Analysis of risk factors associated with pre-myopia among primary school students in the Mianyang Science City.

Objectives To find out the prevalence rate of pre-myopia among primary school students in the Mianyang Science City Area, analyze its related risk factors, and thus provide a reference for local authorities to formulate policies on the prevention and control of myopia for primary school students. Methods From September to October 2021, Cluster sampling was adopted by our research group to obtain the vision levels of primary school students employing a diopter test in the Science City Area. In addition, questionnaires were distributed to help us find the risk factors associated with pre-myopia. Through the statistical analysis, we identify the main risk factors for pre-myopia and propose appropriate interventions. Results The prevalence rate of pre-myopia among primary school students in the Science City Area was 45.27% (1020/2253), of which 43.82% were boys and 46.92% were girls, with no statistically significant difference in the prevalence rate of myopia between boys and girls (2 =2.171, P=0.141). The results of the linear trend test showed that the prevalence rate of pre-myopia tends to decrease with increasing age (Z=296.521, P=0.000). Logistic regression analysis demonstrated that the main risk factors for pre-myopia were having at least one parent with myopia, spending less than 2 hours a day outdoors, using the eyes continuously for more than 1 hour, looking at electronic screens for more than 2 hours, and having an improper reading and writing posture. Conclusion The Science City Area has a high prevalence rate of pre-myopia among primary school students. It is proposed that students, schools, families, and local authorities work together to increase the time spent outdoors, reduce digital screens and develop scientific use of eye habits.

LOC102553417 silencing facilitates the apoptosis of hepatic stellate cells via the miR­30e/MTDH axis.

Hepatic fibrosis is an inevitable pathological process in the progression of multiple chronic liver diseases and remains a major challenge in the treatment of liver diseases. The purpose of the present study was to demonstrate whether silencing of the long non­coding RNA LOC102553417 promoted hepatic stellate cell (HSC) apoptosis via the microRNA (miR)­30e/metadherin (MTDH) axis. A LOC102553417 silencing lentivirus was constructed and transduced into HSC­T6 cells. After confirming the silencing efficiency by reverse transcription­quantitative PCR, cell proliferation was assessed using the Cell Counting Kit­8 assay and apoptosis was assessed using flow cytometry. The interaction between LOC102553417 and miR­30e, and that between miR­30e and MTDH, was demonstrated using the dual­luciferase reporter assay and RNA binding protein immunoprecipitation. The apoptosis of HSC­T6 cells was detected after transfection of miR­30e mimics and inhibitors with or without silencing LOC102553417. Silencing of LOC102553417 curbed HSC­T6 cell proliferation and expedited their apoptosis. LOC102553417 was demonstrated to target miR­30e, whereas miR­30e targeted MTDH. In addition, LOC102553417 silencing significantly upregulated miR­30e expression levels, and significantly downregulated MTDH mRNA and protein expression levels, which resulted in a significantly reduced p­Akt/Akt ratio and significantly elevated p53 protein expression levels. Transfection with miR­30e mimic alone significantly enhanced HSC­T6 cell apoptosis and inhibits LOC102553417 and MTDH expressions, In addition, miR­30e mimic expedites the apoptosis of HSCs stimulated by LOC102553417 silencing; consistent results were obtained by reverse validation of miR­30e inhibitor. In conclusion, the present study demonstrated that LOC102553417 silencing stimulated the apoptosis of HSCs via the miR­30e/MTDH axis.

Serum Homocysteine Levels and Microalbuminuria in Patient with Systemic Lupus Erythematosus.

BACKGROUND: At present, the relationship between serum homocysteine and microalbuminuria (MAU) in systemic lupus erythematosus (SLE) patients is still unclear. Therefore, the aim of our study was to analyze the association between serum homocysteine and MAU in SLE patients. METHODS: The study analyzed 150 patients with SLE at Affiliated Hospital of Youjiang Medical University for Nationalities retrospectively, and we collected for clinical and laboratory data. RESULTS: We found a positive correlation between serum homocysteine and MAU in SLE patients (r = 0.430, p < 0.001). We found that serum homocysteine levels were increased in SLE patients with MAU positive compared to those who were MAU negative (p < 0.001). After adjusting for multiple confounding factors, we found that serum homocysteine maintained a positive correlation with MAU in patients with SLE in multivariate correlation analysis (p = 0.253, r = 0.002). The receiver operating characteristic (ROC) curve with an area under the curve of 0.730, and serum homocysteine had 72.2% sensitivity and 61.9% specificity with cutoff values 9.0 to identify the SLE patients with MAU positive. CONCLUSIONS: The current results found a correlation between serum homocysteine and MAU in SLE patients, suggesting that elevated serum homocysteine levels might be an adverse factor for SLE patients with kidney injury.

Antiviral effects of hepatitis B virus S gene-specific anti-gene locked nucleic acid in transgenic mice.

AIM: To assess the antiviral effects of hepatitis B virus (HBV) S gene-specific anti-gene locked nucleic acid (LNA) in transgenic mice. METHODS: Thirty HBV transgenic mice were acclimatized to laboratory conditions and positive for serum HBV surface antigen (HBsAg) and HBV DNA, were randomly divided into 5 groups (n = 7), including negative control (blank control, unrelated sequence control), positive control (lamivudine, anti-sense-LNA), and anti-gene-LNA experimental group. LNA was injected into transgenic mice by tail vein while lamivudine was administered by gavage. Serum HBV DNA and HBsAg levels were determined by fluorescence-based PCR and enzyme-linked immune sorbent assay, respectively. HBV S gene expression amounts were assessed by reverse transcription polymerase chain reaction. Positive rates of HBsAg in liver cells were evaluated immunohistochemistry. RESULTS: Average rate reductions of HBsAg after treatment on the 3rd, 5th, and 7th days were 32.34%, 45.96%, and 59.15%, respectively. The inhibitory effect of anti-gene-LNA on serum HBsAg peaked on day 7, with statistically significant differences compared with pre-treatment (0.96 ± 0.18 vs 2.35 ± 0.33, P < 0.05) and control values (P < 0.05 for all). Average reduction rates of HBV DNA on the 3rd, 5th, and 7th days were 38.55%, 50.95%, and 62.26%, respectively. This inhibitory effect peaked on the 7th day after treatment with anti-gene-LNA, with statistically significant differences compared with pre-treatment (4.17 ± 1.29 vs 11.05 ± 1.25, P < 0.05) and control values (P < 0.05 for all). The mRNA levels of the HBV S gene (P < 0.05 for all) and rates of HBsAg positive liver cells (P < 0.05 for all) were significantly reduced compared with the control groups. Liver and kidney function, and histology showed no abnormalities. CONCLUSION: Anti-gene-LNA targeting the S gene of HBV displays strong inhibitory effects on HBV in transgenic mice, providing theoretical and experimental bases for gene therapy in HBV.

Serum Bilirubin Concentrations in Patients With Takayasu Arteritis.

CONTEXT: - Bilirubin has strong anti-inflammatory and antioxidative stress action. Progression of inflammation involving arteries is a crucial activator in pathogenesis of Takayasu arteritis (TA). OBJECTIVE: - To investigate the relationship between serum bilirubin and TA. DESIGN: - Our study involved 115 consecutive TA patients. Patients with active-phase disease were followed and received prednisone therapy. RESULTS: - Lower concentrations of serum bilirubin were detected in TA patients compared with healthy subjects (0.6 ± 0.31 versus 0.7 ± 0.22 mg/dL, P = .02). Serum bilirubin concentrations in active TA patients were lower than those in inactive patients (0.5 ± 0.20 versus 0.8 ± 0.32 mg/dL, P < .001). In all patients with TA, serum bilirubin correlated positively with total protein (r = 0.193, P = .04) and negatively with C-reactive protein and erythrocyte sedimentation rate (r = -0.213, P = .03, and r = -0.532, P < .001, respectively). Multiple logistic regression analysis showed that each decrease of 1 mg/dL in serum bilirubin was associated with a 1.10 times increase in the odds for TA compared with the controls (odds ratio = 0.913, 95% CI, 0.856-0.974; P = .006). Serum bilirubin was correlated with erythrocyte sedimentation rate (ß = -0.170, P < .001) in multiple linear regression analysis. The area under the curve for serum bilirubin in predicting active TA patients was 0.802. Serum bilirubin levels were found to be significantly increased after prednisone treatment (0.5 ± 0.20 versus 0.7 ± 0.15 mg/dL, P = .002). CONCLUSIONS: - Lower serum bilirubin levels are associated with TA, and serum bilirubin may be influenced by prednisone therapy in active TA patients. Serum bilirubin levels in TA patients correlate negatively with erythrocyte sedimentation rate.

The role of mean platelet volume in patients with Takayasu arteritis.

Background Takayasu arteritis is a chronic non-specific inflammatory disease and mean platelet volume can either be decreased or increased during inflammation. However, there are no published data to confirm an association between mean platelet volume and Takayasu arteritis. Our aim was to evaluate the role of mean platelet volume in patients with Takayasu arteritis. Methods A total of 119 consecutive patients with Takayasu arteritis and 217 healthy individuals were included in this study. Forty-five Takayasu arteritis patients with active disease were followed with prednisone therapy. Results Mean platelet volume of patients was low compared with control groups (10.1 ± 1.47 fL vs. 11.2 ± 0.91 fL; P < 0.001). Mean platelet volume was lower in active Takayasu arteritis than in inactive Takayasu arteritis patients (9.3 ± 1.39 fL vs. 10.6 ± 1.28 fL; P< 0.001). Mean platelet volume values were significantly increased after prednisone treatment (9.3 ± 1.45 fL vs. 10.5 ± 1.29 fL; P < 0.001). Mean platelet volume negatively correlated with C-reactive protein, erythrocyte sedimentation rate, neutrophil count and platelet count (r = - 0.219, P = 0.018; r = - 0.296, P < 0.001; r = - 0.273, P = 0.003; r =-0.486, P< 0.001), and positively correlated with platelet distribution width (r=0.304, P ≤ 0.001) in patients with Takayasu arteritis. An inverse correlation between mean platelet volume and erythrocyte sedimentation rate was observed in active Takayasu arteritis patients (r = -0.406, P = 0.010). In multiple linear regression analysis, mean platelet volume was independently correlated with erythrocyte sedimentation rate in patients with Takayasu arteritis. Conclusions Our results suggest that mean platelet volume may identify active disease in patients with Takayasu arteritis, and the values of mean platelet volume may help to establish remission of active disease after treatment in Takayasu arteritis patients.

[Prevalence of a high non-high-density lipoprotein cholesterol level in children aged 9-11 years in Mianyang Science City in Sichuan Province, China].

OBJECTIVE: To investigate the non-high-density lipoprotein cholesterol (non-HDL-C) level and the prevalence rate of a high non-HDL-C level in children aged 9-11 years in the Mianyang Science City area in Sichuan Province, China. METHODS: From September to October, 2015, a field investigation was performed for the students from three primary schools in the Mianyang Science City area by cluster sampling. Fasting venous blood was collected for blood lipid tests. The cut-off value of serum non-HDL-C level and prevalence rate of a high non-HDL-C level in children aged 9-11 years in this area were calculated, as well as the prevalence rate of a high non-HDL-C level in obese children. RESULTS: In the children aged 9-11 years in this area, the cut-off value of non-HDL-C level was 3.67 mmol/L, and the prevalence rate of a high non-HDL-C level was 3.7% (22/589). Compared with the non-obese children, the obese children had a significantly higher serum non-HDL-C level (P<0.01) and a significantly higher prevalence rate of a high non-HDL-C level (10.0% vs 2.9%; P<0.01). CONCLUSIONS: The cut-off value of serum non-HDL-C level in children aged 9-11 years in the Mianyang Science City area is established. Obesity is associated with an increased prevalence rate of a high non-HDL-C level in children aged 9-11 years.

[Inhibition of hepatitis B virus (HBV) replication using antisense LNA targeting to both S and C genes in HBV].

OBJECTIVE: To investigate the inhibitory effect on HBV replication of antisense locked nucleic acid (LNA) targeting to both S and C genes in HBV transgenic mice. METHODS: Thirty HBV transgenic mice were randomly divided into five groups (n = 6): glucose control group were treated with 5% glucose solution, liposome control group were treated with liposome alone, S group were treated with LNA targeting to S gene, C group were treated with LNA targeting to C gene, and dual-target group were treated with LNA targeting to both S and C genes. Antisense LNA was injected into mice via the tail vein. Serum HBsAg was quantified by TRFIA. Serum HBV DNA was quantified by real-time PCR. The expression of HBV C-mRNA in the liver was detected by RT-PCR. The expression of HBsAg and HBcAg in the liver was detected by immunohistochemistry. Serum ALB, ALT, BUN and CR were measured using an automatic biochemical analyzer. The effects of antisense LNA on mouse organs were investigated by HE staining. RESULTS: 5 days after LNA injection, serum HBsAg levels in the dual-target group were reduced by 72.8%, and serum HBV DNA levels were decreased by 52.9%. These values were significantly higher than those in the control groups (all P < 0.05). No significant differences were noted in serum ALB, ALT, BUN and CR between the experiment groups and the control groups (all P > 0.05). The expression levels of HBsAg and HBcAg in the liver of dual-target group were significantly lower than those in the control groups. No significant histopathological abnormality was found in liver and kidney tissues in all groups. CONCLUSION: Antisense LNA targeting to both S and C genes can significantly inhibit HBV replication in transgenic mice.

[Bcl-xl blocks tumor necrosis factor alpha-induced caspase 8 activation and apoptosis].

OBJECTIVE: To explore the effect of Bcl-xl on tumor necrosis factor-alpha (TNFalpha)-induced apoptosis signal pathway and apoptosis. METHODS: A dominant negative mutant of ikB (pmi kappaB) and Green Fluorescent Protein (GFP) expression plasmid pEGFP-C1, pmi kappab and pEGFP-C1 and Bcl-xl expression construct pBcl-xl/HA, were co-transfected into HeLa cells. Expression plasmid pBcl-xl/HA was introduced into p65-/-MEF cells in which nuclear factor-kappaB (NF-kappaB)/p65 was deficient, to establish cell line p65-/-Bcl-xl expressing Bcl-xl by selection with puromycin. These cells were treated with TNFalpha at a concentration of 10 ng/ml, and apoptotic cell death was examined microscopically with trypan blue staining. The proteins were abstracted from treated cells, and caspase 8 activation and cleavage of poly (ADP-ribose) polymerase (PARP) were examined by western blot using a specific antibody that recognized cleaved caspase 8 and cleaved PARP, respectively. RESULTS: HeLa cells transfected with pmi kappaB, TNFalpha showed significant cell death as they became rounded, shrank, and detached. However in HeLa cells co-transfected with pBcl-xl and pmi kappaB, no cell death was observed after treatment with TNFalpha. In p65-/- MEF cells; cell death was observed at 4 hours after treatment with TNFalpha, and cell death reached 90% at 12 hours after the treatment. However, in p65-/-Bcl-xl/HA cells expressing Bcl-xl, no cell death was seen even when treated with TNFa for 24 hours. Meanwhile, in pmikB/HeLa cells transfected with pmi kappaB, TNFalpha induced caspase 8 activation and PARP cleavage, but in the HeLa cells co-transfected with pBcl-xl and pmi kappaB, no activated caspase 8 and cleaved PARP were observed after treatment with TNFalpha. CONCLUSION: In the experimental system in which NF-kB was inhibited, Bcl-xl blocked TNFalpha-induced apoptosis signal pathway and apoptosis. These results bring to light that further studies of the pathogenesis and therapy of TNFa-related diseases are needed.