Current practice for pulmonary hypertension

Objective To investigate the current practice of pulmonary hypertension including current epidemiology, diagnosis and treatment. Data sources The review was based on data obtained from the published articles and guidelines. Study selection Articles with high level of evidence or current best evidence in each issue were selected to be reviewed. Results Overall prevalence of pulmonary hypertension was 0.3% to 6% with left heart disease occupying the most proportion, followed by pulmonary disease, pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension. In diagnosis, a flow diagram of diagnosis of pulmonary hypertension, differential diagnosis of pulmonary hypertension and how to determine the severity of pulmonary hypertension are explained including recent development of magnetic resonance imaging and gene abnormality study on bone morphogenetic protein receptor ll. In treatment, newly- developed pulmonary vasodilators and the way to use them are shown to treat pulmonary hypertension. Conclusion Safer and more effective treatment algorithm and basic researches and clinical trials are warranted to be explored.     

Glaucoma secondary to systemic lupus erythematosus

Background Glaucoma secondary to systemic lupus erythematosus （SLE - an uncommon but serious complication that threatens vision and therefore cannot be neglected. A few cases of second, y glaucoma resulting from lupus-induced or iatrogenic ocular impairments have been reported in association with SLE. However, a systematic analysis of the diagnosis and treatment of glaucoma secondary to SLE has not been reported in the literature. The aim of this study is to further investigate the relationship between glaucoma and SLE. Methods In this study, we reviewed nine eyes of five patients diagnosed with secondary glaucoma associated with SLE, including one case of neovascular glaucoma and four cases of steroid-induced glaucoma. Results Neovascular glaucoma was successfully treated by Ahmed glaucoma valve implantation surgery with adjunctive ranibizumab intravitreal injection, followed by panretinal photocoagulation （PRP）. The steroid-induced glaucoma in eight eyes of four cases were controlled by trabeculectomy along with antiproliferative agents. Conclusion Regular follow-up ocular examinations should be conducted to ensure early diagnosis and treatment of secondary glaucoma in SLE patients to improve the prognosis of vision.     

Angiogenesis effect of Astragalus polysaccharide combined with endothelial progenitor cells therapy in diabetic male rat following experimental hind limb ischemia

Background Diabetes mellitus （DM） is a common disease accompanied with a high incidence of hind limb ischemia （HLI）.In recent years,numerous studies demonstrated that endothelial progenitor cells （EPCs） are involved in angiogenesis and maintenance of vascular integrity following HLI.On the other side,it has been proved that Astragalus polysaccharide （APS） could promote angiogenesis.In the present study,we aimed to evaluate the effect of APS and EPCs on enhancing angiogenesis after experimental HLI caused by femoral artery ligation in rats with streptozotocin （STZ）-induced diabetes.Methods Rats （n=110） were randomly assigned to the following groups：sham group,ischemia group,APS group,EPCs group and APS＋EPCs group.APS,EPCs or an equal volume of vehicle was administered intramuscularly after HLI induction,and 6 rats were assessed by angiography at 28 days after induction of HLI,6 rats were sacrificed at the same time point to take histological studies,biochemical tests were also performed at that point in the rest rats.Results APS or EPCs treatment induced an increase,respectively,in the protein expression of vascular endothelial growth factor （VEGF） （36.61%,61.59%）,VEGF receptor-1 （VEGFR-1） （35.50%,57.33%）,VEGFR-2 （31.75%,41.89%）,Angiopoietin-1 （Ang-1） （37.57%,64.66%） and Tie-2 （42.55%,76.94%） （P 〈0.05）,after HLI injury.And combined therapy of APS and EPCs enhanced the effort of angiogenesis after HLI induction in diabetic rats,through elevating protein expression of VEGF （99.67%）,VEGFR-1 （105.33%）,VEGFR2 （72.05%）,Ang-1 （114.30%） and Tie-2 （111.87%） （P〈0.05）.Similarly,mRNA expression of VEGF,VEGFR-1,VEGFR2,Ang-1,Tie-2 also show similar trends as well as protein expression （P〈0.05）.Conclusion APS or EPCs could enhance angiogenesis,and the combined treatment leads to better effort,at least,partially via VEGFNEGFR and Ang-1/Tie-2 signaling pathway.     

Effect of pcDNA3.1- vascular endothelial growth factor 165 recombined vector on vascular buds in rabbit vertebral cartilage endplate

Background  This study aimed to investigate the effect of pcDNA3.1-vascular endothelial growth factor (VEGF)165 vector on vertebral cartilage endplate vascular buds and intervertebral discs.

Methods  Rabbits were randomly assigned to the control and experimental groups with 10 in each. In the experimental group, we anesthetized the rabbits and exposed the front vertebral body. Using the mark of the longitudinal ossature of the front vertebral body of the lumbar vertebrae, we advanced a needle at the central point of the front fourth and fifth lumbar intervertebral discs and injected 20 µl pcDNA3.1-VEGF165. Similarly, in the control group, we injected 20 µl pcDNA3.1. At 4 and 8 weeks post-injection, we examined the changes of the vertebral cartilage endplate using X-ray radiograph, histology, and scanning electron microscopy.

Results  The vertebral cartilage endplate calcification and degeneration in the experimental group were less than those in the control group at 8 weeks post-operation. The average number and diameter of vascular buds obviously increased in the experimental group at 4 and 8 weeks post-operation. The number of vascular buds and the diameter in the region of the inner annulus increased when compared to those in the area near the nucleus pulposus.

Conclusions  The pcDNA3.1-VEGF165 plasmid can increase the average number and diameter of vascular buds and decelerate intervertebral disc degeneration.

     

Impact of vitamin D supplementation on the outcome of tuberculosis treatment: a systematic review and meta-analysis of randomized controlled trials

Background Vitamin D supplementation is believed to be beneficial in the treatment of patients with tuberculosis （TB）,however,results from clinical trials have been inconclusive.Methods We performed a systematic literature search across MEDLINE,EMBASE,the Cochrane Central Register of Controlled Trials,Springer,EBSCO,ProQuest,HighWire Press,and Web of Science,published as of December 2013.We individually inspected citations and extracted data independently.We estimated pooled risk ratios （RR） and 95％ confidence intervals （CI） using random-effect models.We also assessed risk of bias using the Jadad scale and the quality of the evidence using GRADE.We included all randomized controlled trials comparing vitamin D with or without standard TB therapy or placebo.Results A total of five studies were analyzed in our meta analysis covering 841 newly-diagnosed TB cases.Patients receiving vitamin D supplementation had a 39％ reduced risk of sputum smear or culture positive after six weeks of antiTB treatment than those in the control group,although this is not statistically significant （pooled RR 0.61,95％ CI 0.24 to 1.56,P=0.30）.Apart from an increased serum vitamin D level in the supplement group after eight weeks of treatment there was no evidence of any additional adverse effects related to vitamin D.Conclusions The meta analysis results indicate that vitamin D supplementation does not seem to have any beneficial effect in the treatment of TB.Future rigorous randomized controlled trials are needed to explore whether the supplementation of vitamin D could shorten treatment duration and to confirm whether the polymorphisms of vitamin D receptor have any potentially beneficial effect.     

Downregulating activated epidermal growth factor receptor has no effect on RBM5 expression

Background  We were interested in determining how the tumor suppressor gene RBM5 is regulated in lung cancers. Previous studies suggested that the gene expression is related to histological subtype and smoking exposure, since in small cell lung cancers the RBM5 gene is deleted whereas in non-small cell lung carcinomas (NSCLC) RBM5 expression is reduced. Of particular interest was the recent finding that in lung adenocarcinomas, a histological subtype of NSCLC, smoking exposure correlated with mutational activity in the transforming growth factor alpha (TGF-a) signaling pathway. Lung adenocarcinomas from smokers were associated with activating KRAS mutations, whereas lung adenocarcinomas from never-smokers were associated with activating epidermal growth factor receptor (EGFR) mutations. We hypothesized that inhibition of RBM5 in lung adenocarcinomas is achieved indirectly via these activating mutations. The objective of the research described herein was to determine if EGFR activation and RBM5 expression are negatively correlated.

Methods  EGFR expression in the lung adenocarcinoma cell line NCI-H1975 was inhibited using small interfering RNA. RBM5 expression was examined by real-time quantitative polymerase chain reaction and Western blotting.

Results  Reduced EGFR expression did not correlate with any change in RBM5 expression at either the RNA or protein level.

Conclusion  These results suggest that RBM5 expression is not directly regulated by EGFR in non-smoker related lung adenocarinomas, and that some other mechanism operates to inhibit either the expression or function of this potential tumour suppressor in lung cancers that retain the RBM5 gene.

     

Analysis of epidermal growth factor signaling in nasal mucosa epithelial cell proliferation involved in chronic rhinosinusitis

Background Aberrant epithelial repair has been observed in chronic rhinosinusitis （CRS） patients; however, the mechanism of epithelial cell repair regulation is unclear. Epidermal growth factor （EGF） plays an important role in regulating epithelial cell repair in lower airway and may be a critical factor in the remodeling processes of CRS. The objective of our research is to evaluate the differences between CRS and normal subjects and between chronic rhinosinusitis without nasal poiys （CRSsNP） and chronic rhinosinusitis with nasal polys （CRSwNP） in the regulation of EGF pathways and the regulating proliferative position of classic Ras/Raf/MEK/ERK pathways. Methods We evaluated the proliferation rates of ethmoidal mucosal cells before and after stimulation with EGF, epidermal growth factor receptor （EGFR） kinase inhibitor AG1478, and extracellular signal-regulated kinase 1/2 （ERKI/2）inhibitor PD98059 using MTT assays. We also analyzed the sinonasal epithelial cells collected from control subjects and patients with CRS subtypes CRSsNP and CRSwNP for the expression of ERK1/2, phosphorylated ERK1/2, P21, P15, and P27 using western blotting analyses. Results The proliferation rates of sinonasal epithelial cells before and after EGF stimulation were lower in CRS patients than in the controls. AG1478 or PD98059 inhibitor treatment of control epithelial cells did not result in a significant difference in proliferation. Although, AG1478 and PD98059,inhibited the proliferation of CRS cells, the degree of proliferation inhibition was markedly different in CRSsNP. AG1478 suppressed the proliferation of CRSwNP epithelial cells, whereas PD98059 had no effect. The ratio of ERK1/2 phosphorylation in CRS cells was lower than that of the control cells. Cyclin-dependent kinase inhibitors were highly expressed in CRS cells compared with that of control cells. ERK1/2 and P27 showed differential expression in CRSsNP and CRSwNP. Conclusions Differences existed in EGF pathways in CRS patients and normal subjects     

Intravitreal bevacizumab with or without triamcinolone acetonide for diabetic macular edema: a meta-analysis of randomized controlled trials

Background Intravitreal anti-vascular endothelial growth factor （anti-VEGF） drugs and corticosteroids are being widely used to treat diabetic macular edema （DME）. The purpose of this study was to evaluate further the efficacy and safety of intravitreal bevacizumab （IVB） alone in comparison with intravitreal bevacizumab combined with triamcinolone acetonide （IVB/IVT） in the treatment of DME. Methods Pertinent publications were identified through CNKI, PubMed, Medline, EMBASE, and the Cochrane Controlled Trials Register up to November 30, 2013. Two investigators independently assessed the quality of the trials, and changes in central macular thickness （CMT） and best-corrected visual acuity （BCVA） were extracted at 6 weeks and 3, 6, 12, and 24 months after the initial treatment. A meta-analysis was carried out to compare the results between the groups receiving IVB and IVB/IVT using the software RevMan 5.0. Results A total of six randomized controlled trials （RCTs） were identified and included. The meta-analysis revealed that a significant reduction of the CMT was observed at 3 months after the initial treatment in the IVB/IVT group compared to the IVB group （P=-0.001）. Also, changes in CMT at 6 weeks and 6, 12, and 24 months did not vary significantly between the IVB and IVB/IVT groups （P=0.53, 0.76, 0.34, and 0.09, respectively）. Similarly, changes in BCVA at 6 weeks and 3, 6, 12, and 24 months also did not vary significantly between the two groups （P=-0.66, 0.98, 0.81, 0.07, and 0.80, respectively）. The results were robust to sensitivity analyses. However, the rate of intraocular pressure （IOP） rise after intravitreal injections varied significantly between the IVB and IVB/IV＇r groups （P 〈0.01）. A publication bias was not detected by funnel plots, the Egger method, or the Begg method. Conclusions Results of this meta-analysis showed that the treatments with IVB alone and combined IVB/IVT were similarly effective in improving the visual acuity, and, to some degre     

miR-30b and miR-30c expression predicted response to tyrosine kinase inhibitors as first line treatment in non-small cell lung cancer

Background Aberrantly expressed microRNAs are a hallmark of cancer,and microRNA expression profiling is associated with tumor progression and response to chemotherapy,suggesting their potential application as prognostic and predictive biomarkers.The role of microRNAs in lung cancer remains elusive.It has been recently reported that epidermal growth factor receptor （EGFR） and hepatocyte growth factor receptor （MET） tyrosine kinase can regulate expression of specific microRNAs including miR-30b,miR-30c,miR-221,miR-222,miR-103 and miR-203,and induce tumorigenesis and gefitinib resistance in lung cancers.We intend to study the role of miR-30b and miR-30c expression in predicting response to tyrosine kinase inhibitors （TKIs） in non-small cell lung cancer （NSCLC）.Methods We have therefore retrospectively examined expression of miR-30b miR-30c in 41 formalin fixed paraffin embedded tissue samples from NSCLC patients when TKIs were used as first line therapy.Results We found a significant correlation between expression of miR-30b and miR-30c.Furthermore,miR-30b and miR-30c expression correlated with short-term response.Kaplan-Meier analysis further revealed that the expression of miR-30b and miR-30c predicted progression free survival and the overall survival rate in the examined cohort.Conclusion Our study identified miR-30b and miR-30c as useful prognostic predictors in NSCLC patients who underwent first line treatment with TKIs.     

Genetic polymorphism of the phospholipase C epsilon 1 gene and risk of gastric cancer

Background The pathogenesis of gastric cancer （GC） involves environmental and genetic factors.Recently,two genome-wide association studies found that phospholipase C epsilon 1 （PLCE1） polymorphisms might be related to GC risk,and several studies further validated this finding.However,these studies yielded inconsistent results.Methods A comprehensive database search was performed to identify eligible studies.Odds ratios with 95％ confidence intervals were calculated to assess the strength of the association between PLCE1 rs2274223,rs753724,and rs11187842 and risk of GC.Subgroup analyses,publication bias,and sensitivity analyses were also conducted.Results Eleven studies （12 cohorts） were included in the meta-analysis.Based on 13 676 cases and 23 569 controls,a significant association between PLCE1 rs2274223 and GC risk was detected under various genotypic models.In the subgroup analyses,the association was significant for cardia GC,but weak for non-cardia GC.The association under the heterozygote model was detected for PLCE1 rs753724 and rs11187842 based on three studies involving 2768 cases and 3890 controls.Conclusions Our findings demonstrate that the presence of the G allele at rs2274223 of the PLCE1 gene may contribute to susceptibility to GC,especially cardia GC.PLCE1 rs753724 and rs11187842 are associated with GC risk under the heterozygote model.Further well-designed large studies are warranted to validate these findings.     

Current practice of gastric cancer treatment

Objective The aim of this review was to overview the current practice of gastric cancer treatment including surgery and other adjuvant modalities.Data sources The review was based on data obtained from the published articles and main guidelines in the East and West.Study selection Articles with high level of evidence or current best evidence in each issue were selected to be reviewed.Results Although varied adjuvant modalities have been proved to be benefit for treating gastric cancer,surgery is still the most important treatment strategy against gastric cancer.Actively adapting to new technology is important but it should be balanced with an effort to establish sound scientific rationale that adheres to oncologic principles.Conclusions Future treatment of gastric cancer will be focused on tailored,personalized therapy.For achieving it,collaboration across disciplines is essential.Also the philosophy of caring for the patients with gastric cancer should be rooted in the realization of true patient benefit regardless of who is providing the care.With these philosophies,we can shift the scientific and technological advances toward triumph over gastric cancer.     

Antiviral therapy of decompensated hepatitis B virus-related cirrhosis

Objective  To review the development, mechanism, necessity and limitation of antiviral therapy in decompensated hepatitis B virus-related cirrhosis.

Data sources  Most information was pulled from a literature search (Pubmed 2000 to 2011) using the keywords of antiviral and decompensated hepatitis B virus-related cirrhosis. Relevant book chapters were also reviewed.

Study selection  Well-controlled, prospective landmark studies and review articles on antiviral therapy in decompesated hepatitis B virus-related cirrhosis were selected.

Results  Specific antiviral agents not only control viral replication, which permits liver transplantation, but also improve liver function so significantly that patients could be removed from the transplant waiting list. However, the emergence of drug-resistant mutants can result in treatment failure. Combination therapy is a save-strategy in drug-resistant.

Conclusions  Although the treatment of end-stage liver disease is still a challenge worldwide, antiviral therapy has altered the natural history of hepatitis B patients with decompensated cirrhosis. The approval of the new generation of antivirals is opening new perspectives for finding the optimal antiviral treatment for patients with decompensated cirrhosis and preventing antiviral resistance. A combination of antivirals may be one of the future strategies for fulfilling these goals.

     

Effect of c-Met inhibitor SU11274 on human colon cancer cell growth

Background Colon cancer is one of the major malignancies worldwide and it still remains resistant to much of the currently available chemotherapy. Downregulation of HGF/c-Met signaling pathway is an emerging therapy for cancer treatment.

Methods In this study, the inhibitory effects of c-Met phosphorylation were observed with SU11274 on different colon cancer cell lines in vitro.

Results The results revealed the significant inhibitory effects of SU11274 on cell proliferation and cell survival, in a time and dose-dependent manner. Furthermore, the inhibitory effects of SU11274 on different subgroups of colon cancer cells via the HGF/c-Met signaling pathway were implicated in this study.

Conclusion The results suggested the possible selective therapeutic effects of c-Met inhibitor on colon cancer.

     

Fundus artery occlusion caused by cosmetic facial injections

Background With the increasing popularity of cosmetic facial filler injections in recent years, more and more associated complications have been reported. However, the causative surgical procedures and preventative measures have not been studied well up to now. The aim of this stady was to investigate the clinical characteristics and visual prognosis of fundus artery occlusion resulting from cosmetic facial filler injections. Methods Thirteen consecutive patients with fundus artery occlusion caused by facial filler injections were included. Main outcome measures were filler materials, injection sites, best-corrected visual acuity （BCVA）, fundus fluorescein angiography, and associated ocular and systemic manifestations. Results Eleven patients had ophthalmic artery occlusion （OAO） and one patient each had central retinal artery occlusion （CRAO） and anterior ischemic optic neuropathy （AION）. Injected materials included autologous fat （seven cases）, hyaluronic acid （five cases）, and bone collagen （one case）. Injection sites were the frontal area （five cases）, periocular area （two cases）, temple area （two cases）, and nose area and nasal area （4 cases）. Injected autologous fat was associated with worse final BCVA than hyaluronic acid. The BCVA of seven patients with autologous fat injection in frontal area and temple area was no light perception. Most of the patients with OAO had ocular pain, headache, ptosis, ophthalmoplegia, and no improvement in final BCVA. Conclusions Cosmetic facial injections can cause fundus artery occlusion. Autologous fat injection tends to be associated with painful blindness, ptosis, ophthalmoplegia, and poor visual outcomes. The prognosis is much worse with autologous fat injection than hyaluronic acid iniection.     

Effect of angiotensin receptor blockers in the prevention of type 2 diabetes and cardiovascular events: a meta-analysis of randomized trials

Background  As the incidence of type 2 diabetes is rapidly increasing, prevention of the disease should be considered as a crucial objective in the near future. Several studies have shown angiotensin receptor blockers (ARBs) may contribute to the prevention of new-onset type 2 diabetes. This study was conducted to determine if ARBs as monotherapy or combination therapy may experience a decreased incidence of new-onset type 2 diabetes and prevent cardiovascular events.

Methods  Relevant experimental and clinical studies were identified by searching MEDLINE (1969 to May 30, 2011) to extract a consensus of trial data involving the effect of ARBs on prevention of new-onset type 2 diabetes and cardiovascular events. Studies were included if they were randomized controlled trials versus placebo/routine therapy. A random-effects model was utilized. Subgroup and sensitivity analyses were conducted.

Results  Eleven trials were identified, including 82 738 patients. ARBs prevented new-onset type 2 diabetes (odds ratio 0.8 (95% CI 0.76, 0.85)). Regardless of indication for use, essential hypertension (seven trials), impaired glucose tolerance (one trial), cardiocerebrovascular disease (two trials) or heart failure (one trial), reductions in new-onset type 2 diabetes were maintained (0.75 (0.69, 0.82), 0.85 (0.78, 0.92), 0.80 (0.76, 0.85) and 0.80 (0.64, 0.99), respectively). No statistical heterogeneity was observed for any evaluation. However, ARBs did not significantly reduce the odds of all-cause mortality, myocardial infarction and heart failure versus control therapy among all of these studies. But ARBs did reduce the odds of cardiac death and heart failure among the heart failure study versus control therapy.

Conclusion  ARBs have significant ability to reduce risk of developing new-onset type 2 diabetes but does not improve cardiovascular outcomes over the study follow-up periods among all of included studies.

     

Proliferating cell nuclear antigen involved in the repair process of ouabain-induced brain damage independent of hypertension in rats

Background Ouabain is a mammalian adrenocortical hormone that is involved in the pathogenesis of hypertension by inhibiting Na-K ATPase activity.It also participates in a variety of kinase-mediated signaling pathways associated with Na-K ATPase.Previous studies have shown that ouabain can cause cardiac remodeling independent of elevated blood pressure and that proliferating cell nuclear antigen （PCNA） plays a coordinating role for numerous proteins involved in multiple processes associated with DNA synthesis.Therefore,we hypothesized that ouabain might play a role in the cerebral cortex through signaling pathways independent of hypertension.And PCNA might be involved in this process.Methods Male Sprague-Dawley rats were treated with ouabain or with 0.9% nitric sodium as the control group.Systolic blood pressure was recorded weekly.After four weeks of treatment,morphological changes in the cerebral cortex were analyzed using light and transmission electron microscopy.The expression of PCNA in the cerebral cortex was evaluated by immunohistochemistry,real time quantitative PCR,and Western blotting.Results After 4-week treatment,there was no significant difference in systolic blood pressure compared with the control group,but both structural deterioration and up-regulated expression of PCNA in the brain was induced by ouabain treatment.Conclusions These results suggest that ouabain induces alterations in the brain structure,and this effect is independent of blood pressure.PCNA might be involved in the repair process of ouabain-induced brain damage.     

State of the art contemporary treatment of patients with ST elevationmyocardial infarction： pre- and in-hospital organization,devices anddrugs

Objective To review the presentation, diagnosis and recent developments in the pharmacological and invasive treatmentof ST elevation myocardial infarction （STEMI） with a special focus on health-care organization in order to increaseaccessibility of primary percutaneous coronary intervention （PCI）.     

Expression of connexin 36 in central nervous system and its role in epileptic seizure

Objective  This review discusses the experimental and clinical studies those show the expression of connexin 36 in the central nervous system and the possible role of connexin 36 in epileptic seizure.

Data sources  All articles used in this review were mainly searched from PubMed published in English from 1996 to 2012. 

Study selection   Original articles and reviews were selected if they were related to the expression of connexin 36 in the central nervous system and its role in epilepsy.

Results  The distribution of connexin 36 is developmentally regulated, cell-specific and region-specific. Connexin 36 is involved in some neuronal functions and epileptic synchronization. Changes in the connexin 36 gene and protein were accompanied by seizures. Selective gap junction blockers have exerted anticonvulsant actions in a variety of experiments examined in both humans and experimental animals.

Conclusions  Connexin 36 plays an important role in both physiological and pathological conditions in the central nervous system. A better understanding of the role of connexin 36 in seizure activity may contribute to the development of new therapeutic approaches to treating epilepsy.     

Effect of refractive correction on ocular optical quality measurement using double-pass system

Background Optical Quality Analysis System II （OQAS, Visiometrics, Terrassa, Spain） that uses double-pass （DP） technique is the only commercially available device that allows objective measurement of ocular retinal image quality. This study aimed to evaluate the impact of spectacle lenses on the ocular optical quality parameters and the validity of the optometer within OQAS. Methods Seventy eyes of healthy volunteers were enrolled. Optical quality measurements were performed using OQAS with an artificial pupil diameter of 4.0 mm. Three consecutive measurements were obtained from spectacle correction corresponding to subjective refraction and from the OQAS built-in optometer separately. The modulation transfer function cutoff frequency, the Strehl ratio, the width of the point spread function （PSF） at 10% of its maximal height （PSF10）, and the width of the PSF at 50% of its maximal height （PSF50） were analyzed. Results There was no significant difference in any of the parameters between the spectacle correction and the optometer correction （all P 〉0.05, paired t-test）. A good agreement was found between both the methods and a good intraobserver repeatability in both the correction methods. Difference in best focus between two methods was the only parameter associated significantly with optical quality parameter differences. Best focus difference, built-in optometer correction with or without external cylindrical lens, and age were associated significantly with PSF10 difference. No linear correlation between refractive status and optical quality measurement difference was observed. A hyperopic bias （best focus difference of （0.50±0.44） D） and a relatively better optical quality using spectacle correction in high myopia group were found. Conclusions OQAS based on DP system is a clinically reliable instrument. In patients with high myopia, measurements using built-in optometer correction should be considered and interpreted with caution.