Simulating liquids on dynamically warping grids

We introduce dynamically warping grids for adaptive liquid simulation. Our primary contributions are a strategy for dynamically deforming regular grids over the course of a simulation and a method for efficiently utilizing these deforming grids for liquid simulation. Prior work has shown that unstructured grids are very effective for adaptive fluid simulations. However, unstructured grids often lead to complicated implementations and a poor cache hit rate due to inconsistent memory access. Regular grids, on the other hand, provide a fast, fixed memory access pattern and straightforward implementation. Our method combines the advantages of both: we leverage the simplicity of regular grids while still achieving practical and controllable spatial adaptivity. We demonstrate that our method enables adaptive simulations that are fast, flexible, and robust to null-space issues. At the same time, our method is simple to implement and takes advantage of existing highly-tuned algorithms

Novel modification of ceramide: rat glioma ganglioside GM3 having 3-O-acetylated sphingenine

AbstractA novel O-acetylated GM3 containing 3-O-acetyl 4-sphingenine was isolated with one having a non-acetylated base from transplanted rat glioma tissue. The presence and position of the acetyl group were estimated by one- and two-dimensional proton nuclear magnetic resonance, and fast atom bombardmentmass spectrometries. In addition, the O-acetyl showed higher immunological activity toward anti-melanoma antibody in the presence of non-acetylated GM3 in complement-dependent liposome lysis than did non-acetylated or acetylated GM3 alone in the liposome, suggesting enhancement of immunological reactivity of the intact tumor cells by a small amount of O-acetyl GM3

皮質脳波・局所電場電位・単一ニューロン活動に基づく発声時脳活動の復号化に関する研究

学位の種別: 課程博士審査委員会委員 : （主査）東京大学教授 笠井 清登, 東京大学教授 真鍋 俊也, 東京大学准教授 神出 誠一郎, 東京大学講師 湯本 真人, 東京大学教授 芳賀 信彦University of Tokyo(東京大学

Detailed Dynamic Model of Antagonistic PAM System and its Experimental Validation: Sensor-less Angle and Torque Control with UKF

This paper proposes a detailed nonlinear mathematical model of an antagonistic pneumatic artificial muscle (PAM) actuator system for estimating the joint angle and torque using an unscented Kalman filter (UKF). The proposed model is described in a hybrid state-space representation. It includes the contraction force of the PAM, joint dynamics, fluid dynamics of compressed air, mass flows of a valve, and friction models. A part of the friction models is modified to obtain a novel form of Coulomb friction depending on the inner pressure of the PAM. For model validation, offline and online UKF estimations and sensor-less tracking control of the joint angle and torque are conducted to evaluate the estimation accuracy and tracking control performance. The estimation error is less than 7.91 %, and the steady-state tracking control performance is more than 94.75 %. These results confirm that the proposed model is detailed and could be used as the state estimator of an antagonistic PAM system

The heterogeneity of target recognition by lymphokine-activated killer precursor cells.

Lymphokine-activated killer (LAK) cells were generated from peripheral blood lymphocytes (PBL) that were depleted of mature cytotoxic natural killer (NK) cells. PBL NK activity was abolished by pretreatment of effector cells with the toxic lysosomotropic agent L-leucine methyl ester (LME) or by depletion of effector cells by K562 monolayer absorption (MA). Both treatments markedly reduced the proportion of cells expressing NK-associated markers such as CD 16 (Leu 11b, B73.1), Leu 7, and NKH-1 (Leu 19), whereas these treatments had minimal effects on cells expressing T cell markers (CD 3, CD 4, and CD 8). LME and MA also drastically decreased the proportion of K562 target-binding lymphocytes. LAK activity against NK-sensitive and NK-resistant targets can be generated from the NK cell-depleted PBL by incubation with interleukin-2. Peak LAK activity generated from MA-treated PBL was later than the peak of LAK activity generated from either untreated or LME-treated PBL. Although MA of PBL on NK-resistant S4 sarcoma targets had little effect on NK activity, LAK activity against both K562 and S4 targets was reduced. These results suggest that there are at least three LAK precursor subpopulations in PBL: mature NK cells that can bind and kill K562 targets (LME-sensitive and MA-sensitive); "pre-NK" cells that can bind but cannot kill (LME-resistant and MA-sensitive); and non-NK cells that cannot bind and cannot kill K562 targets (MA-resistant)

Biochemical Analysis of Cytokine Effect on the Glycosphingolipid Expression of Human Glioma Cell Lines

We have already found that a human glioma cell line U118MG could modu-late glycosphingolipid (GSL) expression via certain cytokines, though this effect is changeable and very difficult to reproduce even under consistent culture condi-tions. Consecutive analysis of cytokine effect using other 6 glioma (A172, T98G, KG-1C, U87MG, U138MG and U373MG) and one melanoma cell line (Mewo) failed to detect any GSL modulation. A total of ten cytokines were used in this experiment : IL-1beta, IL-2, IL-4, IL-6, IL-8, TNF-alpha, IFN-alpha, IFN-beta, IFN-gamma, and G-CSF, for treating KG-1C mixed glioma cells and 8 cytokines out of those for treating T98G glioblastoma cells. The rest of the cell lines were cultured with IFN-gamma and IL-4 because those two had once shown dramatic effect on GSL expression on U118MG cells. The fact that none of the 6 glioma cell lines responded to cytokines in terms of GSL modulation implies that cytokines do not play a significant role in regulating GSL expression in the glial cell lineage

Cell Density Regulates Antibody Accessibility and Metabolic Turnover of Gangliosides in Human Glioma Cells

The effects of cell density on the gangliosides of 4 human glioma cell lines were studied. The cell lines used were KG-1C (GM3-dominant) , A172 and H4 (GM2-dominant), and Hs683 (GM3, GM2-co-dominant) cells. All these cell lines showed higher immunofluorescence with anti-ganglioside antibodies in FACS analysis at sparse density than at confluent density. Steric hindrance from cell surface proteins had been removed by the pretreatment of the cells with trypsin. The chemical content of gangliosides was consistent throughout the time of cell growth. The mechanisms of crypticity of gangliosides at confluent culture were under investigation. We first evaluated the metabolic turnover rate of gang-liosides at different cell densities. The results clearly showed a more rapid turn-over of gangliosides at sparse density from approximately 2 to 4 fold in terms of radioactivities of incorporated tritium into gangliosides. The profiles of labeled gangliosides were also different between the sparse and confluent cultures. We speculate that better accessibilities of antibodies toward gangliosides should be facilitated by the same mechanism which should, in turn, provide easier access of carbohydrate-hydrolysis enzymes to gangliosides at sparse cell density in order to keep an enhanced turnover rate

Reduction of glycolipids with D-PDMP, a glucosylceramide synthetase inhibitor, caused cell growth inhibition, enhanced cell adhesion, and facilitated cell motility in human glioma cells

Glycolipid synthesis inhibitor, D-PDMP, not only inhibited the production of glycolipid but also inhibited cell growth in human glioma cell line KG-1C in a cell cycle non-dependent manner. The reduction of glycolipid from the cell membrane allowed us to study the biological functions of glycolipids. The ability of cells to adhere to collagen was enhanced by the reduction of glycoli-pids, and random cell migration was also activated by the effect of D-PDMP. The results supported our speculation that glycolipids might function in cell growth, adherence and locomotion