AIM: To study the effect of ocular surface and meibomian gland dysfunction of adolescents before and after wearing overnight orthokeratology, and to explore its effects on adolescent tear film.

METHODS: A prospective clinical study was conducted. 55 cases of 8 to 16-year-old adolescents who met the selection criteria from January 2017 to November 2017 were selected for orthokeratology. Before lens wear and after lens wear 1wk, 1mo, 3mo, 6mo, and 12mo were followed up for Ocular Surface Disease Index(OSDI)questionnaire, slit-lamp examination, and Keratograph 5M.

RESULTS: During the study period, no patients developed infectious keratitis. The OSDI scores were 7.38±1.71 points, 9.21±1.39 points, 10.19±1.02 points, 10.28±1.18 points, 10.29±1.85 points after wearing at 1wk, 1, 3, 6, and 12mo respectively, which were higher than those before wearing(4.80±1.63 points)were increased, and the difference was statistically significant at different times before and after wearing(P<0.05). 1wk, 1, 3, 6, 12mo NIBUT(f)values were 12.39±4.76s, 9.95±5.23s, 11.30±4.58s, 11.21±4.34s, 11.63±5.32s, and NIBUT(av)values were respectively 11.26±6.77s, 11.16±6.48s, 13.09±5.79s, 13.13±5.41s, 13.19±5.21s, NIBUT(f)1mo after wearing compared with before wearing, the difference was statistically significant(P<0.05), NIBUT(av)at 1wk and 1mo after wearing was compared with before wearing, the difference was statistically significant(all P<0.05), and the difference was both at 3, 6, 12mo after wearing and before wearing No statistical significance(all P>0.05).There was no significant change in TMH at 1wk, 1, 3, 6, 12mo after wearing, and the difference was not statistically significant(F=2.168, P>0.05). Corneal fluorescein staining scores were 3.51±1.67 points, 3.54±1.62 points, 4.05±1.52 points, 4.14±1.32 points, 4.50±1.43 points, respectively, 1wk after wearing, 1, 3, 6, and 12mo, which were higher than those before wearing(P<0.05). The meibomian gland lipid secretion score and the meibomian gland loss score did not change significantly at different times before and after wearing(P>0.05).

CONCLUSION: The tear film function in the early period of wearing the orthokeratology is reduced, but it gradually returns to the level before wearing the lens after 6mo, and tends to increase steadily. After wearing the orthokerato-scope, the symptoms of eye discomfort increase and corneal fluorescein stain increased after wearing, no effect on meibomian gland function.

AIM: To observe the therapeutic effect of intravitreal injection of ranibizumab combined with compound Xueshuantong capsule on patients with central exudative chorioretinopathy(CEC).

METHODS: A total of 98 consecutive patients(98 eyes)with CEC treated in our hospital from September 2013 to May 2015 were enrolled in this study and randomly divided into 2 groups. The experimental group received intravitreal injection of ranibizumab treatment, were treated with compound Xueshuantong capsule, 3 consecutive months of treatment; the control group only treated with compound Xueshuantong capsule treatment, the same dosage and course of treatment with the experimental group. Two groups of patients were reviewed monthly, the follow-up time was 6mo. Before and after treatment, visual acuity, foveal retinal thickness and leakage area were measured.

RESULTS: Visual acuity(LogMAR): the visual acuity of the two groups before and after surgery was significantly different(P<0.05); the visual acuity of the experimental group was significantly better than that of the control group, the difference was statistically significant(P<0.05). There was significant difference between experimental group and control group on central macular thickness macular(CMT)(P<0.05), which of experimental group decreased more than that of control group. The improved leakage of the two groups was significant different by χ2 test(P<0.05).

CONCLUSION: Ranibizumab combined with compound Xueshuantong capsule in the treatment of CEC can reduce vascular leakage, reduce macular edema, shorten the course, improve eyesight, which is a safe and effective method for the treatment of CEC. Multiple intravitreal injection of ranibizumab to CEC can improve the vision of patients and keep it stable.

OBJECTIVES: To investigate the roles of cytoskeleton-associated protein 2 (CKAP2) in proliferation, apoptosis, and migration in liver cancer cells and the potential mechanisms. METHODS: Human normal hepatocyte L02 and liver cancer cell lines HepG2, Huh7, and SMMC-7721 were cultured. The CKAP2 expression was detected by real-time PCR and Western blotting. HepG2 cells were randomly divided into a control group, a negative control (NC) group, and a CKAP2 silencing (siCKAP2) group. CCK-8 and BrdU assays were used to evaluate cell viability and proliferation, respectively. Transwell assay was employed to determine cell migration and invasion. The protein levels of cleaved-caspase 3, Bax, E-cadherin, N-cadherin, Vimentin, phosphorylated Janus kinase 2 (p-JAK2), and phosphorylated signal transducer and activator of transcription 3 (p-STAT3) were determined by Western blotting. RESULTS: Compared with normal hepatocyte L02, CKAP2 was highly expressed in liver cancer cell lines HepG2, Huh7, and SMMC-7721 (all <0.05). Compared with the NC group, cell viability and proliferation rate of the siCKAP2 group were decreased (both <0.05). The apoptotic rate, protein expression of cleaved-caspase 3 and Bax in the siCKAP2 group were significantly higher than those in the NC group (all <0.05). Compared with the NC group, cell migration and invasion rates of the siCKAP2 group were significantly attenuated (both <0.05). Compared with the NC group, E-cadherin protein expression in siCKAP2 group was increased, while protein expression levels of Vimentin, N-cadherin, p-JAK2, and p-STAT3 were decreased (all <0.05). CONCLUSIONS CKAP2 gene silence inhibits proliferation, migration, and invasion, and promotes apoptosis in liver cancer cells, while JAK2/STAT3 signaling pathway may be involved in these processes.
Apoptosis ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Cytoskeleton ; Humans ; Liver Neoplasms ; genetics

Objective To evaluate the protective effects elicited by ClpP fusion protein in animal protection tests. Methods Pneumococcal antigens were purified from recombinant Escherichia coli express-ing CIpP cloned gene. 6- to 8-week-old female BALB/c mice were immunized intraperitoneally with either ClpP or PBS plus alum. Every mouse received three doses of 20 μg antigen or PBS in 100 mg of alum adju-vant at 14 d intervals. Sera were collected from mice and analyzed by ELISA 1 week after the third immuni-zation, Intraperitoneal-challenge experiments with 12 different serotypes of Streptococcus pneumoniae were carried out 2 weeks after the third immunization, and we compared their median survival times and survival rates respectively by Mann Whitney U test and Fisher exact test. Results ELISA analysis demonstrated high titer specific antibody responses to ClpP. The median survival times for mice immunized with ClpP pro-tein antigens in adjuvant were significantly longer than those for mice that received the adjuvants alone. Con-clusion A highly expressed recombinant ClpP protein has been successfully obtained and proved to exert the protection against invasive pneumococcal infection without relation of serotype, suggesting ClpP can be a promising candidate vaccine.

The relationship between M3 cholinergic receptor agonist (carbachol) hyperstimulation-induced pancreatic acinar cellular injury and trypsinogen activation or NF-kappaB activation in rats was studied in vitro. Rat pancreatic acinar cells were isolated, cultured and treated with carbachol, the active protease inhibitor (pefabloc), and NF-kappaB inhibitor (PDTC) in vitro. Intracellular trypsin activity was measured by using a fluorogenic substrate. The cellular injury was evaluated by measuring the leakage of LDH from pancreatic acinar cells. The results showed that as compared with control group, 10(-3) mol/L carbachol induced a significant increase of the intracellular trypsin activity and the leakage of LDH from pancreatic acinar cells. Pretreatment with 2 mmol/L pefabloc could significantly decrease the activity of trypsin and the leakage of LDH from pancreatic acinar cells (P < 0.01) following the treatment with a high concentration of carbachol (10(-3) mol/L) in vitro. The addition of 10(-2) mol/L PDTC didn't result in a significant decrease in the activity of trypsin and the leakage of LDH from pancreatic acinar cells treated with a high concentration of carbachol (10(-3) mol/L) in vitro (P > 0.05). It was concluded that intracellular trypsinogen activation is likely involved in pancreatic acinar cellular injury induced by carbachol hyperstimulation in vitro. NF-kappaB activation may not be involved in pancreatic acinar cellular injury induced by carbachol hyperstimulation in vitro.
Carbachol/*pharmacology ; Cholinergic Agonists/pharmacology ; NF-kappa B/*metabolism ; Pancreas/metabolism ; Pancreas/*pathology ; Rats, Wistar ; Receptor, Muscarinic M3/agonists ; Trypsinogen/*metabolism

Objective To introduce the treatment efficacy of using allograft muscle ligament anatomical to rebuild anterior cruciate ligament (ACL) of knee joint under the arthroscopy.Methods Sixty-two cases patients with ACL rupture in anterior cruciate ligament reconstruction under arthroscopy.Allograft ligaments were used as graft,a bone tunnel was established in the proximal tibia and distal femur,and the graft was fixed by the extrusion screw.After the operation,the knee joint was fixed for 12 weeks,and the subjective evaluation was carried out according to the Lysholm and Larson knee score standards;in order to assess the stability of the ligament and the functional recovery of the knee joint,objective evaluation was carried out according to Lachman test in patients.Results The preoperative average Lysholm scale was (43.1±2.1) points,the final average score of 2 years after the reconstruction of the ligament was (91.0+2.3) points,there was significant difference (t=3.460,P=0.001).The preoperative average Larson scale was (41.0±2.9) points,the final average score of 2 years after the reconstruction of the ligament was (90.1±3.5) points,there was significant difference (t=3.232,P=0.001).Lachman test results were negative in 62 patients at the end of the review.No serious postoperative complications occurred,no knee infection,deep vein thrombosis and stiffness.All the patients can be completely straight 1 year after operation,knees up to 120 degrees.All patients were satisfied with the function at the end of the follow-up,no joint instability,no re-rupture occurred during the follow-up period.Conclusion Using the allogeneic single beam anatomy of anterior cruciate ligament reconstruction under arthroscopy can obtain satisfactory clinical efficacy.

Objective To observe the effect of the chitosan tube combined with basic fibroblast growth factor (bFGF) on repairing sciaticnerve injury in rats. Methods 25 adult Wistar rats were divided into modeled sham-operated group (n=10), lesion control group (n=5) andexperiment group (n=10). All of them were operated with a 5-mm sciatic nerve exposed on the left. The lesion control group was intervenedwith the sciatic nerve cut off. The experiment group was intervened with bFGF-chitosan tubes bridged into nerve stumps. The movement behaviorwas observed, the regeneration of the injury nerves and the distal target muscle were detected by morphological staining. Results 5weeks after operation, the movement function of the experiment group was apparently recovered and gaps on the sciatic nerve were connectedby the regeneration nerve in this group and NF and S-100 immunoreactive fibers were observed in regeneration nerve. Masson's trichromestain showed that the target muscle was close to the level of sham-operated group in morphology and density. Conclusion The chitosantube combined with bFGF can repair the peripheral nerve injury effectively and improve the movement function of rats.

To repair the brain of adult rats with traumatic brain injury by inducing neural regeneration with biological scaffolds. Methods 52 adult male Wistar rats were divided into control group, lesion group, blank chitosan carriers group and bioactive material scaffolds group. The neural regeneration and the origin of the newborn neurons in the injury area were detected through histochemistry, immumochemistry and neural tracing on the 3rd day, 7th day, 2nd week, 4th week, 2nd month and 3rd month after operation. Results After application of bioactive material scaffolds, the BrdU+/Nestin+ and BrdU+/Dcx+ cells in gyrus dentatus (DG) of hippocampus and subventricular zone (SVZ) were significantly more than those of the other groups. The BrdU+/Nestin+, BrdU+/Dcx+ and BrdU+/MAP2+ neural cells in injury area of the bioactive material scaffolds group were significantly more than those of the other groups. After application of DiI to label the SVZ cells, DiI+/NeuN+ neurons were observed in the injury areas. Conclusion Bioactive material scaffolds can activate the neural stem cells in SVZ and DG. The neural stem cells in SVZ can migrate to the injury area and then differentiate into mature neurons.

Objective To investigate the effect of MRE11 on the proliferation and apoptosis of esophageal squamous cancer cells and its molecular mechanism. Methods MRE11 expression was downregulated by MRE11 siRNA transfection in esophageal squamous cancer cells. The AKT agonist SC79 (0, 0.1, 0.5, 1, 1.5, 1.8, 2 μg/ml) were used to treat cells with MRE11 inhibition for 24 h. Overexpression vector pcDNA.3.1-c-myc was constructed and co-transfected cells with MRE11 siRNA. Western blot method was used to detect the protein expressions of MRE11, p-AKT and c-myc in esophageal squamous cancer cells Ec9706 and TE-1. The Annexin-V FITC/PI kit was used to detect the apoptosis of Ec9706 and TE-1 cells; the activity of caspase-3 was detected by the Caspase-3 activity detection kit; the proliferation of Ec9706 and TE-1 cells was tested by the BrdU method. Results The protein expressions of MRE11 in Ec9706 and TE-1 cells were significantly increased, compared with human esophageal epithelial Het-1A cells. After MRE11 siRNA transfection, AKT phosphorylation and the protein expressions of MRE11 and c-myc were significantly decreased in esophageal squamous cancer cells. MRE11 inhibition significantly promoted the apoptosis and caspase-3 activity in Ec9706 and TE-1 cells, while inhibited the proliferation of Ec9706 and TE-1 cells. SC79 (1.5, 1.8 and 2 μg/ml) significantly increased AKT phosphorylation in MRE11-suppressed esophageal squamous cancer cells, and reversed the inhibitory effects of MRE11 inhibition on c-myc protein expression and cell proliferation and the promoting effect on cell apoptosis. Overexpression of c-myc inhibited the inhibitory effect of MRE11 down-regulation on cell proliferation and the promotion on caspase-3 activity. Conclusion MRE11 inhibition could effectively inhibit the proliferation of esophageal squamous cancer cells and promote cell apoptosis by regulating AKT and c-myc.

Anti-Inflammatory Agents ; therapeutic use ; Antioxidants ; therapeutic use ; Diabetes Mellitus, Type 2 ; drug therapy ; Drugs, Chinese Herbal ; therapeutic use ; Herbal Medicine ; methods ; Humans ; Hypoglycemic Agents ; therapeutic use