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	1. The roles of serine racemase in excitotoxicity: implication in diabetic retinopathy
	Haiyan Jiang,He Zhang,Shengzhou Wu
	Clinical Medicine 17 April 2018
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (209K B)

	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


	2. Color Doppler Ultrasonography as a Novel Diagnosis for Cyclodialysis Cleft
	Li Haibo,Cai Jinhong,Huang Yanming,Wu Duanxiao,Li Jianan,Huang Yunli,Mao Chunjie,Yan Hua
	Clinical Medicine 26 April 2017
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (4K B)

	Abstract:Several techniques have been described to detect cyclodialysis clefts preoperatively or intraoperatively. We developed a novel tool which presented rapid, convenient images of the cyclodialysis cleft as well as the condition of posterior segment of eyeball using the color Doppler ultrasonography. The location of the cleft was verified using high frequency ultrasound biomicroscopy.
	TO cite this article:Li Haibo,Cai Jinhong,Huang Yanming, et al. Color Doppler Ultrasonography as a Novel Diagnosis for Cyclodialysis Cleft[OL].[26 April 2017] http://en.paper.edu.cn/en_releasepaper/content/4730030


	3. Aberrant levels of circulating endothelial progenitor cells in type 2 diabetes mellitus patients with or without proliferative diabetic retinopathy
	Zhang Jingkai,Chen Qingzhong,Zhang Wei,Mao Chunjie,Zhang Zhuhong,Huang Bo,Yan Hua
	Clinical Medicine 22 April 2017
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (4K B)

	Abstract:Purpose: To investigate the number and function of circulating endothelial progenitor cells (EPC) in patients with type 2 diabetes mellitus (T2DM) with or without proliferative diabetic retinopathy (PDR). Methods: Circulating EPCs were isolated from 30 T2DM patients with PDR (60 eyes), 30 T2DM patients without PDR (60 eyes), as well as age matched control subjects (n=20). EPCs isolated from peripheral blood were quantified using flow cytometric analysis to count the number of CD34+, CD133+and VEGF R2+ cells. Following isolation, the EPCs were cultured in vitro to evaluate proliferation, adhesion and migration. Results: The number of circulating EPCs was significantly decreased in T2DM patients with and without PDR when compared with the healthy control individuals. In addition, the number of EPCs in the cultured samples from T2DM patients with and without PDR was lower compared with the control individuals. Furthermore, impaired proliferation, adhesion and migration were observed in the cultured EPCs from T2DM patients with and without PDR. Notably, increased numbers and aggravated dysfunction of EPCs were detected in T2DM patients with PDR compared with T2DM patients without PDR. In addition, a positive correlation was identified between the EPC number and PDR duration in T2DM patients with PDR.Conclusion: Reduced number and impaired function of circulating EPCs were observed in T2DM patients with or without PDR. In conclusion, EPC levels and aggravated EPC dysfunction in patients with PDR compared with patients without PDR may contribute to the pathogenesis of PDR in T2DM patients. EPC levels may be used as indicators in order to monitor PDR.
	TO cite this article:Zhang Jingkai,Chen Qingzhong,Zhang Wei, et al. Aberrant levels of circulating endothelial progenitor cells in type 2 diabetes mellitus patients with or without proliferative diabetic retinopathy[OL].[22 April 2017] http://en.paper.edu.cn/en_releasepaper/content/4728085


	4. The Effects of Pleiotrophin in Proliferative Vitreoretinopathy
	Ding Xue,Bai Yujing,Zhu Xuemei,Li Tianqi,Jin Enzhong,Huang Lvzhen,Yu Wenzhen,Zhao Mingwei
	Clinical Medicine 09 December 2016
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (4K B)

	Abstract:Purpose: The purpose of our study was to investigate the effects of pleiotrophin (PTN) in proliferative vitreoretinopathy (PVR) both in vitro and in vivo. Methods: Immunofluorescence was used to observe the PTN expression in periretinal membrane samples from PVR patients and controls. ARPE-19 cells were exposed to TGF-β1. The epithelial-to-mesenchymal transition (EMT) of the ARPE-19 cells was confirmed by observed morphological changes and the increased expression of α-SMA and fibronectin at both the mRNA and protein levels. We used specific small interfering (si)RNA to knockdown the expression of PTN. The subsequent effects of PTN inhibition were assessed regarding the EMT, migration, proliferation, cytoskeletal arrangement, TGF-β signaling, PTN signaling, integral tight junction protein expression (e.g., claudin-1 and occludin), p38 MAPK and p-p38 MAPK levels. A

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