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The value of using customized birth-weight centiles to improve the diagnostic accuracy for fetal growth restriction (FGR), in comparison with using population-based charts, remains a matter of debate. One potential explanation for the conflicting data is that most studies used measures of perinatal mortality and morbidity as proxies for placenta-mediated FGR, many of which are not specific and may be confounded by other factors such as prematurity. The aim of this study was to compare the diagnostic accuracy of small-for-gestational age (SGA) at birth, defined according to customized vs population-based charts, for associated abnormal placental pathology.
This was a secondary analysis of data from a prospective cohort study on risk factors for placenta-mediated complications and abnormal placental pathology in low-risk nulliparous women. All placentae were sent for detailed histopathological examination by two perinatal pathologists. The primary exposure was SGA, defined as birth weight < 10
centile d in Obstetrics and Gynecology.
These findings suggest that customized birth-weight centiles may be superior to population-based birth-weight centiles in detecting FGR that is due to underlying placental disease. © 2020 International Society of Ultrasound in Obstetrics and Gynecology.Long non-coding RNAs have important roles in the occurrence and progression of various cancers. However, the molecular mechanism of lncRNAs in colorectal cancer (CRC) is not well illustrated. Thus, we used bioinformatics methods to find potential lncRNAs associated with CRC progression, and chose SH3PXD2A-AS1 as a candidate for further analysis. The roles of SH3PXD2A-AS1 in CRC cells were determined by CCK-8, transwell invasion, wound healing and flow cytometry assays. Besides, we established the CRC tumor models in nude mice to study the effect of SH3PXD2A-AS1 on the tumor growth. Based on the ceRNA hypothesis, we used miRDB and miRTarBase websites to identify the SH3PXD2A-AS1-related ceRNA regulatory network, and measured the roles of this network in CRC cells. The results revealed that the expression profiles of SH3PXD2A-AS1 from GEO and TCGA databases showed an aberrant high level in CRC tissues compared with colorectal normal tissues. SH3PXD2A-AS1 over-expression was also found in CRC cells. SH3PXD2A-AS1 knockdown inhibited the CRC cellular proliferation, invasion and migration but induced apoptosis. Besides, SH3PXD2A-AS1 knockdown also suppressed the growth of CRC tumors. Furthermore, SH3PXD2A-AS1 could function as a ceRNA of miR-330-5p. Additionally, UBA2 was proved to be a target gene of miR-330-5p. Moreover, SH3PXD2A-AS1 knockdown downregulated UBA2 expression through sponging miR-330-5p to inactivate the Wnt/β-catenin signaling pathway, thereby inhibiting the cell growth and promoting apoptosis. Therefore, the SH3PXD2A-AS1/miR-330-5p/UBA2 network could regulate the progression of CRC through the Wnt/β-catenin pathway. These findings offer new sights for understanding the pathogenesis of CRC and provide potential biomarkers for CRC treatment.The innate immune system in the central nervous system (CNS) is mainly represented by specialized tissue-resident macrophages, called microglia. In the past years, various species-, host- and tissue-specific as well as environmental factors were recognized that essentially affect microglial properties and functions in the healthy and diseased brain. Host microbiota are mostly residing in the gut and contribute to microglial activation states, for example, via short-chain fatty acids (SCFAs) or aryl hydrocarbon receptor (AhR) ligands. Thereby, the gut microorganisms are deemed to influence numerous CNS diseases mediated by microglia. In this review, we summarize recent findings of the interaction between the host microbiota and the CNS in health and disease, where we specifically highlight the resident gut microbiota as a crucial environmental factor for microglial function as what we coin "the microbiota-microglia axis."Halide and phenyl substituted germaborenes were shown to react with azides at room temperature and transfer a borylene moiety to give iminoboranes. This iminoborane synthesis based on a borylene transfer route was investigated computationally in the case of the phenyl substituted germaborene.
Selective fetal growth restriction (sFGR) complicating twin to twin transfusion syndrome (TTTS) is associated with 3 to 6 fold increased risk of fetal demise after fetoscopic laser surgery (FLS). Identifying these patients is challenging due to varying definitions used in the literature. Our objective was to determine the association of three currently used definitions for sFGR with demise of the smaller twin, typically the donor, following FLS METHODS Retrospective cohort of monochorionic diamniotic pregnancies undergoing FLS for TTTS between January 2015 to December 2018. The entire cohort was classified as sFGR and non sFGR using 3 different criteria 1- International Society of Ultrasound in Obstetrics and Gynecology (ISUOG) as estimated fetal weight (EFW) of either twin < 10
centile and the intertwin discordance > 25% (Group A); 2- Delphi methods, EFW of either twin < 3
centile (Group B); 3 - Delphi method, presence of 2 of the 4 criteria EFW of either twin < 10
centile, abdominal circ, p = 0.02).
Fetal demise following FLS is increased in the presence of sFGR. Improving diagnosis of sFGR, will improve counseling and may affect management. Delphi method of defining sFGR based on presence of 2 of the 4 criteria had the highest predictive value of donor demise following FLS. This article is protected by copyright. All rights reserved.
Fetal demise following FLS is increased in the presence of sFGR. Improving diagnosis of sFGR, will improve counseling and may affect management. Delphi method of defining sFGR based on presence of 2 of the 4 criteria had the highest predictive value of donor demise following FLS. This article is protected by copyright. APIIIa4 All rights reserved.The synthesis and characterization of new bis(bipyridine)ruthenium(II) ferrocenyl β-diketonate complexes, [(bpy)2 Ru(Fc-acac)][PF6 ] (bpy=2,2'-bipyridine; Fc-acac=functionalized ferrocenyl β-diketonate ligand) are reported. Alongside clinical platinum drugs, these bimetallic ruthenium-iron complexes have been screened for their cytotoxicity against MIA PaCa-2 (human pancreatic carcinoma), HCT116 p53+/+ (human colon carcinoma, p53-wild type) and ARPE-19 (human retinal pigment epithelial) cell lines. With the exception of one complex, the library exhibit nanomolar potency against cancerous cell lines, and their relative potencies are up to 40x, 400x and 72x more cytotoxic than cisplatin, carboplatin and oxaliplatin, respectively. Under hypoxic conditions, the complexes remain cytotoxic (sub-micromolar range), highlighting their potential in targeting hypoxic tumor regions. The Comet assay was used to determine their ability to damage DNA, and results show dose dependent damage which correlates well with the cytotoxicity results.