?AIM:To observe the clinical effect of Ahmed glaucoma valve ( AGV ) implantation for teenagers with refractory glaucoma.?METHODS: Twenty-seven patients ( 27 eyes ) with refractory glaucoma were treated with AGV implantation in our hospital from October 2012 to October 2014. The patients were followed up for 12mo. The success rate of the operation, postoperative intraocular pressure, the best corrected visual acuity, as well as complications were recorded.?RESULTS:The success rate of the operation was 85%. The intraocular pressure of the 27 patients decreased from 48. 3 ± 8. 3mmHg before operations to 21. 4 ± 8. 1mmHg(P<0. 05). Visual field defect was -23. 7±4. 1dB before operations, - 27. 5 ± 4. 7dB at 12mo after operations, and the difference was statistically significant (P<0. 05). There was 85% patients with improved or unchanged vision. Early postoperative complications included shallow anterior chamber ( 5 eyes, 19%) , transient high intraocular pressure ( 3 eyes, 11%) and anterior chamber hemorrhage ( 4 eyes, 15%) , drainage tube obstruction (1 eye, 4%), anterior chamber silicone tube in poor position ( 1 eye, 4%) . There was no ambiopia, drainage erosion and exposed, plate leaked out, choroidal detachment, immune rejection of graft and other complications. Long - term complications included dyscoria ( 8 eyes, 30%) , the back of the plate packed(3 eyes, 11%).?CONCLUSION:AGV implantation is characterized by a high success rate, simple operation, less complications and is an effective treatment for refractory glaucoma in adolescents.

This study was designed to explore the possibility of using ascitic mouse sarcoma cell line(S180) to validate the mouse tumor cell attachment assay for developmental toxicants, and to test the inhibitory effects of various developmental toxicants. The results showed that 2 of 3 developmental toxicants under consideration, sodium pentobarbital and ethanol, significantly inhibited S180cells attachment to Concanavalin A-coated surfaces. Inhibition was dependent on concentration, and the IC5o(the concentration that reduced attachment by 50% ), of these 2 chemicals was 1.2 ×10-3 mol/L and 1.0 mol/L, respectively. Another developmental toxicant, hydrocortisone, did not show inhibitory activity. Two non-developmental toxicants, sodium chloride and glycine were also testedand these did not decrease attachment rates. The main results reported here were generally similar to those obtained with ascitic mouse ovarian tumor cells as a model. Therefore, this study added further evidence to the conclusion that cell specificity does not limit attachment inhibition to Con A-coated surfaces, so S180 cell may serve as an alternative cell model, especially when other cell lines are unavailable. Furthermore, after optimal validation, it can be suggested that an S180 cell attachment assay may be a candidate for a series of assays to detect developmental toxicants.

Objective To establish an simple and convenient animal model of cardiac arrest for studying cerebral resuscitation.Method Clean male Sprague Dawley rats were randomly divided into sham group and experimental group.Cardiac arrest was induced by asphyxiation and ice-cold 0.5 mol KCl with blood flow cut off for 5 minutes.Animals were resuscitated with external cardiopulmonary resuscitation (CPR),mechanical ventilation,and epinephrine injection.Blood pressure,heart rate,successful ratio of resuscitation after 72 hours, time of cardiac arrest (T_(CA)) and return of spontaneous circulation (T_(ROSC)) were recorded.Neural deficit scores (NDS) and levels of maleic dialdehyde (MDA) in plasma were evaluated at 3,6,12,24,48,72 hours after ROSC.The damage score of cortex was measured by transmission electron microscope examination at 3 hours and 72 hours after ROSC.Results All the rats in experimental group had cardiac arrest rapidly.T_(CA) and T_(ROSC) were (137.3?10.2) seconds and (64.4?9.3) seconds,respectively,while the successful rate of resuscitation was 82.5%.The lowest NDS was at 3 hours after ROSC,while the NDS increased gradually.After CPR,the level of MDA in plasma increased significantly,slightly declined at 72 hours after ROSC,but still significantly higher than before the model.Electron microscope examination of cortex showed neuron slightly,organelle and astrocyte,but became better after 72 hours post ROSC.Conclusions The model of cardiac arrest was easy to establish,and the data provided was accurate,which is useful to study the mechanism of cerebral resuscitation.

Animals ; Chlorine Compounds ; toxicity ; Dose-Response Relationship, Drug ; Female ; Lung ; drug effects ; metabolism ; RNA, Messenger ; genetics ; Rats ; Rats, Sprague-Dawley ; Transforming Growth Factor beta1 ; biosynthesis ; genetics ; Tumor Necrosis Factor-alpha ; biosynthesis ; genetics

Dendritic Cell Sarcoma, Follicular ; pathology ; Dendritic Cell Sarcoma, Interdigitating ; pathology ; Female ; Humans ; Middle Aged ; Stomach Neoplasms ; pathology

AIMTo study the effect and mechanism of gonadotrophin-releasing hormone (GnRH) on murine Leydig cell steroidogenesis.

METHODSPurified murine Leydig cells were treated with GnRH-I and -II agonists, and testosterone production and steroidogenic enzyme expressions were determined.

RESULTSGnRH-I and -II agonists significantly stimulated murine Leydig cell steroidogenesis 60%-80% in a dose- and time-dependent manner (P < 0.05). The mRNA expressions of steroidogenic acute regulatory (StAR) protein, P450scc, 3beta-hydroxysteroid dehydrogenase (HSD), but not 17alpha-hydroxylase or 17beta-HSD, were significantly stimulated by both GnRH agonists with a 1.5- to 3-fold increase (P < 0.05). However, only 3beta-HSD protein expression was induced by both GnRH agonists, with a 1.6- to 2-fold increase (P < 0.05).

CONCLUSIONGnRH directly stimulated murine Leydig cell steroidogenesis by activating 3b-HSD enzyme expression.

3-Hydroxysteroid Dehydrogenases ; biosynthesis ; genetics ; Animals ; Blotting, Western ; Cell Separation ; Cells, Cultured ; Cholesterol Side-Chain Cleavage Enzyme ; biosynthesis ; Dose-Response Relationship, Drug ; Gonadotropin-Releasing Hormone ; agonists ; pharmacology ; Leydig Cells ; drug effects ; metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Phosphoproteins ; biosynthesis ; genetics ; RNA ; biosynthesis ; isolation & purification ; Reverse Transcriptase Polymerase Chain Reaction ; Sexual Maturation ; physiology ; Steroids ; biosynthesis ; Testosterone ; biosynthesis

Objective To investigate the influence of dezocine on spinal cord glial fibrillary acidic protein (GFAP) in rats with chronic constriction injury (CCI) of sciatic nerve as well as its protective effect on sciatic nerve.Methods Thirty two SD rats were randomly divided into sham-operation group,model group,experimental-L,-H groups (with 2.5,10 mg · kg-1 dezocine),eight SD rats in each group.The SD rats in experimental groups were treated with dezocine by intraperitoneal injection once every day from the beginning to seven days after operation;but the SD rats in sham-operation group and model group were treated with normal saline.Seven days after operation,the changes of pathological morphological of sciatic nerve in the four groups were detected.And the expression of GFAP in the four groups was detected by immunofluorescence histochemistry.Results After continuous injection of dezocine for 7 days,the sciatic nerve fibers in experimental-L group rats were swelling,the number of sheath cells decreased,and some of them were dissolved.In experimental-H group,there were a few normal myelin in rats,the swelling of nerve fibers is reduced compared with those in model group,but the number of sheath cells decreased compared with those in sham group,axons can be seen in some myelin sheaths.The expression of glial fibrillary acidic protein of spinal cord in sham-operation group,model group,experimental-L,-H groups were 1.03 ± 0.28,2.08 ±0.55,1.61 ±0.14,1.25 ±0.45.Compared with sham group,the difference in model group was significant (P ＜0.001);compared with model group,the difference in experimental-L,-H groups was significant(P ＜ 0.05,P ＜ 0.01).Conclusion Dezocine can inhibit the neuropathic pathologic pain.The mechanism maybe related to the decrease of the expression of GFAP in spinal cord,the activation of astrocytes,and the relief of the edema of sciatic nerve.

Antiviral Agents ; adverse effects ; therapeutic use ; Child ; Hepatitis B, Chronic ; complications ; drug therapy ; Humans ; Interferon Type I ; adverse effects ; therapeutic use ; Male ; Vitiligo ; chemically induced ; etiology

OBJECTIVETo establish a method for evaluating the activity of von Willebrand factor cleaving protease (vWF-cp) and evaluate its clinical application.

METHODSPurified von Willebrand factor polymer was isolated by gel filtration from human fresh-frozen plasma as the enzyme substrate. SDS-PAGE, Western blotting, and luminographic detection were used to evaluate vWF-cp activity of 60 healthy adults, 28 patients with cerebral infarction (CI) and 7 with thrombotic thrombocytopenic purpura (TTP).

RESULTSIn the subjects involved, the method for evaluating vWF-cp activity had intra- and inter-batch coefficient of variation(CV) of 4.81% (n=8) and 8.63% (n=6), respectively. According to this method, the plasma vWF-cp activity in the 60 healthy adults was significantly higher than that in the CI patients [(86.53-/+17.49)% vs (77.15-/+16.72)%, P<0.05]. In TTP patients before plasma replacement, the vWF-cp activity was (9.06-/+7.17)% and increased significantly to (47.00-/+6.27)% 24 h after plasma replacement, respectively, but still significantly lower than that of healthy adults (P<0.01), whereas in the convalescent stage, the activity approached the normal level [(83.18-/+8.83)%, P>0.05].

CONCLUSIONSAccording to the described method, which allows accurate vWF-cp activity measurement with good sensitivity, specificity and reproducibility, vWF-cp activity is lower in CI patients and even more so in TTP patients than that of healthy adults. Plasma replacement can effectively increase the vWF-cp activity in TTP patients.

ADAM Proteins ; blood ; metabolism ; ADAMTS13 Protein ; Adult ; Animals ; Cerebral Infarction ; blood ; enzymology ; Enzyme Assays ; methods ; Female ; Humans ; Male ; Middle Aged ; Purpura, Thrombotic Thrombocytopenic ; blood ; enzymology ; Reproducibility of Results ; Substrate Specificity

OBJECTIVETo investigate the effects of angelicanaphtha on proliferation, cell cycle, apoptosis, and collagen synthesis of human umbilical vein endothelial cells (HUVEC).

METHODSHUVEC was cultured and passaged in Dulbecco's modified Eagle's medium (DMEM) and treated with angelicanaphtha 1 mg/ L, 4 mg/L, and 16 mg/L at 1, 3, 5, and 7 day respectively. The proliferation was measured with MTT method. The cell cycle and apoptosis were analyzed with flow cytometry and collagen synthesis was determined with radioimmunoassay.

RESULTSThe proliferation of the HUVEC was accelerated by angelicanaphtha < or =4 mg/L and inhibited by angelicanaphtha at 16 mg/L (P < 0.05). Lower concentration (< or = 4 mg/L) of Angelicanaphtha decreased cells in G0/G1 phase and increased significantly cells in S phase and inhibited the apoptosis (P < 0.05). However, angelicanaphtha at 16 mg/L increased cells in G0/G1 phase and decreased cells in S phase and induced the apoptosis (P < 0.05). The collagen synthesis of HUVEC was inhibited by angelicanaphtha in concentration-dependent manner (P < 0.05 or 0.01).

CONCLUSIONThe proliferation effects of angelicanaphtha on HUVEC had dualistic regulation of increase by lower-concentration and inhibition by higher-concentration. Collagen synthesis of HUVEC was inhibited by angelicanaphtha in concentration-dependent manner.

Angelica sinensis ; Apoptosis ; drug effects ; Cell Proliferation ; drug effects ; Cells, Cultured ; Collagen Type III ; biosynthesis ; Endothelial Cells ; cytology ; drug effects ; metabolism ; Humans ; Oils, Volatile ; pharmacology ; Umbilical Veins ; cytology