This study investigated a new adhesive system, consisting of soy protein isolate (SPI) and Kymene ® 557H (simply called Kymene) (a commercial wet-strength agent for paper), that was prepared by mixing SPI and Kymene. Wood composites bonded with SPI-Kymene adhesive preparations had shear strengths comparable to or higher than those bonded with commercial phenol formaldehyde resins. Wood composites bonded with the new adhesive system had high water resistance and retained relatively high strength even after they had undergone a boiling-water test. The new adhesive system is formaldehyde-free, easy to use, and environmentally friendly. Kymene was proposed to serve as a curing agent in SPI-Kymene adhesives.

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Remodeling of adipocytes in mesentery (aM) associated with nutritional overload from high fructose diet (hFD) is a source of several comorbidities. however, its pathogenesis is still unclear and there are no specific effective drugs for AM remodeling. Recently hydrogen sulfide (H 2 S) demonstrated potent cytoprotective actions. The purpose of this study was to investigate the effects and underlying mechanisms of AM remodeling in rats fed hFD and with h 2 S pre-treatment. adult male rats on standard diet (SD, control group) or hFD that underwent acute water-immersion restraint stress (WIS) were evaluated for subcellular aM adaptive responses by electron microscopy. The effects on AM of exogenous sodium hydrosulfide (NaHS, 5.6 mg/ kg/day for 9 days) and the Н 2 S-releasing aspirin (aSa) derivative (h 2 S-ASA , 17.5 mg/kg/day) vs conventional ASA (10 mg/kg/day) vs vehicle were investigated. Serum glucose level, thiobarbituric acid reactive substances (TBARS), and activities of cystathionine γ-lyase (CSE) and cystathionine β-synthase (CBS) were examined biochemically using spectrophotometry. In the HFD groups, treatment with NaHS protected aM, as mesenteric microvascular endothelial and sub-endothelial structures were observed vs the vehicletreated group that had signs of endothelial dysfunction, aM damage and dysfunctional mitochondria. The effect of H 2 S-aSa was characterized by protection of aM against hFD and WIS-induced injury, with lower TBARS blood level and increased CSE and CBS activities. Carbohydrate overload for 4 weeks is sufficient to cause AM oxidative damage, mitochondrial dysfunction and endothelial changes. H 2 S plays an important role in mesenteric adipocyte cellular survival against HFD-induced oxidative stress by decreasing overproduction of TBaRS and mitochondrial dysfunction. The use of h 2 S could lead to a novel approach for anti-obesity treatment.K e y w o r d s: hydrogen sulfide (H 2 S), thiobarbituric acid reactive substances (TBaRS), cystathionine gamma-lyase (CSE), cystathionine beta-synthase (CBS), oxidative stress, adipocytes, mesentery, mitochondria.

environmental pollution and technological progress lead to carbon nanoparticles that pose a serious health risk. They are present in soot, dust, and printing toner and can also be formed during grinding and cutting. human neutrophils are able to sequester foreign material by formation of neutrophil extracellular traps (NETs), a process that can cause a strong inflammatory response. In the current work we compared proinflammatory properties of different carbon-based nanostructures: nanodiamonds, graphene oxide, fullerenes c 60 and carbon dots. We tested adjuvant properties of carbon nanoparticles in a murine immunization model by investigating humoral (specific IgG and IgM antibodies) and cellular (delayed type hypersensitivity) immune responses. The ability of NETs to sequester nanoparticles was analyzed in a mouse air pouch model and neutrophil activation was verified by in vivo tracking of near-infrared labeled nanodiamonds and ex vivo fluorescent assays using human blood-derived neutrophils. All carbon nanoparticles exhibited proinflammatory adjuvant-like properties by stimulating production of specific IgG but not IgM antibodies (humoral immune response). The adjuvant-like response decreased in this order: from nanodiamonds, graphene oxide, fullerenes c 60 to carbon dots. None of the studied carbon nanoparticles triggered a delayed type hypersensitivity reaction (cellular immune response). Nanodiamonds and fullerenes c 60 were sequestrated in the body by NETs, as confirmed in the air pouch model and by in vivo fluorescent tracking of near-infrared labeled nanodiamonds. K e y w o r d s: carbon-based nanostructures, immune response, inflammation, neutrophil extracellular traps (NeTs).