Chiroptical Synaptic Perovskite Memristor as Reconfigurable Physical Unclonable Functions.

Physical unclonable functions (PUFs), often referred to as digital fingerprints, are emerging as critical elements in enhancing hardware security and encryption. While significant progress has been made in developing optical and memory-based PUFs, integrating reconfigurability with sensitivity to circularly polarized light (CPL) remains largely unexplored. Here, we present a chiroptical synaptic memristor (CSM) as a reconfigurable PUF, leveraging a two-dimensional organic-inorganic halide chiral perovskite.

A core-shell fiber moisture-driven electric generator enabled by synergetic complex coacervation and built-in potential.

Moisture-driven electricity generators (MEGs) have been extensively researched; however, high-performance flexible variants have seldom been demonstrated. Here we present a novel complex coacervation with built-in potential strategy for developing a high-performance uniaxial MEG, featuring a core of poly(3,4-ethylenedioxythiophene) (PEDOT) with a built-in charge potential and a gel shell composed of poly(diallyldimethylammonium chloride) (PDDA) and sodium alginate (NaAlg) coacervate. The complex coacervation of two oppositely charged polyelectrolytes produces extra mobile carriers and free volume in the device; meanwhile, the PEDOT core's surface charge significantly accelerates carrier diffusion.

Association between hepatocyte TM4SF5 expression and gut microbiome dysbiosis during non-alcoholic fatty liver disease development.

Gut microbiome dysbiosis is involved in non-alcoholic fatty liver disease (NAFLD) development. Hepatic transmembrane 4 L six family member 5 (TM4SF5) overexpression promotes NAFLD. However, how gut microbiota are associated with TM4SF5-mediated NAFLD remains unexplored.

Glucose-mediated mitochondrial reprogramming by cholesterol export at TM4SF5-enriched mitochondria-lysosome contact sites.

Background: Transmembrane 4 L six family member 5 (TM4SF5) translocates subcellularly and functions metabolically, although it is unclear how intracellular TM4SF5 translocation is linked to metabolic contexts. It is thus of interests to understand how the traffic dynamics of TM4SF5 to subcellular endosomal membranes are correlated to regulatory roles of metabolisms.

Methods: Here, we explored the metabolic significance of TM4SF5 localization at mitochondria-lysosome contact sites (MLCSs), using in vitro cells and in vivo animal systems, via approaches by immunofluorescence, proximity labelling based proteomics analysis, organelle reconstitution etc.

TM4SF5-mediated abnormal food-intake behavior and apelin expression facilitate non-alcoholic fatty liver disease features.

Transmembrane 4 L six family member 5 (TM4SF5) engages in non-alcoholic steatohepatitis (NASH), although its mechanistic roles are unclear. Genetically engineered mice fed normal chow or high-fat diet for either an entire day or a daytime-feeding (DF) pattern were analyzed for metabolic parameters. Compared to wild-type and knockout mice, hepatocyte-specific TM4SF5-overexpressing -TG (TG) mice showed abnormal food-intake behavior during the mouse-inactive daytime, increased apelin expression, increased food intake, and higher levels of NASH features.

Systemic TM4SF5 overexpression in Apc mice promotes hepatic portal hypertension associated with fibrosis.

Mutation of the gene for adenomatous polyposis coli (APC), as seen in Apc mice, leads to intestinal adenomas and carcinomas via stabilization of β-catenin. Transmembrane 4 L six family member 5 (TM4SF5) is involved in the development of non-alcoholic fatty liver disease, fibrosis, and cancer. However, the functional linkage between TM4SF5 and APC or β-catenin has not been investigated for pathological outcomes.

Liver-originated small extracellular vesicles with TM4SF5 target brown adipose tissue for homeostatic glucose clearance.

Transmembrane 4 L six family member 5 (TM4SF5) is involved in chronic liver disease, although its role in glucose homeostasis remains unknown. TM4SF5 deficiency caused age-dependent glucose (in)tolerance with no link to insulin sensitivity. Further, hepatic TM4SF5 binding to GLUT1 promoted glucose uptake and glycolysis.

Therapeutic effects of TM4SF5-targeting chimeric and humanized monoclonal antibodies in hepatocellular and colon cancer models.

The transmembrane 4 L six family member 5 (TM4SF5) is aberrantly expressed in hepatocellular and colorectal cancers, and has been implicated in tumor progression, suggesting that it could serve as a novel therapeutic target. Previously, we screened a murine antibody phage-display library to generate a novel monoclonal antibody, Ab27, that is specific to the extracellular loop 2 of TM4SF5. In this study, we evaluated the effects of chimeric Ab27 using cancer cells expressing endogenous TM4SF5 or stably overexpressing TM4SF5 and .

Crosstalk between TM4SF5 and GLUT8 regulates fructose metabolism in hepatic steatosis.

Objective: Transmembrane 4 L six family member 5 (TM4SF5) is likely involved in non-alcoholic steatohepatitis, although its roles and cross-talks with glucose/fructose transporters in phenotypes derived from high-carbohydrate diets remain unexplored. Here, we investigated the modulation of hepatic fructose metabolism by TM4SF5.

Methods: Wild-type or Tm4sf5 knockout mice were evaluated via different diets, including normal chow, high-sucrose diet, or high-fat diet without or with fructose in drinking water (30% w/v).

TM4SF5-mediated liver malignancy involves NK cell exhaustion-like phenotypes.

Aberrant extracellular matrix and immune cell alterations within the tumor microenvironment promote the pathological progression of liver carcinogenesis. Although transmembrane 4 L six family member 5 (TM4SF5) is involved in liver fibrosis and cancer, its mechanism avoiding immune surveillance during carcinogenesis remains unknown. We investigated how TM4SF5-mediated signaling caused immune evasion using in vitro primary cells and in vivo liver tissues from genetic or chemically induced mouse models.

TM4SF5-dependent crosstalk between hepatocytes and macrophages to reprogram the inflammatory environment.

Chronic injury to hepatocytes results in inflammation, steatohepatitis, fibrosis, and nonalcoholic fatty liver disease (NAFLD). The tetraspanin TM4SF5 is implicated in fibrosis and cancer. We investigate the role of TM4SF5 in communication between hepatocytes and macrophages (MΦs) and its possible influence on the inflammatory microenvironment that may lead to NAFLD.

Tetraspanin TM4SF5 in hepatocytes negatively modulates SLC27A transporters during acute fatty acid supply.

Transmembrane 4 L six family member 5 (TM4SF5) is involved in nonalcoholic steatosis and further aggravation of liver disease. However, its mechanism for regulating FA accumulation is unknown. We investigated how TM4SF5 in hepatocytes affected FA accumulation during acute FA supply.

Addition of Cellulose Nanofibers to Control Surface Roughness for Hydrophobic Ceramic Coatings.

Hydrophobic ceramic coatings are used for a variety of applications. Generally, hydrophobic coating surfaces are obtained by reducing the surface energy of the coating material or by forming a highly textured surface. Reducing the surface energy of the coating material requires additional costs and processing and changes the surface properties of the ceramic coating.

Differential TM4SF5-mediated SIRT1 modulation and metabolic signaling in nonalcoholic steatohepatitis progression.

Nonalcoholic fatty liver disease is a chronic condition involving steatosis, steatohepatitis and fibrosis, and its progression remains unclear. Although the tetraspanin transmembrane 4 L six family member 5 (TM4SF5) is involved in hepatic fibrosis and cancer, its role in nonalcoholic steatohepatitis (NASH) progression is unknown. We investigated the contribution of TM4SF5 to liver pathology using transgenic and KO mice, diet- or drug-treated mice, in vitro primary cells, and in human tissue.

Enhanced Interfacial Adhesion of Polydimethylsiloxane (PDMS) by Control of the Crosslink Density.

In this paper, we report a simple, fast, and one-step approach to improve the adhesion force of polydimethylsiloxane (PDMS) by incorporating inorganic nanoparticles that can control the physical, mechanical, and adhesion properties of the PDMS. An organic/inorganic PDMS-based composite was fabricated by the hydrosilylation of vinyl-decorated silica nanoparticles (v-SNPs) and the PDMS. The v-SNP/PDMS composite showed a significantly decreased elastic modulus and increased elongation compared with that of pristine SNPs incorporated with the PDMS composite (SNP/PDMS) and pristine PDMS.

Exploring vitamin D metabolism and function in cancer.

Vitamin D, traditionally known as an essential nutrient, is a precursor of a potent steroid hormone that regulates a broad spectrum of physiological processes. In addition to its classical roles in bone metabolism, epidemiological, preclinical, and cellular research during the last decades, it revealed that vitamin D may play a key role in the prevention and treatment of many extra-skeletal diseases such as cancer. Vitamin D, as a prohormone, undergoes two-step metabolism in liver and kidney to produce a biologically active metabolite, calcitriol, which binds to the vitamin D receptor (VDR) for the regulation of expression of diverse genes.