxidative stress injury in mice or cultured cardiomyocytes with DOX challenge. Cardiomyocytes infected with adenoviral constructs encoding Sirt6 showed reversal of this DOX-induced damage. Intriguingly, Sirt6 reduced oxidative stress injury by upregulating endogenous antioxidant levels, interacted with oxidative stress-stirred p53, and acted as a co-repressor of p53 in nuclei. Sirt6 was recruited by p53 to the promoter regions of the target genes Fas and FasL and further suppressed p53 transcription activity by reducing histone acetylation. Sirt6 inhibited Fas/FasL signaling and attenuated both Fas-FADD-caspase-8 apoptotic and Fas-RIP3 necrotic pathways. These results indicate that Sirt6 protects the heart against DOX-induced cardiotoxicity by upregulating endogenous antioxidants, as well as suppressing oxidative stress and cell death signaling pathways dependent on ROS-stirred p53 transcriptional activation, thus reducing Fas-FasL-mediated apoptosis and necrosis. •Sirt6 is significantly decreased in DOX-insulted mouse hearts and cardiomyocytes. •Sirt6 attenuates DOX-induced cardiac atrophy, dysfunction and oxidative stress. • Sirt6 reduces oxidative stress injury by upregulating endogenous antioxidants. • Sirt6 interacts with p53 as a co-repressor to suppress p53 transcriptional regulation and inhibits Fas-FasL-mediated apoptosis and necrosis downstream of p53.
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http://dx.doi.org/10.1007/s10565-021-09649-2DOI Listing
October 2021

Working life job strain status and cognitive aging in Europe: A 12-year follow-up study.

J Affect Disord 2021 12 4;295:1177-1183. Epub 2021 Sep 4.

Department of Psychology, Stress Research Institute, Stockholm University, Frescati Hagväg 16A, Stockholm 114 19, Sweden. Electronic address:

Background: To examine the association of job strain with cognitive ability and the influence of life-course job strain on later life cognitive decline.

Methods: Data were derived from six waves of the Survey of Health, Aging, and Retirement in Europe. The study sample consists of 13349 participants aged 50 to 98 years at wave 2 and has been followed up for 12-years. Job strain status across working life was assessed using a short demand-control job strain model containing two core dimensions: job demands and job control collected in wave 3. Cognitive abilities concerning episodic memory was assessed by immediate recall and delayed recall tests, executive function was evaluated by verbal fluency test collected in all waves (waves 2-7) except wave 3. Mixed-effects model was used to estimate working life job strain and its cumulative effect on cognitive decline.

Results: Both passive and high strain jobs were associated with lower levels of cognitive ability (episodic memory and verbal fluency) in comparison with active job. Long exposure to active- or low strain-job was associated with higher cognitive ability whereas long exposure to passive job or moderate duration of high strain job was associated with lower cognitive ability. The rate of memory decline was positively related to moderate duration of passive job and negatively related to long-term exposure to low strain job.

Limitations: Information on working conditions was based on self-reported recollections.

Conclusions: Working life variation in job strain status and their duration may explain individual differences in cognitive ability in later life.
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http://dx.doi.org/10.1016/j.jad.2021.08.114DOI Listing
December 2021

Nanomedicine Strategies to Circumvent Intratumor Extracellular Matrix Barriers for Cancer Therapy.

Adv Healthc Mater 2021 Oct 27:e2101428. Epub 2021 Oct 27.

State Key Laboratory of Drug Research & Center of Pharmaceutics, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.

The dense and heterogeneous physical network of the extracellular matrix (ECM) in tumors represents a formidable barrier that limits intratumor drug delivery and the therapeutic efficacy of many anticancer therapies. Here, the two major nanomedicine strategies to circumvent intratumor ECM barriers: regulating the physiochemical properties of nanomedicines and remodeling the components and structure of the ECM are summarized. Nanomedicines can be rationally regulated by optimizing physiochemical properties or designed with biomimetic features to promote ECM permeation capability. Meanwhile, they can also be designed to remodel the ECM by modulating signaling pathways or destroying the components and architecture of the ECM via chemical, biological, or physical treatments. These efforts produce profound improvements in intratumor drug delivery and anticancer efficacy. Moreover, to aid in their anticancer efficacy, feasible approaches for improving ECM-circumventing nanomedicines are proposed.
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http://dx.doi.org/10.1002/adhm.202101428DOI Listing
October 2021

Herbal medicine derived carbon dots: synthesis and applications in therapeutics, bioimaging and sensing.

J Nanobiotechnology 2021 Oct 13;19(1):320. Epub 2021 Oct 13.

Institute of Integrative Medicine, Department of Integrated Chinese and Western Medicine, Xiangya Hospital Central South University, Changsha, China.

Since the number of raw material selections for the synthesis of carbon dots (CDs) has grown extensively, herbal medicine as a precursor receives an increasing amount of attention. Compared with other biomass precursors, CDs derived from herbal medicine (HM-CDs) have become the most recent incomer in the family of CDs. In recent ten years, a great many studies have revealed that HM-CDs tend to be good at theranostics without drug loading. However, the relevant development and research results are not systematically reviewed. Herein, the origin and history of HM-CDs are outlined, especially their functional performances in medical diagnosis and treatment. Besides, we sort out the herbal medicine precursors, and analyze the primary synthetic methods and the key characteristics. In terms of the applications of HM-CDs, medical therapeutics, ion and molecular detection, bioimaging, as well as pH sensing are summarized. Finally, we discuss the crucial challenges and future prospects.
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http://dx.doi.org/10.1186/s12951-021-01072-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8513293PMC
October 2021

Erratum to "The predominant role of pectin in binding Cd in the root cell wall of a high Cd accumulating rice line (Oryza sativa L.)" [Ecotoxicol. Environ. Saf. 206C (2020) 111210].

Ecotoxicol Environ Saf 2021 Dec 7;226:112873. Epub 2021 Oct 7.

College of Resources, Sichuan Agricultural University, Chengdu 611130, Sichuan, China. Electronic address:

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http://dx.doi.org/10.1016/j.ecoenv.2021.112873DOI Listing
December 2021

"The Mental Health Piece is Huge": perspectives on developing a prenatal maternal psychological intervention for congenital heart disease.

Cardiol Young 2021 Sep 30:1-8. Epub 2021 Sep 30.

Department of Psychological and Brain Sciences, George Washington University, Washington, DC, USA.

Objectives: Women carrying a fetus diagnosed with congenital heart disease often experience significant distress because of their medical diagnosis. Given the well-documented impact associated with elevated prenatal stress and critical importance of developing targeted interventions, this study aims to examine stressors, coping and resilience resources, and mental health treatment preferences in pregnant women receiving a congenital heart disease diagnosis to inform the development of a psychological intervention to reduce maternal distress prenatally.

Methods: Three groups of participants were included consisting of two pregnant women carrying a fetus with congenital heart disease, five women of children (4-16 months) with congenital heart disease, and five paediatric cardiology medical providers. Responses were gathered via semi-structured interviews and analysed using qualitative thematic analysis.

Results: Information regarding four broad areas were analysed of emotional distress during pregnancy; experience of initial diagnosis; coping and resilience; and perspectives on a mental health intervention in pregnancy. Anxiety regarding baby's future, guilt following diagnosis, and various coping strategies emerged as primary themes among the participant sample. Medical staff corroborated mothers' heightened anxiety and viewed a psychotherapeutic intervention during the prenatal period as essential and complimentary to standard of care.

Conclusion: We identified salient themes and preferred components for a future psychological intervention delivered prenatally.

Practice Implications: Patients' and providers' perspectives regarding the nature of maternal distress, resilience and treatment preferences can inform the development of interventions to support the emotional well-being of pregnant women carrying a fetus with congenital heart disease to optimise care and potentially improve outcomes for fetal brain development.
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http://dx.doi.org/10.1017/S1047951121004030DOI Listing
September 2021

An ensemble learning framework for potential miRNA-disease association prediction with positive-unlabeled data.

Comput Biol Chem 2021 Aug 24;95:107566. Epub 2021 Aug 24.

School of Management and Economics, Beijing Institute of Technology, Beijing 100081, China.

To explore the pathogenic mechanisms of MicroRNA (miRNA) on diverse diseases, many researchers have concentrated on discovering the potential associations between miRNA and disease using machine learning methods. However, the prediction accuracy of supervised machine learning methods is limited by lacking of experimentally-validated uncorrelated miRNA-disease pairs. Without these negative samples, training a highly accurate model is much more difficult. Different from traditional miRNA-disease prediction models using randomly selected unknown samples as negative training samples, we propose an ensemble learning framework to solve this positive-unlabeled (PU) learning problem. The framework incorporates two steps, i.e., a novel semi-supervised Kmeans (SS-Kmeans) to extract reliable negative samples from unknown miRNA-disease pairs and subagging method to generate diverse training sample sets to make full use of those reliable negative samples for ensemble learning. Combined with effective random vector functional link (RVFL) network as prediction model, the proposed framework showed superior prediction accuracy comparing with other popular approaches. A case study on lung and gastric neoplasms further confirms the framework's efficacy at identifying miRNA disease associations.
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http://dx.doi.org/10.1016/j.compbiolchem.2021.107566DOI Listing
August 2021

Rosmarinic acid ameliorates acetaminophen-induced acute liver injury in mice via RACK1/TNF-α mediated antioxidant effect.

Pharm Biol 2021 Dec;59(1):1286-1293

Department of Pharmacology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, PR China.

Context: Rosmarinic acid (RA) dose-dependently ameliorates acetaminophen (APAP) induced hepatotoxicity in rats. However, whether RA hepatoprotective effect is by regulating RACK1 and its downstream signals is still unclear.

Objective: This study explores the RA protective effect on APAP-induced ALI and its mechanism.

Materials And Methods: Sixty Kunming mice 6-8 weeks old were randomly separated into six groups ( = 10) and pre-treated with normal saline, ammonium glycyrrhetate (AG) or RA (10, 20 or 40 mg/kg i.p./day) for two consecutive weeks. Then, APAP (300 mg/kg, i.g.) was administrated to induce ALI, except for the control. Serum alanine/aspartate aminotransferases (ALT and AST), malondialdehyde (MDA), superoxide dismutase (SOD) and histopathology were used to authenticate RA effect. The liver RACK1 and TNF-α were measured by western blot.

Results: Compared with the APAP group, different dosages RA significantly decreased ALT (52.09 ± 7.98, 55.13 ± 10.19, 65.08 ± 27.61 U/L,  < 0.05), AST (114.78 ± 19.87, 115.29 ± 31.91, 101.78 ± 21.85 U/L,  < 0.05), MDA (2.37 ± 0.87, 2.13 ± 0.87, 1.86 ± 0.39 nmol/mg,  < 0.01) and increased SOD (306.178 ± 90.80, 459.21 ± 58.54, 444.01 ± 78.09 U/mg,  < 0.05). With increasing doses of RA, RACK1 and TNF-α expression decreased. Moreover, the RACK1 and TNF-α levels were positively correlated with MDA ( = 0.8453 and  = 0.9391,  < 0.01).

Discussion And Conclusions: Our findings support RA as a hepatoprotective agent to improve APAP-induced ALI and the antioxidant effect mediated through RACK1/TNF-α pathway.
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http://dx.doi.org/10.1080/13880209.2021.1974059DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8451635PMC
December 2021

Incidence and Prognostic Significance of PD-L1 Expression in High-Grade Salivary Gland Carcinoma.

Front Oncol 2021 26;11:701181. Epub 2021 Aug 26.

Department of Head Neck and Thyroid, Henan Cancer Hospital, Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, China.

Objective: PD-L1 is one of the predictors of immunotherapy efficacy. Our goal was to analyze its expression and prognostic significance in high-grade salivary gland carcinoma (SGC).

Methods: PD-L1 expression was evaluated using paraffin-embedded specimens from patients with surgically treated high-grade SGC, and it was scored by the tumor proportion score (TPS), combined positive score (CPS), and immune cell (IC) score. Associations between clinicopathological variables, disease-free survival (DFS), overall survival (OS) and PD-L1 expression were assessed.

Results: TPS≥1% occurred in 47 patients with an incidence of 43.1%, and it was significantly related to an advanced tumor stage. In patients with TPS<1%, TPS ranging from 1% to 20%, and TPS≥20%, the 5-year DFS rates were 36%, 26%, and 13%, respectively, and the difference was significant. In patients with TPS<1%, TPS ranging from 1% to 20%, and TPS≥20%, the 5-year OS rates were 49%, 24%, and 13%, respectively, and the difference was significant. CPS≥1 occurred in 87 patients with an incidence of 79.8%. IC scores of 0, 1, 2, and 3 were noted in 24 (22.0%), 37 (33.9%), 31 (28.4%), and 17 (15.6%) patients, respectively. Both CPS and IC scores had no impact on DFS or OS.

Conclusions: The expression of PD-L1 in tumor cells of high-grade SGCs was not uncommon, and it was significantly associated with tumor stage. PD-L1 expression in tumor cells rather than in immune cells indicated a poor prognosis.
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http://dx.doi.org/10.3389/fonc.2021.701181DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8427307PMC
August 2021

Antagonism of Cerebral High Mobility Group Box 1 Ameliorates Dendritic Cell Dysfunction in Sepsis.

Front Pharmacol 2021 26;12:665579. Epub 2021 Aug 26.

Trauma Research Center, Fourth Medical Center and Medical Innovation Research Division of the Chinese PLA General Hospital, Beijing, China.

Sepsis has emerged as a global health issue, and accounts for millions of deaths in intensive care units. Dysregulation of the immune response reportedly contributes to the pathogenesis and progression of this lethal condition, which involves both the dysfunction of immune cells and incompetent immunomodulatory mechanisms. High mobility group box 1 (HMGB1) is known as a later inflammatory mediator and is critically involved in the severity and prognosis of sepsis by inducing intractable inflammation and dysfunction of various immune cells. In the present study, we found that intracerebroventricular (ICV) injection of Box A, a specific antagonist of HMGB1, restored the dysregulated response of splenic dendritic cells (DCs) in septic mice by enhancing the expression of surface molecules, including CD80, CD86, and MHC-II, as well as improving DC priming of T lymphocytes. Cerebral HMGB1 was also confirmed to have potent inhibitory effects on DC functions when administrated by ICV injection in normal mice. The brain cholinergic system was found to mediate the immunomodulatory effects of central HMGB1, as it exhibited enhanced activity with persistent HMGB1 exposure. Furthermore, the inhibitory effects of cerebral HMGB1 on the response of peripheral DCs were also blocked by α7nAchR gene knockout. These findings provide novel insight into the relationship between cerebral HMGB1 and splenic DC dysfunction during sepsis, which is, at least in part, dependent on cholinergic system activity.
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http://dx.doi.org/10.3389/fphar.2021.665579DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8427508PMC
August 2021

Surfactant-free synthesis of covalent organic framework nanospheres in water at room temperature.

J Colloid Interface Sci 2022 Jan 7;606(Pt 2):1333-1339. Epub 2021 Jul 7.

National Engineering Research Center for Biomaterials, Sichuan University, Chengdu 610064, PR China. Electronic address:

Covalent organic frameworks (COFs) are a new class of porous materials receiving much attention due to their unique characteristics. However, COFs have been usually synthesized under harsh and complicated conditions, limiting their practical applications. We propose a surfactant-free strategy to controllably synthesize an imine-based covalent organic framework (COF) nanomaterial in water at room temperature. Introduction of tiny amounts of co-solvents not only achieves the morphology and size control of COFs but also ensures stability of COF nanomaterials in aqueous solution. Moreover, water as a solvent plays an important role in the size adjustment of COFs. The surface area of the obtained COFs was approximately 398 m/g with a pore size distribution of about 2.8 nm. In addition, the COFs displayed a good crystallinity.
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http://dx.doi.org/10.1016/j.jcis.2021.07.026DOI Listing
January 2022

Bifunctional magnetic covalent organic framework for simultaneous enrichment of phosphopeptides and glycopeptides.

Anal Chim Acta 2021 Sep 19;1177:338761. Epub 2021 Jun 19.

National Engineering Research Center for Biomaterials, Sichuan University, Chengdu, 610064, PR China. Electronic address:

Protein phosphorylation and glycosylation, which are closely related to various diseases, have been extensively studied recently. Mass spectrometry (MS) based phosphoproteomics and glycoproteomics analysis rely heavily on the pre-treatment. Due to the differences in enrichment conditions, there are still huge challenges in designing and preparing a single affinity material to achieve efficient simultaneous capture and elution of phosphopeptides and glycopeptides. Herein, a novel magnetic covalent organic framework, which was modified with functional molecule 4-(3-(2-(methacryloyloxy)ethyl)-ureido)benzoic acid (MUBA), was designed as a bifunctional enrichment platform for glycopeptides and phosphopeptides. Thanks to the multiple hydrogen bonding interactions between MUBA and hydrogen phosphates, the material possessed excellent enrichment performance for phosphopeptides. In addition, the hydrophilicity of the COF structure and modified molecules endowed this material recognition capability towards glycopeptides based on hydrophilic interaction chromatography. Combining with the inherent properties of COF structure, the established platform achieved simultaneous enrichment of phosphopeptides and glycopeptides with excellent selectivity (1:1:1000 M ratio of α-casein/IgG/BSA), high sensitivity (0.05 fmol/μL α-casein; 0.05 fmol/μL IgG), and good size-exclusion effect (α-casein digests/IgG digests/BSA, 1:1:500). More excitingly, the method was used for the identification of glycopeptides and phosphopeptides from rat liver tissue and the exosomes extracted from liver cancer patients' plasma, proving its specific phosphoproteomics and glycoproteomics study in complex biosamples.
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http://dx.doi.org/10.1016/j.aca.2021.338761DOI Listing
September 2021

Sestrin2 protects dendrite cells against ferroptosis induced by sepsis.

Cell Death Dis 2021 09 4;12(9):834. Epub 2021 Sep 4.

Department of Emergency, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000, People's Republic of China.

Ferroptosis is a nonapoptotic form of programmed cell death triggered by the accumulation of reactive oxygen species (ROS) depended on iron overload. Although most investigations focus on the relationship between ferroptosis and cancer, neurodegenerative diseases, and ischemia/reperfusion injury, research on ferroptosis induced by immune-related inflammatory diseases, especially sepsis, is scarce. Sestrin2 (Sesn2), a highly evolutionary and stress-responsive protein, is critically involved in defense against oxidative stress challenges. Upregulated expression of Sesn2 has been observed in preliminary experiments to have an antioxidative function in the context of an inflammatory response. Nevertheless, the underlying function of Sesn2 in inflammation-mediated ferroptosis in the immune system remains uncertain. The current study aimed to demonstrate the protective effect of Sesn2 on ferroptosis and even correlations with ferroptosis and the functions of ferroptotic-dendritic cells (DCs) stimulated with lipopolysaccharide (LPS). The mechanism underlying DCs protection from LPS-induced ferroptosis by Sesn2 was further explored in this study. We found that the immune response of DCs assessed by co-stimulatory phenotypes was gradually enhanced at the peak time of 12 h upon 1 μg/ml LPS stimulation while ferroptosis in DCs treated with LPS at 24 h was significantly detected. LPS-induced ferroptosis showed a suppressive impact on DCs in phenotypic maturation, which was conversely relieved by the ferroptotic inhibitor. Compared with wild-type (WT) mice, DCs in genetic defective mice of Sesn2 (Sesn2) exhibited exacerbated ferroptosis. Furthermore, the protective effect of Sesn2 on ferroptosis was noticed to be associated with the ATF4-CHOP-CHAC1 pathway, eventually exacerbating ferroptosis by degrading of glutathione. These results indicate that Sesn2 can suppress the ferroptosis of DCs in sepsis by downregulating the ATF4-CHOP-CHAC1 signaling pathway, and it might play an antioxidative role.
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http://dx.doi.org/10.1038/s41419-021-04122-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8418614PMC
September 2021

Distinct roles of miR-34 family members on suppression of lung squamous cell carcinoma.

Biomed Pharmacother 2021 Oct 30;142:111967. Epub 2021 Aug 30.

Department of Thoracic Surgery, Xi'an Chest Hospital, Xi'an 710100, China. Electronic address:

miR-34, whose mimic was used on phase I clinical trial, has been extensively reported since its dysfunction in various cancers including non-small-cell lung cancer (NSCLC). However, the roles of miR-34 family members in the progression of lung squamous carcinoma (SCC) in patients who have occupational-exposure experience are unclear yet. Here, we comprehensively investigated the expression levels of miR-34 family members in SCC patients and compared the roles of them in SCC in vitro and vivo. The results showed that the average levels of miR-34a and miR-34b/c were decreased in patients. The analysis of miR-34a to miR-34b/c levels in patients graded different stages or metastases or recurrence showed that miR-34b/c was reduced earlier and more significantly than miR-34a. In vitro assays demonstrated that both miR-34a and miR-34b/c inhibits SCC cells proliferation, migration and invasion via Notch1 pathway, while miR-34b/c effects more than miR-34a does. As miR-34a was significantly decreased in cancer recurrence, the further analysis of relationship between miR-34a and stem cell adhesion molecular CD44 showed that miR-34a was significantly correlated with CD44 levels in patients. Knockdown of CD44 significantly blocked miR-34a mediated inhibition of cell migration and invasion. Treating the purified CD44 cells with miR-34 overexpression lentivirus inhibited the tumor outgrowth. By contrast, anti-miR-34 facilitated tumor development of CD44 cells. Our study showed that miR-34 family members are negative regulator for SCC development, even though the inhibition is mediated by multiple and complicated signal pathways, which provides theoretical basis for SCC treatment and a biomarker candidate for SCC prognosis.
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http://dx.doi.org/10.1016/j.biopha.2021.111967DOI Listing
October 2021

Maternal mental distress and cortisol levels in pregnancies with congenital heart disease.

Cardiol Young 2021 Aug 31:1-5. Epub 2021 Aug 31.

Developing Brain Institute, Children's National Hospital, Washington, DC20010, USA.

Objectives: Prenatal maternal stress is associated with adverse offspring outcomes, which may be mediated by maternal stress hormones. However, evidence supporting the association between maternal stress and cortisol levels in high-risk pregnancies is limited. This study aims to determine the relationship between self-reported maternal mental distress and maternal salivary cortisol levels in pregnancies complicated by foetal CHD compared with healthy pregnancies.

Methods: We recruited women with pregnancies complicated by foetal CHD and healthy pregnancies. Maternal saliva was collected between 22 and 40 gestational weeks. Standardized questionnaires measuring stress, depression, and anxiety were completed by patients. Generalized estimating equation was used to evaluate associations between maternal mental distress scales and cortisol levels.

Results: We studied 165 women (55 CHD, 110 controls) and collected 504 cortisol samples (160 CHD, 344 controls). Women carrying CHD foetuses had higher stress, anxiety, and depression scores compared to women carrying healthy foetuses. However, maternal cortisol levels did not significantly differ in CHD and controls. Cortisol levels were higher in women carrying foetuses with functionally single-ventricle versus two-ventricle CHD. In both CHD and controls, there was no significant association between maternal stress, depression or anxiety scores and cortisol levels.

Conclusion: Our data suggest that self-reported maternal stress, anxiety, and depression are not associated with maternal salivary cortisol levels in CHD and healthy pregnancies. The impact of maternal mental distress on foetal health may be through other mediating pathways other than maternal cortisol concentrations.
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http://dx.doi.org/10.1017/S1047951121003504DOI Listing
August 2021

Scale-up reactivation of spent S-Zorb adsorbents for gasoline desulfurization.

J Hazard Mater 2022 Feb 13;423(Pt A):126903. Epub 2021 Aug 13.

State Key Laboratory of Heavy Oil Processing, China University of Petroleum, Qingdao 266555, China; College of Chemical Engineering, China University of Petroleum, Qingdao 266555, China.

Reactivating and recycling spent S-Zorb adsorbents reduce fresh adsorbents consumption and hazardous wastes emissions. Though the spent adsorbents have been successfully reactivated in the laboratory, a pilot-scale practice is indispensable before the industrial production. Herein, the reactivation of spent adsorbents was performed at laboratory (1.0 L), middle (10 L) and pilot (3000 L) scale, respectively. The inert ZnSiO and ZnS over the spent adsorbents are recovered to active ZnO, and the NiS is transformed into NiO. There is almost no amplification effect in pore structure and acidity of the reactivated adsorbents, while NiO particle size reduces slightly with the reactivation scales. The computational fluid dynamic simulation indicates that enhanced contact between spent adsorbents and acid/alkaline reagents at larger scale account for the smaller NiO particle. It provides more hydrogenolysis centers for CS bonds breakage after reduction, increasing initial desulfurization activity. More importantly, the adsorbent reactivated at pilot scale exhibits comparable activity to the fresh one in gasoline desulfurization. The sulfur content in the outlet decreases to less than 10 μg g from 1 h of reaction. Thus, the reactivation of spent S-Zorb adsorbents is successfully scaled up to the pilot scale, accelerating industrial practice in recycling the spent adsorbents.
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http://dx.doi.org/10.1016/j.jhazmat.2021.126903DOI Listing
February 2022

Depressive symptoms and cognitive impairment: A 10-year follow-up study from the Survey of Health, Ageing and Retirement in Europe.

Eur Psychiatry 2021 08 27;64(1):e55. Epub 2021 Aug 27.

Stress Research Institute, Department of Psychology, Stockholm University, Stockholm, Sweden.

Background: Depressive symptoms and cognitive impairment often coexisted in the elderly. This study investigates the effect of late-life depressive symptoms on risk of mild cognitive impairment (MCI).

Methods: A total of 14,231 dementia- and MCI free participants aged 60+ from the Survey of Health, Ageing, and Retirement in Europe were followed-up for 10 years to detect incident MCI. MCI was defined as 1.5 standard deviation (SD) below the mean of the standardized global cognition score. Depressive symptoms were assessed by a 12-item Europe-depression scale (EURO-D). Severity of depressive symptoms was grouped as: no/minimal (score 0-3), moderate (score 4-5), and severe (score 6-12). Significant depressive symptoms (SDSs) were defined as EURO-D score ≥ 4.

Results: During an average of 8.2 (SD = 2.4)-year follow-up, 1,352 (9.50%) incident MCI cases were identified. SDSs were related to higher MCI risk (hazard ratio [HR] = 1.26, 95% confidence intervals [CI]: 1.10-1.44) in total population, individuals aged 70+ (HR = 1.35, 95% CI: 1.14-1.61) and women (HR = 1.28, 95% CI: 1.08-1.51) in Cox proportional hazard model adjusting for confounders. In addition, there was a dose-response association between the severity of depressive symptoms and MCI incidence in total population, people aged ≥70 years and women (p-trend <0.001).

Conclusions: Significant depressive symptoms were associated with higher incidence of MCI in a dose-response fashion, especially among people aged 70+ years and women. Treating depressive symptoms targeting older population and women may be effective in preventing MCI.
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http://dx.doi.org/10.1192/j.eurpsy.2021.2230DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8446071PMC
August 2021

Trends and Patterns of Knee Osteoarthritis in China: A Longitudinal Study of 17.7 Million Adults from 2008 to 2017.

Int J Environ Res Public Health 2021 08 23;18(16). Epub 2021 Aug 23.

School of Nursing, Peking University, No. 38 Xueyuan Road, Beijing 100191, China.

Knee osteoarthritis (KOA) provides many challenges on the healthcare system. However, few studies have reported the epidemiology, particularly in a large population. Our study aimed to estimate the prevalence, incidence, trends, and patterns of diagnosed KOA in China. This was a longitudinal study. We used health insurance claims of 17.7 million adults from 2008-2017 to identify people with KOA. Trends in prevalence and incidence were analyzed using joinpoint regression. We identified 2,447,990 people with KOA in Beijing, 60% of which were women. The 10-year average age-standardized prevalence and incidence of KOA was, respectively, 4.6% and 25.2 per 1000 person-years. Prevalence increased with age, surging after 55 years old. The average crude prevalence was 13.2% for people over 55 years old. The prevalence showed an increasing trend from 2008 to 2017, including a period of rapid rise from 2008 to 2011 ( < 0.05); the increase in prevalence was greatest in people under 35 years old ( 0.05). Our analyses showed that the annual prevalence rate of KOA increased significantly from 2008 to 2017 in China. We need to increase our attention to women and the elderly over 55 years old, and also be alert to the younger trend of incidence of KOA.
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http://dx.doi.org/10.3390/ijerph18168864DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8395063PMC
August 2021
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