Objective:To evaluate the efficacy and safety of tirofiban,a platelet glycoproteinⅡb/Ⅲa Inhibitor,in percutaneous coronary intervention(PCI)of patients with acute non-ST segment elevation myocardial infarct(NSTEMI).Methods:A total of 114 patients with acute NSTEMI were enrolled in the trial from Sep.2005 to Jan.2007;they were randomly divided into 2 groups:tirofiban group(n=57)and placebo group(n=57).Patients in tirofiban group were given tirofiban for 24 h after PCI.All patients were routinely given heparin,aspirin and clopidogrel before CPI.The composite occurrence of death,myocardial infarction(MI),need for target vessel revascularization(TVR)after PCI,and the adverse effects(hemorrhage and thrombocypenia)were compared between the 2 groups.Results:One(1.8%)patient had angina pectoris and the other(1.8%)developed subacute thrombus in control group within 24 h after PCl;there was no such event in the tirofiban group.Two(3.6%)patients developed angina pectoris and 2(3.6%) developed subacute thrombus within 30 days after PCI in control group;one patient(1.8%)in birofiban group developed angina pectoris and one patient in birofiban group developed subacute thrombus.Each group had one case(1.8%)of upper digestive tract bleeding during hospitalization.No intracranial hemorrhage,skin/ mucosa hemorrhage,thrombocytopenia,or-death occurred in the 2 groups.Intravenous tirofiban treatment reduced the composite occurrence of death of NSTEMI patients after PCI(P

Objective To investigate the protective effect of pretreatment with Shenfu injectio(SFI)on myocardium against ischemia-reperfusion(I/R)injury in diabetic rabbits.Methods Forty healthy adult male rabbits weighing 2.4-3.2 kg were used in this study.Type I diabetes mellitus was induced by intravenous alloxan 120 mg?kg~(-1) and confirmed by fasting blood glucose＞11.1 mmol?L~(-1).The animals were randomly divided into 5 groups(n=8 each):groupⅠsham operation;groupⅡI/R and groupⅢ,Ⅳ,ⅤSFI+I/R.I/R was produced by occlusion of the anterior descending branch of left coronary artery(LAD)for 60 min.The occlusion of LAD was then released for reperfusion.In sham operation group(Ⅰ)LAD was exposed but not occluded.In groupⅢ,ⅣandⅤSFI 5,10 and 15 ml?kg~(-1) was givenⅣrespectively 30 min before myocardial ischemia.MAP,HR,left ventricular developed pressure(LVDP),?dp/dt_(max),left ventricular end-diastolic pressure(LVEDP)and Vmax were recorded immediately before ischemia(T_0,baseline),at 5 min of ischemia(T_1),immediately before reperfusion(T_2)and at 5,15,60,90,120 min of reperfusion(T_(3-7)).The animals were killed and hearts removed for determination of infarct size and microscopic examination of the ultrastructure of LAD using transmission electron microscope.Results MAP,HR,LVDP,?dp/dt_(max) and Vmax were significantly decreased while LVEDP was significantly increased during reperfusion as compared to the baseline values at T_0 in I/R group. I/R produced myocardial infarct and damage to the endothelial cells of LAD.The harmful effect of I/R was attenuated by different doses of SFI.SFI 10 ml?kg~(-1) provided best effect.Conclusion Pretreatment with SFI can protect the myocardium against I/R injury in diabetic rabbits.SFI 10 ml?kg~(-1) produces better effect.

NS2 and NS3 are two post-transcriptional gene silencing suppressors that are encoded by Rice stripe virus. Gene silencing suppressors are always related to the pathogenicity of viruses. In this study, the cDNA of NS2 and NS3 were recombined by overlapping PCR assays, ligated to the RNAi vector, and inserted into the PXQ expression vector using Pst I; the expressed vector was transferred into calluses induced from seeds of the japonica rice cultivar, 'Nipponbare', using an Agrobacterium-mediated method. Thirty-one T0 transgenic plants were selected by G418 screening. PCR and southern blot analyses confirmed that the target gene was transformed into transgenic rice successfully, and different transgenic plants contained various copies of the gene. The disease resistance assay revealed that T0 transgenic rice had a delayed onset of RSV for approximately 10-20 d, and the accumulation of virus in the transgenic plants was reduced by 30%-50%. This was related to the delayed onset of disease.
Disease Resistance ; Oryza ; genetics ; immunology ; virology ; Plant Diseases ; genetics ; immunology ; virology ; Plants, Genetically Modified ; genetics ; immunology ; virology ; RNA Interference ; Tenuivirus ; genetics ; immunology ; Viral Nonstructural Proteins ; genetics ; immunology

Objective To study the effects of iodine deficiency during pregnancy on fetal iodine metabolism and thyroid function. Methods Wistar dams were randomly divided into four groups: severe iodine deficiency(SID), moderate iodine deficiency(MoID), mild iodine deficiency(MiID) and normal iodine(NI). All the dams were fed with iodine deficient food(iodine contents: 50 μg/kg) and drinking water with different doses of KI (0,54.9,163.8,381.7 μg/L) for 3 months till mating. Iodine was supplied at the dose of 1.24 μg/d(SID), 2.50 μg/d(MoID), 5.00 μg/d(MiID) and 10.00 μg/d(NI), respectively. The dams and their fetuses on gestation of 20 days were studied. Urine iodine of dams and iodine contents in fetal amniotic fluid were measured by As3+-Ce4+catalytic spectrophotometry using ammonium persulfate digestion. And blood iodine in pregnant rats and iodine contents in placental tissue were measured by As3+-Ce4+catalytic spectrophotometry in dry ash of samples in KClO3-ZnSO4-K2CO3-NaCl. Thyroid hormone levels in mother serum and in fetal amniotic fluid were detected by chemiluminascent assay, and their thyroid glands were weighted and carefully observed. Results ①Iodine content in urine and blood of pregnant rats and amniotic fluid of fetal rats reduced along with their decrease of iodine supply. Urine iodine median of rats in 4 groups(NI: 353.7 μg/L; MiID: 115.9 μg/L; MoID: 26.9 μg/L; SID: 0 μg/L) were statistically significant(χ2=32.884, P < 0.01). Blood iodine level in MoID and SID[(29.4±18.6), (11.7± 7.0)μg/L]was significantly lower than that in NI[(49.1±23.0)μg/L, P < 0.05 or < 0.01]. In iodine deficiency groups, there was a decreasing trend in iodine contents of fetal amniotic fluid[MiID: (48.3±23.1)μg/L; MoID: (29.2±14.7)μ/L; SID:(19.5±6.7)μg/L]and an increasing tendency in iodine contents of placental tissue [MiID: (0.57±0.26)μg/g, MoID: (0.53±0.34)μg/g; SID: (0.53±0.15)μg/g], but there was no statistical significance(P>0.05). ②In SID, TT4[(14.3±4.1)nmol/L]and FT4[(10.8±3.6)pmol/L]were lower than that in NI[(28.4±19.3)nmol/L, (20.2±8.0)pmol/L, P < 0.05 or < 0.01], while that in MoID[(22.1±6.1)nmol/L, (18.5±4.1)pmol/L]and MiID[(25.5±13.1)nmol/L, (18.6±8.4)pmol/L]were decreased without statistical significance(P > 0.05). And FT3/FT4 ratio(0.34±0.16), absolute[(48.4±22.7)mg]and relative weights[(144± 76)mg/kg]of thyroid gland in pregnant rats were respectively higher than that in NI[0.16±0.02, (19.5±3.1)mg, (66±10)mg/kg, P<0.01]. But that in MoID[0.19±0.04, (27.0±5.7)mg, (84±19)mg/kg]and MiID[0.17± 0.06, (25.0±8.9)mg, (78±25)mg/kg]were increased without statistical significance(P > 0.05). A visibly congestive enlargement thyroid was found in SID, while thyroid mildly enlarged in MoID and MiID. ③Compared with NI [(2.38±1.55)pmol/L,0.50±0.18], the FT4 levels [(1.07±0.87) pmol/L]in amniotic fluid were significantly decreased (P < 0.05) and the FT3/FT4 ratio (1.96±0.61) was significantly increased (P < 0.01) in SID. There were no statistical significances(P > 0.05) in other 3 groups[MiID: (2.77±0.90)pmol/L,0.46±0.15; MoID: (2.35±0.76)pmoL/L,0.61±0.21]. A visible thyroid enlargement with hyperemia was observed in SID fetus while in other 2 experiment groups their thyroids were only mildly congested. Conclusions Severe iodine deficiency during pregnancy can result in both mother and fetus overt hypothyroidism. The fetal thyroid hormone levels in mild iodine deficiency status is close to normal levels because of maternal and placental compensation. Moreover, both the dam and the fetus suffer from the negative effects in moderate iodine deficiency during pregnancy.

High glucose stimulated angiotensinⅡ(ATⅡ) production in mesangial cells of rat.Both high glucose and ATⅡdecreased expressions of matrix metalloprotein-9 (MMP-9) mRNA and MMP-9/tissue inhibitor of metalloproteinase-1 (TIMP-1) mRNA ratio and increased TIMP-1 mRNA expression in mesangial cells of rat,which could be reversed by an ATⅡreceptor blocker,Saralasin.

Objective To study effect of excessive iodine intake on sodium-iodide symporter(NIS)mRNA and protein expression of breast in lactating rats.Methods60 Wistar rats,having been weaned for one month,were randomly divided into three groups according to their body weights,I.e,①normal iodine(NI,30 rats);②ten fold high iodine(10 HI,15 rats);③one hundred fold high iodine(100 HI,15 rats).Eating food containing iodine of 300μg/L and drinking water of iodine at 5,1845,20 295μg/L,respectively.After fed for 3 months,the rats mated and had offspring,and urine and milk iodine of lactating rats were determined by As-Ce-catalytic spectrophotometric method.Their marmnary glands were sampled at lactation day 10.Then NIS mRNA expression by RT-PCR was determined and NIS protein by immunohistochemistry(SABC)was observed.Results The urine iodine of 10 HI group(3597.5μg/L)and 100HI group(25 404.3μg/L)increased obviously compared with that of NI group(344.7μg/L).The milk iodine of 10HI group(27.1×103μg/L)and 100HI group(191.0×1μg/L)was higher than that of NI group(6.0×103μg/L),but the increased fold of milk iodine was not paralleled with that of urine iodine.Difference of NIS mRNA expression was significant(F=24.19,P＜0.01)among the groups,and the NIS mRNA expression in 10HI(1.250±0.034)and 100HI(1.272±0.039)group were less than that in NI (1.532±0.044)group(P＜0.01).The breast NIS mRNA expression in lactating rats(1.532±0.044)was significantly higher than that in unlactating rats(0.879±0.018,P＜0.01).With the increasing iodine uptake,NIS protein expression decreased.Conclusions The NIS mRNA and protein in rat breasts is down-regulated by excessive iodine intake.So increasing extent of milk iodine concentration is inhibited,which is important to prevent off-spring from getting excessive iodine intake from parental generation.

Objective To investigate the expression of Mta-1 in bladder transitional cell carcinoma (BTCC)and to analyze its correlation with the clinical staging,pathologic grading,metastasis and recur- rence,and to explore the possible molecular mechanisms.Methods Samples of 42 cases of BTCC and 12 normal bladder mueosa tissues were examined with immunohistochemical analysis for the expression of Mta- 1,ER,u-PA and PAI-1.Endothelial cells were stained by anti-CD34,and microvascular density(MVD)of carcinoma tissue was calculated.The correlation of Mta-1 expression with the invasion,metastasis,angiogene- sis and recurrence of BTCCs was analyzed;and the correlation of Mta-1 expression with ER,u-PA,PAI-1,and MVD was also analyzed.Results The positive rate of Mta-1 expression in BTCCs was 73.8%(31/42) , while it was 0.0% in normal bladder mucosa tissues(P＜0.01).The expression level of Mta-l increased with the higher clinical stages and pathologic grades of BTCCs;it was higher in recurrence group(100.0% , 15/15)than in non-recurrence group(59.3%,16/27),and high in metastasis group(100.0%,14/14) than in non-metastasis group(60.7%,17/28)(P＜0.05).The expression level of ER increased with the lower clinical stages and pathologic grades of BTCCs;the positive rate of ER expression was 0.0% in 14 ca- ses with metastasis and was 53.6% in 13 of 28 cases without metastasis(P＜0.05);and the rate was 6.7% in 1 of 15 cases with recurrence and 44.4% in 12 of 27 cases without recurrence(P＜0.05).Negative cor- relation was found between Mta-1 and ER expression(r=-0.739,P＜0.01).The positive rate of u-PA ex- pression(59.5%,25/42)was significantly higher in BTCCs than that in normal bladder mucosa tissues (16.7%,2/12)(P＜0.05).Positive correlation was found between u-PA and Mta-1 expression(r= 0.875),while negative correlation was found between u-PA and PAI-1 expression(r=-0.535).The posi- tive rate of PAI-1 expression in normal bladder mucosa tissues(50.0%,6/12)was significantly higher than that in BTCCs(19.0%,8/42)(P＜0.05).In addition,negative correlation was found between PAI-1 and Mta-1 expression(r=-0.706).And positive correlation was found between MVD in BTCCs marked by an- ti-CD34 and Mta-1 expression(r=0.683).Conclusions Mta-1 is highly expressed in BTCCs,and it correlates closely with tumor pathologic grades,clinical stages,recurrence and metastasis.Mta-1 up-regulates the expression of u-PA and down-regulates that of PAI-1,which is associated with invasion and metastasis and acts as an angiogenic mediator in BTCCs.A negative correlation is found between Mta-1 and ER in inva- sion and metastasis of BTCCs.

Objective Take alkaline ashing method as golden standard to explore the accuracy of chloric acid digestion method in determination of human milk iodine. Methods Sixty one breast milk samples collected in Hexi district of Tianjin was measured by the method for determination of iodine in foodstuff by As3+-Ce4+ catalytic spectrophotometry (referred to as the alkaline ashing method) published in 2008 and the method for determination of iodine in urine by As3+-Ce4+ catalytic spectrophotometry(referred to as acid digestion) published in 1999, respectively. were highly correlated(r = 0.960, t = 26.3, P < 0.01), and the regression equation was (Y) = - 28.1 + 0.808X, in which X was independent variable, that is the results of alkaline ashing method; (Y) was dependent variable, that is the estimated data of chloric acid digestion method. The average difference of the results measured by the two methods was 68.3 μg/L, and the results from chloric acid digestion was 38.9% which lower than that of alkaline samples were diluted by 3,4 and 5-fold and then digested by chloric acid, the liquid clarification rates were 80.3% ashing and chloric acid digestion method were, respectively, 165.4, 110.0 μg/L. Conclusions Compared with alkaline ashing method, the results determined by chloric acid digestion method are significantly lower. It is suggested that there are systemic errors in chloric acid digestion method, which means that alkaline ashing method can not be replaced by the chloric acid digestion method.

Objective To explore the effect of short-term iron deficiency on thyroid function of rat and its mechanism, and to provide new clues and ideas for prevention and control of iodine deficiency disorders. Methods Twenty-two healthy SPF/VAF level weaning male SD rats were randomly divided into control group(iron content in diet was 65 mg/kg) and iron deficiency group(iron content in diet was 15 mg/kg) by body weight, and 11 in each group respectively. After 4 weeks feeding, body weight and thyroid glands weight were measured, and the relative weight of thyroid gland was calculated. Rat whole blood was collected and serum was separated. Hemoglobin, serum iron levels and total iron binding capacity were tested using biochemical assay;serum free iodine thyroid three original acid (FT3), free thyroxine (FT4) and thyroid stimulating hormone (TSH) levels were detected by chemiluminescence;after thyroid were fixed in formalin, embedded with paraffin and sectioned regularly, and immunohistochemical stained, the protein expression of thyroid peroxidase(TPO) was observed. Results Compared with control group [(243.8 ± 16.4)g], iron deficiency group of animals had less body weight[(214.3 ± 18.1 )g, t = 4.002, P ＜ 0.01];there was a lower absolute thyroid weight in iron deficiency group[(11.9 ± 1.6)mg]than in control group[(13.4 ±1.3)mg, t = 2.369, P ＜ 0.01], but no significant changes of the relative weight of thyroid gland between the two groups[(0.055 ± 0.004),(0.055 ± 0.006)g/kg, t = 0.162, P ＞ 0.05]. Hemoglobin and serum iron in iron deficiency group were ( 100.4 ± 8.9)g/L and (7.0 ± 0.8)μmol/L, which were less than that in control group[( 146.5 ±16.3)g/L, (26.1 ± 5.1 )μmol/L, t = 8.233,12.277, all P ＜ 0.01]. Total iron binding capacity in control group was (74.0 ± 4.6)μ mol/L and that in iron deficiency group[(124.8 ± 6.3)μmol/L], and the difference was significant (t = 21.531, P＜ 0.01). At the same time, their serum hormones FT3, FT4 and FT3/FT4[(4.71 ± 0.53), (29.69 ±2.63)pmol/L, 0.16 ± 0.02]were lower than that in control group[(5.69 ± 0.61),(31.98 ± 2.49)pmol/L, 0.18 ±0.01, t = 4.044,2.096,3.255, P ＜ 0.01 or ＜ 0.05]. The expression of TPO protein decreased in iron deficiency group than in control group. Conclusions Iron deficiency reduces thyroid function, which perhaps is due to the reduction of TPO activity. Combined supplementation of iodine and iron will possibly improve the prevention effect on iodine deficiency disorder in iron deficiency areas.

OBJECTIVETo search for a new method of screening for molecular targets for androgen-dependent prostate cancer.

METHODSWe collected tissue samples and paired serum samples from 3 cases of androgen-dependent prostate cancer (ADPC) treated by surgical resection, and included another 3 samples of benign prostatic hyperplasia (BPH) tissue and normal human serum in the control group. The total proteins extracted were separated and transmembrane by two-dimensional gel electrophoresis, followed by hybridization with the sera of the patients with ADPC and those with hormone-independent prostate cancer (HIPC) as the primary antibodies. The differentially expressed proteins were compared by Western blot, analyzed by MALDI-TOF-MS mass spectrography, and verified by RT-PCR and Western blot following bioinformatic identification.

RESULTSThis modified method exhibited a significantly better effect in displaying differentially expressed proteins, by which 12 differentially expressed protein spots were identified, including Beclin1, glutathione S-transferase P (GSTP1-1), ZBTB7, dihydrodiol dehydrogenase 2 (DDH), enolase (ENO1), glucose-dependent insulin-releasing peptide receptor (GIPR), Mn-superoxide dismutase (MnSOD), phosphoglycerate mutase 1 (PGAM1), amino-peptidyl-prolyl cistrons isomerase (PPIA), and phospholipid-PE-binding protein (PEBP). The mRNA and protein expressions of Beclin1 were significantly down-regulated in androgen-dependent prostate cancer tissues.

CONCLUSIONThis modified serum-guided immunoblotting technique has provided a new method for clarifying the molecular mechanisms of the occurrence and progression of HIPC, in which Beclin1-mediated autophagy may play a key role.

Biomarkers, Tumor ; blood ; Blotting, Western ; Humans ; Immunoblotting ; methods ; Male ; Mass Spectrometry ; Prostatic Neoplasms ; genetics ; metabolism ; Proteomics