BACKGROUND: Capsule opacification is a common complication following implantation of intraocular lenses for a long period. Scholars are looking for an ideal intraocular lens so as to reduce the incidence of capsule opacification. OBJECTIVE: To study the effects of three intraocular optic materials with sharp optic edge on anterior and posterior capsule opacification as well as capsulorrhexis contraction. DESIGN, TIME AND SETTING: A randomized controlled study was performed at the Department of Ophthalmology, Affiliated Hospital of Chengde Medical College from May 2005 to December 2006. PARTICIPANTS: A total of 135 patients (148 eyes) with age-related cataract, including 73 males (80 eyes) and 62 females (68 eyes) and aging 52-81 years with the mean age of (71.44 ?6.83) years, were collected in this study. METHODS: All patients were performed with phacoemulsification combining with implantation of foldable intraocular lenses which were characterized by sharp optic edges. Thereafter, they were randomly divided into three groups: lyophobic material group (n=43, 49 eyes), who were implanted with lyophobic acrylic acid intraocular lens; hydrophilic material group (n=42, 46 eyes), who were implanted with hydrophilic acrylic acid intraocular lens; lyophobic/hydrophilic material group (n=50, 53 eyes), who were implanted with lyophobic/hydrophilic acrylic acid intraocular lens. MAIN OUTCOME MEASURES: Anterior and posterior capsule opacification as well as capculorhexis contraction were quantitatively evaluated 1 year postoperatively. RESULTS: At one year postoperatively, incidences of posterior capsule opacification were 8.3% in the lyophobic material group, 26.7% in the hydrophilic material group, and 15.3% in the lyophobic/hydrophilic material group, respectively, and there was significant difference (P 0.05). CONCLUSION: The optic intraocular lens of sharp optic edge does not have any effects on anterior capsule opacification or capsulorrhexis contraction, but has effects on formation of posterior capsule opacification; in particular, lyophobic acrylic acid can reduce the incidence to posterior capsule opacification.

ObjectiveTo evaluate therapeutic effect and the possible mechanism of smecta on paraqual plasma concentrations and multiorgans injury induced by paraquat intoxication in rats. Methods A total of 76 healthy adult SD rats were randomly ( random number) divided into group A (control group n =6),group B ( poisoned group n =30 ),group C (smecta-treated group n=30).Rats in groups B and C were treated intragastrically with PQ at 50 mg/kg,the rats in the group C were given with smecta at 50 mg/kg,while the rats in the other two groups were only intragastrically adminstered with saline.Live rats in groups B and C were sacrificed at 2,6,24,48,72 h after administration of PQ for the determination of paraquat plasma concentrations and for HE staining of lung,stomach and jejunum.The rats were executed at the end of trial by the same way in group A.All measurement data were expressed as means + standard deviation ((x) ±s).The data of pathological score were compared with Independent-samples T test and the data of PQ concentration compared with analysis of variance (ANOVA) followed by LSD-t multiple comparison test.P-values of less than 0.05 were considered statistically significant.ResultsThe paraquat plasma concentration ( ng/ml ) was 440.314 ± 49.776 to 4320.6150 ± 413.947.There were different pathological changes of lung,stomach and jejunum in group B. Lung injuries gradually deteriorated,congestion,edema,leukocyte infiltration,incrassated septa and lung consolidation were observed.The pathological changes were obvious such as abruption of mucosa,hyperemic gastric mucosa and leukocyte infiltration in stomach.Haemorrhage of jejunum mucosa,abruption of villus,gland damage and inflammatory cell infiltration were found. Compared with group B,all the pathological changes mentioned above were obviously alleviated in group C ( P ＜ 0.05 ),and the concentrations reduced ( P ＜ 0.01 ).Conclusions Smecta reduced paraquat plasma concentrations and alleviated pathologic injury of rats with PQ poisoning.

OBJECTIVEThe glucocorticoid dexamethasone (DEX) can induce palatal cleft; however, the mechanism involved remains unclear. E-cadherin is an important cell adhesion molecule, and it can significantly affect cell fate and embryonic development. Recent studies have indicated that E-cadherin expression in palatal epithelial cells is suppressed in normal palate fusion. This study aimed to determine whether the change in E-cadherin expression is related to the incidence of cleft palate in DEX-induced mice.

METHODSMice were divided into the experimental group and the control group. Pregnant mice were injected with DEX on E10.0-E12.0, whereas mice in the control group were injected with normal saline. Hematoxylin and eosin (HE) staining, immunohistochemistry, and real-time quantitative polymerase chain reaction were employed to evaluate the effect of DEX on fetal mouse palatal processes, particularly the changes in E-cadherin and β-catenin expression levels in the phases of the experimental and control groups.

RESULTSData indicated that the incidence of cleft palate in the DEX group was 43.59% (17/39), whereas that in the control group was only 3.03% (1/33). The results of HE staining showed that the obviously shortened palatal processes could not contact and fuse with one another in the DEX-treated mice model compared with those in the control group. The ectopic expression of E-cadherin in embryonic palatal mesenchymal cells was also analyzed. The expression levels of E-cadherin and β-catenin in the experimental group were higher than those in the control group.

CONCLUSIONThese findings indicated that DEX could induce E-cadherin gene upregulation and ectopic expression, as well as high β-catenin expression, thereby inhibiting the growth of mesenchyme cells and cleft palate.

Animals ; Cadherins ; genetics ; metabolism ; Cleft Palate ; chemically induced ; embryology ; Dexamethasone ; adverse effects ; Disease Models, Animal ; Epithelial Cells ; Female ; Glucocorticoids ; Immunohistochemistry ; Mice ; Pregnancy ; beta Catenin ; metabolism

Objective To clarify the relationship between tumor necrosis factor alpha (TNF-α) and leptin in nonalcoholic fatty liver disease.Methods The real-time quantitative PCR (q-PCR) and enzymelinked immunosorbent adsorption experiment(ELISA) were used to detect the expression and correlation of TNFα and leptin in blood cells and serum from the normal group, non-alcoholic simple fatty liver(NAFL) group, nonalcoholic steatohepatitis (NASH) group and cirrhosis group.Results At the level of mRNA, the transcription of TNF-α in cirrhosis group was 14.03 times, 12.07 times and 11.05 times of the normal group, NAFL group and NASH group,and the difference was significant(P＜0.05).Leptin transcription of cirrhosis group was 1.95 times,0.79 times and 1.45 times of normal group, NAFL group and of NASH group(P＞0.05).And in the cirrhosis group, the expression of TNF-α was 7.52 times higher than Leptin (P＜ 0.01).In expression level of protein,TNF-α and leptin in cirrhosis group was 1.98 times and 2.39 times higher than the normal group, 1.24 times and 1.30 times higher than the NAFL group, 1.27 times and 1.37 times higher than NASH, and the difference was significant(P＜0.05).Moreover the expression of TNF-α was significantly higher than that of Leptinin groups above(P＜0.01).Conclusion TNF-α and Leptin are less expression in lymphocytes, but more expression in serum.And TNF-α and Leptin affect the evolution of NAFLD, and present a positive correlation, which lead to the occurrence of NAFLD.Comparing the two methods, detection of serum is more sensitive and more suitable for clinical study than lymphocyte.

[ ABSTRACT] AIM: To study the autophagy of prostate cancer PC-3 cells induced by CD147 in vitro.ME-THODS:Themethod of amino acid starvation to induce autophagy was used.The expression of CD147 was detected by Western blotting.To study the functional effects of CD147 on autophagy in prostate cancer PC-3 cells, the down-regulation of CD147 expression was induced by the technique of RNAi.The conversion of autophagic marker protein LC3-I to LC3-II was determined by Western blotting.The cell death after starvation-induced autophagy was analyzed by trypan blue exclu-sion assay.RESULTS:The CD147 expression gradually increased in starvation-induced autophagy.The down-regulation of CD147 significantly increased the expression of autophagy-related protein LC3-II compared with control group.Mean-while, the cell death rates increased from (19.3 ±3.1)%and (22.3 ±3.5)%in control groups to (38.4 ±3.1)%in si-lencing the expression of CD147 in the PC-3 cells (P<0.05).CONCLUSION:CD147 inhibits starvation-induced auto-phgy and autophagy death in the prostate cancer PC-3 cells.

Community health service centers provide basic medical and public health service for the residents in community with the contract service mode.In the last five years our center started the construction of primary care team.The family physicians,nurses and public health workers formed the basis of health care team,and pharmacists and nutritionists actively joined the team work.The pharmacists provided health education of rational medication,participated in the ward-rounds of home beds and comprehensive management of chronic disease patients,and also conducted counseling clinic of drug use.The clinical nutritionists provided special nutrition guidance for patients,delivered nutrition education and conducted nutrition clinic.The involvement of pharmacists and nutritionist in contract service has greatly ungraded the primary care team,improved the quality of comprehensive care and provided better service for the people in the community.

At present, tumor marker measurement is one of the most important methods for the diagnosis and monitoring of hepatocellular carcinoma (HCC) and prognostic evaluation. This review summarizes the value of tumor markers in the diagnosis of HCC, prediction of biological characteristics, and prognostic evaluation, as well as the diagnostic value of a combination of various tumor markers. With new tumor markers being discovered, the rate of early diagnosis and prognostic evaluation of HCC will be improved.

Objective To analyze the long?term efficacy of intensity?modulated radiotherapy (IMRT) with or without chemotherapy in treatment of 454 patients with nasopharyngeal carcinoma (NPC) and its influencing factors. Methods A retrospective analysis was performed on the clinical data of 454 patients with non?metastatic NPC who received IMRT with or without chemotherapy in our center from 2007 to 2012. Prescribed doses of 69. 96?73. 92 Gy in 33 fractions, 69. 96 Gy in 33 fractions, 60. 06 Gy in 33 fractions, and 50. 96 Gy in 28 fractions were applied to nasopharyngeal gross tumor volume, cervical metastatic lymph nodes, high?risk drainage area, and low?risk drainage area, respectively. In all patients, 438 received induction chemotherapy, 420 concurrent chemotherapy, and 216 adjuvant chemotherapy, most of which were based on cisplatin and taxol. The Kaplan?Meier method was used for calculating survival rates and the log?rank test was used for survival difference analysis and univariate prognostic analysis. The Cox model was used for the multivariate prognostic analysis. Results The 3?year sample size was 210. The 3?year overall survival ( OS ) , local recurrence?free survival, nodal relapse?free survival, progression?free survival, and distant metastasis?free survival ( DMFS) rates were 88. 1%, 91. 0%, 90. 7%, 80. 5%, and 85. 1%, respectively. Age, T stage, and N stage were influencing factors for the OS rate ( P=0. 011;P=0. 005;P=0. 033);T stage and N stage were influencing factors for the disease progression?free survival ( P=0. 017;P=0. 005) and DMFS ( P=0. 012;P=0. 019) . The grade≥3 acute and late adverse reactions included hematological toxicity , oral mucositis , xerostomia , dysphagia , and brain injury . Conclusions IMRT promotes the long?term survival rates in patients with NPC. The distant metastasis is the major reason for treatment failure. The adverse reactions induced by IMRT combined with chemotherapy are tolerable.

Objective To evaluate the role of adenosine A1 receptors in hippocampal neurons in the cognitive dysfunction caused by isoflurane anesthesia in aged mice.Methods Sixteen male adenosine A1 receptor gene knockout homozygote mice (gene knockout mice) and 16 male wild-type mice,aged 18-22 months,weighing 27-32 g,were studied.Each type of mice was randomly divided into 2 groups (n=8 each) using a random number table:control group (group C) and isoflurane anesthesia group (group Ⅰ).Mice inhaled 1.4％ isoflurane in 100％ O2 for 2 h in group Ⅰ,and 100％ O2 for 2 h in group C.All the mice underwent Morris water maze test at 24 h after isoflurane or O2 inhalation.After the test,the mice were sacrificed and the hippocampal tissues were harvested to determine the number of β-amyloid1-42 (Aβ1-42) plaques (using immunohistochemistry) and expression of phosphorylated tau (p-tau) protein,and 2B subunit-containing N-methyl-D-aspartate receptors (NR2B) (by Western blot analysis).Results Compared with group C of wild type mice,the escape latency was significantly prolonged,the number of Aβ1-42 plaques was enlarged,the expression of p-tau protein was up-regulated,and the expression of N R2B was down-regulated in group Ⅰ of wild type mice.Compared with group Ⅰ of wild type mice,the escape latency was significantly shortened,the number of Aβ1-42 plaques was decreased,the expression of p-tau protein was down-regulated,and the expression of NR2B was up-regulated in group Ⅰ of gene knockout mice.There was no significant difference in the parameters mentioned above between group Ⅰ and group C of gene knockout mice.Conclusion Adenosine A1 receptors in hippocampal neurons mediate isoflurane anesthesia-induced cognitive dysfunction in aged mice,and the mechanism may be related to promotion of deposition of Aβ,phosphorylation of tau protein and inhibition of activities of NR2B.

OBJECTIVE To investigate the effect of curcumin on proliferation of neural stem cells (NSCs) of rats and the mechanism. METHODS NSCs derived from the forebrain of rat E15 embryos were cultured in vitro and identified by neuroepithelial stem cell protein ( nestin and SOX2) staining. NSCs were treated with curcumin 0.1, 0.5, 2.5, 12.5 and 62.5 μmol.L-1 for 24 h, respectively. The cyto-toxicity was estimated by measuring the release of lactate dehydrogenase(LDH). Cell viability and prolif-eration were analyzed respectively by MTT and BrdU assay. The mRNA expression levels of glucocorti-coid receptor (GR), Stat3, Notch1 and p21 were detected by qRT-PCR. The protein expression levels of total GR, Stat3 and phosphorylated Stat3 were measured by Western blotting. RESULTS The primary neural stem cells were identified as NSCs. Curcumin 12.5 and 62.5 μmol.L-1 had cell cytotoxicity( P<0.05). Cell viability assay indicated that curcumin 0.5 and 2.5 μmol.L-1 enhanced NSCs viability( P <0.05), but in 62.5 μmol.L-1 group the cell cytotoxicity was inhibited(P<0.05). Curcumin 0.1, 0.5 and 2.5 μmol.L-1 increased NSCs proliferation ( P < 0. 05), whereas 12. 5 and 62. 5 μmol.L-1 caused a decrease in NSCs proliferation(P<0.05). The mRNA expression level of GR in 0.5 μmol.L-1 group was significantly reduced( P<0.05). Western blotting analysis revealed that the protein expression of GR, Stat3 and p-Stat3 was inhibited by curcumin in 0.5 μmol.L-1 group(P<0.05). CONCLUSION Curcumin stimulates NSCs proliferation, possibly by inhibiting GR mRNA and related protein expression.