Modelling the discretization error of initial value problems using the Wishart distribution

This paper presents a new discretization error quantification method for the numerical integration of ordinary differential equations. The error is modelled by using the Wishart distribution, which enables us to capture the correlation between variables. Error quantification is achieved by solving an optimization problem under the order constraints for the covariance matrices. An algorithm for the optimization problem is also established in a slightly broader context

Potential of targeting signal-transducing adaptor protein-2 in cancer therapeutic applications

Adaptor proteins play essential roles in various intracellular signaling pathways. Signal-transducing adaptor protein-2 (STAP-2) is an adaptor protein that possesses pleckstrin homology (PH) and Src homology 2 (SH2) domains, as well as a YXXQ signal transducer and activator of transcription 3 (STAT3)-binding motif in its C-terminal region. STAP-2 is also a substrate of breast tumor kinase (BRK). STAP-2/BRK expression is deregulated in breast cancers and enhances STAT3-dependent cell proliferation. In prostate cancer cells, STAP-2 interacts with and stabilizes epidermal growth factor receptor (EGFR) after stimulation, resulting in the upregulation of EGFR signaling, which contributes to cancer-cell proliferation and tumor progression. Therefore, inhibition of the interaction between STAP-2 and BRK/EGFR may be a possible therapeutic strategy for these cancers. For this purpose, peptides that interfere with STAP-2/BRK/EGFR binding may have great potential. Indeed, the identified peptide inhibitor successfully suppressed the STAP-2/EGFR protein interaction, EGFR stabilization, and cancer-cell growth. Furthermore, the peptide inhibitor suppressed tumor formation in human prostate- and lung-cancer cell lines in a murine xenograft model. This review focuses on the inhibitory peptide as a promising candidate for the treatment of prostate and lung cancers

Magnetic Anisotropy of Quantum Critical Fluctuation in YBa2_2Cu3_3O7_7 at High Magnetic Fields of up to 100 T

The investigation of high-temperature superconductors under high magnetic fields is one of the most important topics in condensed matter physics. For YBa$_2$Cu$_3$O$_7$ (YBCO), the measurements of magnetoresistance under a high magnetic field are technically challenging because the required magnetic field ($B$) is 100 T class. The low temperature (from 52 to 150 K) magnetoresistance is measured in optimally-doped YBCO thin films under the condition $B$$\parallel$CuO$_2$-plane up to 103 T by employing the single-turn coil technique and a radio frequency reflection method. The electrical resistivity $\rho$ exhibits $B$-linear behavior in the normal phase in the high magnetic field region. The field slope coefficient $\beta$ (=$d\rho/dB$) becomes converged at low temperatures. The convergency of $\beta$ below $T_c$ indicates the field-induced strange metal phase, which is determined by the quantum critical fluctuation at high magnetic fields. The $\beta$ value difference under the different directions of the magnetic field suggests the strong anisotropy in quantum critical fluctuations in the strange metal phase of YBCO.Comment: 9 pages, 8 figure

Potential therapeutic applications of targeting signal-transducing adaptor protein-2 in autoimmune diseases

Adaptor proteins are involved in various immune responses via the modulation of many signaling pathways. Signal-transducing adaptor protein-2 (STAP-2) is an adaptor protein that contains typical domains such as the pleckstrin homology (PH) domain, Src homology domain, and a proline-rich region from the N-terminal region. In T cells, STAP-2 positively regulates T cell receptor (TCR)-mediated signaling by associating with CD3ζ immunoreceptor tyrosine-based activation motifs (ITAMs) and lymphocyte-specific protein tyrosine kinase (LCK). Therefore, a peptide that inhibits the interaction between STAP-2 and CD3ζ ITAMs is likely to suppress TCR-mediated T cell activation, as well as T cell-mediated diseases. As expected, the peptide successfully inhibited the STAP-2/CD3ζ ITAM interaction and suppressed TCR-mediated signaling, cell proliferation, and interleukin (IL)-2 production in human/murine T cells. Furthermore, this inhibitor suppressed the pathogenesis of experimental autoimmune encephalomyelitis (EAE), which is widely recognized as a mouse model of multiple sclerosis, via the downregulation of T cell activation and infiltration of T helper (Th) 1/Th17 cells. These results suggest a new strategy for the treatment of multiple sclerosis and other immune diseases