The 2016 Kumamoto earthquake (Kumamoto earthquake sequence) is an extremely high-seismicity event that has been occurring across Kumamoto and Oita Prefectures in Japan since April 14, 2016 (JST). The earthquake early warning system of the Japan Meteorological Agency (JMA) issued warnings for 19 events in the Kumamoto earthquake sequence from April 14 to 19, under some of the heaviest loading conditions since the system began operating in 2007. We analyzed the system performance for cases where a warning was issued and/or strong motion was actually observed. The results indicated that the system exhibited remarkable performance, especially for the most destructive earthquakes in the Kumamoto earthquake sequence. In addition, the system did not miss or seriously under-predict strong motion of any large earthquake from April 14 to 30. However, in four cases, the system issued over-predicted warnings due to the simultaneous occurrence of small earthquakes within a short distance, which implies a fundamental obstacle in trigger-data classifications based solely on arrival time. We also performed simulations using the integrated particle filter (IPF) and propagation of local undamped motion (PLUM) methods, which JMA plans to implement to address over-prediction for multiple simultaneous earthquakes and under-prediction for massive earthquakes with large rupture zones. The simulation results of the IPF method indicated that the IPF method is highly effective at minimizing over-prediction even for multiple simultaneous earthquakes within a short distance, since it adopts a trigger-data classification using velocity amplitude and hypocenter determinations using not-yet-arrived data. The simulation results of the PLUM method demonstrated that the PLUM method is capable of issuing warnings for destructive inland earthquakes more rapidly than the current system owing to the use of additional seismometers that can only be incorporated by this method.
The c-kit proto-oncogene encodes a receptor tyrosine kinase that is known to play a crucial role in hematopoiesis, especially in mast cell growth and differentiation. Although a number of dominant loss-of- function mutations of c-kit gene have been well characterized in mice, rats, and humans, little is known about the c-kit mutations contributing to ligand-independent activation of the c-kit receptor tyrosine kinase (KIT). In a murine mastocytoma cell line, P-815, KIT has been found to be constitutively phosphorylated on tyrosine and activated in a ligand-independent manner. Sequencing of the whole coding region of c-kit cDNA showed that c-kit cDNA of P-815 cells carries a point mutation in codon 814, resulting in amino acid substitution of Tyr for Asp. Murine wild-type c-kit cDNA and mutant- type c-kit cDNA encoding Tyr in codon 814 were expressed in cells of a human embryonic kidney cell line, 293T. In the transfected cells, mutant-form KITTyr814 was strikingly phosphorylated on tyrosine and activated in immune complex kinase reaction regardless of stimulation with a ligand for KIT (stem cell factor), whereas tyrosine phosphorylation and activation was barely detectable in wild-form KIT. The data presented here provide evidence for a novel activating mutation of c-kit gene that might be involved in neoplastic growth or oncogenesis of some cell types, including mast cells.
Homogeneous surface alignment of liquid crystals (5CB) is observed for films formed by coating with aqueous solutions of hydroxypropylcellulose (HPC) for high coating speeds and thin coating thicknesses. On the other hand, for films formed with isotropic ethanol solutions of HPC, 5CB molecules retain the flow-induced alignment created at the formation of the 5CB droplet. The microstructures responsible for the homogeneous surface alignment are not confirmed in the morphological measurement of the film surface with an atomic force microscope, although large grooves corresponding to the banded texture perpendicular to the coating direction exist on the films formed with liquid crystalline solutions of HPC. The possibility of highly oriented HPC molecules in the coating flow is pointed out using the Doi model. These results suggest that the flow-induced anisotropic orientation of HPC molecules is responsible for the homogeneous surface alignment of 5CB.
A peculiar point mutation results in constitutive activation of c-kit receptor tyrosine kinase (KIT) in three different tumor mast cell lines; ie, the HMC-1, P-815, and RBL-2H3. Because constitutive activation of KIT was also observed in the FMA3 mouse mastocytoma cell line, we investigated the molecular mechanism. Sequencing of the whole coding region of the c-kit showed that the point mutation found in HMC- 1, P-815, and RBL-2H3 cells was absent in FMA3 cells and that the c-kit cDNA of FMA3 cells carried an in-frame deletion of 21 base pairs (bp) encoding Thr-Gln-Leu-Pro-Tyr-Asp-His at codons 573 to 579 at the juxtamembrane domain. The FMA3-type c-kit cDNA with 21 bp deletion was introduced into the IC-2 cell line, which was derived from murine cultured mast cells. IC-2 cells were dependent on interleukin (IL)-3 and did not express KIT on the surface. In IC-2 cells introduced with the FMA3-type c-kit cDNA, KIT was constitutively phosphorylated on tyrosines and activated. Moreover, the FMA3-type KIT was dimerized without the stimulation by stem cell factor (SCF), a ligand for KIT. The spontaneously dimerized FMA3-type KIT without SCF binding was not internalized even after the activation. IC-2 cells expressing the FMA3- type KIT grew in suspension culture without IL-3 and SCF and became leukemic in nude athymic mice. The deletion of seven amino acids at the juxtamembrane domain appeared to be a new activating mutation of KIT that might be involved in neoplastic growth of mast cells.
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