Experimental analysis and development of correlations for gas holdup in high pressure slurry co-current bubble columns

The effect of liquid and gas velocities, solid concentrations, and operating pressure has been studied experimentally in a 15 cm diameter air-water-glass beads bubble column. The superficial gas and liquid velocities varied from 1.0 to 40.00 cm/s and 0 to 16.04 cm/s, respectively, while the solid loading varied from 1 to 9%. The gas holdup in the column was reduced sharply as we switched from batch to co-current mode of operation. At low gas velocity, the effect of liquid velocity was insignificant; while at high gas velocity, increasing liquid velocity decreased the gas holdup. Drift flux approach was applied to quantify the combined effect of liquid and gas velocities over gas holdup. For co-current three phase flows, the gas holdup decreased with increase in solid loading for all pressures. But for batch operations, when solid loading was 5% or more, settling started leading to higher gas holdup. Increasing pressure from atmospheric conditions increased the gas holdup significantly, flattening asymptotically.     

Dual-Function Semaphorin 4D Released by Platelets: Suppression of Osteoblastogenesis and Promotion of Osteoclastogenesis

Effects of the antiosteoblastogenesis factor Semaphorin 4D (Sema4D), expressed by thrombin-activated platelets (TPs), on osteoblastogenesis, as well as osteoclastogenesis, were investigated in vitro. Intact platelets released both Sema4D and IGF-1. However, in response to stimulation with thrombin, platelets upregulated the release of Sema4D, but not IGF-1. Anti-Sema4D-neutralizing monoclonal antibody (mAb) upregulated TP-mediated osteoblastogenesis in MC3T3-E1 osteoblast precursors. MC3T3-E1 cells exposed to TPs induced phosphorylation of Akt and ERK further upregulated by the addition of anti-sema4D-mAb, suggesting the suppressive effects of TP-expressing Sema4D on osteoblastogenesis. On the other hand, TPs promoted RANKL-mediated osteoclastogenesis in the primary culture of bone-marrow-derived mononuclear cells (BMMCs). Among the known three receptors of Sema4D, including Plexin B1, Plexin B2 and CD72, little Plexin B2 was detected, and no Plexin B1 was detected, but a high level of CD72 mRNA was detected in RANKL-stimulated BMMCs by qPCR. Both anti-Sema4D-mAb and anti-CD72-mAb suppressed RANKL-induced osteoclast formation and bone resorptive activity, suggesting that Sema4D released by TPs promotes osteoclastogenesis via ligation to a CD72 receptor. This study demonstrated that Sema4D released by TPs suppresses osteogenic activity and promotes osteoclastogenesis, suggesting the novel property of platelets in bone-remodeling processes.     

EAPB0503, an Imidazoquinoxaline Derivative Modulates SENP3/ARF Mediated SUMOylation,and Induces NPM1c Degradation in NPM1 Mutant AML

Nucleophosmin-1 (NPM1) is a pleiotropic protein involved in numerous cellular processes. NPM1 shuttles between the nucleus and the cytoplasm, but exhibits a predominant nucleolar localization, where its fate and functions are exquisitely controlled by dynamic post-translational modifications (PTM). Sentrin/SUMO Specific Peptidase 3 (SENP3) and ARF are two nucleolar proteins involved in NPM1 PTMs. SENP3 antagonizes ARF-mediated NPM1 SUMOylation, to promote ribosomal biogenesis. In Acute Myeloid Leukemia (AML), NPM1 is frequently mutated, and exhibits an aberrant cytoplasmic localization (NPM1c). NPM1c mutations define a separate AML entity with good prognosis in some AML patients, rendering NPM1c as a potential therapeutic target. SENP3-mediated NPM1 de-SUMOylation induces resistance to therapy in NPM1c AML. Here, we demonstrate that the imidazoquinoxaline EAPB0503 prolongs the survival and results in selective reduction in the leukemia burden of NPM1c AML xenograft mice. Indeed, EAPB0503 selectively downregulates HDM2 expression and activates the p53 pathway in NPM1c expressing cells, resulting in apoptosis. Importantly, we unraveled that NPM1c expressing cells exhibit low basal levels of SUMOylation paralleled with high SENP3 and low ARF basal levels. EAPB0503 reverted these molecular players by inducing NPM1c SUMOylation and ubiquitylation, leading to its proteasomal degradation. EAPB0503-induced NPM1c SUMOylation is concurrent with SENP3 downregulation and ARF upregulation in NPM1c expressing cells. Collectively, these results provide a strong rationale for testing therapies modulating NPM1c post-translational modifications in the management of NPM1c AML.     

ER Stress in ERp57 Knockout Knee Joint Chondrocytes Induces Osteoarthritic Cartilage Degradation and Osteophyte Formation

Ageing or obesity are risk factors for protein aggregation in the endoplasmic reticulum (ER) of chondrocytes. This condition is called ER stress and leads to induction of the unfolded protein response (UPR), which, depending on the stress level, restores normal cell function or initiates apoptotic cell death. Here the role of ER stress in knee osteoarthritis (OA) was evaluated. It was first tested in vitro and in vivo whether a knockout (KO) of the protein disulfide isomerase ERp57 in chondrocytes induces sufficient ER stress for such analyses. ER stress in ERp57 KO chondrocytes was confirmed by immunofluorescence, immunohistochemistry, and transmission electron microscopy. Knee joints of wildtype (WT) and cartilage-specific ERp57 KO mice (ERp57 cKO) were analyzed by indentation-type atomic force microscopy (IT-AFM), toluidine blue, and immunofluorescence/-histochemical staining. Apoptotic cell death was investigated by a TUNEL assay. Additionally, OA was induced via forced exercise on a treadmill. ER stress in chondrocytes resulted in a reduced compressive stiffness of knee cartilage. With ER stress, 18-month-old mice developed osteoarthritic cartilage degeneration with osteophyte formation in knee joints. These degenerative changes were preceded by apoptotic death in articular chondrocytes. Young mice were not susceptible to OA, even when subjected to forced exercise. This study demonstrates that ER stress induces the development of age-related knee osteoarthritis owing to a decreased protective function of the UPR in chondrocytes with increasing age, while apoptosis increases. Therefore, inhibition of ER stress appears to be an attractive therapeutic target for OA.     

New developments in the melt rheology of nylons. I: Effect of moisture and molecular weight

Peculiar observations on the melt rheology of ultra-dry nylon resins, nylon 6 in particular, are reported. One aspect of this study deals with a sharp increase in zero shear melt viscosity (e.g. 2 to 5 times) as the nylon 6 resin moisture is taken from 0.10 down to 0.00%; the effect being reversible. Changes of such magnitude are unexpected considering that there are no detectable variations of the chemical/compositional/molecular weight type in the starting resin, when subjected to the imposed drying conditions. Another aspect of this study deals with a deviation of nylons (6, 6,6, and 12) from the Bueche (1952) relationship, well accepted for polymers to date. Under moderate drying conditions (e.g. 50°C/17 h/110 millitorr), the molecular weight exponent is found to be 3.8, which is within the range of 3.4 to 3.8 reported for nylon 6. However, under more severe drying conditions (e.g. 110°C/17 h/110 millitorr), the molecular weight exponents for nylon 6, nylon 66, and nylon 12 are 4.8, 5.4, and 4.6, respectively. We are proposing that a sharp increase in melt viscosity of ultra-dry nylon 6 is partly due to an increase in the molecular weight of the melt (extrudate) which then, has a more pronounced impact on melt viscosity in view of the 4.8 exponent. Such unique results, in contrast to polyethylene (free radical polymer) and poly(ethylene terephthalate) (condensation polymer) are tentatively attributed to H-bonding in nylon melts. Yet another aspect of this study deals with the rheology of supercooled molten polymers that can offer advantages for analytical characterization.     

Influence of the chemical structure of additives poly(ethylene-co-vinyl acetate)-based on the pour point of crude oils

One of the methods to prevent wax precipitation, during petroleum production, transport, and refining, is the use of polymer additives that can reduce the oil pour point. However, no single additive work for all types of crude oil and this relation is not yet well known. In this study, a family of polymers based on poly(ethylene-co-vinyl acetate), containing hydroxyl groups and long pendant hydrocarbon chains (from C6 to C18), were synthesized and characterized by H¹ nuclear magnetic resonance and solubility test. Four crude oil samples containing different amounts and size distribution of the wax were used. The additive's action is favored by higher contents of iso + cycloalkanes and lower contents of n-paraffins with larger chain sizes. The presence of the CH₃COO group in the copolymers promoted the lowering of the pour point, supported by a low OH concentration and the presence of a long pendant hydrocarbon chain: the best results were obtained with C10 and C12 chain lengths. © 2020 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 2020 , 137, 48969.     

Investigation of anti-corrosion behavior of waterborne organosilane–polyester coatings for AA6011 aluminum alloy

Thermal-cured, sol–gel derived, waterborne organosilane–polyester coatings (SiE) have been developed using methyltrimethoxysilane, 3-glycidoxytrimethoxysilane and polyester resin for corrosion protection of aluminum AA6011. The structural and morphological features of the coatings were analyzed by Fourier transform infrared spectroscopy (FT-IR) and atomic force microscopy (AFM). Results show that the coatings on aluminum were smooth, continuous and defect-free. Performance of the SiE coatings were investigated and compared with pure organosilane coating and polyester coating using potentiodynamic polarization studies, contact angle measurement and pencil hardness test. Results from polarization studies have shown that the SiE coated substrate (4.6–13.1 × 10⁻⁷ A/cm²) provided a better corrosion protection than the polyester coated substrate (7.8 × 10⁻⁶ A/cm²) due formation of aluminum–oxygen–silicon covalent bond at aluminum-coating interface. Furthermore, SiE coatings provided better hydrophobicity and hardness than the polyester coating.