Comparative effectiveness of nitro dihydrocapsaicin, new synthetic derivative capsaicinoid, and capsaicin in alleviating oxidative stress and inflammation on lipopolysaccharide-stimulated corneal epithelial cells.

Loss of tear homeostasis, characterized by hyperosmolarity of the ocular surface, induces cell damage through inflammation and oxidation. Transient receptor potential vanilloid 1 (TRPV1), a sensor for osmotic changes, plays a crucial role as a calcium ion channel in the pathogenesis of hypertonic-related eye diseases. Capsaicin (CAP), a potent phytochemical, alleviates inflammation during oxidative stress events by activating TRPV1. However, the pharmacological use of CAP for eye treatment is limited by its pungency. Nitro dihydrocapsaicin (NDHC) was synthesized with aromatic ring modification of CAP structure to overcome the pungent effect. We compared the molecular features of NDHC and CAP, along with their biological activities in human corneal epithelial (HCE) cells, focusing on antioxidant and anti-inflammatory activities. The results demonstrated that NDHC maintained cell viability, cell shape, and exhibited lower cytotoxicity compared to CAP-treated cells. Moreover, NDHC prevented oxidative stress and inflammation in HCE cells following lipopolysaccharide (LPS) administration. These findings underscore the beneficial effect of NDHC in alleviating ocular surface inflammation, suggesting that NDHC may serve as an alternative anti-inflammatory agent targeting TRPV1 for improving hyperosmotic stress-induced ocular surface damage.

Constructed sediment microbial fuel cell for treatment of fat, oil, grease (FOG) trap effluent: Role of anode and cathode chamber amendment, electrode selection, and scalability.

For wastewater treatment, sediment microbial fuel cells (SMFCs) have advantages over traditional microbial fuel cells in cost (due to their membrane-less structure) and operation (less intensive maintenance). Nevertheless, the technical obstacles of SMFCs include their high internal electrical resistance due to sediment in the anode chamber and slow oxygen reduction reaction (ORR) in the cathode chamber, which is responsible for their low power density (PD) (0.2-50 mW/m2). This study evaluated several SMFC improvements, including anode and cathode chamber amendment, electrode selection, and scaling the chamber size up to obtain optimally constructed single-chamber SMFCs to treat fat, oil, and grease (FOG) trap effluent. The chemical oxygen demand (COD) removal efficiency, PD, and electrical energy conversion efficiency concerning theoretically available chemical energy from FOG trap effluent treatment (%ECWW) were examined. Packing biochar in the anode chamber reduced its electrical resistance by 5.76 times, but the improvement in PD was trivial. Substantial improvement occurred when packing the cathode chamber with activated carbon (AC), which presumably catalyzed the ORR, yielding a maximum PD of 109.39 mW/m2, 959 times greater than without AC in the cathode chamber. This SMFC configuration resulted in a COD removal efficiency of 85.80 % and a %ECWW of 99.74 % in 30 days. Furthermore, using the most appropriate electrode pair and chamber volume increased the maximum PD to 1787.26 mW/m2, around 1.7 times greater than the maximum PD by SMFCs reported thus far. This optimally constructed SMFC is low cost and applicable for household wastewater treatment.

Lack of Nck1 protein and Nck-CD3 interaction caused the increment of lipid content in Jurkat T cells.

BACKGROUND: The non-catalytic region of tyrosine kinase (Nck) is an adaptor protein, which is ubiquitously expressed in many types of cells. In T cells, the Nck1 isoform promotes T cell receptor signalling as well as actin polymerisation. However, the role of Nck1 in the lipid metabolism in T cells is unknown. In the present study, we investigated the effect of the Nck1 protein and Nck-CD3 interaction on lipid metabolism and on the physical and biological properties of Jurkat T cells, using a newly developed holotomographic microscope. RESULTS: Holotomographic microscopy showed that Nck1-knocked-out cells had membrane blebs and were irregular in shape compared to the rounded control cells. The cell size and volume of Nck1-deficient cells were comparable to those of the control cells. Nck1-knocked-out Jurkat T cells had a greater lipid content, lipid mass/cell mass ratio, and lipid metabolite levels than the control cells. Interestingly, treatment with a small molecule, AX-024, which inhibited Nck-CD3 interaction, also caused an increase in the lipid content in wild-type Jurkat T cells, as found in Nck1-deficient cells. CONCLUSIONS: Knockout of Nck1 protein and hindrance of the Nck-CD3 interaction cause the elevation of lipid content in Jurkat T cells.