AIM: To explore the clinical application effect of visual training equipment combined with conventional corrective treatment on children with ametropic amblyopia(AMA).METHODS: Prospective randomized control study. A total of 188 children(376 eyes)with AMA treated in our hospital from June 2021 to December 2022 were selected, and they were divided into two groups using a random number table. The conventional correction group(94 cases, 188 eyes)received conventional correction treatment, while the visual training group(94 cases, 188 eyes)received visual training equipment combined with conventional correction treatment, both lasted for 12 mo. The best corrected visual acuity, diopter, eye accommodation function, adverse reactions, amblyopia recurrence rates, and clinical efficacy were compared between the two groups at 6 and 12 mo after treatment.RESULTS:The two groups each had 8 cases(16 eyes)detached, the rate of loss to follow-up was 8.5%, and 86 cases(172 eyes)were included in each group. There were statistically significant differences in the best corrected visual acuity, diopter, amplitude of accommodation, accommodation facility and accommodative lag between the two groups of children before and after treatment(all P<0.05). The total effective rate of the visual training group(98.8%)was higher than that of the conventional correction group(91.9%; P<0.05). There was no statistically significant difference in the total effective rate of clinical efficacy between the two groups in different age groups and different degrees of amblyopia(all P>0.05). There was no statistically significant difference in the incidence of redness and swelling between the two groups(P>0.05). The recurrence rate of amblyopia in the visual training group(1.2%)was lower than that in the conventional correction group(8.1%; P<0.05).CONCLUSION: The combination of visual training equipment and conventional correction therapy has a significant clinical effect on children with AMA, which can effectively correct visual acuity, adjusting diopter and improve eye accommodation function, and recurrence rate of amblyopia is low and safety is high.

Objective:To investigate the protective effect of overexpressed tripartite motif containing (TRIM27) on severe acute pancreatitis (SAP) in mice and its possible mechanism.Methods:Twenty-four mice were randomly divided into the sham operation + control virus group (AAV-GFP group), sham operation + overexpression of TRIM27 group (AAV-TRIM27 group), SAP + control virus group (SAP+AAV-GFP group), SAP + overexpression of TRIM27 group (SAP + AAV-TRIM27 group), with 6 mice in each group. SAP model of mice was established by intraperitoneal injection of L-arginine (4 mg/kg). The sham operation group was injected with equal volume of normal saline, and the virus group was injected with control or TRIM27 overexpression adeno-associated virus (2×10 11 μg/ per mice). The serum and pancreatic tissue samples were collected 72 h after modeling. The levels of serum amylase, lipase, tumor necrosis factor α (TNF-α), interleukin-1b (IL-1b), IL-6, macrophage chemoattractant protein-1 (MCP-1) and the expression of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) in pancreatic tissue were detected by enzyme-linked immunosorbent assay. Hematoxylin eosin staining was used to observe the pathological damage of pancreatic tissue. The expressions of myeloperoxidase (MPO) and Ly6g positive inflammatory cells in mouse pancreas were observed by immunohistochemistry. The expression of p-p65, p65, p-ASK1, ASK1, p-JNK, JNK, p-p38 and p38 in pancreatic tissue were detected by Western blot. Results:The expression of TRIM27 in pancreatic of mice was significantly down regulated after SAP ( P<0.05); after overexpression of TRIM27 by adeno-associated virus, the expression of TRIM27 in mouse pancreas was significantly up-regulated ( P<0.05). There was no significant difference in the indexes of mice between the AAV-GFP group and AAV-TRIM27 group ( P>0.05). Compared with the SAP + AAV-GFP group, the levels of serum amylase, lipase, TNF-α, IL-1b, IL-6 and MCP-1 in mice of the SAP + AAV-TRIM27 group were significantly decreased, MDA in pancreatic tissue was decreased, SOD and GSH were increased, MPO and Ly6g inflammatory cells were significantly decreased, and p-p65, p-ASK1, p-JNK, and p-p38 protein expression were down regulated. Conclusions:Overexpression of TRIM27 alleviates SAP in mice by inhibiting inflammatory response and oxidative stress, and its mechanism may be through inhibiting NFκB/MAPK signaling pathway.

Objective:To investigate the predictive value of dynamic platelet and hemagglutination-related parameters in patients with acute pancreatitis (AP).Methods:The patients admitted to the Department of Emergency Surgery in the First Affiliated Hospital of Zhengzhou University from January 2020 to December 2020 were analyzed. According to the inclusion criteria and exclusion criteria, patients with AP were retrospectively enrolled. According to the Chinese Guidelines for the Diagnosis and Treatment of Acute Pancreatitis (Shenyang, 2019), the patients were divided into two groups: severe acute pancreatitis (SAP group) and non-severe acute pancreatitis (non-SAP group) [including mild acute pancreatitis (MAP) and moderate severe acute pancreatitis (MSAP)]. A normal distribution of the maximum and mean aggregation rates of dynamic platelets (arachiidonic acid), plateletcrit (PCT) and bedside index for severity in acute pancreatitis (BISAP) scores and other measurement data were tested by t test, while measurement data of prothrombin time (PT), fibrinogen (FIB) and D-dimer that did not conform to normal distribution were tested by Mann-Whitney U test. χ 2 test was used for the counting data such as sex, age and etiology of patients in the two groups. The prognostic value of statistically significant indicators for non-SAP group and SAP group was further analyzed by receiver operating characteristic (ROC) curve. Results:A total of 146 patients with AP were enrolled, including 50 patients in SAP group and 96 in non-SAP group. The maximum and average aggregation rates of dynamic platelet (aracidonic acid) in the SAP group were (71.76±17.62) % and (67.91±18.10) %, PT (12.02±1.33) s, FIB (4.76±2.08) g/L, D-dimer (3.75±6.04) μg/L, PCT (0.23±0.08) %, and BISAP scores (1.42±1.18), which were all significantly higher than those in the non-SAP group [the maximum and average aggregation rates of dynamic platelet (arachiidonic acid) (46.65±20.11) % and (42.50±20.71) %, PT (11.50±1.51) s and FIB (3.91±1.48) g/L, D-dimer (1.00±1.37) μg/L, PCT (0.19±0.06) %, BISAP scores (0.45±0.66)] (all P<0.05). According to area under the ROC curve, the maximum and average aggregation rates of dynamic platelets (arachiidonic acid) in serum of patients with SAP were 0.83 and 0.82, respectively, and the sensitivities were 0.56 and 0.68, respectively. The specificity was 0.99 and 0.81, respectively, which was better than PT, FIB, D-dimer, PCT and BISAP scores in predicting the severity of AP. Conclusions:The maximum and average aggregation rates of dynamic platelets (arachidonic acid), PT, FIB, D-dimer, PCT and BISAP scores can be used as predictors of the severity of acute pancreatitis. The maximum and average aggregation rates of dynamic platelets (arachiidonic acid) were the best in predicting the severity of AP.

Background Proline hydroxylase 2 (PHD2) is a degrading enzyme of hypoxia-inducible factor-1α(HIF-1α) and can regulate the expression of vascular endothelial growth factor (VEGF) and erythropoietin that promote hypoxia-induced blood vessel generation.Baicalein is an inhibitor of PHD2.Understanding the inhibitory effects of baicalein on overexpression of PHD2 in hypoxia-induced retinal glial cells is helpful for elucidating the pathogenesis of the ocular nevascular diseases.Objective This study aimed to observe the expression change of PHD2 in hypoxia-induced retinal glial cells and explore the inhibition of baicalein on PHD2.Methods The study protocol was approved by Experimental Animal Ethic Committee.Retinal glial cells were isolated from SPF neonatal SD rats (within 48 hours) and primarily cultured in DEME by explant cell culture.Cultured cells were identified by immunofluorescence staining of glial fibrillary acidic protein.The cells were divided into normal control group,CoCl2 group and CoCl2 +baicalein group.The cells in the normal control group were cultured in the conventional medium,and 200 μmol/L CoCl2 was added in the medium to establish the hypoxia cell models in the CoCl2 group,and 200 μmol/L CoCl2 and 50 μmol/L baicalein were added in the medium in the CoCl2 + baicalein group.The proliferation (absorbancy) of the cells was detected by cell counting kit-8 (CCK-8).The expression of PHD2 and VEGF in the cells was detected and located using immunofluorescence staining.The expressions of PHD2 mRNA and VEGF mRNA and their proteins in the cells were assayed by real-time quantitative PCR and Western blot,respectively.Resnlts The proliferation (absorbancy) of the cells was significantly different among the groups (F=132.05,P=0.00),and the absorbancy was considerably increased in the CoCl2 group compared with normal control group and CoCl2 + baicalein group,with significant differences between the groups (both at P＜ 0.01).Immunofluorescence staining showed that the PHD2 and VEGF were weakly expressed in the cells of the normal control group,and the expression intensity was high in the CoCl2 group.The expression intensities of PHD2 and VEGF in the cells were weakened in the CoCl2 +baicalein group compared with those of the CoCl2 group.The relative expression levels of PHD2 mRNA were 0.366±0.034,0.894 ± 0.015 and 0.445 ± 0.017 and those of PHD2 protein were 131.27 ± 2.61,140.12 ± 4.29,133.14±2.11;those of VEGF mRNA were 1.346 ± 0.008,3.465 ± 0.048 and 2.264 ± 0.073 and those of VEGF protein were 532.25 ± 19.92,601.13 ± 10.21,537.34 ± 5.96 in the normal control group,CoCl2 group and CoCl2 + baicalein group,showing significant differences among the three groups (PHD2:F =905.89,43.18,both at P＜0.01.VEGF:F=27.13,185.79,both at P ＜ 0.01),and the relative expression levels of PHD2 and VEGF mRNA and protein in the CoCl2 group were higher than those in the normal control group and CoCl2 +baicalein group (all at P＜ 0.01).Conclusions Hypoxia stimulates the proliferation of retinal glial cells and increase the expression of PHD2 and VEGF.Baicalein can effectively inhibit the overexpression of PHD2 and VEGF in retinal glial cells and proliferation of retinal glial cells induced by hypoxia.PHD2 is a potential provention and treatment target of hypoxiainduced retinal neovascularization.