Publications by authors named "Qiu Ya"

35 Publications

Role of G Protein-Coupled Estrogen Receptor in Digestive System Carcinomas: A Minireview.

Onco Targets Ther 2021 14;14:2611-2622. Epub 2021 Apr 14.

Department of Breast Surgery, Jiangxi Cancer Hospital, Nanchang University Cancer Hospital, Nanchang, 330029, People's Republic of China.

Digestive system carcinomas are one of the leading causes of cancer-related deaths worldwide. G protein-coupled estrogen receptor (GPER), a novel estrogen receptor, has been recognized as an important mediator in numerous cancer types. Recently, the function and clinical significance of GPER in digestive system carcinomas has been a subject of interest. Increasing evidence has revealed that GPER plays an important role as a potential biomarker in digestive system carcinomas. This work summarizes the recent literature and focuses on the emerging functional role of GPER in digestive system carcinomas, including gastric cancer, hepatocellular carcinoma, pancreatic cancer, and colorectal cancer. The potential application of GPER in novel strategies for the diagnosis and treatment of digestive system carcinomas is discussed and highlighted.
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http://dx.doi.org/10.2147/OTT.S291896DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8055353PMC
April 2021

Current progress and quality of radiomic studies for predicting EGFR mutation in patients with non-small cell lung cancer using PET/CT images: a systematic review.

Br J Radiol 2021 May 12:20201272. Epub 2021 May 12.

Department of Radiology, The First People's Hospital of Kashi Area, Kashi, Xinjiang, China.

Objectives: To assess the methodological quality of radiomic studies based on positron emission tomography/computed tomography (PET/CT) images predicting epidermal growth factor receptor (EGFR) mutation status in patients with non-small cell lung cancer (NSCLC).

Methods: We systematically searched for eligible studies in the PubMed and Web of Science datasets using the terms "radiomics", "PET/CT", "NSCLC", and "EGFR". The included studies were screened by two reviewers independently. The quality of the radiomic workflow of studies was assessed using the Radiomics Quality Score (RQS). Interclass correlation coefficient (ICC) was used to determine inter rater agreement for the RQS. An overview of the methodologies used in steps of the radiomics workflow and current results are presented.

Results: Six studies were included with sample sizes of 973 ranging from 115 to 248 patients. Methodologies in the radiomic workflow varied greatly. The first-order statistics were the most reproducible features. The RQS scores varied from 13.9 to 47.2%. All studies were scored below 50% due to defects on multiple segmentations, phantom study on all scanners, imaging at multiple time points, cut-off analyses, calibration statistics, prospective study, potential clinical utility, and cost-effectiveness analysis. The ICC results for majority of RQS items were excellent. The ICC for summed RQS was 0.986 [95% confidence interval (CI): 0.898-0.998].

Conclusions: The PET/CT-based radiomics signature could serve as a diagnostic indicator of EGFR mutation status in NSCLC patients. However, the current conclusions should be interpreted with care due to the suboptimal quality of the studies. Consensus for standardization of PET/CT-based radiomic workflow for EGFR mutation status in NSCLC patients is warranted to further improve research.

Advances In Knowledge: Radiomics can offer clinicians better insight into the prediction of EGFR mutation status in NSCLC patients, whereas the quality of relative studies should be improved before application to the clinical setting.
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http://dx.doi.org/10.1259/bjr.20201272DOI Listing
May 2021

GPER-Induced ERK Signaling Decreases Cell Viability of Hepatocellular Carcinoma.

Front Oncol 2021 9;11:638171. Epub 2021 Mar 9.

Department of Breast Surgery, Jiangxi Cancer Hospital, Nanchang University Cancer Hospital, Nanchang, China.

Hepatocellular carcinoma (HCC) is an aggressive malignancy with a poor prognosis. Effective biomarkers and specific therapeutic targets for HCC are therefore urgently needed. G protein-coupled estrogen receptor (GPER) plays a crucial role in numerous cancer types; however, its functions in HCC require further exploration. In the present study, we found a remarkable difference in GPER staining between tumor tissue (100/141, 70.9%) and matched non-tumor tissue (27/30, 90.0%). Compared with the GPER-negative patients, the GPER-positive patients with HCC were closely associated with female sex, negative hepatitis B surface antigen, small tumor size, low serum alpha fetoprotein level, and longer overall survival. Treatment with GPER-specific agonist G1 led to the sustained and transient activation of the EGFR/ERK and EGFR/AKT signaling pathways, respectively, in the HCC cell lines HCCLM3 and SMMC-7721, which express high levels of GPER. Interestingly, G1-induced EGFR/ERK signaling, rather than EGFR/AKT signaling mediated by GPER, was involved in decreasing cell viability by blocking cell cycle progression, thereby promoting apoptosis and inhibiting cell growth. Clinical analysis indicated that simultaneous high expression of GPER and phosphorylated-ERK (p-ERK) predicted improved prognosis for HCC. Finally, the activation of GPER/ERK signaling remarkably suppressed tumor growth in an HCC xenograft model, and this result was consistent with the data. Our findings suggest that specific activation of the GPER/ERK axis may serve as a novel tumor-suppressive mechanism and that this axis could be a therapeutic target for HCC.
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http://dx.doi.org/10.3389/fonc.2021.638171DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7985169PMC
March 2021

The Role of Leisure Satisfaction in Serious Leisure and Subjective Well-Being: Evidence From Chinese Marathon Runners.

Front Psychol 2020 10;11:581908. Epub 2020 Nov 10.

Department of Physical Education, College of Education, Zhejiang University, Hangzhou, China.

The topics of serious leisure and subjective well-being have been discussed extensively in previous research. It is generally acknowledged that people prefer to experience deeper satisfaction and happiness through serious participation in leisure-time physical activities. However, it is essential to examine the relationship between serious leisure and subjective well-being in an urban setting as well as the mediating effect of leisure satisfaction. Data were collected from 447 recreational runners at the 2018 Wuxi International Marathon event in China. The study results showed that serious leisure was positively associated with leisure satisfaction and subjective well-being, that leisure satisfaction was positively associated with subjective well-being, and that leisure satisfaction completely mediated the relationship between serious leisure and subjective well-being. Running group membership significantly affected the path from serious leisure to leisure satisfaction, while other demographic variables (e.g., gender and education) did not moderate any paths. These results help explain the intricate relationship between serious leisure and subjective well-being and offer theoretical and managerial implications for serious leisure.
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http://dx.doi.org/10.3389/fpsyg.2020.581908DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7720892PMC
November 2020

Cattle Encephalon Glycoside and Ignotin Protects Neurons Against Microglia-Induced Neuroinflammation via Elevating BDNF Expression and Inhibiting TLR4/NF-κB Pathway.

Neurochem Res 2021 Feb 13;46(2):326-336. Epub 2020 Nov 13.

Department of Geriatrics, Second Hospital of Hebei Medical University, Shijiazhuang, 05000, Hebei, China.

Neuroinflammation is involved in the pathology and progression of Alzheimer's disease (AD) and is closely related to microglial activation. We have previously reported that cattle encephalon glycoside and ignotin (CEGI) could inhibit the activation of microglia in APP/PS1 mice, a mouse model of familial AD. However, the anti-neuroinflammatory mechanisms of CEGI have not yet been fully elucidated. Here, we aimed to investigate the role of CEGI in microglia-mediated neuroinflammation in AD. APP/PS1 mice were treated with CEGI intraperitoneally for 30 days, and then their cognition was assessed. We showed that CEGI alleviated cognitive damage with higher nesting scores, preferential indices, and spontaneous alternation rates in APP/PS1 mice. Moreover, CEGI treatment effectively reduced microglial activation and Iba-1 levels in the cortex of APP/PS1 mice. Additionally, CEGI decreased pro-inflammatory factors production and neuroinflammation-mediated neuronal damage in vivo and in vitro. Finally, CEGI upregulated BDNF levels and downregulated TLR4 and p-NF-κB p65 levels in vivo and in vitro. Taken together, these findings indicated that CEGI could attenuate cognitive deficits in APP/PS1 mice and suppress microglia-induced neuroinflammation via increasing BDNF expression and inhibiting the TLR4/NF-κB pathway.
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http://dx.doi.org/10.1007/s11064-020-03168-yDOI Listing
February 2021

Lipids monitoring in based on terahertz technology.

Biotechnol Biofuels 2020 16;13:161. Epub 2020 Sep 16.

Terahertz Technology Innovation Research Institute, Terahertz Spectrum and Imaging Technology Cooperative Innovation Center, Shanghai Key Lab of Modern Optical System, University of Shanghai for Science and Technology, Shanghai, 200093 China.

Background: Microalgae are considered as a source of low pollution and renewable fuel due to their ability to synthesize an abundance of lipids. Conventional methods for lipid quantification are time-consuming and chemically contaminated, while spectroscopic method combined with mathematical model is much more attractive due to its ability of qualitative and quantitative analysis of material composition, in this sense, terahertz technology provides not only timely and non-destructive testing without chemical pollution, but also provides information on the functional group vibration mode and structure of the measured components. Therefore, terahertz technology is utilized in our investigation and proposed for microalgae metabolism detection.

Results: The aim of this study was to use terahertz spectroscopy to observe lipid content in (). We collected the THz spectra of which were cultivated under nitrogen stress and terahertz spectroscopy was used to analyze changes in substance components (lipids, proteins, carbohydrates and β-carotene). The PLS algorithm was used to model the terahertz data to distinguish the different lipid content of under nitrogen stress. The correlation coefficient of the prediction results of the lipid characteristic band modeling was above 0.991, and the root mean square error was less than 0.132. It indicated that terahertz technology can be used to discriminate cells under different nitrogen stress effectively. The correlation between the terahertz characteristic peak (9.3 THz) and the total lipid content determined by gravimetry reaches 0.960. The final results were compared with the commonly used spectroscopic methods for lipid observation (Raman spectroscopy).

Conclusions: In this article, we demonstrated the effectiveness of terahertz spectroscopy to monitor changes in microalgae lipid content under nitrogen stress. Terahertz spectroscopy is more suitable for industrial production or ordinary laboratories which require intermediate result with low-frequency screening. When quantifying microalgae lipids, the constraint of terahertz spectroscopy is far less than that of Raman spectroscopy, and it is easier for operator to accurately quantify microalgae lipid. In addition, it is still in early stage for the study of microalgae using terahertz spectroscopy technology, there is still much potential for us to explore.
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http://dx.doi.org/10.1186/s13068-020-01801-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7493189PMC
September 2020

Rapamycin Promotes Cardiomyocyte Differentiation of Human Induced Pluripotent Stem Cells in a Stage-Dependent Manner.

Stem Cells Dev 2020 09 18;29(18):1229-1239. Epub 2020 Aug 18.

Department of Cardiology & National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital & Medical School of Chinese PLA, Beijing, China.

Induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) are a promising source for cardiac regenerative therapy, and ideal for in vitro cell modeling of cardiovascular diseases and drug screening. Recent studies have shown that rapamycin can promote cardiomyocyte differentiation in various stem cells. However, how rapamycin affects cardiomyocyte differentiation of iPSCs is still not fully understood. This study aimed to investigate the effect of rapamycin on cardiomyocyte differentiation based on embryoid body (EB) method. First, to determine the autophagy induction protocol, different concentrations of rapamycin were applied in hEBs on day 6. The autophagy was most significant when applying rapamycin at 1 μM for 48 h, demonstrating by the LC3II/LC3I ratio and p62 expression. Then, 1 μM rapamycin was applied for 48 h at different time points of cardiomyocyte differentiation to investigate the role of rapamycin in this process. Compared with control, rapamycin applied on days 0-4 of differentiation significantly decreased the proportion of beating EBs and expression of cardiomyocyte-specific genes, while rapamycin applied on days 4-14 significantly increased them. Among all groups, rapamycin applied on days 4-6 achieved highest cardiomyocyte differentiation efficiency. Furthermore, using autophagy inhibitor NHCl and GSK-3β inhibitor CHIR-99021, we found rapamycin-induced autophagy promoted cardiomyocyte differentiation at middle stage by negatively regulating the Wnt/β-catenin signaling pathway. These results suggest that rapamycin regulates EB-based cardiomyocyte differentiation in a stage-dependent manner, and the negative regulation of Wnt/β-catenin signaling pathway by autophagy was involved in the prodifferentiation effect of rapamycin at middle stage.
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http://dx.doi.org/10.1089/scd.2020.0025DOI Listing
September 2020

Regulation of the cerebrovascular smooth muscle cell phenotype by mitochondrial oxidative injury and endoplasmic reticulum stress in simulated microgravity rats via the PERK-eIF2α-ATF4-CHOP pathway.

Biochim Biophys Acta Mol Basis Dis 2020 08 15;1866(8):165799. Epub 2020 Apr 15.

Department of Cardiology & National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, Beijing 100853, China. Electronic address:

Microgravity exposure results in vascular remodeling and cardiovascular dysfunction. Here, the effects of mitochondrial oxidative stress on vascular smooth muscle cells (VSMCs) in rat cerebral arteries under microgravity simulated by hindlimb unweighting (HU) was studied. Endoplasmic reticulum (ER)-resident transmembrane sensor proteins and phenotypic markers of rat cerebral VSMCs were examined. In HU rats, CHOP expression was increased gradually, and the upregulation of the PERK-eIF2α-ATF4 pathway was the most pronounced in cerebral arteries. Furthermore, PERK/p-PERK signaling, CHOP, GRP78 and reactive oxygen species were augmented by PERK overexpression but attenuated by the mitochondria-targeting antioxidant MitoTEMPO. Meanwhile, p-PI3K, p-Akt and p-mTOR protein levels in VSMCs were increased in HU rat cerebral arteries. Compared with the control, HU rats exhibited lower α-SMA, calponin, SM-MHC and caldesmon protein levels but higher OPN and elastin levels in cerebral VSMCs. The cerebral VSMC phenotype transition from a contractile to synthetic phenotype in HU rats was augmented by PERK overexpression and 740Y-P but reversed by MitoTEMPO and the ER stress inhibitors tauroursodeoxycholic acid (TUDCA) and 4-phenylbutyric acid (4-PBA). In summary, mitochondrial oxidative stress and ER stress induced by simulated microgravity contribute to phenotype transition of cerebral VSMCs through the PERK-eIF2a-ATF4-CHOP pathway in a rat model.
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http://dx.doi.org/10.1016/j.bbadis.2020.165799DOI Listing
August 2020

GPER mediates decreased chemosensitivity via regulation of ABCG2 expression and localization in tamoxifen-resistant breast cancer cells.

Mol Cell Endocrinol 2020 04 19;506:110762. Epub 2020 Feb 19.

Department of Critical Care Medicine, Jiangxi Cancer Hospital, Nanchang, 330029, China. Electronic address:

Rescue chemotherapy is usually the preferred treatment for patients with advanced estrogen receptor-positive (ER+) breast cancer with endocrinotherapy resistance. However, these patients often simultaneously show a poor response to cytotoxic drugs, and thus the detailed mechanism of this resistance needs to be further investigated. Our previous research indicated that the G-protein-coupled estrogen receptor (GPER) is a novel mediator of the development of multidrug resistance, including resistance to both endocrinotherapy and chemotherapy, and ATP binding cassette subfamily G member 2 (ABCG2) has been identified as an engine that confers cancer cells with chemoresistance by expelling xenobiotics and chemotherapeutics. Here, we are the first to show that the expression levels of GPER and ABCG2 are markedly increased in tamoxifen-resistant ER + metastases compared to the corresponding primary tumors. A plasma membrane expression pattern of GPER and ABCG2 was observed in patients with metastases. Furthermore, both ER modulator tamoxifen, GPER-specific agonist G1 and pure ER antagonist ICI 182,780 significantly enhanced ABCG2 expression in tamoxifen-resistant breast cancer cells (MCF-7R) but not in tamoxifen-sensitive cells (MCF-7). The activated downstream GPER/EGFR/ERK and GPER/EGFR/AKT signaling pathways were responsible for regulating the expression and cell membrane localization of ABCG2, respectively, in MCF-7R cells. Interestingly, the above phenomenon could be alleviated by inhibitors of both the indicated signaling pathways and by knockdown of GPER in MCF-7R cells. More importantly, the tamoxifen-induced GPER/ABCG2 signaling axis was shown to play a pivotal role in the development of chemotherapy (doxorubicin) resistance both in vitro and in vivo. The clinical data further revealed that tamoxifen-resistant patients with high GPER/ABCG2 signaling activation had poor progression-free survival (PFS) when given rescue anthracycline chemotherapy. Therefore, our data provide novel insights into GPER-mediated chemoresistance and provide a rationale for the GPER/ABCG2 signaling axis being a promising target for reversing chemoresistance in patients with advanced ER + tamoxifen-resistant breast cancer.
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http://dx.doi.org/10.1016/j.mce.2020.110762DOI Listing
April 2020

The Effect of SNPs, Their Haplotypes, and Gene-Environment Interactions on the Risk of Atherothrombotic Stroke Among the Chinese Population.

Genet Test Mol Biomarkers 2019 Jul 24;23(7):487-494. Epub 2019 Jun 24.

1 Department of Neurology, the Third People's Hospital of Chengdu, the Affiliated Hospital of Southwest Jiaotong University, Chengdu, P.R. China.

Ischemic stroke (IS) is a severe and complex disorder with high morbidity and mortality rates and it has been associated with both environmental and genetic predisposing factors. The purpose of this study was to evaluate the association of the alpha-1-microglobulin/bikunin precursor () gene polymorphisms with IS and any possible interactions between specific alleles and traditional risk factors among a Han Chinese cohort. We conducted a candidate gene study designed to characterize nine (9) single nucleotide polymorphisms (SNPs) of the gene among 195 patients with atherothrombotic stroke (ATS) (a major subtype of IS) and 184 nonstroke controls. Allelic and genotypic frequency differences were evaluated using a logistic regression model. False discovery rate (FDR) correction for multiple comparisons was used. The interactional analyses were performed using the multifactor dimensionality reduction test. We found an association between the rs2567698 CC genotype (odds ratio [OR], 95% confidence interval [CI]: 2.176, 1.159-4.086) and the T allele (OR, 95% CI: 0.654, 0.446-0.960) with risk of ATS in men. However, these associations did not survive FDR correction. In haplotype analyses, the GCCCCCCCC haplotype had a higher frequency (OR, 95% CI: 2.191, 1.048-4.580) in ATS in the ≥45 years of age subgroup, whereas the GCCTCCCCC haplotype decreased the risk for ATS (OR, 95% CI: 0.543, 0.345-0.853) in men. In addition, we also found interactions for ATS risk between SNPs in the gene and modifiable risk factors for ATS, including: rs11788411 and hypertension in the overall population and women; rs2251680 and hypertension in subjects aged 45 years and older, as well as the interaction among hypertension and the rs2567698 and rs10817564 genotypes in men. Our results show a possible association between SNP haplotypes and gene-environment interactions with ATS susceptibility in a Han Chinese cohort.
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http://dx.doi.org/10.1089/gtmb.2018.0248DOI Listing
July 2019

State of charge estimation of vanadium redox battery based on improved extended Kalman filter.

ISA Trans 2019 Nov 20;94:326-337. Epub 2019 Apr 20.

Hefei Wego Electric Automation Co. LTD, Hefei 230051, China.

The accurate state of charge (SOC) estimation can protect the battery from overcharging and over-discharging, and it is useful to make an effective dispatching strategy. The extended Kalman filter (EKF) method is used to estimate SOC widely. But it does not consider the SOC constraints. Moreover, the convergence is influenced by the uncertain initial SOC, which may lead to false alarm, unwanted operation of protection, error dispatching and poor robustness of the system. This paper presents an improved extended Kalman filter (IEKF) method to estimate SOC for vanadium redox battery (VRB) by introducing a gain factor. It can be adjusted automatically according to the output error and SOC boundary. To implement IEKF estimator, a VRB state space model is established and its parameters are identified by recursive least square (RLS) method. Then a VRB of 5kW/30kWh experimental platform is built. Finally, the IEKF method is validated and compared with EKF against unknown initial value through the experiments. The results have shown that IEKF method is superior to EKF in terms of accuracy, convergence speed and robustness. And the estimated SOC remains bounded by using IEKF method. It is more suitable for SOC estimation than EKF algorithm in the industrial applications.
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http://dx.doi.org/10.1016/j.isatra.2019.04.008DOI Listing
November 2019

Activation of melatonin receptor 2 but not melatonin receptor 1 mediates melatonin-conferred cardioprotection against myocardial ischemia/reperfusion injury.

J Pineal Res 2019 Aug 12;67(1):e12571. Epub 2019 Apr 12.

Department of Cardiology, National Clinical Research Center for Geriatric Diseases, 2nd Medical Center, Chinese PLA General Hospital, Beijing, China.

Accumulated pieces of evidence have proved the beneficial effects of melatonin on myocardial ischemia/reperfusion (MI/R) injury, and these effects were largely dependent on melatonin membrane receptor activation. In humans and other mammals, there are two types of melatonin receptors, including the melatonin receptor 1 (MT1, melatonin receptor 1a or MTNR1A) and melatonin receptor 1 (MT2, melatonin receptor 1b or MTNR1B) receptor subtypes. However, which receptor mediates melatonin-conferred cardioprotection remains unclear. In this study, we employed both loss-of-function and gain-of-function approaches to reveal the answer. Mice (wild-type; MT1 or MT2 silencing by in vivo minicircle vector; and those overexpressing MT1 or MT2 by in vivo AAV9 vector) were exposed to MI/R injury. Both MT1 and MT2 were present in wild-type myocardium. MT2, but not MT1, was essentially upregulated after MI/R Melatonin administration significantly reduced myocardial injury and improved cardiac function after MI/R Mechanistically, melatonin treatment suppressed MI/R-initiated myocardial oxidative stress and nitrative stress, alleviated endoplasmic reticulum stress and mitochondrial injury, and inhibited myocardial apoptosis. These beneficial actions of melatonin were absent in MT2-silenced heart, but not the MT1 subtype. Furthermore, AAV9-mediated cardiomyocyte-specific overexpression of MT2, but not MT1, mitigated MI/R injury and improved cardiac dysfunction, which was accompanied by significant amelioration of oxidative stress, endoplasmic reticulum stress, and mitochondrial dysfunction. Mechanistically, MT2 protected primary cardiomyocytes against hypoxia/reoxygenation injury via MT2/Notch1/Hes1/RORα signaling. Our study presents the first direct evidence that the MT2 subtype, but not MT1, is a novel endogenous cardiac protective receptor against MI/R injury. Medications specifically targeting MT2 may hold promise in fighting ischemic heart disease.
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http://dx.doi.org/10.1111/jpi.12571DOI Listing
August 2019

CKIP-1 limits foam cell formation and inhibits atherosclerosis by promoting degradation of Oct-1 by REGγ.

Nat Commun 2019 01 25;10(1):425. Epub 2019 Jan 25.

State Key Laboratory of Proteomics, National Center of Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing, 100850, China.

Atherosclerosis-related cardiovascular diseases are the leading cause of mortality worldwide. Macrophages uptake modified lipoproteins and transform into foam cells, triggering an inflammatory response and thereby promoting plaque formation. Here we show that casein kinase 2-interacting protein-1 (CKIP-1) is a suppressor of foam cell formation and atherosclerosis. Ckip-1 deficiency in mice leads to increased lipoprotein uptake and foam cell formation, indicating a protective role of CKIP-1 in this process. Ablation of Ckip-1 specifically upregulates the transcription of scavenger receptor LOX-1, but not that of CD36 and SR-A. Mechanistically, CKIP-1 interacts with the proteasome activator REGγ and targets the transcriptional factor Oct-1 for degradation, thereby suppressing the transcription of LOX-1 by Oct-1. Moreover, Ckip-1-deficient mice undergo accelerated atherosclerosis, and bone marrow transplantation reveals that Ckip-1 deficiency in hematopoietic cells is sufficient to increase atherosclerotic plaque formation. Therefore, CKIP-1 plays an essential anti-atherosclerotic role through regulation of foam cell formation and cholesterol metabolism.
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http://dx.doi.org/10.1038/s41467-018-07895-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6347643PMC
January 2019

Precise theranostic nanomedicines for inhibiting vulnerable atherosclerotic plaque progression through regulation of vascular smooth muscle cell phenotype switching.

Theranostics 2018 12;8(13):3693-3706. Epub 2018 Jun 12.

Department of Cardiology & National Clinical Research Center of Geriatrics Disease, Chinese PLA General Hospital, Beijing 100853, China.

Coronary heart disease is a prevalent and fatal killer caused by vulnerable atherosclerotic plaques (VASPs). However, the precise detection and treatment of VASPs remains a difficult challenge. Here, we present the development of noninvasive human serum albumin (HSA)-based theranostic nanomedicines (NMs) for the specific diagnosis and effective therapy of VASPs. The ICG/SRT@HSA-pept NMs were formulated to contain payloads of the near-infrared (NIR) fluorescent dye indocyanine green (ICG) and the sirtuin 1 (Sirt1) activator SRT1720, and modified with a peptide moiety targeting osteopontin (OPN). The atherosclerotic mouse model was established with the high-fat diet (HFD). The vascular smooth muscle cells (VSMCs) phenotypic switching was induced using the ox-LDL stimulation. Due to the overexpression of OPN in activated VSMCs and VASPs, the targeted NMs specifically accumulated within the VASPs region after intravenous injection into the atherosclerotic mice, achieving the precise detection of VASPs. In addition, in the presence of SRT1720, the NMs could activate intracellular Sirt1 and activate an antiatherogenesis effect by inhibiting the phenotypic switching of VSMCs, which is an essential contributor to the vulnerability and progression of atherosclerotic plaques. After therapeutic administration of the ICG/SRT@HSA-pept NMs for two weeks, the physiological sizes and plaque compositions of VASPs were markedly improved. Furthermore, ICG/SRT@HSA-pept NMs-treated mice presented a more favorable plaque phenotype than that was observed in free SRT1720-treated mice, suggesting the enhanced delivery of pharmaceutical agents to the atherosclerotic lesions and improved therapeutic efficacy of NMs compared with free SRT1720. The theranostic ICG/SRT@HSA-pept NMs showed great potential for the precise identification and targeted treatment of atherosclerotic diseases.
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http://dx.doi.org/10.7150/thno.24364DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6037040PMC
August 2019

Activation of cannabinoid receptor type II by AM1241 protects adipose-derived mesenchymal stem cells from oxidative damage and enhances their therapeutic efficacy in myocardial infarction mice Stat3 activation.

Oncotarget 2017 Sep 4;8(39):64853-64866. Epub 2017 May 4.

Department of Cardiology, State Key Laboratory of Kidney Diseases, Chinese PLA General Hospital, Beijing, China.

The poor survival of cells in ischemic sites diminishes the therapeutic efficacy of stem cell therapy. Previously we and others have reported that Cannabinoid receptor type II (CB2) is protective during heart ischemic injury for its anti-oxidative activity. However, whether CB2 activation could improve the survival and therapeutic efficacy of stem cells in ischemic myocardium and the underlying mechanisms remain elusive. Here, we showed evidence that CB2 agonist AM1241 treatment could improve the functional survival of adipose-derived mesenchymal stem cells (AD-MSCs) as well as . Moreover, AD-MSCs adjuvant with AM1241 improved cardiac function, and inhibited cardiac oxidative stress, apoptosis and fibrosis. To unveil possible mechanisms, AD-MSCs were exposed to hydrogen peroxide/serum deprivation to simulate the ischemic environment in myocardium. Results delineated that AM1241 blocked the apoptosis, oxidative damage and promoted the paracrine effects of AD-MSCs. Mechanistically, AM1241 activated signal transducers and activators of transcription 3 (Stat3) through the phosphorylation of Akt and ERK1/2. Moreover, the administration of AM630, LY294002, U0126 and AG490 (inhibitors for CB2, Akt, ERK1/2 and Stat3, respectively) could abolish the beneficial actions of AM1241. Our result support the promise of CB2 activation as an effective strategy to optimize stem cell-based therapy possibly through Stat3 activation.
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http://dx.doi.org/10.18632/oncotarget.17614DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5630296PMC
September 2017

Reduced silent information regulator 1 signaling exacerbates sepsis-induced myocardial injury and mitigates the protective effect of a liver X receptor agonist.

Free Radic Biol Med 2017 12 7;113:291-303. Epub 2017 Oct 7.

National Clinical Research Center for Geriatric Diseases & Department of Cardiology, Chinese PLA General Hospital, Beijing 100853, China; Department of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710032, China. Electronic address:

Myocardial injury and dysfunction are critical manifestations of sepsis. Previous studies have reported that liver X receptor (LXR) activation is protective during sepsis. However, whether LXR activation protects against septic heart injury and its underlying mechanisms remain elusive. This study was designed to determine the role of LXR activation in the septic heart with a focus on SIRT1 (silent information regulator 1) signaling. Male cardiac-specific SIRT1 knockout mice (SIRT1-/-) and their wild-type littermates were subjected to sepsis by cecal ligation and puncture (CLP) in the presence or absence of LXR agonist T0901317. The survival rate of mice was recorded during the 7-day period post CLP. Our results demonstrated that SIRT1-/- mice suffered from exacerbated mortality and myocardial injury in comparison with their wild-type littermates. Meanwhile, T0901317 treatment improved mice survival, accompanied by significant ameliorations of myocardial injury and dysfunction in wild-type mice but not in SIRT1-/- mice. Furthermore, the levels of myocardial inflammatory cytokines (TNF-α, IL-6, IL-1β, MCP-1, MPO and HMGB1), oxidative stress (ROS generation, MDA), endoplasmic-reticulum (ER) stress (protein levels of CHOP, GRP78, GRP94, IRE1α, and ATF6), and cardiac apoptosis following CLP were inhibited by T0901317 treatment in wild-type mice but not in SIRT1-/- mice. Mechanistically, T0901317 enhanced SIRT1 signaling and the subsequent deacetylation and activation of antioxidative FoxO1 and anti-ER stress HSF1, as well as the deacetylation and inhibition of pro-inflammatory NF-ΚB and pro-apoptotic P53, thereby alleviating sepsis-induced myocardial injury and dysfunction. Our data support the promise of LXR activation as an effective strategy for relieving heart septic injury.
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http://dx.doi.org/10.1016/j.freeradbiomed.2017.10.005DOI Listing
December 2017

Moderate Autophagy Inhibits Vascular Smooth Muscle Cell Senescence to Stabilize Progressed Atherosclerotic Plaque via the mTORC1/ULK1/ATG13 Signal Pathway.

Oxid Med Cell Longev 2017 21;2017:3018190. Epub 2017 Jun 21.

Department of Cardiology, Chinese PLA General Hospital, Beijing 100853, China.

In order to investigate the effects of autophagy induced by rapamycin in the development of atherosclerosis plaque we established murine atherosclerosis model which was induced in ApoE mice by high fat and cholesterol diet (HFD) for 16 weeks. Rapamycin and 3-Methyladenine (MA) were used as autophagy inducer and inhibitor respectively. The plaque areas in aortic artery were detected with HE and Oil Red O staining. Immunohistochemical staining were applied to investigate content of plaque respectively. In contrast to control and 3-MA groups, rapamycin could inhibit atherosclerosis progression. Rapamycin was able to increase collagen content and a-SMA distribution relatively, as well as decrease necrotic core area. Then we used MOVAS and culture with ox-LDL for 72 h to induce smooth muscle-derived foam cell model in vitro. Rapamycin and 3-MA were cultured together respectively. Flow cytometry assay and SA--Gal staining experiments were performed to detect survival and senescence of VSMCs. Western blot analysis were utilized to analyze the levels of protein expression. We found that rapamycin could promote ox-LDL-induced VSMCs autophagy survival and alleviate cellular senescence, in comparison to control and 3-MA groups. Western blot analysis showed that rapamycin could upregulate ULK1, ATG13 and downregulate mTORC1 and p53 protein expression.
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http://dx.doi.org/10.1155/2017/3018190DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5497616PMC
April 2018

Compound Heterozygous Mutations in the DUOX2/DUOXA2 Genes Cause Congenital Hypothyroidism.

Yonsei Med J 2017 Jul;58(4):888-890

Department of Endocrinology and Metabolism, The Second Hospital Affiliated to Guilin Medical College, Guilin, P.R. China.

The mutations in the dual oxidase 2 (DUOX2) and dual oxidase maturation factor 2 (DUOXA2) genes can cause congenital hypothyroidism (CH). This study reports the pedigree with goitrous congenital hypothyroidism (GCH) due to the coexistence of heterozygous mutations in the DUOX2 and DUOXA2 genes. The two sisters with GCH were diagnosed with CH at neonatal screening and were enrolled in this study. The DUOX2, DUOXA2, and thyroid peroxidase (TPO) genes were considered for genetic defects screening. Family members of the patients and normal controls were also enrolled and evaluated. The two girls harbored compound heterozygous mutations, including a new mutation of c.2654G>T (p.R885L) in the maternal DUOX2 allele and c.738C>G (p.Y246X) in the paternal DUOXA2 allele, that has been previously reported. The germline mutations from the families were consistent with an autosomal recessive inheritance pattern. No mutations in the TPO gene and the controls were observed.
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http://dx.doi.org/10.3349/ymj.2017.58.4.888DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5447125PMC
July 2017

A novel role of CKIP-1 in promoting megakaryocytic differentiation.

Oncotarget 2017 May;8(18):30138-30150

State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Collaborative Innovation Center for Cancer Medicine, Beijing 100850, China.

Casein kinase 2-interacting protein-1 (CKIP-1) is a known regulator of cardiomyocytes and macrophage proliferation. In this study, we showed that CKIP-1 was involved in the process of megakaryocytic differentiation. During megakaryocytic differentiation of K562 cells, CKIP-1 was dramatically upregulated and this upregulation induced by PMA was mediated through downregulation of transcription factor GATA-1. By transient transfection, oligonucleotide-directed mutagenesis and chromatin immunoprecipitation assays, we identified the transcriptional regulation of CKIP-1 by GATA-1. Overexpression of CKIP-1 initiated events of spontaneous megakaryocytic differentiation in K562 cells. Conversely, knockdown of CKIP-1 in cell lines suppressed megakaryocytic differentiation. Mechanistically, overexpression of CKIP-1 changed the expression levels of transcription factors that have been shown to be critical in erythro-megakaryocytic differentiation such as Fli-1, c-Myb and c-Myc. In vivo analysis confirmed that CKIP-1-/- mice had decreased number of CD41+ cells harvested from bone marrow, and lower platelet levels when compared to wild-type littermates. This is the first direct evidence suggesting that CKIP-1 is a novel regulator of megakaryocytic differentiation.
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http://dx.doi.org/10.18632/oncotarget.15619DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5444732PMC
May 2017

Autologous bone marrow stem cell transplantation for the treatment of ulcerative colitis complicated with herpes zoster: a case report.

Front Med 2016 Dec 23;10(4):522-526. Epub 2016 Dec 23.

Institute of Health Management, Institute of Geriatrics, Beijing Key Laboratory of Normal Aging and Geriatrics, Department of Gerontal Gastroenterology, Chinese PLA General Hospital, Beijing, 100853, China.

Ulcerative colitis (UC) is a chronic inflammatory bowel disease with continuous or recurrent symptoms. A 42-year-old male patient with intermittent diarrhea accompanied by bloody mucopurulent stools was admitted to our hospital. The diagnosis of UC was confirmed by a combination of laboratory examination, colonoscopy, and histological assay. The patient developed herpes zoster in the hospital, which challenged traditional treatments. Therefore, we performed an autologous bone marrow cells to modulate the immune system with his permission. Autologous bone marrow mononuclear cells were collected and injected locally into the bowel mucosa, and subsequently injected systemically through a peripheral vein. After the patient underwent auto bone marrow mononuclear cells transplantations twice, the patient's symptoms were alleviated. Furthermore, he recovered from hematochezia, and his hypersensitive C reactive protein decreased. Colonoscopy results showed reduced lesions and decreased areas with bleeding and edema in the sigmoid colon and rectum. No recurrence occurred in the subsequent two years, but long-time monitoring is still necessary for the prophylaxis of colorectal cancer.
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http://dx.doi.org/10.1007/s11684-016-0485-4DOI Listing
December 2016

MRI/optical dual-modality imaging of vulnerable atherosclerotic plaque with an osteopontin-targeted probe based on FeO nanoparticles.

Biomaterials 2017 01 11;112:336-345. Epub 2016 Oct 11.

Department of Cardiology, Chinese PLA General Hospital, Beijing, 100853, China; Department of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, China. Electronic address:

Rupture of vulnerable atherosclerotic plaque is the major pathological cause of luminal thrombosis in acute coronary syndromes. Since foamy macrophages have been identified as a prominent component in vulnerable atherosclerotic lesions and osteopontin (OPN) is reported to be highly expressed in foamy macrophages, OPN could be a potential target for vulnerable atherosclerotic plaque imaging. The current study designed an OPN-specific MRI/optical dual-modality probe to detect vulnerable plaques. Fluorescence imaging revealed that 24 h after injection of the Cy5.5-OPN-DMSA-MNPs (COD-MNPs), the atherosclerotic plaques in carotid artery exhibited significant higher signals in high fat diet (HFD) fed mice in comparison to the group injected with Cy5.5-IgG-DMSA-MNPs (CID-MNPs) or normal diet fed group injected with COD-MNPs (1.87 ± 0.19 × 10 vs. 0.74 ± 0.04 × 10, 0.73 ± 0.03 × 10 p/sec/cm/sr, P < 0.05). Meanwhile, MRI displayed stronger T contrast enhancement 24 h post-injection at the area of atherosclerotic plaques in the carotid of HFD fed group injected with COD-MNPs than group injected with CID-MNPs or normal diet fed group injected with COD-MNPs (post/pre signal ratio: 0.64 ± 0.04 vs. 0.95 ± 0.02, 0.98 ± 0.01, P < 0.05). As a dual-modality molecular probe, the resulting COD-MNPs conjugates exhibit promising potentials for noninvasive detection of vulnerable atherosclerotic plaque in vivo.
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http://dx.doi.org/10.1016/j.biomaterials.2016.10.011DOI Listing
January 2017

[Impurity profile study of cefalotin sodium by two-dimensional liquid chromatography-quadrupole time-of-flight mass spectrometry].

Se Pu 2015 Dec;33(12):1314-9

A two-dimensional liquid chromatography-quadrupole time-of-flight mass spectrometry (2D-LC-QTOF MS) method to profile the impurities of cefalotin sodium was developed. A Symmetry C18 column (250 mm x 4.6 mm, 5 μm) was used in the first dimensional chromatography, with gradient elution using pH 2.5 phosphate buffer and acetonitrile as the mobile phases. The column temperature was maintained at 40 degrees C with an ultraviolet detection of 220 nm for analysis. An ACQUITY UPLC BEH C18 column (50 mm x 2.1 mm, 1.7 μm) was used in the second dimensional chromatography, with gradient elution using water containing 0.1% (v/v) formic acid and acetonitrile containing 0.1% (v/v) formic acid as the mobile phases. The column temperature was maintained at 40 degrees C. An HLB C18 column (30 mm x 2.1 mm, 20 μm) was used as the trap column. The data were collected in positive ion mode. The ion source temperature was set at 100 degrees C and the electrospray ionization (ESI) needle voltage was set at 1 000 V. The nebulizer gas temperature was set at 500 degrees C. The molecular formulas of the impurities were determined by their exact masses and isotope distributions. And the structures were determined by the protonated molecular ions and the manufacturing process of cefalotin sodium. Six impurities of cefalotin sodium were characterized and the origination of the impurities was deduced. Three of them were unknown impurities to the best of our knowledge. It was confirmed that the Chinese Pharmacopoeia 2010 has mistaken impurity A of cefalotin sodium. The results indicated that the 2D-LC-QTOF MS method could be used to investigate the impurity profile of cefalotin sodium, and it is simple and sensitive.
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http://dx.doi.org/10.3724/sp.j.1123.2015.07027DOI Listing
December 2015

A Novel c.554+5C>T Mutation in the DUOXA2 Gene Combined with p.R885Q Mutation in the DUOX2 Gene Causing Congenital Hypothyroidism.

J Clin Res Pediatr Endocrinol 2016 Jun 18;8(2):224-7. Epub 2015 Dec 18.

Huai'an Hospital Affiliated to Xuzhou Medical College and Huai'an Second People's Hospital, Clinic of Endocrinology and Metabolism, Huai'an, China Phone: 86-517-8394 3591 E-mail:

The coexistence of mutations in the dual oxidase maturation factor 2 (DUOXA2) and dual oxidase 2 (DUOX2) genes is rarely identified in congenital hypothyroidism (CH). This study reports a boy with CH due to a novel splice-site mutation in the DUOXA2 gene and a missense mutation in the DUOX2 gene. A four-year-old boy was diagnosed with CH at neonatal screening and was enrolled in this study. The DUOXA2, DUOX2, thyroid peroxidase (TPO), and thyrotropin receptor (TSHR) genes were considered for genetic defects screening. Genomic DNA was extracted from peripheral blood leukocytes, and Sanger sequencing was used to screen the mutations in the exon fragments. Family members of the patient and the controls were also enrolled and evaluated. The boy harbored compound heterozygous mutations including a novel splice-site mutation c.554+5C>T in the maternal DUOXA2 allele and c.2654G>A (p.R885Q) in the paternal DUOX2 allele. The germline mutations from his parents were consistent with an autosomal recessive inheritance pattern. No mutations in the TPO and TSHR genes were detected. A novel splice-site mutation c.554+5C>T in the DUOXA2 gene and a mutation p.R885Q in the DUOX2 gene were identified in a 4-year-old patient with goitrous CH.
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http://dx.doi.org/10.4274/jcrpe.2380DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5096480PMC
June 2016

The potential molecular effects of bursal septpeptide II on immune induction and antitumor activity.

J Vet Sci 2015 30;16(3):325-31. Epub 2015 Jan 30.

Division of Key Lab of Animal Disease Diagnosis and Immunology of China's Department of Agriculture, College of Veterinary Medicine, Nanjing Agriculture University, Nanjing 210095, China.

The bursa of Fabricius (BF) is the acknowledged central humoral immune organ in birds. Bursal septpeptide II (BSP-II) is an immunomodulatory bioactive peptide isolated from BF. To understand the effects of BSP-II on immune induction, gene expression profiles of hybridoma cells treated with BSP-II were evaluated. Pathway analysis showed that regulated genes were involved in cytokine-cytokine receptor interactions, T cell receptor signaling pathway, and pathway in cancer. It was observed that BSP-II reduced tumor cells proliferation and stimulated p53 expression. These results indicate potential mechanisms underlying the effects of the humoral immune system on immune induction, including antitumor activities. Our study has provided a novel insight into immunotherapeutic strategies for treating human tumors.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4588018PMC
http://dx.doi.org/10.4142/jvs.2015.16.3.325DOI Listing
July 2016

The ABCG2 gene Q141K polymorphism contributes to an increased risk of gout: a meta-analysis of 2185 cases.

Mod Rheumatol 2014 Sep 5;24(5):829-34. Epub 2014 Feb 5.

Institute of Rheumatology and Immunology, Affiliated Hospital of North Sichuan Medical College , Nanchong, Sichuan , P. R. China.

Objectives: Individual genetic association studies examining the relationship between the ABCG2 gene polymorphisms and gout have yielded inconsistent results. This study aims to evaluate the association between the ABCG2 gene variants and gout using meta-analysis.

Materials And Methods: Relevant studies were identified by searching databases extensively. The odds ratio (OR) was calculated using a random-effect or fixed-effect model. A Q statistic was used to evaluate homogeneity, and Egger's test and funnel plot were used to assess publication bias. Subgroup analyses on ethnicities and sex were also performed.

Results: A total of 7 studies, including 2185 gout patients and 8028 controls from 5 countries or regions, were included and identified for the current meta-analysis. It was found that the A allele or AA genotype of the ABCG2 Q141K polymorphism (rs2231142) had an increased risk of gout in the general population (A allele, p < 0.00001 and AA genotype, p < 0.00001, respectively). On the contrary, CC homozygote played a protective role against the risk of gout (p < 0.00001). Similar results were found in subgroup analyses. However, there was a significant heterogeneity among studies.

Conclusions: Existing evidence indicates that the Q141K polymorphism (rs2231142, the A allele and AA genotype) is associated with an increased risk of gout.
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http://dx.doi.org/10.3109/14397595.2013.875639DOI Listing
September 2014

A high ratio of dietary n-3/n-6 polyunsaturated fatty acids improves obesity-linked inflammation and insulin resistance through suppressing activation of TLR4 in SD rats.

Nutr Res 2013 Oct 9;33(10):849-58. Epub 2013 Aug 9.

Department of Nutrition and Food Hygiene and the Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, School of Public Health, Fourth Military Medical University, Xi'an 710032, China.

Dietary ratios of n-3/n-6 polyunsaturated fatty acids (PUFAs) have been implicated in controlling markers of metabolic disorders, including obesity, insulin resistance (IR), inflammation, and lipid profiles, which are also presumed to be partly related to type 2 diabetes mellitus (T2DM). However, molecular mechanisms of the different PUFAs related to metabolic disorders have not been systematically addressed. The present study aimed to investigate the impact of dietary n-3/n-6 PUFA ratios on obesity and IR and, further, to determine the underlying mechanisms. For 16 weeks, 32 SD male rats, randomly divided into four groups (n = 8 per group), received one of the following diets: normal chow, high saturated fatty acid (SFA), high n-3/n-6 PUFA ratio (1∶1, PUFA¹:¹), or low n-3/n-6 PUFA ratio (1∶4, PUFA¹:⁴). Following the experimental diet period, metabolic parameters related to obesity and IR were measured. Compared to SFA diet-fed rats, PUFA¹:¹ diet-fed rats exhibited decreased body and visceral fat weight, lowered blood lipids, and improved glucose tolerance and insulin sensitivity. Interestingly, these changes were accompanied with decreased expression levels of circulating pro-inflammatory cytokines, including tumor necrosis factor α, interleukin-6, and C-reactive protein. Moreover, the TLR4 protein and mRNA levels were markedly down-regulated by PUFA¹:¹ compared with SFA; however, PUFA¹:⁴ diet-fed rats failed to exhibit these changes. Cumulatively, our data highlight a role for a PUFA¹:¹ diet in the prevention of obesity and related metabolic disorders by suppressing the activation of TLR4, a critical modulator of pro-inflammatory cytokines.
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http://dx.doi.org/10.1016/j.nutres.2013.07.004DOI Listing
October 2013

[Effects of dietary different ratios of high n - 3/n - 6 polyunsaturated fatty acids on insulin resistance in rats].

Wei Sheng Yan Jiu 2013 Jan;42(1):10-3

Department of Nutrition and Food Hygiene, Fourth Military Medical University, Xi'an 710032, China.

Objective: To study the effects of dietary different ratios of high-fat n - 3/ n - 6 polyunsaturated fatty acids (PUFAs) on insulin sensitivity and pro-inflammatory cytokines expression in serum of rats.

Methods: 40 young male SD rats (n = 10) after adaptive feeding 7d were randomly divided into 4 groups, fed by common diet, high fat diet, high fat with n - 3/n - 6 1 : 1 PUFAs diet, and high fat with n - 3/n - 6 1 : 4 PUFAs diet. The animals were weighted weekly and sacrificed at 16 weeks, then blood lipids, serum insulin sensitivity and pro-inflammatory cytokines (IL-6, TNF-alpha and hs-CRP) were determined.

Results: Compared with normal control group, three high fat groups result in a significant increase of body weight gain. Insulin sensitivity of high fat 1 : 1 group had no significant difference with normal control, but is significantly higher than high-fat and high-fat 1 : 4 group (P < 0.05). Compared with high fat group, pro-inflammatory cytokines expression of high fat 1 : 1 group decreased significantly (P < 0.05).

Conclusion: High dietary polyunsaturated fatty acids appears associated with a trend towards obesity risk, however, increase of the proportion of n - 3 PUFAs dietary composition effectively decreased the expression of pro-inflammatory cytokines, then, improved insulin sensitivity and prevented insulin resistance.
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January 2013

Gene expression profiling of hybridoma cells after bursal-derived bioactive factor BP5 treatment.

Amino Acids 2012 Dec 7;43(6):2443-56. Epub 2012 Jun 7.

Division of Key Lab of Animal Disease Diagnosis and Immunology of China's Department of Agriculture, College of Veterinary Medicine, Nanjing Agriculture University, Nanjing, 210095, China.

Bursa of Fabricius is the acknowledged vital humoral immune system for B cell differentiation and antibody production. To study the molecular mechanism underlying the effect of bursal-derived BP5, we used gene microarray to analyze the genomic expression profiling of BP5-treated hybridoma cells. BP5 exhibited an immunomodulatory effect on antibody production in hybridoma cells and induced alterations in the gene expression profiles related to the immune-related biological processes, such as T cell activation and proliferation, B cell activation, B cell-mediated immunity, and cytokines cytokine production involved in immune response. In addition, 26 biological pathways associated with immunomodulatory functions were regulated in BP5-treated hybridoma cells, in which p53 signal pathway played an important role in antitumor. Among these regulated genes, 12 differentially expressed genes were verified by qRT-PCR. The activation of p53 activity by BP5 was further confirmed by p53 luciferase reporter assay and p53 expression. Our data revealed that bursal-derived BP5 could regulate various immune-related cellular processes, including antitumor factor p53 signal pathway, perhaps partially accounting for the reported immunomodulatory roles and novel antiproliferation on tumor cells functions of bursal-derived bioactive factor BP5.
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http://dx.doi.org/10.1007/s00726-012-1323-xDOI Listing
December 2012

Preauricular transcondylar approach for basal cell adenoma of parotid coexist with ganglion cyst of the ipsilateral temporomandibular joint.

J Craniofac Surg 2011 Nov;22(6):e23-6

Departments of Oral and Maxillofacial Surgery, Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

The concurrence of 2 independent neoplasias in the ipsilateral parotid and the temporomandibular joint (TMJ) region was infrequently reported. In this article, we present a unique case characterized by the coexistence of a rare salivary gland tumor, basal cell adenoma, of the parotid gland with a ganglion cyst in the ipsilateral TMJ region. A special surgical procedure was also presented here using a modified preauricular incision and transcondylar approach for extracapsular dissection of both lesions. Previously published literature are about the traditional treatment of benign parotid tumors using partial or total parotidectomy with the preservation of facial nerve mainly via an S-shaped submandibular incision and approach. Here, for the first time, a special surgical method using preauricular transcondylar approach for this unique case of synchronous occurrence of parotid tumor and TMJ cyst is reported.
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http://dx.doi.org/10.1097/SCS.0b013e31822ec903DOI Listing
November 2011

A bursal pentapeptide (BPP-I), a novel bursal-derived peptide, exhibits antiproliferation of tumor cell and immunomodulator activity.

Amino Acids 2012 Jun 13;42(6):2215-22. Epub 2011 Jul 13.

Division of Key Lab of Animal Disease Diagnosis and Immunology of China's Department of Agriculture, College of Veterinary Medicine, Nanjing Agriculture University, Nanjing, 210095, People's Republic of China.

The bursa of Fabricius (BF) is the central humoral immune organ unique to birds. Here, we isolated a novel bursal pentapeptide I (BPP-I), LGPGP, from BF. BPP-I could play inhibition effect on MCF-7 but not on CEF or Vero cell proliferation in vitro, and enhance antitumor factor p53 protein expression. Also, BPP-I stimulated antibody production in a dose-dependent manner in hybridoma cell. Furthermore, BPP-I could induce various immune responses in mice immunization experiments, including increase antibody production and cytokines IL-4 and IFN-γ level, and induce T-cell immunophenotyping. These results suggest that BPP-I is a potential immunomodulator of antitumor and immunity. The study could provide some novel insights on the probable candidate reagent for the antitumor and immune improvement.
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http://dx.doi.org/10.1007/s00726-011-0961-8DOI Listing
June 2012