The Effect of Changes in the Separation Process for the Performance of Recycled Cement Powder: A Comparison with a Previous Study for Radioactive Waste Immobilization.

Separation of hydrated cement paste from aggregate is a key technology to reduce the amount of radioactive concrete waste during the decommissioning process. If separated cement-paste portions can be recycled as a solidifying agent for other radioactive waste, the amount of radioactive concrete waste could be close to "zero". A study was conducted to achieve circular economy in the area of concrete decommissioning and found it to be successfully used as a solidifying agent for immobilization of liquid radioactive waste. However, previous work used a process that requires large amounts of energy (heat treatment was applied to most of the concrete fraction) because the objective was to completely remove hydrated cement powder from the aggregate. In this work, the separation system was modified to increase energy efficiency (heat treatment was applied to separated powder only), but such a change decreased the surface area of the recycled cement powder due to a higher inclusion of aggregate powder. A relatively lower solution to binder ratio could have been achieved for the preparation of wasteform specimens, and as a result, a 28 day compressive strength of wasteform could have become higher, but the final leachability indices were lower than the results observed from previous work. The results from 28 day compressive strength, thermal cycling and 90 day leaching experiments met the acceptance criteria for wasteform, indicating that this modified system can also be used for immobilization of liquid radioactive waste to meet the "zero" production of concrete waste during the decommissioning of a nuclear power plant. It should be noted that accurate monitoring of aggregate content in recycled cement powder during production is important to maintain proper reactivity of recycled cement powder.

Experimental Study on Time-Dependent Changes in Rheological Properties and Flow Rate of 3D Concrete Printing Materials.

Three-dimensional concrete printing (3DCP) materials require a relatively low water-to-binder ratio (W/B) of 0.3 or less to ensure their buildability and flow properties are sufficiently maintained after mixing. In this study, the rheological properties of 3DCP materials with W/B 0.28 were evaluated up to 60 min after mixing, and the yield stress and plastic viscosity were analyzed over time. A gradual decrease in flow rate with time was observed during the transport of 200 kg of material per batch through a 20 m hose. To examine the time-dependent changes in flow rate and layer volume, a 2200 mm × 1000 mm test specimen was printed. The dependence of the layer width over time during the printing process was measured and analyzed. The experimental analyses showed that the flow rate and layer volume of the 3DCP material gradually decreased with time after mixing, which was correlated with the rheological properties.

X-ray CT Analysis of the Cross-Section of a 3D-Printed Deformed Layer.

In this study, we experimentally analyzed the deformation shape of stacked layers developed using three-dimensional (3D) printing technology. The nozzle traveling speed was changed to 80, 90, 100, and 110 mm/s when printing the layers to analyze its effect on layer deformation. Furthermore, the cross-sectional area and the number of layers were analyzed by printing five layers with overall dimensions of 1000 (w) × 2200 (l) × 50 (h) mm (each layer was 10 mm high) using Vernier calipers. Moreover, we analyzed the interface and cross-sectional area of layers that are difficult to confirm visually using X-ray computed tomography (X-ray CT) analysis. As a result of measuring the deformation at the center of the layer, it was confirmed that the deformation was greater for lower nozzle traveling speeds. Consequently, the X-ray CT analysis verified that the layer had the same cross-sectional area irrespective of the layer printing order at the same nozzle travel speed, even if the layer was deformed.

Evaluation of the Mechanical Properties of a 3D-Printed Mortar.

The mechanical properties of 3D-printed mortars are determined in terms of their compressive and direct tensile bond strengths. To determine such properties using existing methods, a preliminary experiment was conducted. The compressive strength of the printed mortar was compared to mold-casted specimens and it was found that the compressive strength decreased by ~30%. Among the fabrication variables, an increase in nozzle height negatively influenced the direct tensile bond strength. For the same conditions and age, the direct tensile strength decreased by as much as 16-29% when the number of layers increased from 2 to 6. When the specimens were fabricated using a specially designed stainless steel frame and core drill, followed by extraction and the application of physical impact, the 28 days compressive strength of the specimen decreased by ~50%.

Protective effect of Coptidis Rhizoma on S-nitroso-N-acetylpenicillamine (SNAP)-induced apoptosis and necrosis in pancreatic RINm5F cells.

Coptidis rhizoma (CR) is a herb used in many traditional prescriptions against diabetes mellitus in Asia for centuries. Our purpose was to determine the protective effect and its action mechanism of CR on the cytotoxicity of pancreatic beta-cells. Nitric oxide (NO) is believed to play a key role in the process of pancreatic beta-cell destruction leading to insulin-dependent diabetes mellitus (IDDM). Exposure of RINm5F cells to chemical NO donor such as S-nitroso-N-acetylpenicillamine (SNAP) induced apoptotic events such as the disruption of mitochondrial membrane potential (Deltapsim), cytochrome c release from mitochondria, activation of caspase-3, poly (ADP-ribose) polymerase cleavage and DNA fragmentation. Also, exposure of SNAP led to LDH release into medium, one of the necrotic events. However, pretreatment of RINm5F cells with CR extract protected both apoptosis and necrosis through the inhibition of Deltapsim disruption in SNAP-treated RINm5F cells. In addition, rat islets pretreated with CR extract retained the insulin-secretion capacity even after the treatment with IL-1beta. These results suggest that CR may be a candidate for a therapeutic or preventing agent against IDDM.

Scopoletin induces apoptosis in human promyeloleukemic cells, accompanied by activations of nuclear factor kappaB and caspase-3.

Scopoletin (6-methoxy-7-hydroxycoumarin) is a phenolic coumarin and a member of the phytoalexins. In this study we investigated whether scopoletin caused apoptosis in HL-60 promyelocytic cells and, if so, by what mechanisms. We found that scopoletin induced apoptosis as confirmed by a characteristic ladder pattern of discontinuous DNA fragments in a dose-dependent manner. The signal cascade activated by scopoletin included the heterodimeric redox-sensitive transcription factor NF-kappaB, which exhibited an upregulation of nuclear factor-kappa B (NF-kappaB) translocation to the nucleus by increase of IkappaBalpha degradation. In addition, scopoletin activated caspase-3 as was evidenced by both the proteolytic cleavage of the proenzyme and increased protease activity. Activation of caspase-3 resulted in the cleavage of 116 kDa poly(ADP-ribose) polymerase (PARP) to 85 kDa cleavage product in time-and dose-dependent fashions. Prior treatment of the cells with pyrrolidine dithiocarbamate, a potent inhibitor of NF-kappaB activation, or Ac-DEVD-CHO, a specific caspase-3 inhibitor, prevented scopoletin-induced caspase-3 activation, PARP cleavage, and finally DNA fragmentation. Taken together, these results suggest that scopoletin induces NF-kappaB activation, which, in turn, causes activation of caspase-3, degradation of PARP, and eventually leads to apoptotic cell death in HL-60 cells.

Taraxacum officinale protects against cholecystokinin-induced acute pancreatitis in rats.

AIM: Taraxacum officinale (TO) has been frequently used as a remedy for inflammatory diseases. The aim of this study was to investigate the effect of TO on cholecystokinin (CCK)-octapeptide-induced acute pancreatitis in rats. METHODS: TO at 10 mg/kg was orally administered, followed by 75 microg/kg CCK octapeptide injected subcutaneously three times after 1, 3 and 5 h. This whole procedure was repeated for 5 d. We determined the pancreatic weight/body weight ratio, the levels of pancreatic HSP60 and HSP72, and the secretion of pro-inflammatory cytokines. Repeated CCK octapeptide treatment resulted in typical laboratory and morphological changes of experimentally-induced pancreatitis. RESULTS: TO significantly decreased the pancreatic weight/body weight ratio in CCK octapeptide-induced acute pancreatitis. TO also increased the pancreatic levels of HSP60 and HSP72. Additionally, the secretion of IL-6 and TNF-alpha decreased in the animals treated with TO. CONCLUSION: TO may have a protective effect against CCK octapeptide-induced acute pancreatitis.

Molecular mechanisms of apoptosis induced by Scorpio water extract in human hepatoma HepG2 cells.

AIM: To clarify the mechanism underlying the anti-mutagenic and anti-cancer activities of Scorpio water extract (SWE). METHODS: Human hepatoma HepG2 cells were incubated with various concentrations of SWE. After 24-h incubation, cytotoxicity and apoptosis evaluations were determined by MTT and DNA fragmentation assay, respectively. After treatment with SWE, mitochondrial membrane potential (MMP) was determined by measuring the retention of the dye 3,3'-dihexyloxacarbocyanine (DiOC(6)(3)) and the protein expression including cytochrome C and poly-(ADP-ribose) polymerase (PARP) were measured by Western blotting. Caspase-3 and -9 enzyme activities were measured using specific fluorescence dyes such as Ac-DEVD-AFC and Ac-LEHD-AFC. RESULTS: We found that treatment with SWE induced apoptosis as confirmed by discontinuous DNA fragmentation in cultured human hepatoma HepG2 cells. Our investigation also showed that SWE-induced apoptosis of HepG2 cells were associated with intracellular events including disruption of MMP, increased translocation of cytochrome C from mitochondria to cytosol, activation of caspase-3, and PARP. Pre-treatment of N-acetyl-Asp-Glu-Val-Asp-CHO (Ac-DEVD-CHO), a caspase-3 specific inhibitor, or cyclosporin A (CsA), an inhibitor of MMP disruption, completely abolished SWE-induced DNA fragmentation. CONCLUSION: These results suggest that SWE possibly causes mitochondrial damage, leading to cytochrome C release into cytosol and activation of caspases resulting in PARP cleavage and execution of apoptotic cell death in HepG2 cells. These results further suggest that Scorpio may be a valuable agent of therapeutic intervention of human hepatomas.

Herba houttuyniae extract induces apoptotic death of human promyelocytic leukemia cells via caspase activation accompanied by dissipation of mitochondrial membrane potential and cytochrome c release.

Herba houttuyniae has been used as a constituent of herval medicine prescriptions for the treatment of inflammation, cancer, and other diseases. In the present study, we investigated the cellular effects of herba houttuyniae extract (HHE) and the signal pathways of HHE-induced apoptosis in HL-60 human promyelocytic leukemia cell line. HHE treatment caused apoptosis of cells as evidenced by discontinuous fragmentation of DNA, the loss of mitochondrial membrane potential, release of mitochondrial cytochrome c into the cytosol, activation of procaspase-9 and caspase-3, and proteolytic cleavage of poly(ADP-ribose) polymerase. Pretreatment of Ac-DEVD-CHO, caspase-3 specific inhibitor, or cyclosporin A, a mitochondrial permeability transition inhibitor, completely abolished HHE-induced DNA fragmentation. Together, these results suggest that HHE possibly causes mitochondrial damage leading to cytochrome c release into cytosol and activation of caspases resulting in PARP cleavage and execution of apoptotic cell death in HL-60 cells.

Sophorae radix extract inhibits high glucose-induced vascular cell adhesion molecule-1 up-regulation on endothelial cell line.

BACKGROUND: Sophorae radix (SR) has been used for various diseases including atherosclerosis and arrhythmias. Atherosclerosis induced by hyperglycemia is an important factor in the promotion of diabetic complications. An early event in atherosclerosis is the adhesion of monocytes to endothelium via adhesion molecules. Among them, vascular cell adhesion molecule-1 (VCAM-1) expression mediates the binding of monocytes and lymphocytes to vascular endothelial cells. METHODS: The study was performed on vascular endothelial cells (ECV304 cells) that were pretreated with various concentrations of SR extract for 3 h before exposure with high glucose (55.5 mmol/l) for 48 h. The protein expression of VCAM-1 was measured by enzyme-linked immunosorbent assay (ELISA) and its mRNA expression was by reverse transcription polymerase chain reaction (RT-PCR). RESULTS: SR extract significantly inhibited high glucose-induced expression of VCAM-1 in a dose-dependent manner and reduced the level of VCAM-1 mRNA through interfering with translocation of nuclear factor-kappaB (NF-kappaB). Decreased VCAM-1 expression by SR extract was associated reduction of adherence between high glucose-stimulated ECV304 cells and human monocyte-like HL-60 cells. CONCLUSIONS: These data suggest that SR extract inhibits high glucose-mediated monocytes-endothelial cells adhesions and expression of VCAM-1 via inhibition of NF-kappaB translocation.

Induction of apoptosis by takrisodokyeum through generation of hydrogen peroxide and activation of caspase-3 in HL-60 cells.

Takrisodokyeum (TRSDY), a Chinese herbal medicine, has been known to exert anti-tumoral activity in Korea. However, its molecular mechanism of action is not understood. In this study, we found that TRSDY induced apoptosis in HL-60 cells as evidenced by both a characteristic ladder pattern of discontinuous DNA fragments and an increase of annexin V+/PI- stained cell population. Our data demonstrated that TRSDY-induced apoptotic cell death was accompanied by activation of caspase-3 and cleavages of its substrates, poly(ADP-ribose) polymerase (PARP) and RhoGDP dissociation inhibitor (RhoGDI-2; also called D4-GDI) in a time- and concentration-dependent manner. Caspase-3 inhibitor, but not caspase-1 inhibitor, prevented TRSDY-induced apoptosis. Furthermore, treatment with TRSDY increased the production of intracellular hydrogen peroxide and pretreatment of cells with anti-oxidants conferred complete protection against hydrogen peroxide generation and subsequent caspase-3 activation. Taken together, these results suggest that TRSDY induces hydrogen peroxide generation, which, in turn, causes activation of caspase-3, degradation of PARP and D4-GDI, and eventually leads to apoptotic cell death.

Nardostachys jatamansi extract protects against cytokine-induced beta-cell damage and streptozotocin-induced diabetes.

AIM: To investigate the anti-diabetogenic mechanism of Nardostachys jatamansi extract (NJE). METHODS: Mice were injected with streptozotocin via a tail vein to induce diabetes. Rat insulinoma RINm5F cells and isolated rat islets were treated with interleukin-1beta and interferon-gamma to induce cytotoxicity. RESULTS: Treatment of mice with streptozotocin resulted in hyperglycemia and hypoinsulinemia, which was confirmed by immunohistochemical staining of the islets. The diabetogenic effects of streptozotocin were completely abolished when mice were pretreated with NJE. Inhibition of streptozotocin-induced hyperglycemia by NJE was mediated by suppression of nuclear factor (NF)-kappaB activation. In addition, NJE protected against cytokine-mediated cytotoxicity. Incubation of RINm5F cells and islets with NJE resulted in a significant reduction in cytokine-induced NF-kappaB activation and downstream events, inducible nitric oxide synthase expression and nitric oxide production. The protective effect of NJE was further demonstrated by the normal insulin secretion of cytokine-treated islets in response to glucose. CONCLUSION: NJE provided resistance to pancreatic beta-cell damage from cytokine or streptozotocin treatment. The beta-cell protective effect of NJE is mediated by suppressing NF-kappaB activation.