1,1′-[(Hexane-1,6-diyldi­oxy)bis­(nitrilo­methyl­idyne)]dinaphthalene

The title compound, C28H28N2O2, was synthesized by condensation of 1-naphthaldehyde with 1,6-bis­(amino­oxy)hexane in ethanol. The mol­ecule is disposed about a crystallographic centre of symmetry. In the crystal structure, mol­ecules are linked through strong inter­molecular π–π stacking inter­actions [interplana distance = 2.986 (2) Å], forming a three-dimensional network

2,2′-{1,1′-[Pentane-1,5-diyl­bis(oxy­nitrilo)]­diethyl­idyne}diphenol

In the title compound, C21H26N2O4, there is half a mol­ecule in the asymmetric unit with a crystallographic twofold rotation axis passing through the central C atom of the –CH=N—O—(CH2)5—O—N=CH– bridge. The dihedral angle formed by the two benzene rings is 80.85 (2)°. Strong intra­molecular O—H⋯N and C—H⋯O hydrogen bonds help to establish the molecular conformation. There are also weak inter­molecular π–π stacking inter­actions between neighbouring benzene rings [centroid–centroid separation = 3.502 (3) Å]

3,3′-Dibromo-1,1′-[(propane-1,3-diyl­dioxy)­bis(nitrilo­methyl­idyne)]dibenzene

The mol­ecule of the title compound, C17H16Br2N2O2, lies on a twofold axis that passes through the middle atom of the three-atom trimethyl­ene unit. The two aromatic rings are aligned at an angle of 76.02 (4)°

Effects of Yifukang Oral Liquid on Chemotherapy- and Radiotherapy-Induced Toxic and Side Effects of Myelosuppression, Leucopenia and Gastrointestinal Tract Disturbances

Purpose: To investigate the effects of Yifukang oral liquid (YFKOL) on chemotherapy- and radiotherapy-induced myelosuppression, leucopenia and gastrointestinal tract disturbances.Methods: The effects of YFKOL on myelosuppression, leucopenia and gastrointestinal tract disturbances were assessed by cyclophosphamide- and Co60-induced leucopenia in mice, copper sulfate-induced emesis in pigeons, ethanol-induced gastric mucosal lesions in rats, gastric emptying and intestinal propulsion in mice.Results: In cyclophosphamide- and Co60-induced leucopenia assays, the mean white blood cell count (82.6 and 90.1 × 109/L; 7.3 and 8.2 × 109/L, respectively) and thighbone marrow granulocytes (66.1 % and 67.4 %; 60.8 and 66.5 %, respectively) were significantly (p < 0.05) increased after treatment with YFKOL (15 and 30 mL/kg), compared with the respective control (68.2 and 4.7 × 109/L; 58.2 and 53.1 %). In emesis, gastric mucosal lesions, gastric emptying and intestinal propulsion assays, the mean frequency of emesis (30.8 and 22.3 times, respectively) and ulcer index (39.6 and 26.5, respectively) significantly (p < 0.05) decreased, and the mean gastric emptying (25.0 and 24.0 %) and intestinal propulsion (81.9 and 82.8 %) were significantly (p < 0.05) promoted after treatment with YFKOL (10 and 20 mL/kg), compared with the respective control (54.7 times, 62.8, 42.0 and 68.9 %).Conclusion: YFKOL may suppress chemotherapy- and radiotherapy-induced myelosuppression, leucopenia and gastrointestinal tract disturbances.Keywords: Yifukang oral liquid, Gastrointestinal tract disturbances, Leucopenia, Myelosuppression, Tumor, Chemotherapy, Radiotherap

2,2′-Dichloro-1,1′-[(propane-1,3-diyldi­oxy)bis­(nitrilo­methyl­idyne)]dibenzene

The title compound, C17H16Cl2N2O2, assumes a V-shape configuration with a dihedral angle between the two halves of the mol­ecule of 79.60 (4)°. The asymmetric unit comprises one half-mol­ecule with a crystallographic twofold rotation axis passing through the central C atom. There are weak inter­molecular π–π stacking inter­actions between neighbouring benzene rings with inter­molecular plane-to-plane distances of 3.277 (6) and 3.465 (5) Å along the a and c axes, respectively. In the crystal structure, weak inter­molecular C—H⋯O bonds link each mol­ecule to four others to form an infinite three-dimensional network

3,3′-Bis(4-nitro­phen­yl)-1,1′-(p-phenyl­ene)dithio­urea dimethyl sulfoxide disolvate

The asymmetric unit of the title compound, C22H16N6O6S2·2C2H6OS, consists of one half-mol­ecule of the centrosymmetric thiourea derivative and one molecule of dimethyl sulfoxide (DMSO). The carbonyl group forms an intra­molecular hydrogen bond with the NH group, creating a six-membered (C—N—C—N—H⋯O) ring. Two other N—H⋯O hydro­gen bonds link one mol­ecule of the thio­urea to two mol­ecules of DMSO

The relationship between the interactive behavior of industry–university–research subjects and the cooperative innovation performance: The mediating role of knowledge absorptive capacity

IntroductionIndustry–university–research cooperation innovation, which is often characterized by resource complementarity and the sharing technology, has become one of the most preferred innovation cooperation methods for enterprises. However, various problems still occur in the process of industry–university–research cooperations, such as poor innovation performance and difficulty in sustaining cooperation. Existing studies mostly focus on the macroscopic perspectives of geographic location, cooperation scale, concentration, and diversification of industry–university–research cooperation subjects, and fail to explore the microscopic behavioral mechanisms.MethodsTherefore, this paper establishes the interactive behavior of industry–university–research subjects and defines its concepts and dimensions in an attempt to provide a mechanism for improving the cooperative innovation performance of industry–university–research from the micro-behavioral perspective. On the basis of theoretical analysis, this paper develops a model of the relationship between cooperative trust, cooperative communication, and cooperative innovation performance for interactive behavior, while exploring the mediating role of knowledge absorptive capacity. The model was validated by stepwise regression using data from 325 questionnaires.ResultsThe paper found that cooperative trust and cooperative communication in the cooperative interactive behavior of industry–university–research positively contribute to the improvement of cooperative innovation performance. Knowledge absorptive capacity plays a partially mediating role between the interactive behaviors and cooperative innovation performance. More specifically, knowledge absorptive capacity partially mediates cooperative communication in cooperative innovation performance and completely mediates cooperative trust in cooperative innovation performance. The results are largely consistent with the results of the heterogeneity analysis of the sample.DiscussionThis paper not only explains why the cooperative innovation performance of industry–university–research is poor from the perspective of interactive behavior, but also enriches the research perspective of industry–university–research and provides theoretical support for enterprises to optimize the relationship between industry, university, and research institutes

Tulp1 deficiency causes early-onset retinal degeneration through affecting ciliogenesis and activating ferroptosis in zebrafish

Mutations in TUB-like protein 1 (TULP1) are associated with severe early-onset retinal degeneration in humans. However, the pathogenesis remains largely unknown. There are two homologous genes of TULP1 in zebrafish, namely tulp1a and tulp1b. Here, we generated the single knockout (tulp1a(−/−) and tulp1b(−/−)) and double knockout (tulp1-dKO) models in zebrafish. Knockout of tulp1a resulted in the mislocalization of UV cone opsins and the degeneration of UV cones specifically, while knockout of tulp1b resulted in mislocalization of rod opsins and rod-cone degeneration. In the tulp1-dKO zebrafish, mislocalization of opsins was present in all types of photoreceptors, and severe degeneration was observed at a very early age, mimicking the clinical manifestations of TULP1 patients. Photoreceptor cilium length was significantly reduced in the tulp1-dKO retinas. RNA-seq analysis showed that the expression of tektin2 (tekt2), a ciliary and flagellar microtubule structural component, was downregulated in the tulp1-dKO zebrafish. Dual-luciferase reporter assay suggested that Tulp1a and Tulp1b transcriptionally activate the promoter of tekt2. In addition, ferroptosis might be activated in the tulp1-dKO zebrafish, as suggested by the up-regulation of genes related to the ferroptosis pathway, the shrinkage of mitochondria, reduction or disappearance of mitochondria cristae, and the iron and lipid droplet deposition in the retina of tulp1-dKO zebrafish. In conclusion, our study establishes an appropriate zebrafish model for TULP1-associated retinal degeneration and proposes that loss of TULP1 causes defects in cilia structure and opsin trafficking through the downregulation of tekt2, which further increases the death of photoreceptors via ferroptosis. These findings offer insight into the pathogenesis and clinical treatment of early-onset retinal degeneration