Objective To observe whether recombinant human erythropoietin (rhu- EPO) could cross blood- brain barrier (BBB) of premature infants. Methods Thirty - six premature infants, with gestational age 28 - 35 weeks, birth weight0.05).Conclusion Rhu- EPO can cross the BBB of premature infants.

AIM: To investigate the effects of nitric oxide(NO) and caspase-3 on dopamine-induced apoptosis in PC12 cells. METHODS: Flow cytometric assay was used to quantify the apoptotic cells. The morphological of apoptotic cells was evaluated by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL). Nitrite was quantified by Griess reaction. Inducible nitric oxide synthase(iNOS) mRNA was identified by semiquantitative reverse transcription polymerase chain reaction(RT-PCR). Caspase-3 activity was determined by fluorescent spectrofluorometer. RESULTS: Dopamine induced PC12 cells apoptosis in a concentration-dependent manner (0.15-0.60 mmol/L), with positive TUNEL staining. During the development of apoptosis, the expression of iNOS mRNA and the levels of NO increased markedly, so did caspase-3 activity(P

ObjectiveTo investigate the protein expression of ERK1/2,p-ERK1/2,HIF-1α and α-enolase in hypertrophic cardiomyocytes induced by ET-1 and explore the regulation mechanism of overexpression of α-enolase in hypertrophic cardiomyocytes.MethodsET-1-induced abnormal cardiomyocytes were used as model of cardiac hypertrophy.Cellsurface area, [<'3>H]-leucine incorporation and the actin staining were measured to determine the extent of hypertrophy. Cultured cardiomyocytes were divided into 4 groups at random, control group, PD98059 treated group, ET-1 treated group and PD980594- ET-1 treated group. The protein expressions of ERK1/2, p-ERK1/2,HIF-1α and α-enolase were detected by immunoblotting analysis.ResultsCompared with the control group , cell surface area and [<'3>H] leucine incorporation were increased in ET-1 treated group ((1350.7±107.5)μtm<'2> vs. (896.1±70. 2)μtm<'2> , P<0.05; (1387.9±14.8) dpm vs. (787.7±10.2)dpm,P<0.013. Actin staining showed that ET-1-treated cardiomyoeytes had more intense actin staining and clear cross-striations than did control group, which suggested that myocardial cell hypertrophy could be induced by ET-1 in WKY neonatal cardiomyocytes. After MEK 1/2 inhibitor PD98059 was used, the cell surface area and [<'3>H] leucine incorporation were decreased in PD980594-ET-1 treated group compared with ET-1 treated group[(907.0±92.5)μm<'2> vs. (1350.7±107.5)μm<'2>;(841.5±10. 5)dpm vs. (1387.9±14.8)dpm, both P<0.05], which suggested that myocardial cell hypertrophy could be regulated by ERK1/2 signal pathway. Immunoblotting analysis showed that the protein expressions of p-ERK1/2, HIF-1α and α-enolase increased after ET-1 treatment,while PD98059 as an inhibitor of the upstream kinase of ERK1/2 was used, the protein expressions of HIF-1α and α-enolase were partially inhibited.ConclusionsET-1 induces hypertrophic cardiomyocytes through ERK1/2 phosphorylation in cultured neonatal rat cardiac myocytes.ERK1/2 and HIF-1α signal pathway may play an important role in the overexpression of α-enolase in the hypertrophic cardiomyocytes.

Objective To evaluate the neuroprotective effect and possible mechanisms of edaravone(3-methyl-1-phenyl-2-pyrazolin-5-one) in neonatal Harlequin(Hq) mutant mice brain after hypoxia-ischemia brain injury(HIBD) insult.Methods The nine-day-old male Hq mutant mouse pups were assigned randomly either edaravone(n=16) and vehicle(n=17) treatment group.The Hq mice were subjected to left common carotid artery occlusion combined with inhalation 100 mL/L oxygen for 45 minutes.The mice were injected intraperitoneally either with edaravone(10 mg/kg) or equivalent volume of saline immediately after artery occlusion and after hypoxia.Nitrotyrosine and lipid peroxidation formation were evaluated at 3 h and 24 h after hypoxia-ischemia(HI) by using immunohistochemistry staining.Nitrotyrosine formation and caspases activation were evaluated either by immunoblotting or fluorogenic activity measurement at 24 h after HI.Brain injury was evaluated at 72 h by neuropathological score and calculating the infarct volume.Results Brain injury encompassed cortex,hippocampus,striatum and thalamus.Edaravone treatment reduced brain injury significantly in all the brain regions.The total infarct volume was reduced 52.8% in edaravone treatment group compared with vehicle group(P

Objective To explore the correlation between the joint detection of cholinesterase(CHE),alpha-L-fucosidase(AFU) and alpha-fetoprotein(AFP)and primary hepatic cancer(PHC).Methods 56 cases of patients with PHC(PHC group),52 cases of patients with liver cirrhosis(LC group)and 60 cases of healthy individuals(control group)were enrolled in this study,and serum levels of CHE,AFU and AFP were detected and statistically analysed.Results Serum levels of CHE in patients with PHC were negatively correlated with levels of AFU and AFP(correlation coefficient was -0.889 and -0.797 respectively,P <0.05),the ser-um levels of CHE in patients with LC were also negatively correlated with levels of AFU and AFP (correlation coefficient was-0.598 and -0.653 respectively,P <0.05).The positive rates of joint detection of CHE,AFU and AFP in PHC group and LC group were higher than that in the control group,had statistically significant differences(P <0.05 ).Conclusion CHE,AFU and AFP are sensitive indicators of liver lesions,and the joint detection could provide reference value for diagnosis and monitoring pro-gression of PHC.

Objective To evaluate the effect of N- acetylcysteine(NAC) on lipopolysaccharide (LPS) - sensitized neonatal rats with hypoxic- ischemic brain damage(HIBD) and possible mechanism except the antioxidant. Methods With the total number of 98 Wistar pups at postnatal day 8 of either sex was used in this study. There were 86 pups which were divided into three groups to evaluate the brain injury:vehicle group ( n = 29) ,low dose (25 mg/kg) ( n = 31 ) and high dose NAC (200 mg/kg) ( n - 26) treatment group. The pups were injected with LPS(0.1 mg/kg)intraperitoneally 3 days before hypoxic- ischemic(HI) insult. Multiple dose of NAC (25 mg/kg or 200 mg/kg) or vehicle was injected intraperitoneally before and after HI. Brain injury was evaluated 7 days after HI. For the Caspase - 3 activity and immunoblotting analysis, the samples were collected at 24 h after HI treated either with vehicle or high dose NAC ( n = 6 per group). Results The brain injury volume was significantly reduced by high dose NAC (200 mg/kg) treatment compared with that of vehicle (77% reduction, P ＜ 0.001 ). The tissue loss was reduced 67 % ( P ＜ 0.001 ) in high dose NAC treated group compared with that of vehicle. However,there was no significant reduction of brain injury in the low dose NAC treatment group compared with vehicle group. Caspase - 3 like activity measurement showed that the activity decreased 53 % after high dose NAC treatment ( P ＜ 0. 001 ) compared with that of vehicle treatment. The immunoblots showed that the active form of Caspase - 3, 17 kDa band, was abolished by the high dose NAC treatment. Conclusions NAC treatment attenuate LPS - sensitized neonatal HI brain injury is dose dependent. The neuroprotective effect involves Caspase - 3 inhibition.

Objective To investigate the chronic angio-complications of diabetes mellitus(DM)and impared glucosetolerance(IGT)patients were diagnosticated newly.Methods 46 patients with diabetes mellitus and 97 pa- tients of impared glucosetolerance were chosen in the study,and 35 patients were chosen as normal glucose tlerance group.Some biochemical criterion,carotid artery intima-media thickness and plaque condition were measure.Results The group of IGT contract coronary heart disease is 62.9 %,cetebrovascular disease is 20.6%,carotid artery atheromatosis is 50.5 %,the group of DM contract coronary heart disease is 65.2%,cerbrovascular disease is 26,1%,carotid artery atheromatosis is 69.6%,it have statistics significance compared with control group(P

Child ; Child, Preschool ; Contrast Media ; adverse effects ; Coronary Angiography ; Female ; Humans ; Infant ; Iohexol ; adverse effects ; Kidney ; drug effects ; physiology ; Male ; beta 2-Microglobulin ; urine

Objective To study the change of metabolism of serum lipids in patients with mild cognitive impairment(MCI). Methods The serum levels of total cholesterol(TC),triglyceride(TG),low density lipoprotein(LDL) and high density lipoprotein(HDL) were measured in 60 patients with MCI and 100 age-matched normal controls. ResultsThe serum levels of TC,TG and LDL were significantly higher and HDL significantly lower in patients with MCI than in normal controls(P

ObjectiveTo evaluate the neuroprotective effect and possible mechanisms of edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one) in neonatal Harlequin (Hq) mutant mice brain after hypoxia-ischemia brain injury(HIBD) insult.MethodsThe nine-day-old male Hq mutant mouse pups were assigned randomly either edaravone (n=16) and vehicle (n=17) treatment group. The Hq mice were subjected to left common carotid artery occlusion combined with inhalation 100 mL/L oxygen for 45 minutes. The mice were injected intraperitoneally either with edaravone (10 mg/kg) or equivalent volume of saline immediately after artery occlusion and after hypoxia. Nitrotyrosine and lipid peroxidation formation were evaluated at 3 h and 24 h after hypoxia-ischemia(HI) by using immunohistochemistry staining. Nitrotyrosine formation and caspases activation were evaluated either by immunoblotting or fluorogenic activity measurement at 24 h after HI. Brain injury was evaluated at 72 h by neuropathological score and calculating the infarct volume.ResultsBrain injury encompassed cortex, hippocampus, striatum and thalamus. Edaravone treatment reduced brain injury significantly in all the brain regions. The total infarct volume was reduced 52.8% in edaravone treatment group compared with vehicle group (P<0.001). The edaravone treatment reduced nitrotyrosine formation as well as lipid peroxidation formation significantly, but without obviously effect on caspases activation.ConclusionEdaravone affords neuroprotection after neonatal HI insult, which correlated with the reduction of free radical formation.