GLUT1 exacerbates trophoblast ferroptosis by modulating AMPK/ACC mediated lipid metabolism and promotes gestational diabetes mellitus associated fetal growth restriction.

Background: Gestational diabetes mellitus (GDM) has been associated with several fetal complications, such as macrosomia and fetal growth restriction (FGR). Infants from GDM associated FGR are at increased risk for adult-onset obesity and associated metabolic disorders. However, the underlying mechanisms of GDM associated FGR remain to be explored.

Glucose uptake in trophoblasts of GDM mice is regulated by the AMPK-CLUT3 signaling pathway.

GDM, as a metabolic disease during pregnancy, regulates GLUT3 translocation by AMPK, thereby affecting glucose uptake in trophoblasts. It provides a new research idea and therapeutic target for alleviating intrauterine hyperglycemia in GDM. STZ was used to construct GDM mice, inject AICAR into pregnant mice, and observe fetal and placental weight; flow cytometry was employed for the detection of glucose uptake by primary trophoblast cells; immunofluorescence was applied to detect the localization of GLUT3 and AMPK in placental tissue; Cocofal microscope was used to detect the localization of GLUT3 in trophoblast cells;qRT-PCR and Western blot experiments were carried out to detect the expression levels of GLUT3 and AMPK in placental tissue; CO-IP was utilized to detect the interaction of GLUT3 and AMPK.

Blockade of C5a receptor unleashes tumor-associated macrophage antitumor response and enhances CXCL9-dependent CD8 T cell activity.

Macrophages play a crucial role in shaping the immune state within the tumor microenvironment (TME) and are often influenced by tumors to hinder antitumor immunity. However, the underlying mechanisms are still elusive. Here, we observed abnormal expression of complement 5a receptor (C5aR) in human ovarian cancer (OC), and identified high levels of C5aR expression on tumor-associated macrophages (TAMs), which led to the polarization of TAMs toward an immunosuppressive phenotype.

Altered distribution of fatty acid exerting lipid metabolism and transport at the maternal-fetal interface in fetal growth restriction.

Introduction: Fetal growth restriction (FGR) is a common complication of pregnancy. Lipid metabolism and distribution may contribute to the progression of FGR. However, the metabolism-related mechanisms of FGR remain unclear.

Somatic CG6015 mediates cyst stem cell maintenance and germline stem cell differentiation via EGFR signaling in Drosophila testes.

Stem cell niche is regulated by intrinsic and extrinsic factors. In the Drosophila testis, cyst stem cells (CySCs) support the differentiation of germline stem cells (GSCs). However, the underlying mechanisms remain unclear.

Wnt6 regulates the homeostasis of the stem cell niche via Rac1-and Cdc42-mediated noncanonical Wnt signalling pathways in Drosophila testis.

The homeostasis of the stem cell niche is regulated by both intrinsic and extrinsic factors, and the complex and ordered molecular and cellular regulatory mechanisms need to be further explored. In Drosophila testis, germline stem cells (GSCs) rely on hub cells for self-renewal and physical attachment. GSCs are also in contact with somatic cyst stem cells (CySCs).

CG8005 Mediates Transit-Amplifying Spermatogonial Divisions via Oxidative Stress in Testes.

The generation of reactive oxygen species (ROS) widely occurs in metabolic reactions and affects stem cell activity by participating in stem cell self-renewal. However, the mechanisms of transit-amplifying (TA) spermatogonial divisions mediated by oxidative stress are not fully understood. Through genetic manipulation of testes, we demonstrated that CG8005 regulated TA spermatogonial divisions and redox homeostasis.

RpS13 controls the homeostasis of germline stem cell niche through Rho1-mediated signals in the Drosophila testis.

Objectives: Stem cell niche regulated the renewal and differentiation of germline stem cells (GSCs) in Drosophila. Previously, we and others identified a series of genes encoding ribosomal proteins that may contribute to the self-renewal and differentiation of GSCs. However, the mechanisms that maintain and differentiate GSCs in their niches were not well understood.

Excessive reactive oxygen species induce apoptosis via the APPL1-Nrf2/HO-1 antioxidant signalling pathway in trophoblasts with missed abortion.

Aims: Previous evidence has demonstrated that oxidative stress is related to the pathogenesis of missed abortion (MA), but the specific mechanism remains obscure. The adaptor protein APPL1 is one of the differential proteins in chorionic trophoblasts. Thus, this study aimed to assess the potential influence of APPL1 on oxidative stress responses as well the possible molecular mechanisms involving in MA.

Systematic re-analysis strategy of serum indices identifies alkaline phosphatase as a potential predictive factor for cervical cancer.

The aim of the present study was to identify predictive factors for cervical cancer (CC) progression using a multistage approach. The present study obtained data from 390 healthy women and 259 patients with cervical cancer between June 2012 and June 2017, and used a multiple stage re-analysis strategy for clinical detection of CC. A total of seven types of serum indices were used in the present study, including sugar chain antigen 125 (CA-125), sugar chain antigen 199 (CA-199), α fetoprotein (AFP), carcino- embryonic antigen, alkaline phosphatase (ALP), cholesterol and triglyceride (TG).

Precursor RNA processing 3 is required for male fertility, and germline stem cell self-renewal and differentiation via regulating spliceosome function in Drosophila testes.

The nuclear pre-mRNA spliceosome is a large complex containing five small nuclear ribonucleoprotein particles (snRNPs) and many splicing factors. Messenger RNAs (mRNAs) are generated from pre-mRNAs by the process of RNA splicing, which is conserved in eukaryotes. Precursor RNA processing 3 (Prp3) is a U4/U6-associated snRNP whose function remains largely unknown.

Srlp is crucial for the self-renewal and differentiation of germline stem cells via RpL6 signals in Drosophila testes.

Self-renewal and differentiation in germline stem cells (GSCs) are tightly regulated by the stem cell niche and via multiple approaches. In our previous study, we screened the novel GSC regulatory gene Srlp in Drosophila testes. However, the underlying mechanistic links between Srlp and the stem cell niche remain largely undetermined.

Small ribonucleoprotein particle protein SmD3 governs the homeostasis of germline stem cells and the crosstalk between the spliceosome and ribosome signals in .

The ribonucleoprotein (RNP) spliceosome machinery triggers the precursor RNA splicing process in eukaryotes. Major spliceosome defects are implicated in male infertility; however, the underlying mechanistic links between the spliceosome and the ribosome in testes remains largely unresolved. Small ribonucleoprotein particle protein SmD3 (SmD3) is a novel germline stem cell (GSC) regulatory gene identified in our previous screen of testes.

ATP synthase is required for male fertility and germ cell maturation in Drosophila testes.

Germ cell maturation is essential for spermatogenesis and testis homeostasis. ATP synthase serves significant roles in energy storage in germ cell survival and is catalyzed by alterations in the mitochondrial membrane proton concentration. The intrinsic cellular mechanisms governing stem cell maturation remain largely unknown.

Biochemical clinical factors associated with missed abortion independent of maternal age: A retrospective study of 795 cases with missed abortion and 694 cases with normal pregnancy.

The incidence of fertile women with missed abortion dramatically increased in recent years, while very few serum indices have been identified for the diagnosis of missed abortion. The aim of this study was to identify related factors for missed abortion through a retrospective study of serum indices.A total of 795 cases of women with missed abortion and 694 cases of women with normal pregnancy between March 2014 and March 2017 were included in the present study.

Activation of β-catenin causes defects in embryonic development during maternal-to-zygotic transition in mice.

The early stage of embryogenesis is an important and complex cell-remodeling event in reproductive biology. To develop into a normal zygote, maternal-to-zygotic transition (MZT) is especially important for both zygotic genome activation (ZGA) and degradation of maternal products during the early stage of embryonic development. β-Catenin has been identified as an important regulator of embryonic development and adult stem cell division via the canonical Wnt/β-catenin signalling pathway.

Correlation between NM23 protein overexpression and prognostic value and clinicopathologic features of ovarian cancer: a meta-analysis.

Objective: The prognostic value and clinicopathological features of NM23 (non-metastasis 23) have previously been assessed, but the results are controversial. Here, we attempted to clarify the correlation between NM23 expression and its prognostic value and the clinicopathological features in ovarian cancer (OC).

Methods: The relevant studies were identified using PubMed, Embase, and Web of Science.