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[Display omitted] • (E)-2-octenal effectively inhibited the mango pathogen N. Parvum in vitro. • (E)-2-octenal caused cell membrane impairment and ROS increase of N. Parvum. • (E)-2-octenal affected mitochondrial respiration and energy level of N. Parvum. • SDH and MDH are the direct targets of (E)-2-octenal action. • ALO lowered the development of mango stem-end rot and natural storage diseases. Stem-end rot caused by Neofusicoccum parvum is among the most detrimental diseases affecting postharvest mangoes. The present investigation utilized (E)-2-octenal to manage N. parvum infections, elucidating its mechanism of action. The findings revealed that (E)-2-octenal exhibited outstanding antimicrobial potency against N. parvum in vitro within the concentration range of 0.4–1.6 µL/mL. Additionally, (E)-2-octenal significantly compromised the cell membrane integrity and mitochondrial energy metabolism of N. parvum , evidenced by dramatically increased intracellular material leakage and ROS levels, along with reduced mitochondrial membrane potential, ATP, and energy charge. Further experiments showed noteworthy effects on the tricarboxylic acid cycle (TCA) cycle and the key enzyme activities of succinate dehydrogenase (SDH) and malate dehydrogenase (MDH). Molecular docking revealed hydrogen bonding between (E)-2-octenal's aldehyde group and SDH (Trp-307) and MDH (Gly-101), indicating direct targeting of these enzymes for inhibition. To enhance the practical application of (E)-2-octenal, we developed an aerogel-loaded (E)-2-octenal material (ALO) that exhibited superior antimicrobial efficacy in vitro. In vivo , ALO effectively controlled mango stem-end rot, with optimal efficacy at 20 µL/L. This concentration also delayed the natural disease of mango without degrading fruit quality. According to these findings, (E)-2-octenal is a promising preservative against postharvest mango infections, potentially by impeding cellular energy metabolism through direct interaction with SDH and MDH within the TCA pathway, culminating in mitochondrial dysfunction and cell membrane damage. [ABSTRACT FROM AUTHOR]

The elimination of U(VI) from acidic nuclear wastewater is important for solving the problems in environmental and energy fields. However, the adsorbents used for U(VI) extraction/removal usually undergo the issues of high cost, low efficiency, and long adsorption time. In this work, surface-acidified hydroxyapatite (SAHAP) powders were obtained by soaking chicken leg bone in acetic acid combined with hydrothermal treatment, which shows super fast removal/extraction capacity of U(VI) from the solution. The surface of the SAHAP is highly acidified by large quantities of hydrogen phosphate radicals. The characterization and mechanistic investigations indicate that the U(VI) substitute with Ca2+/H+ via an ion-exchange related monolayer chemisorption process. At room temperature, over 99 % of U(VI) could be sequestrated by SAHAP within 20 s at pH 4.0, and the extraction amount could reach 1270 mg/g. Moreover, the SAHAP shows great application potential in the removal/extraction of U(VI) from seawater, and 25 mM CO 3 2- ions could only reduce the adsorption ability by 4.18 % at pH 4.0. This study provides a new approach to fabricating adsorbents for highly effective, selective and low-cost extraction of U(VI) from wastewater. • Surface-acidified hydroxyapatite (SAHAP) was fabricated. • Over 99 % of U(VI) could be sequestrated by SAHAP within 20 s at pH 4.0 • 3.The extraction amount could reach 1270 mg/g. • The extraction rate of U(VI) was 95 % even in the presence of CO 3 2-. [ABSTRACT FROM AUTHOR]

The solid solution between the normal ferroelectric Pb(Zr(sub 1/2)Ti(sub 1/2))O(sub 3) (PZT) and relaxor ferroelectric Pb(Ni (sub 1/3)Nb(sub 2/3))O(sub 3) (PNN) was synthesized by the columbite method. The transistor between relaxor to normal ferroelectricity was typified by a quasilinear relationship between the diffuseness parameter Delta (sub gamma) and PZT mole fraction x.

The composition and cellular heterogeneity of the corpus cavernosum (CC) microenvironment have been characterized, but the spatial heterogeneity at the molecular level remains unexplored. In this study, we integrate single-cell RNA sequencing (scRNA-seq) and spatial transcriptome sequencing to comprehensively chart the spatial cellular landscape of the human and rat CC under normal and disease conditions. We observe differences in the proportions of cell subtypes and marker genes between humans and rats. Based on the analysis of the fibroblast (FB) niche, we also find that the enrichment scores of mechanical force signaling vary across different regions and correlate with the spatial distribution of FB subtypes. In vitro , the soft and hard extracellular matrix (ECM) induces the differentiation of FBs into apolipoprotein (APO)+ FBs and cartilage oligomeric matrix protein (COMP)+ FBs, respectively. In summary, our study provides a cross-species and physiopathological transcriptomic atlas of the CC, contributing to a further understanding of the molecular anatomy and regulation of penile erection. [Display omitted] • The cell-type landscape of the human and rat CC is investigated using spatial transcriptomics • Mechanical force signaling exhibits spatial heterogeneity in the CC • The phenotypic transformation of FBs is regulated by mechanical force signaling Yin et al. map the single-cell and spatial transcriptomes of the human and rat corpus cavernosum. They show that the spatial distribution of fibroblast subpopulations is related to the extracellular matrix stiffness in different regions. In addition, they demonstrate that mechanical force signaling can regulate the transition between fibroblast subpopulations. [ABSTRACT FROM AUTHOR]

Both glymphatic system dysfunction and inflammatory response aggravate neurological dysfunction after subarachnoid hemorrhage (SAH). Studies have shown that β-hydroxybutyrate (BHB) may mitigate painful diabetic neuropathy (PDN) by upregulating SNTA1 expression and reinstating AQP4 polarity. However, the potential of BHB to ameliorate glymphatic system function and inflammatory response in SAH mice remains uncertain. The SAH models were constructed by injection of arterial blood into cisterna Magana. Three groups of C57 mice were randomly assigned: Sham, SAH, and BHB. All mice were subjected to neurological function assessment, western blot, immunofluorescence double staining, and RNA-seq. Glymphatic system function was examined with tracer and immunofluorescence double staining, and the differential genes were examined with RNA-seq. In addition, the expression of related inflammation was detected. Compared with the SAH group, BHB reinstated AQP4 polarization by upregulating SNTA1 protein to enhance the glymphatic system. According to RNA-seq, the different genes were primarily connected to microglia activation, astrocytes, and inflammation. Western blot and immunofluorescence further confirmed that the related inflammatory protein expression levels were upregulated. BHB attenuated neuroinflammation after SAH. Ultimately, it can mitigate the neurological deficits in SAH mice. The study reveals a novel mechanism that BHB treatment mitigates neurologic impairment in SAH mice. We propose that BHB may play a neuroprotective effect by enhancing glymphatic system function and attenuating neuroinflammatory subarachnoid hemorrhage. After subarachnoid hemorrhage(SAH), the polarity of AQP4 decreases and the function of the glymphatic system is impaired, leading to metabolic waste deposition such as Aβ and the accumulation of inflammatory factors. At the same time, astrocyte and microglia activation, and secretion of inflammatory cytokines, such as TNF-α, and IL-1β, aggravate neurological dysfunction. BHB improves neurological dysfunction by improving the glymphatic system and astrocyte and microglial inflammation. [Display omitted] • The downregulation of SNTA1 resulted in the depolarization of AQP4, contributing to impaired glymphatic system function following SAH. • Treatment with β-hydroxybutyrate (BHB) reinstated AQP4 polarization through upregulation of SNTA1 expression, thereby enhancing glymphatic system function in SAH mice. • BHB treatment attenuated the neuroinflammatory response in SAH mice. • BHB treatment mitigated neurological deficits in SAH mice. [ABSTRACT FROM AUTHOR]