RESUMEN

Corrosion protection technology plays a crucial role in preserving infrastructure, ensuring safety and reliability, and promoting long-term sustainability. In this study, we combined experiments and various analyses to investigate the mechanism of corrosion occurring on the epoxy-based anticorrosive coating containing the additive of two-dimensional (2D) and water-stable zirconium-based metal-organic frameworks (Zr-MOFs). By using benzoic acid as the modulator for the growth of the MOF, a 2D MOF constructed from hexazirconium clusters and BTB linkers (BTB = 1,3,5-tri(4-carboxyphenyl)benzene) with coordinated benzoate (BA-ZrBTB) can be synthesized. By coating the BA-ZrBTB/epoxy composite film (BA-ZrBTB/EP) on the surface of cold-rolled steel (CRS), we found the lowest coating roughness (RMS) of BA-ZrBTB/EP is 2.83 nm with the highest water contact angle as 99.8°, which represents the hydrophobic coating surface. Notably, the corrosion rate of the BA-ZrBTB/EP coating is 2.28 × 10-3 mpy, which is 4 orders of magnitude lower than that of the CRS substrate. Moreover, the energy barrier for oxygen diffusion through BA-ZrBTB/EP coating is larger than that for epoxy coating (EP), indicating improved oxygen resistance for adding 2D Zr-MOFs as the additive. These results underscore the high efficiency and potential of BA-ZrBTB as a highly promising agent for corrosion prevention in various commercial applications. Furthermore, this study represents the first instance of applying 2D Zr-MOF materials in anticorrosion applications, opening up new possibilities for advanced corrosion-resistant coatings.

RESUMEN

Imbalanced Sirtuin 1 (SIRT1) levels may lead to liver diseases through abnormal regulation of autophagy, but the roles of SIRT1-regulated autophagy in hepatocellular carcinoma are still controversial. In this study, we found that SIRT1 mRNA and protein levels were upregulated in hepatocellular carcinoma, and high SIRT1 expression hinted an advanced stage and a poor prognosis. The differentially expressed proteins were significantly elevated in autophagy, cellular response to stress, and immune signaling pathways. In a thioacetamide-induced hepatocellular carcinoma mouse model, we found that SIRT1 expression was highly increased with increased autophagy and excessive macrophage inflammatory response. Next, we established a Hepa 1-6 cells and macrophage co-culture system in vitro to model the alteration of tumor microenvironment, and found that the medium from CCl4-treated or SIRT1-overexpressing Hepa 1-6 cells triggered the polarization of macrophage M1, and the culture medium derived from M1 macrophage promoted Hepa 1-6 cells growth and intracellular oxidative stress. The progression of liver fibrosis in the CCl4-induced liver fibrosis mouse model showed that inhibition of SIRT1 alleviated inflammatory response and ameliorated liver fibrosis. These findings suggest that SIRT1-regulated autophagy and inflammation are oncogenic in hepatocarcinogenesis.

Asunto(s)

Autofagia , Carcinoma Hepatocelular , Inflamación , Neoplasias Hepáticas , Sirtuina 1 , Sirtuina 1/metabolismo , Sirtuina 1/genética , Animales , Autofagia/efectos de los fármacos , Ratones , Neoplasias Hepáticas/patología , Neoplasias Hepáticas/metabolismo , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/inducido químicamente , Inflamación/patología , Inflamación/metabolismo , Carcinoma Hepatocelular/patología , Carcinoma Hepatocelular/metabolismo , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/inducido químicamente , Humanos , Macrófagos/metabolismo , Línea Celular Tumoral , Masculino , Carcinogénesis/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , Cirrosis Hepática/inducido químicamente , Cirrosis Hepática/patología , Cirrosis Hepática/metabolismo , Regulación Neoplásica de la Expresión Génica/efectos de los fármacos

RESUMEN

In this study, an array of environmentally friendly and heavy-duty anticorrosion composite coatings were prepared. The synthesis involved amine-capped aniline trimer (ACAT) produced by an oxidative coupling reaction and graphene oxide (GO) prepared based on Hummer's method, and later, the waterborne epoxy thermoset composite (WETC) coatings were prepared by thermal ring-opening polymerization of EP 147w, a commercial waterborne epoxy resin, in the presence of ACAT and/or GO with zinc dust (ZD). A synergistic effect was observed by replacing a significant amount of the ZD loading in the WETC by simultaneously incorporating a small amount of ACAT and GO. The electrochemical corrosion measurements of the as-prepared WETC coatings indicated that incorporating 5% w/w ACAT or 0.5% w/w GO separately replaced approximately 30% w/w or 15% w/w of the ZD, respectively. Moreover, the WETC coatings containing 5% w/w ACAT and 0.5% w/w GO simultaneously were found to replace 45% w/w of the ZD. A salt spray test based on ASTM B-117 also showed a consistent trend with the electrochemical results. Incorporating small amounts of ACAT and GO in WETC coatings instead of ZD not only maintains the anticorrosion performance but also enhances adhesion and abrasion resistance, as demonstrated by the adhesion and abrasion tests.

RESUMEN

PURPOSE: GPX8, which is found in the endoplasmic reticulum lumen, is a member of the Glutathione Peroxidases (GPXs) family. Its role in hepatocellular carcinoma (HCC) is unknown. METHODS: Immunohistochemical staining was used to detect the protein levels of GPX8 in HCC tissue microarrays. A short hairpin RNA lentivirus was used to knock down GPX8, and the main signaling pathways were investigated using transcriptome sequencing and a phosphorylated kinase array. The sphere formation assays, cloning-formation assays and cell migration assays were used to evaluate the stemness and migration ability of HCC cells. Identifying the GPX8-interacting proteins was accomplished through immunoprecipitation and protein mass spectrometry. RESULTS: The GPX8 protein levels were downregulated in HCC patients. Low expression of GPX8 protein was related to early recurrence and poor prognosis in HCC patients. GPX8 knockdown could enhance the stemness and migration ability of HCC cells. Consistently, Based on transcriptome analysis, multiple signaling pathways that include the PI3K-AKT and signaling pathways that regulate the pluripotency of stem cells, were activated after GPX8 knockdown. The downregulation of GPX8 could increase the expression of the tumor stemness markers KLF4, OCT4, and CD133. The in vivo downregulation of GPX8 could also promote the subcutaneous tumor-forming and migration ability of HCC cells. MK-2206, which is a small-molecule inhibitor of AKT, could reverse the tumor-promoting effects both in vivo and in vitro. We discovered that GPX8 and the 71-kDa heat shock cognate protein (Hsc70) have a direct interaction. The phosphorylation of AKT encouraged the translocation of Hsc70 into the nucleus and the expression of the PI3K p110 subunit, thereby increasing the downregulation of GPX8. CONCLUSION: The findings from this study demonstrate the anticancer activity of GPX8 in HCC by inactivating the Hsc70/AKT pathway. The results suggest a possible therapeutic target for HCC.

Asunto(s)

Carcinoma Hepatocelular , Movimiento Celular , Regulación hacia Abajo , Regulación Neoplásica de la Expresión Génica , Neoplasias Hepáticas , Células Madre Neoplásicas , Transducción de Señal , Humanos , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/patología , Carcinoma Hepatocelular/metabolismo , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/patología , Neoplasias Hepáticas/metabolismo , Movimiento Celular/genética , Regulación hacia Abajo/genética , Células Madre Neoplásicas/metabolismo , Células Madre Neoplásicas/patología , Línea Celular Tumoral , Transducción de Señal/genética , Factor 4 Similar a Kruppel , Masculino , Femenino , Animales , Glutatión Peroxidasa/metabolismo , Glutatión Peroxidasa/genética , Persona de Mediana Edad , Ratones Desnudos , Proteínas Proto-Oncogénicas c-akt/metabolismo , Ratones , Ratones Endogámicos BALB C

RESUMEN

In this study, we synthesized a transition metal sulfide (TMS) with a spinel structure, i.e., MnIn2S4 (MIS), using a two-step hydrothermal and sintering process. In the context of lithium-ion battery (LIB) applications, ternary TMSs are being considered as interesting options for anode materials. This consideration arises from their notable attributes, including high theoretical capacity, excellent cycle stability, and cost-effectiveness. However, dramatic volume changes result in the electrochemical performance being severely limited, so we introduced single-walled carbon nanotubes (SWCNTs) and prepared an MIS/SWCNT composite to enhance the structural stability and electronic conductivity. The synthesized MIS/SWCNT composite exhibits better cycle performance than bare MIS. Undergoing 100 cycles, MIS only yields a reversible capacity of 117 mAh/g at 0.1 A/g. However, the MIS/SWCNT composite exhibits a reversible capacity as high as 536 mAh/g after 100 cycles. Moreover, the MIS/SWCNT composite shows a better rate capability. The current density increases with cycling, and the SWCNT composite exhibits high reversible capacities of 232 and 102 mAh/g at 2 A/g and 5 A/g, respectively. Under the same conditions, pristine MIS can only deliver reversible capacities of 21 and 4 mAh/g. The results indicate that MIS/SWCNT composites are promising anode materials for LIBs.

RESUMEN

BACKGROUND: Minimal residual disease (MRD) is proposed to be responsible for tumor recurrence. The role of circulating tumor DNA (ctDNA) to detect MRD, monitor recurrence, and predict prognosis in liver cancer patients undergoing liver transplantation (LT) remains unrevealed. METHODS: Serial blood samples were collected to profile ctDNA mutational changes. Baseline ctDNA mutational profiles were compared with those of matched tumor tissues. Correlations between ctDNA status and recurrence rate (RR) and recurrence-free survival (RFS) were analyzed, respectively. Dynamic change of ctDNA was monitored to predict tumor recurrence. RESULTS: Baseline mutational profiles of ctDNA were highly concordant with those of tumor tissues (median, 89.85%; range 46.2-100%) in the 74 patients. Before LT, positive ctDNA status was associated with higher RR (31.7% vs 11.5%; p = 0.001) and shorter RFS than negative ctDNA status (17.8 vs 19.4 months; p = 0.019). After LT, the percentage of ctDNA positivity decreased (17.6% vs 47.0%; p < 0.001) and patients with positive ctDNA status had higher RR (46.2% vs 21.3%; p < 0.001) and shorter RFS (17.2 vs 19.2 months; p = 0.010). Serial ctDNA profiling demonstrated patients with decreased or constant negative ctDNA status had lower RR (33.3% vs 50.0%; p = 0.015) and favorable RFS (18.2 vs 15.0 months, p = 0.003) than those with increased or constant positive ctDNA status. Serial ctDNA profiling predicted recurrence months ahead of imaging evidence and serum tumor biomarkers. CONCLUSIONS: ctDNA could effectively detect MRD and predict tumor recurrence in liver cancer patients undergone LT.

Asunto(s)

ADN Tumoral Circulante , Neoplasias Hepáticas , Trasplante de Hígado , Humanos , ADN Tumoral Circulante/genética , Recurrencia Local de Neoplasia/genética , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/cirugía , Biomarcadores de Tumor/genética

RESUMEN

Primary liver cancer (PLC) poses a leading threat to human health, and its treatment options are limited. Meanwhile, the investigation of homogeneity and heterogeneity among PLCs remains challenging. Here, using single-cell RNA sequencing, spatial transcriptomic and bulk multi-omics, we elaborated a molecular architecture of 3 PLC types, namely hepatocellular carcinoma (HCC), intrahepatic cholangiocarcinoma (ICC) and combined hepatocellular-cholangiocarcinoma (CHC). Taking a high-resolution perspective, our observations revealed that CHC cells exhibit internally discordant phenotypes, whereas ICC and HCC exhibit distinct tumor-specific features. Specifically, ICC was found to be the primary source of cancer-associated fibroblasts, while HCC exhibited disrupted metabolism and greater individual heterogeneity of T cells. We further revealed a diversity of intermediate-state cells residing in the tumor-peritumor junctional zone, including a congregation of CPE+ intermediate-state endothelial cells (ECs), which harbored the molecular characteristics of tumor-associated ECs and normal ECs. This architecture offers insights into molecular characteristics of PLC microenvironment, and hints that the tumor-peritumor junctional zone could serve as a targeted region for precise therapeutical strategies.

Asunto(s)

Neoplasias de los Conductos Biliares , Carcinoma Hepatocelular , Colangiocarcinoma , Neoplasias Hepáticas , Humanos , Carcinoma Hepatocelular/patología , Neoplasias Hepáticas/patología , Células Endoteliales/metabolismo , Neoplasias de los Conductos Biliares/genética , Colangiocarcinoma/genética , Conductos Biliares Intrahepáticos , Microambiente Tumoral/genética

RESUMEN

BACKGROUND AND AIMS: The recurrence and metastasis of hepatocellular carcinoma (HCC) are mainly caused by microvascular invasion (MVI). Our study aimed to uncover the cellular atlas of MVI+ HCC and investigate the underlying immune infiltration patterns with radiomics features. METHODS: Three MVI positive HCC and three MVI negative HCC samples were collected for single-cell RNA-seq analysis. 26 MVI positive HCC and 30 MVI negative HCC tissues were underwent bulk RNA-seq analysis. For radiomics analysis, radiomics features score (Radscore) were built using preoperative contrast MRI for MVI prediction and overall survival prediction. We deciphered the metabolism profiles of MVI+ HCC using scMetabolism and scFEA. The correlation of Radscore with the level of APOE+ macrophages and iCAFs was identified. Whole Exome Sequencing (WES) was applied to distinguish intrahepatic metastasis (IM) and multicentric occurrence (MO). Transcriptome profiles were compared between IM and MO. RESULTS: Elevated levels of APOE+ macrophages and iCAFs were detected in MVI+ HCC. There was a strong correlation between the infiltration of APOE+ macrophages and iCAFs, as confirmed by immunofluorescent staining. MVI positive tumors exhibited increased lipid metabolism, which was attributed to the increased presence of APOE+ macrophages. APOE+ macrophages and iCAFs were also found in high levels in IM, as opposed to MO. The difference of infiltration level and Radscore between two nodules in IM was relatively small. Furthermore, we developed Radscore for predicting MVI and HCC prognostication that were also able to predict the level of infiltration of APOE+ macrophages and iCAFs. CONCLUSION: This study demonstrated the interactions of cell subpopulations and distinct metabolism profiles in MVI+ HCC. Besides, MVI prediction Radscore and MVI prognostic Radscore were highly correlated with the infiltration of APOE+ macrophages and iCAFs, which helped to understand the biological significance of radiomics and optimize treatment strategy for MVI+ HCC.

Asunto(s)

Carcinoma Hepatocelular , Neoplasias Hepáticas , Humanos , Carcinoma Hepatocelular/patología , Neoplasias Hepáticas/patología , Estudios Retrospectivos , Invasividad Neoplásica , Apolipoproteínas E/genética

RESUMEN

Silicon has the potential to improve lithium-ion battery (LIB) performance substantially by replacing graphite as an anode. The sustainability of such a transformation, however, depends on the source of silicon and the nature of the manufacturing process. Today's silicon industry still overwhelmingly depends on the energy-intensive, high-temperature carbothermal reduction of silica─a process that adversely impacts the environment. Rather than use conventional thermoreduction alone to break Si-O bonds, we report the efficient conversion of SiO2 directly to Mg2Si by a microwave-induced Mg plasma within 2.5 min at merely 200 W under vacuum. The underlying mechanism is proposed, wherein electrons with enhanced kinetics function readily as the reductant while the "bombardment" from Mg cations and electrons promotes the fast nucleation of Mg2Si. The 3D nanoporous (NP) Si is then fabricated by a facile thermal dealloying step. The resulting hierarchical NP Si anodes deliver stable, extended cycling with excellent rate capability in Li-ion half-cells, with capacities several times greater than graphite. The microwave-induced metal plasma (MIMP) concept can be applied just as efficiently to the synthesis of Mg2Si from Si, and the chemistry should be extendable to the reduction of multiple metal(loid) oxides via their respective Mg alloys.

RESUMEN

The tumor microenvironment is a highly heterogeneous circumstance composed of multiple components, while tumor-associated macrophages (TAMs) are major innate immune cells with highly plastic and are always educated by tumor cells to structure an advantageous pro-tumor immune microenvironment. Despite emerging evidence focalizing the role of autophagy in other immune cells, the regulatory mechanism of autophagy in macrophage polarization remains poorly understood. Herein, we demonstrated that hepatocellular carcinoma (HCC) cells educated macrophages toward M2-like phenotype polarization under the condition of coculture. Moreover, we observed that inhibition of macrophage autophagy promoted M2-like macrophage polarization, while the tendency was impeded when autophagy was motivated. Mechanistically, macrophage autophagy inhibition inactivates the NF-κB pathway by increasing the instability of TAB3 via ubiquitination degradation, which leads to the M2-like phenotype polarization of macrophages. Both immunohistochemistry staining using human HCC tissues and experiment in vivo verified autophagy inhibition is correlated with M2 macrophage polarization. Altogether, we illustrated that macrophage autophagy was involved in the process of HCC cells domesticating M2 macrophage polarization via the NF-κB pathway. These results provide a new target to interfere with the polarization of macrophages to M2-like phenotype during HCC progression.

Asunto(s)

Carcinoma Hepatocelular , Neoplasias Hepáticas , Humanos , FN-kappa B/metabolismo , Macrófagos , Autofagia , Línea Celular Tumoral , Microambiente Tumoral

RESUMEN

Zinc (Zn) is an excellent material for use as an anode for rechargeable batteries in water-based electrolytes. Nevertheless, the high activity of water leads to Zn corrosion and hydrogen evolution, along with the formation of dendrites on the Zn surface during repeated charge-discharge (CD) cycles. To protect the Zn anode and limit parasitic side reactions, an artificial solid electrolyte interphase (ASEI) protective layer is an effective strategy. Herein, an ASEI made of a covalent organic framework (COFs: HqTp and BpTp) was fabricated on the surface of a Zn anode via Schiff base reactions of aldehyde and amine linkers. It is seen that COFs can regulate the Zn-ion flux, resulting in dendritic-free Zn. COFs can also mitigate the formation of an irreversible passive layer and the hydrogen evolution reaction (HER). Zn plating/stripping tests using a symmetrical cell suggest that HqTpCOF@Zn shows superior stability and greater coulombic efficiency (CE) compared to bare Zn. The full cell having COFs@Zn also displays much improved cyclability. As a result, the COF proves to be a promising ASEI material to enhance the stability of the Zn anode in aqueous media.

RESUMEN

BACKGROUND AND PURPOSE: Tumor recurrence after liver transplantation (LT) impedes the curative chance for hepatocellular carcinoma (HCC) patients. This study aimed to develop a deep pathomics score (DPS) for predicting tumor recurrence after liver transplantation using deep learning. PATIENTS AND METHODS: Two datasets of 380 HCC patients who underwent LT were enrolled. Residual convolutional neural networks were used to identify six histological structures of HCC. The individual risk score of each structure and DPS were derived by a modified DeepSurv network. Cox regression analysis and Concordance index were used to evaluate the prognostic significance. The cellular exploration of prognostic immune biomarkers was performed by quantitative and spatial proximity analysis according to three panels of 7-color immunofluorescence. RESULTS: The overall classification accuracy of HCC tissue was 97%. At the structural level, immune cells were the most significant tissue category for predicting post-LT recurrence (HR 1.907, 95% CI 1.490-2.440). The C-indices of DPS achieved 0.827 and 0.794 in the training and validation cohorts, respectively. Multivariate analysis for recurrence-free survival (RFS) showed that DPS (HR 4.795, 95% CI 3.017-7.619) was an independent risk factor. Patients in the high-risk subgroup had a shorter RFS, larger tumor diameter and a lower proportion of clear tumor borders. At the cellular level, a higher infiltration of intratumoral NK cells was negatively correlated with recurrence risk. CONCLUSIONS: This study established an effective DPS. Immune cells were the most significant histological structure related to HCC recurrence. DPS performed well in post-LT recurrence prediction and the identification of clinicopathological features.

Asunto(s)

Carcinoma Hepatocelular , Neoplasias Hepáticas , Trasplante de Hígado , Humanos , Trasplante de Hígado/efectos adversos , Recurrencia Local de Neoplasia , Estudios Retrospectivos , Pronóstico , Factores de Riesgo

RESUMEN

Immune-responsive gene 1 (IRG1) encodes aconitate decarboxylase (ACOD1) that catalyzes the production of itaconic acids (ITAs). The anti-inflammatory function of IRG1/ITA has been established in multiple pathogen models, but very little is known in cancer. Here, we show that IRG1 is expressed in tumor-associated macrophages (TAMs) in both human and mouse tumors. Mechanistically, tumor cells induce Irg1 expression in macrophages by activating NF-κB pathway, and ITA produced by ACOD1 inhibits TET DNA dioxygenases to dampen the expression of inflammatory genes and the infiltration of CD8+ T cells into tumor sites. Deletion of Irg1 in mice suppresses the growth of multiple tumor types and enhances the efficacy of anti-PD-(L)1 immunotherapy. Our study provides a proof of concept that ACOD1 is a potential target for immune-oncology drugs and IRG1-deficient macrophages represent a potent cell therapy strategy for cancer treatment even in pancreatic tumors that are resistant to T cell-based immunotherapy.

Asunto(s)

Neoplasias , Macrófagos Asociados a Tumores , Humanos , Animales , Ratones , Macrófagos Asociados a Tumores/metabolismo , Linfocitos T CD8-positivos/metabolismo , Macrófagos/metabolismo , Inmunoterapia , Neoplasias/genética , Neoplasias/terapia , Neoplasias/metabolismo , Hidroliasas/genética

RESUMEN

Hepatocellular carcinoma (HCC) is an immunotherapy-resistant malignancy characterized by high cellular heterogeneity. The diversity of cell types and the interplay between tumor and non-tumor cells remain to be clarified. Single cell RNA sequencing of human and mouse HCC tumors revealed heterogeneity of cancer-associated fibroblast (CAF). Cross-species analysis determined the prominent CD36+ CAFs exhibited high-level lipid metabolism and expression of macrophage migration inhibitory factor (MIF). Lineage-tracing assays showed CD36+CAFs were derived from hepatic stellate cells. Furthermore, CD36 mediated oxidized LDL uptake-dependent MIF expression via lipid peroxidation/p38/CEBPs axis in CD36+ CAFs, which recruited CD33+myeloid-derived suppressor cells (MDSCs) in MIF- and CD74-dependent manner. Co-implantation of CD36+ CAFs with HCC cells promotes HCC progression in vivo. Finally, CD36 inhibitor synergizes with anti-PD-1 immunotherapy by restoring antitumor T-cell responses in HCC. Our work underscores the importance of elucidating the function of specific CAF subset in understanding the interplay between the tumor microenvironment and immune system.

RESUMEN

Hepatocellular carcinoma (HCC) has a complex and changeable tumor microenvironment. Despite emerging evidence focusing on autophagy process within immune cells, the function and regulatory mechanism of macrophage autophagy in tumor progression remains unclear. Our results of multiplex-immunohistochemistry and RNA-sequencing identified the reduced levels of autophagy in tumor macrophages in the HCC microenvironment, associated with a poor prognosis and increased microvascular metastasis in HCC patients. Specifically, HCC suppressed the macrophage autophagy initiation through the up-regulation of mTOR and ULK1 phosphorylation at Ser757. Knockdown of autophagy-related proteins to further inhibit autophagy significantly boosted the metastatic potential of HCC. Mechanistically, the accumulation of NLRP3 inflammasome mediated by autophagy inhibition promoted the cleavage, maturation, and release of IL-1ß, which facilitated the HCC progression, eventually accelerating HCC metastasis via the epithelial-mesenchymal transition. Autophagy inhibition provoked macrophage self-recruitment through the CCL20-CCR6 signaling was also a crucial account of HCC progression. Recruited macrophages mediated the cascade amplification of IL-1ß and CCL20 to form a novel pro-metastatic positive feedback loop through promoting HCC metastasis and increased macrophage recruitment, respectively. Notably, targeting IL-1ß/IL-1 receptor signaling impaired lung metastasis induced by macrophage autophagy inhibition in a mice HCC lung metastasis model. In summary, this study highlighted that inhibition of tumor macrophage autophagy facilitated HCC progression by increasing IL-1ß secretion via NLRP3 inflammasome accumulation and by macrophage self-recruitment through the CCL20 signaling pathway. Interruption of this metastasis-promoting loop by IL-1ß blockade may provide a promising therapeutic strategy for HCC patients.

Asunto(s)

Carcinoma Hepatocelular , Neoplasias Hepáticas , Neoplasias Pulmonares , Animales , Ratones , Autofagia , Carcinoma Hepatocelular/patología , Inflamasomas/metabolismo , Neoplasias Hepáticas/patología , Neoplasias Pulmonares/metabolismo , Macrófagos/metabolismo , Proteína con Dominio Pirina 3 de la Familia NLR/metabolismo , Microambiente Tumoral

RESUMEN

Composite solid electrolytes (CSEs), composed of sodium superionic conductor (NASICON)-type Li1+xAlxTi2-x(PO4)3 (LATP), poly (vinylidene fluoride-hexafluoro propylene) (PVDF-HFP), and lithium bis (trifluoromethanesulfonyl)imide (LiTFSI) salt, are designed and fabricated for lithium-metal batteries. The effects of the key design parameters (i.e., LiTFSI/LATP ratio, CSE thickness, and carbon content) on the specific capacity, coulombic efficiency, and cyclic stability were systematically investigated. The optimal CSE configuration, superior specific capacity (~160 mAh g-1), low electrode polarization (~0.12 V), and remarkable cyclic stability (a capacity retention of 86.8%) were achieved during extended cycling (>200 cycles). In addition, with the optimal CSE structure, a high ionic conductivity (~2.83 × 10-4 S cm-1) was demonstrated at an ambient temperature. The CSE configuration demonstrated in this work can be employed for designing highly durable CSEs with enhanced ionic conductivity and significantly reduced interfacial electrolyte/electrode resistance.

RESUMEN

In this study, we proposed a novel CoIn2S4/reduced graphene oxide (CoIn2S4/rGO) composite anode using a hydrothermal method. By introducing electronic-conductive reduced graphene oxide (rGO) to buffer the extreme volume expansion of CoIn2S4, we prevented its polysulfide dissolution during the lithiation/de-lithiation processes. After 100 cycles, the pristine CoIn2S4 electrode demonstrated poor cycle performance of only 120 mAh/g at a current density of 0.1 A/g. However, the composition-optimized CoIn2S4/rGO composite anode demonstrated a reversible capacity of 580 mAh/g for 100 cycles, which was an improvement of 4.83 times. In addition, the ex situ XRD measurements of the CoIn2S4/rGO electrode were conducted to determine the reaction mechanism and electrochemical behavior. These results suggest that the as-synthesized CoIn2S4/rGO composite anode is a promising anode material for lithium ion batteries.

RESUMEN

Background: Avatrombopag has been approved in patients who have severe thrombocytopenia (<50 × 109/L) and chronic liver disease (CLD) while receiving invasive procedures. The real-world application and effectiveness of avatrombopag in the subgroup patients with liver cancer remain unknown. Methods: Liver cancer patients (including primary liver cancer and colorectal cancer liver metastasis) who had severe thrombocytopenia and received avatrombopag were retrospectively enrolled. Avatrombopag dose, peak and absolute platelet count increase, combination treatment with other thrombopoietic agents, responder (peak count ≥50 × 109/L with absolute increase ≥20 × 109/L) rate, and anticancer treatment effect were analyzed. Thrombosis and bleeding events were assessed. Results: In total, 93 patients were enrolled, with 72 and 21 in the CLD and non-CLD groups, respectively. Patients with CLD had hepatitis B or C, larger spleen volume, and a higher cirrhosis degree. Baseline platelet counts were similar between two groups (median, 37.0 × 109/L vs. 39.0 × 109/L; P=0.594), while patients without CLD had higher peak platelet (median, 134.0 × 109/L vs. 74.0 × 109/L; P=0.015) and absolute increase (median, 101.0 × 109/L vs. 41.0 × 109/L; P=0.020) after avatrombopag treatment. The responder rate was higher in patients without CLD (100% vs. 76.4%; P=0.010). Combined avatrombopag with other thrombopoietic agents significantly increased platelet count; repeated use of avatrombopag produced similar effects with that of initial treatment. Concerning anticancer treatment effect, patients who responded to avatrombopag had a higher disease control rate. No thrombosis or hemorrhagic events were observed, even in patients with portal vein tumor thrombosis. Conclusion: Avatrombopag was safe and effective and ensured successful implementation of anticancer treatment in liver cancer patients with severe thrombocytopenia, accompanied with or without CLD.

RESUMEN

NASICON-type Na4MnCr(PO4)3 (NMCP) wrapped with reduced graphene oxide (rGO) was synthesized via a simple sol-gel method as composite cathode material Na4MnCr(PO4)3/rGO (NMCP/rGO) for Na ion batteries. The surface morphology, crystal structure and pore size distribution of pristine NMCP and as-synthesized NMCP/rGO composite cathode are identified by X-ray diffraction (XRD), field emission-scanning electron microscopy (SEM), transmission electron microscope (TEM), the Brunauer-Emmett-Teller (BET) method and X-ray photoelectron spectroscopy (XPS). The electrochemical performance of composition-optimized NMCP/rGO composite cathode presents stable capacity retention and rate capability. The capacity retention of as-synthesized NMCP/rGO composite is 63.8%, and average coulombic efficiency maintains over 98.7% for 200 cycles. The reversible capacity of as-synthesized NMCP/rGO composite cathode still retained 45 mAh/g and 38 mAh/g under a current density of 0.5 A/g and 1.0 A/g, respectively, which was better than that of pristine NMCP, with only 6 mAh/g and 4 mAh/g. The redox reactions of pristine NMCP and as-synthesized NMCP/rGO composite are studied via cyclic voltammetry. The improved electronic conductivity and structure stability of bare NMCP is attributed to the contribution of the rGO coating.

RESUMEN

Listeria monocytogenes is a life-threatening foodborne pathogen. Here, we report the genomic characterization of a nationwide dataset of 411 clinical and 82 food isolates collected in Taiwan between 2014 and 2019. The observed incidence of listeriosis increased from 0.83 to 7 cases per million population upon implementation of mandatory notification in 2018. Pregnancy-associated cases accounted for 2.8% of human listeriosis and all-cause 7-day mortality was of 11.9% in nonmaternal-neonatal listeriosis. L. monocytogenes was isolated from 90% of raw pork and 34% of chicken products collected in supermarkets. Sublineages SL87, SL5, and SL378 accounted for the majority (65%) of clinical cases. SL87 and SL378 were also predominant (57%) in food products. Five cgMLST clusters accounted for 57% clinical cases, suggesting unnoticed outbreaks spanning up to 6 years. Mandatory notification allowed identifying the magnitude of listeriosis in Taiwan. Continuous real-time genomic surveillance will allow reducing contaminating sources and disease burden. IMPORTANCE Understanding the phylogenetic relationship between clinical and food isolates is important to identify the transmission routes of foodborne diseases. Here, we performed a nationwide study between 2014 and 2019 of both clinical and food Listeria monocytogenes isolates and sequenced their genomes. We show a 9-fold increase in listeriosis reporting upon implementation of mandatory notification. We found that sublineages SL87 and SL378 predominated among both clinical (50%) and food (57%) isolates, and identified five cgMLST clusters accounting for 57% of clinical cases, suggestive of potential protracted sources of contamination over up to 6 years in Taiwan. These findings highlight that mandatory declaration is critical in identifying the burden of listeriosis, and the importance of genome sequencing for a detailed characterization of the pathogenic L. monocytogenes genotypes circulating in Asia.

Asunto(s)

Listeria monocytogenes , Listeriosis , Recién Nacido , Humanos , Listeria monocytogenes/genética , Taiwán/epidemiología , Filogenia , Microbiología de Alimentos , Genoma Bacteriano , Tipificación de Secuencias Multilocus , Secuenciación Completa del Genoma , Listeriosis/epidemiología , Genómica , Brotes de Enfermedades