Abstract Insect tea is consumed as a health beverage in China. The insect tea primary leaf (ITPL) is rich in bioactive substances, which are also used as traditional Chinese medicine. This study investigated the role of ITPL in reducing the oxidative response induced by D‐galactose in mice. Mice were intraperitoneally injected with D‐galactose to induce oxidative damage. The effect of ITPL was tested by pathological observation, serum detection with kits, quantitative polymerase chain reaction, and Western blot. The experimental results show that ITPL increased the thymus, brain, heart, liver, spleen, and kidney indices of oxidized mice. ITPL increased superoxide dismutase, glutathione peroxidase, and glutathione levels and reduced nitric oxide and malondialdehyde levels in the serum, liver, and spleen in oxidative damaged mice. The pathological observations show that ITPL reduced the oxidative damage of the liver and spleen in mice induced with D‐galactose. Simultaneously, ITPL upregulated mRNA expression of neuronal nitric oxide synthase, endothelial nitric oxide synthase, cuprozinc‐superoxide dismutase, manganese superoxide dismutase, catalase, heme oxygenase‐1, nuclear factor‐erythroid 2 related factor 2, γ‐glutamylcysteine synthetase, and NAD(P)H dehydrogenase [quinone] 1, and downregulated the expression of inducible nitric oxide synthase in the liver and spleen of oxidized mice. ITPL had beneficial preventive effects on the oxidative damage caused by D‐galactose in mice and was more effective as an antioxidant than vitamin C. The component analysis test by high‐performance liquid chromatography indicated that ITPL contained the following seven compounds: neochlorogenic acid, cryptochlorogenic acid, rutin, kaempferin, isochlorogenic acid B, isochlorogenic acid A, and hesperidin. ITPL is a plant with excellent antioxidant activities derived from its bioactive substances.
Abstract The metabolome includes not just known but also unknown metabolites; however, metabolite annotation remains the bottleneck in untargeted metabolomics. Ion mobility – mass spectrometry (IM-MS) has emerged as a promising technology by providing multi-dimensional characterizations of metabolites. Here, we curate an ion mobility CCS atlas, namely AllCCS, and develop an integrated strategy for metabolite annotation using known or unknown chemical structures. The AllCCS atlas covers vast chemical structures with >5000 experimental CCS records and ~12 million calculated CCS values for >1.6 million small molecules. We demonstrate the high accuracy and wide applicability of AllCCS with medium relative errors of 0.5–2% for a broad spectrum of small molecules. AllCCS combined with in silico MS/MS spectra facilitates multi-dimensional match and substantially improves the accuracy and coverage of both known and unknown metabolite annotation from biological samples. Together, AllCCS is a versatile resource that enables confident metabolite annotation, revealing comprehensive chemical and metabolic insights towards biological processes.
Objective CLCN7 mutation caused abnormal osteoclasts, resulting in osteopetrosis. Depending on the type of mutation, CLCN7 mutations can lead to severe or relatively benign forms of osteopetrosis. However, the serum metabolic alterations in osteopetrosis caused by CLCN7 mutation are still unknown. We aimed to investigate the differences in the metabolome of osteopetrosis patients caused by CLCN7 mutation versus healthy controls (HC), uncovering potential subtype diagnosis biomarkers. Methods 19 osteopetrosis patients caused by CLCN7 mutation and 19 HC were recruited for liquid chromatography–tandem mass spectrometry analysis. The screened pathway was validated in the myeloid cell specific Clcn7 G763R mutant mouse model by quantitative real-time PCR analysis. Results Three metabolic pathways were significantly enriched, including glycerophospholipid metabolism ( P =0.036948), arachidonic acid metabolism ( P =0.0058585) and linoleic acid metabolism ( P =0.032035). Ten differential expressed metabolites were located in these three pathways and classified ability with areas under the curve over 0.7 in receiver operating characteristic analysis, suggesting a certain accuracy for being the potential biological markers. Especially, we found that the proteins in glycerophospholipid metabolism were predicted to interact with ClC-7 and further verified that the expression of coding genes were significantly up-regulated in myeloid cell specific Clcn7 G763R mutant mouse. Conclusion This study provides data on serum metabolomics in osteopetrosis caused by CLCN7 mutation and provides new potential metabolic markers and pathways for diagnosis and pathogenesis of osteopetrosis.
Drawing on the theoretical frameworks of structural functionalism and relational research perspectives, this study meticulously constructs and analyzes China's inbound tourism flow network spanning the years 2001 to 2023. Employing a diverse array of analytical tools such as the small-world model, rank-size model, structural equivalence model, core-periphery model, and various centrality metrics, the research delves into the structural characteristics and evolution patterns of China's inbound tourism flow network within a comprehensive spatial-temporal framework. Key findings include: 1) Small-world and scale-free properties with tourist flows concentrated in pivotal provinces. 2) Persistence of a U-shaped pattern in inbound tourism, with robust activity in eastern and western regions. 3) Presence of a core-periphery structure, with Beijing, Shanghai, and Guangdong as national hubs. This research enhances understanding of tourism industry spatial organization, offering insights for policymakers and stakeholders in tourism development.
Multimodal data is rapidly growing in many fields of science and engineering, including single-cell biology. We introduce MultiMAP, a novel algorithm for dimensionality reduction and integration. MultiMAP can integrate any number of datasets, leverages features not present in all datasets, is not restricted to a linear mapping, allows the user to specify the influence of each dataset, and is extremely scalable to large datasets. We apply MultiMAP to single-cell transcriptomics, chromatin accessibility, methylation, and spatial data and show that it outperforms current approaches. On a new thymus dataset, we use MultiMAP to integrate cells along a temporal trajectory. This enables quantitative comparison of transcription factor expression and binding site accessibility over the course of T cell differentiation, revealing patterns of expression versus binding site opening kinetics.
San-Huang-Chai-Zhu formula (SHCZF) has been used to improve cholestasis for many years. This study aims to predict the possible gene targets of SHCZF in treating acute intrahepatic cholestasis (AIC) in rats.Eighteen SD rats were randomly assigned to the normal group, ANIT group, and ANIT + SHCZF group. Alpha-naphthylisothiocyanate (ANIT) was used to induce AIC. Serum biochemical indexes were detected in each group. After treatment, the livers were collected and used to extract RNA. The library was constructed by TruSeq RNA, sequenced by Illumina, and analyzed by various bioinformatics methods. qRT-PCR was used to verify the target genes related to the efficacy of SHCZF.Serum ALT, AST, ALP, and TBIL were significantly higher in the ANIT group than in the normal group. Serum ALT and AST levels in the ANIT + SHCZF group were substantially lower than those in the ANIT group. A total of 354 intersected genes were screened by expression level correlation and PCA analysis, GO and KEGG pathway enrichment analysis, and WGCNA and STEM analysis. Then, 4 overlapping genes were found by pathway/BP/gene network construction. SHCZF reversed the downregulation of expression of CYP4A1 and HACL1 and the upregulation of expression of DBI and F11R induced by ANIT. In addition, the qRT-PCR result showed that mRNA expression of CYP4A1, HACL1, and F11R genes in the liver was consistent with the prediction result of bioinformatics analysis.CYP4A1, HACL1, and F11R are genes related to the occurrence of ANIT-induced AIC in rats and may be considered as targets of SHCZF for the treatment of AIC.
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