Objective To evaluate the effect of Eylea (aflibercept) on recombinant adeno-associated virus 2 (AAV2)-vascular endothelial growth factor (VEGF)-induced choroidal neovascularization (CNV).Methods Two normal cynomolgus monkeys were used in this study.Recombinant AAV2-VEGF was delivered by subretinal injection (60 μl/eye,7.0×1011 IU/ml) into both eyes for each cynomolgus monkey.Both eyes of one animal were treated with single intravitreal injection of Eylea (50 μl/eye,40 mg/ml) 3 weeks after AAV2-VEGF injection,and the two eyes of the other animal were untreated.Optical coherence tomography (OCT),electroretinography (ERG),fluorescein angiography (FFA) and ocular photography were conducted.The experiment was approved by the Institutional Animal Care and Use Committee (IACUC) at JOINN Laboratories (Suzhou) (IACUC serial number:ACU15-1112).Results OCT showed that subretinal hyperreflective material,retinal edema,choroid edema and local pigment epithelial detachment were found after injection of recombinant AAV2-VEGF.All of those symptoms were relieved after treated with Eylea,but aggravated after 4 weeks treated with Eylea.FFA showed that the area of fluorescein leakage expanded obviously after 2 weeks treated with AAV2-VEGF,and it was observed at the whole of fundus posterior pole at 5 weeks after injection.After 1 week treated with Eylea,the area of fluorescein leakage decreased obviously,but increased gradually after 4 weeks treated with Eylea.ERG results showed that the amplitude of ERG decreased gradually after injection of recombinant AAV2-VEGF.After intravitreal injection of Eylea,the amplitude of ERG increased gradually,but it decreased again after 4 weeks treated with Eylea.Conclusions Injection of recombinant AAV2-VEGF is capable of inducing CNV and pathological retinal in cynomolgus monkey.Eylea can prevent the development of clinically relevant CNV,but the effect just lasts for a period.

Cardiovascular disease (CVD) is the leading cause of death and a major contributor to disability worldwide. Since the majority of cardiovascular events are preventable, identification of modifiable CVD risk factors and implementation of primordial prevention strategies should be a public health priority. In this aspect, the American Heart Association declared a strategic goal to reduce total CVD mortality in the US by 20% within 10 years via eliminating 7 major CVD risk factors (hypertension, diabetes, dyslipidemia, cigarette smoking, physical inactivity, obesity, and poor-quality diet) in 2010, and their strategy has been achieving. However, the applicability of similar metrics to prevent CVD among East Asians requires an in-depth investigation of the modifiable CVD risk factors based on national and regional evidence-based findings. Herein, this review article aims to discuss several modifiable risk factors for CVDs, using epidemiological evidence from cohort studies and nationally representative data of 2 East Asian countries: Korea and Japan.

Cardiovascular disease (CVD) is the leading cause of death and a major contributor to disability worldwide. Since the majority of cardiovascular events are preventable, identification of modifiable CVD risk factors and implementation of primordial prevention strategies should be a public health priority. In this aspect, the American Heart Association declared a strategic goal to reduce total CVD mortality in the US by 20% within 10 years via eliminating 7 major CVD risk factors (hypertension, diabetes, dyslipidemia, cigarette smoking, physical inactivity, obesity, and poor-quality diet) in 2010, and their strategy has been achieving. However, the applicability of similar metrics to prevent CVD among East Asians requires an in-depth investigation of the modifiable CVD risk factors based on national and regional evidence-based findings. Herein, this review article aims to discuss several modifiable risk factors for CVDs, using epidemiological evidence from cohort studies and nationally representative data of 2 East Asian countries: Korea and Japan.

Purpose To investigate the clinicopathological and molecular genetic features of oncocytic carcinoma of the thy-roid(OCA).Methods The clinicopathological and immuno-histochemical data of 25 patients with oncocytic carcinoma of the thyroid were retrospectively reviewed.Genetic features were determined by fluorescence quantitative PCR.Results The male to female ratio of the 25 patients was 1 ∶ 1.8,and the aver-age age was 49 years.The tumor was confined to the thyroid gland.Of the 22 cases with a single nodule,5 cases were ill-de-marcated and 3 cases were multiple nodular lesions.The average size was 2.7 centimeter in diameter.Cytologically,the tumor cells were arranged in detached clusters with abundant eosino-philic and granular cytoplasm and hyperchromatic nuclei with prominent nucleoli.Histologically,the oncocytic tumor cells mainly arranged in trabecular and solid architecture.Capsular,blood and lymphoid vascular invasion could be observed in a cer-tain extent.Among 25 cases of OCA,8 cases were minimally in-vasive,14 cases were encapsulated angio-invasive and 3 cases were widely invasive.Positive immunoreaction with TTF-1,thy-roglobulin and CD56 supported the thyroid epithelial origination of the tumour.One recurrent case was found to have cervical lymph node metastasis,and another case was presented with bone metastasis,which was determined to harbor TERT promoter mu-tation(C228T)in each case.Different point mutation of RAS gene was determined in 2 cases(8%),respectively.Conclu-sion Oncocytic carcinoma of the thyroid shows typical eosino-philic and granular cytoplasm,immunohistochemical staining is helpful in differential diagnosis with other oncocytic lesions.It lacks BRAF-like mutation.Low frequency of RAS mutations could be found.Rare TERT promoter mutation has significant mutation with clinical behavior of OCA.

【Objective】 To investigate the effects and potential mechanisms of neurodegenerative lesions in male mice caused by ozone exposure. 【Methods】 We divided 23 C57BL/6N male mice aged 8 to 9 months into control group （clean air group， 11） and ozone group （1 mg/m ³， 4h/d， 12）. After 8 weeks of continuous ozone exposure， the Morris water maze experiment was used to detect the mice’s learning and memory ability， HE dyeing to observe pathological changes in hippocampal tissue cells， and immunoprinting tests to detect the expression levels of Tau， p-Tau and α-synuclein proteins in the cerebral cortex tissue. 【Results】 After 8 weeks of ozone exposure， the mice’s spatial learning and memory ability were impaired to a certain extent， the incubation period decreased with time， and the two lines were separated， but the difference was not statistically significant. Ozone exposure caused changes in the morphology of the mice’s hippocampal tissue cells， disorders in the arrangement of hippocampal neuron， and nuclear wrinkles， and significantly increased levels of p-Tau and α-synuclein protein expressions in cerebral cortex tissues （P<0.01）， but there was no statistical significance in the total Tau expression level. 【Conclusion】 Ozone exposure leads to the loss of learning and memory in mice， changes in hippocampal neurocellular pathology， and increased expression levels of neurodegenerative variable-related proteins.