Objective To discuss the combined value of gray-scale ultrasound ( GSUS) and contrast-enhanced ultrasound (CEUS) in the diagnosis of benign and malignant thyroid lesions and to explore the optimal diagnostic point of scoring method .Methods Ultrasound images of 178 thyroid lesions confirmed by pathology were synthetically reviewed by scoring 5 GSUS indicators including shape , orientation, interior echogenicity, halo sign, microcalcification and 6 CEUS indicators including relative arrival time of microbubbles in the periphery and interior, peak periphery and interior echogenicity, peripheral ring-enhancement, and homogeneity of enhancement .One positive indicator scored one point .The optimal diagnostic points and their clinical value were explored according to ROC curves .Results Scores of GSUS, CEUS and the combination of GSUS and CEUS were significantly different (Z =10.188,9.843,10.705,all P <0.001). Areas under ROC curves of GSUS, CEUS and the combination of GSUS and CEUS were 0.936, 0.919 and 0.964, respectively.Three or more positive GSUS indicators of five in a thyroid lesion predicted that the thyroid lesion was malignant , with the sensitivity of 79.6% and the specificity of 91.2%.Two or more positive CEUS indicators of six in a thyroid lesion predicted that the thyroid lesion was malignant , with the sensitivity of 91.8% and the specificity of 81.2%.Five or more positive GSUS and CEUS indicators of eleven in a thyroid lesion predicted that the thyroid lesion was malignant , with the sensitivity of 93.6%and the specificity of 92.3%.The areas under the ROC curve of GSUS and CEUS were 0.936 and 0.919.The area under the ROC curve of the combination of GSUS and CEUS was 0.964, larger than the areas under the GSUS ROC curve and the CEUS ROC curve.Conclusion Ultrasound is valuable in the differential diagnosis of benign and malignant thyroid lesions , and the combination of GSUS and CEUS is the most valuable with 5 points as the optimal diagnostic scoring method .

Objective To analyze the change trends of death situation caused by cerebral apoplexy and myocardial infarction in Chongqing from 2006 to 2010 .Methods All death cases of cerebral apoplexy and myocardial infarction from the five years of 2006 to 2010 were extracted from the direct network report system covering the whole crowd death causes in Chongqing and performed the statistical analysis .Results The constituent ratio of cerebral apoplexy death was increased from 13 .94% to 16 .71% in these five years ,while which of myocardial infarction death in all death causes was stabilized around 4% .The sex ratio of male to female for cerebral apoplexy was descended from 1 .76∶1 .00 to 1 .43∶1 .00 in these five years ,while which for myocardial infarction was dropped from 1 .44∶1 .00 to 1 .30∶1 .00 ;which of cerebral apoplexy and myocardial infarction below 75 years old tended to de-cline ,while which above 75 years old tended to rise .Conclusion The cerebral apoplexy harm to Chongqing people′s life is increas-ing ,while the harm caused by myocardial infarction changes little ;the constituent ratio of female death caused by cerebral apoplexy and myocardial infarction is rising ;the cerebral apoplexy and myocardial infarction damage to old people above 75 years old is grea-ter ,and this damage still continues to grow .

Aged ; Angina, Unstable ; blood ; drug therapy ; pathology ; Capsules ; Drugs, Chinese Herbal ; therapeutic use ; Endothelial Cells ; drug effects ; pathology ; Female ; Humans ; Male ; Middle Aged ; Phytotherapy

AIMTo determine whether activation of kappa-opioid receptor with U50,488H, a selective kappa-opioid receptor agonist, produces any changes in electrical uncoupling during prolonged ischemia and whether these changes in electrical uncoupling is associated with the cardioprotection induced by kappa-opioid receptor activation, and to explore the possible mechanism.

METHODS(1) To observe the effect of U50,488H (10(-7), 10(-6), 3 x10(-6) and 10(-5) mol/L), a selective kappa-opioid receptor agonist, or with a selective kappa-opioid receptor antagonist nor-BNI (5 x 10(-6) mol/L), or with a mitochondrial K(ATP) channel inhibitor 5-HD on myocardium during ischemia/reperfusion in isolated perfused rat heart. Parameters of measurements include hemodynamic data, formazan content, heart rate, coronary flow, and lactate dehydrogenase (LDH). (2) To examine the effect of U50,488H of different concentration on electrical coupling parameters (including onset of uncoupling, plateau time, slope, and fold increase in r1) during 70 min myocardial ischemia in isolated perfused rat heart.

RESULTS(1) Pretreatment with U50,488H concentration dependently increased formazan content and reduced LDH release induced by 30 min of ischemia and 120 min of reperfusion. (2) The onset of electrical uncoupling and plateau time during prolonged ischemia was delayed by kappa-opioid receptor activation with U50,488H. (3) Linear regression analysis shown that the increase in formazan content and decrease in LDH release produced by kappa-opioid receptor activation was associated with delayed electrical uncoupling during prolonged ischemia. (4) The effects of U50,488H on formazan content, LDH release and on electrical coupling were abolished by nor-BNI, or 5-HD.

CONCLUSIONThis results demonstrate that the onset of electrical uncoupling during prolonged ischemia is delayed by kappa-opioid receptor activation with a selective kappa-opioid receptor agonist U50,488H, and that delayed electrical uncoupling is associated with the cardioprotection induced by kappa-opioid receptor activation with U50,488H. These effects of kappa-opioid receptor activation with U50,488H are mediated by mitochondrial K(ATP) channels.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer ; pharmacology ; Animals ; Antihypertensive Agents ; Heart ; drug effects ; physiopathology ; In Vitro Techniques ; Male ; Myocardial Ischemia ; physiopathology ; Myocardium ; metabolism ; Naltrexone ; analogs & derivatives ; pharmacology ; Potassium Channels ; metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Opioid, kappa ; agonists

Objective To investigate the feasibility of 18G trocar for central venous catheterization in adults.Methods Retrospective analyzed the clinical data of 60 patients with central venous catheterization under local anesthesia.These patients were randomly divided into the control group and the observation group.Selected the internal jugular vein as the site of the puncture catheter.The control group was punc-tured by conventional puncture needle while the observation group was punctured by the 18G trocar.Results There was no statistical differ-ence between the two groups in the success rate of final puncture and catheterization(P>0.05).Compared with the control group,the suc-cess rate of guidewire insert was higher,the puncture operation time was shorter,the pain score during puncture operation was lower,and post-operative patient satisfaction was higher in the observation group.The differences of the two groups were statistically significant(P<0.05). Conclusion 18G trocar can perform central venous catheterization successfully.This method has great advantages for awake patients,and it also worked in some cases with difficult wire insertion.

AIMTo determine whether the cardioprotection of ischemic postconditioning and heptanol in ischemic heart against ischemia/reperfusion (I/R) is mediated by gap junction.

METHODSThe effect of ischemic postconditioning, heptanol at different doses (0.03, 0.06, 0.30, and 0.60 mg/kg) and AAP10 (10 mg/kg) on the intact rat heart during 30 min ischemia and 2 h of reperfusion was observed. Ischemic postconditioning was achieved by 3 cycles of 10 s reperfusion/10 s regional ischemia starting at the beginning of the reperfusion. The infarct size and the arrhythmia scores were measured. The effect of ischemic postconditioning, heptanol at different doses (0.05, 0.10, 0.50 and 1.00 mmol/L) and AAP10 (1 x 10(-7)mol/L) on the isolated heart during 30 min ischemia and 2 h of reperfusion was observed. Ischemic postconditioning was achieved by 6 cycles of 10 s reperfusion/10 s global ischemia starting at the beginning of the reperfusion. The arrhythmia scores and conduction velocity of ventricle muscle were measured.

RESULTSIn the intact rat heart model, ischemic postconditioning and heptanol reduced infarct size and arrhythmia scores. In the Langendorff perfused rat heart model, ischemic postconditioning and heptanol reduced arrhythmia scores and conduction velocity of ventricle muscle. Administration of AAP10, an opener of gap junction attenuated the cardioprotection of ischemic postconditioning and heptanol.

CONCLUSIONThe cardioprotection of ischemic postconditioning and heptanol may be related to the attenuation of gap junction communication on myocardiac ischemia/reperfusion injury.

Animals ; Gap Junctions ; physiology ; Heptanol ; pharmacology ; Ischemic Postconditioning ; methods ; Male ; Myocardial Ischemia ; physiopathology ; Myocardial Reperfusion Injury ; physiopathology ; prevention & control ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo determine the effect of activation of lambda-opioid receptor with U50, 488H, a selective kappa-opioid receptor agonist, on the changes in electrical coupling during prolonged ischemia and to explore the possible mechanism.

METHODSThe isolated rat heart was perfused in a Langendorff apparatus. The effect of U50, 488H on electrical coupling parameters including onset of uncoupling, plateau time, slope and fold increase in r(t) was observed in isolated perfused rat heart subjected to global no-flow ischemia. The effect of U50, 488H on connexin 43 (Cx43) expression of ventricular muscle during ischemia was determined by immunohistochemistry.

RESULTSIn the prolonged ischemia model, U50, 488H concentration dependently delayed the onset of uncoupling, increased time to plateau, and decreased the maximal rate of uncoupling during ischemia. The effect of U50, 488H on electrical uncoupling parameters during ischemia was abolished by a selective kappa-opioid receptor antagonist nor-BNI or a PKC inhibitor chelerythrine. The amount of Cx43 immunoreactive signal in ventricular muscle was greatly reduced after ischemia. U50, 488H markedly increased Cx43 expression during ischemia and its effect was also attenuated by nor-BNI or chelerythrine.

CONCLUSIONThese results demonstrated that U50, 488H delayed the onset of uncoupling and plateau time, decreased the maximal rate of uncoupling and increased Cx43 expression of ventricular muscle during ischemia, and these effects of U50, 488H were mediated by kappa-opioid receptor, in which activation of PKC was involved. The effect of U50, 488H on electrical coupling during ischemia was probably correlated with preservation of Cx43 in cardiac muscle.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer ; pharmacology ; Animals ; Benzophenanthridines ; pharmacology ; Connexin 43 ; metabolism ; Female ; Heart ; drug effects ; In Vitro Techniques ; Myocardial Ischemia ; metabolism ; physiopathology ; Myocardium ; metabolism ; Naltrexone ; analogs & derivatives ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Opioid, kappa ; metabolism ; Signal Transduction ; drug effects

Objective To study the effect of different levels of iodine nutrition on secretion of placental hormone in pregnant rats.Methods Two hundred and twenty five Wistar rats (165 female,60 male),weighing about 80 - 100 g were used in the study.Female rats were randomly divided into five groups according to their body weights:low iodine group Ⅰ(LⅠ),low iodine group Ⅱ (LⅡ),adequate iodine(control) group(Al),high iodine group Ⅰ ( HⅠ ),and high iodine group Ⅱ (H Ⅱ ),and 33 rats in each group.Animals in the low iodine groups were fed low-iodine diet,the iodine content was 13.46 μg/kg,in addition,these rats drank deionized water which containing potassium iodated,the dose was 0 and 5 μg/L,respectively.The rats of adequate and the two high iodine groups were fed normal diet,the iodine content was 22.00 μg/kg,they also drank deionized water,containing potassium iodated 50,3000,and 10000 μg/L,respectively.The rats mated after 3 months of feeding,and were respectively sacrificed at early pregnancy(5 ± 2)d,second trimester( 12 ± 2)d,and third trimester of pregnancy(17 ± 2)d,and then their serum was taken.Serum human chorionic gonadotropin(HCG),human chorionic thyrotropin(HCT),and progesterone were measured by enzyme-linked immunosorbent assay (ELISA).Results In the third trimester,the serum levels of rat HCG were significantly different between groups(F =4.16,P ＜ 0.05).The means of rats serum HCG of the two low iodine groups [ (16.08 ± 4.45),(17.43 ± 2.70)U/L] were significantly higher compared with that of AI group[ (13.68 ± 3.52)U/L] in the third trimester(all P ＜ 0.01 ).In the second and third trimester,the levels of rats serum HCT were significantly different between groups(F =3.59,3.40,all P ＜ 0.05).The means of rats serum HCT of HI group [(70.11 ± 10.97)μU/L] in the second trimester and HII group[(74.93 ± 13.22)μU/L] in the third trimester were higher than those of AI group[ (57.14 ± 12.56),(58.17 ± 8.54)μU/L] significantly(all P ＜ 0.01 ).There were statistical differences of the means of serum progesterone among trimester of pregnancy(F =4.06,4.43,all P ＜ 0.05).The level of serum progesterone of the third trimester[ ( 1462.80 ± 286.48 )pmoL/L] compared to those of the first[ (1929.93 ± 158.37) pmol/L] and the second trimester[ (1856.44 ± 542.08)pmol/L] was decreased significantly(all P ＜ 0.05) in LI group.In the control group,the level of serum progesterone of the second trimester [ (2046.45 ± 475.67)pmol/L ] was significantly higher than the first trimester[ (1714.39 ± 461.71 )pmol/L,P ＜ 0.05 ].Conclusions During pregnancy,placenta could promote HCG secretion under iodine-deficient conditions.In addition,the placenta increases the secretion of HCT under conditions of excess iodine.In the condition of severe iodine deficiency,the secretion of serum progesterone decreases,and further decreases with prolongation of pregnancy,but it is opposite to the change of HCG during pregnancy.This phenomenon could lead to harmful pregnant outcomes easily.

ObjectiveTo study the mRNA expression of rat Insulin-like growth factors- Ⅰ (IGF- Ⅰ ) and Transforming growth factor-β1 (TGF-β1) in thyroid and placenta with different iodine intakes during pregnancy.MethodsOne hundred and fifty female Wistar rats,weighting 80 - 100 g,were randomly divided into five groups according to body weight,30 rats in each group.Each group was given deionized water containing different concentrations of iodine,50 μg/L(control group,NI),0 μg/L(iodine deficiency 1 group,LI1 ),5 μg/L(iodine deficiency 2 group,LI2),3000 μg/L(iodine excess 1 group,HI1 ),and 10 000 μg/L(iodine excess 2 group,HI2),respectively.After feeding for 12 weeks,the female rats were mated with male rats.The female rats were sacrificed at first(6,7 days),trimester( 12,13 days),and third trimesters( 19,20 days),respectively,then their thyroid and placenta were collected.The mRNA expressions of IGF- Ⅰ and TGF-1 in thyroid and placenta were detected by real-time quantitative PCR.Results①The actual thyroid weights of LI1 and LI2 groups[ (12.17 ± 5.41 ) × 10-2 g,(3.54 ± 1.21) × 10-2 g] were significantly higher than that of NI group[ (2.05 ± 0.50) × 10-2 g,all P ＜ 0.05] ;actual weights of HI1 and HI 2 groups[ (1.64 ± 0.27) × 10-2 g,(1.66 ± 0.29) × 10-2 g] were compared with that of NI group,the difference was not statistically significant(all P ＞ 0.05).②The mRNA expression of IGF- Ⅰ: at the first trimester,LI1 and LI2 groups(l.98 ± 0.35,1.47 ± 0.22) were all higher than that of NI group(1.01 ± 0.18,all P＜ 0.01 ),HI1 and HI2 groups(0.68 ± 0.16,0.75 ± 0.09) were lower than that of NI group(all P ＜ 0.01 );at the second trimester,HI2 group( 1.14 ± 0.17) was lower than that of NI group( 1.58 ± 0.33,P ＜ 0.01 ) ; at the third trimester,LI2 and HI2 groups(1.47 ± 0.20,1.45 ± 0.35) were lower than that of NI group(2.20 ± 0.37,all P＜0.01).The mRNA expression of IGF- I level in NI group at the first,second,and third trimesters(1.01 ±0.18,1.58 ±0.33,2.20 ± 0.37) was up regulated gradually,pairwise comparisons were statistically significant(all P ＜ 0,01 ).③The mRNA expression of TGF-β1: at the first trimester,LI1 group (1.37 ± 0.13) was higher than NI group (1.05 ±0.18,P ＜ 0.01 ),HI1 and HI2 groups(0.50 ± 0.09,0.44 ± 0.11) were lower than NI group(all P＜ 0.01); at the second trimester,LI1 and HI2 groups(1.39 ± 0.28,1.17 ± 0.12) were higher than NI group(0.63 ± 0.22,all P ＜0.01 ) ; at the third trimester,LI1 and LI2 groups ( 1.57 ± 0.30,1.23 ± 0.20) were higher than NI group ( 0.68 ± 0.17,all P＜ 0.01).TGF-β1 mRNA expressions of NI group at the second (0.63 ± 0.22) and third trimesters(0.68 ± 0.17) were lower than that of the first trimester (1.05 ± 0.18,all P ＜ 0.01).④ Rats' IGF-Ⅰ mRNA expression in placental: at the second trimester HI1 group,HI2 group( 1.48 ± 0.16,1.45 ± 0.25) were all higher than the NI group ( 1.00 ± 0.10,all P ＜ 0.01 ) ; at third trimester,HI1 group ( 1.75 ± 0.15 ) were higher than the NI group ( 1.54 ± 0.29,P＜ 0.05),HI2 group(l.94 ± 0.31) were higher than the NI group(P ＜ 0.01 ).IGF- Ⅰ mRNA expression in placental of NI group at the third trimester was higher than the second trimester(P＜ 0.01).⑤ Rats' TGF-β1 mRNA expression in the placenta: at the second trimester and the third trimester of pregnancy there were no significant difference between the five groups(all P ＞ 0.05) ; NI group at the third trimester(0.83 ± 0.16) was lower than the second trimester(0.98 ± 0.20,P ＜ 0.05).Conclusions During pregnancy,IGF- I mRNA expression increases in thyroid under the conditions of iodine deficiency,and this effect is particularly significant in the first trimester; at the same time,TGF-β1 mRNA expression is increased,and this inhibition becomes clear with the deepening of iodine deficiency.Under the condition of iodine excess,the functions of IGF- Ⅰ and TGF-β1 in thyroid above-mentioned were relatively weak.With the development of gestational period,promoting tissues growth and differentiation effect of placenta's IGF- Ⅰ was more significant gradually,but,inhibited effect of TGF-β1 was weaken.

Objective To study the effects of different iodine intakes on rat iodine metabolism during pregnancy.Methods One hundred and fifty female Wistar rats (body weight 80-100 g) were randomly divided into five groups:control group(NI),lower iodine 1 and 2 groups(LI1 and LI2),High iodine 1 and 2 groups(HI1 and HI2) by weight,30 rats in each group.These rats were given deionized water containing different concentrations of iodine,50(NI),0 (LI1),5(LI2),3000(HI1) and 10000 μg/L(HI2),respectively.After 12 weeks,urine samples were collected before copulation.The rats were sacrificed at the first(6-7 days),second (12-13 days) and third trimesters(19-20 days),respectively,serum and amniotic fluid samples were collected.Urinary iodine and iodine level in the fetal amniotic fluid were measured by As3+-Ce4+ catalytic spectrophotometry.Serum iodine was measured by mild acid digestion method.Results The baseline medians of urinary iodine of LI1 and LI2 groups(5.96,15.92 μg/L) were significantly lower than that of the NI group(43.75 μg/L,all P ＜ 0.01),and the values of HI and HI2 groups(5263.96,20389.64 μg/L) were significantly higher than that of the NI group (all P ＜ 0.01).The median of urinary iodine during pregnancy was significantly lower than that of the baseline of no pregnancy(all P ＜ 0.01).The medians of urinary iodine of the NI group at the first and the second trimesters (28.97,34.34 μg/L) were significantly lower than that of the third trimester(42.31 μg/L,all P ＜ 0.01).The means of serum iodine of LI1 and LI2 groups[(3.68 ± 1.69),(10.45 ± 4.16) μg/L] were significantly lower than that of the NI group [(23.68 ± 3.85)μg/L,all P ＜ 0.05],and the means of serum iodine of HI1 and HT2 groups [(502.67 ± 97.03),(822.15 ± 139.45)μg/L] were significantly higher than that of the NI group (all P ＜ 0.01).Although the mean of serum iodine of HI group gradually decreased with the progression of gestation,the difference was not statistically significant(all P ＞ 0.05).The iodine levels in amniotic fluid of fetal rats at the second and the third trimesters in LI1 group(0.85,3.00 μg/L) were significantly lower than that of the NI group(3.56,7.91 μg/L,all P ＜ 0.01),but the difference was not statistically significant between the iodine level in amniotic fluid of fetal rats of the LI2 and the NI groups at the second and the third trimesters(all P ＞ 0.05).The iodine levels in amniotic fluid of fetal rats at the second and the third trimesters in the HI1 group(49.59,171.21 μg/L) were significantly higher than that of the NI group(all P ＜ 0.01).The iodine levels in amniotic fluid of fetal rats at the second and the third trimesters in HI2 group (98.76,544.77 μg/L) were significantly higher than that of the NI group(all P ＜ 0.01).The iodine level in amniotic fluid of fetal rats in the third trimester was significantly higher than that of the second trimester in all the groups (all P ＜ 0.01).The ratios of serum iodine and urinary iodine of the LI1 and the LI2 groups (1.29 ± 1.14,1.70 ± 1.01) were significantly higher than that of the NI group(0.51 ± 0.37,all P ＜0.01),and that of the HI1 and the HI2 groups(0.21 ± 0.07,0.11 ± 0.07) were significantly lower than that of the NI group (all P ＜ 0.01).The ratios of amniotic fluid iodine and serum iodine of the LI and the LI2 groups (0.19 ± 0.15,0.32 ± 0.17) were significantly higher than that of the NI group(0.13 ± 0.05,P ＜ 0.01),but the difference was not statistically significant between HI1 and HI2 groups(0.09 ± 0.03,0.11 ± 0.04) and NI group(all P ＞ 0.05).The ratio of amniotic fluid iodine and serum iodine of the third trimester was significantly higher than that of the second trimester(all P ＜ 0.05).Conclusions Different iodine intake leads to changes in the levels of maternal iodine metabolism in rats during pregnancy.There probably is a protection mechanism in the mother's body,which protects the mother and the fetal from injury by iodine excess or iodine deficiency.