183 research outputs found
Additive Manufacturing and Topology Optimization Applied to Impeller to Enhance Mechanical Performance
LectureThe paper describes the link between additive manufacturing techniques and topological optimization design process.
An overview of Inconel718 printed material characteristics and as printed quality is given
Finally expander and compressor topological optimization results are shown highlighting the improvement in stress level and dynamic behavior
Design and Production of Innovative Turbomachinery Components via Topology Optimization and Additive Manufacturing
New Challenges and Design for High Mach High Flow Coefficient Impeller for Large Size LNG Plant
LectureThe new generation of LNG plant are moving toward a larger size, that mean larger compression stations, driven by higher power gas turbine that can arrive and exceed 100 MW. This increase of specific power means also increase in compression gas flow and so the need to have compressors that are able to handle it in efficient way. This is true in particular for impeller stages equipping the Propane Compressors that will be selected at higher specific flow coefficient and Mach number. The present paper illustrates an improved impeller stage designed in particular to fit this duty, the need of a multidisciplinary optimization, from aerodynamic, structural mechanic, aeromechanic and rotordynamic. The paper illustrates the main design challenges for this type of impeller design, the validation done by the OEM and the benefits of their usage by mean of dedicated Case studied
Additive Manufacturing and Topology Optimization Applied to Impeller to Enhance Mechanical Performance
LectureThe paper describes the link between additive manufacturing techniques and topological optimization design process.
An overview of Inconel718 printed material characteristics and as printed quality is given
Finally expander and compressor topological optimization results are shown highlighting the improvement in stress level and dynamic behavior
Full Scale Validation Of A High Pressure Ratio Centrifugal Compressor
LectureThe present paper describes the test activities which have validated a new compressor architecture, developed by the OEM, which is able to deliver a higher pressure ratio in a single casing with respect to traditional configurations.
The major differences with respect to the typical technologies used for high pressure machines are in the rotor design: Rotor stacked configuration with impellers connected through high precision toothed joint and a pre-stretched tie-rod; Shrouded and unshrouded impellers on a multistage between-bearings compressor; High peripheral speed journal and thrust bearings. The combination of unshrouded and shrouded impellers allows achieving same pressure ratio in a shorter bearing span, giving the possibility to increase the number of sections for each unit, making possible to reduce the number of casings. A full scale prototype has been built and tested to validate the new machine architecture. The prototype has been designed to fulfill a compression service made of three compression sections with a single unit; the same service could only be performed with at least two units if a standard compressor design was applied. The service requires serial compression of natural gas, characterized as follows: Design inlet volumetric flow close to10800m3/h; Design pressure ratio close to 30; Absorbed power~14MW; Design speed of 17619 RPM (MCS = 18500RPM, mos = 14095 RPM); First section comprises 2 open impellers; second section comprises 3 closed impellers and third section has 2 closed impellers. Impellers for first and second sections are in stacked configuration; third section’s impellers are mounted through shrink fitting. Considering the increased speed requirement, the prototype has been tested in conjunction with an epicyclic gear, which allows for improved efficiency for high gear ratio (12.34 in this case) with respect to standard parallel axes gears
How echinoccocosis affects potential cancer markers in plasma: galectin-3, sN-cadherin and sE-cadherin? a preliminary report
Identification of differentially expressed genes using an annealing control primer system in stage III serous ovarian carcinoma
<p>Abstract</p> <p>Background</p> <p>Most patients with ovarian cancer are diagnosed with advanced stage disease (<it>i.e</it>., stage III-IV), which is associated with a poor prognosis. Differentially expressed genes (DEGs) in stage III serous ovarian carcinoma compared to normal tissue were screened by a new differential display method, the annealing control primer (ACP) system. The potential targets for markers that could be used for diagnosis and prognosis, for stage III serous ovarian cancer, were found by cluster and survival analysis.</p> <p>Methods</p> <p>The ACP-based reverse transcriptase polymerase chain reaction (RT PCR) technique was used to identify DEGs in patients with stage III serous ovarian carcinoma. The DEGs identified by the ACP system were confirmed by quantitative real-time PCR. Cluster analysis was performed on the basis of the expression profile produced by quantitative real-time PCR and survival analysis was carried out by the Kaplan-Meier method and Cox proportional hazards multivariate model; the results of gene expression were compared between chemo-resistant and chemo-sensitive groups.</p> <p>Results</p> <p>A total of 114 DEGs were identified by the ACP-based RT PCR technique among patients with stage III serous ovarian carcinoma. The DEGs associated with an apoptosis inhibitory process tended to be up-regulated clones while the DEGs associated with immune response tended to be down-regulated clones. Cluster analysis of the gene expression profile obtained by quantitative real-time PCR revealed two contrasting groups of DEGs. That is, a group of genes including: <it>SSBP1</it>, <it>IFI6 DDT</it>, <it>IFI27</it>, <it>C11orf92</it>, <it>NFKBIA</it>, <it>TNXB</it>, <it>NEAT1 </it>and <it>TFG </it>were up-regulated while another group of genes consisting of: <it>LAMB2</it>, <it>XRCC6</it>, <it>MEF2C</it>, <it>RBM5</it>, <it>FOXP1</it>, <it>NUDCP2</it>, <it>LGALS3</it>, <it>TMEM185A</it>, and <it>C1S </it>were down-regulated in most patients. Survival analysis revealed that the up-regulated genes such as <it>DDAH2, RNase K and TCEAL2 </it>might be associated with a poor prognosis. Furthermore, the prognosis of patients with chemo-resistance was predicted to be very poor when genes such as <it>RNase K, FOXP1</it>, <it>LAMB2 </it>and <it>MRVI1 </it>were up-regulated.</p> <p>Conclusion</p> <p>The DEGs in patients with stage III serous ovarian cancer were successfully and reliably identified by the ACP-based RT PCR technique. The DEGs identified in this study might help predict the prognosis of patients with stage III serous ovarian cancer as well as suggest targets for the development of new treatment regimens.</p
WEE1 inhibition sensitizes osteosarcoma to radiotherapy
<p>Abstract</p> <p>Background</p> <p>The use of radiotherapy in osteosarcoma (OS) is controversial due to its radioresistance. OS patients currently treated with radiotherapy generally are inoperable, have painful skeletal metastases, refuse surgery or have undergone an intralesional resection of the primary tumor. After irradiation-induced DNA damage, OS cells sustain a prolonged G<sub>2 </sub>cell cycle checkpoint arrest allowing DNA repair and evasion of cell death. Inhibition of WEE1 kinase leads to abrogation of the G<sub>2 </sub>arrest and could sensitize OS cells to irradiation induced cell death.</p> <p>Methods</p> <p>WEE1 expression in OS was investigated by gene-expression data analysis and immunohistochemistry of tumor samples. WEE1 expression in OS cell lines and human osteoblasts was investigated by Western blot. The effect of WEE1 inhibition on the radiosensitivity of OS cells was assessed by cell viability and caspase activation analyses after combination treatment. The presence of DNA damage was visualized using immunofluorescence microscopy. Cell cycle effects were investigated by flow cytometry and WEE1 kinase regulation was analyzed by Western blot.</p> <p>Results</p> <p>WEE1 expression is found in the majority of tested OS tissue samples. Small molecule drug PD0166285 inhibits WEE1 kinase activity. In the presence of WEE1-inhibitor, irradiated cells fail to repair their damaged DNA, and show higher levels of caspase activation. The inhibition of WEE1 effectively abrogates the irradiation-induced G<sub>2 </sub>arrest in OS cells, forcing the cells into premature, catastrophic mitosis, thus enhancing cell death after irradiation treatment.</p> <p>Conclusion</p> <p>We show that PD0166285, a small molecule WEE1 kinase inhibitor, can abrogate the G<sub>2 </sub>checkpoint in OS cells, pushing them into mitotic catastrophe and thus sensitizing OS cells to irradiation-induced cell death. This suggests that WEE1 inhibition may be a promising strategy to enhance the radiotherapy effect in patients with OS.</p
Interaction of galectin-3 with MUC1 on cell surface promotes EGFR dimerization and activation in human epithelial cancer cells
Epidermal growth factor receptor (EGFR) is an important regulator of epithelial cell growth and survival in normal and cancerous tissues and is a principal therapeutic target for cancer treatment. EGFR is associated in epithelial cells with the heavily glycosylated transmembrane mucin protein MUC1, a natural ligand of galectin-3 that is overexpressed in cancer. This study reveals that the expression of cell surface MUC1 is a critical enhancer of EGF-induced EGFR activation in human breast and colon cancer cells. Both the MUC1 extracellular and intracellular domains are involved in EGFR activation but the predominant influence comes from its extracellular domain. Binding of galectin-3 to the MUC1 extracellular domain induces MUC1 cell surface polarization and increases MUC1–EGFR association. This leads to a rapid increase of EGFR homo-/hetero-dimerization and subsequently increased, and also prolonged, EGFR activation and signalling. This effect requires both the galectin-3 C-terminal carbohydrate recognition domain and its N-terminal ligand multi-merization domain. Thus, interaction of galectin-3 with MUC1 on cell surface promotes EGFR dimerization and activation in epithelial cancer cells. As MUC1 and galectin-3 are both commonly overexpressed in most types of epithelial cancers, their interaction and impact on EGFR activation likely makes important contribution to EGFR-associated tumorigenesis and cancer progression and may also influence the effectiveness of EGFR-targeted cancer therapy
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