232 research outputs found

    Thermal performance comparison between microchannel and round tube heat exchangers

    Get PDF
    Alternative round tube profiles to straight microchannel (SMC) tube geometry was explored by gradually applying the microchannel features to fin and tube type heat exchangers. First, previous experimental and computational works related to design and heat transfer analysis of microchannel heat exchanger tubes and testing was reviewed and then a numerical CFD model in FLUENT solver was developed, which was experimentally validated within an error range of 0.1 to 7.8 % based on available data in literature. Single phase, water to water, laminar, counter fluid flow of tube in shell calorimeter heat transfer experiments were numerically simulated to analyze the refrigerant side heat transfer enhancement if round microchannel tubes are used as outdoor coil. According to numerical results, the refrigerant side heat transfer capacity of round tubes of 10.3mm outer diameter with 42 microports of about 0.6 mm port diameter distributed around the tube perimeter (round tube microchannel) was estimated to be about 24% higher than conventional round tube (with no microchannel ports in them) and about 15% lower than conventional straight microchannel tube heat exchangers used in outdoor evaporators. In addition to refrigerant side, parametric studies were performed to investigate the heat transfer effectiveness of 10.3 mm and 5.15 mm outer diameter round (microchannel) tubes (multi port and annular) under cross flow configuration with dry air streams and results were compared with straight microchannel tubes in terms of tube diameter tube spacing effect. It was obtained that the round tube design of 5.15 mm outer diameter having an annular port of 1.6mm hydraulic diameter within 11mm edge to edge tube spacing of vertically parallel fin and tube coil configuration can provide similar air side heat transfer capacity of straight microchannel coil based on its secondary heat transfer area. Additionally, this configuration can provide 50 % better pressure drop performance compared to conventional straight microchannel tube coil.Mechanical & Aerospace Engineerin

    Three-dimensional higher-order Schrödinger algebras and Lie algebra expansions

    Get PDF
    We provide a Lie algebra expansion procedure to construct three-dimensional higher-order Schr\"odinger algebras which relies on a particular subalgebra of the four-dimensional relativistic conformal algebra. In particular, we reproduce the extended Schr\"odinger algebra and provide a new higher-order Schr\"odinger algebra. The structure of this new algebra leads to a discussion on the uniqueness of the higher-order non-relativistic algebras. Especially, we show that the recent d-dimensional symmetry algebra of an action principle for Newtonian gravity is not uniquely defined but can accommodate three discrete parameters. For a particular choice of these parameters, the Bargmann algebra becomes a subalgebra of that extended algebra which allows one to introduce a mass current in a Bargmann-invariant sense to the extended theory.Comment: v3., typos fixed, reference added, version appeared in JHE

    Characterization of Flocs in Dewatering of Coal Plant Tailings

    Get PDF
    Flocculation is a widely used method for dewatering fine coal tailings. Flocs must resist to the shear stresses during the following processes such as flotation, cyclone separation, and pumping. Therefore, the strength of the flocs must be considered during flocculation. In this study, the fine coal tailings were dewatered with an anionic flocculant SNF-923 at various dosages, and the floc size of the coal tailings was characterized using a laser diffraction particle size analyzer with respect to time in order to determine the change in the floc size and hence the floc strength. The results of this study clearly indicated that the determination of the floc size with a laser particle size analyzer could be a simple and good method to observe the flocculation efficiency in terms of the floc strength

    Genome-wide association study of root-lesion nematodes Pratylenchus species and crown rot Fusarium culmorum in bread wheat

    Get PDF
    Triticum aestivum L., also known as common wheat, is affected by many biotic stresses. Root diseases are the most difficult to tackle due to the complexity of phenotypic evaluation and the lack of resistant sources compared to other biotic stress factors. Soil-borne pathogens such as the root-lesion nematodes caused by the Pratylenchus species and crown rot caused by various Fusarium species are major wheat root diseases, causing substantial yield losses globally. A set of 189 advanced spring bread wheat lines obtained from the International Maize and Wheat Improvement Center (CIMMYT) were genotyped with 4056 single nucleotide polymorphisms (SNP) markers and screened for root-lesion nematodes and crown rot resistance. Population structure revealed that the genotypes could be divided into five subpopulations. Genome-Wide Association Studies were carried out for both resistances to Pratylenchus and Fusarium species. Based on our results, 11 different SNPs on chromosomes 1A, 1B, 2A, 3A, 4A, 5B, and 5D were significantly associated with root-lesion nematode resistance. Seven markers demonstrated association with P. neglectus, while the remaining four were linked to P. thornei resistance. In the case of crown rot, eight different markers on chromosomes 1A, 2B, 3A, 4B, 5B, and 7D were associated with Fusarium crown rot resistance. Identification and screening of root diseases is a challenging task; therefore, the newly identified resistant sources/genotypes could be exploited by breeders to be incorporated in breeding programs. The use of the identified markers in marker-assisted selection could enhance the selection process and cultivar development with root-lesion nematode and crown rot resistance

    Identification of novel neutralizing single-chain antibodies against vascular endothelial growth factor receptor 2

    Get PDF
    Human vascular endothelial growth factor (VEGF) and its receptor (VEGFR-2/kinase domain receptor [KDR]) play a crucial role in angiogenesis, which makes the VEGFR-2 signaling pathway a major target for therapeutic applications. In this study, a single-chain antibody phage display library was constructed from spleen cells of mice immunized with recombinant human soluble extracellular VEGFR-2/KDR consisting of all seven extracellular domains (sKDR D1-7) to obtain antibodies that block VEGF binding to VEGFR-2. Two specific single-chain antibodies (KDR1.3 and KDR2.6) that recognized human VEGFR-2 were selected; diversity analysis of the clones was performed by BstNI fingerprinting and nucleotide sequencing. The single-chain variable fragments (scFvs) were expressed in soluble form and specificity of interactions between affinity purified scFvs and VEGFR-2 was confirmed by ELISA. Binding of the recombinant antibodies for VEGFR-2 receptors was investigated by surface plasmon resonance spectroscopy. In vitro cell culture assays showed that KDR1.3 and KDR2.6 scFvs significantly suppressed the mitogenic response of human umbilical vein endothelial cells to recombinant human VEGF 165 in a dose-dependent manner, and reduced VEGF-dependent cell proliferation by 60% and 40%, respectively. In vivo analysis of these recombinant antibodies in a rat cornea angiogenesis model revealed that both antibodies suppressed the development of new corneal vessels (p < 0.05). Overall, in vitro and in vivo results disclose strong interactions of KDR1.3 and KDR2.6 scFvs with VEGFR-2. These findings indicate that KDR1.3 and KDR2.6 scFvs are promising antiangiogenic therapeutic agents. © 2011 International Union of Biochemistry and Molecular Biology, Inc

    Genotype-Phenotype Correlations in Charcot-Marie-Tooth Disease Due to MTMR2 Mutations and Implications in Membrane Trafficking

    Get PDF
    Charcot-Marie-Tooth type 4 (CMT4) is an autosomal recessive severe form of neuropathy with genetic heterogeneity. CMT4B1 is caused by mutations in the myotubularin-related 2 (MTMR2) gene and as a member of the myotubularin family, the MTMR2 protein is crucial for the modulation of membrane trafficking. To enable future clinical trials, we performed a detailed review of the published cases with MTMR2 mutations and describe four novel cases identified through whole-exome sequencing (WES). The four unrelated families harbor novel homozygous mutations in MTMR2 (NM_016156, Family 1: c.1490dupC; p.Phe498IlefsTer2; Family 2: c.1479+1G>A; Family 3: c.1090C>T; p.Arg364Ter; Family 4: c.883C>T; p.Arg295Ter) and present with CMT4B1-related severe early-onset motor and sensory neuropathy, generalized muscle atrophy, facial and bulbar weakness, and pes cavus deformity. The clinical description of the new mutations reported here overlap with previously reported CMT4B1 phenotypes caused by mutations in the phosphatase domain of MTMR2, suggesting that nonsense MTMR2 mutations, which are predicted to result in loss or disruption of the phosphatase domain, are associated with a severe phenotype and loss of independent ambulation by the early twenties. Whereas the few reported missense mutations and also those truncating mutations occurring at the C-terminus after the phosphatase domain cause a rather mild phenotype and patients were still ambulatory above the age 30 years. Charcot-Marie-Tooth neuropathy and Centronuclear Myopathy causing mutations have been shown to occur in proteins involved in membrane remodeling and trafficking pathway mediated by phosphoinositides. Earlier studies have showing the rescue of MTM1 myopathy by MTMR2 overexpression, emphasize the importance of maintaining the phosphoinositides equilibrium and highlight a potential compensatory mechanism amongst members of this pathway. This proved that the regulation of expression of these proteins involved in the membrane remodeling pathway may compensate each other's loss- or gain-of-function mutations by restoring the phosphoinositides equilibrium. This provides a potential therapeutic strategy for neuromuscular diseases resulting from mutations in the membrane remodeling pathway
    corecore