Temporal activation of biological processes by visible light and subsequent return to an inactive state in the absence of light is an essential characteristic of photoreceptor cells. Inspired by these phenomena, light-responsive materials are very attractive due to the high spatiotemporal control of light irradiation, with light being able to precisely orchestrate processes repeatedly over many cycles. Herein, it is reported that light-driven proton transfer triggered by a merocyanine-based photoacid can be used to modulate the permeability of pH-responsive polymersomes through cyclic, temporally controlled protonation and deprotonation of the polymersome membrane. The membranes can undergo repeated light-driven swelling-contraction cycles without losing functional effectiveness. When applied to enzyme loaded-nanoreactors, this membrane responsiveness is used for the reversible control of enzymatic reactions. This combination of the merocyanine-based photoacid and pH-switchable nanoreactors results in rapidly responding and versatile supramolecular systems successfully used to switch enzymatic reactions ON and OFF on demand.Escherichia coli O157H7, a causative agent of haemolytic uremic syndrome, can enter into a viable but non-culturable (VBNC) state in response to harsh stress. Bacteria in this state can retain membrane integrity, metabolic activity and virulence expression, which may present health risks. However, virulence expression and resuscitation ability of the VBNC state are not well understood. Here, we induced E. coli O157H7 into a VBNC state by high temperature, which is commonly used to prevent the proliferation of pathogens in process of soil solarization, composting and anaerobic digestion of organic wastes. The virulence genes were highly expressed in the VBNC state and resuscitated daughter cells. The resuscitation of VBNC cells occurred after the removal of heat stress in Luria-Bertani medium. In addition, E. coli O157 H7 cells can leave the VBNC state and resuscitate with the clearance of protein aggregates. Notably, with the accumulation of protein aggregation and increased levels of reactive oxygen species, cells lost their ability to resuscitate. The results of this study not only can facilitate a better understanding of the health risks associated with the VBNC state but also have the potential to provide a theoretical basis for thermal disinfection processing.Ideonella sakaiensis produces an enzyme, PETase, that is capable of hydrolyzing polyethylene terephthalate (PET) plastic. We demonstrate that although I. Selleck Onametostat sakaiensis can grow on amorphous plastic, it does not grow on highly crystalline plastic under otherwise identical conditions. Both amorphous film and amorphous plastic obtained from commercial food containers support the growth of the bacteria, whereas highly crystalline film and the highly crystalline body of a plastic water bottle do not support growth. Highly crystalline PET can be melted and rapidly cooled to make amorphous plastic which then supports bacterial growth, whereas the same plastic can be melted and slowly cooled to make crystalline plastic which does not support growth. We further subject a plastic water bottle to a top-to-bottom analysis, finding that only amorphous sections are degraded, namely the finish (threading), the topmost portion of the shoulder which connects to the finish, and the area immediately surrounding the centre of the base. Finally, we use these results to estimate that the percentage of non-degradable plastic in plastic water bottles ranges from 52% to 82% (depending on size), demonstrating that most of the plastic found in PET water bottles will not be degraded by I. sakaiensis. Cardiovascular disease (CVD) is the leading cause of death in systemic lupus erythematosus (SLE). B cells play a key role in the pathogenesis of lupus, and anti-BAFF therapy has been approved for use in SLE. Since mature B cells also promote atherosclerosis, we undertook this study to evaluate, in a mouse model and in SLE patients, whether BAFF neutralization has an atheroprotective effect in SLE. The effect of BAFF on atherosclerosis associated with lupus was investigated in the atherosclerosis/lupus-prone apolipoprotein E-knockout D227K mouse model and in a cohort of SLE patients. Mice were treated with a blocking anti-BAFF monoclonal antibody (mAb), while fed a standard chow diet. Carotid plaque and carotid intima-media thickness were assessed by ultrasound at baseline and during follow-up in SLE patients who were asymptomatic for CVD. Anti-BAFF mAb in ApoE D227K mice induced B cell depletion, efficiently treated lupus, and improved atherosclerosis lesions (21% decrease; P = 0.007) in mice with low plasma cholesterol levels but worsened the lesions (17% increase; P = 0.06) in mice with high cholesterol levels. The atheroprotective effect of the BAFF-BAFF receptor signaling inhibition on B cells was counterbalanced by the proatherogenic effect of the BAFF-TACI signaling inhibition on macrophages. In SLE patients, blood BAFF levels were associated with subclinical atherosclerosis (r = 0.26, P = 0.03). Anti-BAFF mAb treatment had a differential effect on the intima-media thickness progression in SLE patients depending on body mass index. Depending on the balance between lipid-induced and B cell-induced proatherogenic conditions, anti-BAFF could be detrimental or beneficial, respectively, to atherosclerosis development in SLE.Depending on the balance between lipid-induced and B cell-induced proatherogenic conditions, anti-BAFF could be detrimental or beneficial, respectively, to atherosclerosis development in SLE.Acute promyelocytic leukemia (APL), a biologically and clinically distinct variant of acute myelogenous leukemia, is characterized by the fusion of the N-terminus of promyelocytic leukemia protein to the C terminus of retinoic acid receptor alpha, mostly due to chromosomal translocation t(15;17). Chidamide, a synthetic analogue of MS-275 identified from a group of benzamide-type compounds, has been found to have efficient anticancer activity in basic and clinical research studies. However, the concrete role and underlying mechanism of Chidamide in the treatment of APL has not been well characterized. Our data demonstrate that Chidamide inhibited the expression of histone deacetylase (HDAC) to induce apoptosis and suppress proliferation in NB4 cells. Mechanistically, Chidamide increases the expression of miR-34a by suppressing HDAC. Furthermore, B-cell lymphoma-2 (Bcl-2) is a direct target of miR-34a, the expression of which is regulated by miR-34a. Functionally, Chidamide inhibits cell proliferation and promotes apoptosis through miR-34a/Bcl-2.