Genome-Wide Identification of bZIP Transcription Factors in Cymbidium ensifolium and Analysis of Their Expression under Low-Temperature Stress.

The basic leucine zipper (bZIP) transcription factors constitute the most widely distributed and conserved eukaryotic family. They play crucial roles in plant growth, development, and responses to both biotic and abiotic stresses, exerting strong regulatory control over the expression of downstream genes. In this study, a genome-wide characterization of the CebZIP transcription factor family was conducted using bioinformatic analysis. Various aspects, including physicochemical properties, phylogenetics, conserved structural domains, gene structures, chromosomal distribution, gene covariance relationships, promoter cis-acting elements, and gene expression patterns, were thoroughly analyzed. A total of 70 CebZIP genes were identified from the C. ensifolium genome, and they were randomly distributed across 18 chromosomes. The phylogenetic tree clustered them into 11 subfamilies, each exhibiting complex gene structures and conserved motifs arranged in a specific order. Nineteen pairs of duplicated genes were identified among the 70 CebZIP genes, with sixteen pairs affected by purifying selection. Cis-acting elements analysis revealed a plethora of regulatory elements associated with stress response, plant hormones, and plant growth and development. Transcriptome and qRT-PCR results demonstrated that the expression of CebZIP genes was universally up-regulated under low temperature conditions. However, the expression patterns varied among different members. This study provides theoretical references for identifying key bZIP genes in C. ensifolium that confer resistance to low-temperature stress, and lays the groundwork for further research into their broader biological functions.

The antihyperuricemia activity of Astragali Radix through regulating the expression of uric acid transporters via PI3K/Akt signalling pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: Astragali Radix (AR) is the dry root of the leguminous plants Astragalus membranaceus (Fisch) Beg. var. mongholicus (Beg) Hsiao, and Astragalus membranaceus (Fisch) Bge., being used as a medicinal and edible resource. AR is used in traditional Chinese medicine prescriptions to treat hyperuricemia, but this particular effect is rarely reported, and the associated mechanism of action is still need to be elucidated. AIM OF THE STUDY: To research the uric acid (UA)-lowering activity and mechanism of AR and the representative compounds through the constructed hyperuricemia mouse and cellular models. MATERIALS AND METHODS: In our study, the chemical profile of AR was analysed by UHPLC-QE-MS, as well as the mechanism of action of AR and the representative compounds on hyperuricemia was studied through the constructed hyperuricemia mouse and cellular models. RESULTS: The main compounds in AR were terpenoids, flavonoids and alkaloids. Mice group treated with the highest AR dosage showed significantly lower (p < 0.0001) serum uric acid (208 ± 9 µmol/L) than the control group (317 ± 11 µmol/L). Furthermore, UA increased in a dose-dependence manner in urine and faeces. Serum creatinine and blood urea nitrogen standards, as well as xanthine oxidase in mice liver, decreased (p < 0.05) in all cases, indicating that AR could relieve acute hyperuricemia. UA reabsorption protein (URAT1 and GLUT9) was down-regulated in AR administration groups, while the secretory protein (ABCG2) was up-regulated, indicating that AR could promote the excretion of UA by regulating UA transporters via PI3K/Akt signalling pathway. CONCLUSION: This study validated the activity, and revealed the mechanism of AR in reducing UA, which provided experimental and clinical basis for the treatment of hyperuricemia with it.

Improved colonic inflammation by nervonic acid via inhibition of NF-κB signaling pathway of DSS-induced colitis mice.

BACKGROUND: Nervonic acid (C24:1∆15, 24:1 ω-9, cis-tetracos-15-enoic acid; NA), a long-chain monounsaturated fatty acid, plays an essential role in prevention of metabolic diseases, and immune regulation, and has anti-inflammatory properties. As a chronic, immune-mediated inflammatory disease, ulcerative colitis (UC) can affect the large intestine. The influences of NA on UC are largely unknown. PURPOSE: The present study aimed to decipher the anti-UC effect of NA in the mouse colitis model. Specifically, we wanted to explore whether NA can regulate the levels of inflammatory factors in RAW264.7 cells and mouse colitis model. METHODS: To address the above issues, the RAW264.7 cell inflammation model was established by lipopolysaccharide (LPS), then the inflammatory factors tumor necrosis factor-α (TNF-α), Interleukin-6 (IL-6), Interleukin-1ß (IL-1ß), and Interleukin-10 (IL-10) were detected by Enzyme-linked immunosorbent assay (ELISA). The therapeutic effects of NA for UC were evaluated using C57BL/6 mice gavaged dextran sodium sulfate (DSS). Hematoxylin and eosin (H&E) staining, Myeloperoxidase (MPO) kit assay, ELISA, immunofluorescence assay, and LC-MS/MS were used to assess histological changes, MPO levels, inflammatory factors release, expression and distribution of intestinal tight junction (TJ) protein ZO-1, and metabolic pathways, respectively. The levels of proteins involved in the nuclear factor kappa-B (NF-κB) pathway in the UC were investigated by western blotting and RT-qPCR. RESULTS: In vitro experiments verified that NA could reduce inflammatory response and inhibit the activation of key signal pathways associated with inflammation in LPS-induced RAW264.7 cells. Further, results from the mouse colitis model suggested that NA could restore intestinal barrier function and suppress NF-κB signal pathways to ameliorate DSS-induced colitis. In addition, untargeted metabolomics analysis of NA protection against UC found that NA protected mice from colitis by regulating citrate cycle, amino acid metabolism, pyrimidine and purine metabolism. CONCLUSION: These results suggested that NA could ameliorate the secretion of inflammatory factors, suppress the NF-κB signaling pathway, and protect the integrity of colon tissue, thereby having a novel role in prevention or treatment therapy for UC. This work for the first time indicated that NA might be a potential functional food ingredient for preventing and treating inflammatory bowel disease (IBD).

Effect of Calcium-based Phosphate Binders Versus Sevelamer on Mortality of Patients with Hemodialysis: A Meta-analysis.

Chronic kidney disease is a public health problem. The purpose of this study was to compare the effects of sevelamer and calciumbased binders on mortality of hemodialysis patients. PubMed, EMBASE and Web of Science were searched for related articles published before May 14, 2020. We included six studies with 43330 participants, of which 21147 and 22183 received calciumbased phosphate binders and sevelamer, respectively. In the analysis of unadjusted data, sevelamer could lower cardiovascular mortality. When adjusted HRs was pooled, the cardiovascular mortality did not differ significantly in the sevelamer and calcium-based phosphate binders groups. Additionally, the all-cause mortality rate in sevelamer group was different from that in calcium-based phosphate binders group. However, sevelamer could not lower all-cause mortality in terms of the adjusted data. No significant difference was found in calcium and phosphorus between calcium-based phosphate binders and sevalmer. Sensitivity analysis showed that partial results of the study were inconsistent. There was no difference in the effect of sevelamer and calciumbased phosphate binders on the risk of all-cause mortality in patients with hemodialysis, after adjusting confounders. However, given the instability of the results, the results need to be further confirmed by a large sample and high quality RCTs.  DOI: 10.52547/ijkd.6814.

Association Between Hemoglobin and Major Adverse Cardiac Events: A Secondary Analysis from A Retrospective Cohort Study.

BACKGROUND: This study aims to investigate the association between hemoglobin and major adverse cardiac events (MACE) in patients with stable coronary artery disease (CAD) who were treated with percutaneous coronary intervention (PCI). METHODS: This was a secondary analysis based on a retrospective cohort study involving 204 patients with stable CAD. Patients were divided into four groups according to hemoglobin levels (Q1: 6.90-12.30 g/dL; Q2: 12.40-13.80 g/dL; Q3: 13.90-14.90 g/dL; Q4: 15.00-19.00 g/dL). Lasso regression analysis was performed to select characteristic variables and reduce dimensions. Odds ratio (OR) and 95% confidence interval (CI) were used for comparing data among groups. RESULTS: After an average follow-up of 783 days, 28/204 (17.72%) patients with CAD developed MACE. Univariate analysis data showed that hemoglobin level was negatively associated with the incidence of MACE in patients with CAD treated with PCI (Q2 vs Q1: OR=0.19, P=0.005; Q3 vs Q1: OR=0.25, P=0.013; Q4 vs Q1: OR=0.13, P=0.002). The negative correlation between hemoglobin and MACE still existed after adjusting selected variables obtained from multivariate regression analysis (Q2 vs Q1: OR= 0.18, P=0.007; Q3 vs Q1: OR=0.29, P=0.038; Q4 vs Q1: OR=0.19, P=0.016). Curve fitting illustrated that hemoglobin level presented a non-linear and negative association with MACE in patients with CAD treated with PCI. CONCLUSIONS: Hemoglobin level can be utilized as a prognostic indicator of MACE in patients with CAD after PCI.

Effect of silencing FBXO2 expression on proliferation, invasion, migration, and EMT of gastric cancer cells / 中国肿瘤生物治疗杂志

@#［摘要］ 目的：探讨F 框蛋白2（F-box only protein 2，FBXO2）基因在人胃癌细胞系中表达及其对胃癌细胞增殖、迁移、侵袭和 EMT 的影响。方法：选择胃癌细胞系MGC-803、AGS、SGC-7901、MKN-28 以及正常胃黏膜上皮细胞株GES-1，qPCR 法检测细 胞中FBXO2 mRNA表达水平。设计靶向抑制FBXO2 表达的特异siRNA，并瞬时转染MGC-803 细胞，转染siRNA无义序列的为 阴性对照。qPCR法检测转染48 h 后MGC-803 细胞中FBXO2 mRNA表达水平；用MTT法、细胞划痕愈合法、Transwell 小室法检 测降低FBXO2 表达对细胞增殖、迁移和侵袭的影响，WB 法检测细胞中EMT 相关蛋白E-cadherin、N-cadherin、vimentin 的表达。 结果：4 种胃癌细胞中FBXO2 mRNA表达水平显著高于胃黏膜上皮细胞GES-1（P<0.05 或P<0.01）。与阴性对照组相比，siRNAFBXO2 组MGC-803 细胞中FBXO2 mRNA表达下调（P<0.01），该细胞的增殖、迁移和侵袭能力受到显著抑制（P<0.05 或P<0.01）， E-cadherin 蛋白表达明显升高（P<0.01），N-cadherin、vimentin 蛋白表达显著降低（均P<0.01）。结论：低表达的FBXO2 可抑制胃 癌细胞的增殖、迁移和侵袭能力，该抑制作用可能与EMT过程有关。

Cognitive Impairment Among Aging People Living With HIV on Antiretroviral Therapy: A Cross-Sectional Study in Hunan, China.

Our cross-sectional study examined the prevalence of cognitive impairment among people living with HIV (PLWH) aged 60 years or older. The sample, composed of 250 PLWH, was recruited from 2 clinics in Hunan, China. Structured questionnaires guided face-to-face interviews, including items addressing demographic characteristics, regimens of antiretroviral therapy, and cognitive status as measured by the Montreal Cognitive Assessment. Findings revealed cognitive function of this population was significantly lower than that of uninfected individuals based on historical comparisons; 87.2% (n = 218) of PLWH in our study had cognitive impairment. Global cognitive function as well as the domains of language and orientation decreased with age. Global cognitive function was associated with sex and education, but not with antiretroviral therapy regimens. These findings support an urgent need to include routine screening for cognitive function in older PLWH and the need to consider the complexity of the evaluation process.

C-Reactive Protein and All-Cause Mortality in Patients with Stable Coronary Artery Disease: A Secondary Analysis Based on a Retrospective Cohort Study.

BACKGROUND The association between C-reactive protein (CRP) and all-cause mortality (ACM) in patients with stable coronary artery disease (CAD) is unclear. Therefore, the aim of the present study was to explore the correlation between CRP and ACM in stable CAD patients. MATERIAL AND METHODS This study was a secondary analysis. Between October 2014 and October 2017, 196 patients aged 43 to 98 years who had a first diagnosis of stable CAD were recruited into this study. We divided the patients into 4 groups (Quartile 1: 0.01-0.03 mg/dL; Quartile 2: 0.04-0.11 mg/dL; Quartile 3: 0.12-0.33 mg/dL; and Quartile 4: 0.34-9.20 mg/dL) according to the concentration of CRP. The indicator surveyed in this research was ACM. RESULTS During a median follow-up of 783 days, ACM occurred in 18 patients, with a mortality rate of 9.18% (18/196). Univariate analysis showed that elevated CRP was closely related to ACM in stable CAD patients (P<0.005). After controlling for potential confounding factors by multivariate logistic regression analysis, this relationship still existed. Pearson correlation analysis showed that elevated CRP log10 transform was associated with LVEF (r=-0.1936, P=0.0067). Receiver operating characteristic (ROC) curve analysis showed that the optimal concentration of CRP for the diagnosis of ACM was 0.345, and the area under the curve (AUC) was 0.735. CONCLUSIONS Elevated CRP is associated with ACM in stable CAD patients, and the best diagnostic threshold is 0.345.

Enhancement of soluble CD28 levels in the serum of Graves' disease.

Graves' disease is an autoimmune disease of the thyroid gland mediated by T cells. CD28, a member of costimulatory molecules, plays a pivotal role in regulating T-cell responses. Plasma-soluble CD28 is one form of CD28 in peripheral blood. To investigate the concentrations of soluble CD28 in patients with Graves' disease, we used a sensitive dual monoclonal antibody sandwich enzyme-linked immunosorbent assay (ELISA) to detect the soluble form of CD28. Our results suggested that mean concentrations of soluble CD28 in plasma of patients with Graves' disease were 1.79 ±1.52 ng/ml, and levels of soluble CD28 in healthy subjects were only 0.83 ±1.35 ng/ml. Concentrations of soluble CD28 detected in patients with Graves' disease were significantly higher than those of healthy subjects (p < 0.01). Moreover, there was a significant positive correlation between the concentrations of soluble CD28 in plasma and levels of FT3 (r = 0.663), FT4 (r = 0.624) and TRAb (r = 0.728) in serum, but a negative correlation was found between sCD28 levels and TSH (r = -0.726). Through in vitro experiments we observed that engagement of soluble CD28 protein and B7-1/B7-2 molecules expressed on dendritic cells could exert the secretion of cytokine IL-6, which may promote the production of autoantibody and aggravate Graves' disease. Therefore, aberrant elevation of plasma-soluble CD28 in patients with Graves' disease may reflect the dysregulation of immune system, and may serve as a useful biomarker in Graves' disease diagnosis.