Numerical Analysis on a Perforated Muffler Applied in the Discharge Chamber of a Twin Screw Refrigeration Compressor Based on Fluid-Acoustic Coupling Method

The twin screw compressor has been widely used in the refrigeration systems due to advantages such as compact structure, stable operation, high efficiency and good adaptability. Intermittent gas flow generates gas pulsation that cause serious problems such as structural vibration and noise in the twin screw refrigeration compressor. Because the mechanical noise can be controlled well with the improvement of machining and assembly accuracy, the aerodynamic noise induced by gas pulsation even has become the main noise source of the twin screw refrigeration compressor. In order to reduce the pressure pulsation, a broadband perforated panel muffler applied in the discharge chamber of the twin screw refrigeration compressor is proposed based on the noise spectrum and flow characteristics of the compressor. In order to obtain the noise spectrum of the twin screw refrigeration compressor, the pressure fluctuation in discharge chamber based on a three-dimensional CFD simulation model is calculated, and the acoustical model is established based on fluid-acoustic coupling method. Then the impacts of different structural parameters on the performance of a perforated panel muffler are investigated, including perforation rate, perforation diameter and panel thickness. Through the optimization of the perforated muffler, a better reduction effect of broadband noise can be achieved. Results of fluid-acoustic coupled analysis can provide guidance on the design and optimization of the perforated muffler and noise reduction of the twin screw refrigeration compressor

Constitutive overexpression of a novel 21 kDa protein by Hodgkin Lymphoma and Aggressive Non-Hodgkin Lymphomas

© 2008 Zhou et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution Licens

The Rotavirus Enterotoxin NSP4 Directly Interacts with the Caveolar Structural Protein Caveolin-1

Rotavirus nonstructural protein 4 (NSP4) is known to function as an intracellular receptor at the endoplasmic reticulum (ER) critical to viral morphogenesis and is the first characterized viral enterotoxin. Exogenously added NSP4 induces diarrhea in rodent pups and stimulates secretory chloride currents across intestinal segments as measured in Ussing chambers. Circular dichroism studies further reveal that intact NSP4 and the enterotoxic peptide (NSP4114-135) that is located within the extended, C-terminal amphipathic helix preferentially interact with caveola-like model membranes. We now show colocalization of NSP4 and caveolin-1 in NSP4-transfected and rotavirus-infected mammalian cells in reticular structures surrounding the nucleus (likely ER), in the cytosol, and at the cell periphery by laser scanning confocal microscopy. A direct interaction between NSP4 residues 112 to 140 and caveolin-1 was determined by the Pro-Quest yeast two-hybrid system with full-length NSP4 and seven overlapping deletion mutants as bait, caveolin-1 as prey, and vice versa. Coimmunoprecipitation of NSP4-caveolin-1 complexes from rotavirus-infected mammalian cells demonstrated that the interaction occurs during viral infection. Finally, binding of caveolin-1 from mammalian cell lysates to Sepharose-bound, NSP4-specific synthetic peptides confirmed the yeast two-hybrid data and further delineated the binding domain to amino acids 114 to 135. We propose that the association of NSP4 and caveolin-1 contributes to NSP4 intracellular trafficking from the ER to the cell surface and speculate that exogenously added NSP4 stimulates signaling molecules located in caveola microdomains

Sub-megabase resolution tiling (SMRT) array-based comparative genomic hybridization profiling reveals novel gains and losses of chromosomal regions in Hodgkin Lymphoma and Anaplastic Large Cell Lymphoma cell lines

<p>Abstract</p> <p>Background</p> <p>Hodgkin lymphoma (HL) and Anaplastic Large Cell Lymphoma (ALCL), are forms of malignant lymphoma defined by unique morphologic, immunophenotypic, genotypic, and clinical characteristics, but both overexpress CD30. We used sub-megabase resolution tiling (SMRT) array-based comparative genomic hybridization to screen HL-derived cell lines (KMH2 and L428) and ALCL cell lines (DEL and SR-786) in order to identify disease-associated gene copy number gains and losses.</p> <p>Results</p> <p>Significant copy number gains and losses were observed on several chromosomes in all four cell lines. Assessment of copy number alterations with 26,819 DNA segments identified an average of 20 genetic alterations. Of the recurrent minimally altered regions identified, 11 (55%) were within previously published regions of chromosomal alterations in HL and ALCL cell lines while 9 (45%) were novel alterations not previously reported. HL cell lines L428 and KMH2 shared gains in chromosome cytobands 2q23.1-q24.2, 7q32.2-q36.3, 9p21.3-p13.3, 12q13.13-q14.1, and losses in 13q12.13-q12.3, and 18q21.32-q23. ALCL cell lines SR-786 and DEL, showed gains in cytobands 5p15.32-p14.3, 20p12.3-q13.11, and 20q13.2-q13.32. Both pairs of HL and ALCL cell lines showed losses in 18q21.32-18q23.</p> <p>Conclusion</p> <p>This study is considered to be the first one describing HL and ALCL cell line genomes at sub-megabase resolution. This high-resolution analysis allowed us to propose novel candidate target genes that could potentially contribute to the pathogenesis of HL and ALCL. FISH was used to confirm the amplification of all three isoforms of the trypsin gene (PRSS1/PRSS2/PRSS3) in KMH2 and L428 (HL) and DEL (ALCL) cell lines. These are novel findings that have not been previously reported in the lymphoma literature, and opens up an entirely new area of research that has not been previously associated with lymphoma biology. The findings raise interesting possibilities about the role of signaling pathways triggered by membrane associated serine proteases in HL and aggressive NHL, similar to those described in epithelial tumors.</p

Constitutively overexpressed 21 kDa protein in Hodgkin lymphoma and aggressive non-Hodgkin lymphomas identified as cytochrome B5b (CYB5B)

<p>Abstract</p> <p>Background</p> <p>We have previously reported a novel constitutively overexpressed 21 kDa protein in Hodgkin Lymphoma (HL) and aggressive Non-Hodgkin Lymphomas (NHL). The objective of the current study was to 1) identify this protein using two independent methods, 2) study the expression of the protein and its encoding mRNA in reactive lymph nodes, normal lymphocytes and CD34+ bone marrow precursor cells, 3) analyse patterns of expression of the protein in tissue microarrays assembled from a large number of diagnostic clinical biopsies from patients with HL, and 4) determine the copy number variation and mutation status of the encoding gene in HL cell lines.</p> <p>Results</p> <p>Peptide sequencing by LC-MS/MS and protein identification by protein array screening identified a single protein, CYB5B. No mutations were detected in the <it>CYB5B </it>gene in HL cell lines. Quantitative PCR showed <it>CYB5B </it>gene expression was increased in HL and NHL cell lines. Array CGH using a submegabase resolution tiling array revealed gains in the <it>CYB5B </it>locus in HL cell lines KMH2 and L428. Membrane expression was seen in Reed-Sternberg cells in clinical biopsies from patients with HL but not in reactive lymph nodes. Bone marrow CD34+ precursor cells were CYB5B negative on the cell surface. RT-PCR assays of RNA extracted from T and B cell enriched fractions obtained from normal peripheral blood mononuclear cells, reactive lymph nodes, tonsils and normal bone marrow samples showed no evidence of increased mRNA levels of <it>CYB5B </it>in comparison to housekeeping gene <it>GAPDH</it>.</p> <p>Conclusions</p> <p>The 21 kDa protein overexpressed in HL and aggressive NHL is identical to CYB5B. <it>CYB5B </it>gene expression is increased in a subset of HL and NHL cell lines tested. This is associated with <it>CYB5B </it>gene amplification in HL cell lines KMH2 and L428. CYB5B may be a potential target for antibody-based therapy of HL and aggressive NHL as although cytoplasmic expression is present in reactive lymphocytes, it is not expressed on the cell surface of non-neoplastic lymphocytes or bone marrow precursor cells.</p

Sterol Carrier Protein-2 Directly Interacts with Caveolin-1 in Vitro and in Vivo

HDL-mediated reverse-cholesterol transport as well as phosphoinositide signaling are mediated through plasma membrane microdomains termed caveolae/lipid rafts. However, relatively little is known regarding mechanism(s) whereby these lipids traffic to or are targeted to caveolae/lipid rafts. Since sterol carrier protein-2 (SCP-2) binds both cholesterol and phosphatidylinositol, the possibility that SCP-2 might interact with caveolin-1 and caveolae was examined. Double immunolabeling and laser scanning fluorescence microscopy showed that a small but significant portion of SCP-2 colocalized with caveolin-1 primarily at the plasma membrane of L-cells and more so within intracellular punctuate structures in hepatoma cells. In SCP-2 overexpressing L-cells, SCP-2 was detected in close proximity to caveolin, 48 ± 4 Å, as determined by fluorescence resonance energy transfer (FRET) and immunogold electron microscopy. Cell fractionation of SCP-2 overexpressing L-cells and Western blotting detected SCP-2 in purified plasma membranes, especially in caveolae/ lipid rafts as compared to the nonraft fraction. SCP-2 and caveolin-1 were coimmunoprecipitated from cell lysates by anti-caveolin-1 and anti-SCP-2. Finally, a yeast two-hybrid assay demonstrated that SCP-2 directly interacts with caveolin-1 in vivo. These interactions of SCP-2 with caveolin-1 were specific since a functionally related protein, phosphatidyinositol transfer protein (PITP), colocalized much less well with caveolin-1, was not in close proximity to caveolin-1 (i.e., \u3e120 Å), and was not coimmunoprecipitated by anti-caveolin-1 from cell lysates. In summary, it was shown for the first time that SCP-2 (but not PITP) selectively interacted with caveolin-1, both within the cytoplasm and at the plasma membrane. These data contribute significantly to our understanding of the role of SCP-2 in cholesterol and phosphatidylinositol targeted from intracellular sites of synthesis in the endoplasmic reticulum to caveolae/lipid rafts at the cell surface plasma membrane

Biochar-based fertilizer: Supercharging root membrane potential and biomass yield of rice

Biochar-based compound fertilizers (BCF) and amendments have proven to enhance crop yields and modify soil properties (pH, nutrients, organic matter, structure etc.) and are now in commercial production in China. While there is a good understanding of the changes in soil properties following biochar addition, the interactions within the rhizosphere remain largely unstudied, with benefits to yield observed beyond the changes in soil properties alone. We investigated the rhizosphere interactions following the addition of an activated wheat straw BCF at an application rates of 0.25% (g·g−1 soil), which could potentially explain the increase of plant biomass (by 67%), herbage N (by 40%) and P (by 46%) uptake in the rice plants grown in the BCF-treated soil, compared to the rice plants grown in the soil with conventional fertilizer alone. Examination of the roots revealed that micron and submicron-sized biochar were embedded in the plaque layer. BCF increased soil Eh by 85 mV and increased the potential difference between the rhizosphere soil and the root membrane by 65 mV. This increased potential difference lowered the free energy required for root nutrient accumulation, potentially explaining greater plant nutrient content and biomass. We also demonstrate an increased abundance of plant-growth promoting bacteria and fungi in the rhizosphere. We suggest that the redox properties of the biochar cause major changes in electron status of rhizosphere soils that drive the observed agronomic benefits

ROBUSTNESS OPTIMIZATION IN PRESCRIPTIVE ANALYTICS

Ph.DDOCTOR OF PHILOSOPHY (BIZ

Nonlinear Flutter Response of Heated Curved Composite Panels with Embedded Macrofiber Composite Actuators

The nonlinear flutter response of heated curved composite panels with embedded macrofiber composite (MFC) actuators in supersonic airflow is investigated. Prescribed voltages are statically applied to the piezoelectric actuators, inducing a prestress field which results in an additional stiffness effect on the curved panel, and it will change the aeroelastic behavior of curved composite panels. The aeroelastic equations of curved composite panels with embedded MFC actuators are formulated by the finite element approach. The von Karman large deflection panel theory and the first-order piston theory aerodynamics are adopted in the formulation. The motion equations are solved by a fourth-order Runge–Kutta numerical scheme, and time history, phase portrait, Poincaré map, bifurcation diagram, and Lyapunov exponent are used for better understanding of the pre/postflutter responses. The results demonstrate that the nonlinear flutter response characteristics of the curved panel differs from those of the flat panels significantly, and the transverse displacement of the curved composite panels with embedded MFC actuators in the preflutter region shows a gradual static displacement; the chaotic motions occur directly after static motion because of the effect of the temperature elevation. The applied voltages can increase the critical dynamic pressure and change the bifurcation diagram of the curved composite panels with embedded MFC actuators, and the response amplitudes can be reduced evidently