Relation of visual field defect with pupil in patients with primary open angle glaucoma / 国际眼科杂志(Guoji Yanke Zazhi)

Abstract?AIM:To evaluate the pupil light reflex in patients with primary open angle glaucoma, and to investigate the relation between pupil and visual field defect.?METHODS:From July 2014 to October 2015, 115 eyes in 86 patients with primary open angle glaucoma and 23 eyes in 16 healthy individuals were continuously enrolled in this study.All the subjects received comprehensive eye examination, visual field examination ( Humphrey, SITA Standard 24-2 ) and dynamic pupil measurement ( MonCV3 Metrovision) .According to the visual field and the Glaucoma Staging System, the patients with glaucoma were divided into 5 subgroups: stage 1, stage 2, stage 3, stage 4 and stage 5. The parameters of pupillary light reflex were as follows: pupil diameter ( minimum, maximum ) , latency and duration of contraction, latency and duration of dilatation, contraction amplitude, contraction and dilatation speed, and percent of pupil contraction ( PPC ). SPSS 19.0 statistical software was used to analyze the measurement results.?RESULTS:The control group significantly differed from the stage 4 subgroup ( P=0.032 ) and stage 5 subgroup (P=0.014) in terms of minimum pupil diameter; there was significant difference in the pupil contraction speed between groups ( F =648.675, P <0.01 ), and the contraction speed in stage 5 subgroup was significantly lower than those in the other subgroups and control group (P<0.05); the control group significantly differed from the stage 3, stage 4, and stage 5 subgroup in terms of PPC ( P<0.05 ).Pupil contraction speed, PPC and minimum diameter showed correlation with the stages of glaucoma.?CONCLUSION:Pupil contraction ability in patients with primary open angle glaucoma was impaired, and the degree of impairment is related with the degree of visual field defect.

Effects of eukaryotic expression plasmid encoding human tumstatin gene on endothelial cells in vitro / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Tumstatin is a novel endogenous angiogenesis inhibitor which is widely studied using purified protein. The current study evaluates the antiangiogenic effects of tumstatin-overexpression plasmid in vitro, reveals the mechanism underlying the vascular endothelial cell growth inhibition and searches for a novel method administering tumstatin persistently.</p><p><b>METHODS</b>The eukaryotic expression plasmid pcDNA-tumstatin encoding tumstatin gene was constructed and transfected to human umbilical vein endothelial cell ECV304 and human renal carcinoma cell ACHN. Expression of tumstatin in the two cell lines was determined by RT-PCR and Western blotting. Vascular endothelial cell proliferation was assessed by CCK-8 assay and cell cycle was analyzed by flow cytometry. To investigate the mechanism by which pcDNA-tumstatin inhibited vascular endothelial cell proliferation in vitro, cyclin D1 protein was detected by Western blotting.</p><p><b>RESULTS</b>DNA sequence confirmed that pcDNA-tumstatin was successfully constructed. RT-PCR and Western blotting indicated that tumstatin could express in the two cell lines effectively. After tumstatin gene transfer, ECV304 cell growth was significantly inhibited and the cell cycle was arrested in G1 phase. And Western blotting showed that pcDNA-tumstatin decreased the level of cyclin D1 protein.</p><p><b>CONCLUSIONS</b>Overexpression of tumstatin mediated by pcDNA 3.1 (+) specially inhibited vascular endothelial cells by arresting vascular endothelial cell in G1 phase resulting from downregulation of cyclin D1 and administration of tumstatin using a gene therapy might be a novel strategy for cancer therapy.</p>

Overexpression of angiotensin converting enzyme 2 inhibits inflammatory response of atherosclerotic plaques in hypercholesterolemic rabbits / 中华心血管病杂志

<p><b>OBJECTIVE</b>Angiotensin converting enzyme 2 (ACE2) efficiently hydrolyses the potent vasoconstrictor angiotensin II to vasodilative angiotensin (1-7). We hypothesized that ACE2 overexpression may inhibit inflammation response in atherosclerotic plaque by degrading Ang II into Ang-(1-7).</p><p><b>METHODS</b>Atherosclerosis (AS) plaques were induced in the abdominal aorta of 38 rabbits by endothelial injury and atherogenic diet for 3 months. Rabbits were then underwent injection of a recombinant adenovirus (2.5 x 10(9) pfu/ml) carrying a murine ACE2 gene (Ad-ACE2) through a catheter into the abdominal aortic segments rich in plaques (n = 19) or injection of a control vector Ad-EGFP (n = 19). One month later, all rabbits were sacrificed and plaques from aortic segments were analyzed.</p><p><b>RESULTS</b>ACE2 expression in aortic tissues of the Ad-ACE2 group were confirmed by immunohistochemistry. Macrophage infiltration (13.6% +/- 4.2% vs. 23.6% +/- 6.9%, P < 0.01) and MCP-1 expression (13.2% +/- 0.4% vs. 25.0% +/- 7.4%, P < 0.01) were significantly reduced in Ad-ACE2 group compared to Ad-EGFP group.</p><p><b>CONCLUSIONS</b>Overexpression of ACE2 inhibited atherosclerotic plaque inflammation response in hypercholesterolemic rabbits.</p>