Objective To evaluate the postoperative complications and visual quality after manual small incision cataract surgery (MSICS) versus phacoemulsification (PHACO).Methods A systematic review of MSICS and PHACO was conducted by a computer search on Medline,Pubmed,CBM and CNKI and a supplementary manual search was also done.The effect was measured as an odds ratio (OR) and weighted mean difference (WMD).RevMan 5.0 software was used to perform the Meta-analysis.Results A total of 9 articles were included in the Meta-analysis.Naked visual acuity at 1 week after surgery (OR =0.93,95％ CI 0.68-1.27),posterior capsular ruptured after surgery (OR =1.07,95％ CI 0.73-1.58),corneal edema after surgery (OR =0.90,95 ％ CI 0.70-1.16),surgically induced astigmatism at 1 month after surgery (WMD =0.08,95％ CI-0.02-0.17) in MSICS and PHACO was no statistically significant difference (P ＞0.05).Conclusion MSICS is safe and reliable surgery as same as PHACO for the patients with cataract,MSICS is more consistent with China' s national conditions.

Objective To investigate the diagnostic value of combined detection of serum gastrin-releasing peptide precursor (ProGRP),neuron specific enolization enzyme(NSE)and carcinoembryonicantigen(CEA)in small cell lung cancer(SCLC). Methods 471 patients with lung tumor from department of respiratory medicine and thoracic surgery and 162 healthy people from medical examination center were studied.Serum levels of ProGRP,NSE and CEA were detected by using electrochemi-cal luminescence method.ROC curves were drawn and the area under the curve (AUC)was calculated.Results The levels of ProGRP and NSE were significantly higher in patients with SCLC than those in NSCLC,lung benign disease group and normal control group (P <0.01).The levels of CEA were significantly higher in SCLC than those in patients with lung be-nign disease group and normal control group (P <0.05).The AUC of ProGRP,NSE and CEA in the diagnosis of SCLC were 0.933,0.777 and 0.554,respectively.The sensitivity of ProGRP,NSE and CEA in the diagnosis of SCLC were 82.6%,60.4%,41.6% and the specificity were 95.2%,83.3% and 71.7% respectively.The sensitivity of combined detec-tion of ProGRP,NSE and CEA was 91.3% and the specificity was 65.3%.Conclusion The serum ProGRP detection has a higher diagnostic value for SCLC.The combined detection of ProGRP,NSE and CEA is useful in the early diagnosis of SCLC.

OBJECTIVETo investigate the effect of CCM3 gene defection on lead induced cell genotoxicity in mouse embryonic fibroblasts.

METHODSC57 female mice were mated with CCM3 gene heterozygous male mice. E13.5 embryos were taken to isolate primary mouse embryonic fibroblasts. After genotyping, wild type and heterozygous cells were treated with different doses of lead acetate. Cell viability, genotoxicity and protein expression were detected by MTS assay, CB micronucleus method and Western blot, respectively.

RESULTSMouse embryonic fibroblasts with lead acetate treatment for 24 h, wild-type cells 100.00 µmol/L lead acetate-treated group (69.16±1.36) and the control group (100.00±2.33) compared to cells decreased by 30%, CCM3 heterozygous type cell 100.00 µmol/L lead acetate-treated group (87.16±5.50) and the control group (100.00±2.06) compared to cells decreased by 13%, the difference was statistically significant (F values were 98.59, 82.63, P<0.001). Lead acetate treatment after 48 h, wild-type cells 100.00 µmol/L lead acetate-treated group (51.99±5.62) and the control group (100.00±3.11) compared to cells decreased by 50%, heterozygous type cells 100.00 µmol/L lead acetate treatment group (66.33±4.06) and the control group (100.00±5.72) compared to cells decreased by 35%, the differences were statistically significant (F values were 82.63, 36.86, P < 0.001). The results of CBMN test showed that with increased dose, micronucleus cell rate of two genotypes showed an increasing trend, in the wild-type cells, the micronucleus cell rate (/1 000) for the control group, 29.6±2.2, 6.25 µmol/L dose group 47.3±6.6, 25 µmol/L dose group 55.5±9.1, 100.00 µmol/L dose group 66.8±3.5; heterozygous cells micronucleus cell rate (/1 000) for the control group, 35.3±5.6, 6.25 µmol/L dose of 50.0±8.3, 25.00 µmol/L dose group 57.0±8.5, 100.00 µmol/L dose group 58.8±2.1. Micronucleus cell rates (/1 000) were significant differences, in 100.00 µmol/L dose groups of two genotypes. Western blot results showed that wild-type cells CCM3 expression 100.00 µmol/L lead acetate-treated group (0.70±0.03) was 1.32 times higher than the control group (0.53±0.07), heterozygous cells CCM3 expression 100.00 µmol/L lead acetate-treated group (0.48±0.02) was 1.77 times higher than control group that of 0.27±0.04, there was statistically significant difference (F values were 14.77, 25.74, P < 0.001); wild-type cells γ-H2AX expression 100.00 µmol/L lead acetate-treated group (0.69±0.03) was 1.06 times higher than the control group (0.65±0.07), heterozygous cells γ-H2AX expression 100.00 µmol/L lead acetate-treated group (0.99±0.04) was 1.55 times higher than the control group CCM3 expression levels (0.64±0.06), there was statistically significant difference (wild-type cells: F = 7.08, P = 0.012, heterozygous type cell: F = 13.49, P = 0.002).

CONCLUSIONCCM3 gene may play a role in lead-induced genetic toxicity of mouse embryonic fibroblasts, CCM3 gene-lead interactions effects on mouse embryonic fibroblasts cell toxicity.

Animals ; Apoptosis Regulatory Proteins ; DNA Damage ; Embryo, Mammalian ; Female ; Fibroblasts ; Genotype ; Male ; Membrane Proteins ; Mice ; Mice, Inbred Strains ; Micronuclei, Chromosome-Defective ; Organometallic Compounds ; Proto-Oncogene Proteins

Objective:To investigate the changes of proopiomelanocortin(POMC) expression in hypothalamus and corresponding metabolism in miR-21 knockout mice.Methods:miR-21 knockout or wild-type C57BL/6J mice were divided into diabetic group and control group, respectively. Diabetic mice model were forged with high-fat diet and low-dose streptozotocin. The changes of body weight and blood glucose in each group were monitored. By the end of the experiment, mice were sacrificed, and POMC protein expression and STAT3 mRNA expression in hypothalamus were detected.Results:There were no significant differences in body weight and blood glucose levels among all groups at baseline( P>0.05). The differences of body weight and blood glucose levels among various groups were compared at 3, 6, 9 and 12 weeks after the model was established. The results showed that body weight of mice in the diabetes group or miR-21 knockout+ diabetes group was higher than that in the control group at each time point( P<0.05). Moreover, there were significant difference in body weight between diabetes group and miR-21 knockout+ diabetes group at 3 and 12 weeks( P<0.05). The blood glucose levels in diabetes group were significantly higher than those in other groups at each time point( P<0.05). The blood glucose level in miR-21 knockout+ diabetes group was lower than that in diabetes group and higher than control group( P<0.05). POMC protein and STAT3 mRNA levels in diabetes group were significantly lower than those in control group, while those in the miR-21 knockout+ diabetes group were higher than those in the diabetes group. Conclusions:The expression of POMC in hypothalamus of miR-21 knockout mice is higher than that of wild-type diabetic mice. miR-21 knockout can decrease blood glucose level and body weight, and improve energy metabolism of diabetic mice.

OBJECTIVE: To explore the genetic basis for a child with metachromatic leukodystrophy (MLD). METHODS: Clinical data of the patient was collected. Genomic DNA was extracted from peripheral blood samples of the child and his family members. Potential variant was screened by whole exome sequencing (WES), and candidate variant was verified by Sanger sequencing. The pathogenicity the variant was analyzed by multiple sequence alignment of the amino acid sequence and three-dimensional model prediction of its protein product. RESULTS: The child was found to harbor compound heterozygous variants c.257G>A (p.R86Q) and c.467del (p.G156Afs*6) of the ARSA gene, among which the c.467del (p.G156Afs*6) frameshift variation was unreported previously. Multiple sequence alignment showed that the site of the c.257G>A (p.R86Q) missense variant is highly conserved. Three-dimensional structure modeling analysis showed that the partial deletion due to the p.G156Afs*6 variant may cause significant alteration of the structure of ARSA protein. CONCLUSION The discovery of novel variant in ARSA has enriched the mutational spectrum of MLD and may facilitate the understanding of the genotype-phenotype correlation of MLD.
Cerebroside-Sulfatase/genetics* ; DNA ; Genetic Association Studies ; Humans ; Leukodystrophy, Metachromatic/genetics* ; Mutation