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1.
ACS Appl Mater Interfaces ; 16(11): 13980-13988, 2024 Mar 20.
Article in English | MEDLINE | ID: mdl-38446715

ABSTRACT

The anisotropic thermal transport properties of low-symmetry two-dimensional materials play an important role in understanding heat dissipation and optimizing thermal management in integrated devices. Examples of efficient energy dissipation and enhanced power sustainability have been demonstrated in nanodevices based on materials with anisotropic thermal transport properties. However, the exploration of materials with high thermal conductivity and strong in-plane anisotropy remains challenging. Herein, we demonstrate the observation of anisotropic in-plane thermal conductivities of few-layer SiP2 based on the micro-Raman thermometry method. For suspended SiP2 nanoflake, the thermal conductivity parallel to P-P chain direction (κ∥b) can reach 131 W m-1 K-1 and perpendicular to P-P chain direction (κ⊥b) is 89 W m-1 K-1 at room temperature, resulting in a significant anisotropic ratio (κ∥b/κ⊥b) of 1.47. Note that such a large anisotropic ratio mainly results from the higher phonon group velocity along the P-P chain direction. We also found that the thermal conductivity can be effectively modulated by increasing the SiP2 thickness, reaching a value as high as 202 W m-1 K-1 (120 W m-1 K-1) for κ∥b (κ⊥b) at 111 nm thickness, which is the highest among layered anisotropic phosphide materials. Notably, the anisotropic ratio always remains at a high level between 1.47 and 1.68, regardless of the variation of SiP2 thickness. Our observation provides a new platform to verify the fundamental theory of thermal transport and a crucial guidance for designing efficient thermal management schemes of anisotropic electronic devices.

2.
Sci China Life Sci ; 67(5): 1027-1034, 2024 May.
Article in English | MEDLINE | ID: mdl-38280143

ABSTRACT

Protein-mediated chromatin interactions can be revealed by coupling proximity-based ligation with chromatin immunoprecipitation. However, these techniques require complex experimental procedures and millions of cells per experiment, which limits their widespread application in life science research. Here, we develop a novel method, Hi-Tag, that identifies high-resolution, long-range chromatin interactions through transposase tagmentation and chromatin proximity ligation (with a phosphorothioate-modified linker). Hi-Tag can be implemented using as few as 100,000 cells, involving simple experimental procedures that can be completed within 1.5 days. Meanwhile, Hi-Tag is capable of using its own data to identify the binding sites of specific proteins, based on which, it can acquire accurate interaction information. Our results suggest that Hi-Tag has great potential for advancing chromatin interaction studies, particularly in the context of limited cell availability.


Subject(s)
Chromatin , Chromatin/metabolism , Chromatin/genetics , Humans , Binding Sites , Protein Binding , Transposases/metabolism , Transposases/genetics , Chromatin Immunoprecipitation/methods , Animals
3.
Nat Commun ; 13(1): 6938, 2022 Nov 14.
Article in English | MEDLINE | ID: mdl-36376300

ABSTRACT

Valence fluctuation of interacting electrons plays a crucial role in emergent quantum phenomena in correlated electron systems. The theoretical rationale is that this effect can drive a band insulator into a superconductor through charge redistribution around the Fermi level. However, the root cause of such a fluctuating leap in the ionic valency remains elusive. Here, we demonstrate a valence-skipping-driven insulator-to-superconductor transition and realize quasi-two-dimensional superconductivity in a van der Waals insulator GeP under pressure. This is shown to result from valence skipping of the Ge cation, altering its average valency from 3+ to 4+, turning GeP from a layered compound to a three-dimensional covalent system with superconducting critical temperature reaching its maximum of 10 K. Such a valence-skipping-induced superconductivity with a quasi-two-dimensional nature in thin samples, showing a Berezinskii-Kosterlitz-Thouless-like character, is further confirmed by angle-dependent upper-critical-field measurements. These findings provide a model system to examine competing order parameters in valence-skipping systems.

4.
Mol Immunol ; 150: 78-89, 2022 10.
Article in English | MEDLINE | ID: mdl-36007354

ABSTRACT

BACKGROUND: Innate immune response constitutes the first line of defense against pathogens. Inflammatory responses involve close contact between different populations of cells. These adhesive interactions mediate migration of cells to sites of infection leading the effective action of cells within the lesions. Cell adhesion molecules are critical to controlling immune response mediating cell adhesion or chemotaxis, as well as coordinating actin-based cell motility during phagocytosis and chemotaxis. Recently, a newly discovered neuroplastin (Np) adhesion molecule is found to play an important role in the nervous system. However, there is limited information on Np functions in immune response. To understand how Np is involved in innate immune response, a mouse model of intraperitoneal infection was established to investigate the effect of Np on macrophage-mediated clearance of E. coli infection and its possible molecular mechanisms. METHODS: Specific deficiency mice with Nptn gene controlling Np65 isoform were employed in this study. The expression levels of mRNA and proteins were detected by qPCR and western blot, or evaluated by flow cytometry. The expression level of NO and ROS were measured with their specific indicators. Cell cycle and apoptosis were detected by specific detection kits. Acid phosphatase activity was measured by flow cytometry after labelling with LysoRed fluorescent probe. Bone marrow derived macrophages (BMDMs) were isolated from bone marrow of mice hind legs. Cell proliferation was detected by CCK8 assay. Cell migration was measured by wound healing assay or transwell assay. RESULTS: The lethal dose of E. coli infection in Np65-/- mice dropped to the half of lethal dose in WT mice. The bacterial load in the spleen, kidney and liver from Np65-/- mice were significantly higher than that from WT mice, which were due to the dramatic reduction of NO and ROS production in phagocytes from Np65-/- mice. Np65 gene deficiency remarkably impaired phagocytosis and function of lysosome in macrophage. Furthermore, Np65 molecule was involved in maturation and proliferation, even in migration and chemotaxis of BMDM in vitro. CONCLUSION: This study for the first time demonstrates that Np is involved in multi-function of phagocytes during bacterial infection, proposing that Np adhesion molecule plays a critical role in clearing pathogen infection in innate immunity.


Subject(s)
Escherichia coli Infections , Escherichia coli , Acid Phosphatase , Actins , Animals , Cell Adhesion Molecules , Escherichia coli/metabolism , Fluorescent Dyes , Macrophages , Membrane Glycoproteins/metabolism , Mice , Protein Isoforms , RNA, Messenger , Reactive Oxygen Species
5.
ACS Appl Mater Interfaces ; 12(41): 46900-46907, 2020 Oct 14.
Article in English | MEDLINE | ID: mdl-32931238

ABSTRACT

Interlayer coupling in two-dimensional (2D) layered materials plays an important role in controlling their properties. 2H- and 3R-MoS2 with different stacking orders and the resulting interlayer coupling have been recently discovered to have different band structures and a contrast behavior in valley physics. However, the role of carrier doping in interlayer coupling in 2D materials remains elusive. Here, based on the electric double layer interface, we demonstrated the experimental observation of carrier doping-enhanced interlayer coupling in 3R-MoS2. A remarkable tuning of interlayer Raman modes can be observed by changing the stacking sequence and carrier doping near their monolayer limit. The modulated interlayer vibration modes originated from the interlayer coupling show a doping-induced blue shift and are supposed to be associated with the interlayer coupling enhancement, which is further verified using our first-principles calculations. Such an electrical control of interlayer coupling of layered materials in an electrical gating geometry provides a new degree of freedom to modify the physical properties in 2D materials.

6.
Mol Immunol ; 117: 189-200, 2020 01.
Article in English | MEDLINE | ID: mdl-31816492

ABSTRACT

BACKGROUND: Tuberculosis (TB) is a chronic infectious disease caused by Mycobacterium tuberculosis (Mtb). Granuloma is a pathological feature of tuberculosis and is a tight immune cell aggregation caused by Mtb. The main constituent cells are macrophages and their derivative cells including epithelioid macrophages. However, the molecular mechanism of the transition has not been reported. The purpose of this study was to investigate whether early secreted antigenic target of 6-kDa (ESAT6) can induce the transition of bone marrow-derived macrophages (BMDMs) into epithelioid macrophages and its possible molecular mechanism. METHODS: The recombinant ESAT6 protein was obtained from E.coli carrying esat6 gene after isopropyl ß-d-thiogalactopyranoside (IPTG) induction. BMDMs were isolated from bone marrow of mice hind legs. Cells viability was detected by Cell Counting Kit 8 (CCK8) assays. The expression levels of mRNA and proteins were detected by qPCR and Western blot, or evaluated by flow cytometry. The expression level of nitric oxide (NO) was measured with a nitric oxide indicator. RESULTS: ESAT6 could significantly induce mRNA and protein expression levels of a group of epithelioid macrophages marker molecules (EMMMs), including E-cadherin, junction plakoglobin, ZO1, desmoplakin, desmoglein3 and catenin porteins, in BMDMs. These events could be abrogated in macrophage from TLR2 deficiency mice. ESAT6 could also markedly induce iNOS/NO production that could significantly inhibit trimethylation of H3K27 in the cells. ESAT6-induced expressions of epithelioid macrophages marker molecules were significantly inhibited in the presence of H3K27 histone demethylase inhibitor GSK J1. Furthermore, ROS scavenging agent N,N'-Dimethylthiourea (DMTU) could markedly inhibit the transition induced by ESAT6 in macrophages. CONCLUSION: This study demonstrates that ESAT6 bound with TLR2 can activate iNOS/NO and ROS signalings to reduce the trimethylation of H3K27 resulting in the increment of EMMMs expression that is beneficial to the transition of macrophages into epithelioid macrophages. However, hypoxia can inhibit this transition event. This study has provided new evidence of pathogenesis of granuloma caused by Mtb and also proposed new ideas for the treatment of TB.


Subject(s)
Antigens, Bacterial/metabolism , Bacterial Proteins/metabolism , Cell Transdifferentiation/physiology , Macrophages/metabolism , Signal Transduction/physiology , Tuberculosis/metabolism , Animals , DNA Methylation/physiology , Down-Regulation , Granuloma/metabolism , Granuloma/microbiology , Granuloma/pathology , Histones , Macrophages/pathology , Mice , Mycobacterium tuberculosis , Nitric Oxide/metabolism , Nitric Oxide Synthase Type II/metabolism , Tuberculosis/pathology
7.
Mol Cell Biochem ; 457(1-2): 179-189, 2019 Jul.
Article in English | MEDLINE | ID: mdl-30911956

ABSTRACT

Mycobacterium tuberculosis (Mtb) is an intracellular pathogen that triggers several survival mechanisms against the host immune system. Many studies show that the diverse components of Mtb can modulate apoptosis in various types of cells differently. So far, apoptosis induced by ESAT-6, an early secreted antigenic target of 6-kDa of Mtb, has been studied but the details of molecular mechanism and signaling pathway remain incompletely defined. This study investigated the role of recombinant ESAT-6 in inducing apoptosis in primary bone marrow-derived macrophages (BMDMs) of mice using Annexin V/PI assay with FACS analysis and Western blotting technique. It has been found that ESAT-6-induced apoptosis in BMDMs in a dose- and time-dependent pattern. Apoptosis induced by ESAT-6 was mainly via the intrinsic pathway with elevated protein levels of cleaved caspase-9 and -3. Furthermore, ESAT-6 also induced Bim activation during this process. Interestingly, this event was TLR2-dependent since the effect of ESAT-6 on apoptosis vanished in BMDM from mice with TLR2 deficiency. Furthermore, ROS generation and MAPKs phosphorylation induced by ESAT-6 were also involved in caspase-9 and caspase-3 activation. Taken together, these data suggest that ESAT-6-mediated apoptosis is involved in ROS-MAPKs signaling and further activating the intrinsic pathway, which provides new insights into the basic physiology of macrophage death in tuberculosis.


Subject(s)
Antigens, Bacterial/pharmacology , Apoptosis/drug effects , Bacterial Proteins/pharmacology , Caspase 3/metabolism , Caspase 9/metabolism , Macrophages/metabolism , Mycobacterium tuberculosis/chemistry , Animals , Antigens, Bacterial/chemistry , Bacterial Proteins/chemistry , Bone Marrow Cells/metabolism , Bone Marrow Cells/pathology , Macrophages/pathology , Male , Mice
8.
Mitochondrial DNA B Resour ; 2(2): 437-438, 2017 Jul 26.
Article in English | MEDLINE | ID: mdl-33473854

ABSTRACT

The complete mitochondrial genome of Heosemys depressa was obtained and characterized in this study. The mitochondrial genome is a circular molecule of 16,773bp in length, and harbours 13 protein-coding genes (PCGs), 2 ribosomal RNA (rRNA) genes, 22 transfer RNA (tRNA) genes, and 1 non-coding D-loop region (control region). Its gene arrangement type is identical to the type of most vertebrate. Phylogenetic analysis suggests that H. depressa is closely related to H. annandalii than to the other species. Our data provide a useful resource for the phylogenetic studies of genus Heosemys.

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