Aortic aneurysm (AA) is a vascular disease involving the progressive dilation of aorta diameter. It is usually asymptomatic but with high mortality once rupture. Currently, there is no effective pharmacologic treatment. MicroRNA specifically refers to non-coding small RNAs consisting of 19-25 nucleotides. The characteristic of microRNA targeting multiple genes seems to form a complicated regulation network, which receives considerable attention. Emerging studies show that microRNAs are closely related to the occurrence and development of AA. Many microRNAs are involved in multiple cell processes and functions and may participate in the pathogenesis of AA, including endothelial cell dysfunction, inflammatory cell infiltration, smooth muscle cell apoptosis, and extracellular matrix degradation. This article will describe the animal models for AA research and the latest progression of microRNA and AA.

Objective To investigate the relationship between corneal hysteresis(CH)and retinal nerve fiber layer(RNFL)thickness in patients with glaucoma.Methods In this study,186 eyes of 133 patients with open-angle glaucoma who attended the ophthalmology department of our hospital were included,with a follow-up of(3.8±0.8)years and an average of 9 visits.The CH measurements were acquired using the Ocular Response Analyzer,and RNFL thickness was measured at each follow-up using spectral domain optical coherence tomography.All statistical analyses were performed with Stata software.Univariate and multivariable linear regression models were used to investigate the relationship between age,baseline CH,intraocular pressure(IOP),central corneal thickness(CCT)and RNFL thickness.Results The aver-age baseline CH was(9.2±1.8)mmHg(1 kPa=7.5 mmHg),average baseline RNFL thickness was(76.4±18.1)μm,the average baseline IOP was(13.8±3.7)mmHg,and the average baseline CCT was(533±42)μm.Univariate model analysis showed that the baseline CH had a positive correlation with RNFL thickness(P＜0.05).The lower the CH,the thinner the RNFL.For every 1 mmHg reduction in CH,the thickness of RNFL was reduced by 0.13 μm,indicating that CH may be involved in the occurrence and development of glaucoma.The univariate model analysis also showed that there was a negative correlation between IOP and RNFL thickness(P＜0.05).The higher the IOP,the thinner the RNFL.However,there was no significant correlation between age,CCT and RNFL thickness(both P＞0.05).The multivariate model analy-sis showed that there was a positive correlation between baseline CH and RNFL thickness during the follow-up,excluding the influence of age,IOP and CCT(P＜0.05).For every l mmHg reduction in CH,the thickness of RNFL was reduced by 0.13 μm.Conclusion There is a positive correlation between baseline CH and RNFL thickness in glaucoma.The lower the CH,the thinner the RNFL.Low CH may be a risk factor for the progression of glaucoma.

AIM:To analyze the expression changes of O-linked N-acetylglucosamine(O-GlcNAc)glycoprotein in the lens capsule of age-related cataract and diabetic cataract and investigate the role of O-GlcNAc glycoprotein in diabetic cataract.METHODS: The lens capsules of 54 patients(56 eyes)with diabetic cataract and 115 patients(120 eyes )with age-related cataract were studied. Immunoblotting was used to detect the expression level of O-GlcNAc protein in the lens capsules of age-related and diabetic cataracts, and mass spectrometry was used to identify the O-GlcNAc glycoproteins in lens capsules.RESULTS: Immunoblotting results showed that the expression level of O-GlcNAc protein in the lens capsule of diabetic cataracts was significantly higher than in the age-related cataracts(P<0.01). With the level of glycosylated hemoglobin increasing, the expression level of O-GlcNAc protein also increased(P<0.01). Totally 5 O-GlcNAc proteins with up-regulated expression(FABP5, KRT16, PGK1, CTSD and S100A7), and 18 O-GlcNAc proteins with down-regulated expression(CRYβB1, etc.)were identified in the lens capsule of patients with diabetic cataract by mass spectrometry. Three new O-GlcNAc glycosylation sites were identified in this study. They were O-GlcNAcylation at T1730 position and S1738 position of PTPRQ and O-GlcNAcylation at T61 position of ATP5MC2.CONCLUSION:O-GlcNAc glycosylation may be involved in the formation and development of diabetic cataract. The differential O-GlcNAc glycoprotein identified by mass spectrometry provided the data for further study about pathogenesis of diabetic cataract.

MethodIn the experiment， 46% vol Red Star Erguotou （10 mL·kg·d^-1） was used to establish the AONFH rat model， and the intervention effect of JPHGP at different doses （2.5， 5.0， 10.0 g·kg^-1） was observed. Jiangusheng pill （JGS， 1.53 g·kg^-1） was selected as the positive control. After 8 weeks of administration， the bone histomorphometry of the femoral head was analyzed by Micro-CT imaging， and the area of medullary microvessels in the femoral head was detected by ink perfusion. The pathological change was observed by hematoxylin and eosin （HE） staining. The protein expressions of Platelet endothelial cell adhesion molecule-1 （CD31）， VEGF， VEGFR2， PI3K， phosphor-Akt （p-Akt） and phosphatase and Tensin homologue deleted on chromosome 10 （PTEN） in the femoral head were determined by immunohistochemistry and Western blot. ResultCompared with normal group， the model group presented the fracture and thinning of trabeculae in the femoral head， increased empty bone lacunae， and elevated number and diameter of adipocytes （P<0.01）. Micro-CT imaging revealed a decrease in bone mineral density （BMD）， bone volume fraction （BV/TV）， trabecular thickness （Tb.Th） and trabecular number （Tb.N） （P<0.05， P<0.01） while an increase in bone surface-to-volume ratio （BS/BV） and trabecular separation （Tb.Sp） （P<0.01）. The results of ink perfusion showed that the area of medullary microvessels in the femoral head was reduced （P<0.01）. Compared with model group， JPHGP lowered the empty bone lacunae rate as well as the number and diameter of adipocytes in the femoral head of AONFH rats. Micro-CT imaging indicated that JPHGP low-dose group had elevated BV/TV， Tb.Th and Tb.N （P<0.05， P<0.01） while decreased BS/BV （P<0.01）， and there was an upward trend in BMD while a downward trend in Tb.Sp， but without statistical difference. In addition， JPHGP medium- and high-dose groups had a rise in BMD， BV/TV， Tb.Th and Tb.N （P<0.05， P<0.01）， a decrease in BS/BV and Tb.Sp （P<0.05， P<0.01） and enlarged area of medullary microvessels in the femoral head （P<0.05， P<0.01）. The expressions of CD31， VEGF， VEGFR2， PI3K， p-Akt in the model group were lower than those in the normal group （P<0.01）， and after medium and high doses of JPHGP treatment， the expressions of CD31， PI3K and p-Akt in the femoral head of rats were up-regulated （P<0.01） while the protein expression of PTEN was down-regulated （P<0.01）. Moreover， JPHGP up-regulated the expressions of VEGF and VEGFR2 （P<0.05， P<0.01）. ConclusionJPHGP can repair the vascular injury in AONFH， and its mechanism may be related to the activation of VEGF/VEGFR2/PI3K/Akt signaling pathway. This study provides certain scientific basis and reference for the clinical application of JPHGP. ObjecctiveTo observe the repair effect of Jianpi Huogu prescription （JPHGP） on vascular injury in experimental alcohol-induced osteonecrosis of femoral head （AONFH）， and to explore its mechanism based on vascular endothelial growth factor （VEGF）/VEGFR2/phosphoinositide 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway.