Studies of glycolysis of poly(ethylene terephthalate) recycled from postconsumer soft‐drink bottles. I. Influences of glycolysis conditions

The glycolysis of recycled poly(ethylene terephthalate) flakes by ethylene glycol (EG) is investigated. Bis‐2‐hydroxyethyl terephthalate (BHET) and oligomers are predominately glycolysis products. The influences of glycolysis temperature, glycolysis time, and the amount of catalyst (cobalt acetate) are illustrated. The BHET, dimer, and oligomers are predominately glycolysis products. The optimum glycolysis temperature is found to be 190°C. If a 190°C glycolysis temperature, 1.5‐h glycolysis time, and 0.002 mol glycolysis catalyst (cobalt acetate) are used, the glycolysis conversion is almost 100%. The glycolysis conversion rate increases significantly with the glycolysis temperature, glycolysis time, and the amount of cobalt acetate. Thermal analyses of glycolysis products are examined by differential scanning calorimetry. In addition, the chemical structures of glycolysis products are also determined by a Fourier transform IR spectrophotometer. © 2001 John Wiley & Sons, Inc. J Appl Polym Sci 80: 943–948, 2001     

The Glioblastoma Microenvironment: Morphology,Metabolism, and Molecular Signature of Glial Dynamics to Discover Metabolic Rewiring Sequence

Different functional states determine glioblastoma (GBM) heterogeneity. Brain cancer cells coexist with the glial cells in a functional syncytium based on a continuous metabolic rewiring. However, standard glioma therapies do not account for the effects of the glial cells within the tumor microenvironment. This may be a possible reason for the lack of improvements in patients with high-grade gliomas therapies. Cell metabolism and bioenergetic fitness depend on the availability of nutrients and interactions in the microenvironment. It is strictly related to the cell location in the tumor mass, proximity to blood vessels, biochemical gradients, and tumor evolution, underlying the influence of the context and the timeline in anti-tumor therapeutic approaches. Besides the cancer metabolic strategies, here we review the modifications found in the GBM-associated glia, focusing on morphological, molecular, and metabolic features. We propose to analyze the GBM metabolic rewiring processes from a systems biology perspective. We aim at defining the crosstalk between GBM and the glial cells as modules. The complex networking may be expressed by metabolic modules corresponding to the GBM growth and spreading phases. Variation in the oxidative phosphorylation (OXPHOS) rate and regulation appears to be the most important part of the metabolic and functional heterogeneity, correlating with glycolysis and response to hypoxia. Integrated metabolic modules along with molecular and morphological features could allow the identification of key factors for controlling the GBM-stroma metabolism in multi-targeted, time-dependent therapies.     

The Hybrid Pyrroloisoindolone–Dehydropyrrolizine Alkaloid (−)‐Chlorizidine A Targets Proteins within the Glycolytic Pathway

The cytotoxic activity of (?)‐chlorizidine A, a marine alkaloid containing a unique fusion between a pyrroloisoindolone and dehydropyrrolizine, was explored by using a combination of cellular and molecular methods. Our studies began by applying preliminary SAR evidence gathered from semisynthetic bioactivity evaluations to prepare an active immunoaffinity fluorescent (IAF) probe. This probe was then used to identify two cytosolic proteins, GAPDH and hENO1, as the targets of (?)‐chlorizidine A.     

Isolation of GCR1, a major transcription factor of glycolytic genes in Saccharomyces cerevisiae, from Kluyveromyces lactis

To study the function of GCR1, a gene involved in the expression of glycolytic genes in Saccharomyces cerevisiae, a Kluyveromyces lactis gene that complements the growth defect of a S. cerevisiae Deltagcr1 mutant was isolated. Introduction of this gene into the Deltagcr1 mutant also restored the activities of glycolytic enzymes. DNA sequencing of KlGCR1 predicted an open reading frame of a 767 amino acid protein with an overall identity of 33% and similarity of 48% to Gcr1p from S. cerevisiae. Its DDBJ/EMBL/GenBank Accession No. is AB046391.     

微波辅助废旧PET聚酯解聚反应研究

采用微波辅助加热的方式研究了回收PET聚酯的乙二醇解聚反应,并对比了相同催化作用下常规加热条件下的解聚反应,对解聚反应产物BHET进行了熔点测定和IFTIR分析.结果显示,两种方法下控制解聚反应至PET聚酯完全转化时单体BHET的收率相差不大,微波辅助条件下单体的收率略高,但是反应时间大大缩短.反应物PET与EG在1:...     

在缩聚阶段加入废长丝醇解物生产纤维级聚酯

选择无油涤纶长丝的废丝,以醋酸锌作催化剂、乙二醇作醇解剂,在220℃左右进行醇解反应,然后经过滤除去未反应的杂质,以一定量添加到预缩聚反应釜中参与缩聚反应,造粒得到质量均匀的聚酯切片。测试结果表明:醇解产物添加量在质量分数0.2%以下时,制得切片的性能达到纤维级聚酯切片标准。     

Inhibition of Cancer Cell Migration by Gold Nanorods: Molecular Mechanisms and Implications for Cancer Therapy

Gold nanorods have received much attention because of their distinct physicochemical properties and promising applications in bioimaging, biosensing, drug delivery, photothermal therapy, and optoelectronic devices. However, little is known regarding their effect on tumor metastasis. In the present investigation, serum protein‐coated gold nanorods (AuNRs) at low concentrations is shown to exhibit no apparent effects on the viability and proliferation of three different metastatic cancer cell lines, that is, MDA‐MB‐231 human breast cancer cells, PC3 human prostate cancer cells, and B16F10 mouse melanoma cells, but effectively inhibit their migration and invasion in vitro. Quantitative proteomics and real‐time PCR array analyses indicate that exposure of cells to AuNRs can down‐regulate the expression of diverse energy generation‐related genes, which accounts for their inhibition of mitochondrial oxidative phosphorylation (OXPHOS) and glycolysis. The impairment of OXPHOS and glycolysis results in a distinctive reduction of ATP production and subsequent inhibition of F‐actin cytoskeletal assembly, which is crucial for the migration and invasion of cancer cells. The inhibitory effect of AuNRs on cancer cell migration is also confirmed in vivo. Taken together, the unique mechanism in inhibiting cancer cell migration by AuNRs might provide a new approach to specific cancer therapeutic treatment.     

Costimulatory CD226 Signaling Regulates Proliferation of Memory-like NK Cells in Healthy Individuals with Latent Mycobacterium tuberculosis Infection

It is now widely accepted that NK cells can acquire memory, and this makes them more effective to protect against some pathogens. Prior reports indicate memory-like NK cells (mlNKs) in murine model of Mycobacterium tuberculosis (Mtb) as well as in healthy individuals with latent TB infection (LTBI). The increased expression of CD226 was evident in mlNKs from LTBI+ people after stimulation with γ-irradiated Mtb (γ-Mtb). We thus evaluated the contribution of costimulatory CD226 signaling in the functionality of mlNKs in LTBI+ people. We found that blockade of CD226 signaling using the antibody- or CRISPR/Cas9-mediated deletion of the CD226 gene in NK cells diminished the proliferation of mlNKs from LTBI+ people. Blocking CD226 signaling also reduced the phosphorylation of FOXO1 and cMyc expression. Additionally, cMyc inhibition using a chemical inhibitor reduced proliferation by mlNKs from LTBI+ people. Moreover, blocking CD226 signaling reduced glycolysis in NK cells, and the inhibition of glycolysis led to reduced effector function of mlNKs from LTBI+ people. Overall, our results provide a role for CD226 signaling in mlNK responses to Mtb.