An Exact Solution of BPS Domain Wall Junction

An exact solution of domain wall junction is obtained in a four-dimensional N=1 supersymmetric U(1) X U(1)' gauge theory with three pairs of chiral superfields which is motivated by the N=2 SU(2) gauge theory with one flavor perturbed by an adjoint scalar mass. The solution allows us to evaluate various quantities including a new central charge Y_k associated with the junction besides Z_k which appears already in domain walls. We find that the new central charge Y_k gives a negative contribution to the mass of the domain wall junction whereas the central charge Z_k gives a dominant positive contribution. One has to be cautious to identify the central charge Y_k alone as the mass of the junction.Comment: LaTeX file, 13 page, 1 ps figur

ALMA Observations of the IRDC Clump G34.43+00.24 MM3: DNC/HNC Ratio

We have observed the clump G34.43+00.24 MM3 associated with an infrared dark cloud in DNC $J$=3--2, HN$^{13}$C $J$=3--2, and N$_2$H$^+$ $J$=3--2 with the Atacama Large Millimeter/submillimeter Array (ALMA). The N$_2$H$^+$ emission is found to be relatively weak near the hot core and the outflows, and its distribution is clearly anti-correlated with the CS emission. This result indicates that a young outflow is interacting with cold ambient gas. The HN$^{13}$C emission is compact and mostly emanates from the hot core, whereas the DNC emission is extended around the hot core. Thus, the DNC and HN$^{13}$C emission traces warm regions near the protostar differently. The DNC emission is stronger than the HN$^{13}$C emission toward most parts of this clump. The DNC/HNC abundance ratio averaged within a $15^{\prime\prime} \times 15^{\prime\prime}$ area around the phase center is higher than 0.06. This ratio is much higher than the value obtained by the previous single-dish observations of DNC and HN$^{13}$C $J$=1--0 ($\sim$0.003). It seems likely that the DNC and HNC emission observed with the single-dish telescope traces lower density envelopes, while that observed with ALMA traces higher density and highly deuterated regions. We have compared the observational results with chemical-model results in order to investigate the behavior of DNC and HNC in the dense cores. Taking these results into account, we suggest that the low DNC/HNC ratio in the high-mass sources obtained by the single-dish observations are at least partly due to the low filling factor of the high density regions.Comment: accepted to Ap

Prostaglandin E2/EP signaling in the tumor microenvironment of colorectal cancer

This article belongs to the Special Issue Molecular and Translational Research on Colorectal CancerThe number of colorectal cancer (CRC) patients is increasing worldwide. Accumulating evidence has shown that the tumor microenvironment (TME), including macrophages, neutrophils, and fibroblasts, plays an important role in the development and progression of CRC. Although targeting the TME could be a promising therapeutic approach, the mechanisms by which inflammatory cells promote CRC tumorigenesis are not well understood. When inflammation occurs in tissues, prostaglandin E2 (PGE2) is generated from arachidonic acid by the enzyme cyclooxygenase-2 (COX-2). PGE2 regulates multiple functions in various immune cells by binding to the downstream receptors EP1, EP2, EP3, and EP4, and plays an important role in the development of CRC. The current therapies targeting PGE2 using non-steroidal anti-inflammatory drugs (NSAIDs) or COX-2 inhibitors have failed due to the global prostanoid suppression resulting in the severe adverse effects despite the fact they could prevent tumorigenesis. Therefore, therapies targeting the specific downstream molecules of PGE2 signaling could be a promising approach. This review highlights the role of each EP receptor in the TME of CRC tumorigenesis and their therapeutic potential

Rational Design of Peptides Derived from Odorant-Binding Proteins for SARS-CoV-2-Related Volatile Organic Compounds Recognition

Peptides are promising molecular-binding elements and have attracted great interest in novel biosensor development. In this study, a series of peptides derived from odorant-binding proteins (OBPs) were rationally designed for recognition of SARS-CoV-2-related volatile organic compounds (VOCs). Ethanol, nonanal, benzaldehyde, acetic acid, and acetone were selected as representative VOCs in the exhaled breath during the COVID-19 infection. Computational docking and prediction tools were utilized for OBPs peptide characterization and analysis. Multiple parameters, including the docking model, binding affinity, sequence specification, and structural folding, were investigated. The results demonstrated a rational, rapid, and efficient approach for designing breath-borne VOC-recognition peptides, which could further improve the biosensor performance for pioneering COVID-19 screening and many other applications

Transforming growth factor-β signaling pathway in colorectal cancer and its tumor microenvironment

Transforming growth factor-beta (TGF-β) signaling is one of the important cellular pathways that play key roles for tissue maintenance. In particular, it is important in the context of inflammation and tumorigenesis by modulating cell growth, differentiation, apoptosis, and homeostasis. TGF-β receptor type 2 (TGFBR2) mutations affected by a mismatch repair deficiency causes colorectal cancers (CRCs) with microsatellite instability, which is, however, associated with relatively better survival rates. On the other hand, loss of SMAD4, a transcription factor in the TGF-β superfamily signaling, promotes tumor progression. Loss of heterozygosity on chromosome 18 can case SMAD4-deficient CRC, which results in poorer patients’ survival. Such bidirectional phenomenon driven by TGF-β signaling insufficiency reflects the complexity of this signaling pathway in CRC. Moreover, recent understanding of CRC at the molecular level (consensus molecular subtype classification) provides deep insight into the important roles of TGF-β signaling in the tumor microenvironment. Here we focus on the TGF-β signaling in CRC and its interaction with the tumor microenvironment. We summarize the molecular mechanisms of CRC tumorigenesis and progression caused by disruption of TGF-β signaling by cancer epithelial cells and host stromal cells