AIM: To investigate the clinical effects of phacoemulsification and surgical techeniques in small pupil cataract after filtering operation of glaucoma.
METHODS: Thirty-six cases ( 36 eyes ) of small pupil cataract after filtering operation of glaucoma were underwent phacoemulsification combined with foldable intraocular lens implantation. Postoperative visual acuity, intraocular pressure filtration bleb and complications were observed. The follow-up time was 3mo.
RESULTS: The preoperative uncorrected visual acuity (UCVA) or best-corrected visual acuity ( BCVA) ≤0. 3 were in all patients. Postoperativerly, the UCVA or BCVA≥0. 3 after 1wk and 3mo were achieved in 23 eyes (63.89%) and 34 eyes (94. 44%). BCVA was <0. 3 in 2 eyes ( 5. 56%) including optic nerve atrophy of one eye and diabetic retinopathy of one eye. All patients were kept the level of normal intraocular pressure and completed filtering bleb, there were no serious complications.
CONCLUSION: Phacoemulsification in small pupil cataract after filtering operation of glaucoma was complex, and reasonable application of operation skills can still achieve better clinical results. The main factor of affecting the visual acuity is pre-existing retinal optic neuropathy.

Bronchogenic Cyst ; Child ; Humans ; Male ; Neck ; pathology ; Young Adult

ObjectiveTo investigate the effect of indomethacin on insulin resistance and metabolic response to surgical injury in patients with gastrointestinal tumor.MethodsFifty-eight cases with gastric cancer or colon cancer were divided into an indomethacin group (n =28) and a control group (n =30).All the operations were performed under general anesthesia.Patients in both groups were given parenteral nutrition 24 hours after operation for 5 ～ 7 days.The patients in the indomethacin group were treated with indomethacin suppository ( 100 mg/12 h).Fasting blood glucose (FBG),fasting serum insulin (FINS),creatinine (Cr),blood urine nitrogen (BUN),triglyceride (TG),free fatty acid (FFA) and C-reactive protein (CRP) of the two groups were detected on the day before operation,and 24,72,120 hours after operation.Insulin resistance index (HOMA-IR) was calculated by using the homeostasis model assessment (HOMA).The vital signs were observed in 72 hours after operation.ResultsThe vital signs in the indomethacin group were more steady.The levels of FBG,FINS,and InHOMA-IR of the control group 24 hours and 72 hours after operation were higher than before operation ( all P =0.000) and those of the indomethacin group ( all P ＜0.01 ).In both of the two groups,the levels of Cr,BUN,TG,and FFA were higher than those before operation,but declined over time.All the indexes in the indomethacin group 120 hours after operation decreased significantly compared with the levels 24 hours after operation ( all P =0.000 ),as well as with the levels in the control group 120 hours after operation ( all P ＜ 0.05 ).No significant difference was found in the level of CRP between the two groups and between before and after operation.ConclusionIndomethacin could reduce the postoperative stress hyperglycemia and insulin resistance in patients with gastrointestinal tumor.

Using the Gram-positive Staphylococcus aureus as the indictor bacterium,fourteen antibacterial strains were initially obtained by the bilayer-media screening method from the raw milk samples,and one isolate was found to exhibit the higher antibacterial activity against the indicator. This isolate was further studied on its individual and cultural morphology features,partial physiological and biochemical reaction activities,G+C content,the sequence features of the 16S rDNA and the species-specific N-acetylmuraminidase gene(acmA) ,consequently,it was identified as the Lactococcus lactis subsp. lactis strain,named as MB191. An evaluation of the antimicrobial spectra of MB191 was subsequently performed,it showed the remarkable activities against not only the tested Gram-positive bacteria,but also several Gram-negative bacteria including Pseudomonas syringae and P. fluorescens,as well as the yeast Debaryomyces hansenii,which was a distinctive feature that was not reported prior to this study.

OBJECTIVE:To evaluate the pharmacoeconomic characteristics of dapagliflozin combined with metformin in the treatment of type 2 diabetes mellitus systematically. METHODS:Retrieved from Health Technology Assessment(HTA),Cochrane Library,PubMed,Embase,CNKI,Wanfang and CBM during database establishment to Jul. 2017,published pharmacoeconomics literatures about dapagliflozin combined with metformin were collected,using"sodium-glucose-transporter-2 inhibitors""SGLT2 inhibitor""metformin""dapagliflozin""cost""benefit""utility""effectiveness""pharmacoeconomic""economic"as English retrieval words and"SGLT2 inhibitor""dage liejing""metformin""cost""benefit""utility""effectiveness"as Chinese retrieval words. Outcome indexes included incremental cost,incremental effect,cost-effectiveness ratio and incremental cost-effectiveness ratio(ICER).The results of the economic research in the included literatures were evaluated systematically. RESULTS:Totally of 4 literatures were included,and all of them were cost-effectiveness analysis. Dapagliflozin was more cost-effective than sulfonylurea because the ICER of dapagliflozin were €2 709/QALY,€10 494/QALY,€7 939/QALY,€5 433/QALY,€4 767/QALY and €6 094/QALY in the UK,Greece,Denmark,Finland,Norway and Sweden,respectively,which were all lower than willingness-to-pay threshold. Dapagliflozin was more cost-effective than DPP-4 inhibitor,and the ICER were €7 200/QALY and €15 120/QALY in the UK and Greece,respectively,which were all lower than willingness-to-pay threshold. CONCLUSIONS:Current economic research shows compared with sulfonylurea and DDP-4 inhibitor,dapagliflozin is a cost-effective treatment alternative for patients with T2DM whose metformin regimen does not provide sufficient glycemic control.

· AIM: To explore the dynamic expression and correlation among telomerase catalytic subunit (TERT), proliferating cell nuclear antigen ( PCNA) and antiapoptosis protein Bd-2 which relate to cell proliferation in epiretinal membrane of rat traumatic proliferative vitreoretinopathy(PVR).· METHODS: S-P technique was applied for immunohistochemical staining of epiretinal membrane of traumatic PVR with TERT, PCNA and Bcl-2 antibody. HE staining was also carried out. The staining results were analyzed with image analysis system.· RESULTS: The positive rate and average A of PCNA protein were upregulated at first and then down-regulated, with the peak value in 14d Group, which was significantly different from those in 7d Group and 28d Group.The positive rate and average A of TERT and Bcl-2 were also upregulated at first and then down-regulated, with the peak value in 14d Group and 21d Group, which were significantly different from those in 7d Group. There was significant correlation among PCNA, Bcl-2 and TERT protein expression (P≤0.01).· CONCLUSTON: TERT and Bcl-2 take part in the regulation of proliferative cells in epiretinal membrane of traumatic proliferative PVR, with high correlation with the dynamic changes of cell proliferation.

Objective To investigate the relationship between genetic polymorphisms in excision repair cross-complementing 1 (ERCC 1 ),xeroderma pigmentosum group D (XPD),xeroderma pigmentosum group C (XPC) and the risk of arsenism caused by coal-burning.Methods Two hundred and twenty-nine patients with arsenism in the endemic area of Jiaole village Xingren county Guizhou province were selected into experimental group.One hundred and ninety-eight inhabitants who had similar living habits but did no burning coal with high arsenic in Dagnoduo village were selected into control group.Two milliliters vein blood samples were taken and analyzed with polymerase chain reaction-restriction frgment length polymorphism technique (PCR-RFLP) to measure the gene polymorphisms of ERCC1 C8092A,XPD Lys751Gln,XPD Asp312Asn,XPD Arg156Arg,and XPC P(AT +/-).Relationship between genotype and the risk of arsenism was also analyzed.Results The frequency of ERCC1 8092CA/AA geno-type in case group [ CA:29.78％ (67/225),AA:10.67％ (24/225) ] was significantly higher than that of control group[CA:23.08％(45/195),AA:5.13％(10/195),x2 =8.116,P ＜ 0.05].The frequency difference of other gene polymorphisms between case and control group was not statistically significant,respectively (x2 =5.649,4.394,0.865,1.490,all P ＞ 0.05).There were 1.780(95％CI:1.174 - 2.698),1.681(95％CI:1.081 - 2.615),and 1.790(95％CI:1.014 - 3.158)-fold increase in risk of arsenism for individuals carrying ERCC1 8092CA + AA,XPD Lys751Gln + Gln751Gln,and XPD Asp312Asn + Asn312Asn genotypes compared respectively with individuals canying ERCC1 8092CC,XPD Lys751Lys,and XPD Asp312Asp(all P ＜ 0.05).The sufferers only with XPD Arg156Arg or XPC P(AT +/-) didn't have higher risk of arsenism(all P ＞ 0.05).Conclusion The results of this study suggest that the gene polymorphisms of ERCC1 C8092A,XPD Lys751Gln,and Asp312Asn are related to the arsenism caused by coal-burning.

Aim We used bone marrow-derived macro-phages ( BMMs ) , to explore the mechanism of macro-phage activation and the effect of TGF-β activated ki-nase-1 ( TAK1 ) inhibitor 5 Z-7-oxozeaenol on it under AGEs conditions. Methods The BMMs were obtained from C57 mice, and purity of BMMs was detected by flow cytometry. Cell viability was tested after treatment with different concentrations of TAK1 inhibitors. Laser confocal microscopy was used to detect macrophage M1 subtype . Flow cytometry was used to analyse the macro-phage activated by AGEs. TNF-α and MCP-1 mRNA levels were evaluated by qRT-PCR. Western blot was used to detect the expression levels of TAK1 signal pathway protein. Results AGEs stimulation could in-crese the activity of M1 macrophages,and 5Z-7-oxoze-aenol could inhibit the differentiation of BMMs. Com-pared with control group, AGEs increased the expres-sion of MCP-1 and TNF-α mRNA(P<0. 01). p-TAK1, TAB1,p-JNK,p-p38MAPK and NF-κBp65 proteins ex-pression also increased significantly ( P <0. 05 ) . After treatment with inhibitor, transcription levels of MCP-1 and TNF-α decreased significantly ( P < 0. 05 , P <0. 01 ) . 5 Z-7-oxozeaenol treatment downregulated the expression of p-TAK1,TAB1,p-JNK,p-p38MAPK and
NF-κBp65 proteins ( P <0. 05 ) . Conclusions AGEs can induce BMMs to M1 phenotypic polarization. 5Z-7-oxozeaenol reduces the expression of inflammatory cyto-kine via inhibiting TAK1/MAPKs, MAPKs/NF-κB pathways.

Objective To investigate the renoprotective effect of transforming growth factor beta activator kinase 1 (TAK1) inhibitor 5Z-7-oxozeaenol (OZ) in diabetic db/db mice and the mechanism.Methods Twenty-four male db/db mice were randomly divided into two groups:db/db mice (db/db,n=12) and db/db mice with 5Z-7-oxozeaenol treatment (db/db+OZ,n=12).Another group of wild type mice (n=12) was held as the control group.OZ 2 mg/kg was administrated by intraperitoneal injection every other day.At week 8 and 12 after 5Z-7-oxozeaenol treatment,blood glucose (BG),body weight (BW),kidney weight (KW) and urinary albumin excretion rate (UAER) were evaluated.Kidney pathological lesions were detected by light and electron microscopy.NF-κB p65,monocyte chemotactic protein-1 (MCP-1) and tumor necrosis factor-ot (TNF-o) were detected by immunohistochemistry.Western blotting was used to detect p-TAK1,TAB1,p-p38MAPK and IL-1β expression,while ICAM-1 and MCP-1 mRNA levels were evaluated by real-time PCR.Results Compared with control group,the levels of BG,BW,KW and UAER were higher (P ＜ 0.01) in db/db mice group,while BW,KW and UAER levels were significantly decreased in db/db + OZ group compared with that in db/db mice group (P ＜ 0.05).In week 8 and 12 db/db mice,glomerular volume and extracellular matrix were increased,while pathological lesions in kidney tissue were positively improved by TAK1 inhibitor.Immunohistochemistry showed that NF-κB p65,MCP-1 and TNF-α expression levels were apparently increased in db/db mice group compared with that in control group (P ＜ 0.05) and were significantly inhibited by TAK1 inhibitor (P ＜ 0.05).Western blotting showed that p-TAK1,TAB1,p-p38MAPK and IL-1β expression levels were higher in db/db mice group than that in control group (P ＜ 0.05) and lower in db/db+ OZ group than that in db/db mice group (P ＜ 0.05).Moreover,real-time PCR showed that the expressions of ICAM-1 and MCP-1 mRNA were higher in db/db mice group than that in control group and lower in db/db+OZ group than that in db/db mice group (P ＜0.05).Conclusions TAK1 Inhibitor can down-regulate MAPK and NF-κB pathway to restrain the reaction of inflammation and alleviate kidney injury in diabetic db/db mice.

Objective To investigate the role of transforming growth factor-β activated kinase-1 (TAK1) signaling pathway in the activation of bone marrow derived macrophages (BMDM) induced by high glucose.Methods Purity of mouse BMDM was detected by flow cytometry.The mice macrophages cultured in vitro were stimulated by high glucose and treated with TAK1 specific inhibitor 5Z-7-oxozeaenol.Cells were divided into normal control group (RPMI 1640),osmolality control group (25 mmol/L mannitol),high glucose group (33 mmol/L D-glucose) and inhibitor group (33 mmol/L D-glucose+300 nmol/L 5Z-7-oxozeaenol).Immunocytochemistry and flow cytometry were used to detect macrophage subtype.The expression of monocyte chemotactic protein-1 (MCP-1) and tumor necrosis Factor-α (TNF-α) mRNA were determined by real time PCR.Expressions of p-TAK1,TAK1 binding protein (TAB1),p-JNK,p-p38 MAPK and NF-κB p65 proteins were analyzed by Western blotting.Results The purity of BMDM was about 99.36％.Compared with normal control group,high glucose group had increased percentage of M1 macrophages,increased expression of MCP-1 and TNF-α mRNA (all P ＜ 0.05).Moreover,p-TAK1,TAB1,p-JNK,p-p38 MAPK and NF-κB p65 proteins expression also increased significantly in high glucose group (all P ＜ 0.05).After treatment with inhibitor 5Z-7-oxozeaenol,the effects induced by high glucose were inhibited (P ＜ 0.05).Conclusions High glucose can induce M1 macrophage activation and expression of inflammatory cytokine of BMDM,which can be inhibited 5Z-7-oxozeaenol through inhibiting TAK1/MAPK and TAK1/NF-κB pathway.