0.05).The recurrence of pterygium was related to the age.If the age increased five years,the risk of recurrence decreased 18.1%. Conclusion The application of MMC(during) the operation could decrease the recurrence rate of pterygium.The recurrence rate of pterygium was not related to the time of application of 0.02% MMC,and detainment for 3 min was enough during the operation.

As one of the first resident standardized training bases, department of ophthalmology of Shanghai Ruijin Hospital participated in this reform process from 2010. Relevant rules and regulations (training management system , training scheme implementation system and evaluation system ) were strictly obeyed. When new problems emerged, under the guidance of department in charge, a series of regimens were formulated and improved gradually by Ophthalmology Professional Committee of Shanghai Resident Standardized Training Department. Based on reviewing and summarizing the work in the last 3 years, some thoughts and suggestions on the resident standardized training in future were put forward ,in-cluding how to better solve the“heavily used, lightly cultured” problem, the“disregarding medical ethics establishment”problem, the“disregarding assessment of teachers”problem and the“disregard-ing obtaining employment”problem.

Objective To investigate the effects of Shenfu injection ( SF,a Chinese herbal medicine preparation made of Codonopsis pilosula and Aconitum carmichaeli) on the cell apoptosis of focal cerebral ischemic-reperfusion injured rats and the expression of heme oxygenase-1 (HO-1). Methods Forty-two male Sprague-Dawley rats used for producing unilateral brain ischemia reperfusion model were randomly divided into three groups:sham operation group ( Sham group),ischemia reperfusion group ( IR group),and SF Injection group (SF group).The model of focal cerebral ischemia-reperfusion injury was induced by transient occlusion of middle cerebral artery (ischemia for 2 h,and reperfusion for 3,6 h respectively).In SF group,SF ( 10 mg/kg) was intraperitoneally injected duri(n)g reperfusion.Cell apoptosis rate in brain tissue was detected by the technique of Annexin-V-PI double staining and was counted in flow cytometer.Expression of HO-1 in brain was measured by RT-PCR,while the pathological and ultra structure changes of cerebral tissue were also observed.Results Cell apoptosis rate of brain tissue were significantly higher in IR group than that in Sham group (P ＜0.01 ),while SF group had less significant changes in cell apoptosis rate, HO-1 level of brain tissue than IR group (P ＜ O.01 ).The ultra structure change of brain tissue was less in SF group than that in IR group.Conclusions During early stage of brain IR injury,SF inhibits cellular apoptosis and in turn protects the brain from injury which is attributed to the increase in HO-1 expression induced by SF.

Objective:To evaluate the effects of dexamethasone on systemic lupus erythematosus complicated with cognitive dysfunction.Methods:Ten wild type mice and 20 MRL/lpr mice were applied for the research.MRL/lpr mice were randomly assigned to a MRL/lpr group and a MRL/lpr + dexamethasone (1.5 mg/kg) group.Interleukin-6 (IL-6),IL-1β,and tumor necrosis factor alpha (TNF-α) in serum and hippocampus were detected.The protein phosphorylation levels of phosphoinositide 3-kinase (P-PI3K),protein kinase B (P-Akt),NF-kappa-B inhibitor alpha (P-IκBa) and nuclear transcription factor kappa-B p65 (P-NF-κB p65) were detected by Western blot,the level of P-NF-κB p65 also was detected by immunohistochemistry.Results:Treatment with dexamethasone (1.5 mg/kg) alleviated the cognitive dysfunction and decreased the levels of IL-6,IL-1 β and TNF-α in serum and hippocampus,and reduced the levels of P-PI3K,P-Akt,P-IκBa and P-NF-κB p65 in hippocampus in MRL/lpr mice.Conclusion:Dexamethasone may play a protective role in the cognitive function by decreasing the levels of TNF-α and IL-1 β in the hippocampus of MRL/lpr lupus mice.

Adult ; Coronary Aneurysm ; complications ; Endocarditis, Bacterial ; complications ; Fistula ; complications ; Humans ; Male

Objective To investigate the effects of naloxone (Na) on pneumocyte apoptosis and expression of heme oxygenase-1 (HO-1) during ischemia reperfusion injury of lung in rats. Method Forty-two male Sprague-Dawley rats were made models of ischemia reperfusion injury of unilateral lung, and were randomly( random number) divided into three groups: sham operation group (Sh group), ischemia reperfusion group (IR group) and naloxone group (Na group). The hilus of lung was clamped for 45 minutes and the clamp was taken off to build the I/R model. After 3-6 hours reperfusion, naloxone in dose of 1 mg/kg was injected intra-peritoneally in rats of Na group. The rate of cell apoptosis in lung tissue was detected with the way of Annexin-V-PI in flow cy-tometer. The wet to dry weight ratio (W/D) of lung tissue was measured. The expression of HO-1 in lung was measured by using RT-PCR and the ultra-structure change of lung tissue was observed under electron microscope. Results The rate of pneumocyte apoptosis and W/D ratio of lung tissue were significantly higher in IR group than in Sh group (P < 0.01), and the rate of pneumocyte apoptosis and W/D ratio of lung tissue were negatively correlated with the expression of HO-1 mRNA in lung tissue. Compared with IR group, the rate of cell apoptosis and W/D ratio were lower and the expression of HO-1 mRNA was higher in Na group (P < 0.01). The ultra- structure changes of lung tissue were lessened in Na group than in IR group. Conclusions During early period of lung IR injury, HO-1 induced by naloxone can inhibit the cellular apoptosis and protect the lung tissue.

Objective To detect the disease-causing mutations in Duchenne muscular dystrophy (DMD) gene of DMD or Becher's muscular dystrophy (BMD) patients or carriers. Methods Multiplex ligation-dependent probe amplification (MLPA) and denaturing high performance liquid chromatography (DHPLC) were coupled to analyze the disease-causing mutations in DMD gene. Results Ten patients were detected to have deletions in different exons; 1 patient was caused by duplication of exon 50 using DHPLC analysis, and 4 patients were found to be caused by non-sense point mutations. However, the disease-causing mutations of other 5 patients remained to be determined. Conclusion MLPA coupled with DHPLC analysis can be used to detect the disease-causing mutations of DMD or BMD systematically, and provide valuable information for the affected families in preventing from recurrence of DMD or BMD.

BACKGROUNDMono-(2-ethylhexyl) phthalate (MEHP), the metabolite of di-(2-ethylhexyl) phthalate (DEHP), was suspected to be toxic to human embryos. This study contributes to investigating its toxic effects by an embryonic stem cell test (EST) based on two human embryonic stem cell (hESCs) lines.

METHODSCH1 established in our own lab and H1, a federally registered cell line were two human embryonic stem cell lines used in this test. Four endpoint measurements were performed consisting of cell viability, proliferation ability, apoptosis as well as changes of gene expression patterns after spontaneous differentiation were determined. For measuring effects on the first three endpoints, the cells were treated with various concentrations of MEHP dissolved in dimethyl sulfoxide (DMSO) and only with DMSO which served as control and harvested after 5 days. For measuring effects during spontaneous differentiation, the RNA of embryoid bodies (EBs) formed after 8 days' MEHP exposure was collected and changes in differentiation specific gene expression patterns were analyzed by quantitative real time RT-PCR.

RESULTSAs a result the viability and proliferation ability of both cell lines decreased significantly at 1000 µmol/L MEHP, while there was no effect on apoptosis or cell morphology. In addition MEHP also changed the gene expression pattern in the EBs of both cell lines.

CONCLUSIONMEHP in a high dose was cytotoxic and affected the development of hESCs, which indicates its embryo toxicity in human embryos.

Apoptosis ; drug effects ; Cell Differentiation ; drug effects ; Cell Proliferation ; drug effects ; Cell Survival ; drug effects ; Cells, Cultured ; Diethylhexyl Phthalate ; analogs & derivatives ; toxicity ; Dose-Response Relationship, Drug ; Embryonic Stem Cells ; drug effects ; pathology ; Humans

BACKGROUNDThe genioglossus (GG) is involved in the maintenance of an open airway for effective breathing. Although the pathogenesis of obstructive sleep apnea hypopnea syndrome (OSAHS) was closely associated with GG dysfunction, its causes and possible treatment have not been elucidated. The aim of the study was to investigate the effects of chronic intermittent hypoxia (CIH) on serum adiponectin levels, electromyograph (EMG) activity and ultrastructure of GG, as well as the effect of an adiponectin supplement in anesthetized rats.

METHODSForty-two healthy male Wistar rats were randomly divided into normal control (A), CIH (B) and adiponectin treatment (C) groups, 14 rats in each group. CIH was performed eight hours per day for five weeks in both groups B and C. Group C received transvenous injection of adiponectin at the dosage of 10 microg per injection, twice a week for five weeks. At the end of the 5th week the GG EMG voltage was measured and compared among the three groups. Transmission electron microscope was used to observe the ultrastructure of the GG.

RESULTSCIH caused significant hypoadiponectinemia, weakened activity of GG EMG at both baseline and hypoxia stimulation, and induced ultrastructural pathological changes, such as, myofibril discontinuities, lysis of myofilament, edema of mitochondria and disruption of cristae, vacuolus and lysis of some mitochondria. Venous supplement of adiponectin improved the above pathological changes resulting from CIH.

CONCLUSIONCIH resulted in pathological changes in GG's EMG and ultrastructure, which could be improved by supplement of adiponectin and be associated with hypoadiponectinemia caused by CIH.

Adiponectin ; administration & dosage ; blood ; Animals ; Electromyography ; Hypoxia ; blood ; physiopathology ; Male ; Microscopy, Electron, Transmission ; Muscle, Skeletal ; physiology ; ultrastructure ; Random Allocation ; Rats ; Rats, Wistar ; Sleep Apnea, Obstructive ; blood ; physiopathology ; Tongue ; physiology ; ultrastructure

After treating with chemotherapy or immunosuppressant, malignant diseases of hematopoietic system such as leukemia, malignant lymphoma and aplastic anemia usually induced severe infection such as sepsis. Sepsis which is hard to be diagnosed causes high death rate. This study was purposed to establish an experimental sepsis mouse model so as to provide a basis for pathogenesis and intervention study. A classic caecal ligation and puncture (CLP) was used to establish experimental sepsis model. ELISA was used to detect levels of C5a, IL-6, TNFalpha, and IFN-gamma. Flow Cytometry was applied to measure apoptosis of lymphocytes in thymus and mesentery. The pathologic changes of thymus and spleen were confirmed by HE staining. The results showed that almost 70%-80% mice died at 72 hours after CLP. Only approximate 20% animal survived during finite time, mice in CLP group had significant weight lose. Meanwhile large release of different inflammatory mediators which are related with sepsis (C5a, IL-6, TNF-alpha, and IFN-gamma) was observed after CLP. Apoptosis of lymphocytes in thymus and mesentery lymphonodus was enhanced markedly after CLP. Significantly pathologic injury was also observed in thymus and spleen. It is concluded that a mouse model of experimental sepsis was successfully established by caecal ligation and puncture which can well mimic the clinical symptom of sepsis. The experimental sepsis mouse model provides an excellent tool for exploring the pathogenesis and intervention ways for sepsis accompanied with complicated malignant hematological diseases in vivo.
Animals ; Apoptosis ; Cecum ; injuries ; Complement C5a ; metabolism ; Disease Models, Animal ; Interferon-gamma ; metabolism ; Interleukin-6 ; metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Sepsis ; metabolism ; pathology ; Spleen ; pathology ; Thymus Gland ; pathology ; Tumor Necrosis Factor-alpha ; metabolism