The malignant pleural mesothelioma is kind of tumor that has close contact with theasbestos to oncolytic,and its attack is very strong.Because the reasons of it iS not obviously and always be found in the middle of late period,the present treatment plan dosnt have a satisfied effect.However oncolytic herpes simplex viruses and obliging platinum induction to oncolyti herpes simplex viruses that generate the GADD34 protein may have the relative specificity to themesothelioma cancer cell,therefore is a prospect ive treatment plan.

Objective To observe the inhibit effect of triplex forming oligonucleotide (TFO)(platelet-derived growth factor-B chain, PDGF) on tumor growth and angiogenesis in rats with glioma.Methods 1?10~6 C_6 glioma cells with high-flow microinfusion were seed into right caudate putamens of 18 rats by stereotaxic technique. TFO was injected in situ 1 week after glioma cells inoculation. Treat group Ⅰ and treat group Ⅱ received TFO at dose of 1.5 mg/20 ?l and 3.0 mg/20 ?l, respectively. The same doses were given again at 8, 11 and 14th day after glioma cells inoculation. The control group was treated with 20 ?l normal saline at same time like treat groups. Three weeks after glioma cells inoculation, all the rats were killed. The expressions of, PDGF-B, vascular endothelial growth factor (VEGF) and proliferating cell nuclear antigen (PCNA) were detected with microscopic histology.Results The inhibition rate of tumor growth was 66.0% in treat groupⅠand 92.2% in treat group Ⅱ. There was significant difference between the two groups ((P

To correlate the ultrasound and MR imaging of carotid atherosclerotic plaque with its histologic compositions,20 patients(22 lesions) scheduled for carotid endarterectomy were examined by B mode ultrasound and MRI preoperatively. The specimens were also examined postoperatively and the images of carotid plaque were recorded. The transverse pathological sections of plaques were made and matched with images of ultrasound and MRI. 256 gray scale ultrasound densitometric analysis of carotid plaque compositions was performed. Ultrasonic density of calcium, fibrous tissue, hemorrage/thrombus and lipid deposits was (89?12), (53?8), (37?6) and (39?3) respectively in vivo , and was (168?11), (136?12), (85?12) and (89?10) respectively in vitro . In vivo relative signal intensities of calcium, fibrous tissue, old hemorrhage/thrombus and lipid deposits were low, equal, equal and very high respectively on T 1 W MR image, and very low, equal, high and high respectively on PDW MR image, and low, equal or slightly high, high and high respectively on T 2 W MR image. Signal intensities of plaque contents ex vivo were correlated to signal intensities in vivo. Densitometric analysis of ultrasound images of carotid plaques can quantify possible components of plaque, and MRI has the feasibility to identify the components of plaque.

Objective To discuss the image characters and the technical manipulation of endovascular embolization for cerebral AVM with bleeding. Methods The cerebral AVMs with bleeding in 56 cases were confirmed by CT, MRI, and whole cerebral DSA. Depended on the nidus of AVM, the superselective endovascular embolization with NBCA or embolization combined with radiological surgery was chosen. Results The nidus was eliminated for 100% in 36 cases after embolization for 1 to 3 processes. The rebleeding was found in 2 cases with new growth and survival aneurysm in nidus during the follow-up period and treatment with X-knife, and was cured by the second embolization. Conclusion The main causes of AVM bleeding included aneurysm and aneurysm-like dilation beside and located at the nidus, fine draining veins, and growth in the ventricles. To prevent the brain from bleeding, it is favourable to eliminate the aneurysm in AVM during embolization.

Objective:To observe the effect of triplex forming oligonucleotide(TFO) of PDGF-B chain on cell proliferation and cell cycle of rat glioma.Methods:1?10 6 C 6 glioma cells with high-flow microinfusion were seeded into right caudate putamen of rats.TFO was used in situ a week after glioma cell inoculation.The treatment groupⅠandⅡwere treated with 1.5 mg/20 ?l and 3.0 mg/20 ?l TFO respectively on 8,11 and 14 d after cell inoculation.The control group was treated with 20 ?l normal saline with the same procedure.Three weeks after cell inoculation all rats were killed and samples were detected with macroscopic,microscopic histology and immunofluorescence flow cytometric analysis.Results:The inhibition rates of tumor growth were 66.1% in the treatment groupⅠand 91.8% in the treatment group Ⅱ.TFO specifically blocked expressions of PDGF-B and PCNA of glioma cells in a concentration-dependent fashion. TFO obviously inhibited the transit of cells from the G 0-G 1 to S phase in a concentration-dependent fashion.Conclusion:TFO can commendably block PDGF-B expression,inhibit cell proliferation and induce C 6 glioma cells arrest in the G 1 phase,and thus inhibit tumor growth of glioma.

Purpose To investigate the diagnostic value of the arrhythmogenic right ventricular dysplasia (ARVD) using multi-slice spiral CT (MSCT). Materials and Methods Thirty-four patients who were suspected as ARVD received right ventricular radiography, including 16 ARVD patients and 15 non-ARVD patients regarded as control group. The structural and shaped change of heart on reconstructed images of long axis, short axis and four cavity surface and analyze were observed, and MSCT features of right ventricular radiography characteristics were analyzed for ARVD patients. Results Sixteen cases of ARVD were correctly diagnosed by MSCT, and 14 cases had fatty infiltration including 11 cases of apex of heart, 8 cases of inferior wall, 5 cases of anterior wall, 5 cases of anterior wall of funnel area, 3 cases of diagram, 4 cases of papillary muscle, 6 cases of muscular trabecula and moderator band and 1 case of whole right ventricular free wall. Five cases showed scallop sign, 16 cases excessive trabecular change, 11 cases thinned changes, and 16 cases enlarged changes of right ventricular wall. Conclusion MSCT features of right ventricular for ARVD have relative diagnostic characteristics, and the scallop sign and excessive trabecular change of right ventricular wall are its specific imaging characteristics.

Objective:To investigate the feasibility and adverse reactions of simultaneous integrated boost (SIB) in volumetric modulated arc therapy (VMAT) for early breast cancer after breast-conserving surgery.Methods:A total of 67 patients with early breast cancer after breast-conserving surgery at Zhongshan People's Hospital from September 2019 to May 2021 were enrolled. All patients received VMAT-SIB to the whole breast and tumor bed. The total breast dose and tumor bed dose were 40.5Gy/15 times every 3 weeks and 48 Gy/15 every 3 weeks respectively. The exposure dose of organs at risk and acute adverse reactions of radiotherapy were evaluated.Results:The average doses of planning target volume of the whole brease (PTV WB) and planning target volume of the boost(PTV BOOST) were (42.0±2.1) Gy and (49.9±0.8) Gy, respectively. The V 95% and V 105% of PTV WB and PTV BOOST were (98.8±1.2)% and (31.4±11.3)%, (99.8±0.6)% and (22.9±10.2)%, respectively. The V 5Gy, V 20Gy, V 30Gy and mean dose (D mean) of ipsilateral lung were (52.4±12.0)%, (15.3±4.5)%, (6.7±2.2)% and (11.0±2.4) Gy respectively. The V 18Gy, V 40Gy and D mean of heart were 3.80% (0.48%,9.60%), 0 (0,0.16%) and (6.7±2.1) Gy respectively. At the end of radiotherapy, 19 patients (29%) of all 67 patients had no acute skin toxicity, 41 patients (61%) showed radiation erythema, 5 patients (7%) had radioactive dry peeling and 2 patients (3%) had wet peeling mainly located in the nipple, areola area and breast folds. None of the patients had grade 3-4 acute skin reactions. Breast swelling and breast pain were found respectively in 9 patients (13%) and 7 patients (10%). No local recurrence or distant metastases were observed during the follow-up period. The 2-year disease-free survival rate was 100%. Conclusions:VMAT combined with SIB is feasible in the treatment of early breast cancer. The adverse reactions of radiotherapy are mild and well tolerated.

BACKGROUNDTo explore the possibility of targeting blockage of Wnt signal transduction pathway of nm23-H1 gene transfection in human high-metastatic large cell lung cancer cell line L9981, and to provide evidence to elucidate the signal conductive mechanism of nm23-H1 mediated tumor metastasis suppression.

METHODSThe expression of GSK-3β and β-catenin of Wnt signal pathway was detected in cytoplasm and nucleus in L9981 cell line with nm23-H1 deletion, L9981-pLXSN cell line transfected with vector and L9981-nm23-H1 cell line transfected with nm23-H1 gene by Western blot.

RESULTS(1)GSK-3β expression in L9981-nm23-H1 cytoplasm (6 341±541) was significantly higher than those in L9981 (3 736±298) and L9981-pLXSN (3 613±383) cell lines ( P < 0.001); (2)GSK-3β expression in L9981-nm23-H1 nucleus (4 356±490) was significantly higher than those in L9981 (657±57) and L9981-pLXSN (705±75) cell lines ( P < 0.001); (3)β-catenin expression in L9981-nm23-H1 cytoplasm (3 649±118) was significantly higher than those in L9981 (1 401±31) and L9981-pLXSN (1 350±55) cell lines ( P < 0.001); (4)No statistical difference of the β-catenin expression in nucleus was observed among L9981-nm23-H1 (2 945±68), L9981 (2 604±23) and L9981-pLXSN (2 652±53)( P > 0.05); (5)No significant difference of GSK-3β or β-catenin expression in cytoplasm and nucleus was observed between L9981 and L9981-pLXSN ( P > 0.05).

CONCLUSIONS(1)nm23-H1 gene can remarkably upregulate the expression of GSK-3β in cytoplasm and nucleus, and β-catenin expression in cytoplasm in L9981-nm23-H1 cell, but can not induce the nucleus accumulation of β-catenin. (2)Regulation of GSK-3β and β-catenin expression, and targeting blockage of Wnt signaling pathway may be one of molecular mechanisms that nm23-H1 contributes to play a vital role in the "Lung Cancer Metastasis Suppressive Cascade".

BACKGROUNDTo explore the effects of nm23-H1 gene transfection and forskolin on PKA activity in human high-metastasis large cell lung cancer cell line L9981.

METHODSThree cell lines, primary human large cell lung cancer cell line (L9981), vector transfection cell line (L9981-pLXSN) and nm23-H1 gene transfection cell line (L9981-nm23-H1-pLXSN), were treated with PKA activator forskolin. The PKA activity at different time points after treatment with forskolin was detected in the three lung cancer cell lines by radioimmunological method with SignaTECT cAMP-dependent PKA assay system.

RESULTS(1) Before forskolin treatment, the activity of PKA of L9981-nm23-H1-pLXSN was remarkably higher than those of L9981 and L9981-pLXSN (P < 0.01), but no significant difference in the PKA activity was observed between L9981 and L9981-pLXSN (P > 0.05). (2)The PKA activity was remarkably increased in all the three lung cancer cell lines after treatment with different concentration of forskolin (P < 0.01), and up to the highest level at the concentration of 100 μmol/L. It showed a dose-dependent relationship between the PKA activity and forskolin concentration; (3) The PKA activity in all the three cell lines was elevated to the highest level at 30 minutes after treatment with forskolin of 100 μmol/L, and it showed a time-dependent relationship between the PKA activity and action time of forskolin.

CONCLUSIONS(1)Transfection of nm23-H1 gene can up-regulate the PKA activity of human high-metastasis large cell lung cancer cell line L9981, and its function as a tumor metastasis suppressor gene may be related to its effects on regulation of PKA signal transduction pathways; (2)Forskolin can remarkably up-regulate the PKA activity of L9981 cell line, and the elevation of PKA activity has a time-dependent and dose-dependent relation to forskolin.

BACKGROUNDTo explore the influences of nm23-H1 gene transfection and protein kinase C (PKC) inhibitor Calphostin C on PKC signal transduction pathway in human high-metastasis large cell lung cancer cell line L9981, and to evaluate the effects of nm23-H1 gene on translocation and activation in subcellular region.

METHODSThe translocation of PKC in subcellular region was observed in L9981 before and after nm23-H1 gene transfection and Calphostin C treatment by Laser scanning confocal microscope (LSCM) method.

RESULTSPKC-α and PKC-βII were found to locate in different subcellular site in L9981 before and after nm23-H1 gene transfection. PKC-α and PKC-βII mainly located in nucleus and perinucleus in L9981 and L9981-pLXSN cell lines, which were in active status. PKC-α and PKC-βII mainly located in soluble cytosolic fraction in L9981-nm23-H1 cell line and were inactive status. PKC-α and PKC-βII mainly located in cytosolic fraction and were in inactive status in all the three cell lines after treatment with Calphostin C.

CONCLUSIONSThe results suggest that nm23-H1 gene might make PKC to translocate from nucleus and perinucleus to soluble cytosolic fraction in L9981 cell line. PKC inhibitor, Calphostin C, can also make PKC to translocate from nucleus and perinucleus to soluble cytosolic fraction in L9981, L9981-pLXSN cell lines. Both transfection of nm23-H1 gene and treatment with Calphostin C can suppress the PKC signal transduction in L9981 cell line.