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- Li, Jingwen, et al.
(författare)
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Emerging Food Packaging Applications of Cellulose Nanocomposites : A Review
- 2022
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Ingår i: Polymers. - : MDPI AG. - 2073-4360. ; 14:19
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Forskningsöversikt (refereegranskat)abstract
- Cellulose is the most abundant biopolymer on Earth, which is synthesized by plants, bacteria, and animals, with source-dependent properties. Cellulose containing beta-1,4-linked D-glucoses further assembles into hierarchical structures in microfibrils, which can be processed to nanocellulose with length or width in the nanoscale after a variety of pretreatments including enzymatic hydrolysis, TEMPO-oxidation, and carboxymethylation. Nanocellulose can be mainly categorized into cellulose nanocrystal (CNC) produced by acid hydrolysis, cellulose nanofibrils (CNF) prepared by refining, homogenization, microfluidization, sonification, ball milling, and the aqueous counter collision (ACC) method, and bacterial cellulose (BC) biosynthesized by the Acetobacter species. Due to nontoxicity, good biodegradability and biocompatibility, high aspect ratio, low thermal expansion coefficient, excellent mechanical strength, and unique optical properties, nanocellulose is utilized to develop various cellulose nanocomposites through solution casting, Layer-by-Layer (LBL) assembly, extrusion, coating, gel-forming, spray drying, electrostatic spinning, adsorption, nanoemulsion, and other techniques, and has been widely used as food packaging material with excellent barrier and mechanical properties, antibacterial activity, and stimuli-responsive performance to improve the food quality and shelf life. Under the driving force of the increasing green food packaging market, nanocellulose production has gradually developed from lab-scale to pilot- or even industrial-scale, mainly in Europe, Africa, and Asia, though developing cost-effective preparation techniques and precisely tuning the physicochemical properties are key to the commercialization. We expect this review to summarise the recent literature in the nanocellulose-based food packaging field and provide the readers with the state-of-the-art of this research area.
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| 2. |
- Song, Byong-Sop, et al.
(författare)
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Mitoribosomal defects aggravate liver cancer via aberrant glycolytic flux and T cell exhaustion
- 2022
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Ingår i: Journal for ImmunoTherapy of Cancer. - : BMJ. - 2051-1426. ; 10:5
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Tidskriftsartikel (refereegranskat)abstract
- Background Mitochondria are involved in cancer energy metabolism, although the mechanisms underlying the involvement of mitoribosomal dysfunction in hepatocellular carcinoma (HCC) remain poorly understood. Here, we investigated the effects of mitoribosomal impairment-mediated alterations on the immunometabolic characteristics of liver cancer.Methods We used a mouse model of HCC, liver tissues from patients with HCC, and datasets from The Cancer Genome Atlas (TCGA) to elucidate the relationship between mitoribosomal proteins (MRPs) and HCC. In a mouse model, we selectively disrupted expression of the mitochondrial ribosomal protein CR6-interacting factor 1 (CRIF1) in hepatocytes to determine the impact of hepatocyte-specific impairment of mitoribosomal function on liver cancer progression. The metabolism and immunophenotype of liver cancer was assessed by glucose flux assays and flow cytometry, respectively.Results Single-cell RNA-seq analysis of tumor tissue and TCGA HCC transcriptome analysis identified mitochondrial defects associated with high-MRP expression and poor survival outcomes. In the mouse model, hepatocyte-specific disruption of the mitochondrial ribosomal protein CRIF1 revealed the impact of mitoribosomal dysfunction on liver cancer progression. Crif1 deficiency promoted programmed cell death protein 1 expression by immune cells in the hepatic tumor microenvironment. A [U-13C6]-glucose tracer demonstrated enhanced glucose entry into the tricarboxylic acid cycle and lactate production in mice with mitoribosomal defects during cancer progression. Mice with hepatic mitoribosomal defects also exhibited enhanced progression of liver cancer accompanied by highly exhausted tumor-infiltrating T cells. Crif1 deficiency induced an environment unfavorable to T cells, leading to exhaustion of T cells via elevation of reactive oxygen species and lactate production.Conclusions Hepatic mitoribosomal defects promote glucose partitioning toward glycolytic flux and lactate synthesis, leading to T cell exhaustion and cancer progression. Overall, the results suggest a distinct role for mitoribosomes in regulating the immunometabolic microenvironment during HCC progression.
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