3-(4-Methoxy­phen­yl)-1-(2-nitrophen­yl)prop-2-en-1-one

The title compound, C16H13NO4, was prepared from 2-nitrylhypnone [systematic name: 1-(2-nitrophenyl)ethanone] and 4-methoxy­benzophenone by a Claisen–Schmidt condensation. The dihedral angle formed by the two benzene rings is 80.73 (2). The crystal packing is stabilized by inter­molecular C—H⋯O hydrogen bonds

3-(4-Fluoro­phen­yl)-1-(4-methoxy­phen­yl)prop-2-en-1-one

The title compound, C16H13FO2, was prepared from 4-methoxy­hypnone and 4-fluoro­benzophenone by Claisen–Schmidt condensation. All the bond lengths and bond angles are in normal ranges. The dihedral angle formed by the two benzene rings is 33.49 (2)°. The crystal packing is stabilized by inter­molecular C—H⋯O hydrogen-bonding inter­actions

1-[3-(2-Nitro­phen­yl)-5-phenyl-2-pyrazolin-1-yl]ethanone

The title compound, C17H15N3O3, was prepared from 1-(2-nitro­phen­yl)-3-phenyl­prop-2-en-1-one and hydrazine. The dihedral angle between the benzene and phenyl rings is 74.55 (2)°. The pyrazoline ring is in a slight envelope conformation with the C atom bonded to the phenyl ring forming the flap. In the crystal structure, weak inter­molecular C—H⋯O hydrogen bonds connect mol­ecules into chains along [100]

Tetra­imidazole­bis(trichloro­acetato)copper(II)

The title compound, [Cu(C2Cl3O2)2(C3H4N2)4], was prepared by the reaction of imidazole and trichloro­acetatocopper(II). The CuII atom adopts a distorted octa­hedral coordination geometry, binding the N atoms of four imidazole ligands and the carboxyl­ate O atoms of two trichloro­acetate anions. The mol­ecular structure and packing are stabilized by N—H⋯O hydrogen-bonding inter­actions. Close inter­molecular Cl⋯Cl contacts [3.498 (3) Å] are also found in the structure

(1R,1′S)-1,1′-Dihydr­oxy-1,1′-biisobenzofuran-3,3′(1H,1′H)-dione

In the title compound, C16H10O6, the complete mol­ecule is generated by a crystallographic centre of symmetry. In the crystal, O—H⋯O hydrogen bonds link the mol­ecules into (100) sheets and C—H⋯O links also occur

3-(5-Methyl-2-fur­yl)-1-(p-tol­yl)-2-propen-1-one

The title compound, C15H14O2, was prepared from 4-methyl­hypnone and 5-methyl­furfural by Clasion–Schmidt condensation. All of the bond lengths and bond angles are in normal ranges. The dihedral angle formed by the benzene ring and furan ring is 5.31 (2)

2,7-Dibromo-9,9-bis­[(pyridin-1-ium-4-yl)meth­yl]fluorene dinitrate

In the title compound, C25H20Br2N2 2+·2NO3 −, the cation lies on a twofold rotation axis which imposes disorder of the dibromo­fluorene unit. In addition, the unique nitrate anion is disordered over two general sites of equal occupancy. The crystal structure is stabilized by inter­molecular N—H⋯O hydrogen bonds

Modulation of epithelial sodium channel in human alveolar epithelial cells by lipoxin A4 through AhR-cAMP-dependent pathway

Purpose: To investigate the effect of lipoxin A4 (LXA4) on the expressions of protein and mRNA of alveolar epithelial sodium channel (ENaC) in normal and lipopolysaccharide (LPS)-stimulated A549 cells.Methods: A549 cell-lines were randomized into 11 groups (N = 8) and treated. EnaC level was evaluated by Western blot. Total RNA was extracted and reverse-transcribed and then levels of ENaC mRNA, cGMP and cAMP in the cells were determined.Results: LXA4 (10-7mol/L) increased the expressions of α-subunit of ENaC relative to LPS group. In addition, LXA4 significantly up-regulated the expression of mRNAs of α, β and γ subunits of ENaC (p < 0.01). The level of cAMP was increased in LXA4 group, but significantly reduced in LPS group relative to control group (p < 0.05). However, treatment with LXA4 annulled the increased cAMP concentration, compared with LPS group (p < 0.05)Conclusion: These results show that LXA4 influences ENaC up-regulation in normal and LPS stimulated A549 alveolar epithelial cells.Keywords: Acute lung injury, Alveolar epithelial sodium channel, Lipoxin A4, AhR, cAMP, cGM

The impacts of dietary sphingomyelin supplementation on metabolic parameters of healthy adults: a systematic review and meta-analysis of randomized controlled trials

BackgroundStudies have shown that sphingomyelin (SM) and its metabolites play signaling roles in the regulation of human health. Endogenous SM is involved in metabolic syndrome (MetS), while dietary SM supplementation may maintain lipid metabolism and prevent or alleviate MetS. Therefore, we hypothesized that dietary SM supplementation is beneficial for human health.AimsIn order to examine the impacts of dietary SM on metabolic indexes in adults without MetS, we performed a meta-analysis to test our hypothesis.MethodsA comprehensive search was performed to retrieve randomized controlled trials that were conducted between 2003 and 2023 to examine the effects of dietary SM supplementation on metabolic parameters in the Cochrane Library, PubMed, Web of Science, Embase, and ClinicalTrials.gov databases. RevMan 5.4 and Stata 14.0 software were used for meta-analysis, a sensitivity analysis, the risk of bias, and the overall quality of the resulted evidence.ResultsEventually, 10 articles were included in this meta-analysis. Dietary SM supplementation did not affect the endline blood SM level. When compared to the control, SM supplementation reduced the blood total cholesterol level [MD: −12.97, 95% CI: (−14.57, −11.38), p < 0.00001], low-density lipoprotein cholesterol level [MD: −6.62, 95% CI: (−10.74, −2.49), p = 0.002], and diastolic blood pressure [MD: −3.31; 95% CI (−4.03, −2.58), p < 0.00001] in adults without MetS. The supplementation also increased high-density lipoprotein level [MD:1.41, 95% CI: (0.94, 1.88), p < 0.00001] and muscle fiber conduction velocity [MD: 95% 1.21 CI (0.53, 1.88), p = 0.0005]. The intake of SM had no effect on the blood phospholipids and lyso-phosphatidylcholine, but slightly decreased phosphatidylcholine, phosphatidylethanolamine, and phosphatidylinositol concentrations. Dietary SM supplementation reduced insulin level [MD: −0.63; 95% CI (−0.96, −0.31), p = 0.0001] and HOMA-IR [MD: −0.23; 95% CI (−0.31, −0.16), p < 0.00001] without affecting blood levels of glucose and inflammatory cytokines.ConclusionOverall, dietary SM supplementation had a protective effect on blood lipid profiles and insulin level, but had limited impacts on other metabolic parameters in adults without MetS. More clinical trials and basic research are required.Systematic review registrationPROSPERO, identifier CRD42023438460

Etiological Analysis of Neurodevelopmental Disabilities: Single-Center Eight-Year Clinical Experience in South China

Etiology determination of neurodevelopmental disabilities (NDDs) currently remains a worldwide common challenge on child health. We herein reported the etiology distribution feature in a cohort of 285 Chinese patients with NDDs. Although concrete NDD etiologies in 48.4% of the total patients could not be identified, genetic diseases (with the proportion of 35.8% in the total cases) including inborn errors of metabolism (IEM) and congenital dysmorphic diseases, constituted the commonest etiology category for NDDs in this study. The two key experimental technologies in pediatric metabolomics, gas chromatography-mass spectrometry (GC-MS), and tandem mass spectrometry (MS-MS), proved to be substantially helpful for the exploration of the NDD etiologies in this clinical investigation. The findings in this paper provided latest epidemiologic information on the etiology distribution of NDDs in Chinese, and the syndromic NDDs caused by citrin deficiency and the novel chromosomal karyotype, respectively, further expanded the etiology spectrum of NDDs