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Fetal abdominal subcutaneous soft tissue thickness (FASSTT) is a key indicator in evaluating fetal growth, development, and nutritional status. Currently, manual measurement in FASSTT faces the problems of difficulty in positioning, time consumption, and inaccurate measurement. Therefore, this article proposes an automatic measurement scheme for FASSTT. Firstly, a U‐shaped attention network VGG‐SeUnet is proposed to automatically segment the subcutaneous soft tissue area of the fetal abdomen. Secondly, based on the segmentation results, a morphological method is proposed to obtain FASSTT. Specifically, the segmentation network uses VGG16 as the encoder and connects the decoder through jump connections for multi‐scale fusion. We introduce channel attention to jump connections, which enables the model to select key channels for feature fusion. At the same time, the model uses the proposed DF_Loss function for training to solve the problem of sample imbalance. Based on the segmentation results, a morphological distance transformation algorithm is proposed to obtain FASSTT by drawing the maximum inscribed circle and calculating its diameter. The method is evaluated on a fetal abdominal circumference ultrasound dataset containing 135 samples. The DSC, mIOU, mPA, Precision and Recall of the segmentation experiments reache 88.9%, 81.02%, 90.44%, 86.38%, and 90.44% respectively. The difference between FASSTT's result from that provided by radiologist is 0.0615 cm in Average Error (AVE) and 0.081 cm in Root Mean Square Error (RMSE). The overall performance of this algorithm is superior to existing methods with excellent performance, and the measurement error is less than 1 millimeter. This result proves that the proposed scheme in this paper can achieve automated measurement of FASSTT and assist doctors in subsequent evaluation of fetal development and nutritional status. [ABSTRACT FROM AUTHOR]

Osteoarthritis (OA) is a prevalent and disabling disease that affects a significant proportion of the global population. Urine-derived stem cells (USCs) have shown great prospects in the treatment of OA, but there is no study that has compared them with traditional stem cells.This study aimed to compare the therapeutic efficacy and mechanisms of USCs and adipose-derived stem cells (ADSCs) for OA treatment.Controlled laboratory study.We compared the biological properties of USCs and ADSCs using CCK-8, colony formation, EdU, adhesion, and apoptosis assays. We evaluated the protective effects of USCs and ADSCs on IL-1β–treated OA chondrocytes by chemical staining, immunofluorescence, and Western blotting. We assessed the effects of USCs and ADSCs on chondrocyte autophagy by transmission electron microscopy, immunofluorescence, and Western blotting. We also compared the therapeutic efficacy of intra-articular injections of USCs and ADSCs by gross, histological, micro–computed tomography, and immunohistochemical analyses in an OA rat model induced by anterior cruciate ligament transection.USCs showed higher proliferation, colony formation, DNA synthesis, adhesion, and anti-apoptotic abilities than ADSCs. Both USCs and ADSCs increased the expression of cartilage-specific proteins and decreased the expression of matrix degradation–related proteins and inflammatory factors in OA chondrocytes. USCs had a greater advantage in suppressing MMP-13 and inflammatory factors than ADSCs. Both USCs and ADSCs enhanced autophagy in OA chondrocytes, with USCs being more effective than ADSCs. The autophagy inhibitor 3-MA reduced the enhanced autophagy and protective effects of USCs and ADSCs on OA chondrocytes.To our knowledge, this is the first study to explore the efficacy of USCs in the treatment of knee OA and to compare them with ADSCs. Considering the superior properties of USCs in terms of noninvasive acquisition, a high cost-benefit ratio, and low ethical concerns, our study suggests that they may be a more promising therapeutic option than ADSCs for OA treatment under rigorous regulatory pathways.USCs may be a superior cell source for stem cells to treat knee OA, and this study strengthens the evidence for the application of USCs. [ABSTRACT FROM AUTHOR]

Benefiting from high safety, low cost, and competitive energy density, aqueous zinc ion batteries (AZIBs) have emerged as very promising technology for grid energy storage. However, the lifetime of AZIBs is severely affected by uncontrolled zinc dendritic growth and undesirable side reaction. To address the problem, natural aluminum silicate hydroxide covered glass fibers separator (AlSi‐GF) is prepared herein using a simple spraying method. Aluminum silicate hydroxide is a complex oxide, where a large number of adsorption sites can adsorb Zn2+ and guide its deposition process. In particular, the Maxwell–Wagner polarization of aluminum silicate hydroxide under an applied electric field contributes to homogenizing the electric field distribution around the interface, thereby modulating zinc deposition and reducing the nucleation overpotential. Impressively, AlSi‐GF separator enables high‐performance zinc‐metal batteries. The symmetric battery with AlSi‐GF separator has a stable voltage polarization and an ultra‐long cycle life of 2280 h at a current density of 1 mA cm−2, and the Zn//V2O5 full cell based on AlSi‐GF separator can exhibit a high specific capacity of 123 mAh g−1 after 1500 cycles at 1 A g−1. This study provides new insights into the design of reliable and cost‐effective separators for metal anodes in energy storage devices. [ABSTRACT FROM AUTHOR]

In this study, a 4-(hydroxymethyl)-2,6,7-trioxa-1-phosphabicyclo[2.2.2]octane 1-oxide (PEPA)-functionalized acrylate monomer, PEPAA, is designed and utilized for the synthesis of macromolecular flame retardants poly(PEPAA-co-AM) with varying PEPAA/AM ratio through copolymerization with acrylamide (AM). The poly(PEPAA-co-AM) is then incorporated into polypropylene (PP) to prepare PP/poly(PEPAA-co-AM) composites. The flame retardant effect of poly(PEPAA-co-AM) on PP is investigated using cone calorimetric test (CCT), and compared with that of PEPAA homopolymer (P-PEPAA), AM homopolymer (PAM), and blends of P-PEPAA/PAM. The results demonstrate that, in comparison with P-PEPAA, PAM, and blends of P-PEPAA/PAM, the incorporation of poly(PEPAA-co-AM) significantly enhances the flame retardancy of PP. Notably, the best flame retardancy is achieved when the ratio of PEPAA/AM copolymerization in poly(PEPAA-co-AM) is 2/8. The morphology and composition of residual chars from combustion are analyzed using SEM-EDS while the residual graphitization degree is examined through Raman spectroscopy. Additionally, TG-FTIR-MS is utilized to investigate the pyrolysis products in gas phase during thermal decomposition of poly(PEPAA-co-AM). Based on these experimental results, a flame retardant mechanism for poly(PEPAA-co-AM) is proposed. The PP/poly(PEPAA-co-AM) composites not only retain the excellent processing properties of pure PP but also exhibit enhanced mechanical properties., (© 2024 Wiley‐VCH GmbH.)

Targeting cell surface molecules using radioligand and antibody-based therapies has yielded considerable success across cancers. However, it remains unclear how the expression of putative lineage markers, particularly cell surface molecules, varies in the process of lineage plasticity, wherein tumor cells alter their identity and acquire new oncogenic properties. A notable example of lineage plasticity is the transformation of prostate adenocarcinoma (PRAD) to neuroendocrine prostate cancer (NEPC)-a growing resistance mechanism that results in the loss of responsiveness to androgen blockade and portends dismal patient survival. To understand how lineage markers vary across the evolution of lineage plasticity in prostate cancer, we applied single-cell analyses to 21 human prostate tumor biopsies and two genetically engineered mouse models, together with tissue microarray analysis on 131 tumor samples. Not only did we observe a higher degree of phenotypic heterogeneity in castrate-resistant PRAD and NEPC than previously anticipated but also found that the expression of molecules targeted therapeutically, namely PSMA , STEAP1 , STEAP2 , TROP2, CEACAM5 , and DLL3 , varied within a subset of gene-regulatory networks (GRNs). We also noted that NEPC and small cell lung cancer subtypes shared a set of GRNs, indicative of conserved biologic pathways that may be exploited therapeutically across tumor types. While this extreme level of transcriptional heterogeneity, particularly in cell surface marker expression, may mitigate the durability of clinical responses to current and future antigen-directed therapies, its delineation may yield signatures for patient selection in clinical trials, potentially across distinct cancer types., Competing Interests: Competing interests statement:P.S.N. has received consulting fees from Janssen, Merck and Bristol Myers Squibb and research support from Janssen for work unrelated to the present studies. S.Z. has received consulting fees from Guidepoint and GLG consulting. J.L.Z. is a current employee of AstraZeneca. M.C.H served as a paid consultant/received honoraria from Pfizer and has received research funding from Merck, Novartis, Genentech, Promicell and Bristol Myers Squibb. C.L.S is on the board of directors of Novartis, is a co-founder of ORIC Pharmaceuticals, and is a co-inventor of the prostate cancer drugs enzalutamide and apalutamide, covered by U.S. patents 7,709,517, 8,183,274, 9,126,941, 8,445,507, 8,802,689, and 9,388,159 filed by the University of California. C.L.S. is on the scientific advisory boards of the following biotechnology companies: Beigene, Blueprint, Cellcarta, Column Group, Foghorn, Housey Pharma, Nextech, PMV.

Multiple sclerosis (MS) is an autoimmune disease characterized by inflammatory demyelination occurring in the central nervous system (CNS). Inulin is a common prebiotic that can improve metabolic disorders by modulating the gut microbiota. However, its capacity to affect CNS autoimmunity is poorly recognized. Experimental autoimmune encephalomyelitis (EAE) is a classical mouse model of MS. Herein, we found that oral administration of inulin ameliorated the severity EAE in mice, accompanied by reductions in inflammatory cell infiltration and demyelination in the CNS. These reductions were associated with decreased proportion and numbers of Th17 cells in brain and spleen. Consistent with the findings, the serum concentrations of IL-17, IL-6, and TNF-α were reduced in inulin treated EAE mice. Moreover, the proliferation of auto-reactive lymphocytes, against MOG 35-55 antigen, was attenuated ex vivo . Mechanistically, inulin treatment altered the composition of gut microbiota. It increased Lactobacillus and Dubosiella whereas decreased g_ Prevotellaceae_NK3B31_group at the genus level, alongside with elevated concentration of butyric acid in fecal content and serum. In vitro , butyrate, but not inulin, could inhibit the activation of MOG 35-55 stimulated lymphocytes. Furthermore, fecal microbiota transplantation assay confirmed that fecal contents of inulin-treated normal mice had an ameliorative effect on EAE mice. In contrast, antibiotic cocktail (ABX) treatment diminished the therapeutic effect of inulin in EAE mice as well as the reduction of Th17 cells, while supplementation with Lactobacillus reuteri restored the amelioration effect. These results confirmed that the attenuation of inulin on Th17 cells and inflammatory demyelination in EAE mice was dependent on its modulation on gut microbiota and metabolites. Our findings provide a potential therapeutic regimen for prebiotic inulin supplementation in patients with multiple sclerosis.