Publications by authors named "Zhonghui Liu"

70 Publications

Enhanced North Pacific subtropical gyre circulation during the late Holocene.

Nat Commun 2021 Oct 12;12(1):5957. Epub 2021 Oct 12.

Department of Earth Sciences, The University of Hong Kong, Hong Kong SAR, China.

The North Pacific Subtropical Gyre circulation redistributes heat from the Western Pacific Warm Pool towards the mid- to high-latitude North Pacific. However, the driving mechanisms of this circulation and how it changed over the Holocene remain poorly understood. Here, we present alkenone-based sea surface temperature reconstructions along the Kuroshio, California and Alaska currents that cover the past ~7,000 years. These and other paleorecords collectively demonstrate a coherent intensification of the boundary currents, and thereby the basin-scale subtropical gyre circulation, since ~3,000-4,000 years ago. Such enhanced circulation during the late Holocene appears to have resulted from a long-term southward migration of the Intertropical Convergence Zone, associated with Holocene ocean cooling. Our results imply that the North Pacific Subtropical Gyre circulation could be weakened under future global warming.
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http://dx.doi.org/10.1038/s41467-021-26218-7DOI Listing
October 2021

Matrine ameliorates the inflammatory response and lipid metabolism in vascular smooth muscle cells through the NF-κB pathway.

Exp Ther Med 2021 Nov 16;22(5):1309. Epub 2021 Sep 16.

Department of Emergency Medicine, Yidu Central Hospital of Weifang, Weifang, Shandong 262500, P.R. China.

Atherosclerosis is a chronic inflammatory disease associated with inflammatory responses and the uncontrolled proliferation and excessive apoptosis of vascular smooth muscle cells. However, the effects of matrine on the inflammatory response, abnormal lipid metabolism and cell proliferation and apoptosis marker proteins in human aortic vascular smooth muscle cells (HAVSMCs) have not been elucidated. Therefore, the present study aimed to investigate the effect of matrine on an model of atherosclerosis using HAVSMCs. The HAVSMCs were divided into normal, model and matrine groups. The model group was treated with oxidized low-density lipoprotein (oxLDL), the matrine group was treated with oxLDL and matrine and the normal group was treated with physiological saline. Total cholesterol (TC), free cholesterol (FC) and cholesterol ester (CE) levels were measured in the cell supernatant. In addition, the relative mRNA levels of inflammatory factors were quantified using reverse transcription-quantitative PCR, and the cell proliferation and apoptosis rates were evaluated using Cell Counting Kit-8 and flow cytometry assays, respectively. The expression levels of proteins associated with proliferation and apoptosis were also determined using western blotting. The levels of TC, FC and CE and the mRNA levels of IL-1β, IL-6, and TNF-α in the matrine group were lower than those in the model group, but higher than those in the normal group. After 48 and 96 h of treatment, the cell proliferation and apoptotic rates were lower in the matrine group compared with the model group. The relative expression levels of Ki-67, proliferating cell nuclear antigen and Bax were decreased, while that of Bcl-2 was increased in the matrine group compared with the model group. In addition, the relative protein expression of nuclear factor κB (NF-κB) in the matrine group was lower than that in the model group, but higher than that in the normal group. In summary, matrine inhibited activation of the NF-κB pathway and reduced cell proliferation and apoptosis in the oxLDL-induced atherosclerosis model, and exhibited anti-inflammatory effects. These results suggest that matrine attenuated abnormal biological reactions in HAVSMCs through the NF-κB pathway.
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http://dx.doi.org/10.3892/etm.2021.10744DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8461614PMC
November 2021

The protective effect and potential mechanism of NRXN1 on learning and memory in ADHD rat models.

Exp Neurol 2021 Oct 3;344:113806. Epub 2021 Jul 3.

Department of Child Healthcare, Women's Hospital of Nanjing Medical University (Nanjing Maternity and Child Health Care Hospital), Nanjing 210004, China. Electronic address:

The learning and memory network is highly complex and remains unclear. The hippocampus is the location of learning and memory function. Impairment of synaptic morphology and synaptic plasticity (i.e., long-term potentiation) appears to cause learning and memory deficits. Several studies have indicated the role of NRXN1 in regulating the synaptic function, but little is known on its role in learning and memory dysfunction associated with attention deficit and hyperactivity disorder (ADHD). Our results showed that overexpression and interference of NRXN1 in vivo, respectively, affected learning and memory, as was assessed by Morris water maze tests, in spontaneously hypertensive rats (SHRs) and Sprague Dawley (SD) rats. We found that SD rats performed better after methylphenidate (MPH) treatment in salvage trials. Accordingly, the change of NRXN1 led to altered synapse-related gene (PSD95, SYN1, GAP43, NLGN1) expression, further providing evidence of its role in the maintenance of synaptic plasticity. We also verified that the expression of synapse-related genes synchronously changed with NRXN1expression in the behavioral assessment. The expression of NRXN1 was confirmed to affect the expression of synapse-related genes after its interference and overexpression in the primary hippocampal neurons in vitro. These results confirmed our hypothesis that NRXN1 might nucleate an overall trans-synaptic signaling network that controls synaptic plasticity and is responsible for impairments in learning and memory in ADHD. These findings suggest a possible protective role of NRXN1 in learning and memory in ADHD. Further RNA-seq sequencing revealed significant differences in the expression of 5-hydroxytryptamine receptor (5-HTR), which was further verified at the cellular level, and the mechanism of NRXN1 affecting synaptic plasticity was preliminarily discussed.
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http://dx.doi.org/10.1016/j.expneurol.2021.113806DOI Listing
October 2021

Activin A as a Novel Chemokine Induces Migration of L929 Fibroblasts by ERK Signaling in Microfluidic Devices.

Front Cell Dev Biol 2021 21;9:660316. Epub 2021 May 21.

Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun, China.

Activin A, a member of the transforming growth factor-beta (TGF-β) superfamily, contributes to tissue healing and fibrosis. As the innate tissue cells, fibroblasts also play an important role in wound healing and fibrosis. Herein, this study was aimed to investigate how activin A exhibited regulatory effects on adhesion and migration of fibroblasts. We found that activin A induced the migration of fibroblast cell line L929 cells in transwell chamber and microfluidic device. Activin A also promoted L929 cells adhesion, but did not affect L929 cells viability or proliferation. In addition, activin A induced α-SMA expression and TGF-β1 release, which were factors closely related to tissue fibrosis, but had no effect on IL-6 production, a pro-inflammatory cytokine. Furthermore, activin A elevated calcium levels in L929 cells and increased p-ERK protein levels. Activin A-induced migration of L929 cells was attenuated by ERK inhibitor FR180204. To conclude, these data indicated that activin A as a novel chemokine induced the chemotactic migration of L929 cells via ERK signaling and possessed the pro-fibrosis role. These findings provide a new insight into understanding of activin A in tissue fibrosis.
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http://dx.doi.org/10.3389/fcell.2021.660316DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8175620PMC
May 2021

The screening of immune-related biomarkers for prognosis of lung adenocarcinoma.

Bioengineered 2021 12;12(1):1273-1285

Department of Geriatrics, Peking University First Hospital, Beijing, China.

Lung adenocarcinoma (LUAD) accounts for a frequently seen non-small cell lung cancer (NSCLC) histological subtype, and it is associated with dismal prognostic outcome. However, the benefits of traditional treatment are still limited, and the efficacies of immunotherapy are quite different. Therefore, it is of great significance to identify novel immune-related therapeutic targets in lung adenocarcinoma. In this study, we identified a set of immune-related biomarkers for prognosis of lung adenocarcinoma, which could provide new ideas for immunotherapy of lung adenocarcinoma. Datasets related to LUAD were filtered from the GEO database. The appropriate packages were used to identify differentially expressed genes (DEGs) and to carry out enrichment analysis, followed by the construction of prognostic biomarkers. The Kaplan-Meier (K-M) curves were plotted to analyze patient survival based on hub genes. Associations between the expression of selected biomarkers and six types of tumor-infiltrating immune cells were evaluated based on the online tool TIMER. After analyzing five GEO datasets(GSE32867, GSE46539, GSE63459, GSE75037 and GSE116959), we discovered altogether 67 DEGs, among which, 15 showed up-regulation while 52 showed down-regulation. Enrichments of integrated DEGs were identified in the ontology categories. CAV1, CFD, FMO2 and CLEC3B were eventually selected as independent prognostic biomarkers, they were correlated with clinical outcomes of LUAD patients. Moreover, a positive correlation was observed between biomarker expression and all different types of immune infiltration, and the expression level of the four biomarkers was all positively related to macrophage.
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http://dx.doi.org/10.1080/21655979.2021.1911211DOI Listing
December 2021

Activin A impairs ActRIIA neutrophil recruitment into infected skin of mice.

iScience 2021 Feb 21;24(2):102080. Epub 2021 Jan 21.

Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun 130021, China.

Activin A levels are elevated during multiple severe infections and associated with an increased risk of death. However, the role of activin A in bacterial infection is still unclear. Here, we found that activin A levels were increased during skin infection in mice. Administration of activin A increased the bacterial burden and promoted the spread of bacteria . Moreover, activin A inhibited neutrophil chemotaxis to N-formylmethionine-leucyl-phenylalanine via the type IIA activin receptor (ActRIIA) and impaired ActRIIA neutrophil recruitment to infection foci . Additionally, we identified a novel subpopulation of neutrophils, ActRIIA neutrophils, which exhibit superior phagocytic capacity compared to ActRIIA neutrophils and possess an N2-like immunoregulatory activity via secreting IL-10 and TGF-β. Taken together, these findings indicate that activin A inhibits the recruitment of ActRIIA neutrophils to infected foci, leading to the impairment of bacterial clearance, and thus may hamper early infection control.
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http://dx.doi.org/10.1016/j.isci.2021.102080DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7873648PMC
February 2021

Antagonistic effects of activin A and TNF-α on the activation of L929 fibroblast cells via Smad3-independent signaling.

Sci Rep 2020 11 26;10(1):20623. Epub 2020 Nov 26.

Department of Immunology, College of Basic Medical Sciences, Jilin University, 126 Xinmin Street, Changchun, 130021, Jilin, China.

Fibroblasts play an important role in inflammation and tissue fibrosis. Both activin A and TNF-α can activate immune cells, however, the roles and relationship of them in activating fibroblasts in inflammation remain unclear. Here, this study revealed that TNF-α promoted the release of NO and IL-6 by L929 fibroblast cells, but co-treatment with activin A attenuated these effects. In contrast, activin A induced cell migration and increased the production of tissue fibrosis-related TGF-β1 and fibronectin, while TNF-α inhibited these function changes of L929 cells induced by activin A. Moreover, this study revealed that activin A and TNF-α regulated the activities of L929 cells via ERK1/2/MAPK pathway, rather than Smad3-dependent signaling pathway. Taken together, these data indicate that activin A and TNF-α exert mutually antagonistic effects on regulating fibroblasts activities, and the balance between their action may determine the process and outcome of fibroblasts-mediated inflammation.
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http://dx.doi.org/10.1038/s41598-020-77783-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7693280PMC
November 2020

Orbital climate variability on the northeastern Tibetan Plateau across the Eocene-Oligocene transition.

Nat Commun 2020 10 16;11(1):5249. Epub 2020 Oct 16.

State Key Laboratory of Loess and Quaternary Geology, Institute of Earth Environment, Chinese Academy of Sciences, Xi'an, China.

The first major build-up of Antarctic glaciation occurred in two consecutive stages across the Eocene-Oligocene transition (EOT): the EOT-1 cooling event at ~34.1-33.9 Ma and the Oi-1 glaciation event at ~33.8-33.6 Ma. Detailed orbital-scale terrestrial environmental responses to these events remain poorly known. Here we present magnetic and geochemical climate records from the northeastern Tibetan Plateau margin that are dated precisely from ~35.5 to 31 Ma by combined magneto- and astro-chronology. These records suggest a hydroclimate transition at ~33.7 Ma from eccentricity dominated cycles to oscillations paced by a combination of eccentricity, obliquity, and precession, and confirm that major Asian aridification and cooling occurred at Oi-1. We conclude that this terrestrial orbital response transition coincided with a similar transition in the marine benthic δO record for global ice volume and deep-sea temperature variations. The dramatic reorganization of the Asian climate system coincident with Oi-1 was, thus, a response to coeval atmospheric CO decline and continental-scale Antarctic glaciation.
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http://dx.doi.org/10.1038/s41467-020-18824-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7567875PMC
October 2020

Does the time from symptom onset to surgery affect the outcomes of patients with acute appendicitis? A prospective cohort study of 255 patients.

Asian J Endosc Surg 2021 Jul 29;14(3):361-367. Epub 2020 Sep 29.

Department of Surgery, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China.

Introduction: The objective of this study was to evaluate the impact of operative timing on outcomes of acute appendicitis.

Methods: This study examined adult patients who had presented to the hospital with acute appendicitis and had undergone appendectomy from December 2017 to February 2019. Time delay and outcomes of perforated and non-perforated appendicitis were compared. Patients were classified into five groups based on the period from symptom onset to operation: group 1, <24 hours; group 2, ≥24 and <48 hours; group 3, ≥48 and <72 hours; group 4, ≥72 and <96 hours; and group 5, ≥96 hours. The five groups were compared, with risk of perforation assessed in particular.

Results: A total of 255 patients were included in the analysis. Symptom duration, operative time, and length of postoperative hospital stay (P < .001) were significantly longer in the perforated group (n = 49) than in the non-perforated group (n = 206). The perforated group also had a higher conversion rate to open procedures (P = .002) and a higher rate of wound infection (P = .034). Group 1 had 53 patients, group 2 had 95 patients, group 3 had 57 patients, group 4 had 32 patients, and group 5 had 18 patients. The incidence of appendiceal perforation and median operative time progressively increased along with symptom duration in the five groups. In multivariate analyses, independent risk factors for appendiceal perforation were male gender (odds ratio = 2.33, 95% confidence interval [CI]: 1.07-5.08) and symptom duration ≥48 hours (relative to ≥24 and <48 hours) (odds ratio = 4.64, 95%CI: 1.76-12.27). Patients with symptom duration ≥72 hours had a significantly longer operative time than those with symptom duration ≥48 and <72 hours (β = 21.38, 95%CI: 5.66-37.11, P = .008).

Conclusion: The risk of perforation increased significantly 48 hours after the onset of appendicitis. Symptoms duration ≥72 hours was associated with a longer operative time.
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http://dx.doi.org/10.1111/ases.12870DOI Listing
July 2021

Distinct long non-coding RNA and mRNA expression profiles in the hippocampus of an attention deficit hyperactivity disorder model in spontaneously hypertensive rats and control wistar Kyoto rats.

Brain Res Bull 2020 08 25;161:177-196. Epub 2020 Apr 25.

Department of Child Healthcare, Women's Hospital of Nanjing Medical University (Nanjing Maternity and Child Health Care Hospital), Nanjing, 210004, China. Electronic address:

The incidence of attention deficit hyperactivity disorder (ADHD) in children is increasing. Long non-coding RNAs (lncRNAs) participate in many biological processes involved in the regulation of gene expression. Although numerous lncRNAs have been proven to be crucial in brain development and associated with its degeneration, changes in lncRNA expression profiles during ADHD progression and their possible roles remain unclear. The purpose of this study is to investigate the expression profiles of lncRNAs in hippocampus from an ADHD model in spontaneously hypertensive rats (SHRs) and in normal control Wistar Kyoto (WKY) rats. We determined the expression profiles of lncRNAs and mRNAs in SHRs and WKY rats using microarray analysis technology. Then, differentially expressed lncRNAs were confirmed by real-time polymerase chain reaction (RT-PCR). Gene Ontology (GO) and pathway analysis of differentially expressed mRNAs or nearby genes was used to predict the possible functions of the lncRNAs. A gene co-expression network was established to study the relationship between expression of lncRNAs and related mRNAs. A total of 267 differentially expressed lncRNAs (including 144 upregulated and 123 downregulated) and 311 differentially expressed mRNAs were identified in SHRs, compared to those in WKY rats. Subsequently, 15 lncRNAs were selected and confirmed by RT-PCR analysis. GO and Kyoto Encyclopedia of Genes and Genome (KEGG) pathway analysis showed that the dysregulated lncRNAs are involved in brain developmental processes and neuronal function and maintenance. Co-expression network analysis revealed the close relationship between the differentially expressed lncRNAs and mRNAs. Additionally, co-expression analysis of dysregulated lncRNAs with their downstream genes, which are reported in nervous system and regulation of learning and memory, indicated that lncRNA NONRATT0006598.2 was related to Baiap2 gene, which may participate in ADHD progress. Our findings contribute to understand the importance of lncRNAs and mRNAs in the progression of ADHD, and identify potential therapeutic targets for ADHD treatment.
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http://dx.doi.org/10.1016/j.brainresbull.2020.03.015DOI Listing
August 2020

Overexpression of Krüppel-Like Factor 4 Suppresses Migration and Invasion of Non-Small Cell Lung Cancer Through c-Jun-NH2-Terminal Kinase/Epithelial-Mesenchymal Transition Signaling Pathway.

Front Pharmacol 2019 8;10:1512. Epub 2020 Jan 8.

Department of Geriatrics, Peking University First Hospital, Beijing, China.

Krüppel-like factor 4 (KLF4) is a transcription factor and plays a vital role in cancer initiation and development. However, the role of Krüppel-like factor 4 in the metastasis of non-small cell lung cancer (NSCLC) is not clear. Here, we demonstrated that the expression of Krüppel-like factor 4 was significantly decreased in human non-small cell lung cancer tissues compared with that in normal tissues using Western blot. We performed immunohistochemical staining and observed the decreased expression of Krüppel-like factor 4 in human lung cancer tissues, and metastatic tumor tissues located in the trachea and main bronchus. We also found that the E-cadherin expression was decreased, while vimentin expression was increased in human NSCLC tissues and metastatic tumor tissues located in the trachea and main bronchus. Additionally, enforced expression of Krüppel-like factor 4 in mouse lungs significantly inhibited the metastasis of circulating Lewis lung carcinoma cells to the lungs by attenuating mesenchymal-epithelial transition (MET). Furthermore, cell scratch assays and Matrigel invasion assays revealed that overexpression of Krüppel-like factor 4 inhibited the migration and invasion of non-small cell lung cancer cell lines A549, H1299, H226, and H1650 cells. Moreover, overexpression of Krüppel-like factor 4 attenuated TGF-β1-induced epithelial-mesenchymal transition (EMT) in A549, and inhibited the phosphorylation of c-Jun-NH2-terminal kinase (JNK), an important pathway in metastasis in non-small cell lung cancer. Our and findings illustrate that Krüppel-like factor 4 inhibited metastasis and migration of non-small cell lung cancer, and indicate that Krüppel-like factor 4 could be a potential therapeutic target for the treatment of non-small cell lung cancer.
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http://dx.doi.org/10.3389/fphar.2019.01512DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6960180PMC
January 2020

FOXO3a is stabilized by USP18-mediated de-ISGylation and inhibits TGF-β1-induced fibronectin expression.

J Investig Med 2020 03 23;68(3):786-791. Epub 2019 Dec 23.

Department of Anesthesia, Jilin University First Hospital, Changchun, China

FOXO3a belongs to a family of transcription factors characterized by a conserved forkhead box DNA-binding domain. It has been known to regulate various cellular processes including cell proliferation, apoptosis and differentiation. Post-translational modifications of FOXO3a and their roles in the regulation of FOXO3a activity have been well-documented. FOXO3a can be phosphorylated, acetylated and ubiquitinated, however, the ISGylation of FOXO3a has not been reported. Protein overexpression, ISGylation and half-life were measured to determine the post-translational modification of FOXO3a. Human fibroblast cells were treated with transforming growth factor (TGF)-β1 to determine the role of FOXO3a ISGylation in TGF-β1 signaling. FOXO3a's half-life is around 3.7 hours. Inhibition of the proteasome, not lysosome, extends its half-life. ISGylation, but not ubiquitination of FOXO3a, is increased in the presence of the proteasome inhibitor. Overexpression of ISG15 increases FOXO3a degradation, while overexpression of USP18 stabilizes FOXO3a through de-ISGylation. These results suggest that FOXO3a is degraded in the ISGylation and proteasome system, which can be reversed by USP18, an ISG15-specific deubiquitinase. This study reveals a new molecular mechanism by which ISGylation regulates FOXO3a degradation. Furthermore, we show that the overexpression of FOXO3a attenuated TGF-β1-induced fibronectin expression in human lung fibroblast cells without altering Smad2/3 expression and activation. FOXO3a can be ISGylated, which can regulate FOXO3a stability. USP18/FOXO3a pathway is a potential target for treating TGF-β1-mediated fibrotic diseases such as idiopathic pulmonary fibrosis.
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http://dx.doi.org/10.1136/jim-2019-001145DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7057795PMC
March 2020

Spatial distribution of fluoride in drinking water and health risk assessment of children in typical fluorosis areas in north China.

Chemosphere 2020 Jan 7;239:124811. Epub 2019 Sep 7.

Institute of Environment and Health, Tianjin Centers for Disease Control and Prevention, Tianjin, 300011, China. Electronic address:

China has been suffering from endemic fluorosis for the past 30 years. This study investigated fluoride concentrations in 10 districts of Tianjin, China, to illustrate their spatial distribution characteristics and potential human health risks. The results showed fluoride concentration of 0.01-6.30 mg L with a mean value of 0.99 mg L, and 78.82% of water fluoride reaches the standard for drinking water (1.5 mg L). Higher fluoride levels were recorded in deep well pumps supply zones, and more potential changes in fluoride occurred was positively correlated with pH in groundwater. Mean value of fluoride in drinking water in 10 districts followed the order of WQ > BC > JZ > NH > BD > BH > JN > JH > DL > XQ. Estimations of non-carcinogenic risk for drinking water indicated that mean hazard quotient values of fluoride for combined pathways (i.e., oral ingestion and dermal absorption) were >1.0 for all age groups of WQ and BC. The results also showed that the estimated risk primarily came from the ingestion pathway. Risk levels for children varied obviously, generally in the order of 1-4y > 4-7y > 7-9y (years old). In the central tendency center and reasonable maximum exposure conditions, estimated risks were 1.25, 1.12, 0.771 and 3.66, 3.29, 2.27, respectively. The results supply material information for health authorities in fluorosis areas to put forward more efficient policies to control the endemic diseases. Attention should be paid to the formulation of health promotion strategies and measures to reduce fluoride intake in order to protect the health of residents.
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http://dx.doi.org/10.1016/j.chemosphere.2019.124811DOI Listing
January 2020

Involvement of CHOP in activin A‑induced myeloma NS‑1 cell apoptosis.

Oncol Rep 2019 Dec 22;42(6):2644-2654. Epub 2019 Oct 22.

Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.

Activin A, a multifunctional cytokine, is a member of transforming growth factor‑β (TGF‑β) superfamily. It is associated with a variety of pathophysiological processes, including inflammation, fibrosis, and tumorigenesis. Chronic or prolonged endoplasmic reticulum (ER) stress can lead to cells apoptosis. However, whether ER stress‑related proteins, such as CHOP, GADD34 are involved in activin A‑induced myeloma cell apoptosis remains unknown. In the present study, it was revealed that activin A inhibited the proliferation of myeloma cell line NS‑1 cells and induced NS‑1 cell apoptosis. Activin A upregulated the expression of CHOP, GADD34, caspase‑3, and caspase‑12. Moreover, both Smad3 and p‑Smad3 levels were increased with treatment of activin A. Further studies revealed that the overexpression of activin signaling protein Smad3 in NS‑1 cells increased the levels of CHOP, caspase‑3, and p‑Smad3. These data indicated that the CHOP protein of the ER stress pathway may be involved in activin A‑induced NS‑1 cell apoptosis, and also indicated the potential therapy of activin A‑induced apoptosis via CHOP signaling for multiple myeloma.
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http://dx.doi.org/10.3892/or.2019.7382DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6859442PMC
December 2019

Inhibitory effect of activin A on IL-9 production by mouse NK cells through Smad3 signaling.

Biol Chem 2020 02;401(2):297-308

Department of Immunology, College of Basic Medical Sciences, Jilin University, 126 Xinmin Street, Changchun 130021, China.

Interleukin-9 (IL-9) is a cytokine secreted by T-helper (Th)9 cells, and activin A can enhance Th9 cell differentiation. However, whether activin A affects IL-9 production by natural killer (NK) cells remains unclear. Herein, we found that not only Th cells, but also CD3-CD49b+NKp46+ NK cells of Balb/c mice produced IL-9. Although activin A promoted IL-9 expression in CD4+ Th cells, it inhibited IL-9 production by CD49b+NKp46+ NK cells in mice. Furthermore, the enzyme-linked immunosorbent assay (ELISA) results showed that mouse NK cells could secrete mature IL-9 protein, and activin A inhibited IL-9 release by NK cells. Additionally, activin A inhibited interferon (IFN)-γ production in splenic NK cells in mice, but promoted IL-2 production, and did not alter the production of IL-10. Western blotting results showed that levels of activin type IIA receptor (ActRIIA), Smad3 and phosphorylated-Smad3 (p-SMAD3) protein increased in activin A-treated splenic NK cells, compared with that in control NK cells. The inhibitory effects of activin A on IL-9 production by NK cells were attenuated in the presence of activin antagonist follistatin (FST) or Smad3 knockdown to NK cells. These data suggest that although activin A up-regulates IL-9 expression in Th cells, it inhibits IL-9 production in NK cells through Smad3 signaling.
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http://dx.doi.org/10.1515/hsz-2019-0245DOI Listing
February 2020

Profiling the long noncoding RNA interaction network in the regulatory elements of target genes by chromatin in situ reverse transcription sequencing.

Genome Res 2019 09 17;29(9):1521-1532. Epub 2019 Jul 17.

Key Laboratory of Organ Regeneration and Transplantation of Ministry of Education, Cancer Center, The First Hospital of Jilin University, Changchun, Jilin 130061, P.R. China.

Long noncoding RNAs (lncRNAs) can regulate the activity of target genes by participating in the organization of chromatin architecture. We have devised a "chromatin-RNA in situ reverse transcription sequencing" (CRIST-seq) approach to profile the lncRNA interaction network in gene regulatory elements by combining the simplicity of RNA biotin labeling with the specificity of the CRISPR/Cas9 system. Using gene-specific gRNAs, we describe a pluripotency-specific lncRNA interacting network in the promoters of and , two critical stem cell factors that are required for the maintenance of pluripotency. The promoter-interacting lncRNAs were specifically activated during reprogramming into pluripotency. Knockdown of these lncRNAs caused the stem cells to exit from pluripotency. In contrast, overexpression of the pluripotency-associated lncRNA activated the promoters of core stem cell factor genes and enhanced fibroblast reprogramming into pluripotency. These CRIST-seq data suggest that the and promoters are organized within a unique lncRNA interaction network that determines the fate of pluripotency during reprogramming. This CRIST approach may be broadly used to map lncRNA interaction networks at target loci across the genome.
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http://dx.doi.org/10.1101/gr.244996.118DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6724666PMC
September 2019

Perspectives of small molecule inhibitors of activin receptor‑like kinase in anti‑tumor treatment and stem cell differentiation (Review).

Mol Med Rep 2019 Jun 30;19(6):5053-5062. Epub 2019 Apr 30.

Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.

Activin receptor‑like kinases (ALKs), members of the type I activin receptor family, belong to the serine/threonine kinase receptors of the transforming growth factor‑β (TGF‑β) superfamily. ALKs mediate the roles of activin/TGF‑β in a wide variety of physiological and pathological processes, ranging from cell differentiation and proliferation to apoptosis. For example, the activities of ALKs are associated with an advanced tumor stage in prostate cancer and the chondrogenic differentiation of mesenchymal stem cells. Therefore, potent and selective small molecule inhibitors of ALKs would not only aid in investigating the function of activin/TGF‑β, but also in developing treatments for these diseases via the disruption of activin/TGF‑β. In recent studies, several ALK inhibitors, including LY‑2157299, SB‑431542 and A‑83‑01, have been identified and have been confirmed to affect stem cell differentiation and tumor progression in animal models. This review discusses the therapeutic perspective of small molecule inhibitors of ALKs as drug targets in tumor and stem cells.
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http://dx.doi.org/10.3892/mmr.2019.10209DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6522871PMC
June 2019

800-kyr land temperature variations modulated by vegetation changes on Chinese Loess Plateau.

Nat Commun 2019 04 29;10(1):1958. Epub 2019 Apr 29.

State Key Laboratory of Loess and Quaternary Geology, Institute of Earth Environment, Chinese Academy of Sciences, 710061, Xi'an, China.

The complicity of long-term land surface temperature (LST) changes has been under investigated and less understood, hindering our understanding of the history and mechanism of terrestrial climate change. Here, we report the longest (800 thousand years) LSTs based on distributions of soil fossil bacterial glycerol dialkyl glycerol tetraethers preserved in well-dated loess-paleosol sequences at the center of the Chinese Loess Plateau. We have found a previously-unrecognized increasing early and prolonged warming pattern toward the northwestern plateau at the onset of the past seven deglaciations, corresponding to the decrease in vegetation coverage, suggesting underlying surface vegetation or lack of has played an important role in regulating LSTs, superimposed on the fundamental global glacial-interglacial changes. Our results support that LSTs in semi-humid and semi-arid regions with little vegetation will be more sensitive to the anticipated global temperature rise, while improving vegetation coverage would reduce LSTs and thus ecological impacts.
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http://dx.doi.org/10.1038/s41467-019-09978-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6488643PMC
April 2019

Eastern equatorial Pacific cold tongue evolution since the late Miocene linked to extratropical climate.

Sci Adv 2019 Apr 3;5(4):eaau6060. Epub 2019 Apr 3.

College of Earth, Ocean, and Atmospheric Sciences, Oregon State University, Corvallis, OR 97331, USA.

The timing and mechanisms of the eastern equatorial Pacific (EEP) cold tongue development, a salient feature of the tropical ocean, are intensely debated on geological time scales. Here, we reconstruct cold tongue evolution over the past 8 million years by computing changes in temperature gradient between the cold tongue and eastern Pacific warm pool. Results indicate that the cold tongue remained very weak between 8 and 4.3 million years ago, implying much weaker zonal temperature gradients prevailing during the late Miocene-Pliocene, but then underwent gradual intensification with apparently increasing sensitivity of the cold tongue to extratropical temperature changes. Our results reveal that the EEP cold tongue intensification was mainly controlled by extratropical climate.
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http://dx.doi.org/10.1126/sciadv.aau6060DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6447375PMC
April 2019

Activin A regulates activities of peripheral blood natural killer cells of mouse in an autocrine and paracrine manner.

Exp Cell Res 2019 01 17;374(1):114-121. Epub 2018 Nov 17.

Department of Physiology, College of Basic Medical Sciences, Jilin University, Changchun 130021, China. Electronic address:

Activin A, a multifunctional cytokine of transforming growth factor-β (TGF-β) superfamily, can be produced by the diverse immune cells. NK cells in peripheral blood are one of the major immune cells applied to cancer therapy in recent years. However, whether activin A can be produced by natural killer (NK) cells and be involved in regulation of peripheral blood NK cells activities of mouse are not well characterized. Here, we found that activin type IIA and IIB receptors and signaling molecules Smad2, 3 were expressed in peripheral blood NK cells of mouse by flow cytometry and RT-PCR. The cultured blood NK cells of mouse not only produced activin βA chain protein by intracellular cytokine staining, but also secreted mature activin A protein by enzyme-linked immunosorbent assay (ELISA), and the production was promoted by IL-2. In addition, IL-2 as a positive control obviously promoted IFNγ production of mouse blood NK cells in vitro. However, activin A suppressed IFNγ production, but enhanced IL-2 synthesis and did not alter IL-10 production. Moreover, we found that activin A significantly suppressed the ability of NK cells to lyse target cells. These data revealed that blood NK cells of mouse were not only the target cells in response to activin A, but also the source of activin A, suggesting that activin A may play an important role in regulation of NK cells activities of mouse in an autocrine / paracrine manner.
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http://dx.doi.org/10.1016/j.yexcr.2018.11.013DOI Listing
January 2019

Colorectal Surgery Training in the Hong Kong Special Administrative Region and China.

Ann Coloproctol 2018 Jun 30;34(3):111-118. Epub 2018 Jun 30.

Department of Surgery, The University of Hong Kong - Shenzhen Hospital, Shenzhen, China.

Until 1st July 1997, Hong Kong was under the governance of the British Government; therefore, the British system of education was followed. After internship, 7 years of general surgical training is required to obtain registration and fellowship qualifications of the College of Surgeon of Hong Kong and Edinburg. After having become a specialist in general surgery, the surgeon could choose to specialize in colorectal surgery with an additional 3 to 5 years of specialist training in an accredited centre and 6 months of overseas training with subsidies. On the contrary, China has more than 600 medical schools, and students can enroll in different programs to become a medical practitioner. Despite a great discrepancy exists in the quality of teaching and supervision but there are comprehensive regulations governing the accreditation of hospitals, credentialing of operations, medical records, etc. to ensure medical and patient safety. Vast amounts of resources are being invested to strengthen the quality and to advance the technology used in patient care, not only by supporting basic and clinical research but also by providing extra resources to "import" experts and help develop services with clinical excellence. To accomplish this, the aim of the "three fames project" with a 5-year funding of 3 million United States dollar is to invite overseas experts to help build medical teams in specific areas. Due to its huge population (more than 1.3 billion people), China is a country full of potential for development in clinical research, collaboration, knowledge exchange, and the provision of premier medical services.
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http://dx.doi.org/10.3393/ac.2018.05.28DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6046540PMC
June 2018

Interferon regulatory factor 3 mediates Poly(I:C)-induced innate immune response and apoptosis in non‑small cell lung cancer.

Int J Oncol 2018 May 5;52(5):1623-1632. Epub 2018 Mar 5.

Department of Geriatrics, Peking University First Hospital, Beijing 100034, P.R. China.

Immunotherapy is considered one of the most promising treatments for lung cancer. The cell signalling molecules melanoma differentiation-associated protein 5 (MDA5) and retinoic acid-inducible gene I protein (RIG‑I) are essential receptors that recognise intracellular pathogen-associated nucleic acids, whereas interferon regulatory factor 3 (IRF3) controls the expression of innate immunity-associated genes in macrophages. However, the innate immune response to polyinosinic:polycytidylic acid [Poly(I:C)] in lung cancer remains to be elucidated. In the present study, western blot analysis, reverse transcription-quantitative polymerase chain reaction, RNA interference, IRF3 plasmid construction, ELISA and apoptosis analysis were employed to study the innate immune response and apoptosis of non‑small cell lung cancer (NSCLC) cells. Poly(I:C) transfection in NSCLC cells triggered apoptosis via the extrinsic apoptotic pathway, and activated the innate immune response by promoting interferon-β and C-X-C motif chemokine ligand 10 expression. Treatment with the IκB kinase ε/tumour necrosis factor receptor-associated factor family member-associated nuclear factor-κB activator-binding kinase 1 inhibitor BX795, which inhibits IRF3 phosphorylation, or transfection with small interfering RNA/short hairpin RNA to downregulate MDA5, RIG‑I or IRF3, prior to Poly(I:C) transfection inhibited the innate immune response and apoptotic pathway. Conversely, IRF3 overexpression promoted activation of the apoptotic pathway, thus indicating that the MDA5/RIG‑I/IRF3 axis may mediate responses to Poly(I:C) transfection. Furthermore, phosphorylation of the transcription factor signal transducer and activator of transcription 1 (STAT1) was associated with the alterations in IRF3 phosphorylation and apoptosis, thus suggesting that STAT1 may be involved in Poly(I:C)-induced apoptosis. In NSCLC surgical samples, MDA5, RIG‑I and IRF3 were highly expressed, whereas the expression levels of phosphorylated‑IRF3 were reduced. These findings indicated that the function of the MDA5/RIG‑I/IRF3 axis may be impaired in some lung cancers. In conclusion, the present findings suggested that the MDA5/RIG‑I/IRF3 axis, which is associated with innate immunity, is intact in NSCLC cells, and IRF3 is involved in regulating the apoptotic pathway in NSCLC cells.
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http://dx.doi.org/10.3892/ijo.2018.4300DOI Listing
May 2018

Activin A induces apoptosis of mouse myeloma cells via the mitochondrial pathway.

Oncol Lett 2018 Feb 11;15(2):2590-2594. Epub 2017 Dec 11.

Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.

Activin A is a pleiotropic cytokine belonging to the transforming growth factor β superfamily. Abnormal expression of activin A is associated with tumorigenesis. Multiple myeloma is characterized by the development of osteolytic disease, which ultimately leads to cachexia. However, the involvement of activin A in myeloma cell viability and apoptosis remains to be fully elucidated. For this purpose, mouse myeloma NS-1 cells were treated with activin A, and subsequently subjected to 5-bromo-2'-deoxyuridine analysis, Hoechst 33342 staining, flow cytometry and western blot analysis. The results revealed that activin A significantly suppressed NS-1 cell viability, and induced NS-1 cell apoptosis. In addition, activin A-induced promotion of NS-1 cell apoptosis was accompanied by upregulated expression of BCL2 associated X, apoptosis regulator (Bax), but downregulated expression of B cell lymphoma-2 (Bcl-2), resulting in an increase of the Bax/Bcl-2 ratio. Furthermore, cytochrome and caspase-3 protein expression also increased following treatment with activin A. These data suggest that activin A induces apoptosis in mouse myeloma NS-1 cells via the mitochondrial pathway, providing a novel insight into multiple myeloma treatment.
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http://dx.doi.org/10.3892/ol.2017.7584DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5777288PMC
February 2018

Identification of risk factors for sepsis-associated mortality by gene expression profiling analysis.

Mol Med Rep 2018 Apr 25;17(4):5350-5355. Epub 2018 Jan 25.

Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.

Sepsis is a common cause of mortality due to systemic infection. Although numerous studies have investigated this life-threatening condition, there remains a lack of suitable markers to evaluate the severity of sepsis. The present study focused on the identification of risk factors for sepsis‑associated mortality by genome‑wide expression profiling. Initially, the GEO2R web tool was used to identify the differentially expressed genes (DEGs) between sepsis survivors and nonsurvivors. It was identified that the upregulated DEGs in the nonsurvivors compared with survivors were highly enriched in the type I interferon (IFN‑I) signaling pathway. Furthermore, the associations of the upregulated genes were analyzed by STRING and the results demonstrated that a set of proteins in IFN‑I signaling pathway closely interacted with each other. To further investigate whether the IFN‑I signaling pathway is dysregulated in a subset of patients with a high risk of mortality due to sepsis, in this case neonates, the DEGs between the cord blood mononuclear cells of neonates and adult peripheral blood mononuclear cells were analyzed. It was identified that DEGs were not enriched in IFN‑I signaling in the blood of untreated neonates and adults; however, IFN‑I signaling was upregulated in the lipopolysaccharide (LPS)‑treated cord blood mononuclear cells of healthy neonates compared with the LPS‑treated peripheral blood mononuclear cells of adults. In addition, these data revealed that the proteins involved in the IFN‑I signaling pathway possessed a higher number of interacting partners. These results indicated that upregulated IFN‑I signaling may be a high-risk factor for mortality due to sepsis.
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http://dx.doi.org/10.3892/mmr.2018.8491DOI Listing
April 2018

Krüpple-like-factor 4 Attenuates Lung Fibrosis via Inhibiting Epithelial-mesenchymal Transition.

Sci Rep 2017 Nov 20;7(1):15847. Epub 2017 Nov 20.

The Geriatrics Department, Peking University First Hospital, Beijing, China.

Epithelial-mesenchymal transition (EMT) plays an important role in the pathogenesis of idiopathic pulmonary fibrosis (IPF). Krüpple-like-factor 4 (KLF4), has been suggested to play an important role in the phenotype transition. However, its function in pulmonary fibrosis and EMT of human alveolar epithelial cells (AECs) remains unclear. This study aimed to examine the role of KLF4 in pulmonary fibrosis and EMT. Decreased expression of KLF4 was first observed in human IPF lung tissues and models of bleomycin-induced pulmonary fibrosis. Transgenic mice with overexpression of KLF4 were subjected to bleomycin-induced pulmonary fibrosis model and showed attenuated lung fibrosis and EMT compared to wild type group. Furthermore, the effects overexpression and knockdown of KLF4 on TGF-β1-induced EMT were examined in AECs. Adenovirus-mediated overexpression of KLF4 attenuated TGF-β1-induced EMT and activation of Smad2/3 and Dvl in AECs. Conversely, knockdown of KLF4 promoted the activation of pathways above mentioned and TGF-β1-induced EMT. Our results demonstrates that KLF4 plays an important role in bleomycin-induced lung fibrosis through suppressing TGFβ1-induced EMT. Thus, it may serve as a potential target for the treatment of pulmonary fibrosis.
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http://dx.doi.org/10.1038/s41598-017-14602-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5696468PMC
November 2017

Catch me if you can-How to make the best use of pleural effusion.

J Thorac Dis 2017 Aug;9(8):E664-E668

The Geriatrics Department, Peking University First Hospital, Beijing 100034, China.

Etiology diagnosis of pleural effusion is a commonly encountered yet challenging problem. How to make the best use of pleural effusion evokes thinking. Myelomatous pleural effusion (MPE) is a rare condition and has been reported sporadically. We report an extremely rare case of multiple myeloma (MM) [IgD-lambda (λ) type, stage III B] with MPE as initial presentation and complicated with massive pericardial effusions during the progression of the disease. Cytological identification of malignant plasma cells in pleural effusion is the most direct method to diagnose MPE. What we learn from this case is that cell block can increase the sensitivity of detecting malignancies compared with conventional smear. Doctors should make best use of pleural effusion before further invasive procedure.
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http://dx.doi.org/10.21037/jtd.2017.06.65DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5594196PMC
August 2017

Expression and anti-inflammatory role of activin receptor-interacting protein 2 in lipopolysaccharide-activated macrophages.

Sci Rep 2017 09 4;7(1):10306. Epub 2017 Sep 4.

Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun, China.

The bacterial endotoxin lipopolysaccharide (LPS), a key pathogenic stimulator, can induce the activation of macrophages. Activin receptor-interacting protein 2 (ARIP2), an intracellular signaling protein, has a wide histological distribution, however, whether ARIP2 is involved in regulation of activation of macrophages was not well characterized. Here, by immunocytochemical staining, we found that ARIP2 protein existed in monocyte-macrophage cell line RAW264.7 cells and peritoneal macrophages of mouse, and ARIP2 expression in RAW264.7 cells was up-regulated by LPS. Furthermore, the results revealed that ARIP2 overexpression in the LPS-activated RAW264.7 cells inhibited the productions of IL-1β and TNFα, phagocytic activities and CD14 expression, whereas did not alter expressions of MyD88, TLR2 and TLR4. Additionally, in vivo ARIP2 overexpression also reduced the productions of IL-1β and TNFα from the LPS-stimulated peritoneal macrophages of mouse. These data suggest that ARIP2 may play an anti-inflammatory role in macrophages via inhibiting CD14 expression.
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http://dx.doi.org/10.1038/s41598-017-10855-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5583376PMC
September 2017

Activin A regulates activation of mouse neutrophils by Smad3 signalling.

Open Biol 2017 05;7(5)

Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun 130021, People's Republic of China

Activin A, a member of the transforming growth factor beta superfamily, acts as a pro-inflammatory factor in acute phase response, and influences the pathological progress of neutrophil-mediated disease. However, whether activin A can exert an effect on the activities of neutrophils remains unclear. In this study, we found that the release of activin A was enhanced from neutrophils of mouse when stimulated with lipopolysaccharide. Furthermore, neutrophils were not only the source of activin A but also the target cells in response to activin A, in which canonical activin signalling components existed, and levels of ACTRIIA, SMAD3 and p-SMAD3 proteins were elevated in activin A-treated neutrophils. Next, the role of activin A was determined in regulation of neutrophils activities. Our data revealed that activin A induced O release and reactive oxygen species production, promoted IL-6 release, and enhanced phagocytosis, but failed to attract neutrophils migrating across the trans-well membrane. Moreover, we found that effect of activin A on IL-6 release from the peritoneal neutrophils of mouse was significantly attenuated by knockdown. In summary, these data demonstrate that activin A can exert an effect on neutrophils activation in an autocrine/paracrine manner through Smad3 signalling, suggesting that activin A is an important regulator of neutrophils.
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http://dx.doi.org/10.1098/rsob.160342DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5451541PMC
May 2017

The effects of activin A on the migration of human breast cancer cells and neutrophils and their migratory interaction.

Exp Cell Res 2017 08 4;357(1):107-115. Epub 2017 May 4.

Department of Physics and Astronomy, University of Manitoba, Winnipeg, MB, Canada R3T 2N2. Electronic address:

Activin A belongs to the superfamily of transforming growth factor beta (TGFβ) and is a critical regulatory cytokine in breast cancer and inflammation. However, the role of activin A in migration of breast cancer cells and immune cells was not well characterized. Here, a microfluidic device was used to examine the effect of activin A on the migration of human breast cancer cell line MDA-MB-231 cells and human blood neutrophils as well as their migratory interaction. We found that activin A promoted the basal migration but impaired epidermal growth factor (EGF)-induced migration of breast cancer cells. By contrast, activin A reduced neutrophil chemotaxis and transendothelial migration to N-Formyl-Met-Leu-Phe (fMLP). Finally, activin A promoted neutrophil chemotaxis to the supernatant from breast cancer cell culture. Collectively, our study revealed the different roles of activin A in regulating the migration of breast cancer cells and neutrophils and their migratory interaction. These findings suggested the potential of activin A as a therapeutic target for inflammation and breast cancers.
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http://dx.doi.org/10.1016/j.yexcr.2017.05.003DOI Listing
August 2017

Clinical application value of impulse oscillometry in geriatric patients with COPD.

Int J Chron Obstruct Pulmon Dis 2017 15;12:897-905. Epub 2017 Mar 15.

Geriatrics Department, Peking University First Hospital, Beijing, People's Republic of China.

Background: The diagnosis and assessment of COPD rely mainly on the use of spirometry, which is an effort-dependent test and requires good patient cooperation. Impulse oscillometry (IOS) is a non-volitional method that requires less effort and cooperation and presents advantages for geriatric patients. However, the clinical application value of IOS in geriatric patients with COPD remains unclear.

Aim: The aim of this study was to investigate the clinical application value of IOS in geriatric patients with COPD.

Subjects And Methods: A total of 234 subjects were retrospectively enrolled in this study, including 133 patients with COPD and 101 healthy volunteers. All the participants underwent IOS and spirometry examination. The data were collected and analyzed in the overall group, the geriatric group (aged ≥65 years), and the advanced elderly group (aged ≥80 years).

Results: 1) In COPD patients, a significant increase in respiratory impedance (Z5), resonant frequency (Fres), and respiratory resistance (R5, R20, R5-R20) and a decrease in respiratory reactance (X5) were observed in the overall group, the geriatric group, and the advanced elderly group compared with the healthy control subjects. 2) The IOS parameters correlated well with spirometry in COPD. In particular, R5-R20 showed the best correlation with forced expiratory volume in 1 second (FEV) in the different age groups. 3) Fres and R5-R20 had the best diagnostic efficiency for COPD. The area under the curve (AUC) values for Fres, expressed by the receiver operating characteristic (ROC) curve, were 0.905, 0.909, and 0.914, for the different age groups, respectively. 4) The optimal cutoff values for Fres to diagnose airflow obstruction from ROC curves was 17.715 in the COPD patients. Its sensitivity and specificity were 0.789 and 0.931, respectively, and the cutoff values were similar in geriatric and advanced elderly patients.

Conclusion: IOS demonstrated good relevance compared with spirometry for geriatric patients with COPD. IOS may serve as an alternative method for spirometry in elderly subjects for the evaluation of the state of COPD.
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http://dx.doi.org/10.2147/COPD.S129974DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5358990PMC
August 2017
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