The maize ZmVPS23-like protein relocates the nucleotide-binding leucine-rich repeat protein Rp1-D21 to endosomes and suppresses the defense response.

Plants often utilize nucleotide-binding leucine-rich repeat (NLR) proteins to perceive pathogen infections and trigger a hypersensitive response (HR). The endosomal sorting complex required for transport (ESCRT) machinery is a conserved multisubunit complex that is essential for the biogenesis of multivesicular bodies and cargo protein sorting. VPS23 is a key component of ESCRT-I and plays important roles in plant development and abiotic stresses. ZmVPS23L, a homolog of VPS23-like in maize (Zea mays), was previously identified as a candidate gene in modulating HR mediated by the autoactive NLR protein Rp1-D21 in different maize populations. Here, we demonstrate that ZmVPS23L suppresses Rp1-D21-mediated HR in maize and Nicotiana benthamiana. Variation in the suppressive effect of HR by different ZmVPS23L alleles was correlated with variation in their expression levels. ZmVPS23 also suppressed Rp1-D21-mediated HR. ZmVPS23L and ZmVPS23 predominantly localized to endosomes, and they physically interacted with the coiled-coil domain of Rp1-D21 and mediated the relocation of Rp1-D21 from the nucleo-cytoplasm to endosomes. In summary, we demonstrate that ZmVPS23L and ZmVPS23 are negative regulators of Rp1-D21-mediated HR, likely by sequestrating Rp1-D21 in endosomes via physical interaction. Our findings reveal the role of ESCRT components in controlling plant NLR-mediated defense responses.

Maize requires arogenate dehydratase 2 for resistance to Ustilago maydis and plant development.

Maize (Zea mays) smut is a common biotrophic fungal disease caused by Ustilago maydis and leads to low maize yield. Maize resistance to U. maydis is a quantitative trait. However, the molecular mechanism underlying the resistance of maize to U. maydis is poorly understood. Here, we reported that a maize mutant caused by a single gene mutation exhibited defects in both fungal resistance and plant development. maize mutant highly susceptible to U. maydis (mmsu) with a dwarf phenotype forms tumors in the ear. A map-based cloning and allelism test demonstrated that 1 gene encoding a putative arogenate dehydratase/prephenate dehydratase (ADT/PDT) is responsible for the phenotypes of the mmsu and was designated as ZmADT2. Combined transcriptomic and metabolomic analyses revealed that mmsu had substantial differences in multiple metabolic pathways in response to U. maydis infection compared with the wild type. Disruption of ZmADT2 caused damage to the chloroplast ultrastructure and function, metabolic flux redirection, and reduced the amounts of salicylic acid (SA) and lignin, leading to susceptibility to U. maydis and dwarf phenotype. These results suggested that ZmADT2 is required for maintaining metabolic flux, as well as resistance to U. maydis and plant development in maize. Meanwhile, our findings provided insights into the maize response mechanism to U. maydis infection.

Random Forest for Predicting Treatment Response to Radioiodine and Thyrotropin Suppression Therapy in Patients With Differentiated Thyroid Cancer But Without Structural Disease.

BACKGROUND: We aimed to develop a machine-learning model for predicting treatment response to radioiodine (131I) therapy and thyrotropin (TSH) suppression therapy in patients with differentiated thyroid cancer (DTC) but without structural disease, based on pre-treatment information. PATIENTS AND METHODS: Overall, 597 and 326 patients with DTC but without structural disease were randomly assigned to "training" cohorts for predicting treatment response to 131I therapy and TSH suppression therapy, respectively. Six supervised algorithms, including Logistic Regression, Support Vector Machine, Random Forest (RF), Neural Networks, Adaptive Boosting, and Gradient Boost, were used to predict effective response (ER) to 131I therapy and biochemical remission (BR) to TSH suppression therapy. RESULTS: Stimulated and suppressed thyroglobulin (Tg) and radioiodine uptake before the current course of 131I therapy were mostly attributed to ER to 131I therapy, while thyroid remnant available on the post-therapeutic whole-body scan at the last course of 131I therapy and TSH were greatly contributed to Tg decline under TSH suppression therapy. RF showed the best performance among all models. The accuracy and area under the receiver operating characteristic curve (AUC) for segregating ER from non-ER during 131I therapy with RF were 81.3% and 0.896, respectively. The accuracy and AUC for predicting BR to TSH suppression therapy with RF were 78.7% and 0.857, respectively. CONCLUSION: This study demonstrates that machine learning models, especially the RF algorithm are useful tools that may predict treatment response to 131I therapy and TSH suppression therapy in DTC patients without structural disease based on pre-treatment routine clinical variables and biochemical markers.

Impaired bisecting GlcNAc reprogrammed M1 polarization of macrophage.

The functions of macrophages are governed by distinct polarization phenotypes, which can be categorized as either anti-tumor/M1 type or pro-tumor/M2 type. Glycosylation is known to play a crucial role in various cellular processes, but its influence on macrophage polarization is not well-studied. In this study, we observed a significant decrease in bisecting GlcNAc during M0-M1 polarization, and impaired bisecting GlcNAc was found to drive M0-M1 polarization. Using a glycoproteomics strategy, we identified Lgals3bp as a specific glycoprotein carrying bisecting GlcNAc. A high level of bisecting GlcNAc modification facilitated the degradation of Lgals3bp, while a low level of bisecting GlcNAc stabilized Lgals3bp. Elevated levels of Lgals3bp promoted M1 polarization through the activation of the NF-кB pathway. Conversely, the activated NF-кB pathway significantly repressed the transcription of MGAT3, leading to reduced levels of bisecting GlcNAc modification on Lgals3bp. Overall, our study highlights the impact of glycosylation on macrophage polarization and suggests the potential of engineered macrophages via glycosylated modification. Video Abstract.

Integrating transcriptomics, glycomics and glycoproteomics to characterize hepatitis B virus-associated hepatocellular carcinoma.

BACKGROUND: Hepatocellular carcinoma (HCC) ranks as the third most common cause of cancer related death globally, representing a substantial challenge to global healthcare systems. In China, the primary risk factor for HCC is the hepatitis B virus (HBV). Aberrant serum glycoconjugate levels have long been linked to the progression of HBV-associated HCC (HBV-HCC). Nevertheless, few study systematically explored the dysregulation of glycoconjugates in the progression of HBV-associated HCC and their potency as the diagnostic and prognostic biomarker. METHODS: An integrated strategy that combined transcriptomics, glycomics, and glycoproteomics was employed to comprehensively investigate the dynamic alterations in glyco-genes, N-glycans, and glycoproteins in the progression of HBV- HCC. RESULTS: Bioinformatic analysis of Gene Expression Omnibus (GEO) datasets uncovered dysregulation of fucosyltransferases (FUTs) in liver tissues from HCC patients compared to adjacent tissues. Glycomic analysis indicated an elevated level of fucosylated N-glycans, especially a progressive increase in fucosylation levels on IgA1 and IgG2 determined by glycoproteomic analysis. CONCLUSIONS: The findings indicate that the abnormal fucosylation plays a pivotal role in the progression of HBV-HCC. Systematic and integrative multi-omic analysis is anticipated to facilitate the discovery of aberrant glycoconjugates in tumor progression.

Sialylation on vesicular integrin ß1 determined endocytic entry of small extracellular vesicles into recipient cells.

BACKGROUND: Small extracellular vesicles (sEV) are closely associated with the development and metastasis of many types of mammalian cancer. Glycoconjugates are highly expressed on sEV and play important roles in sEV biogenesis and their interaction with other cells. However, the study on vesicular glycoconjugates are far behind proteins and nucleic acids. Especially, the functions of sialic acids which are the terminal components of glycoconjugates, are poorly understood in sEV. METHODS: Sialic acid levels on sEV from plasma and bladder cancer cells were determined by ELISA and lectin blotting. Effects of sialylation on sEV uptake were determined by flow cytometry. Vesicular glycoproteins bearing sialic acids responsible for sEV uptake was identified by proteomics and density gradient centrifugation, and their site-specific sialylation functions were assayed by N-glycosylation site mutation. Effects of integrin ß1 bearing sialic acids on the pro-metastatic function of sEV in vivo were explored using Balb/c nu/nu mice. RESULTS: (1) Increased sialic acid levels were observed in sEV from malignant bladder cancer cells. (2) Elimination of sialic acids on sEV impaired sEV uptake by recipient cells. (3) Vesicular integrin ß1 bearing sialic acids was identified to play a key role in sEV uptake. (4) Desialylation of the hybrid domain of vesicular integrin ß1 inhibited its binding to matrix fibronectin, and reduced sEV entry into recipient cells. (5) Sialylation on integrin ß1 affected pro-metastatic function of sEV in Balb/c nu/nu mice. CONCLUSIONS: Taken together, our findings indicate important functional roles of sialic acids in sEV uptake and reprogramming plasticity of surrounding normal epithelial cells.

Metabolome Revealed the Potential Mechanism of Fusarium Wilt Resistance in Bitter Gourd (Momordica charantia) Based on Liquid Chromatography with Mass Spectrometry.

Fusarium wilt fungus infection of bitter gourd, a major melon vegetable crop, results in massive yield reduction. Through extensive testing, some Fusarium wilt-resistant bitter melon varieties have been produced, but the molecular mechanism of their resistance to the fungus remains unknown. Importantly, after bitter melon plants are infected with Fusarium oxysporum f. sp. momordicae (FOM), apart from altering their gene expression levels, numerous metabolites are produced because of the interaction with the fungus. In the current study, an untargeted metabolomics analysis was performed to investigate the metabolic difference between resistant and susceptible bitter gourd varieties at various timepoints postinoculation with FOM based on liquid chromatography with mass spectrometry. A total of 1,595 positive ion mode and 922 negative ion mode metabolites were identified. Between the resistant and susceptible bitter gourd varieties, 213 unique differentially abundant metabolites (DAMs) were identified, and they were mainly enriched in the alpha-linolenic acid metabolism pathway. By comparing the postinoculation with preinoculation timepoints in the resistant and susceptible bitter gourd varieties, 93 and 159 DAMs were identified, respectively. These DAMs were mainly related to beta-alanine metabolism, among others. Multiple metabolites in the biosynthesis of the phenylpropanoid pathway showed greater variability in the susceptible than the resistant varieties, which may be related to senescence and mortality in the susceptible variety. These results provide new insights into the understanding of metabolite changes after FOM infection and a theoretical foundation for the elucidation of the bitter gourd disease resistance mechanism.

Transcriptome analysis provides insights into lignin synthesis and MAPK signaling pathway that strengthen the resistance of bitter gourd (Momordica charantia) to Fusarium wilt.

Fusarium wilt is a typical soil-borne disease caused by Fusarium oxysporum f. sp. momordicae (FOM) in bitter gourd. In this study, by comparing sequencing data at multiple time points and considering the difference between resistant (R) and susceptible (S) varieties, differentially expressed genes were screened out. Short time-series expression miner analysis revealed the upregulated expression trend of genes, which were enriched in phenylpropanoid biosynthesis, plant-pathogen interaction, and mitogen-activated protein kinase signaling pathway. Further, observation of the microstructure revealed that the R variety may form tyloses earlier than the S variety to prevent mycelium diffusion from the xylem vessel. After Fusarium wilt infection, the enzymatic activities of superoxide dismutase, peroxidase, phenylalanine ammonia lyase, and catalaseas well as levels of superoxide anion and malondialdehyde were increased in the R variety higher than those in the S variety. This study provides a reference to elucidate the disease resistance mechanism of bitter gourd.

Modulation Mechanism of Wuniuzao Dark Tea Polysaccharide on Lipid Metabolism in Hyperlipidemic Mice Induced by High-Fat Diet.

The aim of this study was to investigate the functional mechanism of Wuniuzao dark tea polysaccharide (WDTP) that protect against hyperlipidemia in mice induced by high-fat diet. WDTP was extracted by hot water, isolated and purified by DEAE-52 chromatography and characterized by high-performance liquid chromatograph (HPLC), Fourier transform infrared spectroscopy (FT-IR) and scanning electron microscope (SEM). Different doses (200 or 800 mg/kg/day) of WDTP were orally administered to mice induced by high-fat diet to evaluate the mechanism of WDTP regulating lipid metabolism. And these results showed that average molecular weight of WDTP was nearly 63,869 Da. And WDTP intervention significantly reduced body weight, lipid accumulation, and modulated blood lipid levels. The mechanism of WDTP ameliorating lipid metabolism was associated with regulating the expression of lipid metabolism-related genes and serum exosomes miR-19b-3p, and modulating the community structure of gut microbiota in mice.

When Glycosylation Meets Blood Cells: A Glance of the Aberrant Glycosylation in Hematological Malignancies.

Among neoplasia-associated epigenetic alterations, changes in cellular glycosylation have recently received attention as a key component of hematological malignancy progression. Alterations in glycosylation appear to not only directly impact cell growth and survival, but also alter the adhesion of tumor cells and their interactions with the microenvironment, facilitating cancer-induced immunomodulation and eventual metastasis. Changes in glycosylation arise from altered expression of glycosyltransferases, enzymes that catalyze the transfer of saccharide moieties to a wide range of acceptor substrates, such as proteins, lipids, and other saccharides in the endoplasmic reticulum (ER) and Golgi apparatus. Novel glycan structures in hematological malignancies represent new targets for the diagnosis and treatment of blood diseases. This review summarizes studies of the aberrant expression of glycans commonly found in hematological malignancies and their potential mechanisms and defines the specific roles of glycans as drivers or passengers in the development of hematological malignancies.

Photoactivated Hydrogen Sulfide Donor with a Near-Infrared Fluorescence Report System for Accelerated Chronic Wound Healing.

Delayed wound healing is one of the major diabetes complications that occur in 25% of diabetic patients. Specific wound management and combination treatment are required to repair the wound, which still remains a challenge with few effective therapies available currently. In this work, a new H2S donor PRO-F, which is characterized by the capability to promote wound healing in diabetes, was designed. PRO-F can be activated by light without consuming endogenous substances and the accompanying fluorescent signal makes the real-time tracking of released H2S possible. PRO-F is able to deliver H2S in an intracellular environment with moderate release efficiency (50%), which presents cytoprotective effects against excessive reactive oxygen species (ROS) induced damage. Furthermore, the potential of PRO-F to enhance chronic wound healing was validated by employing diabetic models. This work provides new insights into the therapeutic role of H2S donors in complex wound conditions, which should advance the pathophysiological research associated with H2S.

Smart Target-Initiated Catalytic DNA Junction Circuit Amplification Strategy for the Ultrasensitive Electrochemiluminescence Detection of MicroRNA.

One of the highly attractive research directions in the electrochemiluminescence (ECL) field is how to regulate and improve ECL efficiency. Quantum dots (QDs) are highly promising ECL materials due to their adjustable luminescence size and strong luminous efficiency. MoS2 NSs@QDs, an ECL emitter, is synthesized via hydrothermal methods, and its ECL mechanism is investigated using cyclic voltammetry and ECL-potential curves. Then, a stable and vertical attachment of a triplex DNA (tsDNA) probe to the MoS2 nanosheets (NSs) is applied to the electrode. Next, an innovative ECL sensor is courageously empoldered for precise and ultrasensitive detection of target miRNA-199a through the agency of ECL-resonance energy transfer (RET) strategy and a dextrous target-initiated catalytic three-arm DNA junction assembly (CTDJA) based on a toehold strand displacement reaction (TSDR) signal amplification approach. Impressively, the ingenious system not only precisely regulates the distance between energy donor-acceptor pairs leave energy less loss and more ECL-RET efficiency, but also simplifies the operational procedure and verifies the feasibility of this self-assembly process without human intervention. This study can expand MoS2 NSs@QDs utilization in ECL biosensing applications, and the proposed nucleic acid amplification strategy can become a miracle cure for ultrasensitive detecting diverse biomarkers, which helps researchers to better study the tumor mechanism, thereby unambiguously increasing cancer cure rates and reducing the risk of recurrence.

Transfer of miR-4755-5p through extracellular vesicles and particles induces decitabine resistance in recipient cells by targeting CDKN2B.

Decitabine (5-aza-2-deoxycytidine, DAC), a DNA-hypomethylating agent, has been one of the frontline therapies for clonal hematopoietic stem cell disorders, such as myelodysplastic syndrome and acute myeloid leukemia, but DAC-resistance often occurs and leads to treatment failure. Therefore, elucidating the mechanisms of DAC resistance is important for improving its therapeutic efficacy. The extracellular vesicles and particles (EVPs) have been reported to be involved in mediating drug resistance by transporting diverse bioactive components. In this study, we established the DAC-resistant cell line (KG1a-DAC) from its parental human leukemia-derived cell line KG1a and observed that EVPs released from KG1a-DAC can promote DAC-resistant in KG1a cells. Moreover, treatment with KG1a-DAC EVPs reduced the expression of cyclin-dependent kinase inhibitor 2B (CDKN2B) in KG1a cells. miRNA-Seq analysis revealed that miR-4755-5p is overexpressed in EVPs from KG1a-DAC. Dual-luciferase reporter assay and flow cytometry analysis confirmed that miR-4755-5p rendered KG1a cells resistant to the DAC by targeting CDKN2B gene. Taken together, miR-4755-5p in EVPs released from the DAC-resistant cells plays an essential role in inducing DAC-resistance, and is a potential therapeutic target for suppression of DAC resistance.

Reciprocal regulation of TWIST1 and OGT determines the decitabine efficacy in MDS/AML.

Chemoresistance poses a significant impediment to effective treatment strategies for myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). Our previous study unveiled that oncogene TWIST1 interacted with DNA methyltransferase 3a (DNMT3a) to regulate the decitabine (DAC) resistance in MDS/AML. However, the underlying mechanism of TWIST1 dysregulation in DAC resistance remained enigmatic. Here, we found that O-GlcNAc modification was upregulated in CD34+ cells from MDS/AML patients who do not respond to DAC treatment. Functional study revealed that O-GlcNAcylation could stabilize TWIST1 by impeding its interaction with ubiquitin E3 ligase CBLC. In addition, as one typical transcription factor, TWIST1 could bind to the promoter of O-GlcNAc transferase (OGT) gene and activate its transcription. Collectively, we highlighted the crucial role of the O-GlcNAcylated TWIST1 in the chemoresistance capacity of MDS/AML clonal cells, which may pave the way for the development of a new therapeutic strategy targeting O-GlcNAcylated proteins and reducing the ratio of MDS/AML relapse. Video Abstract.

Fully endoscopic microvascular decompression for the treatment of hemifacial spasm, trigeminal neuralgia, and glossopharyngeal neuralgia: a retrospective study.

BACKGROUND: Microvascular decompression (MVD) is already the preferred surgical treatment for medically refractory neurovascular compression syndromes (NVC) such as hemifacial spasm (HFS), trigeminal neuralgia (TN), and glossopharyngeal neuralgia (GPN). Endoscopy has significantly advanced surgery and provides enhanced visualization of MVD. The aim of this study is to analyze the efficacy and safety of fully endoscopic microvascular decompression (E-MVD) for the treatment of HFS, TN, and GPN, as well as to present our initial experience. MATERIALS AND METHODS: This retrospective case series investigated fully E-MVD performed in 248 patients (123 patients with HFS, 115 patients with TN, and 10 patients with GPN ) from December 2008 to October 2021 at a single institution. The operation duration, clinical outcomes, responsible vessels, intra- and postoperative complications, and recurrences were recorded. Preoperative and immediate postoperative magnetic resonance imaging (MRI) and computerized tomography (CT) were performed for imageological evaluation. The Shorr grading and Barrow Neurological Institute (BNI) pain score were used to evaluate clinical outcomes. The efficacy, safety, and risk factors related to the recurrence of the operation were retrospectively analysed, and the surgical techniques of fully E-MVD were summarised. RESULTS: A total of 248 patients (103 males) met the inclusion criteria and underwent fully E-MVD were retrospectively studied. The effective rate of 123 patients with HFS was 99.1%, of which 113 cases were completely relieved and 9 cases were significantly relieved. The effective rate of 115 patients with TN was 98.9%, of which 105 cases had completely pain relieved after surgery, 5 cases had significant pain relieved, 4 cases had partial pain relieved but still needed to be controlled by medication. The effective rate of 10 patients with GPN was 100%, 10 cases of GPN were completely relieved after surgery. As for complications, temporary facial numbness occurred in 4 cases, temporary hearing loss in 5 cases, dizziness with frequent nausea and vomiting in 8 cases, headache in 12 cases, and no cerebral hemorrhage, intracranial infection, and other complications occurred. Follow-up ranged from 3 to 42 months, with a mean of 18.6 ± 3.3 months. There were 4 cases of recurrence of HFS and 11 cases of recurrence of TN. The other effective patients had no recurrence or worsening of postoperative symptoms. The cerebellopontine angle (CPA) area ratio (healthy/affected side), the length of disease duration, and the type of responsible vessels are the risk factors related to the recurrence of HFS, TN, and GPN treated by fully E-MVD. CONCLUSIONS: In this retrospective study, our results suggest that the fully E-MVD for the treatment of NVC such as HFS, TN, and GPN, is a safe and effective surgical method. Fully E-MVD for the treatment of NVC has advantages and techniques not available with microscopic MVD, which may reduce the incidence of surgical complications while improving the curative effect and reducing the recurrence rate.

Clusterin Is a Prognostic Biomarker of Lower-Grade Gliomas and Is Associated with Immune Cell Infiltration.

Dysregulation of clusterin (CLU) has been demonstrated in many cancers and has been proposed as a regulator of carcinogenesis. However, the roles of CLU in gliomas remain unclear. The expression of CLU was assessed using TIMER2.0, GEPIA2, and R package 4.2.1 software, leveraging data from TCGA and/or GTEx databases. Survival analysis and Cox regression were employed to investigate the prognostic significance of CLU. Immune infiltration was evaluated utilizing TIMER2.0, ESTIMATE, and CIBERSORT. The findings reveal the dysregulated expression of CLU in many cancers, with a marked increase observed in glioblastoma and lower-grade glioma (LGG). High CLU expression indicated worse survival outcomes and was an independent risk factor for the prognosis in LGG patients. CLU was involved in immune status as evidenced by its strong correlations with immune and stromal scores and the infiltration levels of multiple immune cells. Additionally, CLU was co-expressed with multiple immune-related genes, and high CLU expression was associated with the activation of immune-related pathways, such as binding to the antigen/immunoglobulin receptor and aiding the cytokine and cytokine receptor interaction. In conclusion, CLU appears to play crucial roles in tumor immunity within gliomas, highlighting its potential as a biomarker or target in glioma immunotherapy.

Species Identification of Caviar Based on Multiple DNA Barcoding.

This study aimed to explore the applicability of DNA barcoding for assessing the authenticity of caviar on the Chinese market. A set of universal COI primers and two sets of designed primers based on COI and D-loop genes were used to identify maternal species of samples from 21 batches of caviar. The results showed that the PCR products from three sets of primers had more than 98% similarity to the sequences in database. The COI gene could not distinguish sturgeons with closed genetic relationships, while D-loop gene could effectively improve the accuracy of DNA barcoding and was more suitable to the identification of interspecific sturgeon than the COI gene. The neighbor-joining dendrogram further confirmed the applicability and accuracy of COI and D-loop genes in identifying maternal relatives of caviar (Acipenser baerii/Acipenser gueldenstaedtii/Acipenser schrenckii/Huso dauricus/Huso huso). Despite the limitations of mitochondrial DNA in identifying hybrid sturgeon species, the presence of counterfeit caviar of non-sturgeon ingredients could be excluded. All the caviar samples were identified successfully as sturgeon species, but the mislabeling rate of species was 33.4%, indicating that there were illegal phenomena such as disorderly labeling, mislabeling, and adulteration on the market.

Chemical Modification of Polysaccharides: A Review of Synthetic Approaches, Biological Activity and the Structure-Activity Relationship.

Natural polysaccharides are macromolecular substances with great potential owing to their wide biological activity and low toxicity. However, not all polysaccharides have significant pharmacodynamic activity; hence, appropriate chemical modification methods can be selected according to the unique structural characteristics of polysaccharides to assist in enhancing and promoting the presentation of their biological activities. This review summarizes research progress on modified polysaccharides, including common chemical modification methods, the change in biological activity following modification, and the factors affecting the biological activity of chemically modified polysaccharides. At the same time, the difficulties and challenges associated with the structural modification of natural polysaccharides are also outlined in this review. Thus, research on polysaccharide structure modification is critical for improving the development and utilization of sugar products.

[Complete chloroplast genome sequencing and phylogeny of wild Atractylodes lancea from Yuexi, Anhui province].

This study investigated the choroplast genome sequence of wild Atractylodes lancea from Yuexi in Anhui province by high-throughput sequencing, followed by characterization of the genome structure, which laid a foundation for the species identification, analysis of genetic diversity, and resource conservation of A. lancea. To be specific, the total genomic DNA was extracted from the leaves of A. lancea with the improved CTAB method. The chloroplast genome of A. lancea was sequenced by the high-throughput sequencing technology, followed by assembling by metaSPAdes and annotation by CPGAVAS2. Bioiformatics methods were employed for the analysis of simple sequence repeats(SSRs), inverted repeat(IR) border, codon bias, and phylogeny. The results showed that the whole chloroplast genome of A. lancea was 153 178 bp, with an 84 226 bp large single copy(LSC) and a 18 658 bp small single copy(SSC) separated by a pair of IRs(25 147 bp). The genome had the GC content of 37.7% and 124 genes: 87 protein-coding genes, 8 rRNA genes, and 29 tRNA genes. It had 26 287 codons and encoded 20 amino acids. Phylogenetic analysis showed that Atractylodes species clustered into one clade and that A. lancea had close genetic relationship with A. koreana. This study established a method for sequencing the chloroplast genome of A. lancea and enriched the genetic resources of Compositae. The findings are expected to lay a foundation for species identification, analysis of genetic diversity, and resource conservation of A. lancea.

[Distribution of memory B cell subsets in peripheral blood of children with frequently relapsing nephrotic syndrome]. / é¢‘å¤å‘è‚¾ç— ç»¼åˆå¾æ‚£å„¿å¤–å‘¨è¡€è®°å¿†B细胞亚群分布变化.

OBJECTIVES: To investigate the change in the distribution of memory B cell subsets in children with frequently relapsing nephrotic syndrome (FRNS) during the course of the disease. METHODS: A total of 35 children with primary nephrotic syndrome (PNS) who attended the Department of Pediatrics of the Affiliated Hospital of Xuzhou Medical University from October 2020 to October 2021 were enrolled as subjects in this prospective study. According to the response to glucocorticoid (GC) therapy and frequency of recurrence, the children were divided into two groups: FRNS (n=20) and non-FRNS (NFRNS; n=15). Fifteen children who underwent physical examination were enrolled as the control group. The change in memory B cells after GC therapy was compared between groups, and its correlation with clinical indicators was analyzed. RESULTS: Before treatment, the FRNS and NFRNS groups had significantly increased percentages of total B cells, total memory B cells, IgD+ memory B cells, and IgE+ memory B cells compared with the control group, and the FRNS group had significantly greater increases than the NFRNS group (P<0.05); the FRNS group had a significantly lower percentage of class-switched memory B cells than the NFRNS and control groups (P<0.05). After treatment, the FRNS and NFRNS groups had significant reductions in the percentages of total B cells, total memory B cells, IgM+IgD+ memory B cells, IgM+ memory B cells, IgE+ memory B cells, IgD+ memory B cells, and IgG+ memory B cells (P<0.05) and a significant increase in the percentage of class-switched memory B cells (P<0.05). The FRNS group had a significantly higher urinary protein quantification than the NFRNS and control groups (P<0.05) and a significantly lower level of albumin than the control group (P<0.05). In the FRNS group, urinary protein quantification was negatively correlated with the percentage of class-switched memory B cells and was positively correlated with the percentage of IgE+ memory B cells (P<0.05). CONCLUSIONS: Abnormal distribution of memory B cell subsets may be observed in children with FRNS, and the percentages of IgE+ memory B cells and class-switched memory B cells can be used as positive and negative correlation factors for predicting recurrence after GC therapy in these children.