Thermal conductivities of water-agar gels were determined at concentrations with mass fractions between w = 0.001 and w = 0.1 and temperatures from (278.15 to 323.15) K by means of a specifically designed probe system based on the line heat source principle. The thermal conductivity probe was calibrated and validated using glycerin (with mass fraction w = 0.99), glycol (with mass fraction w = 0.99), and ultra pure water (with resistivity 18.4 MΩ 3 cm, electric conductivity 0.055 μS 3 cm -1 ). Their measured and recommended values of thermal conductivity were in good agreement. The experimental data of thermal conductivity values of water-agar gels were sensitive to both concentration and temperature. The thermal conductivity of water-agar gels decreased with increasing concentration, while it increased as temperature increased. Predictive regression models were proposed to give a good fit for thermal conductivity with concentration and temperature.

Liquid–liquid Phase Separation (LLPS) of proteins and nucleic acids has emerged as a new paradigm in the study of cellular activities. It drives the formation of liquid-like condensates containing biomolecules in the absence of membrane structures in living cells. In addition, typical membrane-less condensates such as nuclear speckles, stress granules and cell signaling clusters play important roles in various cellular activities, including regulation of transcription, cellular stress response and signal transduction. Previous studies highlighted the biophysical and biochemical principles underlying the formation of these liquid condensates. The studies also showed how these principles determine the molecular properties, LLPS behavior, and composition of liquid condensates. While the basic rules driving LLPS are continuously being uncovered, their function in cellular activities is still unclear, especially within a pathological context. Therefore, the present review summarizes the recent progress made on the existing roles of LLPS in cancer, including cancer-related signaling pathways, transcription regulation and maintenance of genome stability. Additionally, the review briefly introduces the basic rules of LLPS, and cellular signaling that potentially plays a role in cancer, including pathways relevant to immune responses and autophagy.

The tumor microenvironment (TME) has attracted attention owing to its essential role in tumor initiation, progression, and metastasis. With the emergence of immunotherapies for various cancers, and their high efficacy, an understanding of the TME in gastric cancer (GC) is critical. The aim of this study was to investigate the effect of various components within the GC TME, and to identify mechanisms that exhibit potential as therapeutic targets. The ESTIMATE algorithm was used to quantify immune and stromal components in GC samples, whose clinicopathological significance and relationship with predicted outcomes were explored. Low tumor mutational burden and high M2 macrophage infiltration, which are considered immune suppressive characteristics and may be responsible for unfavorable prognoses in GC, were observed in the high stromal group (HR = 1.585; 95% CI, 1.112-2.259; P = 0.009). Furthermore, weighted correlation network, differential expression, and univariate Cox analyses were used, along with machine learning methods (LASSO and SVM-RFE), to reveal genome-wide immune phenotypic correlations. Eight stromal-relevant genes cluster (FSTL1, RAB31, FBN1, ANTXR1, LRRC32, CTSK, COL5A2, and ENG) were identified as adverse prognostic factors in GC. Finally, using a combination of TIMER database and single-sample gene set enrichment analyses, we found that the identified genes potentially contribute to macrophage recruitment and polarization of tumor-associated macrophages. These findings provide a different perspective into the immune microenvironment and indicate potential prognostic and therapeutic targets for GC immunotherapies.

Magnetic Fe3O4@C/Co nanocomposites exhibited high efficiency and reusability in activation of PMS for decolorization of AO II solution.

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N6-Methyladenosine (m 6 A) is the most common RNA internal modification in eukaryotic cells. Its regulatory effects at the post-transcriptional level on both messenger RNAs (mRNAs) and noncoding RNAs have been widely studied; these include alternative splicing, stability, translation efficiency, nucleus export, and degradation. m 6 A modification is implicated in a series of physiological and pathological activities, such as embryonic stem cell differentiation, immunoregulation, adipogenesis, and cancer development. Recently, the significance of m 6 A methylation has been identified in both viral hepatitis and non-alcohol fatty liver disease (NAFLD), which are major risk factors in the development of hepatocellular carcinoma (HCC). Given the high incidence and mortality rate of HCC worldwide, it is of great importance to elucidate the mechanisms underlying HCC initiation and progression. m 6 A as an emerging research focus has great potential to facilitate the understanding of HCC, particularly from an etiological perspective. Thus, in this review, we summarize recent progress in understanding m 6 A modification related to viral hepatitis, NAFLD, and HCC, including their mechanisms and clinical applications.

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