Objective To investigate the geographical distribution of excessive iodine in drinking water and to demarc aI|e the excessive iodine regions in Hebei Province.Methods In 173 counties of Hebei Province, town was surveyed as an elementary unit.Five villages were sampled according to the direction of east,west, south,north,center in every town.If the water sources were more than 5 in a village,water was sampled according to the direction ofeast,west, south,north, center, respectively;If the water sources were less than 5 in a village, all were sampled:If the village used water of cental supply,only one sample wag collected.Arsenic-cerium catalysis was used to determine the iodine concentration of drinking water.Results Two thousands and forty-nine towns were investigated and 19 352 water samples were determined in Hebei Province.One hundred and seventy- two towns were confirmed to be excessive iodine areas,where the range of water iodine Wag 0.1～2840.4μg/L The water 8amDle with 18 358 had a water iodine median less than 150.0μg/L The areas with water iodine median less than 150.0μg/L,in between 150.0μg/L and less than 300.0μg/L,and equal to or more than 300.0 μg/L accounted for 94.86%,2.92%and 2.22%,respectively.There were 110 towns with water iodine median being between 150.0μg/L and iess than 300.0 μg/L and 62 towns with water iodine median equal to or more than 300 gμ/L.Exeessive iodine towns distributed in 33 counties of 6 cities involving 5 854 960 residents in'Hebei Provmce. MOBt of the water sources with excessive iodine Cangzhou were deep wells and there was a positive correlation between we depth and water iodine concentration (r=0.430,P<0.01), while they were shallow wells in Handan, Xingtai.Hengshui,and no correlation was found between well depth and water iodine concentration(r=-0.060,-0.119.-0.121,P>0.05).Conclusions Six cities have excessive iodine water resotlrees in Hebei Province, mostly in Handan.xingtai,Hengshui and Cangzhou Cities,which all are low-lying land.The water with excessive iodine is hypogene,and the towns with excessive iodine water distributein patchy or spot pattern.

Objective To investigate the effect of exogenous kallikrein on apoptosis of the neurons aroundthe cerebralinfarctareain rats. Methods Thirty rats wjth cerebral infarction induced by middle cerebral artery occlusion(MCAO)were assigned randomly into 3 groups(n=10),namely the blank control group,saline group,and pAdCMV-HTK group.In the pAdCMV-HTK group,kallikrein gene was delivered into the cerebral ischemie lesion via a replication-defective adenovims using stereotaetic injection technique, and the expression of exogenous kallikrein was detected immunohistoehemically.TUNEL staining was performed to evaluate the neuronal apoptosis around the infarct area,and RT-PCR used to detect the mRNA expressions ofbcl-2,bax and caspase-3 in the brain tissues. Results At 24 h aftertreatment there were some HTK expressed cells found in group C and peal(at 72 h after treatment.While compare with group B and group C,there existed significant difference(112±6.1,68±4.2,59±3.9,P<0.05).At 72 h after treatment,the NSS of group C was significantly lower than that ofgruop B and A(6.70±0.16,8.13±0.16,7.93±0.20,P<0.05);7 days after the treatment,the difference was more significant(5.14±0.18,7.82±0.14,7.91±0.10,P<0.01).Apoptotic cells were mostly seen around the infarct area.The ratsinpAdCMV-HTK group showed significantly reduced number of cells positive for TUNEL staining as compared to those in the saline and blank control groups at 3 days(10.1±0.9,16.7±1.1,and 20.4±0.8,respectively)and 7 days after the treatment(15.2±1.2,33.6±1.3,and 28.8±1.7,respectively)(P<0.05).The mRNA levels ofbc1-2.bax and caspasc-3 were elevated in all the groups at 24 h,peaked at 72 h,and decreased gradually till 7 days alter the treatment.Compared with those in the other two groups，bcl-2 mRNA level in the pAdCMV-HTK group increased slightly P>0.05) while bax and caspase-3 mRNA levels decreased markedly(P<0.05) 72 h and 7 days after the treatment.Conclusion Kallikrein can inhibit neuronal apoptosis around the cerebral infarct and improve the neurological fimction of rats following cerebral infarction probably by reducing the expressions of such apoptotic factors as bax and caspase-3.

Objective To investigate the effects ofkallikrein gene transfer on microvascularproliferation around the cerebral infarct and on the recovery of regional cerebral blood flow (rCBF)following ischemia/reperfusion injury in rats. Methods The rats with cerebral ischemia/reperfusioninjury induced by middle cerebral artery occlusion (MCAO) were randomly assigned into blank controlgroup, saline group, and pAdCMV-HTK treatment group and received corresponding injections into thetissues around the infarct area. Each group was divided into 3 subgroups (n=10) for observation at 12, 24and 72 h after the treatment. The neurological deficits of the rats before and after the treatment wereevaluated using neurological severity scores (NSS), and the expressions of exogenous human tissuekallikrein (HTK) and vascular endothelial growth factor (VEGF) in the brain tissues were detectedimmunohistochemically. TIC staining was performed to measure the changes in the infarct size.14C-iodoantipyrine tracing technique was used to define the rCBF in the rats. Results Compared tothe blank control group, the cerebral infarct size was significantly reduced in pAdCMV-HTK group 24 hafter the treatment, and was further reduced at 72 h (P<0.05). At 24 h after the treatment, the NSS inpAdCMV-HTK group was significantly lower than that in the blank euntrol and saline groups (P<0.05),and was further reduced at 72 h (P<0.01). After MCAO, the VEGF-positive cells were found mostly inthe cortex and the white matter around the infarct area. The expression of VEGF in pAdCMV-HTK groupwas markedly higher than that in the other two groups at 12, 24, and 72 h after the treatment (P<0.05). Inall the 3 groups, the rCBF around the infarct was slightly decreased as compared to that in thecontralateral hemisphere, pAdCMV-HTK slightly increased the rCBF 12 h after the injection (P>0.05),and significant increase in the rCBF occurred 24 h and 72 h after the injection (P<0.05). ConclusionKallikrein gene transfer following cerebral ischemia/reperfusion injury promotes vascular proliferationaround the infarct and increases the rCBF to reduce the infarct volume and attenuate neurological deficitsin rats.

Objective To explore the associations between fasting serum lipids and high-sensitivity C-reactive protein ( hsCRP).Methods Serum triglyceride ( TG),high-density lipoprotein cholesterol (HDL-C) and hsCRP were measured in residents of Chengdu,China.Subjects with potential factors which might influence lipids and hsCRP were excluded,580 subjects [ mean age ( 62.3 ± 6.6 ) years ; male:58.7％ ] were finally recruited by random sampling methods.Results There was a weak positive relationship between TG and hsCRP ( r =0.108,P =0.01 ) and a weak negative relationship between HDLC and hsCRP (r =- 0.197,P ＜ 0.001 ),this was also true in the sub-group with BMI ＜ 24 kg/m2 ( r =0.236,-0.140 respectively,all P ＜0.001 ).In subjects with BMI ＜24 kg/m2,the hsCRP concentration was significantly higher in subjects with higher TG or lower HDL-C ( all P ＜ 0.05 ).hsCRP increased in proportion with the degree of dyslipidemia.After adjusting for gender,age,TC,LDL-C,fasting blood glucose,systolic blood pressure,diastolic blood pressure,history of hypertension and diabetes,smoking and alcohol drinking,logistic regression analysis showed that the odds ratio for increased hsCRP was 1.970 in subjects with either increased TG or lower HDL-C (P =0.105) and 9.098 in subjects with both higher TG or lower HDL-C levels (P =0.031 ).However,the observed relationship between TG,HDL-C and hsCRP in subjects with BMI ＜ 24 kg/m2 could not be observed in subjects with subjects with BMI ＞ 24 kg/m2despite significant more cardiovascular risk factors in these subjects.Conclusions A weak positive correlation between TG and hsCRP as well as a weak negative correlation between HDL-C and hsCRP was evidenced in the whole cohort suggesting dyslipidemia might be related to enhanced inflammatory status.However,this relationship is not observed in subjects with BMI ＞ 24 kg/m2 despite existence of more cardiovascular risk factors in these subjects.

Objective The impact of late incomplete stent apposition(ISA)post sirolimus eluting stent(SES)implantation in patients with acute coronary syndrome(ACS)on long-term clinical outcomes remainB controversial.The alm of the present study was to eva]uate the association between late ISA and clinical outcomes in patients with ACS compared with that with stable angina(SA).Methods From February 2005 to March 2007,54 ACS patients and 83 SA patients were enrolled in this study,late ISA was determined by meallS of threc-dimensional volumetric intravaaculair ultrasound(IVUS)analyses one year after SES implantation and clinical outcomes one year post IVUS were obtained in these patients.Results In 219 treated lesions of the 137 patients,late ISA wag documented in 25 lesions in 16 patients(20 ISA in 12 ACS patients vs.5 ISA in 4 SA patients,P＜0.001).Thoush lunlen area in reference and stented segment,neointimal hyperplasia(NIH)area and percentage of NIH in stented segment,and external elastic membrane(EEM)area in reference segment were similar between two groups,EEM area in stented segment [(15.34±5.44)mm2vs.(13.83±4.51)mm2,P=0.026],stented/reference segment EEM area ratio (1.13±0.22 vs.1.02±0.18,P＜0.001),plaque and media area[(8.43±3.93)mm2vs.(7.01±2.93)mm2,P=0.002]was significantly lager in ACS group than that in SA group.Multivariable logistic analysis showed that ACS(OR 6.477 with 95%CI from 2.297 to 18.263,P＜0.001)and stent length≥23 mm(OR 3.680 with 95% CI from 1.181 to 11.469,P=0.025)were main independent factors of occurrence of late ISA.Incidence of main adverse cardiac events(MACE)one year post IVUS Wag similar between the two groups.Conclusion Compared with patients with SA,ACS patients had larger stented segment EEM area,plaque and media areaas well as increased incidence of ISA.However,the incidence of MACE was similar in ACS and SA patients one year after IVUS.

Objective To evaluate the pharmacokinetics of multiple dose of antofloxacin hydroehloride tablet under fast and food state in Chinese healthy subjects.Methods A randomized,open and multiple dose study was conducted.Three dose groups with 16 subjects per group were given the dose of 200,400 and 600 mg antofloxacin hydrochloride tablet,once daily for 7 days respectively.8 subjects (4 male and 4 female) were administrated under fast state and 8 subjects (4 male and 4 female) under food state in each dose.The concentrations of antofloxacin in plasma and urine were determined by HPLC method.Results The main pharmacokinetics parameters of three dose (200,400 and 600 mg) under fast at first day were as follows:Cmax were (2.23 ±0.38),(4.59 ± 1.40),(5.03 ±0.77)mg · L-1,t1/2βwere(11.99 ±3.31),(10.97 ±5.33),(14.39 ± 1.63)h,tmax were (1.37 ±0.78),(2.04 ± 1.42),(2.90 ±2.02)h,AUC0-t were (27.61 ±6.14),(51.77 ±22.09),(73.62 ±10.14)mg · L-1 · h,AUC0-∞ were (38.28 ± 13.49),(72.28 ± 42.80),(108.91 ± 13.26) mg · L-1 · h,V/F were (92.84 ± 12.98),(91.90±14.55),(116.28±22.62)L,CL/F were (5.73 ±1.71),(7.67 ±4.65),(5.58 ±0.66)L· h-1,respectively;under food state at first day,Cmax were (2.36 ± 0.43),(4.11 ± 1.53),(5.60 ± 1.00) mg · L-1,t1/2β were (14.37 ±4.34),(11.25 ±5.39),(15.53 ±2.94) h,tmax were (2.69 ± 1.62),(2.40 ± 1.50),(2.65 ±1.29)h,AUC0-t were (33.69 ±4.00),(48.07 ±22.19),(78.01 ±17.18)mg · L-1 · h,AUC0-∞ were (50.71 ± 8.86),(67.37 ± 41.98),(121.31.66 ± 33.54) mg · L-1 · h,V/F were (81.04 ± 16.35),(106.32 ±34.33),(114.08±20.00)L,CL/Fwere (4.07 ±0.82),(8.28 ±5.29),(5.23 ±1.18)L · h-1,respectively.After 7 days,the main pharmacokinetics parameters of three dose (200,400 and 600 mg) under fast were as follows:Cmax were (3.69 ± 1.39),(7.54 ± 2.95),(8.50 ± 0.93) mg · L-1,t1/2β were (25.22 ± 3.34),(19.56 ±12.47),(15.95 ±2.85)h,tmax were (1.64±1.29),(1.31 ±0.79),(1.60±1.07)h;AUC0-twere (72.29 ± 24.00),(142.96 ± 67.20),(180.81 ± 35.33) mg · L-1 · h,AUC0-∞ were (75.90 ± 25.46),(148.26 ±69.86),(183.30±35.11)mg · L-1 · h,V/F were (184.77 ±52.51),(119.22 ±53.92),(118.91 ±30.13) L,CL/F were (5.06 ± 1.18),(4.75 ± 1.72),(5.15 ±0.72)L · h-1;under food state,Cmax were (3.53 ± 1.06),(6.54 ±1.43),(8.52 ±1.80)mg · L-1,t1/2βwere (24.08 ±6.12),(20.64 ±9.16),(18.69 ±6.49)h,tmax were (2.94 ± 1.02),(1.96 ± 1.05),(2.69 ±0.96)h,AUC0-t were (94.71 ±31.03),(142.17 ±52.46),(211.34.01 ±52.99)mg · L-1 · h,AUC0-∞were (99.32 ±33.93),(149.77 ±55.19),(213.76 ±53.00)mg· L-1 · h,V/F were (139.40±37.39),(140.24±71.11),(130.20 ±71.09)L;CL/F were (4.11 ±1.13),(4.81 ± 1.17),(4.69 ± 0.88)L · h-1.Urinary recovery rates after 7 days doses from zero to 120 h were (67.24±13.56)％,(68.62±14.45)％ and (74.31 ±12.99)％,respectively.Conclusion Food had no obvious influence on pharmacokinetics parameters after multiple oral dose of 200,400 and 600 mg antofloxacin hydrochloride tablet under fast and food state,except that tmax increased.There was no accumulation in human body.It can be considered that food had no effect in the clinical use of antofloxacin hydrochloride tablet.