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C24H48N2O3, monoclinic, P21 (no. 4), a = 14.805(3) Å, b = 10.0557(18) Å, c = 18.061(3) Å, β = 98.935(5)°, V = 2656.3(8) Å3, Z = 4, Rgt(F) = 0.0674, wRref(F2) = 0.1955, T = 173 K.

C29H54N2O3, monoclinic, P21 (no. 4), a = 9.8091(11) Å, b = 7.6661(8) Å, c = 19.095(2) Å, β = 93.171(4)°, V = 1433.7(3) Å3, Z = 2, Rgt(F) = 0.0657, wRref(F2) = 0.1362, T = 250 K.

C31H48N2O, orthorhombic, P212121 (no. 19), a = 6.530(2) Å, b = 11.728(4) Å, c = 35.236(12) Å, V = 2698.6(15) Å3, Z = 4, Rgt(F) = 0.0492, wRref(F2) = 0.1034, T = 173 K.

C28H42N2O2, monoclinic, P21 (no. 4), a = 12.679(3) Å, b = 6.9067(14) Å, c = 15.577(3) Å, β = 113.821(4)°, V = 1247.8(5) Å3, Z = 2, Rgt(F) = 0.0485, wRref(F2) = 0.1266, T = 173 K.

Lithium lanthanum titanate (Li3xLa2/3−xTiO3, abbreviated as LLTO, where x = 0.08, 0.1, 0.12, 0.14, 0.16, and 0.167) is prepared using a conventional solid-phase method, and its crystal structure, phase composition, microstructure, and electrical properties are investigated. Experimental results indicate that when the Li content is low (x = 0.8), there exist tetragonal, cubic, and orthogonal phases in LLTO. As the Li content increases (x ≥ 0.1), the orthogonal phase disappears, and there are changes in the phase composition of tetragonal and cubic phases. When the occupancy rates of Li and La are low, the number of A-site vacancies increases, as does the electrical conductivity of LLTO. At room temperature, the ionic conductivity of LLTO increases and then decreases. The Li0.30La0.56TiO3 ceramic electrolyte exhibits the highest total ionic conductivity of 7.22 × 10−5 S/cm, a minimum activation energy of 0.31 eV, and an electrical conductivity of 6.26 × 10−11 S/cm. This paper provides a theoretical basis for subsequent research on solid Li3xLa2/3−xTiO3 electrolytes. [ABSTRACT FROM AUTHOR]

Lithium lanthanum titanate (Li3xLa2/3−xTiO3, abbreviated as LLTO, where x = 0.08, 0.1, 0.12, 0.14, 0.16, and 0.167) is prepared using a conventional solid-phase method, and its crystal structure, phase composition, microstructure, and electrical properties are investigated. Experimental results indicate that when the Li content is low (x = 0.8), there exist tetragonal, cubic, and orthogonal phases in LLTO. As the Li content increases (x ≥ 0.1), the orthogonal phase disappears, and there are changes in the phase composition of tetragonal and cubic phases. When the occupancy rates of Li and La are low, the number of A-site vacancies increases, as does the electrical conductivity of LLTO. At room temperature, the ionic conductivity of LLTO increases and then decreases. The Li0.30La0.56TiO3 ceramic electrolyte exhibits the highest total ionic conductivity of 7.22 × 10−5 S/cm, a minimum activation energy of 0.31 eV, and an electrical conductivity of 6.26 × 10−11 S/cm. This paper provides a theoretical basis for subsequent research on solid Li3xLa2/3−xTiO3 electrolytes. [ABSTRACT FROM AUTHOR]

Antimony (Sb) has recently been identified as a novel nerve poison, although the cellular and molecular mechanisms underlying its neurotoxicity remain unclear. This study aimed to assess the effects of the nuclear factor kappa B (NF-κB) signaling pathway on antimony-induced astrocyte activation. Protein expression levels were detected by Western blotting. Immunofluorescence, cytoplasmic and nuclear fractions separation were used to assess the distribution of p65. The expression of protein in brain tissue sections was detected by immunohistochemistry. The levels of mRNAs were detected by Quantitative real-time polymerase chain reaction (qRT-PCR) and reverse transcription-polymerase chain reaction (RT-PCR). Antimony exposure triggered astrocyte proliferation and increased the expression of two critical protein markers of reactive astrogliosis, inducible nitric oxide synthase (iNOS) and glial fibrillary acidic protein (GFAP), indicating that antimony induced astrocyte activation in vivo and in vitro. Antimony exposure consistently upregulated the expression of inflammatory factors. Moreover, it induced the NF-κB signaling, indicated by increased p65 phosphorylation and translocation to the nucleus. NF-κB inhibition effectively attenuated antimony-induced astrocyte activation. Furthermore, antimony phosphorylated TGF-β-activated kinase 1 (TAK1), while TAK1 inhibition alleviated antimony-induced p65 phosphorylation and subsequent astrocyte activation. Antimony activated astrocytes by activating the NF-κB signaling pathway. [ABSTRACT FROM AUTHOR]

The compound 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD), a persistent organic pollutant, is harmful to the nervous system, but its effects on the brain are still unclear. This study aimed to investigate the effects of TCDD on astrocytes proliferation and underlying molecular mechanism. The cell proliferation was measured by EdU-based proliferation assay and PI staining by flow cytometry. Protein expression levels were detected by Western blotting. Immunofluorescence, cytoplasmic and nuclear fractions separation were used to assess the distribution of signal transducer and activator of transcription 3 (STAT3). C6 cells treated with 10 and 50 nmol/L TCDD for 24 h showed significant promotion of the proliferation of. The exposure to TCDD resulted in the upregulation in the expression levels of phosphorylated protein kinase B (p-Akt), phosphorylated STAT3, and cyclin D1 in a dose- and time-dependent manner. The inhibition of Akt expression with LY294002 or STAT3 expression with AG490 abolished the TCDD-induced cyclin D1 upregulation and cell proliferation. Furthermore, LY294002 suppressed the activation of STAT3. Finally, TCDD promoted the translocation of STAT3 from the cytoplasm to the nucleus, and LY294002 treatment blocked this effect. TCDD exposure promotes the proliferation of astrocyte cells via the Akt/STAT3/cyclin D1 pathway, leading to astrogliosis. [ABSTRACT FROM AUTHOR]

C29H54N2O3, monoclinic, P21 (no. 4), a = 9.8091(11) Å, b = 7.6661(8) Å, c = 19.095(2) Å, β = 93.171(4)°, V = 1433.7(3) Å3, Z = 2, Rgt(F) = 0.0657, wRref(F2) = 0.1362, T = 250 K. [ABSTRACT FROM AUTHOR]

C28H42N2O2, monoclinic, P21 (no. 4), a = 12.679(3) Å, b = 6.9067(14) Å, c = 15.577(3) Å, β = 113.821(4)°, V = 1247.8(5) Å3, Z = 2, Rgt(F) = 0.0485, wRref(F2) = 0.1266, T = 173 K. [ABSTRACT FROM AUTHOR]

C24H41NO, orthorhombic, P212121 (no. 19), a = 6.3752(16) Å, b = 12.607(3) Å, c = 26.943(7) Å, V = 2165.4(10) Å3, Z = 4, Rgt(F) = 0.0573, wRref(F2) = 0.1232, T = 173 K. [ABSTRACT FROM AUTHOR]

C28H42N2O2, monoclinic, P21 (no. 4), a = 12.679(3) Å, b = 6.9067(14) Å, c = 15.577(3) Å, β = 113.821(4)°, V = 1247.8(5) Å3, Z = 2, Rgt(F) = 0.0485, wRref(F2) = 0.1266, T = 173 K. [ABSTRACT FROM AUTHOR]

Aim: To investigate the role of serum-and-glucocorticoid-inducible-kinase-1 (SGK1) in colitis and its potential pathological mechanisms., Methods: SGK1 expression in mucosal biopsies from patients with active Crohn's disease (CD) and normal controls was detected by immunohistochemistry. We established an acute colitis model in mice induced by 2,4,6-trinitrobenzene sulfonicacid, and demonstrated the presence of colitis using the disease activity index, the histologic activity index and hematoxylin and eosin staining. The cellular events and potential mechanisms were implemented with small interference RNA and an inhibitor of signaling molecule (i.e., U0126) in intestinal epithelial cells (IECs). The interaction between SGK1 and the signaling molecule was assessed by co-immunoprecipitation., Results: SGK1 expression was significantly increased in the inflamed epithelia of patients with active CD and TNBS-induced colitis model (0.58 ± 0.055 vs 0.85 ± 0.06, P < 0.01). At the cellular level, silencing of SGK1 by small interference RNA (siSGK1) significantly inhibited the phosphorylation of mitogen-activated protein kinase kinase 1 (MEK1) and the downstream molecule extracellular signal regulated protein kinase (ERK) 1/2, which induced the upregulation of p53 and Bcl-2-associated X protein, mediating the subsequent cellular apoptosis and proliferation in IECs. Cells treated with MEK1 inhibitor (i.e., U0126) before siSGK1 transfection showed a reversal of the siSGK1-induced cellular apoptosis., Conclusion: Our data suggested that SGK1 may protect IECs in colitis from tumor necrosis factor-α-induced apoptosis partly by triggering MEK/ERK activation.