47 research outputs found
Highly Porous Core–Shell Structured Graphene-Chitosan Beads
Graphene oxide (GO) sheets have been
assembled into various three-dimensional porous structures and composites,
with potential applications in energy and environmental areas. Here,
we show the combination of GO and chitosan (CTS) into inorganic–organic
heterocomposites as ∼3 mm diameter core–shell beads
with controlled microstructure. The spherical GO-CTS beads, made by
a two-step freeze-casting method, consist of a GO core wrapped by
a CTS shell with abrupt interface; both parts have high porosities
(94–96%) and mesopores volume (0.246 cm<sup>3</sup>/g) yet
with different pore morphologies. Incorporation of a GO core into
the CTS beads significantly improved the methyl orange adsorption
capacity (353 mg/g at 318 K) compared with pure CTS beads. Key factors
such as the pH value, adsorbent dosage, concentration, time, and temperature
have been studied in detail, whereas adsorption isotherm and kinetic
studies reveal a Langmuir model following the pseudo-second order
Image1_Downregulation of MARC2 Promotes Immune Escape and Is Associated With Immunosuppression of Hepatocellular Carcinoma.TIF
The N-reductive enzyme system (NRES), composed of MARC1, MARC2, CYB5, and CYB5R, is responsible for the reduction of N-oxygenated compounds and participates in several physiological processes. For example, MARC2 serves as an important prognostic indicator and is downregulated in hepatocellular carcinoma, and the downregulation of MARC2 is critical to the regulation of lipid metabolism and cell cycle progression. However, the role of MARC2 in tumor immune microenvironment modification had not previously been investigated. In this study, we found that downregulation of MARC2 was associated with the differentiation of CD4+T cells into regulatory T cells (Tregs). Furthermore, restoring the expression of MARC2 could increase the expression of HLA-C and B2M via PPARA-related lipid metabolism signaling pathways, which could facilitate tumor antigen presentation to the tumor-infiltrating T cells. Additionally, MARC2 expression negatively correlated with several immune checkpoints. The immune checkpoint burden was generated based on 28 MARC2-related immune checkpoints. Patients with a higher immune checkpoint burden were predicted to have a poorer prognosis and a lower level of activated CD8+ T cells. The results showed that expression of the NRES is a prognostic indicator of hepatocellular carcinoma and MARC2 contributes significantly to predict the prognosis. Finally, loss of MARC2 in HCC patients was found to facilitate immune escape and was associated with immunosuppression.</p
Selective Ion Transport through Functionalized Graphene Membranes Based on Delicate Ion–Graphene Interactions
Recently, graphene
oxide (GO) membranes have been reported with
the ability to separate different solutes in aqueous suspensions by
a molecular sieving effect. On the other hand, we propose that the
chemical interactions between ions and GO membranes might also take
effect in selective ion transmembrane transportation. In this paper,
on the basis of the permeation of Cu<sup>2+</sup> and Mg<sup>2+</sup> sources through hydroxyl-, carboxyl-, and amino-functionalized graphene
membranes, the delicate ion–graphene interactions which might
be responsible for the selective ion permeation are investigated.
We demonstrate experimentally that the coordination between transition-metal
cations and carboxyl functionalities and the cation−π
interactions between main-group cations and sp<sup>2</sup> regions
are responsible for the selective transport of small ions through
graphene-based membranes, which is beyond the scope of molecular sieving
effect proposed previously. Notably, by grafting amino groups onto
the graphene basal planes, the permeations of Cu<sup>2+</sup> and
Mg<sup>2+</sup> cations are both weakened. These results not only
throw light upon the mechanism for the selective ion permeation through
graphene-based membranes but also lay a foundation for the separation
of target ions by grafting specific functionalities
Image3_Downregulation of MARC2 Promotes Immune Escape and Is Associated With Immunosuppression of Hepatocellular Carcinoma.TIF
The N-reductive enzyme system (NRES), composed of MARC1, MARC2, CYB5, and CYB5R, is responsible for the reduction of N-oxygenated compounds and participates in several physiological processes. For example, MARC2 serves as an important prognostic indicator and is downregulated in hepatocellular carcinoma, and the downregulation of MARC2 is critical to the regulation of lipid metabolism and cell cycle progression. However, the role of MARC2 in tumor immune microenvironment modification had not previously been investigated. In this study, we found that downregulation of MARC2 was associated with the differentiation of CD4+T cells into regulatory T cells (Tregs). Furthermore, restoring the expression of MARC2 could increase the expression of HLA-C and B2M via PPARA-related lipid metabolism signaling pathways, which could facilitate tumor antigen presentation to the tumor-infiltrating T cells. Additionally, MARC2 expression negatively correlated with several immune checkpoints. The immune checkpoint burden was generated based on 28 MARC2-related immune checkpoints. Patients with a higher immune checkpoint burden were predicted to have a poorer prognosis and a lower level of activated CD8+ T cells. The results showed that expression of the NRES is a prognostic indicator of hepatocellular carcinoma and MARC2 contributes significantly to predict the prognosis. Finally, loss of MARC2 in HCC patients was found to facilitate immune escape and was associated with immunosuppression.</p
Image7_Downregulation of MARC2 Promotes Immune Escape and Is Associated With Immunosuppression of Hepatocellular Carcinoma.TIF
The N-reductive enzyme system (NRES), composed of MARC1, MARC2, CYB5, and CYB5R, is responsible for the reduction of N-oxygenated compounds and participates in several physiological processes. For example, MARC2 serves as an important prognostic indicator and is downregulated in hepatocellular carcinoma, and the downregulation of MARC2 is critical to the regulation of lipid metabolism and cell cycle progression. However, the role of MARC2 in tumor immune microenvironment modification had not previously been investigated. In this study, we found that downregulation of MARC2 was associated with the differentiation of CD4+T cells into regulatory T cells (Tregs). Furthermore, restoring the expression of MARC2 could increase the expression of HLA-C and B2M via PPARA-related lipid metabolism signaling pathways, which could facilitate tumor antigen presentation to the tumor-infiltrating T cells. Additionally, MARC2 expression negatively correlated with several immune checkpoints. The immune checkpoint burden was generated based on 28 MARC2-related immune checkpoints. Patients with a higher immune checkpoint burden were predicted to have a poorer prognosis and a lower level of activated CD8+ T cells. The results showed that expression of the NRES is a prognostic indicator of hepatocellular carcinoma and MARC2 contributes significantly to predict the prognosis. Finally, loss of MARC2 in HCC patients was found to facilitate immune escape and was associated with immunosuppression.</p
AES characterizations (the C and O concentration distributions along the thickness) for GO membranes after annealing at 80°C for (a) 0 and (b) 9 days, respectively.
<p>The sputter rate is 35 nm/min. (c) The comparison of O/C ratio distributions along the depth within GO membranes after 0- and 9-day annealing. (d, e) C (red) and O (green) mappings of GO membranes after 0- and 9-day annealing, respectively. The mappings were performed after sputtering the GO membranes for 5 min to exclude the effect of surface O physisorption.</p
Image2_Downregulation of MARC2 Promotes Immune Escape and Is Associated With Immunosuppression of Hepatocellular Carcinoma.TIF
The N-reductive enzyme system (NRES), composed of MARC1, MARC2, CYB5, and CYB5R, is responsible for the reduction of N-oxygenated compounds and participates in several physiological processes. For example, MARC2 serves as an important prognostic indicator and is downregulated in hepatocellular carcinoma, and the downregulation of MARC2 is critical to the regulation of lipid metabolism and cell cycle progression. However, the role of MARC2 in tumor immune microenvironment modification had not previously been investigated. In this study, we found that downregulation of MARC2 was associated with the differentiation of CD4+T cells into regulatory T cells (Tregs). Furthermore, restoring the expression of MARC2 could increase the expression of HLA-C and B2M via PPARA-related lipid metabolism signaling pathways, which could facilitate tumor antigen presentation to the tumor-infiltrating T cells. Additionally, MARC2 expression negatively correlated with several immune checkpoints. The immune checkpoint burden was generated based on 28 MARC2-related immune checkpoints. Patients with a higher immune checkpoint burden were predicted to have a poorer prognosis and a lower level of activated CD8+ T cells. The results showed that expression of the NRES is a prognostic indicator of hepatocellular carcinoma and MARC2 contributes significantly to predict the prognosis. Finally, loss of MARC2 in HCC patients was found to facilitate immune escape and was associated with immunosuppression.</p
Formation energies and reaction barriers for proposed evolution paths (a–c) of oxygen containing functional groups on GO, calculated by DFT based calculations.
<p>Formation energies and reaction barriers for proposed evolution paths (a–c) of oxygen containing functional groups on GO, calculated by DFT based calculations.</p
Image9_Downregulation of MARC2 Promotes Immune Escape and Is Associated With Immunosuppression of Hepatocellular Carcinoma.TIF
The N-reductive enzyme system (NRES), composed of MARC1, MARC2, CYB5, and CYB5R, is responsible for the reduction of N-oxygenated compounds and participates in several physiological processes. For example, MARC2 serves as an important prognostic indicator and is downregulated in hepatocellular carcinoma, and the downregulation of MARC2 is critical to the regulation of lipid metabolism and cell cycle progression. However, the role of MARC2 in tumor immune microenvironment modification had not previously been investigated. In this study, we found that downregulation of MARC2 was associated with the differentiation of CD4+T cells into regulatory T cells (Tregs). Furthermore, restoring the expression of MARC2 could increase the expression of HLA-C and B2M via PPARA-related lipid metabolism signaling pathways, which could facilitate tumor antigen presentation to the tumor-infiltrating T cells. Additionally, MARC2 expression negatively correlated with several immune checkpoints. The immune checkpoint burden was generated based on 28 MARC2-related immune checkpoints. Patients with a higher immune checkpoint burden were predicted to have a poorer prognosis and a lower level of activated CD8+ T cells. The results showed that expression of the NRES is a prognostic indicator of hepatocellular carcinoma and MARC2 contributes significantly to predict the prognosis. Finally, loss of MARC2 in HCC patients was found to facilitate immune escape and was associated with immunosuppression.</p
Image10_Downregulation of MARC2 Promotes Immune Escape and Is Associated With Immunosuppression of Hepatocellular Carcinoma.TIF
The N-reductive enzyme system (NRES), composed of MARC1, MARC2, CYB5, and CYB5R, is responsible for the reduction of N-oxygenated compounds and participates in several physiological processes. For example, MARC2 serves as an important prognostic indicator and is downregulated in hepatocellular carcinoma, and the downregulation of MARC2 is critical to the regulation of lipid metabolism and cell cycle progression. However, the role of MARC2 in tumor immune microenvironment modification had not previously been investigated. In this study, we found that downregulation of MARC2 was associated with the differentiation of CD4+T cells into regulatory T cells (Tregs). Furthermore, restoring the expression of MARC2 could increase the expression of HLA-C and B2M via PPARA-related lipid metabolism signaling pathways, which could facilitate tumor antigen presentation to the tumor-infiltrating T cells. Additionally, MARC2 expression negatively correlated with several immune checkpoints. The immune checkpoint burden was generated based on 28 MARC2-related immune checkpoints. Patients with a higher immune checkpoint burden were predicted to have a poorer prognosis and a lower level of activated CD8+ T cells. The results showed that expression of the NRES is a prognostic indicator of hepatocellular carcinoma and MARC2 contributes significantly to predict the prognosis. Finally, loss of MARC2 in HCC patients was found to facilitate immune escape and was associated with immunosuppression.</p
