Study of reactive dyes and their hydrolyzed forms in a real trichromatic dyeing process by capillary electrophoresis with UV detection.

Detecting the concentration of reactive dyes and their hydrolyzed products is essential for controlling the dyeing process and is an important guide for upgrading and improving textile dyeing technology. In this study, capillary electrophoresis (CE) with UV detection was for the first time applied in a real trichromatic dyeing process to provide qualitative and quantitative determination of reactive dyes and their hydrolyzed forms. Here, three original reactive dyes (SES-Cl-red-195, SES-Cl-yellow-145, and SES-Cl-blue-194), their vinyl sulfone forms (VS-Cl-red-195, VS-Cl-yellow-145, and VS-Cl-blue-194), and complete hydrolyzed forms (HES-OH-red-195, HES-OH-yellow-145, and HES-OH-blue-194) could be baseline separated in our developed BGE comprised of 10.0 mol/L Na2B4O7, 15% (V/V) ACN at pH 8.50 that adjusted by 0.50 mol/L H3BO3. The LODs (S/N = 3) of nine analytes ranged from 0.3 to 1.3 mg/L, and high sensitivities were achieved with UV detection. The RSDs of peak area and migration time were in the ranges of 1.4-3.8% and 0.39-1.29%, which indicated the CE methods were reliable for studying different dye forms in complex dye baths, and for evaluating dyeing process quality. Thus, the percentage of dye-uptake in single and trichromatic combination dyes was calculated based on the concentration of the original and their vinyl sulfone and hydrolyzed forms, and the result was consistent with the traditional UV-Vis method.

Dual Function of Par3 in Tumorigenesis.

Cell maintenance and the establishment of cell polarity involve complicated interactions among multiple protein complexes as well as the regulation of different signaling pathways. As an important cell polarity protein, Par3 is evolutionarily conserved and involved in tight junction formation as well as tumorigenesis. In this review, we aimed to explore the function of Par3 in tumorigenesis. Research has shown that Par3 exhibits dual functions in human cancers, both tumor-promoting and tumor-suppressive. Here, we focus on the activities of Par3 in different stages and types of tumors, aiming to offer a new perspective on the molecular mechanisms that regulate the functions of Par3 in tumor development. Tumor origin, tumor microenvironment, tumor type, cell density, cell-cell contact, and the synergistic effect of Par3 and other tumor-associated signaling pathways may be important reasons for the dual function of Par3. The important role of Par3 in mammalian tumorigenesis and potential signaling pathways is context dependent.

Arginase II Promotes Intervertebral Disc Degeneration Through Exacerbating Senescence and Apoptosis Caused by Oxidative Stress and Inflammation via the NF-κB Pathway.

Intervertebral disc degeneration (IDD) has been generally accepted as the major cause of low back pain (LBP), which imposes massive clinical and socioeconomic burdens. Previous studies have demonstrated that oxidative stress and inflammation-induced senescence and apoptosis of nucleus pulposus cells (NPCs) are the main cellular processes that cause IDD. Arginase II (ARG2), an enzyme involved in a variety of pathological processes, including cellular senescence, apoptosis, oxidative stress, and inflammation, has been shown to promote degeneration in several degenerative diseases, including osteoarticular diseases. Based on previous studies, we hypothesized that ARG2 deficiency might be conducive to the treatment of IDD by inhibiting the dyshomeostasis of the extracellular matrix (ECM), and the oxidative stress and inflammatory response-induced senescence and apoptosis via NF-κB. In this study, we found that ARG2 deficiency inhibited senescence and apoptosis of NPCs, and degeneration of the ECM induced by oxidative stress and the inflammatory response. Similar results were found with the selective NF-κB pathway inhibitor JSH-23. In contrast, overexpression of ARG2 had the opposite effect. Taken together, our results suggest that ARG2 deficiency prevents IDD via NF-κB, and may therefore, be a potential therapeutic strategy for IDD.

uPAR: An Essential Factor for Tumor Development.

Tumorigenesis is closely related to the loss of control of many genes. Urokinase-type plasminogen activator receptor (uPAR), a glycolipid-anchored protein on the cell surface, is controlled by many factors in tumorigenesis and is expressed in many tumor tissues. In this review, we summarize the regulatory effects of the uPAR signaling pathway on processes and factors related to tumor progression, such as tumor cell proliferation, adhesion, metastasis, glycolysis, tumor microenvironment and angiogenesis. Overall, the evidence accumulated to date suggests that uPAR induction by tumor progression may be one of the most important factors affecting therapeutic efficacy. An improved understanding of the interactions between uPAR and its coreceptors in cancer will provide critical biomolecular information that may help to better predict the disease course and response to therapy.