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"Liang, Xiao-Na"
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التخفيف من حدة الفقر في الصين المعاصرة
استنادا إلى نظرة عامة على أوضاع الفقر، يقدم هذا الكتاب مسار التخفيف من حدة الفقر والتنمية في الصين، ويشرح نموذج التنمية والتخفي من حدة الفقر بخصائص صينية والتمسك بمباديء (سيطرة الحكومة ومشاركة المجتمع والاعتماد على الذات والتنمية الموجهة والتنمية الشاملة) كما يقدم الكتاب تلخيصا شاملا لإنجازات الصين العظيمة وخبراتها الهامة وإسهاماتها الرئيسية في قضية التخفيف من حدة الفقر في العالم، ويعرض بإيجاز نظرات وممارسات التخفيف المستهدف من الفقر في العصر الجديد من أجل توفير مراجع لكسب المعركة ضد الفقر في الصين وقضية التخفيف من حدة الفقر في العالم.
Book
A New HPLC-UV Method Using Hydrolyzation with Sodium Hydroxide for Quantitation of Trans-p-Hydroxycinnamic Acid and Total Trans-p-Hydroxycinnamic Acid Esters in the Leaves of Ligustrum robustum
Trans-p-hydroxycinnamic acid and its esters in the leaves of Ligustrum robustum might be a new resource to prevent diabetes and its complications. In the present study, a new HPLC-UV method using hydrolyzation with sodium hydroxide for quantitation of trans-p-hydroxycinnamic acid and total trans-p-hydroxycinnamic acid esters in the leaves of L. robustum was developed, since it was difficult and troublesome to analyze no less than 34 trans-p-hydroxycinnamic acid esters by usual HPLC. The extract of L. robustum was hydrolyzed with sodium hydroxide at 80 °C for 2 h, and then, hydrochloride was added. HPLC analysis was performed in reverse phase mode using a C-18 column, eluting with methanol-0.1% acetic acid aqueous solution (40:60, v/v) in isocratic mode at a flow rate of 1.0 mL·min−1 and detecting at 310 nm. The linear range for trans-p-hydroxycinnamic acid was 11.0–352.0 μg·mL−1 (r2 = 1.000). The limit of detection and limit of quantification were 2.00 and 6.07 μg·mL−1, respectively. The relative standard deviations of intra-day and inter-day variabilities for trans-p-hydroxycinnamic acid were less than 2%. The percentage recovery of trans-p-hydroxycinnamic acid was 103.3% ± 1.1%. It is the first HPLC method using hydrolyzation for quantification of many carboxylic esters. Finally, the method was used successfully to determine trans-p-hydroxycinnamic acid and total trans-p-hydroxycinnamic acid esters in various extracts of the leaves of L. robustum. The 60–70% ethanol extracts of L. robustum showed the highest contents of free trans-p-hydroxycinnamic acid (3.96–3.99 mg·g−1), and the 50–80% ethanol extracts of L. robustum displayed the highest contents of total trans-p-hydroxycinnamic acid esters (202.6–210.6 mg·g−1). The method can be applied also to the quality control of the products of L. robustum.
Journal Article
Upregulation of interferon-γ activation in patients with anti-interferon-γ autoantibodies immunodeficiency syndrome: insights from single-cell analysis
Anti-interferon-γ autoantibodies (AIGAs) immunodeficiency syndrome is an emerging adult-onset immunodeficiency causing opportunistic infections. However, its comprehensive immune landscape remains elusive. This study presents the first single-cell RNA sequencing (scRNA-seq) analysis of AIGAs immunodeficiency syndrome, aiming to delineate its pathogenic mechanisms.
We performed scRNA-seq on peripheral blood mononuclear cells (PBMCs) from 8 AIGAs immunodeficiency syndrome patients (4 infective, 4 stable phase) and 3 healthy controls. Findings were validated by flow cytometry in an expanded cohort (15 patients vs. 10 controls).
Single-cell RNA sequencing of PBMCs from patients with AIGAs immunodeficiency syndrome identified a comprehensive immune subset profile, including effector memory CD4
T cells, naive CD4
T cells, regulatory T cells, GNLY
CD8
Tem, GZMK
CD8
Tem, naive CD8
T cells, naive B cells, memory B cells, plasma cells, ISG
atypical B cells, monocytes, and NKT cells. ScRNA-seq analysis revealed a significantly higher proportion of Th1 cells (16.62% vs. 6.94% in controls) and ISG
B cells (2.95% vs. 0.53%), alongside a lower proportion of plasma cells (9.30% vs. 17.79%) and memory B cells (9.54% vs. 27.35%). Flow cytometry consistently confirmed the increase in Th1 cells (21.84% [14.87-27.57] vs. 11.96% [7.19-15.74]) and decreases in marginal zone B cells (2.87% [1.71-4.45] vs. 8.60% [6.77-15.65]), memory B cells (13.85% [5.72-20.23] vs. 22.96% [16.39-33.83]), and class-switched B cells (6.11% [2.39-9.10] vs. 10.18% [5.35-15.77]). Transcriptome analysis demonstrated upregulated expression of interferon-response and HLA genes (e.g., HLA-DQB1, HLA-DQA1, HLA-DRB1), whereas IRF1 was downregulated across all subsets; functional enrichment analyses further highlighted significant activation in IFN signaling and B cell activation pathways. CellChat and pseudotime analyses indicated that CD4
Tem and CD14
monocytes drive sustained Th1 inflammation and monocyte hyperactivation through enhanced pro-inflammatory and antigen-presenting interactions, with T-cell differentiation skewed toward terminal effectors and B-cell development disrupted by ISG
B cell emergence, premature plasma cell formation, and IGLC3-biased class switching, collectively delineating the interferon-mediated immunopathology of AIGAs immunodeficiency syndrome.
In summary, this first single-cell atlas maps AIGAs immunodeficiency syndrome as a Th1-skewed, IFN-γ-driven disorder sustained by CD4
Tem-CD14
monocyte crosstalk. It combines T-cell activation, expanded Th1 and ISG
B cells, and loss of memory/plasma B cells to drive autoantibody generation. Skewed T- and B-cell trajectories and polygenic up-regulation of interferon/HLA genes provide a clear mechanistic rationale for targeted therapy.
Journal Article
Clinicopathological role of miR-30a-5p in hepatocellular carcinoma tissues and prediction of its function with bioinformatics analysis
It has been reported that deregulation or dysfunction of microRNAs (miRNAs) plays an essential part in the hepatocarcinogenesis. However, the contribution and mechanism of microRNA-30a-5p (miR-30a-5p) in hepatocellular carcinoma (HCC) remains largely unknown. Therefore, our aim was to investigate the clinicopathological role of miR-30a-5p in HCC tissues and explore its potential pathways in this study.
The expression of miR-30a-5p was measured in 95 HCC and adjacent noncancer tissues by real-time reverse transcription quantitative polymerase chain reaction. The relationship between miR-30a-5p expression levels and clinicopathological parameters was also analyzed. Furthermore, the potential target genes of miR-30a-5p were collected via online prediction and literature searching. Gene ontology and pathway enrichment analyses were used to identify the possible function of miR-30a-5p in HCC.
Compared with adjacent noncancer tissues (2.23±0.77), expression level of miR-30a-5p was significantly lower in HCC tissues (1.26±0.66, P<0.001). MiR-30a-5p expression was evidently correlated with tumor nodes, metastasis, tumor-node-metastasis stage, portal vein tumor embolus, vascular invasion, and status of tumor capsule (all P<0.05). A total of 878 genes were finally used for the biological informatics analyses. These prospective target genes were highly enriched in various key pathways, for instance, Ubiquitin-mediated proteolysis, Axon guidance, Neurotrophin signaling pathway, Amyotrophic lateral sclerosis, and ErbB signaling pathway.
In conclusion, this study clarifies that the downregulation of miRNA-30a-5p might play a vital part in the incidence and progression of HCC via targeting various prospective genes and pathways. Future validation is required to further explore the prospective molecular mechanism of miR-30a-5p in HCC.
Journal Article
Relationship between TRAF6 and deterioration of HCC: an immunohistochemical and in vitro study
Objective
To explore the relationship between tumor necrosis factor receptor-associated factor 6 (TRAF6) and the clinicopathological features in HCC as well as its biological function.
Methods
Totally, 412 liver tissues were collected, including 171 hepatocellular carcinoma (HCC) and their corresponding non-tumor tissues, 37 cirrhosis and 33 normal liver tissues. The expression of TRAF6 was assessed by immunohistochemistry. Then, analysis of the correlations between TRAF6 expression and clinicopathological parameters in HCC was conducted. Furtherer, in vitro experiments on HepG2 and Hep3B cells were performed to validate the biological function of TRAF6 on HCC cells. TRAF6 siRNA was transfected into HepG2 and Hep3B cell lines and TRAF6 expression was evaluated with RT-qPCR and western blot. The assays of cell viability, proliferation, apoptosis and caspase-3/7 activity were carried out to investigate the effects of TRAF6 on HCC cells with RNA interference. Cell viability was assessed with Cell Titer-Blue kit. Cell proliferation was tested with MTS kit. Cell apoptosis was checked through morphologic detection with fluorescence microscope, as well as caspase-3/7 activity was measured with fluorogenic substrate detection.
Results
The positive expression rate of TRAF6 protein was 49.7 % in HCC, significantly higher than that of normal liver (12.1 %), cirrhosis (21.6 %) and adjacent non-cancerous tissues (36.3 %, all
P
< 0.05). Upregulated TRAF6 was detected in groups with metastasis (Z = −2.058,
P
= 0.04) and with low micro-vessel density (MVD) expression (Z = −2.813,
P
= 0.005). Spearman correlation analysis further showed that the expression of TRAF6 was positively correlated with distant metastasis (r = 0.158,
P
= 0.039) and negatively associated with MVD (r = −0.249,
P
= 0.004). Besides, knock-down of TRAF6 mRNA in HCC cell lines HepG2 and Hep3B both resulted in cell viability and proliferation inhibition, also cell apoptosis induction and caspase-3/7 activity activation.
Conclusions
TRAF6 may contribute to metastasis and deterioration of the HCC via influencing cell growth and apoptosis. Thus, TRAF6 might become a predictive and therapeutic biomarker for HCC.
Journal Article
Correction to: Relationship between TRAF6 and deterioration of HCC: an immunohistochemical and in vitro study
Following the publication of the original article [1], the authors reported that they had supplied the incorrect figure 6 for publication. The correct figure 6 is given in this correction article. The results and conclusions described therein are not affected by these corrections. The authors sincerely apologize for the error. This has now been included in this correction article.
Journal Article
Proteogenomic verifies targets underlying erythromycin alleviate neutrophil extracellular traps-induced inflammation
Background
Neutrophil Extracellular Traps (NETs) are closely related to the progression of inflammation in Chronic Obstructive Pulmonary Disease (COPD). Erythromycin (EM) has been shown to inhibit inflammation in COPD, but its molecular mechanisms is still unclear. The aim of our study is investigate the molecular mechanisms of EM's anti-inflammatory effects in NETs-induced inflammation.
Methods
Transcriptomics and proteomics data were obtained from U937 cells treated with NETs and EM. Differentially expressed genes (DEGs) and differentially expressed proteins (DEPs) were identified using R software. Pathway enrichment analyses, were employed to identify inflammation-related pathways. Cytoscape were utilized to construct network of hub targets regulated by EM which related with oxidative stress and inflammation. Additionally, Cytoscape and STRING were used to construct protein–protein interaction (PPI) network of key targets regulated by EM. The expression levels of key targets were further confirmed through WB and PCR experiments.
Results
Both transcriptomics and proteomics indicate that EM decrease NETs –induced AKT1 expression. Enrichment analysis of DEGs and DEPs reveal multiple common pathways involved in EM’s regulation inflammation, including the PI3K/AKT pathway, response to oxidative stress, IKK/NF-κB signaling and PTEN signaling pathway. Nine key targets in PI3K/AKT-related inflammatory pathways regulated by EM and ten targets of EM-regulated oxidative stress were identified. WB and PCR results confirmed that EM reversing the NETs-induced inflammation by modulating the activity of these targets. Furthermore, clinical samples and vitro experiments confirm that EM alleviates NETs-induced glucocorticoid resistance via inhibiting PI3K/AKT, thereby repressing inflammation.
Conclusions
Our study provides a comprehensive proteogenomic characterization of how EM alleviates NET-related inflammation, and identify PI3K/AKT play a critical role in the mechanism by which EM inhibits inflammation.
Journal Article
Wheat Drought-Responsive Grain Proteome Analysis by Linear and Nonlinear 2-DE and MALDI-TOF Mass Spectrometry
A comparative proteomic analysis of drought-responsive proteins during grain development of two wheat varieties Kauz (strong resistance to drought stress) and Janz (sensitive to drought stress) was performed by using linear and nonlinear 2-DE and MALDI-TOF mass spectrometry technologies. Results revealed that the nonlinear 2-DE had much higher resolution than the linear 2-DE. A total of 153 differentially expressed protein spots were detected by both 2-DE maps, of which 122 protein spots were identified by MALDI-TOF and MALDI-TOF/TOF mass spectrometry. The identified differential proteins were mainly involved in carbohydrate metabolism (26%), detoxification and defense (23%), and storage proteins (17%). Some key proteins demonstrated significantly different expression patterns between the two varieties. In particular, catalase isozyme 1, WD40 repeat protein, LEA and alpha-amylase inhibitors displayed an upregulated expression pattern in Kauz, whereas they were downregulated or unchanged in Janz. Small and large subunit ADP glucose pyrophosphorylase, ascorbate peroxidase and G beta-like protein were all downregulated under drought stress in Janz, but had no expression changes in Kauz. Sucrose synthase and triticin precursor showed an upregulated expression pattern under water deficits in both varieties, but their upregulation levels were much higher in Kauz than in Janz. These differentially expressed proteins could be related to the biochemical pathways for stronger drought resistance of Kauz.
Journal Article
A New HPLC-UV Method Using Hydrolyzation with Sodium Hydroxide for Quantitation of ITrans/I-Ip/I-Hydroxycinnamic Acid and Total ITrans/I-Ip/I-Hydroxycinnamic Acid Esters in the Leaves of ILigustrum robustum/I
Trans-p-hydroxycinnamic acid and its esters in the leaves of Ligustrum robustum might be a new resource to prevent diabetes and its complications. In the present study, a new HPLC-UV method using hydrolyzation with sodium hydroxide for quantitation of trans-p-hydroxycinnamic acid and total trans-p-hydroxycinnamic acid esters in the leaves of L. robustum was developed, since it was difficult and troublesome to analyze no less than 34 trans-p-hydroxycinnamic acid esters by usual HPLC. The extract of L. robustum was hydrolyzed with sodium hydroxide at 80 °C for 2 h, and then, hydrochloride was added. HPLC analysis was performed in reverse phase mode using a C-18 column, eluting with methanol-0.1% acetic acid aqueous solution (40:60, v/v) in isocratic mode at a flow rate of 1.0 mL·min[sup.−1] and detecting at 310 nm. The linear range for trans-p-hydroxycinnamic acid was 11.0–352.0 μg·mL[sup.−1] (r[sup.2] = 1.000). The limit of detection and limit of quantification were 2.00 and 6.07 μg·mL[sup.−1], respectively. The relative standard deviations of intra-day and inter-day variabilities for trans-p-hydroxycinnamic acid were less than 2%. The percentage recovery of trans-p-hydroxycinnamic acid was 103.3% ± 1.1%. It is the first HPLC method using hydrolyzation for quantification of many carboxylic esters. Finally, the method was used successfully to determine trans-p-hydroxycinnamic acid and total trans-p-hydroxycinnamic acid esters in various extracts of the leaves of L. robustum. The 60–70% ethanol extracts of L. robustum showed the highest contents of free trans-p-hydroxycinnamic acid (3.96–3.99 mg·g[sup.−1]), and the 50–80% ethanol extracts of L. robustum displayed the highest contents of total trans-p-hydroxycinnamic acid esters (202.6–210.6 mg·g[sup.−1]). The method can be applied also to the quality control of the products of L. robustum.
Journal Article
Clinicopathological significance of STAT4 in hepatocellular carcinoma and its effect on cell growth and apoptosis
Recent studies showed that signal transducer and activator of transcription 4 (STAT4) was downregulated in hepatocellular carcinoma (HCC) tissues. However, the role of STAT4 in HCC is still unknown. The aim of this study is to explore the association between STAT4 expression and other clinicopathological features in HCC and to test the effect of STAT4 on cell growth and apoptosis in vitro.
STAT4 was evaluated by immunohistochemistry in 171 HCC and corresponding paraneoplastic liver, 37 cirrhosis, and 33 normal liver tissues. Association between STAT4 and clinicopathological parameters was analyzed. Meta-analysis on STAT4 in cancer was performed. The effect of STAT4 small interfering RNA (siRNA) on cell growth and cell apoptosis was also detected.
Positive rate of STAT4 was 29.2% (50/171) in HCC tissues, 53.2% (91/171) in paraneoplastic liver tissues, 64.9% (24/37) in cirrhosis tissues, and 72.7% (24/33) in normal liver tissues. STAT4 was upregulated in younger patients who were female, with single tumor node, early TNM stage, without portal vein tumor embolus, and α-fetoprotein (AFP)-positive tumors compared with the groups comprising older patients, males, and those with multiple tumor nodes, advanced TNM stage, with portal vein tumor embolus, and AFP negative tumors. Meta-analysis showed STAT4 was correlated with TNM stage (OR =0.50, 95% CI =0.30, 0.83, P=0.008) and age (OR =0.58, 95% CI =0.38, 0.95, P=0.032) in malignant tissues, and with AFP level (OR =1.76, 95% CI =1.06, 2.94, P=0.03) in HCC. STAT4 siRNA promoted growth and suppressed apoptosis of HepG2 cells.
STAT4 might play a vital role in development of HCC, via influencing cell growth and apoptosis, as a tumor suppressor.
Journal Article