Objective To learn the control status of iodine deficiency disorders in Baoji City of Shaanxi Province.Methods From 2009 to 2011,according to the National Iodized Salt Monitoring Program,the iodized salt was monitored,and thyroid was examined in 12 counties(areas) of Baoji City.According to rural and urban area stratification,60 children aged 8 to 10 were selected in each county(district),and their urine samples were collected for determination of iodine content.In 2011,per capita daily salt intake was surveyed by the three weighing method at children's home whose urine was collected.Chencang Area,Fufeng County and Taibai County,representatives of Baoji City different geomorphic features were selected for investigation of water iodine,and urinary iodine of pregnant and lactating women,and 15 people were selected in each county (district).Results From 2009-2011,in the 12 counties(areas) in Baoji City,the coverage rate of iodized salt was all 100.00％(3468/3468); the qualified rate of iodized salt and the consumption rate of qualified iodized salt were all ＞ 99.00％.Children's goiter rate was 3.41％(87/2548),3.06％(77/2520) and 3.33％(84/2520),and they were all less than that of the national standard (＜ 5％).Medians of urinary iodine of 8-10 years old children were 368.20,293.80 and 332.50 μg/L,respectively,and the ratios of urine iodine ≥300 μg/L were accounted for 66.42％ (797/1200),48.05％(692/1440) and 56.67％(816/1440),respectively.Median urinary iodine of pregnant women was 301.81 μg/L and lactating women was 329.79 μg/L.A total of 1116 households were investigated,the median of per capita daily salt intake was 8.9 g.Eighteen water samples were collected,range of water iodine value were 0.60-10.25 μg/L.Conclusions Iodine nutrition in general population of Baoji City is exceeded the optimum level,and the current iodized salt concentration has some down space,but fully consideration should be taken on iodine needs in different iodine deficiency areas and among different groups of people.

Objective To learn the existing state of Keshan disease and its trend in Baoji City,and to provide a scientific basis for control of the disease.Methods Feng,Qianyang,Linyou and Long Counties,the Keshan disease affected areas were selected to carry out the case study,and Keshan cases were searched from all registered cases of myocardial patients of the past three years at county-level medical institutions and hospitals of townships(towns).Thirteen villages affected by Keshan disease in Qianyang,Fengxiang,Feng,Linyou and Long Counties were selected as monitoring points to carry out a intensified monitoring.All subjects were surveyed by comprehensive clinical physical examination and 12-lead ECG tracings,and they were diagnosed according to the Keshan disease diagnostic criteria.Ten households were selected randomly in each monitoring point(village),and self-produced wheat samples and adult subject's occipital hair samples were collected for detecting selenium levels.Results Seven hundred and forty-six cardiac cases which containing 17 cases of chronic Keshan disease were discovered in 32 medical institutions,and there were no acute and subacute type of Keshan disease patients.Five thousand seven hundred and twenty-three subjects were examined in the 13 monitoring sites,and 65 cases of Keshan disease were diagnosed which including 17 cases of slow and 48 cases of potential Keshan disease,and no acute or subacute case was found.The total detection rate was 1.14％,and the detection rate ranged from 0 to 2.86％.Hair selenium mean was 0.420 mg/kg; wheat selenium mean was 0.079 mg/kg.Conclusions The Keshan disease detection rate of Baoji City is at a low level.The selenium level of local residents has reached the level of non-endemic area.Constant detection of patient with Keshan disease means various control measures should be reinforced.The comprehensive monitoring program,such as monitoring people's in vivo and in vitro selenium level and others,should be established as soon as possible.

Objective To investigate the causes and preventive measures of hepatic failure during perioperative period of liver resection for primary hepatic carcinoma in the elderly patients, and to explore its diagnosis and treatment. Methods The 62 patients with primary hepatic carcinoma undergoing hepatectomy were analyzed retrospectively, and they were divided into two groups: elderly group (age≥60 years) and non-elderly group (age＜60 years). The influencing factors for damage of hepatic function were analyzed using single variant and multivariate stepwise regression analysis in elderly and non-elderly group, pringle maneuver and non-pringle maneuver group, more (≥500 ml)and less (＜500 ml) amount of bleeding group. Results The incidence of hepatic damage and mortality rate induced by hepatic failure were 32. 6% and 1.6% respectively after liver resection for primary hepatic carcinoma. Single variant analysis showed that pringle maneuver, intraoperative blood loss, blood transfusion and size of tumor were associated with postoperative hepatic function.Furthermore, multivariate stepwise regression analysis revealed that pringle maneuver was the independent risk factor associated with postoperative hepatic function (β = 0. 314, t= 2. 272, P ＜0. 05). Conclusions The postoperative hepatic damage is significantly correlated with pringle maneuver and intraoperative bleeding in liver resection for hepatocellular carcinoma in senile people.And improving operative techniques, shorting the time of pringle maneuver, decreasing intraoperative bleeding were the main preventive measures for hepatic damage after liver resection for primary hepatic carcinoma in the elderly patients.

Objective To investigate the protective effects of midazolam on noise-induced hearing loss in guinea pigs by testing reactive oxygen species (ROS) level in the cochlea and plasma SOD and MDA. Methods Totally forty male pigmented guinea pigs were randomly divided into four groups: control (C) , midazolam (M), normal saline (S) and noise-induced deafened (D) groups, with ten guinea pigs in each. Groups M, S and D were exposed to a continuous noise (4kHz , octave band, 100dB SPL) 3h every day for 3 consecutive days. Group M was treated with midazolam, which was administered intramuscularly (0.1mg/kg) 24h before noise exposure, and immediately upon and during noise exposure. Group S was exposed to noise and treated with the same volume of normal saline intramuscularly, the time of injection was the same as that of Group M. Group C was not exposed to noise, but was treated with midazolam intramuscularly, the time of injection and the dosage were the same as those of Group M. Group S was exposed to noise and treated with normal saline intramuscularly ,the time of injection was same with that of Group M.Group D was exposed to noise only. All animals received auditory brainstem response (ABR) threshold recording before and immediately after noise exposure. Blood was collected when the guinea pigs were killed after the last ABR threshold recording, and serum SOD activity and MDA content were detected. Both the cochleae were removed and prepared for ROS assay. Results After noise exposure, ABR threshold shift (1.6±1.5) and ROS content [(291.10±2.30)u/mL] in Group M were significantly lower than those in Groups S and D [41.7±3.3, 44.3±3.9; (348.52±3.60)u/mL, (315.56±6.70)u/mL, P<0.05]. Serum SOD activity and MDA content were significantly increased in Group M, but the amplitude was less than that in Groups S and D.Conclusion Midazolam can prevent noise-induced hearing loss by reducing the increased ROS level in the cochlea after noise exposure.

Humans ; Infant, Extremely Low Birth Weight ; Infant, Newborn ; Infant, Premature ; Treatment Outcome

Female ; Fluoroscopy ; Humans ; Intubation, Intratracheal ; Male ; Middle Aged ; Tracheotomy ; methods

OBJECTIVE: To investigate the self-renewal mechanism of CD133+ cancer stem cells from Hep-2 cell line. METHOD: The CD133+ cells were sorted by flow cytometry from Hep-2 cell line. Then the sorted CD133+ cells were cultured in RPMI1640. The ability of self-renewal of CD133+ cells were tested by MTT assay. mRNA and protein expression of self-renewal related genes were detected by western blot and RT- PCR. RESULT: (3.10 ± 0.21)% of Hep-2 cells expressed the membrane antigen CD133. CD133+ fraction was raised to (90.20 ± 5.51)% by flow cytometry. In vitro culture and growth curve showed CD133+ cells had more active proliferation ability than CD133- cells, which showed statistically significant difference between these two group (P < 0.01). RT- PCR and western blot results showed upregulated mRNA and protein expression of Fas, c-myc, survivin in CD133+ group (P < 0.01). In the same time, the ratio of Bcl-2/Bax gene expression was obviously increased in CD133+ group. Self-renewal related gene such as β-catenin, SHH, SMOH and Bmi-1,Gli-1 were all up-regulated in CD133+ group both in mRNA and protein. On the contrary, PTCH gene was down-regulated. CONCLUSION CD133 positive cells are a small proportion of a Hep-2 cell line. The results of this experiment verified that CD133 positive cells owned the properties of cancer stem cells. Upregulated anti-apoptotic gene is the foundatiom of self-renewal mechanism of CD133+ cells. Cancer stem cells related signal pathways such as Hedgehog, Wnt and Bmi-1 pathway are in state of activation. The identification of self-renewal mechanism about cancer stem cell provides a powerful tool to investigate the tumorigenic process in the larynx and to develop therapies targeting to these signal pathways.
AC133 Antigen ; Antigens, CD ; Apoptosis ; Cell Physiological Phenomena ; physiology ; Down-Regulation ; Flow Cytometry ; Glycoproteins ; Humans ; Laryngeal Neoplasms ; Neoplastic Stem Cells ; physiology ; Patched Receptors ; Patched-1 Receptor ; Peptides ; Receptors, Cell Surface ; genetics ; metabolism ; Signal Transduction ; beta Catenin ; genetics

AIM: To elucidate the role of mitochondrial DNA (mtDNA) deletion in the pathogenesis of viral myocarditis in mice. METHODS: 50 BALB/c mice were divided into two groups randomly. 40 were experimental group, each of them was injected 0.1 mL Eagle liquids with CVB_3 (TCID_ 50=108) intraperitoneally. Another 10 mice were given equal volume Eagle liquids as control group. Cardiac functions in vivo and mtDNA 3867 deletion rate in myocytes were detected separately at the day 3, 11 and 24 after injection. The correlation of mtDNA 3867 deletion rate to cardiac functions was analyzed using Spearman method. RESULTS: At the day 3 after injection, mtDNA 3867 deletion rate in experimental group was 8.3 times higher than that in control group [(0.01970?0.00118)% vs (0.00211?0.00032)%,P

In order to investigate the impairment of mitochondrial membrane phospholipid localization and DNA(3867) (mtDNA(3867)) deletion and the correlation between cardiac and skeletal muscle cells in mice with viral myocarditis, 50 BALB/c mice were divided into two groups randomly. In experimental group (n=40), the mice were intraperitoneally injected with 0.1 mL Eagle liquid with CVB3(TCID50=10(8)), while in the control group (n=10), the mice were subjected to equal volume of Eagle liquid. The impairment of mitochondrial membrane phospholipid localization and mtDNA(3867) deletion rate of cardiac and skeletal muscle were detected separately at day 3, 11 and 24 after injection. The correlation of mitochondrial membrane phospholipid localization and mtDNA(3867) deletion rate between cardiac and skeletal muscle cells cells was analyzed using Spearman method. At the day 3 after injection, in both cardiac and skeletal muscle cells, mtDNA(3867) deletion rate was significantly higher in experimental group than in control group (P<0.05), but the localization of mitochondrial membrane phospholipid showed no difference between two groups (P>0.05). At day 11 after injection, the mtDNA(3867) deletion rate of both cells in experimental group was increased to the peak level (P<0.05), and the impairment of mitochondrial membrane phospholipid localization of both cells also increased markedly in experimental group as compared with control group (P>0.05). At the day 24 after injection, the impairment of mitochondrial membrane phospholipid localization and mtDNA(3867) deletion of both cells showed a recovery tendency, but still severer than those at the day 3 after injection (P<0.05). The impairment of mitochondrial membrane phospholipid localization and mtDNA(3867) deletion were consistent and synchronistic between cardiac and skeletal muscle cells, and showed good correlations (P<0.05). The impairment of mitochondria plays an important role in the pathogenesis of viral myocarditis, and the skeletal muscle cells might act as a peripheral "window" to reflect the mitochondrial damage of cardiac myocytes.

Objective: To investigate the effects of human tissue inhibitor of matelloproteinase 4 (TIMP 4) on vascular smooth muscle cells (VSMCs) migration and the neointimal formation after balloon injury in rats. Methods: The cultured VSMCs were transfected with an adenoviral vector containing human TIMP 4 gene, AdTIMP 4. Effect of TIMP 4 on VSMC migration was investigated by monolayer cell scrape. AdTIMP 4, control adenoviral vector or PBS was transduced into the rat carotid artery from the adventitial after carotid artery injury. Cell number within the internal elastic lamina 4 days after gene transfer was counted and neointima/media area ratio 28 days after gene transfer was calculated. Results: The migration distance of VSMCs infected with AdTIMP 4 was inhibited markedly. Morphometric analysis demonstrated a statistically significant reduction in the number of cells migrated into neointima compared with controls [(32.5?4.8) cells per section, (33.8?7.0) cells per section and (8.2?2.4) cells per section for uninfected, AdGFP treated and AdTIMP 4 treated arteries, respectively]. There was a reduction of intima/media ratio of TIMP 4 treated group by 66.5% compared with control groups 28 days after gene transfer ( P