Search

Gallic acid (GA) is a common phenolic acid that is widely used as an antibacterial agent in the food industry. In order to increase its applicability, this study investigated the antibacterial effects and mechanisms of GA on Escherichia coli O157:H7 (E. coli O157:H7) after UV-C light treatment combined with photodynamic therapy. This study evaluated the photodynamic effects of GA after UV-C irradiation (UVC-GA) based on changes in substances and ROS generation. Using E. coli O157:H7 as a model bacterium, the antibacterial effects were evaluated from various aspects, including MIC, MBC, time-kill curve, cell membrane damage, DNA damage, protein damage, motility changes, biofilm formation, and activity. In addition, the antibacterial mechanisms were further investigated by combining RT-qPCR analysis of gene expression. The results of this study demonstrated that GA has the ability to exert photodynamic effects, even after the removal of the UV-C light source, and can effectively reduce the number of viable E. coli O157:H7 cells. Moreover, UVC-GA caused significant damage to the cell membrane, DNA, and proteins, and according to the RT-qPCR results, the antibacterial mechanisms of UVC-GA and GA on E. coli O157:H7 were completely different. Based on the above results, food-sterilizing detergents can be developed and applied to contaminated oyster to provide an effective food cleaning effect. [ABSTRACT FROM AUTHOR]

Current hydrophilic modification strategies improve the antifouling ability of membranes but fail to completely eliminate the fouling of emulsified oil droplets with a wide size distribution. Constructing membranes with superior anti‐oil‐fouling ability to resist various oil droplets especially at high permeation fluxes is challenging. Here, the fabrication of a zero‐oil‐fouling membrane by grafting considerably high coverage of zwitterionic polymer and building defect‐free hydration defense barrier on the surface is reported. A uniform layer of protocatechuic acid with COOH as abundant as existing in every molecule is stably deposited on the membrane so as to provide sufficient reactive sites and achieve dense grafting of the zwitterionic polymer. The coverage of zwitterionic polymer on the membrane plays a crucial role in promoting the antifouling ability to emulsified oil droplets. The poly(vinylidene fluoride) membrane with 93% coverage of the zwitterionic polymer exhibits zero oil fouling when separating multitudinous oil‐in‐water emulsions with ≈0% flux decline, ≈100% flux recovery, and a high water flux of ≈800 L m−2 h−1 bar−1. This membrane outperforms almost all of the reported membranes in terms of the comprehensive antifouling performance. This work provides a feasible route for manufacturing super‐antifouling membranes toward oil/water separation application. [ABSTRACT FROM AUTHOR]

Acute myeloid leukemia (AML) is a common malignancy worldwide. Human immune deficiency virus type 1 enhancer-binding protein 3 (HIVEP3) was verified to play a vital role in types of cancers. However, the functional role of HIVEP3 in AML was rarely reported. In this study, CCK-8, colony formation assay, flow cytometry, and Trans-well chamber experiments were applied for detecting cell proliferation, apoptosis, and invasion in AML cells. The expression of proteins related to TGF-β/Smad signaling pathway was determined by western blot. Our data showed that the expression level of HIVEP3 was closely related to the risk classification and prognosis of AML patients. Moreover, HIVEP3 was highly expressed in AML patients and cells. Knockdown of HIVEP3 significantly repressed cell proliferation invasion, and enhanced cell apoptosis in HL-60 and THP-1 cells. In addition, HIVEP3 donwreglation could inhibit the TGF-β/Smad signaling pathway. TGF-β overexpression could reverse the inhibition effects of HIVEP3 knockdown on AML development and the TGF-β/Smad signaling pathway. These findings indicated that HIVEP3 contributed to the progression of AML via regulating the TGF-β/Smad signaling pathway and had a prognostic value for AML. [ABSTRACT FROM AUTHOR]