Background: Coronavirus disease 2019 (COVID-19) is posing a huge threat to human health worldwide. We aim to investigate the immune status of CD8 + T and NK cells in COVID-19 patients. Methods: The count and immune status of lymphocytes were detected by flow cytometry in 32 COVID-19 patients and 18 healthy individuals. Results: As the disease progression in COVID-19 patients, CD8 + T and NK cells were significantly decreased in absolute number but highly activated. After patients' condition improved, the count and immune status of CD8 + T and NK cells restored to some extent. GrA + CD8 + T and perforin + NK cells had good sensitivity and specificity for assisting diagnosis of COVID-19. Conclusions: As the disease progression, the declined lymphocytes in COVID-19 patients might lead to compensatory activation of CD8 + T and NK cells. GrA + CD8 + T and perforin + NK cells might be used as meaningful indicators for assisting diagnosis of COVID-19.
Reusing polluted water through various decontamination techniques has appeared as one of the most practical approaches to address the global shortage of clean water. Rather than relying on single decontamination mechanism, herein we report the preparation and utilization of paper-based composites for multifunctional solar-driven clean water generation that is inspired by the multiple water purification approaches in biological systems. The reduced graphene oxide (rGO) sheets within such composites can efficiently remove organic contaminants through physical adsorption mechanism. Under solar irradiation, the floating rGO composites can instantly generate localized heating, which not only can directly generate clean water through distillation mechanism but also significantly enhance adsorption removal performance with the assistance of upward vapor flow. Such porous-structured paper-based composites allow for facile incorporation of photocatalysts to regenerate clean water out of contaminated water with combined adsorption, photodegradation, and interfacial heat-assisted distillation mechanisms. Within a homemade all-in-one water treatment device, the practical applicability of the composites for multifunctional clean water generation has been demonstrated.
Aberrant activation of β-catenin in the nucleus has been implicated in a variety of human cancers but the fate of nuclear β-catenin is unknown. Here we demonstrate that tripartite motif-containing protein 33 (TRIM33), acting as an E3 ubiquitin ligase, reduces the abundance of nuclear β-catenin protein. TRIM33-mediated β-catenin is destabilized and is GSK-3β or β-TrCP independent. TRIM33 interacts with and ubiquitylates nuclear β-catenin. Moreover, protein kinase Cδ, which directly phosphorylates β-catenin at Ser715, is required for the TRIM33–β-catenin interaction. The function of TRIM33 in suppressing tumour cell proliferation and brain tumour development depends on TRIM33-promoted β-catenin degradation. In human glioblastoma specimens, endogenous TRIM33 levels are inversely correlated with β-catenin. In summary, our findings identify TRIM33 as a tumour suppressor that can abolish tumour cell proliferation and tumorigenesis by degrading nuclear β-catenin. This work suggests a new therapeutic strategy against human cancers caused by aberrant activation of β-catenin.
Emerging evidences have shown that GSK3β plays oncogenic roles in multiple tumor types; however, the underlying mechanisms remain largely unknown. Herein, we show that nuclear GSK3β is responsible for the accumulation of the histone demethylase KDM1A and critically regulates histone H3K4 methylation during tumorigenesis. GSK3β phosphorylates KDM1A serine 683 upon priming phosphorylation of KDM1A serine 687 by CK1α. Phosphorylation of KDM1A induces its binding with and deubiquitination by USP22, leading to KDM1A stabilization. GSK3β and USP22-dependent KDM1A stabilization is required for the demethylation of histone H3K4, thereby repression of BMP2, CDKN1A, and GATA6 transcription, cancer stem cell self-renewal, and glioblastoma tumorigenesis. In human glioblastoma specimens, KDM1A levels are correlated with nuclear GSK3β and USP22 levels. Furthermore, a GSK3 inhibitor tideglusib sensitizes tumor xenograft to chemotherapy in mice via KDM1A down-regulation and improves survival. Our findings demonstrate that nuclear GSK3β and USP22-mediated KDM1A stabilization is essential for glioblastoma tumorigenesis.
Modern microelectronics and emerging technologies such as wearable devices and soft robotics require conformable and thermally conductive thermal interface materials to improve their performance and longevity. Gallium‐based liquid metals (LMs) are promising candidates for these applications yet are limited by their moderate thermal conductivity, difficulty in surface‐spreading, and pump‐out issues. Incorporation of metallic particles into the LM can address these problems, but observed alloying processes shift the LM melting point and lead to undesirable formation of additional surface roughness. Here, these problems are addressed by introducing a mixture of tungsten microparticles dispersed within a LM matrix (LM‐W) that exhibits two‐ to threefold enhanced thermal conductivity (62 ± 2.28 W m−1 K−1 for gallium and 57 ± 2.08 W m−1 K−1 for EGaInSn at a 40% filler volume mixing ratio) and liquid‐to‐paste transition for better surface application. It is shown that the formation of a nanometer‐scale LM oxide in oxygen‐rich environments allows highly nonwetting tungsten particles to mix into LMs. Using in situ imaging and particle dipping experimentation within a focused ion beam and scanning electron microscopy system, the oxide‐assisted mechanism behind this wetting process is revealed. Furthermore, since tungsten does not undergo room‐temperature alloying with gallium, it is shown that LM‐W remains a chemically stable mixture.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.