Objective To assess the value of peripheral blood thyroid stimulating hormone receptor(TSHR) mRNA determination in differential diagnosis of benign and malignant thyroid nodules.Methods Fine needle aspiration cytology (FNAC) and (or) postoperative histopathology as the gold standard were carried out,the expression of circulating TSHR mRNA was determined by RT-PCR in 33 patients with benign thyroid nodules,39 patients with thyroid cancer,and 20 normal controls.Results TSHR mRNA signals were not detected in normal controls,the positive rate of TSHR mRNA was higher in the group with malignant nodules than the group of benign nodules (91.2％ vs 48.5％,P＜0.01).TSHR mRNA level in the preoperative malignant group was significantly higher than that in the normal,benign,and postoperative cancer groups (all P ＜ 0.01).Using peripheral blood TSHR mRNA for differentiating benign or malignant of thyroid nodule had a sensitivity,specificity,and accuracy of 91.2％,51.5％ and 71.6％,respectively.The sensitivities of TSHR mRNA,FNAC,and these two methods combined in detecting malignant nodules were 91.3％,86.9％,and 100.0％ respectively,while diagnostic accuracies were respectively 84.0％,80.0％,and 92.0％.TSHR mRNA expression showed no significant relationship with sex,age,size,and number of nodule in these patients (all P ＞ 0.05),but it did exhibit significant difference between benign and malignant nodules(P＜0.01).Conclusion The peripheral blood TSHR mRNA could be used as a molecular marker for thyroid cancer,and it would help enhance the preoperative differentiation of benign and malignant thyroid nodules.

ObjectiveToestablisharatmodelofincreasedbloodflow-inducedpulmonaryarterialhypertension generatedbyanastomosisoftheleftcommoncarotidarterytoleftexternaljugularvein.Methods 45maleSDratswere divided into three groups:the shunt group , the ligation group and the sham group .At twelve weeks after the procedure , the general status of the rats was observed . Heart conditions , cardiac output and shunt patency were measured by echocardiography .Right ventricular systolic pressure ( RVSP ) and Qp/Qs were checked by catheterization . Right ventricular hypertrophy index ( RVHI) was calculated and lung tissues were examined by pathology using hematoxylin -eosin and elastin Van Gieson staining .All data were analyzed statistically by one-way ANOVA test using SPSS 16.0.Results There was no significant difference in body weight gains between the groups .The patency rate of shunt was 84.6%.The heart was enlarged in the group shunt .Cardiac output increased significantly in the shunt group than that in the other two groups [(309.8 ±33.1) mL/min?kg vs.(245.6 ±31.9) mL/min?kg, (240.8 ±30.9)mL/min?kg, respectively, P<0.05].In the shunt group Qp/Qs was 2.16 ±0.38 and RVSP increased to (35.8 ±4.9) mmHg, RVHI was 0.3263 ± 0.0342, significantly higher than that of the other groups .The pulmonary arteriolar wall was evidently thickened in contrast to that in the sham group [ ( 22.3 ±1.7 )% vs.( 10.6 ±1.7 )%, P <0.05 ) .Conclusions Anastomosis of the left common carotid artery to left external jugular vein can successfully establish pulmonary arterial hypertension model induced by high blood flow in rats .

Objective To study the clinical effects and side effects of recombinant human vascular endostatin combined with pemetrexed and cisplatin in the treatment of advanced lung adenocarcinoma.Methods Forty-seven patients with advanced lung adenocarcinoma were recruited from Jan 2011 to Jan 2013,and they were randomly divided into experimental group and control group.The experimental group (n =24) was added with recombinant human vascular endostatin based on pemetrexed and cisplatin,whereas the control group(n =23) was administered with pemetrexed and cisplatin only.The objective response rate (ORR),disease control rate (DCR),progressive disease (PD) rate,progression-free survival (PFS),overall survival (OS) and the side effects of 2 groups were evaluated.Results In the experimental group,ORR,DCR,PD rate,PFS and OS were 41.7 ％ (10/24),79.2 ％ (19/24),20.8 ％ (5/24),8.0 months and 12.5 months respectively,while those of control group were 34.7 ％ (8/23),47.8 ％ (11/23),52.2 ％ (12/23),6.2 months and 10.0 months.DCR,PD rate and PFS of experimental group had significant differences compared with control group (P ＜ 0.05).OS of experimental group had no significant difference compared with control group (P ＞ 0.05).The side effects of 2 groups were mainly hematologic toxicities,digestive reactions and fatigue,and the incidence rates were not significantly different between 2 groups (P ＞ 0.05).Conclusions Recombinant human vascular endostatin combined with pemetrexed and cisplatin in treatment of patients with advanced lung adenocarcinoma improves the DCR,decreases the PD rate,prolongs the PFS.There is an increasing trend in the OS of experimental group,and with tolerable side effects.

AIM:To investigate the effect of ionizing radiation on epithelial-mesenchymal transition in lung cancer cell line A549 and its possible mechanism.METHODS:The lung cancer A549 cells were irradiated with different doses (0 Gy, 1 Gy, 2 Gy, 4 Gy and 8 Gy) of X-ray for different time.The morphological changes of the cells were observed under inverted microscope at time points of 12 h, 24 h and 48 h.The expression of vimentin, N-cadherin, E-cadherin and transcription factor c-Myc was detected by Western blot at the time points of 12 h and 24 h.RESULTS:After ionizing radiation, the contours of the A549 cells were unclear, the protrusions increased, and the edges were irregular, with fried egg-like collapses.The mesenchymal morphology of the A549 cells was most obvious after irradiation at 8 Gy for 48 h.Compared with 0 Gy irradiation group, the expression of vimentin was down-regulated seemingly 12 h after irradiation, but up-regulated in 2 Gy, 4 Gy and 8 Gy irradiation groups for 24 h, and the most obvious effect was observed in 2 Gy irradiation group (P<0.01).Compared with 0 Gy irradiation group, the expression of N-cadherin was up-regulated in 1 Gy, 2 Gy and 4 Gy irradiation groups for 24 h (P<0.05), while the expression of E-cadherin was not influenced.The up-regulation of vimentin expression in lung cancer cell line A549 was positively correlated with c-Myc expression.CONCLUSION:Ionizing radiation may promotes epithelial-mesenchymal transition in the lung cancer cell line A549 by up-regulating the c-Myc expression.

Objective To develop a new type of blast injury simulator to establish a mouse model of brain blast injury and study its damage mechanism. Methods Thirty healthy Kunming mice were randomly(random number) divided into the normal control group and brain blast injury model (TBI) group. A mouse model of traumatic brain injury was prepared by a self-developed explosive injury simulator. Morris water maze, Evans blue experiment and HE staining were used to observe the effects of shockwave exposure on spatial memory, blood-brain barrier, and pathological changes of brain tissues. T test was used for statistical analysis. Western blot method was used for detecting expression of brain injury markers Tau, S100β, Choline, inflammatory factors IL-1β, IL-4, IL-6, IL-10, NF-κB, apoptosis factors Bcl-2, Bax, Caspase3, and oxide protein stress-related factors IREα, MDA5, COX2 SOD1, and SOD2. Results Compared with the normal control group, (11.2±2.1) s, the time of searching platform in the TBI group was (54.6±8.4) s, was significantly longer (t=-19.330, P<0.05), and the EB exudation in the TBI group was 3.22 times (t=-13.903, P<0.05). Pathological staining revealed neuronal damage in the hippocampus, and TBI induced brain injury markers Tau(0.26±0.03 vs 0.46±0.04,t=-9.788, P<0.05), S100β(0.54±0.03 vs 0.74±0.02,t=-12.433, P<0.05) and Choline(0.54±0.05 vs 0.80±0.04, t=-7.970, P<0.05), inflammatory cytokines IL-1β(0.22±0.04 vs 0.31±0.05,t=-3.431, P<0.05), IL-4(0.65±0.02 vs 0.97±0.03, t=-18.927, P<0.05), IL-6(0.88±0.05 vs 1.07±0.08, t=-9.488, P<0.05) and NF-κB(0.80±0.06 vs 1.03±0.07,t=-4.507, P<0.05), and pro-apoptotic cytokines Bax(0.66±0.04 vs 0.78±0.04, t=-13.007, P<0.05) and Caspase3(0.44±0.03 vs 0.60±0.05, t=-4.472, P<0.05), oxidative stress-related factor pro IREα(0.72±0.06 vs 1.07±0.04, t=-9.665, P<0.05), MDA5(0.47±0.02 vs 0.77±0.02, t=-23.678, P<0.05) and expression of COX2(0.70±0.07 vs 0.86±0.02, t=-6.421, P<0.05), inhibition of inflammation inhibitory factor IL-10(1.14±0.06 vs 0.74±0.07, t=13.729, P<0.05), inhibition of apoptosis factors Bcl-2(0.72±0.05 vs 0.46±0.02, t=11.491, P<0.05) and inhibition of oxidative stress factors SOD1(1.17±0.05 vs 0.99±0.01, t=7.731, P<0.05) and SOD2(0.81±0.05 vs 0.61±0.04, t=10.257, P<0.05) expression. Conclusions The brain injury induced by blast exposure can induce spatial learning and memory loss, blood brain barrier disruption, neuronal damage hippocampus in mice, and promote the expression of brain injury markers, induce inflammation, oxidative stress and apoptosis. The self-developed explosive shock simulator successfully establishes a mouse brain blast injury model.