2,079 research outputs found
Activation of Ras-ERK pathway by Fgf8 and its downregulation by Sprouty2 for the isthmus organizing activity
In the previous studies, we showed that strong Fgf8 signaling activates the Ras-ERK pathway to induce cerebellum. Here, we show importance of negative regulation of this pathway. 'Prolonged' activation of ERK by misexpression of _Fgf8b_ and dominant-negative _Sprouty2_ (_dnSprouty2_) did not change the fate of the mesencephalic alar plate. Downregulation of ERK activity using a MEK inhibitor, U0126, or by tetracycline dependent Tet-off system after co-expression of _Fgf8b_ and _dnSprouty2_, forced the mesencephalic alar plate to differentiate into cerebellum. We then paid attention to Mkp3. After misexpression of _dnMkp3_ and _Fgf8b_, slight downregulation of ERK activity occurred, which may be due to Sprouty2, and the mesencephalon transformed to the isthmus-like structure. The results indicate that ERK must be once upregulated and then be downregulated for cerebellar differentiation, and that differential ERK activity level established by negative regulators receiving Fgf8 signal may determine regional specificity of mesencephalon and metencephalon
Formulation and Application of Quantum Monte Carlo Method to Fractional Quantum Hall Systems
Quantum Monte Carlo method is applied to fractional quantum Hall systems. The
use of the linear programming method enables us to avoid the negative-sign
problem in the Quantum Monte Carlo calculations. The formulation of this method
and the technique for avoiding the sign problem are described. Some numerical
results on static physical quantities are also reported.Comment: Proceedings of The 15th International Conference on Electronic
Properties of Two-Dimensional Systems (EP2DS-15
Shape transformations of lipid vesicles by insertion of bulky-head lipids
Lipid vesicles, in particular Giant Unilamellar Vesicles (GUVs), have been increasingly
important as compartments of artificial cells to reconstruct living cell-like systems in a
bottom-up fashion. Here, we report shape transformations of lipid vesicles induced by
polyethylene glycol-lipid conjugate (PEG lipids). Statistical analysis of deformed vesicle
shapes revealed that shapes vesicles tend to deform into depended on the concentration
of the PEG lipids. When compared with theoretically simulated vesicle shapes, those
shapes were found to be more energetically favorable, with lower membrane bending
energies than other shapes. This result suggests that the vesicle shape transformations
can be controlled by externally added membrane molecules, which can serve as a
potential method to control the replications of artificial cells
Non-commutative hypergroup of order five
We prove that all hypergroups of order four are commutative and that there
exists a non-comutative hypergroup of order five. These facts imply that the
minimum order of non-commutative hypergroups is five even though the minimum
order of non-commutative groups is six
LPS-Toll-Like Receptor-Mediated Signaling on Expression of Protein S and C4b-Binding Protein in the Liver
Protein S (PS), mainly synthesized in hepatocytes and endothelial cells, plays a critical role as a cofactor of anticoagulant activated protein C (APC). PS activity is regulated by C4b-binding protein (C4BP), structurally composed of seven α-chains (C4BPα) and a β-chain (C4BPβ). In this paper, based primarily on our previous studies, we review the lipopolysaccharide (LPS)-induced signaling which affects expression of PS and C4BP in the liver. Our in vivo studies in rats showed that after LPS injection, plasma PS levels are significantly decreased, whereas plasma C4BP levels first are transiently decreased after 2 to 12 hours and then significantly increased after 24 hours. LPS decreases PS antigen and mRNA levels in both hepatocytes and sinusoidal endothelial cells (SECs), and decreases C4BP antigen and both C4BPα and C4BPβ mRNA levels in hepatocytes. Antirat CD14 and antirat Toll-like receptor (TLR)-4 antibodies inhibited LPS-induced NFκB activation in both hepatocytes and
SECs. Furthermore, inhibitors of NFκB and MEK recovered the LPS-induced decreased expression of PS in both cell types and the LPS-induced decreased expression of C4BP in
hepatocytes. These data suggest that the LPS-induced decrease in PS expression in hepatocytes and SECs and LPS-induced decrease in C4BP expression in hepatocytes are mediated by MEK/ERK signaling and NFκB activation and that membrane-bound CD14 and TLR-4 are involved in this mechanism
Deep Point-to-Plane Registration by Efficient Backpropagation for Error Minimizing Function
Traditional algorithms of point set registration minimizing point-to-plane
distances often achieve a better estimation of rigid transformation than those
minimizing point-to-point distances. Nevertheless, recent deep-learning-based
methods minimize the point-to-point distances. In contrast to these methods,
this paper proposes the first deep-learning-based approach to point-to-plane
registration. A challenging part of this problem is that a typical solution for
point-to-plane registration requires an iterative process of accumulating small
transformations obtained by minimizing a linearized energy function. The
iteration significantly increases the size of the computation graph needed for
backpropagation and can slow down both forward and backward network
evaluations. To solve this problem, we consider the estimated rigid
transformation as a function of input point clouds and derive its analytic
gradients using the implicit function theorem. The analytic gradient that we
introduce is independent of how the error minimizing function (i.e., the rigid
transformation) is obtained, thus allowing us to calculate both the rigid
transformation and its gradient efficiently. We implement the proposed
point-to-plane registration module over several previous methods that minimize
point-to-point distances and demonstrate that the extensions outperform the
base methods even with point clouds with noise and low-quality point normals
estimated with local point distributions.Comment: 25 pages, 10 figure
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