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Abstract This study examined the relationship between radon (222Rn) concentrations in seawater and crustal activity in the Yatsushiro Sea by investigating the submarine fault zone situated at the southern end of the Futagawa–Hinagu fault zone, activated by the 2016 Kumamoto earthquake (M7.3). We conducted an analysis of 222Rn concentration in samples of bottom water just above the seafloor and pore water in sediments, utilizing multiple and piston cores from the Hakuho Maru Expedition KH18-3. The findings revealed significantly elevated 222Rn concentrations in the central sites of the Yatsushiro Sea, coinciding with a high-stress field exhibiting dense active faults. Seismicity analysis revealed heightened moment release and a low b-value post the 2016 Kumamoto earthquake, indicative of increased seismic activity and the potential for substantial earthquakes in the Yatsushiro Sea vicinity. Our results indicate that heightened concentrations of 222Rn in seawater can serve as an effective tracer for identifying and estimating submarine fault activities. Moreover, our research highlights the utility of 222Rn concentrations in detecting active submarine faults and assessing their activity. It contributes to a comprehensive understanding of the potential for significant earthquakes in the Yatsushiro Sea in the future.

Abstract Integrating two-dimensional (2D) layered materials with wide bandgap β-Ga2O3 has unveiled impressive opportunities for exploring novel physics and device concepts. This study presents the epitaxial growth of 2D β-In2Se3/3D β-Ga2O3 heterostructures on c-Sapphire substrates by plasma-assisted molecular beam epitaxy. Firstly, we employed a temperature-dependent two-step growth process to deposit Ga2O3 and obtained a phase-pure $$(\overline{2 }01)$$ ( 2 ¯ 01 ) β-Ga2O3 film on c-Sapphire. Interestingly, the in-situ reflective high-energy electron diffraction (RHEED) patterns observed from this heterostructure revealed the in-plane ‘b’ lattice constant of β-Ga2O3 ~ 3.038Å. In the next stage, for the first time, 2D In2Se3 layers were epitaxially realized on 3D β-Ga2O3 under varying substrate temperatures (Tsub) and Se/In flux ratios (RVI/III). The deposited layers exhibited (00l) oriented β-In2Se3 on $$(\overline{2 }01)$$ ( 2 ¯ 01 ) β-Ga2O3/c-Sapphire with the epitaxial relationship of $$[11\overline{2 }0]$$ [ 11 2 ¯ 0 ] β-In2Se3 || [010] β-Ga2O3 and $$[10\overline{1 }0]$$ [ 10 1 ¯ 0 ] β-In2Se3 || [102] β-Ga2O3 as observed from the RHEED patterns. Also, the in-plane ‘a’ lattice constant of β-In2Se3 was determined to be ~ 4.027Å. The single-phase β-In2Se3 layers with improved structural and surface quality were achieved at a Tsub ~ 280 °C and RVI/III ~ 18. The microstructural and detailed elemental analysis further confirmed the epitaxy of 2D layered β-In2Se3 on 3D β-Ga2O3, a consequence of the quasi-van der Waals epitaxy. Furthermore, the β-Ga2O3 with an optical bandgap (Eg) of ~ 5.04 eV (deep ultraviolet) when integrated with 2D β-In2Se3, Eg ~ 1.43eV (near infra-red) can reveal potential applications in the optoelectronic field.

Abstract Background The tumour microenvironment (TME) is a specialised niche involving intercellular communication among cancer cells and various host cells. Among the host cells, the quantity and quality of immune cells within the TME play essential roles in cancer development and management. The immunologically suppressive, so‐called ‘cold’ TME established by a series of tumour–host interactions, including generating immunosuppressive cytokines and recruiting regulatory host immune cells, is associated with resistance to therapies and worse clinical outcomes. Main body Various therapeutic approaches have been used to target the cold TME, including immune checkpoint blockade therapy and adoptive T‐cell transfer. A promising, less explored therapeutic strategy involves targeting TME‐associated exosomes. Exosomes are nanometer‐sized, extracellular vesicles that transfer material from donor to recipient cells. These particles can reprogram the recipient cells and modulate the TME. In particular, exosomes from haematopoietic cells are known to promote or suppress cancer progression under specific conditions. Understanding the effects of haematopoietic cell‐secreted exosomes may foster the development of therapeutic exosomes (tExos) for personalised cancer treatment. However, the development of exosome‐based therapies has unique challenges, including scalable production, purification, storage and delivery of exosomes and controlling batch variations. Clinical trials are being conducted to verify the safety, feasibility, availability and efficacy of tExos. Conclusion This review summarises our understanding of how haematopoietic cell‐secreted exosomes regulate the TME and antitumour immunity and highlights present challenges and solutions for haematopoietic cell‐derived exosome‐based therapies.

Legumes acquire access to atmospheric nitrogen through nitrogen fixation by rhizobia in root nodules. Rhizobia are soil-dwelling bacteria and there is a tremendous diversity of rhizobial species in different habitats. From the legume perspective, host range is a compromise between the ability to colonize new habitats, in which the preferred symbiotic partner may be absent, and guarding against infection by suboptimal nitrogen fixers. Here, we investigate natural variation in rhizobial host range across Lotus species. We find that Lotus burttii is considerably more promiscuous than Lotus japonicus, represented by the Gifu accession, in its interactions with rhizobia. This promiscuity allows Lotus burttii to form nodules with Mesorhizobium, Rhizobium, Sinorhizobium, Bradyrhizobium, and Allorhizobium species that represent five distinct genera. Using recombinant inbred lines, we have mapped the Gifu/burttii promiscuity quantitative trait loci (QTL) to the same genetic locus regardless of rhizobial genus, suggesting a general genetic mechanism for symbiont-range expansion. The Gifu/burttii QTL now provides an opportunity for genetic and mechanistic understanding of promiscuous legume-rhizobia interactions. [Graphic: see text] Copyright © 2022 The Author(s). This is an open access article distributed under the CC BY 4.0 International license.

Abstract Immune checkpoint blockade therapy has revolutionized non-small cell lung cancer treatment. However, not all patients respond to this therapy. Assessing the tumor expression of immune checkpoint molecules, including programmed death-ligand 1 (PD-L1), is the current standard in predicting treatment response. However, the correlation between PD-L1 expression and anti-PD-1/PD-L1 treatment response is not perfect. This is partly caused by tumor heterogeneity and the common practice of assessing PD-L1 expression based on limited biopsy material. To overcome this problem, we developed a novel method that can make formalin-fixed, paraffin-embedded tissue translucent, allowing three-dimensional (3D) imaging. Our protocol can process tissues up to 150 μm in thickness, allowing anti-PD-L1 staining of the entire tissue and producing high resolution 3D images. Compared to a traditional 4 μm section, our 3D image provides 30 times more coverage of the specimen, assessing PD-L1 expression of approximately 10 times more cells. We further developed a computer-assisted PD-L1 quantitation method to analyze these images, and we found marked variation of PD-L1 expression in 3D. In 5 of 33 needle-biopsy-sized specimens (15.2%), the PD-L1 tumor proportion score (TPS) varied by greater than 10% at different depth levels. In 14 cases (42.4%), the TPS at different depth levels fell into different categories (

In this paper, we propose an end-to-end key-player-based group activity recognition network specially applied to the identification of basketball offensive tactics in limited data scenarios. Our previous studies show that basketball tactics can be better recognized via key player detection with multiple instance learning (MIL) using the support vector machine (SVM). However, the SVM in that work is required to extract features depending on basketball- and tactic-specific knowledge for good performance. Thus, in this study, we develop an end-to-end trainable neural network without prior knowledge and integrate MIL into it. As long as a tactic label is given, MIL can train the network to identify tactic’s key players. For testing, our network can recognize the key players in a video clip and provide a tag of the tactic related to them. Like other neural network models, our network requires a large annotated dataset. At the same time, we could collect only a few labeled data, which is common in dealing with group activity recognition. To overcome such a limitation, we propose a novel data augmentation framework, the tactical-based conditional generative adversarial network (GAN), for generating new labeled trajectories. The experimental results show that our method significantly improves 9.13 % in tactic recognition and 4.965 % in key player detection.

PKC-mediated inflammation is important in ovarian physiology. The roles of Akt and protein phosphatase 2A (PP2A) in PKC-mediated inflammation in ovarian granulosa cells (GCs) remain mostly unclear. PKC activator phorbol 12-myristate 13-acetate induced the Akt phosphorylation in rat primary GCs but reduced the Akt phosphorylation in KGN human GCs. In rat GCs, an inhibitory effect of PI3K inhibitor wortmannin and a stimulatory effect of Akt activator SC79 on PKC-induced cyclooxygenase-2 (COX-2)/PGE2production were noted; wortmannin and SC79 acted oppositely in human GCs. In rat GCs, PP2A inhibitor okadaic acid further enhanced the PKC-mediated promoter activation and elevation of mRNA and protein levels of the COX-2 gene, whereas PP2A activator sodium selenate attenuated the PKC-mediated COX-2 expression and promoter activation. PKC activation did not affect PP2A phosphorylation, but okadaic acid indeed augmented the PKC-induced NF-κB nuclear translocation. Thus, PP2A appears to act as a negative modulator in PKC-mediated cellular inflammation in rat GCs, at least in part due to its attenuating effect on the PKC-induced NF-κB activation.

The purpose of this research was to study the effects of complex functional strength training (whole-body vibration + unstable surface training) on overall shooting performance, including the shooters’ stability of hold, time on target, and the body sway. We compared the shooters’ performances at three time intervals: (a) pretraining, (b) 6 weeks post-WBV+UST, and (c) 6 weeks detraining. The study participants were eight rifle shooters. Training was c on an unstable surface with vibration frequency of 30 Hz and amplitude of 2 mm. Six weeks after complex training, participants’ shooting performance and body sway significantly improved. Specifically, shooting scores and total time improved by 5.50% and 7.34%, respectively, as did the DevTotal values between performances at different times: 10 ms (p = 0.01), 20 ms (p = 0.04), 30 ms (p = 0.02), and 40 ms (p = 0.02). The DevY values also showed significant differences between performances at different times: 10 ms (p < 0.01), 20 ms (p < 0.01), 30 ms (p < 0.01), 40 ms (p < 0.01), and 50 ms (p < 0.01). A 6 week complex training method can effectively improve shooting stability, fluency, and scores.

Despite a moderate magnitude, Mw = 6.4, the 5 February 2016 Meinong, Taiwan, earthquake caused significant damage in Tainan City and the surrounding areas. Several seismograms display an impulsive S-wave velocity pulse with an amplitude of about 1 m s-1, which is similar to large S-wave pulses recorded for the past several larger damaging earthquakes, such as the 1995 Kobe, Japan, earthquake (Mw = 6.9) and the 1994 Northridge, California, earthquake (Mw = 6.7). The observed PGV in the Tainan area is about 10 times larger than the median PGV of Mw = 6.4 crustal earthquakes in Taiwan. We investigate the cause of the localized strong ground motions. The peak-to-peak ground-motion displacement at the basin sites near Tainan is about 35 times larger than that at a mountain site with a similar epicentral distance. At some frequency bands (0.9 - 1.1 Hz), the amplitude ratio is as large as 200. Using the focal mechanism of this earthquake, typical “soft” and “hard” crustal structures, and directivity inferred from the observed waveforms and the slip distribution, we show that the combined effect yields an amplitude ratio of 17 to 34. The larger amplitude ratios at higher frequency bands can be probably due to the effects of complex 3-D basin structures. The result indicates that even from a moderate event, if these effects simultaneously work together toward amplifying ground motions, the extremely large ground motions as observed in Tainan can occur. Such occurrences should be taken into consideration in hazard mitigation measures in the place with frequent moderate earthquakes.

The 2013 ML 6.4 Ruisui earthquake struck a seismic gap around the northern part of the Longitudinal Valley where rare earthquakes have occurred for at least two decades. Seismic data with different frequency bands connote a diverse scale of source characteristics. The slip model derived by a previous study using long-period seismic data provided us with the preliminary earthquake source properties in low-frequency energy radiation. However, the high-frequency part of the seismic energy needs to be considered for the strong motions in the comprehensive frequency band. As a case study, we carried out broadband strong motion simulations through the hybrid scheme, which simulated waveforms combining the low-frequency motions (frequency-wavenumber integration method) and high-frequency motions (empirical Green’s function method) to reveal the strong ground motion and source characteristics of the 2013 Ruisui earthquake. The results show that even though the local structure is complicated this hybrid simulation can effectively rebuild the overall broadband strong ground motion characteristics for the 2013 Ruisui earthquake. Additional study issues are required to better understand the nature of localized high peak ground acceleration and the related seismic hazards for future earthquakes.

A 47-year-old woman presented with spontaneous right side pneumothorax. Image studies showed consolidations and reticular opacities involving the pleural and subpleural regions of bilateral lungs. Wedge biopsy specimens of right upper, middle and lower lobes showed fibrosis of the visceral pleura and subpleural area in all three lobes, more significant in the upper lobe. Elastic Van Gieson stain showed a pattern of alveolar septal elastosis with intra-alveolar fibrosis. The clinical presentation and pathological findings are compatible with pleuroparenchymal fibroelastosis, a rare and distinct type of interstitial lung disease. This entity is different from usual interstitial pneumonia by its relationship to pleura, upper lobe predominance and temporal homogeneity. It is different from non-specific interstitial pneumonia by its pleural involvement and scanty inflammatory cell infiltration. Pleuroparenchymal fibroelastosis is a slowly progressive disease; about half of the patients die in 10 years. No curative treatment is available at present time.

Much evidence has indicated that matrix metalloproteinases (MMPs) participate in the progression of neuroinflammatory disorders. The present study was undertaken to investigate the inhibitory effect and mechanism of the antipsychotic haloperidol on MMP activation in the stimulated THP-1 monocytic cells. Haloperidol exerted a strong inhibition on tumor necrosis factor- (TNF-) α-induced MMP-9 gelatinolysis of THP-1 cells. A concentration-dependent inhibitory effect of haloperidol was observed in TNF-α-induced protein and mRNA expression of MMP-9. On the other hand, haloperidol slightly affected cell viability and tissue inhibition of metalloproteinase-1 levels. It significantly inhibited the degradation of inhibitor-κB-α (IκBα) in activated cells. Moreover, it suppressed activated nuclear factor-κB (NF-κB) detected by a mobility shift assay, NF-κB reporter gene, and chromatin immunoprecipitation analyses. Consistent with NF-κB inhibition, haloperidol exerted a strong inhibition of lipopolysaccharide- (LPS-) induced MMP-9 gelatinolysis but not of transforming growth factor-β1-induced MMP-2. In in vivo studies, administration of haloperidol significantly attenuated LPS-induced intracerebral MMP-9 activation of the brain homogenate and the in situ in C57BL/6 mice. In conclusion, the selective anti-MMP-9 activation of haloperidol could possibly involve the inhibition of the NF-κB signal pathway. Hence, it was found that haloperidol treatment may represent a bystander of anti-MMP actions for its conventional psychotherapy.