ObjectiveTo investigate the effect of PTEN on cell proliferation in human breast cancer cell BT549.MethodsThe plasmid pcDNA3-PTEN was used to transfect the PTEN - null breast cancer cell BT549 by lipo - transfection.After G418 selection,BT549 cells which stably expressed PTEN were obtained and amplified.Western blot were used to determine the target protein expression,the cell viability was tested by MTT assay.Results(1)Compared with the control,PTEN-BT549 cells demonstrated high expression of PTEN protein ;(2)The proliferation speed of PTEN-BT549 was obviously slower than BT549 and pcDNA3-BT549 cells( P ＜ 0.05 ).ConclusionAnti-oncogene PTEN suppresses the growth of breast cancer cell BT549.

Objective To observe the application value of cardiac troponin I (cTnI),cardiac troponin T (cTnT) and creatine kinase MB (CK MB) for the early diagnosis of acute myocardial infarction (AMI).Methods The same serum sample was measured to detect the indexes of cTnI,cTnT and CK MB levels in 60 patients with AMI and 40 patients with UA.Comparison between AMI and UA was performed and all the indexes were analysed contrastively.Results The sensitivity of cTnI and cTnT was higher than that of CK MB,and their positive rates were 63.3%,46.7% and 18.3% respectively (P0.05) and the specificity of the three indexes were almost the same without significant difference.Conclusion cTnI and cTnT,as specific markers of cardiac damage,are more sensitive and specific in the early diagnosis of AMI.As a convenient,swift and accurate measurement method,cTnI has significant clinical value.

Objective To analyze the clinical effect of brevisapine injection on high sensitivity C-reaction protein level in the treatment of acute myocardial infarction.Methods The patients were randomly divided into treatment group(n=80)and control group(n=80).Both groups were treated with routine midication,but treatment group were given intravenous drip of 100 mg brevisapine once a day.for 14 days.80 paients who came for diagnosis were selected for healthy control group.The selqlm high sensitivity C-reaction protein levels were measured at 2 d,7 d,and 14 d by ELLSA in treatment group,control group and healthy control group.Mortality,heart function status (Killip class),revaseularization and clinical adverse cardic events including postinfartion angina,new arrhythmia,reinfarction and bleeding complication at 4 weeks were observed.Results Treatment group had a significantly high level of hs-CRP compared with healthy subjects[(6.37±1.43)vs.(2.17±1.12)mmol/L,P＜0.01]at the second day.The serum hs-CRP content of treatment group was obviously lower than that of control group(3.21±1.31)and(2.25±0.34)mmol/L vs.(5.87±1.16)、(3.97±1.21)mmol/L,(P＜0.01)]on the 7th,14th days;The revascularization rate of treatment group was obviously higher than that of control group[62.50%(50/80)vs.51.25% (45/80),P ＜0.01];There was no difference between the two groups in mortality(3.75% vs.4.10%,P ＞0.05).No difference was found in the rate of bleeding between the two groups(6.25% vs.7.50%,P ＞0.05);Patients with Killip class＜Ⅱ of treatment group was obviously higher than that of control group (83.75% vs 61.25%,P ＜ 0.05 );Clinical adverse cardic events rates at 4 weeks of treatment group were obviously lower than those of control group (P ＜ 0.01 ).No obvious adverse reactions related to the treatment group were observed.Condusion The serum hs-CRP level is in close relation with acute myocardial infarction,which is the risk factor.It is effective and safe of brevisapine injection in the treatment of acute myocardial infarction.The effects of brevisapine on acute myocardial infarction might be involved in decreasing the level of hs-CRP and inhibiting the vascular inflammatory reaction.

BACKGROUND:Although incidents of organophosphate-induced delayed neurotoxicity have been documented for over a century, the molecular mechanisms underlying the axonopathy remain poorly understood.
OBJECTIVE:To discuss the effects of tri-ortho-cresyl phosphate (TOCP) on homeostasis of the glutamate-glutamine cycle and the expression of key enzymes in the brains of hens.
METHODS:Twenty-four adult hens were randomly divided into three groups (n=8). TOCP group was treated with TOCP by gavage at a single dosage of 1 000 mg/kg, and control group was given an equivalent volume vehicle by gavage, while hens in the phenylmethylsulfonyl fluoride (PMSF)+TOCP group were subcutaneously injected with 40 mg/kg PMSF fol owed by 1 000 mg/kg TOCP 24 hours later. The hens were kil ed on days 5 and 21 post-dosing. The brains were taken out quickly and preserved in a-80℃deep freezer. ELISA was used to determination the content of glutamine synthetase and glutaminase and the activity of glutamine synthetase. Corresponding kits were used to measure the level of glutamate and glutamine. Fluo3-AM was used to measure cytosolic calcium concentration. RESULTS AND CONCLUSION:The activity and content of glutamine synthetase and the concentration of glutamine were down-regulated, while the concentrations of the intracellular Ca2+and glutamate were up-regulated in the early stage after TOCP administration. It is also suggested that the downregulated expression of glutamine synthetase may be associated with organophosphate-induced delayed neurotoxicity through the disruption of homeostasis of the glutamate-glutamine cycle and cytosolic calcium concentration.

BACKGROUND:Although incidents of organophosphorus poisoning-induced delayed neuropathy (OPIDN) have been documented for over a century, the molecular mechanisms underlying the axonopathy remain poorly understood. Therefore, OPIDN treatment has been increasingly concerned. OBJECTIVE:To construct the OPIDN hen model induced by triorthocresyl phosphate (TOCP) and to explore the effect of phenylmethylsulfonyl fluoride (PMSF) intervention. METHODS:Adult hens were randomly divided into four groups: two TOCP groups, a PMSF group and a control group. TOCP groups were treated with TOCP by gavage at a single dosage of 1 000 mg/kg and 750 mg/kg respectively; control group was given an equivalent volume of saline by gavage while hens in the PMSF group were subcutaneously injected with 40 mg/kg PMSF 24 hours after 1 000 mg/kg TOCP injection. OPIDN neurological signs were assessed by a six-point graded scale. The changes of the hen weight were recorded. The hens were kiled on day 5 and 21 post-dosing. The samples were cut into 50 nm thick sections and examined by transmission electron microscopy. RESULTS AND CONCLUSION:OPIDN neurological signs such as abnormal gaits progressed in severity with time (P < 0.05), and the hen weight was significantly decreased in TOCP groups (P < 0.05). However, no clinical signs of delayed neurotoxicity were observed in hens of the PMSF group and the control group during the experiment period. The mild mitochondrial sweling and the fragmentation of microfilament and microtubule arrangement in axons were observed on day 5 post-dosing, leaving the other organeles remained unchanged. On day 21, neuronal degeneration was apparent, including sweling of endoplasmic reticulum, abnormal change of mitochondria, and disordered arrangement of cytoskeleton. The optimal dose of TOCP was 1 000 mg/kg. Experimental findings indicate that, OPIDN hen model induced by TOCP and PMSF intervention hen model were successfuly constructed. PMSF intervention significantly improved the pathologic changes and clinical symptoms of OPIDN induced by TOCP in hens.

Objective: To establish a content determination method for ferric iron and ferrous iron in ferrous succinate tablets.Methods: Using a Dionex RFICTM protection column (4 mm×50 mm)and a Dionex RFICM Ion PacRCS5A analytical column (4 mm×250 mm), the eluent solution consisted of 7 mmol·L-1 dipicolinic acid, 66 mmol·L-1 potassium hydroxide, 5.6 mmol·L-1 potassium phosphate monobasic and 74 mmol·L-1 formic acid.The flow rate was 1.5 ml·min-1, the column temperature was 30.0℃ and the injection volume was 1.3 μl.Results: Fe3+ showed good linearity within the range of 0.5-15 μg·ml-1(r=1.000 0), Fe2+ showed good linearity within the range of 25-200 μg·ml-1(r=1.000 0), and the average recovery was 103.6%(RSD=2.7%, n=9)and 98.3%(RSD=1.9%, n=9), respectively.Conclusion: The method is simple, reliable and accurate, and can be used for the determination of Fe3+and Fe2+ in ferrous succinate tablets.

Objective To evaluate the changes and significances of malondialdehyde(MDA)and Superoxide dismutase(SOD)in unstable angina pectoris(UAP)patient after percutaneous coronary intervention(PCI). Methods MDA and SOD were tested in 25 UAP patients before and 1h,24h,72h after PCI.20 UAP patients who were performed on coronary angiography(CAG) and 20 normal individuals entered this study as contrasts.All the UAP patients were followed up for 3 months。 Results Level of MDA in UAP cases significantly increased compared with the normal individuals, P

Carcinoembryonic antigen(CEA)is an oncofetal antigen which has been widespraad studied.A murine stage-Specific embryonic antigen(SSEA-l)is a new oncodeveloptnental antigen which appears at 8-cell stage of mouse embryo.The expression of CEA and SSEA-1 in gastric malignant and nonmalignant tissues by using immunofluorescence technique were reported in this study. Most of gastric carcinoma stained intensively for CEA (68 of 78 cases. 87. 2%) and SSEA-l(89.0%).But CEA only expressed in 15.0% of normal gastric mucosa (3/20) and SSEA-1 in 30.0%. In non-malignant gastric tissues, CEA was expressed in 61.5% (8 of 13 cases)of chronic atrophic gastritis (CAG) and 87.5%(7/8)of chronic superiicial gastritis (CSG)with intestinal metaplasia,but only 38.2% and 29.2% in CSG without intestinal metaplasia and peptic ulcer seperately. SSEA-1 existed in more than 80% of all kind of son-malignant gastric tissues, including CAG, CSG with or without intestinal metaplasia and peptic ulcer. These results indicated that CEA will be of more benefit for the diagnosis of gastric carcinoma or premalignant gastric lesions than that of SSEA-1.

Adolescent ; Adult ; Audiometry, Pure-Tone ; Ear Protective Devices ; utilization ; Humans ; Middle Aged ; Noise, Occupational ; prevention & control ; Young Adult

Chromosome Deletion ; Chromosomes, Human, Pair 15 ; genetics ; Humans ; Infant ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; genetics ; Male ; Mutation