β-conglycinin has been identified as one of the major feed allergens. However, studies of β-conglycinin on fish are scarce. This study investigated the effects of β-conglycinin on the growth, digestive and absorptive ability, inflammatory response, oxidative status and gene expression of juvenile Jian carp (Cyprinus carpio var. Jian) in vivo and their enterocytes in vitro. The results indicated that the specific growth rate (SGR), feed intake, and feed efficiency were reduced by β-conglycinin. In addition, activities of trypsin, chymotrypsin, lipase, creatine kinase, Na+,K+-ATPase and alkaline phosphatase in the intestine showed similar tendencies. The protein content of the hepatopancreas and intestines, and the weight and length of the intestines were all reduced by β-conglycinin. β-conglycinin increased lipid and protein oxidation in the detected tissues and cells. However, β-conglycinin decreased superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), glutathione peroxidase (GPx) and glutathione reductase (GR) activities and glutathione (GSH) content in the intestine and enterocytes. Similar antioxidant activity in the hepatopancreas was observed, except for GST. The expression of target of rapamycin (TOR) gene was reduced by β-conglycinin. Furthermore, mRNA levels of interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and transforming growth factor-β (TGF-β) genes were increased by β-conglycinin. However, β-conglycinin increased CuZnSOD, MnSOD, CAT, and GPx1b gene expression. In conclusion, this study indicates that β-conglycinin induces inflammation and oxidation, and causes dysfunction of intestinal digestion and absorption in fish, and finally reduces fish growth. The results of this study provide some information to the mechanism of β-conglycinin-induced negative effects.

Molecular hydrogels have attracted extensive research interest in recent years because of their inherent properties (e.g., formation by the self-assembly of small molecules and their gel-sol/sol-gel phase transitions can be easily manipulated by external stimulus). [1] They have shown great potential in fields such as three-dimensional (3D) cell culture [2] and controlled drug delivery. [3] During the formation of a molecular hydrogel, a small molecule (molecular hydrogelator) needs to selfassemble into a 3D matrix of nanofibers, nanorods, or nanospheres that can hold water molecules within the cavities of the 3D matrix. To form the 3D matrix, there should be strong or at least medium interactions between self-assembled nanostructures. Otherwise, nanostructures with weak interactions between them will only form dispersions or solutions in the aqueous phase. Actually, there are many examples of this kind of self-assembled system that lack strong interactions between the self-assembled structures. [4] This type of solution/dispersion containing self-assembled nanostructures could change to a hydrogel if the interaction between the nanostructures could be enhanced. For example, several groups have demonstrated that zinc and calcium ions can be used to cross-link self-assembled nanofibers to form molecular hydrogels. [5] In this study, we rationally designed a fusion protein with four binding sites and used the proteinpeptide interaction to enhance interactions between selfassembled nanofibers, thus leading to the formation of molecular hydrogels (Figure 1).There are only a few examples of polymeric hydrogels formed by specific protein-peptide interactions. [6] Specific protein-peptide interaction has also been used to direct selfassembly of peptide nanowires into micrometer-sized crystalline cubes. [7] However, there are no reports about the formation of molecular hydrogels through protein-peptide interactions up to now. As mentioned above, the formation of a 3D matrix is crucial to the formation of molecular hydrogels. To use protein-peptide interactions to enhance interfiber interactions to support 3D structures, fusion proteins with multiple binding sites are needed. These kinds of fusion proteins usually contain two parts, one for multimer formation and the other for peptide binding. However, these fusion proteins are usually in the balance between multimers with multiple binding sites and monomer with only one binding site. The dissociation constants of protein-peptide interactions are also usually in the micro-to millimolar range. It remains a challenge to develop a protein that can predominantly (> 95 %) form multimers with multiple binding sites. It would also be highly interesting for researchers in the field of biomaterials to develop a protein-peptide interaction with Figure 1. Protein-peptide interaction can be used to enhance interactions between self-assembled fibers, thus leading to molecular hydrogelation. A) Chemical structure of Nap-GFFYGGGWRESAI (1: nongelator) with a possible self-assembly a...

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This study investigated the effects of glycinin on the growth, intestinal oxidative status, tight junction components, cytokines and apoptosis signalling factors of fish. The results showed that an 80 g/kg diet of glycinin exposure for 42 d caused poor growth performance and depressed intestinal growth and function of juvenile Jian carp (Cyprinus carpio var. Jian). Meanwhile, dietary glycinin exposure induced increases in lipid peroxidation and protein oxidation; it caused reductions in superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx) activities; and it increased MnSOD, CuZnSOD, GPx1b and GPx4a mRNA levels, suggesting an adaptive mechanism against stress in the intestines of fish. However, dietary glycinin exposure decreased both the activity and mRNA levels of nine isoforms of glutathione-S-transferase (GST) (α, μ, π, ρ, θ, κ, mGST1, mGST2 and mGST3), indicating toxicity to this enzyme activity and corresponding isoform gene expressions. In addition, glycinin exposure caused partial disruption of intestinal cell-cell tight junction components, disturbances of cytokines and induced apoptosis signalling in the distal intestines > mid intestines > proximal intestines of fish. Glycinin exposure also disturbed the mRNA levels of intestinalrelated signalling factors Nrf2, Keap1a, Keap1b, eleven isoforms of protein kinase C and target of rapamycin/4E-BP. Interestingly, glutamine was observed to partially block those negative influences. In conclusion, this study indicates that dietary glycinin exposure causes intestinal oxidative damage and disruption of intestinal physical barriers and functions and reduces fish growth, but glutamine can reverse those negative effects in fish. This study provides some information on the mechanism of glycinin-induced negative effects.

TianQin is a geocentric space-based gravitational-wave observatory mission consisting of three drag-free controlled satellites in an equilateral triangle with an orbital radius of [Formula: see text][Formula: see text]km. The constellation faces the white-dwarf binary RX J0806.3[Formula: see text]1527 located slightly below the ecliptic plane, and is subject to gravitational perturbations that can distort the formation. In this study, we present combined methods to optimize the TianQin orbits so that a set of 5-year stability requirements can be met. Moreover, we discuss slow long-term drift of the detector pointing due to orbital precession, and put forward stable orbits with six other pointings along the lunar orbital plane. Some implications of the findings are pointed out.