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ترصد موسوعة \"تاريخ التبادلات الأدبية الصينية العربية\" مسيرة التبادلات الثقافية والأدبية منذ القدم بين الحضارتين الصينية والعربية، والترجمات الصينية الأولى للأدب العربي، كما تسلط الضوء على الأدب الصيني في الدول العربية، ورحلة التبادلات بين الأدباء العرب والصينيين والأحداث التاريخية التي واكبت محطات حركة التبادلات الأدبية بين الجانبين. كما ترصد التاريخ الطويل للأمة العربية في التواصل التجاري والثقافي والأدبي مع الصين، حيث عرفت الصين العرب منذ القرن الثاني قبل الميلاد مع رحلة المبعوث الصيني تشانغ تشيان إلى الغرب في عصر الإمبراطور هان وو دي، ثم عبر طريق الحرير البري القديم وطريق الحرير البحري \"طريق التوابل\" اللذين شهدا تدفقا للتجار العرب على الصين لتنتعش التبادلات الثقافية والأدبية إلى جانب التجارية بين الجانبين يوما بعد يوم.

Oncogene‐derived metabolic reprogramming is important for anabolic growth of cancer cells, which is now considered to be not simply rely on glycolysis. Pentose phosphate pathway and tricarboxylic acid cycle also play pivotal roles in helping cancer cells to meet their anabolic and energy demands. The present work focused on gankyrin, a relatively specific oncogene in hepatocellular carcinoma (HCC), and its impact on glycolysis and mitochondrial homeostasis. Metabolomics, RNA‐seq analysis, and subsequent conjoint analysis illustrated that gankyrin regulated the pentose phosphate pathway (PPP), tricarboxylic acid (TCA) cycle, and mitochondrial function and homeostasis, which play pivotal roles in tumor development. Mechanistically, gankyrin was found to modulate HCC metabolic reprogramming via TIGAR. Gankyrin positively regulated the transcription of TIGAR through Nrf2, which bound to the antioxidant response elements (AREs) in the promoter of TIGAR. Interestingly, TIGAR feedback regulated the transcription of Nrf2 and subsequently gankyrin by promoting nuclear importation of PGC1α. The loop between gankyrin, Nrf2, and TIGAR accelerated glucose metabolism toward the PPP and TCA cycle, which provided vital building blocks, such as NADPH, ATP, and ribose of tumor and further facilitated the progression of HCC. Gankyrin positively regulated the transcription of TIGAR through Nrf2, which bound to the antioxidant response elements (AREs) in the promoter of TIGAR. Interestingly, TIGAR feedback regulated the transcription of Nrf2 and subsequently gankyrin by promoting nuclear importation of PGC1a. The loop between gankyrin, Nrf2, and TIGAR accelerated glucose metabolism toward the pentose phosphate pathway (PPP) and tricarboxylic acid (TCA) cycle, which provided vital building blocks, such as NADPH, ATP, and ribose of tumor and further facilitated tumorigenesis of hepatocellular carcinoma (HCC).

The activation of C—C bonds enables rapid construction of new organic frameworks owing to facile structural reorganization. Nevertheless, enantioselective C—C activation remains heavily underexplored and has been predominantly limited to intramolecular reactions. We herein report two categories of asymmetric intermolecular [4 + 2] annulations between benzocyclobutenones (BCBs) and unsaturated reagents, namely, alkynes and cyclic dicarbonyl compounds. The atroposelective coupling of BCB with several classes of sterically hindered alkynes afford C—N and C—C axially chiral 2-naphthols. The [4 + 2] annulation of BCBs and α -dicarbonyls afford spirocyclic products. Both coupling systems proceed efficiently with excellent regio-, chemo- and enantioselectivity via substrate activation and judicious choice of chiral bidentate phosphine ligands. Synthetic transformations of selected products are demonstrated, and the derived chiral products are shown to be useful additives in C—H bond activation or as ligands in Pd-catalyzed C—C coupling. Enantioselective C—C activation remains heavily underexplored and has been predominantly limited to intramolecular reactions. Here the authors report two categories of asymmetric intermolecular [4+2] annulations between benzocyclobutenones and unsaturated reagents, namely, alkynes and cyclic dicarbonyl compounds.

Doxorubicin (DOX) is a highly potent chemotherapeutic agent, but its usage is limited by dose-dependent cardiotoxicity. DOX-induced cardiotoxicity involves increased oxidative stress and activated endoplasmic reticulum-mediated apoptosis. Alginate oligosaccharide (AOS) is a non-immunogenic, non-toxic and biodegradable polymer, with anti-oxidative, anti-inflammatory and anti-endoplasmic reticulum stress properties. The present study examined whether AOS pretreatment could protect against acute DOX cardiotoxicity, and the underlying mechanisms focused on oxidative stress and endoplasmic reticulum-mediated apoptosis. We found that AOS pretreatment markedly increased the survival rate of mice insulted with DOX, improved DOX-induced cardiac dysfunction and attenuated DOX-induced myocardial apoptosis. AOS pretreatment mitigated DOX-induced cardiac oxidative stress, as shown by the decreased expressions of gp91 (phox) and 4-hydroxynonenal (4-HNE). Moreover, AOS pretreatment significantly decreased the expression of Caspase-12, C/EBP homologous protein (CHOP) (markers for endoplasmic reticulum-mediated apoptosis) and Bax (a downstream molecule of CHOP), while up-regulating the expression of anti-apoptotic protein Bcl-2. Taken together, these findings identify AOS as a potent compound that prevents acute DOX cardiotoxicity, at least in part, by suppression of oxidative stress and endoplasmic reticulum-mediated apoptosis.

The standard regimen of gemcitabine combined with cisplatin offers limited clinical benefits in the treatment of advanced intrahepatic cholangiocarcinoma (ICC) due to intrinsic or acquired resistance. Currently, effective biomarkers to predict and improve chemotherapy resistance in ICC are lacking. Here, it is reported that a long non‐coding RNA (lncRNA), PAX8‐AS1, reduces the efficacy of standard chemotherapeutic drugs. Mechanistically, PAX8‐AS1 activates NRF2 by binding to p62, thereby promoting GPX4 transcription, and stabilizes GPX4 mRNA through interaction with IGF2BP3. The PAX8‐AS1/GPX4 axis inhibits ferroptosis and promotes resistance to gemcitabine and cisplatin. In preclinical models, the combination of the GPX4 inhibitor JKE‐1674 with gemcitabine and cisplatin exhibits superior antitumor efficacy. These findings suggest a promising therapeutic strategy to improve chemotherapy efficacy in advanced ICC. PAX8‐AS1 drives chemoresistance in intrahepatic cholangiocarcinoma by activating NRF2‐mediated GPX4 transcription and stabilizing GPX4 mRNA via IGF2BP3. Targeting the PAX8‐AS1/GPX4 axis with a GPX4 inhibitor enhances the efficacy of gemcitabine and cisplatin in preclinical models, offering a promising strategy to overcome chemotherapy resistance in advanced intrahepatic cholangiocarcinoma.

Background Microvascular invasion (MVI) adversely affects postoperative long-term survival outcomes in patients with hepatocellular carcinoma (HCC). There is no study addressing genetic changes in HCC patients with MVI. We first screened differentially expressed genes (DEGs) in patients with and without MVI based on TCGA data, established a prediction model and explored the prognostic value of DEGs for HCC patients with MVI. Methods In this paper, gene expression and clinical data of liver cancer patients were downloaded from the TCGA database. The DEG analysis was conducted using DESeq2. Using the least absolute shrinkage and selection operator, MVI-status-related genes were identified. A Kaplan-Meier survival analysis was performed using these genes. Finally, we validated two genes, HOXD9 and HOXD10, using two sets of HCC tissue microarrays from 260 patients. Results Twenty-three MVI-status-related key genes were identified. Based on the key genes, we built a classification model using random forest and time-dependent receiver operating characteristic (ROC), which reached 0.814. Then, we performed a survival analysis and found ten genes had a significant difference in survival time. Simultaneously, using two sets of 260 patients’ HCC tissue microarrays, we validated two key genes, HOXD9 and HOXD10. Our study indicated that HOXD9 and HOXD10 were overexpressed in HCC patients with MVI compared with patients without MVI, and patients with MVI with HOXD9 and 10 overexpression had a poorer prognosis than patients with MVI with low expression of HOXD9 and 10. Conclusion We established an accurate TCGA database-based genomics prediction model for preoperative MVI risk and studied the prognostic value of DEGs for HCC patients with MVI. These DEGs that are related to MVI warrant further study regarding the occurrence and development of MVI.

This study was carried out to explore the roles of circular RNAs (circRNAs) in nucleus pulposus (NP) tissues in intervertebral disc degeneration (IDD). Differentially expressed circRNAs in IDD and normal NP tissues were identified based on the results of microarray analysis. Bioinformatics techniques were employed to predict the direct interactions of selected circRNAs, microRNAs (miR), and mRNAs. CircRNA_104670 was selected as the target circRNA due to its large multiplier expression in IDD tissues. After luciferase reporter and EGFP/RFP reporter assays, we confirmed that circRNA_104670 directly bound to miR-17-3p, while MMP-2 was the direct target of miR-17-3p. The receiver-operating characteristic (ROC) curve showed that circRNA_104670 and miR-17-3p had good diagnostic significance for IDD (AUC circRNA_104670  = 0.96; AUC miRNA-17-3p  = 0.91). A significant correlation was detected between the Pfirrmann grade and expression of circRNA_104670 ( r  = 0.63; p  = 0.00) and miR-17-3p ( r  = −0.62; p  = 0.00). Flow-cytometric analysis and the MTT assay showed that interfering with circRNA_104670 using small interfering RNA (siRNA) inhibited NP cell apoptosis ( p  < 0.01), and this inhibition was reduced by interfering with miR-17-3p. Interfering with circRNA_104670 suppressed MMP-2 expression and increased extracellular matrix (ECM) formation, which were also reduced by interfering with miR-17-3p. Finally, an MRI evaluation showed that circRNA_104670 inhibition mice had a lower IDD grade compared with control mice ( p  < 0.01), whereas circRNA_104670 and miRNA-17-3p inhibition mice had a higher IDD grade compared with circRNA_104670 inhibition mice ( p  < 0.05). CircRNA_104670 is highly expressed in the NP tissues of IDD and acts as a ceRNA during NP degradation. Spinal disease: A roundabout route to disc degeneration ‘RNA sponges’ may provoke lower back pain by soaking up regulatory RNAs that normally protect the protein infrastructure surrounding cells in intervertebral discs. Many people suffer from lower back pain arising from disc degeneration (IDD). A team led by Fei-Zou and Jian-Yuan Jiang at Fudan University, Shanghai, China set out to identify molecular mechanisms that might contribute to IDD. They focused on circular RNAs, non-protein coding RNAs that have been linked to a variety of diseases. The researchers learned that IDD is associated with strongly elevated expression of a circular RNA that acts as an ‘RNA sponge’, binding to and thereby inactivating other RNA molecules. This inactivation ultimately results in the excessive production of an enzyme that can damage the protein matrix that supports cells within spinal discs, potentially setting up the conditions for IDD.

CKAP4, one kind of type II trans-membrane protein, plays an important role to maintain endoplasmic reticulum structure and inhibits the proliferation of bladder cancer cells by combining its ligand anti-proliferative factor (APF). However, the biological function of CKAP4 in the progression of liver cancer has not been clearly demonstrated. In the present study, we knocked down or overexpressed CKAP4 in hepatocellular carcinoma (HCC) cells and cell proliferation, invasion, and migration capacities were investigated by CCK-8 and transwell assays. In vivo tumor model in mice was used to evaluate the role of CKAP4 on growth and metastasis of HCC. The data documented that HCC cells with high CKAP4 levels were featured by low proliferation capability as well as low invasion potential. Interestingly, we found that CKAP4 suppressed the activation of epithelial growth factor receptor (EGFR) signaling, which may partly explain the role of CKAP4 in cell biological behavior of HCC. Further study revealed that CKAP4 could associate with EGFR at basal status and the complex was reduced upon EGF stimulation, leading to release EGFR into cytoplasm. Thus, we demonstrate the novel mechanism, for the first time, expression of CKAP4 regulates progression and metastasis of HCC and it may provide therapeutic values in this tumor.

The aim of the present study was to measure the expression of Cochlin (COCH) and analyze its association with survival, recurrence and the benefits from adjuvant transarterial chemoembolization (TACE) in patients with hepatocellular carcinoma (HCC) following hepatectomy. Patients with high COCH expression levels had a poorer prognosis in terms of overall and disease-free survival rate compared with those with low COCH expression levels. Further analysis revealed that patients with low COCH expression who received TACE experienced markedly lower early recurrence rates compared with those who did not receive TACE. However, patients with high COCH expression with and without adjuvant TACE after resection experienced no difference in disease recurrence rates. The expression of COCH was found to be associated with hepatitis B virus infection, portal vein tumor thrombosis and Barcelona Clinic Liver Cancer stage in HCC. Therefore, the findings of the present study indicated that clinical detection of COCH expression may help estimate the prognosis of patients with HCC, as well as determine whether to administer TACE after surgery to prevent recurrence.

The activation of C-C bonds enables rapid construction of new organic frameworks owing to facile structural reorganization. Nevertheless, enantioselective C-C activation remains heavily underexplored and has been predominantly limited to intramolecular reactions. We herein report two categories of asymmetric intermolecular [4 + 2] annulations between benzocyclobutenones (BCBs) and unsaturated reagents, namely, alkynes and cyclic dicarbonyl compounds. The atroposelective coupling of BCB with several classes of sterically hindered alkynes afford C-N and C-C axially chiral 2-naphthols. The [4 + 2] annulation of BCBs and α-dicarbonyls afford spirocyclic products. Both coupling systems proceed efficiently with excellent regio-, chemo- and enantioselectivity via substrate activation and judicious choice of chiral bidentate phosphine ligands. Synthetic transformations of selected products are demonstrated, and the derived chiral products are shown to be useful additives in C-H bond activation or as ligands in Pd-catalyzed C-C coupling.The activation of C-C bonds enables rapid construction of new organic frameworks owing to facile structural reorganization. Nevertheless, enantioselective C-C activation remains heavily underexplored and has been predominantly limited to intramolecular reactions. We herein report two categories of asymmetric intermolecular [4 + 2] annulations between benzocyclobutenones (BCBs) and unsaturated reagents, namely, alkynes and cyclic dicarbonyl compounds. The atroposelective coupling of BCB with several classes of sterically hindered alkynes afford C-N and C-C axially chiral 2-naphthols. The [4 + 2] annulation of BCBs and α-dicarbonyls afford spirocyclic products. Both coupling systems proceed efficiently with excellent regio-, chemo- and enantioselectivity via substrate activation and judicious choice of chiral bidentate phosphine ligands. Synthetic transformations of selected products are demonstrated, and the derived chiral products are shown to be useful additives in C-H bond activation or as ligands in Pd-catalyzed C-C coupling.