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Objective To explore the value of diffusion kurtosis imaging (DKI) in predicting radiotherapy sensitivity of esophageal cancer from the animal model level.Methods BALB/c nude mice were subcutaneously injected with Eca-109 cell lines to form xenograft tumors.The tumors received a single dose of 15 Gy (6 MV X-rays) in the experimental group or had no any treatment as control.The volume of transplanted tumor,the change of ADC,MK and MD values,and the tumor cell density and necrosis ratio of these two groups were observed at the corresponding time points.Results The growth of xenograft volume in the experimental group was suppressed and it was significantly smaller than that in the control group (t=3.206-6.149,P＜0.05) at the 7th day after radiotherapy.From the 3rd day after radiotherapy,the ADC and MD values of the experimental group were significantly higher than those of the control group,and the MK values was lower than those in the control group (tADC =-11.018--2.049,tMD =-6.609--2.052,tMK =2.492-9.323,P＜0.05).Meanwhile,the tumor cell density of the control group was higher than that of the experimental group,and the proportion of necrosis in the experimental group was higher than that in the control group (tdensity =-8.387--2.239,t is =2.980-17.430,P＜0.05).Conclusions A single large dose radiation could inhibit the growth of xenograft.ADC,MK,MD values changed at the early stage prior to morphological changes of tumor in consistent with the change of cell density and necrosis ratio.DKI has the potential value in predicting radiotherapy sensitivity of esophageal carcinoma.
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The paper presented the characteristics of ambulatory surgery and the construction of a standardized management system in pediatrics. Every step of the process is standardized. Admission criteria cover all, including the children patients, surgeons, anesthesiologists, and surgical procedures, while preoperative postoperative evaluation is made and upon discharge as well. Surgery cancellation rate is reduced at all dimensions. Such rapid rehabilitation measures as preventive anti-vomiting, and shorter perioperative fasting time were introduced, along with effective post-discharge support. These efforts aim at exploring the safety and efficacy of standardized management approaches for pediatric day surgery, providing references for specialized pediatric hospitals.
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Objective To discuss the commonly used puncturing approaches in CT-guided 125I seed implantation for lumbar lymph node metastases in order to provide safe and reliable technical guidance for clinical practice.Methods Under CT guidance,125I seed implantation for lumbar lymph node metastases was performed.According to different locations of metastatic lymphadenopathy (left waist,right waist or middle waist),the corresponding puncture route and implantation method were adopted.Meanwhile,different puncturing approach was designed in order to avoid damage to vital organs.Results For the performance of 125I seed implantation for the lymphadenopathy located at the left waist,right waist and middle waist,the commonly used puncturing approaches were percutaneous transthoracic lumboiliac costal muscle method (i.e.back approach),trans-hepatic trans-duodenal method (i.e.lateral approach) or back approach method,and trans-mesenteric approach together with coaxial needle method (i.e.anterior approach) respectively.Conclusion It is clinically feasible to use different puncturing approaches in performing 125I seed implantation for lumbar lymph node metastases,the suitable puncturing approach can ensure a successful and safe operation.
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<p><b>OBJECTIVE</b>To explore the role of the hydatidiform mole-related gene F10 in the tumorigenicity of choriocarcinoma cell lines JEG-3 in nude mice.</p><p><b>METHODS</b>Choriocarcinoma JEG-3 cell lines with stable F10 gene over-expression and F10 gene silencing were established using cell transfection and RNA interference techniques, respectively. Thirty SPF nude mice (4-5 weeks old) were equally randomized into F10 over-expression group, control group, and F10 gene-silenced group for subcutaneous injection of 0.2 ml cell suspension (5 × 10⁷ cells) of F10 gene over-expressing JEG-3 cells, non-treated JEG-3 cells, and F10 gene-silenced JEG-3 cells, respectively. The mice were observed and weighed every 3-4 days, and the tumor formation time was recorded to draw the tumor growth curve and calculate the tumor formation rate.</p><p><b>RESULTS</b>The tumor formation rates were 100% in all the 3 groups. No significant difference was found in the tumor formation time among the F10 over-expression, F10-silenced and control groups (6.2 ± 0.78 vs 7 ± 2.49 vs 6.3 ± 0.67 days; F=0.781, P=0.468). A significantly greater tumor growth rate was noted in the F10 over-expression group compared with the other two groups (P<0.05), and the growth rate was significantly slower in F10-silenced group than in the control group (P<0.05). The subcutaneous tumor weight at 5 weeks after JEG-3 cell injection differed significantly among F10 over-expression, F10-silenced and control groups (571.1 ± 221.10 vs 136.2 ± 66.25 vs 354.5 ± 116.23 mg; F=21.199, P=0.000).</p><p><b>CONCLUSION</b>F10 gene plays a role in the regulation of choriocarcinoma JEG-3 cell proliferation and might enhance its tumorigenicity in nude mice.</p>
Subject(s)
Animals , Female , Humans , Mice , Pregnancy , Cell Line, Tumor , Cell Proliferation , Choriocarcinoma , Pathology , Gene Expression , Gene Expression Regulation, Neoplastic , Genes, Neoplasm , Hydatidiform Mole , Genetics , Mice, Nude , Transfection , Uterine Neoplasms , PathologyABSTRACT
Objective The F10 gene was found in the initial stage of our study to be highly expressed in hydatidiform mole. The aim of this study was to investigate the effects of theoverexpression or depletion of F10 on the invasiveness of the choriocarcinoma cell line JAR and explore the relationship of F10 expression with the invasiveness and metastasis ofchoriocarcinoma. Methods Using cell transfection and RNA interference technology, we established JAR choriocarcinoma cell lines with stablyoverexpressedor silenced F10 gene.We randomly and equally assigned 30 SPF nude mice into the three groups to receive the injection of JAR cellswith overex-pressed F10 ( F10 overexpression group) , untreated JAR cells ( control group) , and JAR cells with silenced F10( F10 silence group) . At 5 weeks after the JAR cell injection, we harvested the subcutaneous tumor tissues from the mice, determined the expressions of ma-trix metalloproteinases (MMP), tissue inhibitors of metalloproteinase-1(TIMP-1), and plasminogen activator inhibitor-1(PAI-1), and compared by Western blot and immunohistochemistry, and compared the expressions among the three groups of mice. Results Im-munohistochemistryshowed significantlyup-regulated expressions of MMP-2, -8, -11, -16, and-19 and down-regulated expressions of TIMP-1 and PAI-1 in the subcutaneous tumor tissues in the F10 overexpression group as compared with the control and F10 silence groups ( P<0.05) .Western blot also exhibitedextremely significantly up-regulated expressions of MMP-2,-8,-11,-16, and -19 pro-teins anddown-regulated expressions of TIMP-1 and PAI-1 proteins in the F10 overexpression groupin comparison with the control and F10 silence groups( P<0.01 ) . Conclusion By up-regulating the expressions of MMPs and down-regulating the expressions of TIMP-1 and PAI-1, the F10 gene might be an upstream stimulating factor involved in the proliferation, invasiveness, and metastasis of-choriocarcinoma cells.
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Objective To analyze the invasion and metastasis of endometrial stromal cells in endometriosis through assessing the transcription levels of COX-2, PGE2, Snail and E-cadherin mRNA. Methods Ectopic and eutopic endometri?al tissues from patients with EMs (endometriosis) or uterine fibroids were collected and cultured. The fourth generation of pu?rified endometrial stromal cells were used for research, and the transcription levels of COX-2, PGE2, Snail and E-cadherin mRNA were analyzed by RT-PCR. Results There were no statistical differences in transcription levels of COX-2, PGE2, Snail and E-cadherin mRNA in eutopic endometrial stromal cells from patients with EMs or uterine fibroids between secra?tion stage and proliferation stage(P>0.05). The transcription levels of COX-2, PGE2 and Snail mRNA were significantly in?creased while transcription level of E-cadherin mRNA was decreased in eutopic and ectopic endometrial stromal cells in pa?tients with EM compared with those in patients with uterine fibroid. And the difference was statistically significant(P<0.05 or P<0.01). The transcription levels of COX-2, PGE2 and Snail mRNA were obviously higher while transcription level of E-cadherin mRNA was lower in ectopic endometrial stromal cells than those in eutopic endometrial stromal cells from pa?tients with EMs. And the difference was statistically significant(P<0.05 or P<0.01). Conclusion The invasion and me?tastasis of endometrial stromal cells of patients with EMs were remarkable than those cell of patients without EMs. What ’s more, the invasion and metastasis in ectopic endometrial stromal cells were more obvious than those cells in the pathogenesis of EMs.
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Objective To observe the effect of rosuvastatin on serum hs-CRP,IL-18 levels in patients with acute myocardial infarction.Methods By randomized,double-blind,controlled study,102 patients with acute myocardial infarction were randomly divided into the treatment group(rosuvastatin 10mg/d,continuous medication 14d) and the control group(not used rosuvastatin,other treatment and care were same with the treatment group).Before treatment,24h after treatment,after 2 months of follow-up,the serum hs-CRP and IL-18 levels were detected and compared.Results After treatment,the serum hsCRP level increased and then decreased,24h after treatment,the serum hsCRP level of the treatment group increased to (15.54 ±2.51) mg/L,which was significantly lower than the control group (19.26 ±.2.92) mg/L (t =4.65,all P ＜ 0.05).2 months after treatment,the serum hs-CRP levels of the two groups were decreased to (3.21 ± 1.39) mg/L and (7.67 ± 2.07) mg/L,the difference was statistically significant (t =5.54,4.63,all P ＜ 0.05).After treatment,the serum IL-18 level decreased,24h after treatment,the serum IL-18 level ofthe treatment group decreased to (29.13 ±6.34)pg/L,which was significandy lower than the control group (33.01 ± 7.34) pg/L(t =3.59,P ＜ 0.05).2 months after treatment,serum IL-18 levels of the two groups were decreased to (27.52 ± 5.33) pg/L and (32.01 ± 6.24) pg/L,the difference was statistically significant (t =3.87,3.28,P ＜0.05).Conclusion Rosuvastatin can significantly reduce the serum hsCRP and IL-18 levels in patients with acute coronary syndrome,it has better anti-inflammatory effect and can be used as a new therapeutic target for acute myocardial infarction.
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Objective The purpose of the present study was to investigate the effect of peroxisome proliferator-activated receptors δ（PPAR δ）activation with dietary GW610742X on the expression of tenascin-C in the infarcted and remodeling myocardium.Methods Sixty male Wistar rats were divided into four groups,including control group,sham group,myocardial infarction（MI） group,and MI＋GW610742X（GW）group.The left coronary artery was ligated to establish the MI model.PPAR δ activator GW610742X（100mg/kg/d）was administrated into the rats of GW group.At 3 months after procedure,the expression and distribution of tenascin-C in left ventricular free wall from each group were examined by Western blotting and immunofluorescence,respectively.Results After 3 months following procedure,there were obvious necrosis and fibrosis in left ventricular free wall from MI group.The expression of tenascin-C in MI and GW group was significantly higher than those in control and sham group（P 〈 0.01）.Moreover,tenascin-C expression in GW group was remarkably decreased compared to MI group（P 〈 0.05）.Additionally,tenascin-C expression in sham group was similar to that in control group（P 〉 0.05）.Conclusion The tenascin-C is upregulated in infarcted myocardium during the remodeling process,which can be significantly attenuated by PPAR δ activation.
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AIM: To investigate the contribution of angiotensin-converting enzyme inhibitor (ACEI) to the regulation of calpain system in infarcted myocardium. METHODS: Rat myocardial infarction (MI) model was established by permanent ligation of the left coronary artery. The treatment with the ACEI inhibitor rampril (1 mg?kg~-1 ?d~-1 ) was started 7 days prior to surgery. On day 1, 3, 7 and 14 after MI, protein levels of calpainⅠ, Ⅱ and calpastatin were determined in left ventricular free wall (LVFW), interventricular septum (IS) and right ventricule. RESULTS: CalpainⅠprotein level was increased in IS 14 d post MI, whereas the protein level of calpainⅡ was maximally increased in LVFW 3 d post MI. Rampril decreased protein up-regulation of calpainⅠ and Ⅱ, and reduced infarct size and interstitial fibrosis. Calpastatin protein expression was not affected by ACEI. CONCLUSIONS: CalpainⅠ is involved in cardiac remodelling in the late and calpainⅡ contributes to cardiac tissue damage in the early phase of MI. The heart protective effect of ACEI may be related to the inhibition of calpain system in the pathogenesis of myocardial infarction.
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Aim To investigate the contribution of cardiac L-and L/T-type Ca~2+ channels in the calpain mediated myocardial damage following myocardial infarction(MI).Methods Rat MI model was established by permanent ligation of the left coronary artery, infarcted rats were orally treated with placebo, amlodipine(L-channel blockade, 4 mg?kg~-1 ?d~-1 ) or mibefradil(L/T-Channel blockade, 10 mg?kg~-1 ?d~-1 ) beginning 7 d before induction of myocardial infarction. Protein levels of u-calpain and m-calpain were measured 1,3,7 and 14 d post coronary occlusion in the noninfarcted and infarcted myocardium.Infarcted size,left ventricular dilation were determined in picrosirius red stained hearts.Results Myocardial infarction induced an up regulation of u-calpain protein and activity in the noninfarcted myocardium(maximum day 14 days post infarction), whereas protein and activity of m-calpain were increased in the infarcted myocardium 3 d post infarction. Amlodipine inhibited protein up-regulation of u-calpain and decreased left ventricular dilation and interventricular septal thickness. Mibefradil attenuated protein up regulation of m-calpain 14 days post infarction, reduced infarct size more obviously.Conclusions Infarction-induced cardiac hypertrophy was accompanied by an up-regulation of u-calpain, whereas m-calpain was up-regulated in the infarcted myocardium in the processing of cardiac infarcted pathogensisi. Cardiac L and L/T-type Ca~2+ channel blockade differentially reduced post infarction remodeling associated with selective inhibition of cardiac u-calpain and m-calpain, respectively.
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The role of DS-182 in protection of cellular damages induced by oxygen free radicals was studied in rat cardiac mitochondria. The changes of cardiac mitochondrial enzyme (cytochrome oxidase) and P/O, RCR were used as indices of mitohondrial injury. The experimental animals were divided into three groups: control group, injury group (Fe~(2+)+ascorbic acid), and protection group (DS-182+Fe~(2+)+ascobic acid). Results obtained showed that incubation of mitochondrial suspension with ascorbic acid and Fe~(2+) resulted in decrease of activity of cytochrome oxidase, P/O (with ?-ketoglutarate andsuccinate as substrate respectively) and RCR, which indicated that the structure and function of mitochondria were damaged. Danshensu (DS-182) can inhibit the decrease of cytochrome oxidase activity, P/O and RCR. Thus, DS-182 with acts as an effective scavenger for oxygen free radicals prevented the mitochondrial injury.