The bacterial strain JI6, which has plant growth-promoting characteristics, was isolated from ginseng rhizosphere soil. It can produce indoleacetic acid (IAA), dissolve phosphorus, dissolve potassium and fix nitrogen and significantly promoted the growth of ginseng. The strain was identified as Pseudomonas thivervalensis by morphological, physiological and biochemical characteristics and 16S rDNA sequence analysis. The bud length of ginseng seeds treated with 109 CFU/mL JI6 suspension increased significantly by 42.76% after 15 days. The fresh weight and the ginsenoside content of 3-year-old ginseng roots significantly increased by 38.72% with the 108 CFU/mL JI6 suspension for five months in the field. The strain JI6 can inhibit the six fungal pathogens and control rusty root rot of ginseng. For the biocontrol mechanism, the strain JI6 can colonize in ginseng rhizosphere soil. After treatment with JI6, the activitie of five ginseng defence enzymes of β-1.3 glucanase, peroxidase and phenylalanine ammonia-lyase, chitinase and superoxide dismutase and four soil enzymes of urease, phosphatase, invertase, and catalase significantly increased. The effect of strain JI6 on soil microbial community showed that the microbial diversity increased and the abundance of beneficial microorganisms elevated, while the abundance of pathogenic microorganisms decreased. This study indicate the great potential of P. thivervalensis JI6 for use as a biological agent for the control of ginseng rusty root rot.
Background: Despite the implementation of the universal salt iodization (USI) program for correction of iodine deficiency in China for ∼20 years, the actual iodine nutrition status of Chinese residents and the prevalence of iodine deficiency and iodine excess are issues that need to be addressed. This nationally representative cross-sectional study was conducted across all 31 provinces of mainland China to gather extensive data on iodine nutrition status and the influential factors. Methods: This study included 78,470 participants, aged 18 years or older, who were interviewed and asked to answer a questionnaire. Urine iodine concentration (UIC) was measured by the inductively coupled plasma mass spectrometry method, and goiter was examined by thyroid ultrasonography. In addition, sixty 9-11 years old school children in each province were randomly selected to evaluate the UIC and thyroid ultrasonography. The iodine nutrition status was determined according to the World Health Organization guidelines. Results: The iodized salt coverage was 95.37%. The median urine iodine (MUI) was 177.89 μg/L (interquartile range [IQR], 117.89-263.90 μg/L) and goiter prevalence was 1.17% (confidence interval [95% CI 0.95-1.43]) in the adult population. The MUI was 199.75 μg/L (IQR, 128.41-303.37 μg/L) in school-age children, and goiter prevalence was 3.50% [95% CI, 2.93-4.13]. The percentage of individuals with UIC <50 μg/L was 3.43%, <20%. Analysis indicated that sex, age, geographic factors, body mass index, and smoking habits influence the iodine nutrition level. Conclusion: The mandatory USI program has successfully eliminated iodine deficiency disorders, and the findings indicate that the iodine nutrition level in the general population is within the safe range.
Abstract ENCODE comprises thousands of functional genomics datasets, and the encyclopedia covers hundreds of cell types, providing a universal annotation for genome interpretation. However, for particular applications, it may be advantageous to use a customized annotation. Here, we develop such a custom annotation by leveraging advanced assays, such as eCLIP, Hi-C, and whole-genome STARR-seq on a number of data-rich ENCODE cell types. A key aspect of this annotation is comprehensive and experimentally derived networks of both transcription factors and RNA-binding proteins (TFs and RBPs). Cancer, a disease of system-wide dysregulation, is an ideal application for such a network-based annotation. Specifically, for cancer-associated cell types, we put regulators into hierarchies and measure their network change (rewiring) during oncogenesis. We also extensively survey TF-RBP crosstalk, highlighting how SUB1, a previously uncharacterized RBP, drives aberrant tumor expression and amplifies the effect of MYC, a well-known oncogenic TF. Furthermore, we show how our annotation allows us to place oncogenic transformations in the context of a broad cell space; here, many normal-to-tumor transitions move towards a stem-like state, while oncogene knockdowns show an opposing trend. Finally, we organize the resource into a coherent workflow to prioritize key elements and variants, in addition to regulators. We showcase the application of this prioritization to somatic burdening, cancer differential expression and GWAS. Targeted validations of the prioritized regulators, elements and variants using siRNA knockdowns, CRISPR-based editing, and luciferase assays demonstrate the value of the ENCODE resource.
To investigate the efficacy of bevacizumab combined with chemotherapy in the treatment of colorectal cancer (CRC) and to analyze the effects on brain peptides, intestinal flora, and oxidative stress in CRC patients.Eighty two patients with CRC who were admitted to our hospital from March 2018 to June 2021 were selected as the research subjects and divided into the control group (n = 41) and the observation group (n = 41). The control group was treated with XELOX chemotherapy, and the observation group was additionally treated with bevacizumab, which was repeated every 3 weeks for a total of two treatments. The therapeutic effects of the two groups were evaluated after treatment. The brain-gut peptide index, intestinal flora index and oxidative stress index were detected, and the adverse reactions of the two groups were recorded.In the control group, ER was 36.59% (15/41) and DCR was 73.17% (30/41). In the observation group, ER was 63.41% (26/41) and DCR was 90.24% (37/41). ER and DCR in the observation group were higher than those in the control group (P < 0.05). After treatment, the levels of motilin and gastrin in the observation group were lower than those in the control group, and ghrelin was higher than that in the control group (P < 0.05). After treatment, the levels of Bifidobacterium, Lactobacilli and Enterococcus in the observation group were higher than those in the control group, and the level of Escherichia coli was lower than that in the control group (P < 0.05). After treatment, the SOD level of the observation group was lower than that of the control group, and the MDA level was higher than that of the control group.Bevacizumab combined with chemotherapy has good efficacy in the treatment of colorectal cancer patients, which can effectively improve the gastrointestinal motility of patients, regulate the intestinal flora of the body, rebuild the microecological balance, effectively reduce the oxidative stress response of patients, and reduce the incidence of adverse reactions.
Abstract Background radiation-induced intestinal injury (RIII) is an important cause of death in nuclear accidents and common complication after radiotherapy in patients with pelvic, abdominal, or retroperitoneal tumors. Up to now there is no effective means to prevent or treat RIII due to its complex mechanism, in which the death of intestinal cells is the main reason. Recently, GSDMD-mediated pyroptosis was identified as an important type of cell death and play a role in many diseases. However, the effect of pyroptosis on RIII is still unclear. Method using GSDMD knockout mice, the role of pyroptosis in the RIII was investigated. By detecting the release of LDH, expression of GSDMD, Caspase-11, Caspase-1 and absorption rate of SYTOX Green, the pyroptosis of radiated Mode-k cells was determined, simultaneously the common pyroptosis induced by LPS was conducted as positive control. Further, the upstream of GSDMD were screened by predictive analysis of transcription factors combing RNA-seq. Results we showed that GSDMD-mediated pyroptosis is involved in the process of RIII, and unexpectedly found that radiation induced a delayed pyroptosis that is substantially different from common pyroptosis induced by such as LPS. Further investigation revealed that radiation-induced DNA damage up-regulated the expression of P53, which subsequently transcribes GSDMD. In addition, the up-regulated GSDMD led to pyroptosis simultaneously promoting Ca 2+ influx that afterwards enhanced apoptosis induced by radiation. Finally, targeting GSDMD, disulfiram displayed a potential protection for RIII. Conclusion radiation could induce delayed pyroptosis in the intestinal epithelial cell that is greatly different from common pyroptosis. During that process, GSDMD was cleaved and had inducible high expression which was mainly mediated by P53 transcription.
<abstract><p>A two-patch model with additive Allee effect is proposed and studied in this paper. Our objective is to investigate how dispersal and additive Allee effect have an impact on the above model's dynamical behaviours. We discuss the local and global asymptotic stability of equilibria and the existence of the saddle-node bifurcation. Complete qualitative analysis on the model demonstrates that dispersal and Allee effect may lead to persistence or extinction in both patches. Also, combining mathematical analysis with numerical simulation, we verify that the total population abundance will increase when the Allee effect constant $ a $ increases or $ m $ decreases. And the total population density increases when the dispersal rate $ D_{1} $ increases or the dispersal rate $ D_{2} $ decreases.</p></abstract>
A vegetarian diet may prevent elevation of blood pressures and lower the risk for hypertension through lower degrees of obesity, inflammation, and insulin resistance. This study investigated the association between a vegetarian diet and hypertension incidence in a cohort of Taiwanese adult nonsmokers and examined whether this association was mediated through inflammation, abdominal obesity, or insulin resistance (using fasting glucose as a proxy).This matched cohort study was from the 1994-2008 MJ Health Screening Database. Each vegetarian was matched with five nonvegetarians by age, sex, and study site. The analysis included 4109 nonsmokers (3423 nonvegetarians and 686 vegetarians), followed for a median of 1.61 years. The outcome includes hypertension incidence, as well as SBP and DBP levels. Regression analysis was performed to assess the association between vegetarian diet and hypertension incidence or future blood pressure levels in the presence/absence of potential mediators.Vegetarians had a 34% lower risk for hypertension, adjusting for age and sex (odds ratio: 0.66, 95% confidence interval: 0.50-0.87; SBP: -3.3 mmHg, P < 0.001; DBP: -1.5 mmHg, P < 0.001). The results stay statistically significant after further adjustment for C-reactive protein, waist circumference, and fasting glucose (odds ratio: 0.72, 95% confidence interval: 0.55-0.86; SBP: -2.4 mmHg, P < 0.05; DBP: -1.1 mmHg, P < 0.05). The protective association between vegetarian diet and hypertension appeared to be consistent across age groups.Taiwanese vegetarians had lower incidence of hypertension than nonvegetarians. Vegetarian diets may protect against hypertension beyond lower abdominal obesity, inflammation, and insulin resistance.
Resistance to thyroid hormone beta (RTHβ) is an autosomal dominant hereditary disorder that is difficult to diagnose because of its rarity and variable clinical features, which are caused by mutations in the thyroid hormone receptor beta (THRB) gene. Recent studies have indicated a close association between THRB mutations and human cancers, but the mechanistic role of THRB mutations in carcinogenesis is unknown. Herein, we report two cases of RTHβ coexisting with papillary thyroid carcinoma (PTC) and their follow-up results. Two female patients presented with elevated serum thyroid hormone levels and nonsuppressed thyrotropin (TSH). Genetic analysis showed that each patient had a THRB gene mutation (p.P453T and p. R320H). Based on the results of ultrasound-guided fine-needle aspiration biopsy, the thyroid nodules were suspected to be PTC. Intraoperative pathology confirmed that the two patients had PTC with multifocal carcinoma of both lobes. One patient underwent total thyroidectomy and central lymph node dissection, and the other underwent total thyroidectomy alone. Following surgery, large doses of levothyroxine were administered to suppress TSH levels and prevent recurrent or persistent disease. However, it is difficult to continually suppress TSH levels below the upper limit of the normal range. To date, the two patients have experienced no recurrence of PTC on ultrasound.
To explore the differential metabolites in the serum of infants with iron deficiency anemia(IDA) and non iron deficiency anemia, and to explore the potential biomarkers.Non-targeted metabolomics of 30 infants with iron deficiency anemia aged 6-11 months and 30 infants with non iron deficiency anemia aged 6-11 months were analyzed by ultra-high performance liquid chromatography with time of flight mass spectrometry using Acquity UPLC BEH C_(18) column(100 mm×2.1 mm, 1.8 μm). The differences of metabolites between the two groups were analyzed by principal component analysis(PCA) and orthogonal partial least squares discriminant analysis(OPLS-DA). Differential metabolites were screened according to OPLS-DA variable importance projection(VIP) >1. The related metabolic pathways involved in the markers were analyzed based on the KEGG database.Differences in serum metabolic profiles between iron deficiency anemia group and non iron deficiency anemia group were observed. The 44 potential biomarkers were mainly lipids. Combined with pathway analysis, the metabolic pathways related to different metabolites included glycerophosphingolipid metabolism and sphingolipid metabolism.There are differences in lipid metabolites between infants with non iron deficiency anemia and iron deficiency anemia, suggesting that the occurrence and progress of iron deficiency anemia are related to lipid metabolism.
DNA methylation is thought to be extensively involved in the pathogenesis of many diseases, including major psychosis. However, most studies focus on DNA methylation alteration at promoters of protein-coding genes, despite the poor correlation between DNA methylation and gene expression.We analyzed differentially methylated regions and differentially expressed genes in patients with schizophrenia and bipolar disorder and normal subjects. Gene expression and DNA methylation were analyzed with RNA-seq and MeDIP-seq of post-mortem brain tissue (brain region BA9) cohort in five schizophrenia, seven bipolar disorder cases and six controls, respectively.Here, we performed a large-scale integrative analysis using MeDIP-seq, coupled with RNA-seq, on brain samples from major psychotic and normal subjects and observed obvious discrepancy between DNA methylation and gene expression. We found that differentially methylated regions (DMRs) were distributed across different types of genomic elements, especially introns. These intronic DMRs were significantly enriched for diverse regulatory elements, such as enhancers and binding sites of certain transcriptional factors (e.g., Pol3). Notably, we found that parts of intronic DMRs overlapped with some intragenic miRNAs, such as hsa-mir-7-3. These intronic DMR-related miRNAs were found to target many differentially expressed genes. Moreover, functional analysis demonstrated that differential target genes of intronic DMR-related miRNAs were sufficient to capture many important biological processes in major psychosis, such as neurogenesis, suggesting that miRNAs may function as important linkers mediating the relationships between DNA methylation alteration and gene expression changes.Collectively, our study indicated that DNA methylation alteration could induce expression changes indirectly by affecting miRNAs and the exploration of DMR-related miRNAs and their targets enhanced understanding of the molecular mechanisms underlying major psychosis.
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