Ping Sun

Ping Sun


Research Focus & Metrics

Academic Career Length

14Years (2013-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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22 February 2013 in Experimental and Therapeutic Medicine
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Journal Article
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SZShiguang Zhu
Shiguang Zhu
PSPing Sun
Ping Sun
YZYingxin Zhang
Yingxin Zhang
LYLiping Yan
Liping Yan
BLBing Luo
Bing Luo
The aim of this study was to detect the expression of proliferatng cell nuclear antigen (PCNA) and c-myc in Epstein‑Barr virus (EBV)-associated gastric carcinoma (EBVaGC) and EBV-negative gastric carcinoma (EBVnGC), as well as the expression of EBV-encoded proteins in EBVaGC and their effect on carcinogenesis and the development of gastric cancer. The PCNA and c-myc protein levels were assessed by immunohistochemistry in 13 EBVaGC and 45 EBVnGC specimens. The expression of related genes of EBV, including EB nuclear antigen (NA)-1 and EBNA2 genes, latent membrane protein 1 (LMP1) and early genes BARF1 and BHRF1 were tested by reverse transcription-polymerase chain reaction (RT-PCR) and southern blotting. The PCNA labeling index (LI) of EBVaGCs, EBVnGCs and the corresponding adjacent tissues of EBVaGCs were 49.3768±12.1832, 14.839±7.1847, 35.613±8.3831 and 24.2735±10.1332, respectively. The PCNA LI was significantly different between EBVaGC and EBVnGC of EBVaGC (t=4.686, P<0.01). The difference between EBVaGC and corresponding adjacent tissues of EBVaGC was also significant (t=8.805, P<0.01). The expression of c-myc protein was detected in 33 of 58 (55.39%) gastric carcinomas and in 21 of 58 (36.21%) adjacent tissues. There was a significant difference between the two groups (χ2=4.989, P0.05). EBNA1 mRNA was detected in all 13 EBVaGC cases, while EBNA2 and LMP1 mRNA was not detected in these cases. Of the 13 EBV-positive samples, 6 exhibited BARF1 transcripts and 2 exhibited BHRF1 transcripts. c-myc expression did not correlate with the presence of EBV in EBVaGC. EBV infection may induce PCNA expression. The lack of EBNA2 and LMP1 protein expression in EBVaGC suggests that EBNA2 and LMP1 do not correlate with cell apoptosis and c-myc expression. Early genes BARF1 and BHRF1 may play an important role in the development and progression of gastric carcinomas by immortalizing epithelial cells.

1 February 2017 in International Journal of Gynecological Cancer
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Journal Article
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PSPing Sun
Ping Sun
YSYong Shen
Yong Shen
JGJiao-Mei Gong
Jiao-Mei Gong
Lili ZhouLili Zhou
Lili Zhou
JSJia-He Sheng
Jia-He Sheng
FDFujiao Duan
Fujiao Duan

30 October 2017 in PLOS ONE
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HHHairong Huang
Hairong Huang
ZXZanzan Xu
Zanzan Xu
XSXianhong Shao
Xianhong Shao
DWDaniel Wismeijer
Daniel Wismeijer
PSPing Sun
Ping Sun
GWGang Wu
Gang Wu
This study identified potential general influencing factors for a mathematical prediction of implant stability quotient (ISQ) values in clinical practice. We collected the ISQ values of 557 implants from 2 different brands (SICace and Osstem) placed by 2 surgeons in 336 patients. Surgeon 1 placed 329 SICace implants, and surgeon 2 placed 113 SICace implants and 115 Osstem implants. ISQ measurements were taken at T1 (immediately after implant placement) and T2 (before dental restoration). A multivariate linear regression model was used to analyze the influence of the following 11 candidate factors for stability prediction: sex, age, maxillary/mandibular location, bone type, immediate/delayed implantation, bone grafting, insertion torque, I-stage or II-stage healing pattern, implant diameter, implant length and T1-T2 time interval. The need for bone grafting as a predictor significantly influenced ISQ values in all three groups at T1 (weight coefficients ranging from -4 to -5). In contrast, implant diameter consistently influenced the ISQ values in all three groups at T2 (weight coefficients ranging from 3.4 to 4.2). Other factors, such as sex, age, I/II-stage implantation and bone type, did not significantly influence ISQ values at T2, and implant length did not significantly influence ISQ values at T1 or T2. These findings provide a rational basis for mathematical models to quantitatively predict the ISQ values of implants in clinical practice.

19 May 2021 in Pharmaceuticals
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changjing shichangjing shi
changjing shi
Yu YaoYu Yao
Yu Yao
LWLei Wang
Lei Wang
PSPing Sun
Ping Sun
JFJianying Feng
Jianying Feng
GWGang Wu
Gang Wu
The avascular structure and lack of regenerative cells make the repair of osteochondral defects in the temporomandibular joint (TMJ) highly challenging in the clinic. To provide a viable treatment option, we developed a methacrylated gelatin (Gel-MA) hydrogel functionalized with human salivary histatin-1 (Hst1). Gel-MA is highly biocompatible, biodegradable, and cost-effective. Hst1 is capable of activating a series of cell activities, such as adhesion, migration, differentiation, and angiogenesis. To evaluate the efficacy of Hst1/Gel-MA, critical-size osteochondral defects (3 mm in diameter and 3 mm in depth) of TMJ in New Zealand white rabbits were surgically created and randomly assigned to one of the three treatment groups: (1) control (no filling material); (2) Gel-MA hydrogel; (3) Hst1/Gel-MA hydrogel. Samples were retrieved 1, 2, and 4 weeks post-surgery and subjected to gross examination and a series of histomorphometric and immunological analyses. In comparison with the control and Gel-MA alone groups, Hst1/Gel-MA hydrogel was associated with significantly higher International Cartilage Repair Society score, modified O’Driscoll score, area percentages of newly formed bone, cartilage, collagen fiber, and glycosaminoglycan, and expression of collagen II and aggrecan. In conclusion, Hst1/Gel-MA hydrogels significantly enhance bone and cartilage regeneration, thus bearing promising application potential for repairing osteochondral defects.

7 August 2017 in Oncotarget
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Lili ZhouLili Zhou
Lili Zhou
YSYong Shen
Yong Shen
JGJiao-Mei Gong
Jiao-Mei Gong
PSPing Sun
Ping Sun
JSJia-He Sheng
Jia-He Sheng
// <![CDATA[ $('.header-date').hide();$('#titleAuthors').hide();$('#abstractHeader').hide(); // ]]> Li-Li Zhou1, *, Yong Shen1, *, Jiao-Mei Gong2, *, Ping Sun1 and Jia-He Sheng1 1Department of Clinical Laboratory, Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, Henan, China 2Department of Clinical Laboratory, Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China *These authors have contributed equally to this work Correspondence to: Li-Li Zhou, email: zhoulilimy@126.com Keywords: microRNA-466, cervical cancer, tumor marker, screening, diagnoses Received: June 20, 2017 Accepted: July 13, 2017 Published: August 07, 2017 ABSTRACT Cervical cancer is the second most common cancer in women in the world. In this study, we explore tumor markers and microRNA-466 combination for cervical cancer screening. Tumor markers were measured by the methods of electro-chemiluminescent immunoassay and enzyme immunoassay. The microRNA-466 was performed by quantitative real-time polymerase chain reaction. Among normal group, hyperplasia group and cancer group, the CEA expression levels were 2.26 ng/ml, 3.85 ng/ml and 16.08 ng/ml, respectively. While the CA125 expression levels were 13.61 u/ml, 27.32 u/ml and 44.93 u/ml, respectively. The SCCA expression levels were 13.61 ng/ml, 27.32 ng/ml and 44.93 ng/ml, respectively. The expression levels of tumor markers were all gradually increased with the development of cervical lesions. The expression levels of microRNA-466 in cervical cancers (0.62) were greater than that in normal (0.076) and hyperplasia (0.24). The expression of microRNA-466 was correlated with lymphnode metastasis (P=0.000). There is a lower overall survival rate of patient with large tumor or lymphnode metastasis. Thus, the combination of tumor markers and microRNA-466 can be useful for early detection of cervical cancer and indicators for advanced stage and prognosis of the disease.

12 March 2018 in PLOS ONE
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JLJakub Lubiński
Jakub Lubiński
WMWojciech Marciniak
Wojciech Marciniak
MMMagdalena Muszynska
Magdalena Muszynska
EJEwa Jaworowska
Ewa Jaworowska
MSMieczyslaw Sulikowski
Mieczyslaw Sulikowski
JLJan Lubiński
Jan Lubiński
[This corrects the article DOI: 10.1371/journal.pone.0184873.].