(E)-3-(9-Anthr­yl)-1-(4-fluoro­phen­yl)-2-(1H-1,2,4-triazol-1-yl)prop-2-en-1-one

The C=C double-bond in the title compound, C25H16FN3O, has an E configuration. The dihedral angle between the fluoro­phenyl and triazole rings is 80.57 (2)°

Aspirin protects against preeclampsia via p38MAPK signaling pathway

Purpose: To investigate the protective effect of aspirin against preeclampsia and the involvement of p38MAPK signaling pathway in the process.Methods: Sixty pregnant women who underwent antenatal care and delivery at Chancheng Central Hospital from September 2020 to September 2022 were selected and equally assigned to control group (CG) and experimental group (EG). From the 12th week of gestation, EG was administered 100 mg of aspirin and 1000 mg of calcium carbonate daily, while CG was given only 1000 mg of calcium carbonate daily. Both groups were treated up to the 35th week of gestation. Thereafter, blood samples were taken for measurement of serum levels of p38MAPK. In addition, the blood pressure of the women was measured. The incidence of preeclampsia and maternal-infant outcomes were assessed.Results: EG had a lower p38MAPK level at week 35 of pregnancy, and lower blood pressure levels at the 27th and 35th weeks of gestation, than CG (p < 0.05). There were 5 cases of preeclampsia (16.7 %) in EG, and 13 cases (43.3 %) of preeclampsia in CG, with a lower incidence of preeclampsia in EG than in CG (ꭓ2 = 5.079, p < 0.05). The numbers of newborns through premature delivery and cesarean section, as well as Apgar score ≤ 7 were lower in EG than in CG (p < 0.05).Conclusion: Aspirin exerts a protective effect against preeclampsia through via p38MAPK signaling pathway. Therefore, aspirin treatment may be useful in reducing the incidence of preeclampsia and improving maternal-infant outcomes. However, further clinical trials are recommended prior to application in clinical practice

Complexity measures and uncertainty relations of the high-dimensional harmonic and hydrogenic systems

In this work we find that not only the Heisenberg-like uncertainty products and the R\'enyi-entropy-based uncertainty sum have the same first-order values for all the quantum states of the $D$-dimensional hydrogenic and oscillator-like systems, respectively, in the pseudoclassical ($D \to \infty$) limit but a similar phenomenon also happens for both the Fisher-information-based uncertainty product and the Shannon-entropy-based uncertainty sum, as well as for the Cr\'amer-Rao and Fisher-Shannon complexities. Moreover, we show that the LMC (L\'opez-Ruiz-Mancini-Calvet) and LMC-R\'enyi complexity measures capture the hydrogenic-harmonic difference in the high dimensional limit already at first order

Molecular cytogenetic analyses of Epinephelus bruneus and Epinephelus moara (Perciformes, Epinephelidae)

Genus Epinephelus (Perciformes, Epinephelidae), commonly known as groupers, are usually difficult in species identification for the lack and/or change of morphological specialization. In this study, molecular cytogenetic analyses were firstly performed to identify the closely related species Epinephelus bruneus and E. moara in this genus. The species-specific differences of both fish species showed in karyotype, chromosomal distribution of nucleolar organizer regions (NORs) and localization of 18S rDNA. The heterochromatin (interstitial C-bands) and distribution pattern of telomere (TTAGGG)n in E. bruneus revealed the chromosomal rearrangements and different karyotypic evolutionary characteristics compared to those in E. moara. The cytogenetic data suggested that the lineages of E. bruneus and E. moara were recently derived within the genus Epinephelus, and E. moara exhibited more plesiomorphic features than E. bruneus. All results confirmed that E. moara, which has long been considered a synonym of E. bruneus, is a distinct species in the family Epinephelidae. In addition, molecular cytogenetic analyses are useful in species differentiation and phylogenetic reconstruction in groupers

HDAC3-Dependent Epigenetic Pathway Controls Lung Alveolar Epithelial Cell Remodeling and Spreading via miR-17-92 and TGF-β Signaling Regulation

SummaryThe terminal stages of pulmonary development, called sacculation and alveologenesis, involve both differentiation of distal lung endoderm progenitors and extensive cellular remodeling of the resultant epithelial lineages. These processes are coupled with dramatic expansion of distal airspace and surface area. Despite the importance of these late developmental processes and their relation to neonatal respiratory diseases, little is understood about the molecular and cellular pathways critical for their successful completion. We show that a histone deacetylase 3 (Hdac3)-mediated epigenetic pathway is critical for the proper remodeling and expansion of the distal lung saccules into primitive alveoli. Loss of Hdac3 in the developing lung epithelium leads to a reduction of alveolar type 1 cell spreading and a disruption of lung sacculation. Hdac3 represses miR-17-92 expression, a microRNA cluster that regulates transforming growth factor β (TGF-β) signaling. De-repression of miR-17-92 in Hdac3-deficient lung epithelium results in decreased TGF-β signaling activity. Importantly, inhibition of TGF-β signaling and overexpression of miR-17-92 can phenocopy the defects observed in Hdac3 null lungs. Conversely, loss of miR-17-92 expression rescues many of the defects caused by loss of Hdac3 in the lung. These studies reveal an intricate epigenetic pathway where Hdac3 is required to repress miR-17-92 expression to allow for proper TGF-β signaling during lung sacculation

Activation of the Extracellular Signal-Regulated Kinase Signaling Is Critical for Human Umbilical Cord Mesenchymal Stem Cell Osteogenic Differentiation

Human umbilical cord mesenchymal stem cells (hUCMSCs) are recognized as candidate progenitor cells for bone regeneration. However, the mechanism of hUCMSC osteogenesis remains unclear. In this study, we revealed that mitogen-activated protein kinases (MAPKs) signaling is involved in hUCMSC osteogenic differentiation in vitro. Particularly, the activation of c-Jun N-terminal kinases (JNK) and p38 signaling pathways maintained a consistent level in hUCMSCs through the entire 21-day osteogenic differentiation period. At the same time, the activation of extracellular signal-regulated kinases (ERK) signaling significantly increased from day 5, peaked at day 9, and declined thereafter. Moreover, gene profiling of osteogenic markers, alkaline phosphatase (ALP) activity measurement, and alizarin red staining demonstrated that the application of U0126, a specific inhibitor for ERK activation, completely prohibited hUCMSC osteogenic differentiation. However, when U0126 was removed from the culture at day 9, ERK activation and osteogenic differentiation of hUCMSCs were partially recovered. Together, these findings demonstrate that the activation of ERK signaling is essential for hUCMSC osteogenic differentiation, which points out the significance of ERK signaling pathway to regulate the osteogenic differentiation of hUCMSCs as an alternative cell source for bone tissue engineering. Copyright © 2016 Chen-Shuang Li et al

Ustekinumab treats psoriasis by suppressing RORC and T-box but its suppression of GATA restrains its efficacy

Psoriasis is a T-cell mediated disease that involves IL-23/Th17 and IL-12/Th1 axes. Ustekinumab, a fully human monoclonal antibody targeting the p40 subunit of both IL-12 and IL-23, has proven to be efficient and safe for treating patients with psoriasis. Yet, there have been no reports with human skin/blood samples that would elucidate the molecular mechanisms by which ustekinumab calms psoriasis skin lesions. To investigate the efficacy and molecular pathway (RORC, t-BOX and GATA) of ustekinumab in treating patients with psoriasis skin lesions. A total of 30 patients with psoriasis were randomized into placebo group and treatment group. PASI of each patient was calculated at 0, 12 and 24 weeks post-treatment. The mRNA levels of RORC, t-BOX and GATA in peripheral blood mononuclear cells separated from patients’ whole blood were analyzed using qPCR. Decreased mRNA of RORC, t-BOX and GATA were observed after continuous injections, indicating that ustekinumab exerts its effect by interacting with these molecules; while no significant difference in foxp3 mRNA levels were found between placebo group and treatment group