Objective To explore the influence of electrical stimulation on prefrontal cortical neurons and synaptic ultramicrostructure of hypoxic-ischemic brain damage(HIBD)in neonatal rats.Methods The sixty 7-day-old newborn healthy SD rats were randomly divided into hypoxic-ischemic group(model group),electrical stimulation(intervention)group and sham operation group(control group),which 20 for each group.The models of perinatal HIBD rats were prepared by ligation of left common carotid artery with a temporary systemic hypoxia for 2 hours.Intervention group was subject to electric stimulation for 30 minutes,once everyday after surgery.Control group and model group were not subject to electric stimulation but caught to fix in corresponding period.Fastigial nucleus electric stimulations were performed for 3 d,14 d and 21 d.Five rats were killed in each group after the application of electron microscope to observe the brain cortex neurons and synaptic ultrastructure changes.Results In model group,the neuronal shrinkage,the amount of organelles dacrease,ob-vious edema of cytoplasm,obvious swellen mitochondria,and synapse quantity decrease,synaptic space fusion,obvious synaptic vesicle were observed.Intervention group different times,mitochondria hydrops gradually alleviated,synaptic space gradually cleared,synaptic vesicle increased,pathological changes obviously lessened compared to model group at the same time,and there was no apparent abnormality compared with control group on the 21st d.Conclusion Electric stimulation can promote the ultramicrostructures recovery of HIBD rats.

Objective To investigate the effects of electrical stimulation on vascular endothelial growth factor(VEGF) and its receptor expressions of neonatal rat brain with hypoxic-ischemic brain damage(HIBD).Methods Seventy-five 7-day-old newborn health SD rats were randomly divided into sham operation group(control group,n=25),hypoxia-ischemia group(model group,n=25) and the electrical sti-mulation group(intervention group,n=25).To bulid HIBD animal model of neonatal rats,the left common carotid artery was ligated and nitrogen-oxygen gas mixture was inhaled 2 hours.Fastigial nucleus stimulation was given 12 hours after the operation in intervention group,30 min?time-1,1 time?d-1,the time length was 1 d,3 d,7 d,14 d or 21 d,respectively.There was no electrical stimulation in model group and control group.The rats in these groups were captured at the corresponding time.Five rats in each group were killed at the corresponding pe-riods after electrical stimulation,the expression of VEGF and its receptor fam-like tyrosine kinase receptor(flt-1 / VEGFR1),fetal liver kinase receptor(flk-1/KDR/VEGFR2) in hippocampus were observed by immunohistochemistry.SPSS 15.0 software was used to analyze the data.Results The expression of VEGF,VEGFR1,VEGFR2 at every time point in electrical stimulation group were higher significantly than those in model group and control group(Pa0.05).Conclusion Electrical stimulation can promote the expression of VEGF and its receptors VEGFR1,VEGFR2.

Abstract?AIM: To investigate the effect of epigallocatechin-3-gallate ( EGCG ) against oxidative stress induced by high glucose in human lens epithelium ( HLE) cells.? METHODS: The HLE cell oxidative damage model induced by high concentration glucose was established, and was intervented with different concentrations of EGCG. Cell viability was determined by MTT assay, cell morphology was investigated by convert microscope, cells apoptosis was assayed by flow cytometry with Hoechst-PI staining. Moreover, the levels of super oxide dismutase ( SOD) , glutathione peroxidase ( GSH-Px) and malondialdehyde ( MDA) in supernatant were also tested after different treatment either with high concentration glucose or with different concentrations of EGCG.?RESULTS: MTT results showed that HLE cells activity increased to 50. 33%± 3. 52% and 63. 33%± 4. 63% after treated with 10 μmol/L and 100 μmol/L EGCG respectively, the difference was statistically significant compared with oxidative injury group(32. 67%±3. 10%)(P<0. 05 ); HLE cells maintained better morphology intervented with EGCG under high glucose conditions, the number of apoptotic cells reduced, SOD and GSH-Px level within HLE cells increased and MDA levels decreased.?CONCLUSION:EGCG plays its strong antioxidant effect by increasing SOD, GSH-Px content and decreasing MDA content in cells, therefore provides a reliable experimental basis for the search for effective prevention and treatment of cataract drug.

Objective To investigate the level and value of serum IgE, anti-IgE, FcεRⅠα, anti-FcεRⅠin autoimmune liver disease ( AILD) .Methods In this case-control study, the serum samples and clinical data of 77 patients with hepatosis were collected between May and November 2014 from the department of gastroenterology of Shanghai First People′s Hospital.These patients had positive results about the liver-related autoimmune antibodies, including 33 cases of AILD, 44 cases of other chronic liver disease. 64 healthy persons were collected as control group.Serum mast cell-associated anti-IgE, FcεRⅠα, anti-FcεRⅠwere detected by Enzyme-linked Immuno sorbent Assay ( ELISA) .Serum IgE, IgM and IgG were detected by rate scatter nephelometry.Differences among AILD, other chronic liver disease and healthy control were assessed.Results were compared using Mann-Whitney U test.Results Mast cell-associated anti-IgE, FcεRⅠα, anti-FcεRⅠin liver-related autoimmune antibodies positive patients were significantly higher than healthy control [1.74(1.16 -2.88)mg/L, 14.86(4.39 -26.23)mg/L, 47.22(36.89 -55.29)mg/L and 1.23(0.95-1.58)mg/L, 1.87(1.52-2.33)mg/L, 35.40(24.74-44.89)mg/L, respectively;U=1614,556.5,1319.5, P<0.01].FcεRⅠαwas significantly higher in other chronic liver disease patients than AILD patients [18.40(7.35-30.64)mg/L and 6.25(2.49-22.29), respectively;U=445, P<0.01] .Conclusion Mast cell-associated anti-IgE, FcεRⅠα, anti-FcεRⅠwere increased in liver-related autoimmune antibodies positive hepatosis patients.However, FcεRⅠαwas lower in AILD than other chronic liver disease.Mast cell-associated anti-IgE、FcεRⅠαand anti-FcεRⅠ molecules involved in the inflammatory lesion of liver disease.

Aims To study the changes of serum me-tabolites in systemic lupus erythematosus ( SLE ) mice ( MRL/lpr) by treatment of Qinghao-Biejia and to ex-plore the pathogenesis of SLE and mechanism of drug action. Methods The serum samples of control group, SLE model group and Qinghao-Biejia treatment group ( low and high dose ) were collected, the metabolic profile of samples was analyzed by high performance liquid chromatography-quadrupole-time of flight mass spectrometry system ( HPLC-Q-TOF/MS ) . Software of Mass Hunter and Mass Profiler Professional ( MPP ) were used to process the data. A supervised mode of partial least squares-discriminant analysis ( PLS-DA ) was applied to recognize the data pattern. Results There were obvious disorders of lipid metabolism in SLE model. Compared with control group, Qinghao-Biejia treatment group improved lipid metabolism, af-fected the thrombosis development of SLE; and Qing-hao-Biejia treatment group reduced the pathological damage by improving inflammatory acute phase of SLE in mice. Conclusion Qinghao-Biejia treatment plays a therapeutic role in repairing the imbalance by multidi-mensional metabolic pathways in SLE mice.

OBJECTIVETo observe the acute hemodynamic effects of intravenous diltiazem in patients with congenital heart defect (CHD) and severe pulmonary hypertension (HP) post cardiac surgery.

METHODSFrom November 2003 to September 2005, 12 patients with CHD and severe HP (4 male, mean age 17.8 +/- 9.8 years) after cardiac surgery received intravenous diltiazem (3 - 5 microg x kg(-1) x min(-1)) in the Intensive Care Unit. Mean pulmonary artery pressure (mPAP), mean arterial pressure (MAP), heart rate (HR), stroke volume (SV), systemic vascular resistance (SVR), pulmonary vascular resistance (PVR) were monitored with Swan-Ganz catheter before (T1) and 6 hours (T2) after diltiazem injection, before weaning patients off of ventilator (T3), 1 hour (T4) and 24 hour (T5) after extubation.

RESULTSAll patients survived during the observation period and no patient developed pulmonary hypertension crisis. The average ventilation time was (88.7 +/- 50.1) hours. Mean ICU stay time was (5.8 +/- 3.1) days. Compared to T1, mPAP was significantly decreased at T3 and T5, MAP significantly increased at T4 and T5, HR significantly reduced at T2 and thereafter, SV significantly increased at T3, T4 and T5 and PVR significantly increased at T3 and T5 while SVR remained unchanged after diltiazem therapy.

CONCLUSIONIntravenous use of diltiazem is safe and effective for patients with CHD with severe HP post cardiac surgery.

Adolescent ; Adult ; Child ; Child, Preschool ; Diltiazem ; therapeutic use ; Female ; Heart Defects, Congenital ; complications ; drug therapy ; Humans ; Hypertension, Pulmonary ; complications ; drug therapy ; Injections, Intravenous ; Male ; Young Adult

Aged ; Carcinoma, Small Cell ; genetics ; Case-Control Studies ; Cytochrome P-450 CYP2E1 ; genetics ; Female ; Humans ; Lung Neoplasms ; genetics ; Male ; Middle Aged ; Polymorphism, Single Nucleotide

The deubiquitinating enzyme ubiquitin specific peptidase 15 (USP15) is regarded as a regulator of TGFβ signaling pathway. This process depends on Smad7, the inhibitory factor of the TGFβ signal, and type I TGFβ receptor (TβR-I), one of the receptors of TGFβ. The expression level of USP15 seems to play vital roles in the pathogenesis of many neoplasms, but so far there has been no report about USP15 in psoriasis. In this study, immunohistochemical staining of USP15, TβR-I and Smad7 was performed in 30 paraffin-embedded psoriasis specimens and 10 normal specimens to investigate the expression of USP15, TβR-I and Smad7 in psoriasis and to explore the relevance among them. And USP15 small interfering RNA (USP15 siRNA) was used to transfect Hacat cells to detect the mRNA expression of TβR-I and Smad7. Of 30 cases of psoriasis in active stage, 28, 24 and 26 cases were positive for USP15, TβR-I and Smad7 staining, respectively. The positive rates of USP15 and Smad7 were significantly higher in psoriasis specimens than in normal skin specimens (44.1%±26.0% vs. 6.1%±6.6%, 47.2%±27.1% vs. 6.6%±7.1%), and positive rate of TβR-I (20.3%±22.2%) in psoriasis was lower than that in normal skin specimens (46.7%±18.2%). There was a significant positive correlation between USP15 and Smad7 expression, and significant negative correlations between USP15 and TβR-expression, an I d between TβR- and Smad7 expression I in psoriasis. After transfection of USP15 siRNA in Hacat cells, the expression of TβR-mRNA was up I -regulated and that of Smad7 was down-regulated. It is concluded that USP15 may play a role in the pathogenesis of psoriasis through regulating the TβR-I/Smad7 pathway and there may be other cell signaling pathways interacting with USP15 to take part in the development of psoriasis.

Objective To evaluate the effect of dexamethasone to the cultured rat thoracic aortic smooth muscle cells(SMC)in vitro,and explore the role on it's prevention and cure for the in-stent restenosis after vascular intervention.Methods The rat thoracic aortic SMC were harvested and cultured for six to ten passages.The cultured SMC were synchronized and then restimulated to enter the cell cycle,and treated with incremental concentrations of dexamethasone or without dexamethasone as control.The proliferative assay was performed with MTT method in the different time points after treatment.RT-PCR was performed to assay the level of proliferating cell nuclear antigen(PCNA)mRNA.Results 1.Dexamethasone progressively inhibited rat aortic SMC proliferation in a concentration-dependent fashion.The A value was statistically significant for different concentrations(F=36.02,P＜0.001).The effect was not significant for dexamethasone concentrations either between 10~(-6)and 10~(-5)mol/L(P=0.065)or between 10~(-11)mol/L and control group(P= 0.567).2.RT-PCR suggested dexamethasone significantly decreased rat aortic SMC PCNA mRNA transcription in a concentration-dependent fashion.Statistical analysis indicated F=15.407 and P＜0.001 by ANOVA. Comparing to the control,the corrected A value was not statistically significant at 10~(-9)or 10~(-11)mol/L groups by post hoc analysis.Conclusions Dexamethasone inhibits rat aortic SMC proliferation in a concentration- dependent fashion.The data suggest that effective action concentration is 10~(-7)mol/L with persistent time up to 96 hours or more.Dexamethasone may play the inhibit role to SMC at lower concentration with prolonging action time.

OBJECTIVETo investigate the effect of p65 gene inhibited by siRNA on neuronic differentiation in the marrow mesenchymal stem cells (MSCs).

METHODSThe MSCs were transfected with Rn-p65-siRNA. Fasudil hydrochloride induced MSCs differentiating into neurons. The non-transfected group and negative control group (transfected with negative control siRNA marked by Cy3) were used as controls. The fluorescence expressed by transfected MSCs were observed under inverted fluorescence microscope at 24 h,48 h and 72 h after transfected with negative control siRNA. The viability of MSCs was detected by MTT at 24 h, 48 h and 72 h after transfected with Rn-p65-siRNA. The expressions of p65 mRNA and protein in MSCs were detected by RT-PCR and Western blot respectively. The expressions of p65 protein, NSE, MAP-2 and glial fibrillary acidic protein (GFAP) were detected by immunocytochemical method after transfection for 6 h.

RESULTSThe fluorescence of MSCs was mostly displayed after transfection of 72 hours and the efficiency of transfection was up to 83.3% ± 3.8%. Meanwhile, the p65 mRNA and p65 protein expressed by MSCs of transfected group were significantly decreased (P < 0.05); MTT displayed that the viability of MSCs was also significantly reduced (P < 0.05). The best efficiency of induction was observed in the transfected group. There were higher expressions of NSE and MAP-2 than the other group (P < 0.05).

CONCLUSIONThe p65 gene inhibited by siRNA can promote the marrow mesenchymal stem cells to differentiate into neurons.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine ; analogs & derivatives ; Animals ; Cell Differentiation ; Glial Fibrillary Acidic Protein ; metabolism ; Mesenchymal Stromal Cells ; cytology ; Neurons ; cytology ; RNA, Messenger ; RNA, Small Interfering ; Rats ; Transcription Factor RelA ; antagonists & inhibitors ; metabolism ; Transfection