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Objective To construct the LyP-1 targeted MR fluorescence dual-modality molecular probe for pancreatic cancer,and to observe its features and MRI charicteristics.Methods The 50 nm MR-fluorescent dual-modality molecular probe with surface modified with cyclic nine-amino acid peptide LyP-1 (Cys-Gly-Asn-Lys-Arg-Thr-Arg-Gly Cys) was rationally designed.Whether the molecular probe could specifically recognize the pancreatic cancer cells were validated by the combination of fluorescent imaging and MR T2WI.Results The new MR-fluorescent dual-modality molecular probe anchored with LyP-1 could be used for the fluorescent imaging and MR T2WI of pancreatic cancer in mouse.And the molecular probe was demonstrated to be effective in conjugating with pancreatic cancer cells on fluorescent images and caused obvious MR signal reduction under T2 relaxometry in vitro.In vivo experiment,the molecular probe could be used for fluorescent labeling tumor tissue and detecting orthotopic pancreatic cancer in C57BL/6 mouse as MR contrast agent.Conclusion The LyP1 immobilized MR-fluorescent dual-modality molecular probe can actively target to mouse orthotopic xenograft of pancreatic cancer,which is hopeful to the application in early probing and diagnosis of pancreatic cancer by multimodal imaging.
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Objective To construct the LyP-1 targeted MR fluorescence dual-modality molecular probe for pancreatic cancer,and to observe its features and MRI charicteristics.Methods The 50 nm MR-fluorescent dual-modality molecular probe with surface modified with cyclic nine-amino acid peptide LyP-1 (Cys-Gly-Asn-Lys-Arg-Thr-Arg-Gly Cys) was rationally designed.Whether the molecular probe could specifically recognize the pancreatic cancer cells were validated by the combination of fluorescent imaging and MR T2WI.Results The new MR-fluorescent dual-modality molecular probe anchored with LyP-1 could be used for the fluorescent imaging and MR T2WI of pancreatic cancer in mouse.And the molecular probe was demonstrated to be effective in conjugating with pancreatic cancer cells on fluorescent images and caused obvious MR signal reduction under T2 relaxometry in vitro.In vivo experiment,the molecular probe could be used for fluorescent labeling tumor tissue and detecting orthotopic pancreatic cancer in C57BL/6 mouse as MR contrast agent.Conclusion The LyP1 immobilized MR-fluorescent dual-modality molecular probe can actively target to mouse orthotopic xenograft of pancreatic cancer,which is hopeful to the application in early probing and diagnosis of pancreatic cancer by multimodal imaging.
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Objective To investigate the correlation between IL‐18 and deep venous thrombosis disease and its clinical significa‐tion .Methods To detect the expression of IL‐18 by ELISA ,we collected the blood samples of DVT patients as the experimental group(n=40) compared to the control group(n=40) and normal group(n=20) .IL‐18 over expression/interference vectors were constructed and transfected human vein endothelial cells ,analyzed by microarray and KEGG Pathway as biology information tech‐nology .Then discuss the association between IL‐18 and DVT .Results Results of ELISA showed that compared with control group and normal group ,the expression of IL‐18 gene in DVT patient were up‐regulated(F=11 .248 ,P0 .05) .Immunofluorescence detected IL‐18 gene expression in cytoplasm of human umbilical vein endothelial cells (HUVECs) .According to the microarray analysis we found in the IL18‐pCDH‐GFP transfected cells 17 signaling pathways were down‐expressed while 16 signaling pathways were up‐expressed .Compared with normal group cells ,in the IL18‐LMP‐shRNAmir1 transfected cells 23 signaling pathways were down‐ex‐pressed and 9 signaling pathways were up‐expressed .Conclusion Based on the above experimental data ,it is very clear that IL‐18 influenced HUVECs and plays an important role in DVT ,it is possible to predict the diagnosis of DVT and act as candidate molecu‐lar markers .
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Objective To study and establish a high quality digital 3D anatomical modeling of the mandible with full teeth.Methods A set of accurate digital models of standard anatomical specimens of mandibular teeth were obtained by laser scanning, and the 3D mandible model was reconstructed by CT scan data;then, a registration deformation method based on the geometry and image anatomical landmark was employed to do the registration of each tooth to the mandible model, and finally the tooth enamel , dentin, periodontal ligament were generated .Results A high quality digital 3D anatomical modeling of the mandible with full teeth was built , each tooth had detail crown and whole root , the distinction between the enamel , dentin, periodontal ligament , and any anatomical regions can be zoomed and rotately displayed . Conclusion The digital 3D anatomical modeling of the mandible with full teeth has realistic 3D imaging view and convenient teaching-learning function , and has tremendous apllication futures in the stomatology , maxillofacial and other medical departments .
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Objective To investigate the association between the signaling pathways of MCP-1-pCDH-GFP-trans?fected cells and deep venous thrombosis (DVT). Methods The cultured human umbilical vein endothelial cells (HUVECs) were tested by immunofluorescence and co-immunoprecipitation methods. The constructed MCP-1 over-expression/interfer?ence vector, and the change of transcription profile were detected by microarray assay and biological information technology analysis. Results MCP-1 over-expression/interference vector MCP-1-pCDH-GFP/MCP-1-LMP shRNAmir1 was con?structed and HUVECs were transfected. According to the microarray analysis we found that there were 18 down-expressed signaling pathways and 7 up-expressed signaling pathways in MCP-1-pCDH-GFP-transfected cells. There were 60 down-expressed signaling pathways and 15 up-expressed signaling pathways in the MCP-1-LMP shRNAmir1 transfected cells. Conclusion Signaling pathways of MCP-1 plays an important role in DVT formation,which may provide us a new way to study molecular mechanism of DVT.
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Objective To build rat DVT inferior vena cava partial stasis (narrow) model, to detected the expression ofβ2-GP1, VEGF and TF in rat blood, and to investigat the correlation betweenβ2-GP1, VEGF and TF with DVT. Meth?ods SD rats (n=70) are divided into control group (n=10), sham operation group (n=30) and the model group (n=30) ran?domly and DVT model was built by the inferior vena cava partial stasis (narrow) after 2 h, 8 h and 24 h respectively. In each time point, ten rats were taken in each group, inferior vena cava blood were collected whileβ2-GP1, VEGF and TF expres?sion were detected by ELISA. Results In rat experiment, compared with control group, there was no significant change in?expression of β2-GP1, VEGF and TF in sham operation group (P > 0.05). Levels of β2-GP1, VEGF and TF were in?creased at the 2nd hour and 8th hour then peak at the 24th hour which was higher than those in the 24th hour control group and in Sham group and it was also higher than those in the 2nd hour and the 8th hour in model group with statistical signifi?cant difference (P<0.01). Conclusion Based on the above experimental data, in rat DVT formation process, β2-GP1, VEGF and TF may play an important role in promote DVT formation.
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BACKGROUND:Studies in recent years have demonstrated that arginase Ⅰ contribute to the process of numerous cardiovascular diseases,however,most of studies focus on arteries,few regarding venous diseases.OBJECTIVE:To explore the changes of arginase Ⅰ expression in rat traumatic deep venous thrombosis models,and to analyze the possible function of arginase Ⅰ in deep venous thrombosis formation.METHODS:Totally 100 Sprague Dawley rats were randomly divided into the control and model groups.Traumatic deep venous thrombosis models were established by clamping the femoral vein and immobilizing the bilateral hind limbs (hip spica cast fixation),and assigned into initial thrombosis,peak thrombosis and non-thrombosis groups according to different observing time points and pathophysiological situations of thrombosis.Whole blood RNA of each group was extracted,and the change of arginase I expression in blood cells of each group was detected by real-time PCR.RESULTS AND CONCLUSUON:Expression of arginase Ⅰ in the peak thrombosis group was significantly increased compared with other 3 groups (P < 0.01).There were no significances among control,initial thrombosis and non-thrombosis groups (P > 0.05).The finding demonstrated that arginase Ⅰ is closely related to deep vein thrombosis formation.
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BACKGROUND:The molecular mechanism of traumatic deep vein thrombosis is complex.Numerous studies focus on clinical observation and epidemiology,but its molecular mechanism has not been a new breakthrough.OBJECTIVE:By use of gene array technology,this study was aimed to study the expression changes of matrix metalloproteinases in rat models of traumatic deep vein thrombosis,and to explore the roles of matrix metalloproteinases in traumatic deep venous thrombosis.METHODS:A total of 150 SD rats,SPF grade,of 8-12 weeks old,body weight of 250-300 g,were divided at random into normal control group (n=10) and model group (n=140).Rat traumatic deep venous thrombosis models were set up by clamping the femoral vein and fixing the bilateral hind limbs,and the fixation of hip spica with plaster bandage was conducted in each group.Then rats were divided into 7 subgroups:post-traumatic 0.5 hours,post-traumatic 2.5 hours (initial period of thrombosis),post-traumatic 25 hours (thrombogenesis at thrombotic crest-time),post-traumatic 25 hours non-thrombogenesis at the thrombotic crest-time),post-traumatic 72 hours (thrombus resolution),post-traumatic 72 hours thrombus insolution) and post-traumatic 168 hours (nonthrombosis).At the corresponding phasess,the femoral vein tissues were incised,and total RNA of femoral vein was extracted using Trizol one-step method.Applying Genechip Rat Genome 430 2.0 genechips,the gene expressions in femoral vein were detected in different groups.The rate of traumatic deep venous thrombogenesis and non-thrombogenesis,the rate of thrombi solution and insolution were observed;the expressions of matrix metalloproteinases and tissue inhibitor of metalloproteinases at different time phases was detected by gene array data analysis.RESULTS AND CONCLUSION:Three model rats died and the remaining 147 rats were involved in the final analysis.At the post-traumatic 25 hours,the rate of thrombogenesis was 50.5% and nonthrombogenesis was 49.5%.To the post-traumatic 168 hours,the rate of thrombus solution was 56.7% and thrombus insolution was 43.3%.Both matrix metalloproteinases and tissue inhibitor of metalloproteinases exhibited differential expressions in the course of traumatic deep venous thrombosis.Under the thrombus insolution state,matrix metalloproteinases continued to show a high expression,tissue inhibitor of metalloproteinase expression was down-regulated in the thrombus formation,was significantly inhibited in the thrombus insoluUon process.In the process of traumatic deep vein thrombosis and insolution,matrix metalloproteinase was closely related to traumatic deep vein thrombosis,the matrix metalloproteinase/tissue inhibitor of metalloproteinases are likely to affect the biological state of thrombosis.
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<p><b>OBJECTIVE</b>To study the expression changes of matrix metalloproteinases (MMPs) in traumatic deep vein thrombosis (TDVT) in a rat model with the aid of gene chip technology and to explore the roles of MMPs in TDVT.</p><p><b>METHODS</b>Totally 150 Sprague Dawley rats were randomly divided into control group (n equal to 10) and model group (n equal to 140). Rat models of TDVT were established by clamping the femoral vein and fixing the bilateral hind limbs. Then fixation of the hip spica with plaster bandage was conducted. According to the observation phases and/or biological situations of the femoral vein thrombosis, the model rats were further divided into 7 groups. Vascular tissues were obtained from each group through noninvasive incision into the femoral vein at corresponding time points. We adopted the Trizol one-step method for total RNA extraction, Affymetrix RAT 230 2.0 array for detection of RNA expressions and fold change (FC) analysis for changes of differential expressions of MMPs in each group. The main outcome parameters measured included expressions of MMP-2, MMP-3, MMP-7, MMP-8, MMP-9, MMP-10, MMP-11, MMP-12, MMP-13, MMP-14, MMP-16, MMP-23 and MMP-24. Gene array data of these MMPs were analyzed by the Affymetrix Microarray Analysis software (Version 5.0).</p><p><b>RESULTS</b>FC analysis showed differential expressions of MMPs in each group during the course of TDVT. At the initial period of thrombosis, MMP-2, MMP-3, MMP-7, MMP-8, MMP-9, MMP-10, MMP-11, and MMP-24 had significantly high expression, while MMP-12, MMP-13, MMP-14, MMP-16 and MMP-23 had relatively low expression. MMPs were all highly expressed at the peak time of thrombosis. In the process of thrombus resolution, MMP-2, MMP-10, MMP-16 and MMP-24 have relatively low expression, while MMP-12, MMP-13, MMP-14, MMP-16 and MMP-23 have significantly high expression.</p><p><b>CONCLUSION</b>MMPs may affect the process of TDVT through transcription regulation of the fibrinolysis-anti-fibrinolytic system during the course of thrombosis and thrombus resolution.</p>
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Animais , Ratos , Modelos Animais de Doenças , Metaloproteinases da Matriz , Fisiologia , Ratos Sprague-Dawley , Trombose Venosa , Ferimentos e LesõesRESUMO
We report on 2 siblings with a partial trisomy of 7q (7q22-->qter) and concomitant partial monosomy of 8p (8p23.3-->pter), which were shown by FISH using probes located at the telomere region of each chromosome. All the balanced translocation carriers (father and a sister) in this family had a normal phenotype. The 2 siblings with the same abnormal karyotype had similar multiple congenital anomalies and dysmorphic features. During the follow-up, the first male patient died in the neonatal period, but the female sibling is still alive at 2 years and 6 months of age.