Abstract: Background: Chronic periodontitis are associated with the resorption of alveolar bone. Sclerostin participates in the process of bone resorption through the RANKL/RANK/OPG pathway. However, the mechanism of bone resorption and sclerostin expression in chronic periodontitis is unclear. In this study, the purpose was to evaluate the mechanism of action of sclerostin in human chronic periodontitis. Methods: Saliva and gingival crevicular fluid were collected from systemically healthy non-periodontitis (n=30) and chronic periodontitis subjects (n=30). The protein levels of sclerostin, RANKL and OPG in saliva and gingival crevicular fluid were detected by enzyme linked immunosorbent assay (ELISA). Results: Sclerostin levels in saliva and gingival crevicular fluid were significantly higher in the chronic periodontitis group than the non-periodontitis group (P < 0.05). The level of OPG is significantly lower but the RANKL level and the ratio of RANKL/OPG was significantly higher than that in the non-periodontitis group in saliva and gingival crevicular fluid (P < 0.05). Sclerostin levels in saliva and gingival crevicular fluid were significantly positively correlated with PD, CAL and BOP (P < 0.05). Conclusions: The results showed that sclerostin may affect bone tissue damage of chronic periodontitis through RANKL/RANK/OPG pathway. It will provide a new insight into the diagnosis and treatment of periodontitis patients.

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	1. The role of sclerostin and receptor activator of nuclear factor κB ligand/osteoprotegerin signalling pathways in chronic periodontitis
	Wang Tiantian,Yuan Xuemin,Zhang Xingxing,LI Yue,Pang Yunqing,Wang Xuemei,Wang Jing
	Clinical Medicine 20 April 2018
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	Abstract: Background: Chronic periodontitis are associated with the resorption of alveolar bone. Sclerostin participates in the process of bone resorption through the RANKL/RANK/OPG pathway. However, the mechanism of bone resorption and sclerostin expression in chronic periodontitis is unclear. In this study, the purpose was to evaluate the mechanism of action of sclerostin in human chronic periodontitis. Methods: Saliva and gingival crevicular fluid were collected from systemically healthy non-periodontitis (n=30) and chronic periodontitis subjects (n=30). The protein levels of sclerostin, RANKL and OPG in saliva and gingival crevicular fluid were detected by enzyme linked immunosorbent assay (ELISA). Results: Sclerostin levels in saliva and gingival crevicular fluid were significantly higher in the chronic periodontitis group than the non-periodontitis group (P < 0.05). The level of OPG is significantly lower but the RANKL level and the ratio of RANKL/OPG was significantly higher than that in the non-periodontitis group in saliva and gingival crevicular fluid (P < 0.05). Sclerostin levels in saliva and gingival crevicular fluid were significantly positively correlated with PD, CAL and BOP (P < 0.05). Conclusions: The results showed that sclerostin may affect bone tissue damage of chronic periodontitis through RANKL/RANK/OPG pathway. It will provide a new insight into the diagnosis and treatment of periodontitis patients.
	TO cite this article:Wang Tiantian,Yuan Xuemin,Zhang Xingxing, et al. The role of sclerostin and receptor activator of nuclear factor κB ligand/osteoprotegerin signalling pathways in chronic periodontitis[OL].[20 April 2018] http://en.paper.edu.cn/en_releasepaper/content/4744647


	2. The roles of serine racemase in excitotoxicity: implication in diabetic retinopathy
	Haiyan Jiang,He Zhang,Shengzhou Wu
	Clinical Medicine 17 April 2018
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	Abstract:Excitotoxicity is a pathologic process when excitatory amino acids such as glutamate kill neurons or nerve; this process is largely ascribed to over-activation of glutamate receptors including the NMDA/non-NMDA receptors. Activation of the NMDA receptor is dependent on the binding of glutamate to GluN2 subunit and of D-serine/glycine to GluN1 subunit. Excitotoxicity accounts for neurodegeneration in stroke, traumatic brain injury, neurodegenerative diseases including Alzheimer\'s disease and amyotrophic lateral sclerosis, even in diabetic retinopathy (DR). DR is characterized with retinal neurodegeneration and retinal microvascular abnormalities; a plethora of data indicate that retinal neurodegeneration precedes microvascular abnormalities. In the last decade, neurodegeneration in DR has been highlighted; inflammation and oxidation due to hyperglycemia have been connected with retinal neuronal loss. Although the underlying mechanisms remain elusive, convincing data suggest the critical role of over-activation of NMDAR underlying retinal neurodegeneration. Recent data including ours demonstrate that overexpression of serine racemase and excessive D-serine contributes to neurodegeneration in DR; SR deficiency significantly rescues this retinal neuropathy. Herein, the role of serine racemase in excitotoxicity and the contribution to retinal neurodegeneration in DR have been reviewed.
	TO cite this article:Haiyan Jiang,He Zhang,Shengzhou Wu. The roles of serine racemase in excitotoxicity: implication in diabetic retinopathy[OL].[17 April 2018] http://en.paper.edu.cn/en_releasepaper/content/4744636

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	3. Derivation of a 17 myocardial segment angiographic scoring system and its validation
	XU Mingxing,HE Yongming
	Clinical Medicine 09 September 2017
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	Abstract:The Syntax Score has been devised to characterize the number of lesions, and their functional impact, location, and complexity in terms of coronary artery trees. An obvious fallacy is that the Syntax Score system over simply divided coronary artery circulation system into right or left dominant coronary artery circulation, which fails to reflect the great variability of coronary artery trees. Furthermore, the Syntax Score is in essence blood vessel-based rather than blood vessel importance-based. Finally, the scores assigned for the lesion characteristics, such as calcification, tortuosity, angulation, and thrombosis, etc, are largely arbitrary in the Syntax score. In the current study, we have aimed to devise a new scoring system, the 17 myocardial segment based coronary scoring system, to accurately describe the anatomical characteristics of the native coronary artery trees, to grade the complexity of the acquired coronary artery diseases according to the importance of a blood vessel, and to collect the treatment information on lesions. We have successfully completed a program to realize the above-mentioned aims based on the following preexisting or initiated classifications or rules: 54 coronary artery circulations; a 17 myocardial segment model; the 3 areas delineated by 3 anatomical landmarks on the left heart surface; law of competitive myocardial blood supply for the 3 areas; and blood flow for parent vessels equals the summation of blood flow for daughter vessels. The utility of the 17 myocardial segment based coronary scoring system for prediction of outcomes will be investigated prospectively in the conduct of the trial: in acute myocardial infarction patients undergoing emergency percutaneous coronary intervention trial (AMI-EPCI trial). Once validated and standardized, the 17 myocardial segment based coronary scoring system will be available online.
	TO cite this article:XU Mingxing,HE Yongming. Derivation of a 17 myocardial segment angiographic scoring system and its validation[OL].[ 9 September 2017] http://en.paper.edu.cn/en_releasepaper/content/4741405


	4. Clinicopathological and prognostic significance of circulating tumor cells in patients with esophageal cancer : A meta-analysis
	Hou Jinxuan,Zou Kun,Xu Yu
	Clinical Medicine 09 September 2017
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	Abstract:The aim of this meta-analysis was to assess the clinicopathological and prognostic significance of circulating tumor cells (CTCs) in patients with esophageal cancer. We searched PubMed, EMBASE, Science Citation Index Expanded, Cochrane library (from inception to October 2016) with the key words "esophageal cancer", "circulating tumor cells", "prognosis" and "peripheral blood". Hazard ratio, risk ratio, odds ratio and their 95% confidence intervals were set as effect measures. All analyses were performed by STATA 12.0. 17 studies were retrieved, CTCs positive was significant associated with poor progression-free survival (HR = 2.55; 95%CI: 2.12-3.06) and overall survival (HR = 2.46; 95%CI: 1.94-3.11). CTCs positive were also associated with high recurrence (OR=2.66; 95%CI: 1.63-4.35) and poor response of chemoradiotherapy (RR=0.80; 95%CI: 0.66-0.97). For clinicopathological characteristics, CTCs positive was significantly associated with TNM staging, depth of infiltration, regional lymph nodes metastasis, distant metastasis, lymphatic invasion and venous invasion. The meta-analysis has confirmed the significant clinicopathological and prognostic value of CTCs positive for both PFS and OS in patients with esophageal cancer.
	TO cite this article:Hou Jinxuan,Zou Kun,Xu Yu. Clinicopathological and prognostic significance of circulating tumor cells in patients with esophageal cancer : A meta-analysis[OL].[ 9 September 2017] http://en.paper.edu.cn/en_releasepaper/content/4741316


	5. Novel Functions of MicroRNA-17-92 Cluster in the Endocrine System
	Wan Shan,Chen Xiang,He Yuedong,Yu Xijie
	Clinical Medicine 26 June 2017
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	Abstract:MiR-17-92 cluster is coded by MIR17HG in chromosome 13, which can be further processed to form six mature miRNAs and is highly conserved in vertebrates. Published literatures have proved that miR-17-92 cluster is expressed at a wide range of tissues and cells, and plays important functions during lung, heart and immune system development. MiR-17-92 cluster is deregulated in various types of tumors and crtically regulates tumorigenesis and metastsis. Recent research shows that miR-17-92 cluster also plays novel functions in the endocrine system. Mutations of MIR17HG are responsible for the skeletal abnormalities in the Feingold Syndrome. Circulating levels of miR-17-92 cluster are abnormal in obesity and diabetes patients. MiR-17-92 cluster is essential for glucose-stimulated insulin secretion and β cell adaptation under metabolic stress. In the present review, we summarized recent findings in the physiological and pathological roles of miR-17-92 cluster in the glucose, bone and lipid metabolisms, and discussed the possibility of using miR-17-92 cluster signaling pathway as the diagnostic and therapeutic options for related disorders.
	TO cite this article:Wan Shan,Chen Xiang,He Yuedong, et al. Novel Functions of MicroRNA-17-92 Cluster in the Endocrine System[OL].[26 June 2017] http://en.paper.edu.cn/en_releasepaper/content/4737877


	6. Current approaches and challenges for regenerative endodontic therapy
	ZHENG Yi,GAO Bo
	Clinical Medicine 19 May 2017
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	Abstract:Immature teeth are susceptible to infections due to trauma, anatomic anomalies, and caries. Traditional endodontic therapy such as apexification and pulpotomy have several disadvantages, including the unpredictability of apical barrier formation and the long duration of treatment. Regenerative endodontic therapy provides an alternative treatment approach that builds on the principles of regenerative medicine and biological tissue engineering process. This process includes two key parts: one is pulp revascularization, regenerating new vital pulp tissue in the root canal to promote continuous root growth and development; the other is tissue engineering, stem cells under the induction of suitable biological active scaffold and growth factors promote pulp dentin complex regeneration. The aim of the therapy is not only for a resolution of pain, inflammation and periapical lesions, but also for regenerating functional pulpal tissue to promote root development in terms of both length and thickness. This review summarizes the recent concept of pulp revascularization in the treatmet of immature teeth with nonvital pulps and the emerging research on pulp tissue engineering, and put insight of the challenges and clinical outcomes of regenerative endodontic therapy.
	TO cite this article:ZHENG Yi,GAO Bo. Current approaches and challenges for regenerative endodontic therapy[OL].[19 May 2017] http://en.paper.edu.cn/en_releasepaper/content/4735088


	7. Perspectives of traditional Chinese medicine in pancreas protection for acute pancreatitis
	LI Jun,ZHANG Shu,ZHOU Rui,ZHANG Jian,LI Zongfang
	Clinical Medicine 10 May 2017
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	Abstract:Acute pancreatitis (AP) is one of the most common diseases. AP is associated with significant morbidity and mortality, but it lacks specific and effective therapies. Traditional Chinese medicine (TCM) is one of the most popular complementary and alternative medicine modalities worldwide for the treatment of AP. The current evidence from basic research and clinical studies has shown that TCM has good therapeutic effects on AP. This review summarizes the widely used formulas, single herbs and monomers that are used to treat AP and the potential underlying mechanisms of TCM. Because of the abundance, low cost, and safety of TCM as well as its ability to target various aspects of the pathogenesis, TCM provides potential clinical benefits and a new avenue with tremendous potential for the future treatment of AP.
	TO cite this article:LI Jun,ZHANG Shu,ZHOU Rui, et al. Perspectives of traditional Chinese medicine in pancreas protection for acute pancreatitis[J].


	8. The establishment of gene expression profiling-guided clinical precision treatment for patients with endometrial carcinoma
	ZHOU Jingyi,Yin Fufen,LI Xiaoping,YAO Yuanyang,CHEN Yonghua,GAO Baorong,YANG Yuan,YANG Yingchao,LI Mingzhu,ZHAO Lijun,WANG Zhiqi,SHEN Danhua,WEI Lihui,WANG JianLiu
	Clinical Medicine 08 May 2017
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	Abstract:Endometrial carcinoma (EC) is a common gynaecologic cancer. Most EC patients, especially those with early stage endometrioid endometrial adenocarcinoma (EEC), will have a good prognosis. Studies showed that similar staging and histology results in early stage EC patients had completely different prognoses postoperatively. EC is a highly heterogeneous disease, and different genetic alterations may exist in the same histological phenotype of carcinoma, indicating that some flaws exist in the current therapy strategy based on the clinical pathological classification and Bokhman's classification. It's necessary to establish new molecular type of the EC. 492 EC-related genes from the NCBI database were selected, and oligoprobes were then designed with the UniGene Database and the Human Reference Sequence (RefSeq) Database. An EC-related, 492-gene microarray was constructed with the oligoprobes. A hierarchical cluster algorithm was used to sort tumour samples according to gene expression patterns. Significance analysis of microarrays (SAM) was used to select the different expressed genes. Genes' expression were tested by immunohistochemistry assay. Results showed that the UPSC samples exhibited distinct gene expression profiles compared to those of EEC and 46 genes that could highly discriminate UPSC from EEC. 21 genes were selected and defined as EC prognosis-related genes and some of the genes. Our data suggests seeking new molecular type of the EC different from the traditional clinical pathological classification and Bokhman's classification, will help in the accurate prognosis and practice of precise therapy of EC.?????
	TO cite this article:ZHOU Jingyi,Yin Fufen,LI Xiaoping, et al. The establishment of gene expression profiling-guided clinical precision treatment for patients with endometrial carcinoma[OL].[ 8 May 2017] http://en.paper.edu.cn/en_releasepaper/content/4729555


	9. The roles of mitoferrin-2 in the process of arsenic trioxide-induced cell damage in human gliomas
	WANG Ligang
	Clinical Medicine 08 May 2017
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	Abstract:Background: Among glioma treatment strategies, arsenic trioxide (As2O3) has shown efficacy as a therapeutic agent against human gliomas. However, the exact antitumor mechanism of action of As2O3 is still unclear. Mitochondria are considered to be the major source of intracellular reactive oxygen species (ROS), which are known to be associated with As2O3-induced cell damage. Therefore, we investigated whether mitoferrin-2, a mitochondrial iron uptake transporter, participates in As2O3-induced cell killing in human gliomas. Methods: Human glioma cell lines were used to explore the mechanism of As2O3's antitumor effects. First, expression of mitoferrin-2 was analyzed in glioma cells that were pretreated with As2O3. Changes in ROS production and apoptosis were assessed. Furthermore, cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). Results: In the present study we found that As2O3 induced ROS production and apoptosis in glioma cells. In addition, gene expression of mitoferrin-2, a mitochondrial iron uptake transporter, was increased 4 to 5 fold after exposure to As2O3 (5 μM) for 48 hours. Furthermore, apoptosis and cytotoxicity induced by As2O3 in glioma cells were decreased after silencing the mitoferrin-2 gene. Conclusions: Our findings indicated that mitoferrin-2 participates in mitochondrial ROS-dependent mechanisms underlying As2O3-mediated damage in glioma cells.
	TO cite this article:WANG Ligang. The roles of mitoferrin-2 in the process of arsenic trioxide-induced cell damage in human gliomas[OL].[ 8 May 2017] http://en.paper.edu.cn/en_releasepaper/content/4733708


	10. ACVR1-Fc Suppresses BMP Signaling and Chondro-osseous Differentiation in an in vitro Model of Fibrodysplasia Ossificans Progressiva
	Zhang Keqin,Pang Jing,Zuo Yue
	Clinical Medicine 06 May 2017
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	Abstract:Fibrodysplasia ossi?cans progressiva (FOP) is a rare and devastating genetic disease of heterotopic endochondral ossi?cation (HEO), and currently no effective therapies are available for this disease. A recurrent causative heterozygous mutation (c.617 G>A; R206H) for FOP was identified in activin receptor type IA (ACVR1), a bone morphogenetic protein (BMP) type I receptor. This mutation aberrantly activates the BMP-Smad1/5/8 signaling pathway and leads to HEO in FOP patients. Here we report development of a soluble recombinant ACVR1-Fc fusion protein by combining the extracellular domain of human wild type ACVR1 and the Fc portion of human immunoglobulin gamma 1 (IgG1). The ACVR1-Fc fusion protein significantly down-regulated the dysregulated BMP signaling caused by the FOP ACVR1 mutation and effectively suppressed chondro-osseous differentiation in a previously described cellular FOP model, human umbilical vein endothelial cells (HUVECs) that were infected with adenovirus-ACVR1R206H (HUVECR206H). This ACVR1-Fc fusion protein holds great promise for prevention and treatment of HEO in FOP and related diseases.
	TO cite this article:Zhang Keqin,Pang Jing,Zuo Yue. ACVR1-Fc Suppresses BMP Signaling and Chondro-osseous Differentiation in an in vitro Model of Fibrodysplasia Ossificans Progressiva[OL].[ 6 May 2017] http://en.paper.edu.cn/en_releasepaper/content/4731860

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