ChemInform Abstract: The Monoclinic Form of Trilithium Dichromium(III) Tris(orthophosphate).

Monoclinic Li₃Cr₂(PO₄)₃ is prepared by melting equimolar amounts of Cr and P in a reactive LiCl/CsCl (4:1) flux (reactant/flux ratio of 1:3, evacuated silica tube, 1123 K, 2 d, 4 K/h cooling rate).     

Dexamethasone Attenuates Oncostatin M Production via Suppressing of PI3K/Akt/NF-κB Signaling in Neutrophil-like Differentiated HL-60 Cells

Oncostatin M (OSM) plays a role in various inflammatory reactions, and neutrophils are the main source of OSM in pulmonary diseases. However, there is no evidence showing the mechanism of OSM production in neutrophils. While dexamethasone (Dex) has been known to exert anti-inflammatory activity in various fields, the precise mechanisms of OSM downregulation by Dex in neutrophils remain to be determined. Here, we examined how OSM is produced in neutrophil-like differentiated HL-60 cells. Enzyme-linked immunosorbent assay, real-time polymerase chain reaction, and Western blot analysis were utilized to assess the potential of Dex. Granulocyte-macrophage colony-stimulating factor (GM-CSF) stimulation resulted in OSM elevation in neutrophil-like dHL-60 cells. OSM elevation induced by GM-CSF is regulated by phosphatidylinositol 3-kinase (PI3K)/Akt/nuclear factor (NF)-kB signal cascades. GM-CSF stimulation upregulated phosphorylated levels of PI3K or Akt or NF-κB in neutrophil-like dHL-60 cells. Treatment with Dex decreased OSM levels as well as the phosphorylated levels of PI3K or Akt or NF-κB in neutrophil-like dHL-60 cells. Our findings show the potential of Dex in the treatment of inflammatory diseases via blocking of OSM.     

Synergistic induction of cancer cell migration regulated by Gβγ and phosphatidylinositol 3-kinase

Phosphatidylinositol 3-kinase (PI3K) is essential for both G protein-coupled receptor (GPCR)- and receptor tyrosine kinase (RTK)-mediated cancer cell migration. Here, we have shown that maximum migration is achieved by full activation of phosphatidylinositol 3,4,5-trisphosphate-dependent Rac exchanger 1 (P-Rex1) in the presence of Gβγ and PI3K signaling pathways. Lysophosphatidic acid (LPA)- induced migration was higher than that of epidermal growth factor (EGF)-induced migration; however, LPA-induced activation of Akt was lower than that stimulated by EGF. LPA-induced migration was partially blocked by either Gβγ or RTK inhibitor and completely blocked by both inhibitors. LPA-induced migration was synergistically increased in the presence of EGF and vice versa. In correlation with these results, sphingosine-1-phosphate (S1P)-induced migration was also synergistically induced in the presence of insulin-like growth factor-1 (IGF-1). Finally, silencing of P-Rex1 abolished the synergism in migration as well as in Rac activation. Moreover, synergistic activation of MMP-2 and cancer cell invasion was attenuated by silencing of P-Rex1. Given these results, we suggest that P-Rex1 requires both Gβγ and PI3K signaling pathways for synergistic activation of Rac, thereby inducing maximum cancer cell migration and invasion.     

ChemInform Abstract: (Sr1-xBax)FeO2 (0.4 ≤ x ≤ 1): A New Oxygen-Deficient Perovskite Structure.

The new oxygen-deficient perovskites of title are prepared by reaction of (Sr_1-xBa_x)FeO_3-δ (x = 0.4, 0.5, 0.6, 0.7, 0.8, 0.9; δ ≤ 0.5; obtained from stoichiometric mixtures of SrCO₃, BaCO₃, and Fe₂O₃ at 1473 K in air for 48 h) with an excess of CaH₂ at 593 K for 3—14 d (0.4 ≤ x ≤ 0.9) and NaH at 413 K for 3 d (x = 1.0).     

6,7,4′-Trihydroxyflavanone Mitigates Methamphetamine-Induced Neurotoxicity in SH-SY5y Cells via Nrf2/heme Oxyganase-1 and PI3K/Akt/mTOR Signaling Pathways

Methamphetamine (METH) is a synthetic psychostimulant drug that has detrimental effects on the health of its users. Although it has been investigated as a cause of neurodegenerative disease due to its neurotoxicity, whether small molecules derived from natural products attenuate these side effects remains elusive. 6,7,4′-trihydroxyflavanone (THF) is a flavanone family that possesses various pharmacological activities, including anti-rheumatic, anti-ischemic, anti-inflammatory, anti-osteoclastogenic, and protective effects against METH-induced deactivation of T cells. However, little is known about whether THF protects neuronal cells from METH-induced neurotoxicity. Here, we investigated the protective effects of THF on neurotoxicity induced by METH exposure by enhancing the Nrf2/HO-1 and PI3K/Akt/mTOR signaling pathways in SH-SY5y cells. Treatment with THF did not lead to cytotoxicity, but attenuated METH-induced neurotoxicity by modulating the expression of apoptosis-related proteins, METH-induced oxidative stress, and PI3K/Akt/mTOR phosphorylation in METH-exposed SH-SY5y cells. Moreover, we found THF induced Nrf2 nuclear translocation and HO-1 expression. An inhibitor assay confirmed that the induction of HO-1 by THF attenuates METH-induced neurotoxicity. Therefore, we suggest that THF preserves neuronal cells from METH-induced neurotoxicity by upregulating HO-1 expression through the Nrf2 and PI3K/Akt/mTOR signaling pathways. Thus, THF has therapeutic potential for use in the treatment of METH-addicts suffering from neurodegenerative diseases.     

IR spectroscopic study of the interaction between trimethylgallium and arsine in the liquid phase

The formation of a donor-acceptor complex Me₃Ga · AsH₃ in a solution in liquid krypton at 130 K and in a binary liquid solution of those substances at 263 K was established by IR spectroscopy. In the latter case, Me₃Ga and AsH₃ react at an appreciable rate to form an amorphous product of composition Me_3-x ,GaAsH_3-x .Translated fromIzvestiya Akademii Nauk. Seriya Khimicheskaya, No. 9, pp. 2259–2262, September, 1996.     

ChemInform Abstract: Tetrayttrium Difluoride Disilicate Orthosilicate,Y4F2[Si2O7][SiO4].

Colorless lath-shaped single crystals of the title compound are obtained from a melt of Y₂O₃, YF₃, and SiO₂ (2:5:3 molar ratio) using CsCl as a flux (evacuated silica tube, 973 K, 9 d, 10 K/h cooling rate).     

ChemInform Abstract: Supertetrahedral Networks and Lithium‐Ion Mobility in Li2SiP2 and LiSi2P3.

Polycrystalline Li₂SiP₂ (I) and LiSi₂P₃ (II) are prepared by solid state reaction of stoichiometric amounts of the elements at 1123 K and 1223 K (II), resp.     

ChemInform Abstract: Identification of Diborane(4) with Bridging B—H—B Bonds.

Photolysis of B₂H₆ dispersed in solid neon with far‐UV light (120—220 nm) at 3 K leads to the formation of B₂H₄, which is characterized by IR spectroscopy and B3LYP quantum chemical computations.     

ChemInform Abstract: Barium Dierbium(III) Tetrasulfide.

Orange needles of BaEr₂S₄ are obtained during an investigation of the Ba/Er/U/S system by solid state reaction of a mixture of ²³⁸U, Er, BaS, and S in the ratio 1:1:3:3 (evacuated C‐coated fused silica tube, 1273 K, 8 d, cooling rate 3 K/h) together with black crystals of Sb₂S₃ and US₂.     

ChemInform Abstract: Redetermination of Na3TaF8.

The crystal structure of Na₃TaF₈ is redetermined at 153 K and well determined bond distances and angles are provided.     

Resveratrol Enhances Inhibition Effects of Cisplatin on Cell Migration and Invasion and Tumor Growth in Breast Cancer MDA-MB-231 Cell Models In Vivo and In Vitro

Triple-negative breast cancer (TNBC) is a refractory type of breast cancer that does not yet have clinically effective drugs. The aim of this study is to investigate the synergistic effects and mechanisms of resveratrol combined with cisplatin on human breast cancer MDA-MB-231 (MDA231) cell viability, migration, and invasion in vivo and in vitro. In vitro, MTS assays showed that resveratrol combined with cisplatin inhibits cell viability as a concentration-dependent manner, and produced synergistic effects (CI < 1). Transwell assay showed that the combined treatment inhibits TGF-β1-induced cell migration and invasion. Immunofluorescence assays confirmed that resveratrol upregulated E-cadherin expression and downregulated vimentin expression. Western blot assay demonstrated that resveratrol combined with cisplatin significantly reduced the expression of fibronectin, vimentin, P-AKT, P-PI3K, P-JNK, P-ERK, Sma2, and Smad3 induced by TGF-β1 (p < 0.05), and increased the expression of E-cadherin (p < 0.05), respectively. In vivo, resveratrol enhanced tumor growth inhibition and reduced body weight loss and kidney function impairment by cisplatin in MDA231 xenografts, and significantly reduced the expressions of P-AKT, P-PI3K, Smad2, Smad3, P-JNK, P-ERK, and NF-κB in tumor tissues (p < 0.05). These results indicated that resveratrol combined with cisplatin inhibits the viability of breast cancer MDA231 cells synergistically, and inhibits MDA231 cells invasion and migration through Epithelial-mesenchymal transition (EMT) approach, and resveratrol enhanced anti-tumor effect and reduced side of cisplatin in MDA231 xenografts. The mechanism may be involved in the regulations of PI3K/AKT, JNK, ERK and NF-κB expressions.     

On the matrix effect in the determination of main components of dolomite by atomic flame emission and absorption spectrometry

Summary The matrix effects in the determination of the main components of dolomite by flame emission (Na, K) and atomic absorption spectrometry (Ca, Mg, Fe, Mn) have been examined according to the methodology based on the theory of design of experiments. The influence of some auxiliary compounds added to a sample solution has been investigated. The determination of Fe and Mn proved to be specific. The matrix effect has been eliminated in the determination of K by adding a mixture of NaCl and H₃PO₄, in the determination of Na by KCl spectral buffer, in the determination of Mg by NaCl buffer and in the case of Ca by SrCl₂ as a spectral buffer.

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Untersuchung über den Matrixeffekt bei der Bestimmung der Hauptbestandteile von Dolomit durch Atomemissions- und -absorptionsspektrometrie

Zusammenfassung Mit Hilfe methodisch geplanter Versuche wurde der Einfluß der Matrix auf die Bestimmung von Na und K (Emission) sowie Ca, Mg, Fe und Mn (Absorption) untersucht. Ebenso wurde der Einfluß verschiedener Zusätze geprüft. Die Bestimmung von Fe und Mn erwies sich als spezifisch. In den anderen Fällen konnte die Matrixstörung durch folgende Zusätze behoben werden: Gemisch von NaCl und H₃PO₄ für K, KCl für Na, NaCl für Mg, SrCl₂ für Ca.

     

Study of phase separation in polyurethane using paramagnetic labels. Effect of soft segment molecular weight,structure, and thermal history

The morphology of segmented polyurethane (PU) elastomers was studied by means of ESR at various temperatures ranging from 100K-450K. The PU's were based on 4,4'-diphenylmethane diisocyanate (MDI), poly (oxytetramethylene) glycols (PTMO) and hydroxyl-terminated random compolymers of tetrahydrofuran and 3-methyl-tetrahydrofuran (THF/Me-THF). Purified 1,4-butanediol (BD) was used as a chain extender. The nitroxide probe, 4-hydroxy-2-2',6-6'-tetramethylpiperidine-1-oxyl (TEMPOL), was used to label the polyurethanes by reaction with an NCO group of MDI. Analysis of the electron spin resonance (ESR) spectra suggested that the label situates at heterogeneous sites, which means that a two-phase domain is present. The morphologies at 300K and 400K were compared. It was found from ESR spectra that polyurethanes made from soft segments having higher MW exhibited greater phase separation at 300K than their corresponding elastomers made from lower MW soft segments. However, at 400K the more isotropic ESR spectra for the PUs containing higher MW soft segments suggested that the PUs were more mobile than their analogs having lower MW soft segments. The introduction of 3-methyl side groups decreased the phase mixing at 400K due to steric hindrance.     

Protective Effects of Jujubosides on 6-OHDA-Induced Neurotoxicity in SH-SY5Y and SK-N-SH Cells

6-hydroxydopamine (6-OHDA) is used to induce oxidative damage in neuronal cells, which can serve as an experimental model of Parkinson’s disease (PD). Jujuboside A and B confer free radical scavenging effects but have never been examined for their neuroprotective effects, especially in PD; therefore, in this study, we aimed to investigate the feasibility of jujubosides as protectors of neurons against 6-OHDA and the underlying mechanisms. 6-OHDA-induced neurotoxicity in the human neuronal cell lines SH-SY5Y and SK-N-SH, was used to evaluate the protective effects of jujubosides. These findings indicated that jujuboside A and B were both capable of rescuing the 6-OHDA-induced loss of cell viability, activation of apoptosis, elevation of reactive oxygen species, and downregulation of the expression levels of superoxide dismutase, catalase, and glutathione peroxidase. In addition, jujuboside A and B can reverse a 6-OHDA-elevated Bax/Bcl-2 ratio, downregulate phosphorylated PI3K and AKT, and activate caspase-3, -7, and -9. These findings showed that jujubosides were capable of protecting both SH-SY5Y and SK-N-SH neuronal cells from 6-OHDA-induced toxicity via the rebalancing of the redox system, together with the resetting of the PI3K/AKT apoptotic signaling cascade. In conclusion, jujuboside may be a potential drug for PD prevention.     

ChemInform Abstract: Two New Compounds, β-ScTe and Y3Au2, and a Reassessment of Y2Au.

The title compounds are prepared by solid state reaction of the elements (Ta containers; 1573 K, 200 h for β-ScTe and 1323 K, 7 d for Y₃Au₂ and Y₂Au).     

ChemInform Abstract: Synthesis and Crystal Structure of the A6B5O18 Perovskite-Like Compounds.

Single phase Ba₅KNb₅O₁₈ (I) is prepared by solid state reaction of Ba₅Nb₄O₁₅ and KNbO₃ (1370 K, 2 h), while Sr₆Nb₄SnO₁₈ (II) results from calcination of the coprecipitated metal hydroxycarbonates (1570 K, 2 h).     

ChemInform Abstract: On Squaring Triangles — Structural Motifs in Cu—In—Sb Compounds.

Two new compounds, Cu₇In_2.5Sb_0.5 (I) and Cu₂In_0.75Sb_0.25 (II) are prepared from the elements (silica ampules, 1173 K, 3 d, followed by annealing at 573—773 K for 220 d).     

ChemInform Abstract: Synthesis and Characterization of a Disordered Variant of KB5O7(OH)2.

The title compound is hydrothermally synthesized from a mixture of KNO₃, B₂O₃, and Ce(NO₃)₃·6H₂O with a molar ratio of 1:1:0.07 (autoclave, 513 K, 3 d).