Simulation and optimization of scrap wagon dismantling system based on Plant Simulation.

Based on the existing plant layout and process flow, a simulation analysis was conducted using the Plant Simulation platform with the utilization efficiency of each station and production capacity of the dismantling system as indicators. A problem with long-term suspension in the disassembly process was determined. Based on the two optimization directions of increasing material transportation equipment and expanding the buffer capacity, a cost-oriented optimization model is established.

Sulforaphane suppresses in vitro and in vivo lung tumorigenesis through downregulation of HDAC activity.

Background: Sulforaphane (SFN), an isothiocyanate isolated from broccoli, has been reported to have chemopreventive activity. However, the effects of SFN on lung cancer have not been investigated. In this study, we investigate the chemopreventive role of SFN through the inhibition of histone deacetylase (HDAC) in two different lung cancer cells by in vitro and in vivo mouse models.

Meta-analysis of HLA matching and the outcome of unrelated umbilical cord blood transplantation (CBT).

Objective: The aim of this meta-analysis is to compare the HLA disparities and the outcome of UCBT, i.e. the disease-free survival (DFS), engraftment, graft-versus-host disease, (GVHD), and transplantation related mortality (TRM).

Novel roles for palmitoylation of Ras in IL-1 beta-induced nitric oxide release and caspase 3 activation in insulin-secreting beta cells.

We recently demonstrated that functional inactivation of H-Ras results in significant reduction in interleukin 1 beta (IL-1 beta)-mediated effects on isolated beta cells. Since palmitoylation of Ras has been implicated in its membrane targeting, we examined the contributory roles of palmitoylation of Ras in IL-1 beta-induced nitric oxide (NO) release and subsequent activation of caspases. Preincubation of HIT-T15 or INS-1 cells with cerulenin (CER, 134 microM; 3 hr), an inhibitor of protein palmitoylation, significantly reduced (-95%) IL-1 beta-induced NO release from these cells.

Novel roles for the rho subfamily of GTP-binding proteins in succinate-induced insulin secretion from betaTC3 cells: further evidence in support of the succinate mechanism of insulin release.

We have previously demonstrated regulatory roles for Rho subfamily of G-proteins in glucose- and calcium-induced insulin secretion. Herein, we examined regulation by these proteins of insulin secretion from betaTC3 cells elicited by mitochondrial fuels, such as the succinic acid methyl ester (SAME). Preincubation of these cells with Clostridium difficile toxin-B (200 ng/mL), which monoglucosylates and inactivates Cdc42 and Rac1, markedly decreased (> 70%) SAME-induced insulin secretion.

Mastoparan-induced insulin secretion from insulin-secreting betaTC3 and INS-1 cells: evidence for its regulation by Rho subfamily of G proteins.

Mastoparan, a tetradecapeptide from wasp venom, stimulates insulin secretion from the islet beta-cells, presumably via activation of trimeric G proteins. Herein, we used Clostridial toxins, which selectively modify and inactivate the Rho subfamily of G proteins, to examine whether mastoparan-induced insulin secretion also involves activation of these signaling proteins. Mastoparan, but not mastoparan 17 (an inactive analog of mastoparan), significantly stimulated insulin secretion from betaTC3 and INS-1 cells.

Inhibition of glucose- and calcium-induced insulin secretion from betaTC3 cells by novel inhibitors of protein isoprenylation.

The majority of low molecular weight G proteins undergoes a series of post-translational modification steps, e.g., isoprenylation, at their C-terminal cysteine, which seem to be critical for the transport of the modified proteins to the membrane sites for interaction with their respective effector proteins.

Localization and characterization of the mitochondrial isoform of the nucleoside diphosphate kinase in the pancreatic beta cell: evidence for its complexation with mitochondrial succinyl-CoA synthetase.

Nucleoside diphosphate kinase (NDPK) catalyzes the transfer of terminal phosphates from nucleoside triphosphates to nucleoside diphosphates to yield nucleotide triphosphates. The present study was undertaken to localize and characterize the mitochondrial isoform of NDPK (mNDPK) in the pancreatic beta cell since it could contribute to the generation of mitochondrial nucleotide triphosphates and, thereby, to the mitochondrial high-energy phosphate metabolism of the pancreatic beta cell. Mitochondrial fractions from the insulin-secreting beta cells were isolated by differential centrifugation.