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High-density polyethylene (HDPE)/polypropylene (PP) composites with graphenes were prepared by meltcompounding method. Graphene sheets were prepared through thermally reduced graphene oxide (TRG) and surfactant exfoliated graphene (SEG), respectively. Structural characterization showed that the TRG sheets exhibited a few-layers composition with more defects compared to the SEG sheets. Morphological observations of the composites demonstrated that the graphene was preferentially dispersed in the HDPE phase and the addition of graphene (TRG and SEG) influenced the phase structure of the HDPE/PP composites. The distribution of the TRG sheets in the HDPE phase was better than the SEG sheets, and the obtained HDPE/PP composites exhibited a low electrical percolation threshold with the highly dispersed graphene. The TRG/HDPE/PP composite showed a low electrical percolation threshold of 3 wt% (1.25 vol%). For the SEG/HDPE/PP system, the percolation threshold was 7 wt% (2.98 vol%). Differences in the behavior of the two graphene components (TRG and SEG) in the HDPE/PP composites influenced the formation of percolation networks and electrical properties. [ABSTRACT FROM AUTHOR]

Multiple sclerosis is characterized by the presence of multiple plaques within the central nervous system, manifesting as remission and exacerbation of neurologic dysfunction over variable time courses. We present the case of a 20-ycar-old woman. Before treatment, her auditory brain stem response (ABR) test revealed bilateral prolongation. A caloric test showed canal paresis of the right ear and a normal response on the left. A vestibular evoked myogenic potential (VEMP) test displayed an absent response in the right ear and a delayed response in the left. A magnetic resonance imaging (MRI) scan demonstrated multiple diffuse high signal lesions in the hemispheres, brain stem, and cerebellum. Six months after treatment, the demyelinating plaques were shown to have resolved spontaneously on MRI. Recovery of caloric responses was anticipated. Bilateral prolongation of ABRs remained, but the VEMP test disclosed a normal response in the right ear and a delayed response in the left. Accordingly, in addition to MRI, calorie tests and ABR and VEMP tests arc useful in monitoring the evolution of audiovestibular function in patients with multiple sclerosis. [ABSTRACT FROM AUTHOR]

Graphene‐skinned fiber fabric is prepared by chemical vapor deposition (CVD) of continuous graphene on fabric, which enables conformal graphene coverage on fibers and inherits high electrical and thermal conductivity of graphene. However, in the fabric‐shaped configuration, high electrical and thermal contact resistances between fibers, and the lack of conductive and thermal pathways along radial direction of fibers limit the improvement of electrical and thermal conductivity. Herein, carbon nanotubes (CNTs), due to the 1D structure with excellent electrical and thermal conductivity, are introduced to build rich “bridges” to connect the isolated fibers to build new electron and phonon transport channels. Thus, the conceptual design of CNT/graphene‐skinned glass fiber fabric (CNT/GGFF) is creatively proposed and realized by a carefully designed CVD. Constructing the 3D electrically and thermally conductive network in CNT/GGFF leads to >90% decrease of sheet resistance, 4.5 times increase of tensile strength, and >70% decrease of thermal resistance compared with GGFF, making it promising for applications in composite materials, heat dissipation, and de‐icing. Moreover, the thermal resistance of CNT/GGFF exhibits temperature‐independent, extending applications to aviation and space because changes in thermal conductivity of traditional materials with environmental temperatures can adversely affect the thermal stability, reliability, and lifetime of aircrafts. [ABSTRACT FROM AUTHOR]

Background: Targeting glucose uptake by glucose transporter (GLUT) inhibitors is a therapeutic opportunity, but efforts on GLUT inhibitors have not been successful in the clinic and the underlying mechanism remains unclear. We aim to identify the key metabolic changes responsible for cancer cell survival from glucose limitation and elucidate its mechanism., Methods: The level of phosphorylated YAP was analyzed with Western blotting and Phos-tag immunoblotting. Glucose limitation-induced metabolic changes were analyzed using targeted metabolomics (600MRM). The anti-cancer role of metabolite was examined using colony formation assay and APC min/+ mice. Co-immunoprecipitation, LS-MS, qRT-PCR, and immunofluorescence were performed to explore the underlying mechanisms., Results: We found that D-Ribose-5-phosphate (D5P), a product of the pentose phosphate pathway connecting glucose metabolism and nucleotide metabolism, functions as a metabolic checkpoint to activate YAP under glucose limitation to promote cancer cell survival. Mechanistically, in glucose-deprived cancer cells, D5P is decreased, which facilitates the interaction between MYH9 and LATS1, resulting in MYH9-mediated LATS1 aggregation, degradation, and further YAP activation. Interestingly, activated YAP further promotes purine nucleoside phosphorylase (PNP)-mediated breakdown of purine nucleoside to restore D5P in a feedback manner. Importantly, D5P synergistically enhances the tumor-suppressive effect of GLUT inhibitors and inhibits cancer progression in mice., Conclusions: Our study identifies D5P as a metabolic checkpoint linking glucose limitation stress and YAP activation, indicating that D5P may be a potential anti-cancer metabolite by enhancing glucose limitation sensitivity., Competing Interests: Declarations. Ethics approval and consent to participate: All animal experiments were approved by the Institutional Animal Care and Use Committee of the Zhengzhou University. All animal experiments were performed in compliance with the Guide for the Care and Use of Laboratory Animals (National Academies Press, 2011) and according to the institutional ethical guidelines for animal experiments. Competing interests: The authors declare no competing interests., (© 2025. The Author(s).)

Tumors can use metabolic reprogramming to survive nutrient stress. Epigenetic regulators play a critical role in metabolic adaptation. Here we screened a sgRNA library to identify epigenetic regulators responsible for the vulnerability of colorectal cancer (CRC) cells to glucose deprivation and found that more EZH2-knockout cells survived glucose deprivation. Then, we showed that EZH2 expression was significantly downregulated in response to glucose deprivation in a glucose-sensitive CRC cell line, and EZH2-knockdown cells were more resistant to glucose deprivation. Mechanistically, EZH2 deficiency upregulated the expression of glutaminase (GLS) and promoted the production of glutamate, which in turn led to increased synthesis of intracellular glutathione (GSH) and eventually attenuated the reactive oxygen species (ROS)-mediated cell death induced by glucose deprivation. Although EZH2 functioned as an oncogene in cancer progression and EZH2 knockout abolished colorectal cancer development in a mouse model, here we revealed a mechanistic link between EZH2 and metabolic reprogramming via the direct regulation of GLS expression and observed a negative correlation between EZH2 and GLS expression in colorectal cancer tissues. These findings further confirmed the importance of heterogeneity, provided an explanation for the clinical tolerance of cancer cells to EZH2 inhibitors from the perspective of metabolism, and proposed the possibility of combining EZH2 inhibitors and glutamine metabolism inhibitors for the treatment of cancer., (© 2021. The Author(s).)

The tumor microenvironment significantly affects tumor progression, and tumor cells can also remodel the tumor microenvironment through complex interaction. Inflammasomes are innate immune system receptors/sensors that regulate an inflammatory response mainly mediated by the nucleotide-binding oligomerization domain-like receptors in macrophages, which can also influence the formation, progression and therapeutic response of cancer. However, the effects of tumor-derived factors in the microenvironment on inflammasomes have rarely been reported. In this study, we found that lactate, as the main metabolite of tumor cells could specifically activate the nucleotide-binding oligomerization domain, leucine rich repeat and pyrin domain-containing protein 3 inflammasome through increasing the level of reactive oxygen species (ROS) in THP-1-derived macrophages. Furthermore, we showed that transforming growth factor-β (TGF-β), a cytokine accumulated in the tumor microenvironment, could be induced by lactate treatment in tumor cells, and in turn inhibit inflammasome activation induced by lactate and other canonical ligands in macrophages. In addition, TGF-β might induce autophagy of macrophages in a SMAD-dependent manner, leading to ROS clearance and eventually inhibiting the activation of inflammasomes. Collectively, these results indicated that in the tumor microenvironment, tumor-derived lactate could act as a danger signal alerting innate immunity, but nevertheless tumor cells produced more TGF-β to avoid immune surveillance., (© 2020 Wiley Periodicals LLC.)

Background: Inflammation has been found to be associated with many neurodegenerative diseases, including Parkinson's and dementia. Attenuation of microglia-induced inflammation is a strategy that impedes the progression of neurodegenerative diseases., Methods: We used lipopolysaccharide (LPS) to simulate murine microglia cells (BV2 cells) as an experimental model to mimic the inflammatory environment in the brain. In addition, we examined the anti-inflammatory ability of corylin, a main compound isolated from Psoralea corylifolia L. that is commonly used in Chinese herbal medicine. The production of nitric oxide (NO) by LPS-activated BV2 cells was measured using Griess reaction. The secretion of proinflammatory cytokines including tumor necrosis factor (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) by LPS-activated BV2 cells was analyzed using enzyme-linked immunosorbent assay (ELISA). The expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3), apoptosis-associated speck-like protein containing a caspase-activation and recruitment domain (ASC), caspase-1, IL-1β and mitogen-activated protein kinases (MAPKs) in LPS-activated BV2 cells was examined by Western blot., Results: Our experimental results demonstrated that corylin suppressed the production of NO and proinflammatory cytokines by LPS-activated BV2 cells. In addition, corylin inhibited the expression of iNOS and COX-2, attenuated the phosphorylation of ERK, JNK and p38, decreased the expression of NLRP3 and ASC, and repressed the activation of caspase-1 and IL-1β by LPS-activated BV2 cells., Conclusion: Our results indicate the anti-inflammatory effects of corylin acted through attenuating LPS-induced inflammation and inhibiting the activation of NLRP3 inflammasome in LPS-activated BV2 cells. These results suggest that corylin might have potential in treating brain inflammation and attenuating the progression of neurodegeneration diseases.

Cytoplasmic STAT3, after activation by growth factors, translocates to different subcellular compartments, including nuclei and mitochondria, where it carries out different biological functions. However, the precise mechanism by which STAT3 undergoes mitochondrial translocation and subsequently regulates the tricarboxylic acid (TCA) cycle-electron transport chain (ETC) remains poorly understood. Here, we clarify this process by visualizing STAT3 acetylation in starved cells after serum reintroduction or insulin stimulation. CBP-acetylated STAT3 undergoes mitochondrial translocation in response to serum introduction or insulin stimulation. In mitochondria, STAT3 associates with the pyruvate dehydrogenase complex E1 (PDC-E1) and subsequently accelerates the conversion of pyruvate to acetyl-CoA, elevates the mitochondrial membrane potential, and promotes ATP synthesis. SIRT5 deacetylates STAT3, thereby inhibiting its function in mitochondrial pyruvate metabolism. In the A549 lung cancer cell line, constitutively acetylated STAT3 localizes to mitochondria, where it maintains the mitochondrial membrane potential and ATP synthesis in an active state.

Purpose: To apply a battery of audiovestibular function tests and magnetic resonance imaging (MRI) to investigate the causes of oscillopsia in nasopharyngeal carcinoma (NPC) patients after irradiation (RT)., Methods and Materials: Of 300 NPC patients, 12 (4%) developed oscillopsia after RT. The mean accumulated radiation dose to the nasopharynx was 112 +/- 30 Gy. Each patient underwent a battery of audiovestibular function tests, including audiometry and the dynamic illegible E, caloric, and rotational tests., Results: Excluding 3 patients with neck fibrosis who could not perform the head turning movement, the remaining 9 patients displayed 100% abnormal dynamic illegible E test results and 100% abnormal refixation saccades. All 12 patients presented with bilateral hearing loss, caloric reductions, and reduced gains of the vestibular ocular reflex (VOR) on the rotational test, indicating bilateral VOR loss. After excluding tumor relapse and radiation necrosis of the brain by MRI, the oscillopsia in these 12 irradiated NPC patients was attributed to bilateral VOR loss., Conclusion: Radiation-induced oscillopsia in our NPC patients was attributed to bilateral VOR loss, possibly as a result of higher radiation doses. Hence, the therapeutic benefits of a second course of RT are associated with the potential risk of oscillopsia after RT.