Hypoxia-inducible factor-1 (HIF-1) is an essential transcription factor, which mediates the transcription of multiple target genes to adapt the body for hypoxia.Oxygen-induced retinal neovascularization (RNV) is an important pathological process of retinopathy of prematurity (ROP). By mediating the transcription of vascular endothelial growth factors, angiopoietin and platelet-derived growth factors, HIF-1 can promote RNV and then lead to ROP.Therefore, HIF-1 plays a vital role in the pathological process of ROP.In this paper, the recent research progress on the role of HIF-1 in oxygen-induced RNV was summarized in order to further the understanding of ROP pathogenesis and treatment.

Objective:We applied a hypoxia-induced model of human fetal retinal microvascular endothelial cell (RMEC) to study the effect of carbonic anhydrase 9 (CA9) on cell proliferation.Methods:The eyeballs of spontaneously aborted fetuses in Guangdong Women and Children's Hospital were obtained, and the retinas were isolated. RMEC was obtained by trypsin and collagenase two-step enzyme digestion, and endothelial cells were identified by CD34. The fetal RMEC and the purchased adult RMEC were cultured in normoxic and hypoxic incubators (1%O 2+5%CO 2+94%N 2), and the expression of CA9 was detected by qPCR and Western blot. After knocking down the CA9 by small interference RNA technique, the cell proliferation was detected by CCK-8 method, and the cell viability was detected by CCK-8 after adding CA9 inhibitor U-104. Results:The primary RMEC was extracted successfully. Immunofluorescence staining showed the percentage of CD34 positive cells in the third-generation cells was nearly 100%. The expression of CA9 mRNA in immature fetus and adult RMEC under hypoxia culture was higher than that under normoxic culture (fetal 1% O 2 group vs. fetal 21% O 2 group: 67.80±10.31 vs. 1.00±0.04, P<0.001; adult 1% O 2 group vs. adult 21% O 2 group: 1.72±0.22 vs. 1.00±0.02, P=0.014). Western blot analysis showed significantly increased expression of CA9 in the fetal RMEC exposed to hypoxia, which aligned with the expression of CA9 mRNA. When fetal RMEC was transfected with siCA9 20 nM, the knockdown rate of CA9 was 95% ( P<0.001). CCK-8 assay showed significantly lower proliferation of fetal RMEC cells in siCA9 group compared to siNC group (0.57±0.05 vs. 0.90±0.03, P<0.001), which was reflected by the OD value. With the addition of 100 μM CA9 inhibitor U-104, the viability of fetal RMEC in the treated groupwas significantly lower than that in the untreated group (99.16%±3.82% vs. 119.10% ±1.72%, P=0.002). Conclusions:The expression of CA9 differed between adult and preterm fetus in our hypoxia-induced RMEC model. Inhibiting CA9 can inhibit the proliferation of retinal microvascular endothelial cells of preterm fetus.

Objective: To analyze the anatomical structure and distribution of the fused renal pyramid (FRP) in cadaveric kidney, and discuss its appearances by CT and ultrasonic examinations. Methods: From June 2018 to September 2018, 108 cadaveric kidneys were proceeded for regional anatomy. The distribution and anatomical manifestations of FRP was recorded. The renal pyramid was sliced and HE stained to explore the vascular distribution in FRP. From October 2018 to January 2019, ultrasound imaging data of 112 patients with 224 kidneys were collected, including 60 males and 52 females, age (39.0±15.1), ranging from 16 to 73 years old. The renal imaging data of 89 patients and 178 patients with enhanced renal CT were collected, including 48 males and 41 females. Age (45.4±13.6), ranging from 23 to 69 years old. The imaging findings of FRP in ultrasound and enhanced CT was summarized. Results: In cadaver kidneys, the proportion of FRP in upper and lower calyces was 68.6% (74/108) and 64.8% (70/108), respectively, higher than that in middle calyces 34.3% (37/108). In the middle group, the incidence of mild fusion was 39.0% (16/41) and severe fusion was 48.8% (20/41). The incidence of fusion of two renal pyramidal structures was 90.2% (37/41). HE staining showed that the boundary between the artery in FRP and the surrounding renal pyramidal was unclear, and the protection of connective tissue was lacking. In Ultrasound, the FRP presented as a large trapezoidal hypo-echoic area with red and blue color signals in doppler mode. In ultrasound, the incidence of FRP was 18.8% (42/224). In enhanced CT, the FRP presented as enhanced cord-like high density shade in large low density area in cortex phase. In enhanced CT, the incidence of FRP 27.5%(49/178). Conclusions The FRP is a common structure in human kidney. The arteries localize within the FRP and are absence of sufficient connective tissue protection which are different from normal arteries. Ultrasound and enhanced CT have recognition ability for FRP.