Publications by authors named "Haibin Cui"

12 Publications

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Dexmedetomidine ameliorates lipopolysaccharide-induced acute lung injury by inhibiting the PI3K/Akt/FoxO1 signaling pathway.

J Anesth 2021 Apr 5. Epub 2021 Apr 5.

Department of Anesthesiology, School and Hospital of Stomatological, China Medical University, Liaoning Provincial Key Laboratory of Ora Disease, No. 117 Nanjing North Street, Heping District, Shenyang, 110002, China.

Purpose: Dexmedetomidine (DEX) has been associated with inflammation, oxidative stress, and apoptosis, but its effects on lipopolysaccharide (LPS)-induced lung injury remain uncertain. The present study explored the effects of DEX on LPS-induced lung injury and studied the possible molecular mechanisms by testing the effects of the phosphoinositide-3 kinase (PI3K) inhibitor LY294002 and BEZ235.

Methods: Seventy C57BL/6 mice were randomly divided into the control, LPS, LPS + DEX, LPS + LY294002, LPS + BEZ235, LPS + DEX + LY294002, and LPS + DEX + BEZ235groups. Lung samples were collected 48 h after LPS treatment.

Results: DEX significantly inhibited LPS-induced increases in the lung weight/body weight ratio and lung wet/dry weight ratio, decreased inflammatory cell infiltration, and decreased the production of proinflammatory factors, such as interleukin-1β (IL-1β), IL-6, and tumor necrosis factor α (TNF-α)in the lungs. DEX also markedly attenuated the increases in malondialdehyde 5 (MDA 5) and inositol-dependent enzyme a (IRE-a), attenuated the decrease in superoxide dismutase 1(SOD-1), reversed the low expression of B-cell lymphoma-2 (Bcl-2), and the high expressions of Bax and Caspase-3. DEX also decreased the expression of phosphorylated PI3K and phosphorylated Akt and increased the expression of phosphorylated forkhead box-O transcription factor 1 (FoxO1). More interestingly, LY294002 or BEZ235 pretreatment significantly abolished the inhibitory effects of DEX on LPS-induced lung inflammation, oxidative stress, and apoptosis.

Conclusions: These data suggest that DEX ameliorates LPS-induced acute lung injury partly through the PI3K/Akt/FoxO1 signaling pathway.
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http://dx.doi.org/10.1007/s00540-021-02909-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8021217PMC
April 2021

Effect of Notch1 on neural tube defects and neural stem cell differentiation induced by all‑trans retinoic acid.

Mol Med Rep 2021 Mar 21;23(3). Epub 2021 Jan 21.

Department of Pediatrics, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250021, P.R. China.

Neural tube defects (NTDs) are the most serious and common birth defects in the clinical setting. The Notch signaling pathway has been implicated in different processes of the embryonic neural stem cells (NSCs) during neural tube development. The aim of the present study was to investigate the expression pattern and function of Notch1 (N1) in all‑trans retinoic acid (atRA)‑induced NTDs and NSC differentiation. A mouse model of brain abnormality was established by administering 28 mg/kg atRA, and then brain development was examined using hematoxylin and eosin (H&E) staining. The N1 expression pattern was detected in the brain of mice embryos via immunohistochemistry and western blotting. NSCs were extracted from the fetal brain of C57 BL/6 embryos at 18.5 days of pregnancy. N1, Nestin, neurofilament (NF), glial fibrillary acidic protein (GFAP) and galactocerebroside (GALC) were identified using immunohistochemistry. Moreover, N1, presenilin 1 (PS1), Nestin, NF, GFAP and GALC were detected via western blotting at different time points in the NSCs with control media or atRA media. H&E staining identified that the embryonic brain treated with atRA was more developed compared with the control group. N1 was downregulated in the embryonic mouse brain between days 11 and 17 in the atRA‑treated group compared with the untreated group. The distribution of N1, Nestin, NF, GFAP and GALC was positively detected using immunofluorescence staining. Western blotting results demonstrated that there were significantly, synchronous decreased expression levels of N1 and PS1, but increased expression levels of NF, GFAP and GALC in NSCs treated with atRA compared with those observed in the controls (P<0.05). The results suggested that the N1 signaling pathway inhibited brain development and NSC differentiation. Collectively, it was found that atRA promoted mouse embryo brain development and the differentiation of NSCs by inhibiting the N1 pathway.
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http://dx.doi.org/10.3892/mmr.2021.11859DOI Listing
March 2021

Sensitive detection of NO using a compact portable CW DFB-QCL-based WMS sensor.

Appl Opt 2020 Oct;59(30):9491-9498

This paper introduces a compact and portable sensor based on mid-infrared absorption spectroscopy for NO detection employing a room-temperature continuous wave (CW) distributed feedback quantum cascade laser (DFB-QCL) emitting at 1900.08. A software-based digital signal generator and lock-in amplifier, in combination with the wavelength modulation spectroscopy (WMS) technique, were used for the concentration measurement of NO. In addition, a Gabor filter denoising method was developed to improve the performance of the measurement system. As a result, a minimum detection limit of 42 ppbv can be achieved at 3 s integration time, and a measurement precision of 450 ppbv can be reached with a time resolution of 0.1 s. The performance of the compact portable sensor was verified by a series of experiments, denoting great potential of field application for sensitive NO sensing.
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http://dx.doi.org/10.1364/AO.402484DOI Listing
October 2020

CircDHDDS/miR-361-3p/WNT3A Axis Promotes the Development of Retinoblastoma by Regulating Proliferation, Cell Cycle, Migration, and Invasion of Retinoblastoma Cells.

Neurochem Res 2020 Nov 31;45(11):2691-2702. Epub 2020 Aug 31.

Department of Ophthalmology, Shanghai Pudong Hospital, Shanghai, China.

Retinoblastoma (RB) is a common intraocular malignant tumor. The growing evidence has reported that circular RNAs (circRNAs) play critical roles in RB development. Therefore, the purpose of the study is to investigate the regulatory mechanism of circDHDDS in RB. The real-time quantitative polymerase chain reaction (RT-qPCR) assay was used to quantify the expression levels of circDHDDS, miR-361-3p, and WNT3A in RB tissues and cells (RPCs, Y-79, and WERI-Rb-1). The proliferation and cell cycle of RB cells were assessed by colony formation assay and flow cytometry assays, respectively. The migration and invasion of RB cells were measured by transwell assay. The protein expression levels of Nectin-3 (CD113), SOX2, Nanog, and WNT3A were measured by Western blot assay. The functional targets of circDHDDS and miR-361-3p were predicted by bioinformatics databases, and the dual-luciferase reporter assay was used to confirm the interaction relationship between miR-361-3p and circDHDDS or WNT3A. The functional role of circDHDDS silencing in vivo was evaluated by xenograft experiment. We found that circDHDDS was overexpressed in RB tissues and cells compared with normal retinas tissues and retinal pigment epithelial cells, correspondingly. Furthermore, silencing of circDHDDS impeded proliferation, migration, invasion, and induced cell cycle arrest in vitro, which were abolished by knockdown of miR-361-3p. The in vivo experiments also suggested that tumor growth was inhibited by knockdown of circDHDDS. Moreover, we also found that miR-361-3p specifically bound to WNT3A, and overexpression of miR-361-3p suppressed RB development by decreasing WNT3A expression. Summarily, circDHDDS, a molecule sponge of miR-361-3p, regulated the expression of WNT3A. Therefore, circDHDDS/miR-361-3p/WNT3A axis stimulated the development of RB by regulation of proliferation, cell cycle program, migration, and invasion of RB cells.
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http://dx.doi.org/10.1007/s11064-020-03112-0DOI Listing
November 2020

NUSAP1 gene silencing inhibits cell proliferation, migration and invasion through inhibiting DNMT1 gene expression in human colorectal cancer.

Exp Cell Res 2018 06 30;367(2):216-221. Epub 2018 Mar 30.

The First Department of Oncology, Cangzhou Central Hospital, Cangzhou, Hebei, China.

Colorectal cancer (CRC) is one of the most common cause of cancer-related death in both female and male patients, with a high capacity for tumor migration and invasion. Recently, aberrant nucleolar and spindle-associated protein 1 (NUSAP1) expression has been reported in several cancers. However, the biological function and molecular mechanism of NUSAP1 in CRC have not been reported. Here, we demonstrated that NUSAP1 gene expression was notably upregulated in CRC tissues and cell lines (Caco2, LS174T, SW480, and LoVo). Subsequently, SW480 and LoVo cells were transfected with NUSAP1 siRNA, respectively, and the biological function of NUSAP1 was investigated. Results indicated that NUSAP1 silencing by siRNA inhibited CRC cell proliferation, and induces cell apoptosis. Moreover, NUSAP1 knockdown suppressed cell migration, cell invasion, and epithelial-to-mesenchymal transition (EMT). Furthermore, NUSAP1 silencing notably inhibited the mRNA and protein expression level of DNA methyltransferase 1 (DNMT1). DNMT1 overexpression partly rescued the effect of NUSAP1 silencing on colorectal cancer biological function. Taken together, NUSAP1 gene silencing induced cell apoptosis, and inhibited cell proliferation, cell migration, cell invasion, and EMT in colorectal cancer through inhibiting DNMT1 gene expression. These findings indicat that NUSAP1 is a promising molecular target for CRC treatment.
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http://dx.doi.org/10.1016/j.yexcr.2018.03.039DOI Listing
June 2018

Lack of ClC-2 Alleviates High Fat Diet-Induced Insulin Resistance and Non-Alcoholic Fatty Liver Disease.

Cell Physiol Biochem 2018 10;45(6):2187-2198. Epub 2018 Mar 10.

2ndDepartment of Endocrinology, Hebei, China.

Background/aims: Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease. This study aims to investigate whether chloride channel 2 (ClC-2) is involved in high fat diet (HFD)-induced NAFLD and possible molecular mechanisms.

Methods: ClC-2 expression was liver-specifically downregulated using adeno-associated virus in C57BL/6 mice treated with a chow diet or HFD for 12 weeks. Peripheral blood and liver tissues were collected for biochemical and pathological estimation respectively. Western blotting was applied to detect the protein expressions of lipid synthesis-related enzymes and the phosphorylated level of IRS-1, Akt and mTOR.

Results: ClC-2 mRNA level was significantly increased in patients with non-alcoholic steatohepatitis, which positively correlated with the plasma levels of alanine transaminase (ALT), aspartate transaminase (AST) and insulin. Knockdown of ClC-2 in liver attenuated HFD-induced weight gain, obesity, hepatocellular ballooning, and liver lipid accumulation and fibrosis, accompanied by reduced plasma free fatty acid (FFA), triglyceride (TG), total cholesterol (TC), ALT, AST, glucose and insulin levels and homeostasis model of insulin resistance (HOMA-IR) value. Moreover, HFD-treated mice lacking ClC-2 showed inhibited hepatic lipid accumulation via regulating lipid metabolism through decreasing sterol regulatory element binding protein (SREBP)-1c expression and its downstream targeting enzymes such as fatty acid synthase (FAS), HMG-CoA reductase (HMGCR) and acetyl-Coenzyme A carboxylase (ACCα). In addition, in vivo and in vitro results demonstrated that ClC-2 downregulation in HFD-treated mice or HepG2 cells increased the sensitivity to insulin via activation of IRS-1/Akt/mTOR signaling pathway.

Conclusion: Our present study reveals a critical role of ClC-2 in regulating metabolic diseases. Mice lacking ClC-2 are associated with a remarkably beneficial metabolic phenotype, suggesting that decreasing ClC-2 may be an attractive therapeutic strategy for the treatment of NAFLD.
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http://dx.doi.org/10.1159/000488164DOI Listing
June 2018

Long noncoding RNA CCAT2 is activated by E2F1 and exerts oncogenic properties by interacting with PTTG1 in pituitary adenomas.

Am J Cancer Res 2018 1;8(2):245-255. Epub 2018 Feb 1.

The First Department of Oncology Surgery, Cangzhou Central Hospital, Hebei Medical UniversityCangzhou, China.

Pituitary adenomas, arising from the pituitary gland cells, are one of the most frequent tumors found in the sella region. However, the molecular mechanisms involved in the carcinogenesis and progression of pituitary adenomas is still not understood in detail. Long noncoding RNA (lncRNA) colon cancer-associated transcript 2 (CCAT2), a newly identified lncRNA, has been reported to be abnormally expressed in some cancers. In the present study, we found that CCAT2 was significantly upregulated in pituitary adenomas tissues. Elevated CCAT2 expression was correlated with poor prognosis in patients with pituitary adenomas. Moreover, CCAT2 expression was activated by E2F1. Loss-of-function and gain-of-function assays showed that CCAT2 positively regulated pituitary adenoma cell proliferation, migration, and invasion. Further investigation demonstrated that CCAT2 interacted with PTTG1, and promoted its stability. Furthermore, CCAT2 affected the expression of downstream genes regulated by PTTG1, including , , , and . Cumulatively, CCAT2 functions as an oncogene in pituitary adenomas and its overexpression contributes to pituitary adenoma carcinogenesis and progression.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5835692PMC
February 2018

A novel percutaneous achievement and maintenance of reduction and screw fixation for acute displaced scaphoid fractures: minimum two-year follow-up.

Int Orthop 2018 08 10;42(8):1911-1916. Epub 2018 Jan 10.

Hand Surgery, The Third Hospital Of Hebei Medical University, No.139, Ziqiang Road, Qiaoxi District, Shijiazhuang, Hebei, 050051, People's Republic of China.

Purpose: The purpose of this study was to introduce a novel method of percutaneous achievement and maintenance of reduction for acute displaced scaphoid fractures and evaluate the feasibility of this method in treating acute displaced scaphoid fractures as well as explore its indications.

Methods: From February 2012 to March 2014, 15 patients with acute displaced scaphoid fractures were treated with our technique. Two Kirschner wires were used to achieve and maintain the reduction of the scaphoid fractures throughout the entire process of the traditional percutaneous screw fixation process. The following parameters including function scores according to modified Mayo wrist scoring system, range of motion (ROM) of the wrist, grip strength, pinch strength, healing time, time to return to work, and final outcomes were recorded.

Result: All patients were followed up with a mean period of 2.5 years (range, 2-3.5 years). All fractures healed with a mean of 9.3 weeks (range, 7-11.5 weeks). All patients returned to pre-injury level of activity within six weeks. The functional scores averaged 90.3 (range, 80-100). ROM of the wrist was equal to that of the contralateral side at three months postoperatively. Grip strength and pinch strength compared with contralateral were 98% and 92%, respectively. All were satisfied with the final outcomes.

Conclusions: Our technique is successfully performed in acute displaced scaphoid fractures resulting in shortened immobilization and prompt functional recovery. It broadens the indications of the percutaneous method, which means the advantages of the percutaneous method are maximally reserved whilst the drawbacks of open reduction were avoided.
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http://dx.doi.org/10.1007/s00264-018-3758-5DOI Listing
August 2018

A two-step approach for copper and nickel extracting and recovering by emulsion liquid membrane.

Water Sci Technol 2016 Nov;74(10):2454-2461

China Petroleum Engineering Co., Ltd Beijing Company, Beijing 100010, China.

The recycling of copper and nickel from metallurgical wastewater using emulsion liquid membrane (ELM) was studied. P507 (2-ethylhexyl phosphonic acid-2-ethylhexyl ester) and TBP (tributyl phosphate) were used as carriers for the extraction of copper and nickel by ELMs, respectively. The influence of four emulsion composition variables, namely, the internal phase volume fraction (ϕ), surfactant concentration (Wsurf), internal phase stripping acid concentration (Cio) and the carrier concentration (Cc), and the process variable treat ratio on the extraction efficiencies of copper or nickel were studied. Under the optimum conditions, 98% copper and nickel were recycled by using ELM. The results indicated that ELM extraction is a promising industrial application technology to retrieve valuable metals in low concentration metallurgical wastewater.
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http://dx.doi.org/10.2166/wst.2016.393DOI Listing
November 2016

Meta-analysis in the association between obesity and risk of thyroid cancer.

Int J Clin Exp Med 2014 15;7(12):5268-74. Epub 2014 Dec 15.

First Department of Tumor Surgery, The Center Hospital of Cangzhou Cangzhou 061001, Hebei, China.

Although many epidemiologic studies have investigated obesity and thyroid cancer risk, definite conclusions cannot be drawn. To clarify the effects of obesity on the risk of thyroid cancer, a meta-analysis was performed. Related studies were identified from PubMed, Springer Link, Ovid, Chinese Wanfang Data Knowledge Service Platform, Chinese National Knowledge Infrastructure (CNKI), and Chinese Biology Medicine (CBM) till 16 Aug 2014. Pooled RRs and 95% CIs were used to assess the strength of the associations. A total of 16 studies including 12616154 subjects were involved in this meta-analysis. A significantly elevated thyroid cancer risk was found in overall analysis (RR = 1.29, 95% CI 1.20-1.37, P < 0.00001). In the gender subgroup analyses, a statistically significant association was found in male patients (RR = 1.35, 95% CI 1.16-1.58, P = 0.0001) and in female patients (RR = 1.29, 95% CI 1.19-1.40, P < 0.00001). When we limited the meta-analysis to studies that controlled for age (RR = 1.34, 95% CI 1.24-1.44, P < 0.00001), smoke (RR = 1.36, 95% CI 1.22-1.52, P < 0.00001), alcohol use (RR = 1.40, 95% CI 1.15-1.71, P = 0.0009), and history of benign thyroid disease (RR = 1.51, 95% CI 1.24-1.83, P < 0.0001), a significant association between obesity and thyroid cancer risk remained. This meta-analysis provides the evidence that obesity may contribute to the thyroid cancer development.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4307477PMC
February 2015

[Advantage of D2+ lymph node dissection for distal advanced gastric cancer].

Zhonghua Wei Chang Wai Ke Za Zhi 2015 Feb;18(2):127-30

Department of Gastrointestinal Oncology Surgery, Key Lab of Cancer Treatment and Prevention of Tianjin, Tianjin Cancer Hospital, Tianjin Medical University, Tianjin 300060, China.

Objective: To evaluate the value of D2+ lymph node dissection for patients with distal advanced gastric cancer.

Methods: Clinicopathological data of 305 cases with distal advanced gastric cancer receiving D2+(n=68) or D2(n=237) lymph node dissection in the Tianjin Cancer Hospital from January 2003 to December 2007 were analyzed retrospectively. The overall 5-year survival rate between the 2 groups.

Results: The median survival was 36 months and the 5-year overall survival rate was 40.3% in all patients. The 5-year overall survival rates in the D2+ and D2 groups were 50.4% and 37.4% respectively, and the difference was statistically significant(P=0.049). In multivariate prognostic analysis however, the extent of lymph node dissection was not identified as an independent prognostic factor(P=0.174). Subgroup analysis showed that 5-year survival rate of D2+ group was significantly higher as compared to D2 group for the following subgroups: maximum diameter of tumor larger than 4 cm(43.9% vs. 27.0%), Borrmann type III(-IIII((55.5% vs. 30.1%), poorly differentiated and undifferentiated tumor (49.8% vs. 37.0%), T4 stage (47.8% vs. 31.0%), N2 stage (53.3% vs. 13.9%), N3 stage (20.0% vs. 9.6%) and positive No.6 lymph nodes (33.1% vs. 16.0%).

Conclusion: Compared with D2 lymph node dissection, D2+ lymph node dissection may benefit some patients with large, poorly differentiated, or late-stage tumor.
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February 2015

Association between matrix metalloproteinase 1 -1607 1G>2G polymorphism and cancer risk: a meta-analysis including 19706 subjects.

Int J Clin Exp Med 2014 15;7(9):2992-9. Epub 2014 Sep 15.

The First Department of Tumor Surgery, The Center Hospital of Cangzhou Cangzhou 061001, Hebei, P. R. China.

The association between MMP1 -1607 1G>2G polymorphism and cancer risk has been reported, but results remained controversial and ambiguous. To assess the association between MMP1 -1607 1G>2G polymorphism and cancer risk, a meta-analysis was performed. Based on comprehensive searches of the PubMed, Elsevier Science Direct, Excerpta Medica Database (Embase), and Chinese Biomedical Literature Database (CBM), we identified outcome data from all articles estimating the association between MMP1 -1607 1G>2G polymorphism and cancer risk. The pooled odds ratio (OR) with 95% confidence intervals (CIs) were calculated. Thirty-eight studies involving 10178 cases and 9528 controls were included. Overall, significant association between MMP1 -1607 1G>2G polymorphism and cancer susceptibility was observed for additive model (OR = 1.21, 95% CI 1.09-1.35), for codominant model (OR = 1.34, 95% CI 1.10-1.63), for dominant model (OR = 1.17, 95% CI 1.01-1.34), for recessive model (OR = 1.31, 95% CI 1.14-1.52). In the subgroup analysis by ethnicity, the significant association was found among Asians but not among Caucasians. In the subgroup analysis by site of cancer, significant associations were found among lung cancer, colorectal cancer, head and neck cancer and bladder cancer. This meta-analysis demonstrated that the MMP1 -1607 1G>2G polymorphism was significantly associated with cancer risk.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4211823PMC
October 2014