Effects of 1-methylcyclopropene on superficial scald and related metabolism in ‘Wujiuxiang’ pears during cold storage

‘Wujiuxiang’ (Pyrus bretschneideri R. × Pyrus communis L.) pears often suffer from superficial scald after long-term cold storage. In this study, harvested ‘Wujiuxiang’ pear fruits were fumigated with 1-MCP at concentrations of 0.5 μL/L and 1.0 μL/L and subsequently stored at low temperature (0 °C). The superficial scald index; flesh firmness; total soluble solids (TSS) content; respiration and ethylene production rates; relative membrane permeability; concentrations of α-farnesene, conjugated trienols (CTols), and hydrogen peroxide (H2O2); and activities of superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), and lipoxygenase (LOX) of the peel were investigated. The results showed that compared with control, 1-MCP reduced the index of superficial scald; maintained a higher firmness and a lower TSS content; inhibited the accumulation of H2O2, α-farnesene and conjugated trienols and the increase in cell membrane permeability; and maintained a higher activity of APX, SOD and CAT and a lower activity of LOX. These findings indicate that 1-MCP regulates the activities of H2O2-scavenging enzymes to inhibit the accumulation of H2O2 and thereby reduces cell membrane damage and inhibits the accumulation of conjugated trienols. Thus, 1-MCP could decrease the incidence of superficial scald in ‘Wujiuxiang’ pears

The involvement of phenolic metabolism in superficial scald development in ‘Wujiuxiang’ pear

Superficial scald often occurs after a long term of cold storage in apples and pears. In this study, the superficial scald index, the contents of major phenolic compounds, polyphenol oxidase (PPO) activity and its related genes expression in peel was investigated during cold storage period and at shelf life in ‘Wujiuxiang’ pear (Pyrus communis L. cv. Wujiuxiang) with or without 1-MCP treatment. It showed that arbutin, chlorogenic acid, catechin and epi-catechin were the main phenolic compounds in the peel, and 1-MCP treatment significantly inhibited scald development while altering the composition of phenolic compounds, inhibited PPO activity and the expression of phenylalanine ammonia ligase (PAL1, PAL2), cinnamate 4-hydroxylase (C4H1, C4H2) and PPO (PPO1, PPO5) and up-regulated the expression of hydroxycinnamoyl-CoA shikimate/quinate hydroycinnamoyltransferase (HCT1), p-coumarate-3-hydro-xylase (C3H) and PPO (PPO4 and PPO6) in the peel. These results suggested that the phenolic metabolism is closely related to the scald development, and several genes related to phenolic metabolism were involved in scald development

CAFE Learning to Condense Dataset by Aligning Features

Dataset condensation aims at reducing the network training effort through condensing a cumbersome training set into a compact synthetic one. State-of-the-art approaches largely rely on learning the synthetic data by matching the gradients between the real and synthetic data batches. Despite the intuitive motivation and promising results, such gradient-based methods, by nature, easily overfit to a biased set of samples that produce dominant gradients, and thus lack global supervision of data distribution. In this paper, we propose a novel scheme to Condense dataset by Aligning FEatures (CAFE), which explicitly attempts to preserve the real-feature distribution as well as the discriminant power of the resulting synthetic set, lending itself to strong generalization capability to various architectures. At the heart of our approach is an effective strategy to align features from the real and synthetic data across various scales, while accounting for the classification of real samples. Our scheme is further backed up by a novel dynamic bi-level optimization, which adaptively adjusts parameter updates to prevent over-/under-fitting. We validate the proposed CAFE across various datasets, and demonstrate that it generally outperforms the state of the art: on the SVHN dataset, for example, the performance gain is up to 11%. Extensive experiments and analyses verify the effectiveness and necessity of proposed designs.Comment: The manuscript has been accepted by CVPR-2022

Improved 11α-hydroxycanrenone production by modification of cytochrome P450 monooxygenase gene in Aspergillus ochraceus

Eplerenone is a drug that protects the cardiovascular system. 11α-Hydroxycanrenone is a key intermediate in eplerenone synthesis. We found that although the cytochrome P450 (CYP) enzyme system in Aspergillus ochraceus strain MF018 could catalyse the conversion of canrenone to 11α-hydroxycanrenone, its biocatalytic efficiency is low. To improve the efficiency of 11α-hydroxycanrenone production, the CYP monooxygenase-coding gene of MF018 was predicted and cloned based on whole-genome sequencing results. A recombinant A. ochraceus strain MF010 with the high expression of CYP monooxygenase was then obtained through homologous recombination. The biocatalytic rate of this recombinant strain reached 93 % at 60 h without the addition of organic solvents or surfactants and was 17–18 % higher than that of the MF018 strain. Moreover, the biocatalytic time of the MF010 strain was reduced by more than 30 h compared with that of the MF018 strain. These results show that the recombinant A. ochraceus strain MF010 can overcome the limitation of substrate biocatalytic efficiency and thus holds a high potential for application in the industrial production of eplerenone

Characterization of expression and enzyme activity of lipoxygenases during fruit softening and superficial scald development in ‘Wujiuxiang’ pear

Lipoxygenases (LOXs; EC 1.13.11.12) have been implicated in fruit ripening and senescence; however, little is known regarding the specific LOX genes involved in fruit softening and scald develop- ment in pear. In this study, two 9-lipoxygenase genes, PcLOX1 and PcLOX7, were characterized in silico in the Pyrus communis draft genome. The expression pattern of PcLOX1 and PcLOX7, LOX ac-tivity, respiration rate and ethylene production were analyzed during fruit softening and superficial scald development in ‘Wujiuxiang’ pear with or without 1-MCP treatment. The results demonstrated that PcLOX1 and PcLOX7 belong to the type-1 LOX subfamily, and their expression levels, enzyme activity, respiration rate and ethy-lene production were increased during fruit softening and scald de­velopment. In contrast, 1-MCP treatment could effectively suppress respiration rate and ethylene production and inhibit expression of PcLOX1 and PcLOX7 and LOX enzyme activity, resulting in de- layed fruit softening and scald development. These findings indicate that PcLOX1 and PcLOX7 are involved in fruit ripening and scald development in ‘Wujiuxiang’ pear

Pinocembrin protects against β-amyloid-induced toxicity in neurons through inhibiting receptor for advanced glycation end products (RAGE)-independent signaling pathways and regulating mitochondrion-mediated apoptosis

BACKGROUND: It is known that amyloid-β peptide (Aβ) plays a pivotal role in the pathogenesis of Alzheimer's disease (AD). Interaction between Aβ and the receptor for advanced glycation end products (RAGE) has been implicated in neuronal degeneration associated with this disease. Pinocembrin, a flavonoid abundant in propolis, has been reported to possess numerous biological activities beneficial to health. Our previous studies have demonstrated that pinocembrin has neuroprotective effects on ischemic and vascular dementia in animal models. It has been approved by the State Food and Drug Administration of China for clinical use in stroke patients. Against this background, we investigated the effects of pinocembrin on cognitive function and neuronal protection against Aβ-induced toxicity and explored its potential mechanism. METHODS: Mice received an intracerebroventricular fusion of Aβ(25-35). Pinocembrin was administrated orally at 20 mg/kg/day and 40 mg/kg/day for 8 days. Behavioral performance, cerebral cortex neuropil ultrastructure, neuronal degeneration and RAGE expression were assessed. Further, a RAGE-overexpressing cell model and an AD cell model were used for investigating the mechanisms of pinocembrin. The mechanisms underlying the efficacy of pinocembrin were conducted on target action, mitochondrial function and potential signal transduction using fluorescence-based multiparametric technologies on a high-content analysis platform. RESULTS: Our results showed that oral administration of pinocembrin improved cognitive function, preserved the ultrastructural neuropil and decreased neurodegeneration of the cerebral cortex in Aβ(25-35)-treated mice. Pinocembrin did not have a significant effect on inhibiting Aβ(1-42 )production and scavenging intracellular reactive oxygen species (ROS). However, pinocembrin significantly inhibited the upregulation of RAGE transcripts and protein expression both in vivo and in vitro, and also markedly depressed the activation of p38 mitogen-activated protein kinase (MAPK)-MAPKAP kinase-2 (MK2)-heat shock protein 27 (HSP27) and stress-activated protein kinase (SAPK)/c-Jun N-terminal kinase (JNK)-c-Jun pathways and the downstream nuclear factor κB (NFκB) inflammatory response subsequent to Aβ-RAGE interaction. In addition, pinocembrin significantly alleviated mitochondrial dysfunction through improving mitochondrial membrane potential and inhibiting mitochondrial oxidative stress, and regulated mitochondrion-mediated apoptosis by restoration of B cell lymphoma 2 (Bcl-2) and cytochrome c and inactivation of caspase 3 and caspase 9. CONCLUSIONS: Pinocembrin was shown to infer cognitive improvement and neuronal protection in AD models. The mechanisms of action of the compound were illustrated on RAGE-dependent transduction inhibition and mitochondrion protection. It appears to be a promising candidate for the prevention and therapy of AD

Echinacoside Protects against 6-Hydroxydopamine-Induced Mitochondrial Dysfunction and Inflammatory Responses in PC12 Cells via Reducing ROS Production

Parkinson’s disease (PD) is a neurodegenerative disorder characterized by progressive loss of dopaminergic (DA) neurons at the substantia nigra. Mitochondrial dysfunction and inflammatory responses are involved in the mechanism of cell damage in PD. 6-Hydroxydopamine (6-OHDA), a dopamine analog, specifically damages dopaminergic neurons. Echinacoside (ECH) is a phenylethanoid glycoside isolated from the stems of Cistanche salsa, showing a variety of neuroprotective effects in previous studies. The present study was to investigate its effect against 6-OHDA-induced neurotoxicity and possible mechanisms in PC12 cells. The results showed that 6-OHDA reduced cell viability, decreased oxidation-reduction activity, decreased mitochondrial membrane potential, and induced mitochondria-mediated apoptosis compared with untreated PC12 cells. However, echinacoside treatment significantly attenuated these changes induced by 6-OHDA. In addition, echinacoside also could significantly alleviate the inflammatory responses induced by 6-OHDA. Further research showed that echinacoside could reduce 6-OHDA-induced ROS production in PC12 cells. These results suggest that the underlying mechanism of echinacoside against 6-OHDA-induced neurotoxicity may be involve in attenuating mitochondrial dysfunction and inflammatory responses by reducing ROS production