?AlM:To understand the clinical effect of trabeculectomy with mitomycin and interferon therapy on neovascular glaucoma.? METHODS: Neovascular glaucoma patients in our hospital from January 2011 to January 2013 were sampled, from them, 57 cases ( 57 eyes ) were randomly divided into two groups, control group received routine trabeculectomy for treatment, the experimental group accepted combination therapy of trabeculectomy +mitomycin + interferon. The clinical efficacy of two groups were observed.?RESULTS:The total effective rate (96%) in experimental group was significantly better than that in the control group ( 76%) , and the visual acuity, filtering bleb and postoperative 1wk, 1a of intraocular pressure changes were better than those of the control group, there was a statistically significant difference (P<0. 05). The rate of complications in experimental group ( 10%) was slightly higher than that of the control group (7%), but there was no statistically significant difference (P>0. 05).? CONCLUSlON: Trabeculectomy combined mitomycin and interferon treatment of neovascular glaucoma has exact clinical effect, and is worthy of clinical popularization and application.

Objective To synthesize 628F-Py-AMD3465,to investigate its biodistribution in mice and to perform the microPET/CT imaging on mice bearing human lung cancer cell (A549).Methods AMD3465 quaternary ammonium salt precursor was directly labeled with 18F,then 628F-Py-AMD3465 was synthesized through nucleophilic reaction,hydrolysis,neutralization and the product was purified using HPLC.The labeling yield and radiochemical purity were analyzed by HPLC.Fifteen Kunming mice were injected with 5.55 MBq of 628F-Py-AMD3465 and sacrificed at 5,20,40,60 and 120 min postinjection.The selected tissues were harvested and weighed,and the radioactivity in the tissues was measured by an automated γ-spectrometer.The ％ID/g was calculated.MicroPET/CT studies were performed on A549-bearing mice after injecting 6-18F-Py-AMD3465 through vena caudal.Paired t test was used.Results 6-18F-Py-AMD3465 was successfully synthesized with the labeling yield of (9.0±2.0)％,the total synthesis time was about 60 min,and the radiochemical purity was more than 98％.Biodistribution studies showed that the radiouptake was higher in the kidneys and bladder of normal mice,which demonstrated that 6-18 F-Py-AMD3465 was mainly excreted through the kidneys.Biodistribution in A549-bearing mice was similar to that in normal mice.The tumor/muscle ratio at 40 min was 5.0,but the radiouptake of the tumor was still lower than that of the normal lung:(8.05±0.35) ％ID/g vs (9.33±0.66) ％ID/g;t=5.26,P＜0.05.MicroPET/CT imaging showed that the high-uptake location of 6-18F-Py-AMD3465 in tumor-bearing mice was similar to the normal mice,and the tumor uptake reached the maximum level at 45 min post-injection (SUV 0.67).Conclusions 6-18F-Py-AMD3465 can be synthesized by a simple method.A lower uptake could be shown in the tumor compared to that in the lung and the tracer has limited diagnostic value for lung cancer.

Objective To survey and analyze characteristics of brucellosis epidemic in Dalian City for the purpose of setting up prevention and control measures for the disease. Methods In 2007, the basic situation of people of 7-60 years old and in close contact with livestock was surveyed in Dalian according to the "Surveillance standard for brucellosis"(GB 16885-1997). Blood was collected in brucellosis suspicious or high-risk groups for the laboratory examination, using rose bengal test for qualitative detection and test-tube agglutination test(SAT) method for quantitative detection of serum antibodies; At the same time, brucellosis cases found in the routine monitoring and confirmed in and this survey in the department of endemic disease prevention in the center for disease control and prevention of Dalian City underwent questionnaire surveys. Results All 1563 people were epidemiologically surveyed of brucellosis, 1310 were male, 253 female,livestock care givers accounted for 56.05% (876/1563). 240 blood samples were serologically surveyed, the detection rate was 3.75%(9/240). This survey confirmed 2 cases of brucellosis patients, 3 cases confirmed in routine monitoring. 3 cases were infected via contacting infected brucellosis cows, and the 2 cases were imported. Conclusions To strengthen the quarantine of livestock and timely treat the infected livestock should be the key of control of brucellosis. At the same time, professionals of livestock should be educated to protect themselves.

Adult ; Humans ; Male ; Neck Injuries ; complications ; Pharynx ; injuries ; Trachea ; injuries

AIM:To investigate the effect and the mechanism of tanshinone ⅡA in attenuating PM2.5-induced human umbilical vein endothelial EA.hy926 cell injury.METHODS:The samples of fine particulate matter (PM2.5) were collected in Guangzhou and made into suspension.Different concentrations (0, 20, 200 and 400 mg/L) of PM2.5 were added to EA.hy926 cells.The viability and apoptosis of EA.hy926 cells, the protein levels of p-p38 MAPK, Bax and Bcl-2 in the EA.hy926 cells, the contents of interleukin-6 (IL-6), tumor necrosis factor-α(TNF-α) and malonaldehyde ( MDA) , and the activity of superoxide dismutase ( SOD) and lactic dehydrogenase ( LDH) in the EA.hy926 cell culture supernatant were measured by MTT assay, flow cytometry, Western blot, ELISA and colorimetry, respectively.Tanshinone ⅡA at different concentrations (5, 10 and 20 μmol/L) or a specific inhibitor of p38 MAPK pathway, SB203580 (20μmol/L) , was added into the EA.hy926 cells to observe the effect of tanshinone ⅡA.RESULTS:Compared with control group, PM2.5 significantly increased the apoptosis, the contents of IL-6, TNF-αand MDA, the activity of LDH, and the protein levels of p-p38 MAPK and Bax/Bcl-2 ratio, but decreased the viability and SOD activity in the EA.hy926 cells (P<0.05).Compared with PM2.5 group, tanshinone IIA significantly decreased the apoptosis, the contents of IL-6, TNF-αand MDA, the activity of LDH, and the protein levels of p-38 MAPK and Bax/Bcl-2 ratio, but increased the viabil-ity and SOD activity in the EA.hy926 cells (P<0.05).CONCLUSION:Tanshinone ⅡA attenuates PM2.5-induced EA. hy926 cell injury via the inhibition of p38 MAPK pathway.

OBJECTIVE:To study the inhibitory effects of berberine on EA.hy926 human umbilical vein endothelial cells (EA. hy926 cells) injury induced by particulates with no more than 2.5 μm air aerodynamic diameter in atmospheric (PM2.5),and its p38 mitogen-activated protein kinase(MAPK)signal pathway mechanism. METHODS:PM2.5 samples were collected and hatched EA.hy926 cells with concentrations of 0(blank control),20,200 and 400 mg/L for 24 h. The survival rate and apoptosis rate of cells,contents of IL-6,TNF-α and MDA,activities of SOD and LDH,protein levels of p-p38 MAPK,Bcl-2 and Bcl-2 associated X protein (Bax) were detected. The above indexes of EA.hy926 cells in blank control group,PM2.5 group (200 mg/L PM2.5), p38 MAPK pathway-specific blocker SB203580 group (20 μmol/L SB203580+200 mg/L PM2.5),berberine low-,medium- and high-concentrations groups(5,10,20 μmol/L berberine+200 mg/L PM2.5)were also determined. RESULTS:Compared with blank control,survival rate of cells,SOD activity and Bcl protein decreased after 200,400 mg/L PM2.5 hatched;apoptosis rate of cells, contents of IL-6,TNF-α and MDA,LDH activity,protein levels of p-p38 MAPK and Bax increased (P<0.05),in concentra-tion-dependent manner. Compared with PM2.5 group,survival rate of cells,SOD activity and Bcl-2 protein increased in berberine medium-,high-concentrations groups and SB203580 group;apoptosis rate of cells,contents of IL-6,TNF-α and MDA,LDH ac-tivity,protein levels of p-p38 MAPK and Bax decreased (P<0.05). CONCLUSIONS:Berberine attenuates PM2.5-induced EA. hy926 cells injury via the inhibition of p38 MAPK pathway.

Adult ; Aged ; Female ; Heart Failure ; complications ; therapy ; Humans ; Hypothyroidism ; complications ; therapy ; Middle Aged

Aim To investigate the protective effect of allicin against EA. hy926 endothelial cell injury in-duced by PM2. 5 and the possible mechanism. Meth-ods The samples of fine particulate matter ( PM2. 5 ) were collected and made into suspension. Different concentrations of PM2. 5 ( 20 , 200 , 400 mg · L-1 ) were added to EA. hy926 cell. The viability and apop-tosis of EA. hy926 cell, the protein levels of p-ERK1/2, Bax and Bcl-2 in the EA. hy926 cell, the contents of tumor necrosis factor-α( TNF-α) , interleukin-6 ( IL-6 ) , and malonaldehyde ( MDA ) , the activities of su-peroxide dismutase ( SOD ) and lactic dehydrogenase ( LDH) in the EA. hy926 cell culture supernatant were measured by MTT assay, flow cytometry, Western blot, enzyme-linked immunosorbent assay ( ELISA ) and colorimetry, respectively. Allicin at different con-centrations(5,20,40 mg·L-1 ) or a specific inhibitor of ERK1/2 signaling pathway PD98059 ( 20 μmol · L-1 ) was added into the EA. hy926 cell to observe the effect of allicin. Results Compared with control group, PM2. 5 significantly increased the apoptosis, the contents of TNF-α, IL-6 and MDA, the activity of LDH, the protein levels of p-ERK1/2 and Bax/Bcl-2 ratio, but decreased the viability and SOD activity in the EA. hy926 cell(P<0. 05). Compared with PM2. 5 group, allicin significantly decreased the apoptosis, the contents of TNF-α, IL-6 and MDA, the activity of LDH, the protein levels of p-ERK1/2 and Bax/Bcl-2 ratio, but increased the viability and SOD activity in the EA. hy926 cell ( P <0. 05 ) . Conclusion Allicin displays a significant protective effect against EA. hy926 endothelial cell injury induced by PM2 . 5 and its mechanism may be related to the attenuations of in-flammation and oxidative stress via the inhibition of ERK1/2 pathway.

P75 was the risk factor (PP50 were risk factors (P

Objective: To examine the association between the cross-resistance to ethionamide (Eto) and isoniazid (INH) and mutations of drug resistant genes in Mycobacterium tuberculosis (MTB), so as to provide the evidence for clinical diagnosis and treatment for multidrug-resistant (MDR) tuberculosis. Methods: Totally 126 MTB clinical isolates were selected, including 88 MDR-MTB clinical isolates and 38 INH- and rifampicin (RFP)-sensitive isolates. The resistance to INH and Eto was tested in MTB clinical isolates using the drug susceptibility test, and the mutations in the spacer region of INH and Eto resistance-related katG, inhA, ethA, mshA, ndh, spacer region of oxyR-ahpC and inhA promoter were detected using PCR assay. The phenotypic resistance served as a gold standard, and the sensitivity, specificity and accuracy of gene mutation tests were calculated for detection of MTB clinical isolates cross-resistant to INH and Eto. Results: Of the 126 MTB clinical isolates, there were 37 isolates cross-resistant to INH and Eto (29.37%), 51 isolates with resistance to INH and susceptibility to Eto (40.48%), 4 isolates with susceptibility to INH and resistance to Eto (3.17%) and 34 isolates with susceptibility to INH and Eto (26.98%). Among the 41 Eto-resistant MTB clinical isolates, there were 37 isolates with resistance to INH (90.24%). There were 64 MTB clinical isolates detected with katG mutations (50.79%), 4 isolates with mutation in the spacer region of oxyR-ahpC (3.17%), 2 isolates with inhA mutations (1.59%), and these isolates were all resistant to INH. There were 11 MTB clinical isolates detected with mutation in the inhA promoter (8.73%) and one isolate with ndh mutation, and all these isolates were cross-resistant to INH and Eto. There were 23 MTB clinical isolates detected with ethA mutations (18.25%) and 40 isolates with mshA mutations (31.75%), in which Eto-susceptible and -resistant isolates were detected. The diagnostic sensitivity, specificity and accuracy of inhA promoter tests for detection of cross-resistance to INH and Eto were 29.73% (95%CI: 16.44%-47.17%), 100.00% (95%CI: 87.36%-100.00%) and 63.38% (95%CI: 51.76%-73.63%) in MTB clinical isolates. Conclusions The prevalence of INH resistance is high in Eto-resistant MTB clinical isolates. Mutation in the inhA promoter region correlates with the cross-resistance to INH and Eto in MTB clinical isolates, and detection of mutation in the inhA promoter may be feasible to detect the cross-resistance to INH and Eto in MTB clinical isolates.