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Objective:To explore the innovative measures of scientific and technological achievements transformation in hospital by taking the practical experience of scientific and technological achievements transformation of West China Hospital of Sichuan University (WCH).Methods:The data of patents and technological achievements transformation of WCH was analyzed.Results:WCH applied for 1 800 patents and granted 1 145 during January 2015 and December 2019. By 2019, the conversion rate of scientific and technological achievements of WCH reached 14%.Conclusions:WCH has achieved remarkable results in promoting the scientific and technological achievements transformation through a series of innovative explorations and practices, including building professional technology transfer organizations and teams, establishing achievement transformation incentive policies, developing technology transformation standard process and regulations, creating a positive atmosphere of achievement transformation , as well as actively cultivating high-value patents.
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<p><b>BACKGROUND</b>It has been proved that Tanshinone has obvious anticancer effect, but its mechanisms of anticancer are still unknown. Anticancer Ketonon is complex antitumor drug which Tanshinone is combined with other anticancer elements. This study aims to explore the antineoplastic effects of Anticancer Ketonon on Lewis lung cancer and the mechanisms in mice.</p><p><b>METHODS</b>The mice were divided into three groups: Ketonon group, 5-fluorouracil (5-Fu) group and control group. The former two groups were treated with responsive drugs after subcutaneous inoculation of Lewis lung cancer. The last group was only treated with normal saline after inoculation. Apoptosis index and cell cycle were measured by flow cytometry.</p><p><b>RESULTS</b>Two experiments were carried out in male and female mice respectively. The tumor inhibitory rates of Anticancer Ketonon were 38.9% and 32.2% respectively, those of 5-FU were 59.6% and 53.9%. Compared with those of control groups, the tumor weights in Ketonon group and 5-Fu group were statistically decreased (P < 0.05). Metastasis rates of the lung in the three groups were not statistically different (P > 0.05). The apoptosis index of Ketonon group was significantly higher than that of control group (P < 0.05), but the cell cycle was not statistically changed compared with that of control group (P > 0.05).</p><p><b>CONCLUSIONS</b>Anticancer Ketonon has antineoplastic effect on Lewis lung cancer in mice and the mechanism may be associated with inducing apoptosis of tumor cells.</p>
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<p><b>BACKGROUND</b>To study chemosensitivity of anticancer drugs in the peripheral blood lymphocytes(PBL) of lung cancer patients and evaluate the correlation of chemosensitivity of tumor cells and peripheral blood lymphocytes in vitro.</p><p><b>METHODS</b>The sensitive rate of 15 kinds of anticancer drugs in the peripheral blood lymphocytes and the tumor cells of 74 cases of lung cancer in vitro were tested by the MTT method.</p><p><b>RESULTS</b>There was no significant difference in the sensitivity of 12 anticancer drugs between PBL and tumor cells of patients with lung cancer (P > 0.05).</p><p><b>CONCLUSIONS</b>The chemosensitive test of the peripheral blood lymphocytes is valuable for reference of selecting anti-cancer drugs in clinic for lung cancer.</p>
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<p><b>BACKGROUND</b>To observe the growth-inhibiting effect of anticancer ketonon on A549 cell line and PLA-801D cell line and to explore its mechanism based on the antineoplastic effects of Tanshinon.</p><p><b>METHODS</b>A549 and PLA-801D cell lines were treated with anticancer ketonon by techniques of cell culture in vitro . The growth curves and dose-effect curves were drawn up. The ability of clone formation was determined. It was observed and analysed by light microscopy and flow cytometry.</p><p><b>RESULTS</b>The growth of A549 and PLA 801D cell lines was evidently inhibited. Ability of clone formation was inhibited. The apoptosis index of cells was increased after treated with anticancer ketonon and the cell cycle was blocked at G0/G1 phase.</p><p><b>CONCLUSIONS</b>Anticancer ketonon can significantly inhibit the growth of human lung cancer cells probably through inducing the apoptosis of cancer cells.</p>
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<p><b>BACKGROUND</b>To study the growth-inhibiting effect and its molecular mechanism of Tanshinone on human lung carcinoma cell line.</p><p><b>METHODS</b>Human lung adenocarcinoma cell line (SPC-A-1) was treated in vitro with 0.5μg/ml Tanshinone IIA for five days, and the cells treated with all trans retinoic acid (RA) and DDP as control. Changes in cell morphology, proliferation dynamics, cell cycle distribution and tumor-related gene expression were detected.</p><p><b>RESULTS</b>The cell growth and rate of clone formation of SPC-A-1 cells were markedly inhibited in Tanshinone group than RA group. Flow cytometry demonstrated that S phase cells decreased and G₀/G₁ phase cells increased in Tanshinone group. Expression of p53, p21 was up-regulated obviously but CDKN₂ was down-regulated markedly by Tanshinone IIA.</p><p><b>CONCLUSIONS</b>Tanshinone IIA can inhibit cell growth and clone formation in human lung cancer cell line (SPC-A-1) and its possible molecular mechanism may be inhibiting DNA synthesis by up-regulating p53, p21 and down-regulating CDKN₂.</p>
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<p><b>BACKGROUND</b>To study the apoptosis-inducing effect of Tanshinone and its molecular mechanism on human lung cancer cells.</p><p><b>METHODS</b>Human lung cancer cell line (SPC-A-1) was treated in vitro with 0.5 mg/L Tanshinone IIA for five days, and the cells treated with all trans retinoic acid (RA) or DDP as controls. Changes in cell morphology, apoptotic index and apoptosis related gene expression were detected by electron microscope, FCM and DNA-end-labeling.</p><p><b>RESULTS</b>Many apoptotic cells were observed by light and electron microscopes. FCM examination showed that apoptotic index in Tanshinone group was much higher than that of DDP and control groups, but no difference was found statistically compared with RA group. The expression of p53, Fas and Bax genes in Tanshinone group was up-regulated markedly, but Bcl-2 was obviously down-regulated.</p><p><b>CONCLUSIONS</b>Tanshinone IIA can induce apoptosis in human lung cancer cell line (SPC-A-1) . Up-regulating expression of p53, Bax, Fas and down-regulating Bcl-2 expression might be its molecular mechanisms.</p>
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<p><b>OBJECTIVE</b>To explore the role of fragile histidine triad(FHIT) gene in the proliferation, apoptosis and tumorigenesis of human lung cancer cells.</p><p><b>METHODS</b>FHIT gene packaged with lipofectin was transfected into the cells of a human lung adenocarcinoma cell line (A549), which stably expressed ectogenous FHIT gene. The FHIT mRNA and protein expression of A549-FHIT, A549-vector and A549 cell were detected by reverse transcription-PCR(RT-PCR), Western blot and immunocytochemical methods. The cell cycle pattern and apoptosis were assayed by using flow cytometry.</p><p><b>RESULTS</b>After transfection of FHIT gene, cell growth was obviously inhibited (P<0.01). The apoptosis index of A549-FHIT (8.42%) was significantly higher than that of A549-vector (5.45%) and A549 cells (5.71%)(P<0.01). The clone-formation rate of A549-FHIT cell (21.84%) was significantly lower than that of A549-vector (28.70%) and A549 cells (31.68%, P<0.01). Compared with control cell lines, larger scale of A549-FHIT cells accumulated in G0/G1, presenting that the proportion of the cells in G0/G1 phase was obviously increased from 67.78 % to 82.35 %. Tumorigenicity of the A549 cells in nude mice was greatly inhibited by expression of ectogenous FHIT gene, the weight and volume of A549-FHIT(1.61 g/1.37 cm(3)) were significantly lower than that of A549-vector (2.45 g/1.99cm(3)) and A549 cells (2.77 g/2.27 cm(3))(P<0.05).</p><p><b>CONCLUSION</b>Expression of ectogenous FHIT gene can obviously inhibit the proliferation and tumorigenesis of A549 cells, and can induce A549 cells into programmed cell death. The result of this study suggests that FHIT gene may be a tumor suppressor gene in human lung cancer cells.</p>
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Animals , Female , Humans , Male , Mice , Acid Anhydride Hydrolases , Adenocarcinoma , Genetics , Pathology , Apoptosis , Physiology , Cell Cycle , Physiology , Cell Division , Physiology , Genes, Tumor Suppressor , Physiology , Lung Neoplasms , Genetics , Pathology , Mice, Nude , Neoplasm Proteins , Genetics , Physiology , Neoplasm Transplantation , Phenotype , Transfection , Transplantation, Heterologous , Tumor Cells, CulturedABSTRACT
1?g/ml)could inhibit osteoblasts to grow and proliferate, and showed cytotoxic activity. Conclusion aFGF possesses the effect of triggering osteoblasts to grow and proliferate, and its effective concentration is 10-100 ng/ml.
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OBJECTIVE:To study the in vitro sensitivity of lung cancer tissue to commonly-used antineoplas?tics.METHODS:The sensitivity of45fresh samples of human lung cancer to15commonly-used antineoplastics was deter?mined by MTT method.RESULTS:Lung cancer was more sensitive to CBP,VM26,THP,DDP,BLM,MTX and HCPT.However,there was individual difference in sensitivity to the same drug.CONCLUSION:The sensitivity assay of chemotherapeutic agents could provide important information for selection of the agents and MTT assay is a rapid and simple method for detecting the sensitivity of antineoplastics.