Choroidal metastasis is one of the most common malignant tumors inside the eyes. It causes pain, hypopsia and some other related symptoms. It reduces the quality of the patients' life. It's significant for the patients to be detected and treated early, therefore they will have better vision and longer life. The treatments of choroidal metastasis are developing quickly. Both the vitreous cavity injection of targeted drug and gene therapy are hot topics of research. This paper summarizes the etiology, development, diagnosis and treatment of choroidal metastasis nowadays.

Myeloid differentiation protein-2(MD-2)can separately and simultaneously bind lipopolysaccharide(LPS)and toll-like receptor 4(TLR4)has been shown to play critical roles in mediated recognition responses to LPS by TLR4 and signal transduction induced by LPS.MD-2 can be bound by LPS,not TLR4.The cells have no responsiveness or weak responsiveness to LPS without MD-2.MD-2 can be secreted into blood plasma,formed soluble MD-2 and remotely regulated cells that contained TLR4 without MD-2.MD-2 has been shown to play important roles in endotoxin signal transduction.MD-2 is a small molecular,short nucleic acid fragment,easily regulated should become a new potential anti-inflammatory target.

Adult ; Bronchoalveolar Lavage ; methods ; Humans ; Male ; Pulmonary Surfactants ; therapeutic use ; Silicosis ; therapy

Objective To explore the effect of age on neurogenesis of dentate gyrus granule cell and the impact on differentiation of newborn cells in rats.Methods SD rats were selected and divided into 5 groups according age of 7,14,28,60,180 d(n=8),and the neurogenesis of dentate gyrus granule cell in hippocampus with normal development was detected,using 5-bromo-BrdU(BrdU) labled newborn neuron and ?-tubulin protein(TuJ1) and glial fibrillary acidic protein(GFAP) labeled glial cells,and understood the newborn cells to neurons and glial cell differentiation ratio.Results Neurogenesis was found in dentate gyrus granule cell layer with hippocampus of all different age rats.Various forms of cells with a larger nucleus that were round,oval,diamond were distributed over the entire granule cell layer.BrdU-positive cells within each group were 158.07?5.37,141.28?7.27,116.93?9.24,76.56?6.88,41.42?4.45,the number of BrdU-positive cells were reduced with the growth of rats(P0.05);4%-5% newborn cells expressed GFAP.In addition,some of the BrdU-positive cells at the same time did not express TuJ1 or GFAP.Conclusions There are neurogenesis in dentate gyrus granule cell in rats of different age.The new born cells mostly differentzate into granule neuron cell.The capability of cell proliferation are decreased with the growth of age.

Based on the standards for mental developmental re-tardation set up by WHO in 1985,by applying IQ andadaptation to social behavior as indexes for observa-tion with testing methods for intelligence commonlyaccepted,we have observed the effects in 128 suchcases treated by combined use of acupuncture,adhe-sive—pressing therapy at auricular points and drugplastering at points.Results showed that our therapyis conducive to the improvement of intelligence in suchcases.

OBJECTIVETo explore the effect of Qingyi Granule (QYG) on high mobility group box-1 (HMGB1) expressions in liver and renal tissues of severe acute pancreatitis (SAP) rats.

METHODSFifty-four Sprague-Dawley (SD) rats were divided into the sham-operation (SO) group, the SAP group, and the QYG group according to random digits table. Rats in the SAP group were induced by injecting 5% sodium taurocholate (STC). Liver and renal pathological changes were observed by HE staining. Serum contents of amylase (AMS), MDA, IL-1, and HMGB1 were detected by ELISA. HMGB1 protein expressions in liver and renal tissues were tested by immunohistochemistry. HMGB1 mRNA expressions in liver and renal tissues were detected by reversed transcription PCR.

RESULTSThe pathological scores, serum levels of AMS, MDA, IL-1 and HMGB1, and protein and mRNA HMGB1 expressions in liver and renal tissues were increased more obviously in the SAP group than in the SO group (P < 0.05, P < 0.01). All of them could be down-regulated by QYG intervention, with the most significant effect seen at 72 h (P < 0.05, P < 0.01) in a time-effect relationship.

CONCLUSIONSHMGB1 participated in SAP complicated liver and renal injuries. QYG could effectively inhibit HMGB1 expressions, thereby attenuating SAP complicated liver and renal injuries.

Amylases ; Animals ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; HMGB1 Protein ; metabolism ; Interleukin-1 ; Kidney ; metabolism ; Liver ; metabolism ; Pancreatitis ; drug therapy ; metabolism ; RNA, Messenger ; Rats ; Rats, Sprague-Dawley ; Taurocholic Acid

Objective To explore the application value of DOSE index score in the peitients with chronic obstructive pulmonary disease.Methods 122 cases of plateau COPD patients were followed up for 12 months,and we recorded and analyzed the patient's health and life.We also recorde FEV 1 and DOSE scores of the patients with COPD,and record the COPD risk events,including the number of respiratory failure and death,and the times of hospitalization,total such confinement,outpatient expenses,hospitalization expenses,mMRC,and scored in the number of exacerbations,etc.Results The DOSE index score was negatively correlated with FEV1％ pred (r=0.73,P ＜ 0.05) for 122 COPD patients,and were positively correlated with mMRC (r=085,P ＜ 0.01),the annual number of exacerbations (r=0.71,P ＜ 0.01),respiratory failure (r=0.65,P ＜ 0.01),heart failure (r=0.50,P ＜ 0.01),number of outpatient service (r=0.12,P＜0.01),hospitalization time (r=0.70,P＜0.01),the totalsuchconfinement (r=0.66,P＜0.01),outpatient expenses (r=0.13,P＞ 0.13),hospitalization expenses (r=0.65,P＜0.01).ROC curve was used to analyzed the cut-off point and curve area of COPD DOSE index.Conclusion The DOSE index is a simple COPD assessment tools,and is closely related to the prognosis of patients and health.

AIM: To investigate the effect of digoxin on apoptosis and growth in human gastric carcinoma SGC7901 cells and its possible mechanism.METHODS: SGC7901 cells were incubated in the medium containing digoxin at different concentrations for 24 h.CCK-8 assay was employed to detect the anti-tumor effect of digoxin on SGC7901 cells, and IC50 value of digoxin was calculated.Flow cytometry was used to determine the apoptosis and the cell cycle.Western blot was used to analyze the protein levels of c-Src, p-c-Src(Tyr416), Akt, p-Akt(Ser473), ERK1/2 and p-ERK1/2 (Tyr204).The mRNA expression of c-Src was by RT-PCR.RESULTS: As the concentration of digoxin increased, the cell viability was reduced gradually starting at 50 nmol/L digoxin treatment (P<0.05).The cell viability was reduced to the lowest extent by exposure to 500 nmol/L digoxin (P<0.05).The IC50 value of digoxin was 191.45 nmol/L for 24 h.After treatment with 200 nmol/L digoxin for 24 h, the apoptotic rate and the proportion of G0/G1 phase were significantly increased (P<0.05), the phosphorylated levels of c-Src, ERK1/2 and Akt declined (P<0.05), the mRNA and protein levels of c-Src were down-regulated (P<0.05) and the ability of migration was weaker (P<0.05) than that in control group.CONCLUSION: Digoxin may suppress the growth and induce the apoptosis of human gastric carcinoma SGC7901 cells by inhibiting the expression of c-Src gene and down-regulating the phosphorylated levels of ERK1/2 and Akt.

Background:Intestinal ischemia-reperfusion( I/R)is a surgical abdomen,which not only leads to intestinal tissue necrosis,but also induces systemic inflammatory response,resulting in a serious impact on other organs and tissues. Aims:To investigate the role and mechanism of rosiglitazone( ROS)on intestinal I/R injury. Methods:Eighteen male C57BL/6 mice were randomly divided into three groups:sham operation group,I/R injury group and ROS pretreatment group. Mice in ROS pretreatment group received ROS(0. 3 mg/kg,IV)30 minutes before I/R injury. I/R injury model was established by clamping superior mesenteric artery for 30 minutes,followed by 4 hours reperfusion. All the mice were sacrificed. The pathology of intestinal tissue was examined by HE staining. The mRNA expressions of tumor necrosis factor( TNF )-α, interferon(IFN)-γ,interleukin( IL)-1β,transforming growth factor( TGF)-β and Smad3 were measured by real-time quantitative PCR. The protein expressions of TGF-βand Smad3 were measured by Western blotting. Serum levels of TNF-α, IFN-γand IL-1βwere measured by ELISA. Results:Compared with the sham operation group,pathological score of small intestinal mucosa in I/R injury group was significantly increased(P<0. 05),and the mRNA expressions of TNF-α,IFN-γand IL-1β were significantly increased( P < 0. 05 ),the mRNA and protein expressions of TGF-β and Smad3 were significantly increased(P<0. 05),the serum levels of TNF-α,IFN-γand IL-1β were significantly increased(P<0. 05). With the pretreatment of ROS,all the above-mentioned indices were significantly ameliorated(P<0. 05). Conclusions:ROS pretreatment can attenuate intestinal I/R injury by inhibiting TGF-β/Smad3 signal pathway to reduce inflammation.

AIM: To investigate the effect of suberoylanilide hydroxamic acid (SAHA) on the apoptosis of hu-man small-cell lung cancer H446 cells and its possible mechanism.METHODS: H446 cells were incubated in the medi-um containing SAHA.CCK-8 assay was used to detect the anti-tumor effect of SAHA on the H446 cells, and IC50 values of SAHA were calculated.Flow cytometry was used to analyze the apoptosis.After Notch3 gene was silenced, the pro-apopto-tic effect of SAHA on the H446 cells was inhibited ( P <0.05).Eukaryotic expression plasmid containing N3ICD was transfected into the H446 cells, so that N3ICD was expressed in the H446 cells.The mRNA expression of Notch3 was measured by RT-PCR.The protein levels of Notch3, N3ICD, Puma and cleaved caspase-3 were determined by Western blot.RESULTS: SAHA remarkably reduced the cell viability in a dose-dependent manner (P <0.05), and the IC50 value of SAHA was 1.91 μmol/L.SAHA induced apoptosis in a dose-dependent manner (P <0.05).The expression of Notch3 gene was negative in the H446 cells, SAHA reactivated Notch3 gene and Notch3 pathway in a dose-dependent manner (P <0.05).Notch3 knockdown inhibited apoptosis induced by SAHA (P <0.05).Over-expression of N3ICD up-regula-ted the protein levels of Puma and cleaved caspase-3.CONCLUSION: SAHA induces apoptosis in human small-cell lung cancer H446 cells by activating Notch3 pathway and up-regulating the protein level of Puma.