AEBP1 upregulation contributes to cervical cancer progression by facilitating cell proliferation, migration, and invasion.

Background: Aberrant expression of adipocyte enhancer-binding protein 1 (AEBP1) has been demonstrated to be involved in the tumorigenesis and progression of numerous cancers. This study was aimed to investigate the mechanism of AEBP1 in the development of cervical cancer.

Methods: The expression of AEBP1 in cervical cancer was assessed by immunohistochemistry.

GLP1R boosts survival, migration and invasion of endometrial cancer cells and protects against ferroptotic cell death.

Background: Despite the strong evidence concerning carcinogenic roles of glucagon-like peptide 1 receptor (GLP1R), the role of this gene in endometrial cancer (EC) remains elusive. This study investigated the properties of GLP1R on EC .

Methods: The expression of GLP1R in EC was detected by RT-qPCR, immunohistochemistry, and western blotting.

Effects of metalloprotease ADAMTS12 on cervical cancer cell phenotype and its potential mechanism.

ADAMTS12 is a gene widely expressed in human tissues. We studied the expression level of ADAMTS12 in cervical cancer tissue and its relationship with clinicopathological features. We also explored the function of ADAMTS12 in cervical cancer cells and its underlying mechanisms.

Suppressing electron-phonon coupling in organic photovoltaics for high-efficiency power conversion.

The nonradiative energy loss (∆E) is a critical factor to limit the efficiency of organic solar cells. Generally, strong electron-phonon coupling induced by molecular motion generates fast nonradiative decay and causes high ∆E. How to restrict molecular motion and achieve a low ∆E is a sticking point.

Paeonol ameliorates endometrial hyperplasia in mice via inhibiting PI3K/AKT pathway-related ferroptosis.

Background: Paeonol (Pae) is one of the active ingredients from components of Guizhi Fuling Capsule, a traditional Chinese medicine widely used for the treatment of women's diseases, which exhibits various biological and pharmacological activities.

Purpose: The objective of this study was to investigate the molecular mechanism underlying the role of Pae in protecting against endometrial hyperplasia (EH).

Methods: CCK-8 assay was performed to detect the effect of Pae on cell proliferation.

GLP1R inhibits the progression of endometrial carcinoma through activation of cAMP/PKA pathway.

Background: This study strived to explore the role and mechanism of glucagon-like peptide-1 receptor (GLP1R) in endometrial carcinoma (EC).

Methods: In detail, after transfection of GLP1R overexpression vector and small interfering RNA targeting PKA, the mRNA expressions of GLP1R and PKA in EC cells (Ishikawa and RL95-2) were quantified by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The cell biological behaviors, including proliferation, migration, invasion, and apoptosis, were detected using 5-ethynyl-2'-deoxyuridine (EdU), wound healing, transwell, and flow cytometry assays, respectively.

Analysis on clinical association of uterine scar diverticulum with subsequent infertility in patients underwent cesarean section.

To evaluate the relationship between uterine cesarean scar diverticulum (CSD) and subsequent infertility in patients who underwent cesarean section, and determine the effects of pelvic fluid-releasing inflammations on infertility.A retrospective analysis was designed among patients with CSD who were admitted to our hospital from January 1, 2018 to December 31, 2019. A total of 60 patients with CSD and uterine fibroids or benign ovarian tumors who underwent cesarean section were included, and divided into the CSD group and control group.

Analysis of risk factors for cesarean scar diverticulum: A STROBE-compliant case-control study.

The purpose of this study was to explore the relevant factors that affect the risk of cesarean scar diverticulum (CSD).A retrospective, case-control study was designed among women with a history of cesarean section (CS) who were admitted in Zhejiang Tongde Hospital from January 2017 to December 2019. Women with missing information were excluded.

Guizhi Fuling Capsule ameliorates endometrial hyperplasia through promoting p62-Keap1-NRF2-mediated ferroptosis.

Ethnopharmacological Relevance: Guizhi Fuling Capsule (GFC) is a classical traditional Chinese medicine officially recorded in Synopsis of the Golden Chamber and has long been used to treat gynecological diseases in China. However, scientific evidence for the anti-endometrial hyperplasia potential of GFC used in traditional medicine is lacking.

Aim Of The Study: This study evaluated whether GFC protects against endometrial hyperplasia and its potential mechanism in mice.

Curcumin analogue AI-44 alleviates MSU-induced gouty arthritis in mice via inhibiting cathepsin B-mediated NLRP3 inflammasome activation.

NOD-like receptors (NLRs), as a part of intracellular pattern recognition receptors (PRR), are important regulators in innate immune system. The NLRP3 inflammasome which is a member of NLRs has been linked to several human inflammatory diseases. Gouty arthritis is triggered when the deposition of monosodium urate (MSU) crystals in joints induces acute inflammation characterized by the recruitment of macrophages and neutrophils.

Laparoscopic repair with hysteroscopy of cesarean scar diverticulum.

Aim: The aim of this study was to investigate the clinical data of laparoscopic repair with hysteroscopy of cesarean scar diverticulum (CSD).

Methods: We retrospectively evaluated 49 patients with CSD in our hospital who had undergone laparoscopic repair with hysteroscopy from January 2014 to June 2015. All patients had a history of cesarean section deliveries and prolonged postmenstrual spotting (duration 16.

[Protective effects and its mechanism of lipoxins on human umbilical vein endothelial cells under hypoxia].

Objective: To investigate protective effects and mechanisms of lipoxinA(4) (LXA(4)) on human umbilical vein endothelial cells (HUVEC) under hypoxia in vitro.

Methods: The HUVEC culture were divided into groups as followed: added M199 culture medium as normal control groups, added CoCl2 to mimic hypoxia in vitro as hypoxia group and added different concentrations of LXA(4) (1, 10, 100 nmol/L) were added to the induced hypoxial HUVEC as agents intervention group. Morphological changes of HUVEC were observed by using inverted phase contrast microscope.

Effects of lipoxin A(4) on CoCl(2)-induced angiogenesis and its possible mechanisms in human umbilical vein endothelial cells.

Lipoxin A(4) (LXA(4)), a 'stop signal' for inflammation, is endogenously produced by eicosanoids, mainly via cell-to-cell interactions. At present, its influence on hypoxic angiogenesis, which is responsible for tumor growth and metastasis, has not been determined. Hypoxia regulates a variety of transcription factors including hypoxia-inducible factor (HIF)-1alpha, which plays a role in the expression of vascular endothelial growth factor (VEGF) and is considered a target for anti-angiogenic therapy.

Formyl-peptide receptor like 1: a potent mediator of the Ca2+ release-activated Ca2+ current ICRAC.

In electrically non-excitable cells, one major source of Ca(2+) influx is through the store-operated (or Ca(2+) release-activated Ca(2+)) channel by which the process of emptying the intracellular Ca(2+) stores results in the activation of Ca(2+) channels in the plasma membrane. Using both whole-cell patch-clamp and Ca(2+) imaging technique, we describe the electrophysiology mechanism underlying formyl-peptide receptor like 1 (FPRL1) linked to intracellular Ca(2+) mobilization. The FPRL1 agonists induced Ca(2+) release from the endoplasmic reticulum and subsequently evoked I(CRAC)-like currents displaying fast inactivation in K562 erythroleukemia cells which expresses FPRL1, but had almost no effect in K562 cells treated with FPRL1 RNA-interference and HEK293 cells which showed no FPRL1 expression.