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Objective@#To explore the relationship between lifestyle and myopia and construct Nomogram model to predict myopia risk among primary school students in Tianjin, so as to provide a scientific basis for precision myopia prevention and control.@*Methods@#From April to July of 2022, a census method was used to conduct vision testing and lifestyle related questionnaires among 373 180 primary school students in 15 districts of Tianjin. The relationship between lifestyle and myopia was analyzed by the multivariate Logistic regression, and a nomogram prediction model was constructed to predict myopia risk.@*Results@#The detection rate of myopia among primary school students in Tianjin was 37.6%. The results of the multivariate Logistic regression showed that daily outdoor activity time of 1-2 h ( OR =0.94) and >2 h ( OR =0.84), time of using daily electronic devices of >2 h ( OR =1.03), daily paper materials reading and writing time of 1-2 h ( OR =1.02) and >2 h ( OR =1.09), weekly fresh vegetable intake of 2-6 times ( OR =0.93) and ≥7 times ( OR =0.88) were statistically correlated with myopia ( P <0.01). The Nomogram prediction model showed that the factors associated with myopia were grade, family history of myopia, gender, daily outdoor activity time, weekly frequency of fresh vegetable intake, daily paper materials reading and writing time, and time of using daily electronic devices time.@*Conclusions@#The lifestyle of primary school students in Tianjin is associated with myopia. The constructed nomogram model could provide a scientific basis for identifying key intervention populations for myopia prevention and taking targeted prevention and control measures.
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Objective:To investigate the effect of hyperbaric oxygen combined with RNA interference (RNAi) technology targeting aquaporin-4 (AQP-4) on improving cognitive function in rats with traumatic brain injury (TBI), and to explore its mechanism.Methods:Totally 112 adult male SD rats were randomly divided into four groups: control group, hyperbaric oxygen(HBO) group, AQP-4 RNAi group and combined treatment group, with 28 rats in each group.The TBI model of rat was established by hydraulic percussion and siRNA targeting aquaporin 4 was constructed. Rats were given corresponding intervention according to their groups.Then the modified neurological severity scores(mNSS)was evaluated on the 7th day and 21th day after operation. Morris water maze test was carried out from the 21st day to 25th day after operation and the percentage of target quadrant and daily escape latency were recorded.The changes of the brain permeability of blood-brain barrier and moisture in brain tissues were measured by Evans blue fluorometry and a wet-dry-weighing technique respectively. The protein expression levels of AQP-4, Caspase-3, Bcl-2, MMP-2 and MMP-9 were detected by Western blot method. The mRNA expression of AQP-4 in TBI brain tissue was measured by RT-PCR method, and the apoptosis rate of TBI brain cells was detected by TUNEL and AnnexinV methods on the 7th day after operation. SPSS 23.0 and Graphpad Prism 7.0 softwares were used for data analysis.One-way ANOVA was used for inter group comparison.Repeated measurement ANOVA was used for Morris results, and the LSD- t test was used for pairwise comparisons. Results:The results of mNSS showed that there were significant differences among the groups on the 7th day and 21st day after operation ( F=4.89, 7.59, both P<0.05). The scores of each treatment group were lower than that of the control group, and the effect of the combined treatment group was the best (7th day: t=3.98, -7.75, both P<0.05; 21st day: t=47.82, 7.94, both P<0.05). The results of Morris water maze test showed that the time and group interaction of rats in the target quadrant residence time and escape latency were not statistically significant( F=1.83, 8.42, both P>0.05). The escape latency and the percentage of stay in the target quadrant in the combined treatment group were better than those in other groups on the 24th and 25th day after operation (all P<0.05). Evans blue staining showed that the contents of Evans blue in AQP-4 RNAi group, hyperbaric oxygen group and combined treatment group were lower than that in the control group(all P<0.05), and that in the combined treatment group was the lowest( t=6.19, P<0.05). The results of dry-wet specific gravity method showed that the water content of brain tissue in the combined treatment group((68.15±1.52)%) was the lowest, and that in the AQP-4 RNAi group((76.71±1.06)%) was lower than that in the HBO group ((80.23±1.43)%)( t=4.38, P<0.05). The results of Western blot showed that the protein levels of AQP-4, Caspase-3, MMP-2 and MMP-9 in the combined treatment group were significantly lower than those in other groups(all P<0.05), while the expression of Bcl-2 was increased in the combined treatment group( P<0.05). RT-PCR results (gray value ratio) showed that AQP-4 mRNA levels in AQP-4 RNAi group(0.61±0.21), HBO group (0.83±0.12), combined treatment group(0.22±0.05) and CON group (1.31 ± 0.25) were significantly different( F=175.05, P<0.05), while the AQP-4 mRNA levels decreased in AQP-4 RNAi group which was better than that in hyperbaric oxygen group ( t=5.25, P<0.05). The decrease was the most obvious in the combined treatment group ( t=58.94, P<0.05). The results of TUNEL and AnnexinV showed that the treatment groups were more effective than the control group in inhibiting neuronal apoptosis, especially in the combined treatment group ( P<0.01). Conclusion:The combination of targeted AQP-4 RNAi and hyperbaric oxgen can effectively promote the recovery of neurological and cognitive function, and the mechanism may be related to protecting the integrity of blood-brain barrier, alleviating brain edema and inhibiting apoptosis of nerve cells after TBI.
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Objective:To investigate the effect and mechanism of bone marrow mesenchymal stem cell (BMSC)-derived exosomal microRNA-1297 (miR-1297) on hippocampal neuron damage in depressed rats.Methods:BMSCs and BMSCs-derived exosomes were prepared and identified. Rats were first injected with corticosterone to establish the model of depression, and then injected with BMSCs-derived exosomes. Superoxide dismutase (SOD), malondialdehyde (MDA), lactate dehydrogenase (LDH), TNF-α and IL-1β in rat serum samples, hippocampal tissues and neurons were detected. Expression of miR-1297 in hippocampal tissues and neurons was detected by RT-qPCR. A rat hippocampal neuron injury model was established to investigate the role of BMSC-derived exosomes and miR-1297 in neuronal apoptosis and proliferation. The targeting relationship between miR-1297 and connective tissue growth factor (CTGF) was analyzed using dual luciferase reporter genes.Results:In the hippocampus of depressed rats, the expression of miR-1297 was low, while the expression of CTGF was elevated. Exosomes derived from BMSCs can inhibit the expression of CTGF by up-regulating the level of miR-1297, thereby inhibiting neuronal cell apoptosis in the hippocampus of depressed rats, while increasing the level of SOD, and reducing inflammatory damage, and ultimately improving the behavioral function of depressed rats.Conclusions:Depressed rats showed decreased expression of miR-1297 and increased expression of CTGF. BMSC-derived exosomes inhibited CTGF expression through up-regulating miR-1297, thereby improving hippocampal neuron damage in rats with depression.
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Thrombolytic therapy is one of the standard treatments of acute ischemic stroke.The patients with acute ischemic stroke often complicated with cerebral microbleed.Whether thrombolytic therapy will increase the risks of bleeding and early neurological deterioration in such patients are not conclusive.This article reviews the impact of cerebral microbleed burden on the outcome after thrombolytic therapy in patients with acute ischemic stroke.
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Objective To examine the effects and mechanisms of siRNA targeting aquaporin 4 (AQP 4) in combination with hyperbaric oxygen therapy(HBO) on cerebral edema and apoptosis in the brain tissue of rats after hemorrhage.Methods Rats were randomly divided into four groups,the control group,the hyperbaric oxygen group,the AQP-4 siRNA group and the combination therapy group (24 rats).Thrombin Ⅶ was injected into the caudate nucleus to establish the hemorrhage model.Construction of siRNA targeting aquaporin 4 was conducted.The mRNA expression of AQP-4 was detected by RT-PCR at day 3.Changes in brain moisture and blood-brain barrier perme ability were measured by a wet/dry weight method and Evans blue fluorometry.The nerve cell apoptosis rate was analyzed by Annexin V andTdT-mediated dUTP-biotin nick end labeling (TUNEL).The expression of proteins including AQP-4,MMP-2,MMP-9,Bcl-2 and caspase-3 was detected by Western Blotting.All the animals were given a score for their nerve function at day 3.Results AQP-4 siRNA treatment obtained better effects than HBO in decreasing the brain edema leveland silencing AQP-4 mRNA(P＜0.05)while,the combination therapy group achieved the best results(P＜ 0.05).Compared with the control group,the percentage of apoptotic cells decreased in all the three treatment groups,with the most marked decrease observed in the combination treatment group(4.24± 0.04)％(F=13.76,P=0.001).The expression of AQP-4,MMP-2,MMP-9 and caspase-3 was lower (P＜0.05) and the expression of Bcl-2 was higher(P＜0.01)in the combination treatment group than in the other three groups.Compared with the control group,all the other three groups received better scores on nerve function defect evaluation at day 3 after hemorrhage(P＜0.05),with the combination treatment group again achieving the most favorable score (4.7 ± 1.1) (F=7.21,P =0.013).Conclusions Targeted siRNA interference combined with hyperbaric oxygen can effectively reduce cerebral edema after cerebral hemorrhage,inhibit neuronal apoptosis and promote neuron function recovery.The underlying mechanisms may be related to down-regulation of AQP-4,MMP 2,MMP-9 and caspase-3 expression and up-regulation of Bcl-2 expression.
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Objective To investigate the role of glycogen synthase kinase -3beta(GSK3β)on invasion and metastasis of human osteosarcoma cells .Methods Expression and phosphorylation of GSK 3βwere examined in osteosarcoma cell lines and tumor tissue from osteosarcoma patients by Western blot .The effects of small mole-cule GSK3βinhibitors on cell metastasis were detected by cell invasion assay and cell migration assay .Results Osteosarcoma cell lines showed increased GSK 3βexpression and abnormal activity regulation .In tumor tissue of patients with osteosarcoma metastasis and non -metastasis,GSK3βwere detected expression and abnormal activi-ty,especially in tumor tissue of the patients with osteosarcoma metastasis .Inhibition of GSK3βactivity resulted in inhibiting cells invasion and migration in osteosarcoma cell line .Conclusion In this research,we demonstrated that GSK3βencouraged osteosarcoma cells metastasis .The result will open up a potential target for clinical treat-ment of osteosarcoma .
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Objective To explore SIRT4 gene expression in tumor tissue and investigate the clinicol-pathological features in osteosarcoma .Methods In this study ,SIRT4 protein expression was detected in 106 os-teosarcoma tissues and 36 paired neighboring non -tumorous tissues by immunohistochemistry and determined the correlation between the SIRT 4 expression and the clinicopathological features .Results SIRT4 protein was dra-matically decreased in osteosarcoma cells compared with neighboring non -tumorous bone cells .The low expres-sion of SIRT4 was notably associated with a poor overall survival and disease -free survival in osteosarcoma pa-tients.By using univariate and multivariate analyses ,we confirmed that the increased SIRT 4 expression was an in-dependent factor in predicting better prognosis for patients .Conclu is on SIRT4 expression might be an inde-pendent biomarker for prognostic evaluation of osteosarcoma .
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Objective To investigate the molecular mechanisms of effect of glycogen synthase kinase -3beta( GSK3β) on proliferation of human osteosarcoma cells .Methods Normal osteoblast hFO and osteosarcoma cell lines were examined for GSK 3βexpression and activity by Western blot and in vitro kinase assay ( NIRKA) . The effects of small molecule GSK3βinhibitors on cell proliferation and apoptosis were examined .Depletion of en-dogenous GSK3βby GSK 3βsiRNA detected the expression and phosphorylation of p 27 and its downstream cy-clinD1-CDK-Rb pathway factor by Western blot .Human osteosarcoma cell xenografts ,in athymic mice model , were treated with DMSO as control or with GSK 3βinhibitor SB-216763 or AR-A014418 by intraperitoneal in-jection,3 times a week.The tumor growth and body weight were observed in nude mice .Results Osteosarcoma cell lines showed increased GSK 3βexpression and decreased serine 9 phosphorylation compared with normal oste-oblast cells.Inhibition of GSK3βresulted in attenuated cell proliferation and increased apoptosis in most osteosar-coma cell lines in vitro and in vivo in MG 63 xenografts in rodents but not in hFOB cells .We decreased endoge-nous GSK3b activity,tumor growth was inhibited in SB216763,AR -A014418 group compared with control group.There was statistical significance(P<0.05).GSK3βinhibition in osteosarcoma cells was associated with decreased p27 expression, Rb expression and phosphorylation level of decline , CDK2, 4, 6 protein level de-creased,the upregulation of cyclin D1 expression but the phosphorylation level of no effect .Conclusion In this research,we demonstrate that deregulated GSK 3βsustains osteosarcoma cells survival through modulation of p27and cyclinD1-CDK-Rb pathway.The result will open up a potential target for clinical treatment of osteosar -coma.
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Osteosarcoma is a common malignant bone tumor in the skeletal system of minors .The five-year survival rate of patients with osteosarcoma is significanty improved by neoadjuvant chemotherapy combined with surgery.However,its mortality and morbidity rates remain quite high .With the development of molecular bi-ology and genetics ,gene therapy provides a new hope for patients with osteosarcoma .Researchers at home and a-broad have actively explored effective therapeutic targets .In this paper ,new progress in the study of gene -targe-ted therapy for osteosarcoma is reviewed .
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Objective To investigate the effects of dextran sulfate on lung ischemia-reperfusion injury after lung transplantation in rats.Method A total of 32 male Wistar rats were subjected to unilateral left lung orthotopic transplantation.They were randomly divided two groups (n =16 each):DXS group [DXS (10 mg/kg) was given prior to the reperfusion],and the control group (the same volume of normal saline was given).After animals were sacrificed,the lung graft was harvested 2 h after reperfusion.Oxygenation indexes,wet/dry ratio (W/D),myeloperoxidase (MPO) activity,malondialdehyde (MDA) and endothelin 1 (ET-1) in the transplanted lung,and tumor necrosis factor a (TNF-α) and interleukin 8 (IL-8) in serum were measured.The lung injury scores were evaluated and complement deposition was observed.Result After 2-h reperfusion,compared to the control group,oxygenation indexes were improved significantly in DXS group (P＜0.05),but there were no significant differences in W/D between two groups.In DXS group,the activity of MPO was significantly reduced,and the contents of MDA and ET-1 in the lung tissue were significantly reduced as compared with the control group.DXS reduced the level of TNF-α and IL-8 markedly in serum (P ＜0.05).There was no significant difference in lung injury score between two groups (4.53 ± 0.46 vs.5.28 ±0.49,P＞0.05).Compared to the control group,DXS reduced the deposition of C3c (0.8 ±0.2vs1.5±0.3) andC6 (1.2±0.4vs.2.4±0.5) (P＜0.05).Conclusion Administration of DXS attenuated ischemia-reperfusion injury after lung transplantation by inhibiting complement deposition,and improved the oxygenation of the transplanted lung.This protection was associated with inhibition of inflammation and oxidation and endothelial cytoprotection.
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Objective To investigate the effects of desflurane on the delayed rectifier potassium current (Ik ) in acutely dissociated rat parietal cortical neurons. Methods Wistar rats between 10- and 14-day old of both sexes were used. The parietal cortical neurons were acutely dissociated enzymatically. The extracellular fluid saturated with 0.3,0.6 and 0.9 mmol/L desflurane was added to the culture dish, then the effects of different concentrations of desflurane on Ik were investigated by using the whole-cell patch-clamp technique in acutely dissociated rat parietal cortical neurons. Results IK was inhibited by desflurane in a concentration-dependent manner ( P ＜0.01). The V1/2 of the activation and inactivation curves and the slop factor had no change after giving 0.6 mmol/L desflurane (P ＞ 0.05). Conclusion Desflurane inhibits delayed rectifier potassium channels of parietal cortical neurons of rats in a concentration-dependent manner, and has no effect on the activation and inactivation of delayed rectifier potassium channels, indicating that the change in the excitability of the channel is not involved in the mechanism of inhibitory effect of desflurane, and the other reasons may be involved in the mechanism.
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AIM: To explore the change of the amount of GLUT4 protein at the plasma membrane of the rat skeletal muscle after high-fat feeding. METHODS: The animals were divided into three groups (ten for each): group I: control; group II: high-fat feeding; group III: high-fat feeding + dietary treatment. The rat model of insulin resistance (IR) was made by feeding high-fat diet for eight weeks. And then insulin-resistant rats were fed with chow diet for 4 weeks. Fasting plasma glucose and fasting serum insulin levels were measured before and after dietary treatment, respectively. Insulin treatment was achieved by intraperitoneal injection of insulin (10 unit insulin per kg body weight) 15 minutes before killing the animals. The right hindlimb skeletal muscle was rapidly dissected. Then the expression of GLUT4 protein at the plasma membrane in all the animals was assessed with Western bloting. RESULTS: The GLUT4 content at the plasma membrane in high-fat-fed rat skeletal muscle was significantly lower (about 31%) than that in controls (P
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Objective To investigate the effects of aerosolized prostaglandin E1 (PGE1) inhalation on oxygenation and intrapulmonary shunt in acute lung injury (ALI) .Methods Eighteen healthy male pigs weighing 14-18 kg were anesthetized with intraperitoneal pentobarbital 50 mg?kg-1, intubated and mechanically ventilated (VT=10-15 ml?kg-1, RR= 16 bpm, FiO2=100%) . PaCO2 was maintained at 34-45 mm Hg. Anesthesia was maintained with intravenous infusion of ketamine-procaine-succinyl-choline. Swan-Ganz catheter was placed via right femoral vein. Right femoral artery was cannulated for BP monitoring and blood sampling. ALI was induced by intratracheal instillation of HCl (0.1 mol?L-1) until PaO2 was
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Objective To investigate the protective effect of desflurane on the brain against ischemia-reperfusion (I/R) injury and the underlying mechanism. Methods Ninety-six male Wistar rats weighing 250-300 g were randomly divided into 4 groups (n = 24 each) : group A sham operation; group B I/R; group C desflurane + I/R and group D 5-HD + desflurane + I/R. I/R was induced by occlusion of bilateral common carotid arteries combined with controlled hypotension for 10 min. In C group 1 MAC desflurane (5.9% ) was inhaled for 60 min before I/R. In group D 5-HD 5 mg?kg-1 was given i.v. before desflurane inhalation. The animals recovered from anesthesia at 30 min of reperfusion. The neurological behavior was evaluated by the clambering test, the overhanging test, the inclined plane test and the beam balance test. Animals were killed at 6, 24 and 48 h ( n = 8 each) of reperfusion in each group and the brains were removed for microscopic examination of area CA1 of hippocampus for the number of normal pyramidal neurons surviving I/R. Results Neurological behavior was greatly compromised by I/R at 6, 24 and 48 h of reperfusion. The animals behaved significantly better at 6,24 and 48h in C group but only at 6 h in D group than in B group. The number of normal pyramidal neurons in CA1 of hippocampus was significantly decreased by I/R at 6, 24 and 48 h of reperfusion. The number was significantly larger at 6, 24 and 48 h in C group but only at 6h in D group than in B group. Conclusion Desflurane preconditioning has protective effect on the brain against I/R injury. Activation of KATP channel is involved in the mechanism.
