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Abstract Background Colorectal cancer (CRC) is a prevalent malignancy with high morbidity and mortality rates. Previous studies have demonstrated that interleukin (IL)-22 is involved in CRC progression; however, the exact mechanism remains unclear. This study aimed to investigate the effects of IL-22 on CRC cell proliferation and metastasis. Methods IL-22 levels in the serum and tissues of CRC patients were measured using enzyme-linked immunosorbent assay (ELISA). Cell counting kit-8 (CCK-8) assay was used to detect the viability of CRC (HCT116) cells treated with different IL-22 concentrations. Colony formation, Transwell invasion, and scratch assays were employed to assess the effects of IL-22 on cell proliferation, invasion, and migration. Western blotting was performed to measure the expression levels of phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT), p-PI3K, p-AKT, E-cadherin, matrix metalloproteinase (MMP)-2, MMP-9, SNAI1, and TWIST1 in HCT116 cells treated with IL-22 or a PI3K inhibitor. Results ELISA results showed that the expression of IL-22 was significantly increased in the serum and tissues of CRC patients compared to controls. IL-22 treatment increased cell viability and colony formation in a concentration-dependent manner and enhanced cell invasion and migration. Western blotting analysis revealed that IL-22 stimulation upregulated p-PI3K and p-AKT expression, while total PI3K and AKT levels remained unchanged. Additionally, IL-22 also decreased E-cadherin expression and increased the expression of MMP-2, MMP-9, SNAI1, and TWIST1. Conclusions IL-22 activates the PI3K-AKT pathway and promotes HCT116 cell proliferation and metastasis. Targeting the regulation of the PI3K/AKT pathway may be a potential therapeutic strategy for CRC.

The elucidation of the structural characteristics of deoxyribonucleic acid (DNA) by Watson and Crick, the advent of polymerase chain reaction technology, and the development of primer-synthesis methods, enable DNA to be replicated and transformed in an increasingly easy manner, such that it is among the most directed and evolving nanomaterials in molecular biology. Traditional cancer diagnosis methods are somewhat limited and are unable to meet existing needs; consequently, DNA nanostructures with wide ranging properties are receiving increasingly more attention because a number of DNA materials have been shown to exhibit diagnostic properties. Some DNA materials can functionally alter the biological behavior of cells, such as cell migration, cell proliferation, cell differentiation, autophagy, and anti-inflammatory effects. Some single-stranded DNA or ribonucleic acid with secondary structure through self-pairing, called aptamer, systematic evolution of ligands by exponential enrichment (SELEX), have targeting capabilities and can be applied to tumor targeted diagnosis and therapy. Several DNA nanomaterials with three-dimensional nanostructures and stable structures are being investigated as drug carrier systems to act on a variety of antitumor drugs or gene therapy agents. This article reviews the use of functionalized DNA nanostructures in cancer diagnosis and treatment applications. Various biosensors and carriers based on DNA nanostructures are introduced and chemical reactions related to the preparation of the carrier and the signal transduction mechanism of the sensor are discussed. Efficient carrier/biosensor platforms based on various structural developments and current DNA nanomaterial developments are also presented.

Background: 1,2,3,4,6-Penta-O-galloyl-β-D-glucose (β-PGG) is a polyphenol ellagic compound with a variety of pharmacological effects and has an inhibitory effect on lots of cancers. Objective: To explore the antitumor effects and mechanism of 1,2,3,4,6-Penta-O-galloyl-β-D-glucose on human hepatocellular carcinoma HepG2 cells. Design: A network pharmacology method was first used to predict the possible inhibition of hepatocellular carcinoma growth by 1,2,3,4,6-Penta-O-galloyl-β-D-glucose (β-PGG) through the p53 signaling pathway. Next, the Cell Counting Kit (CCK-8) assay was performed to evaluate changes in the survival rate of human hepatocellular carcinoma HepG2 cells treated with different concentrations of the drug; flow cytometry was used to detect changes in cell cycle, apoptosis, mitochondrial membrane potential (MMP) and intracellular Ca2+ concentration; real-time fluorescence quantification and immunoblotting showed that the expression of P53 genes and proteins associated with the p53 signaling pathway was significantly increased by β-PGG treatment. Reasult: It was found that β-PGG significantly inhibited survival of HepG2 cells, promoted apoptosis, decreased MMP and intracellular Ca2+ concentration, upregulated P53 gene and protein expression, increased CASP3 expression, and induced apoptosis in HepG2 cells. Conclusion: This study has shown that network pharmacology can accurately predict the target of β-PGG’s anti-hepatocellular carcinoma action. Moreover, it was evident that β-PGG can induce apoptosis in HepG2 cells by activating the p53 signaling pathway to achieve its anti-hepatocellular carcinoma effect in vitro.

Objective The clinical characteristics and imaging information of insular glioma patients were collected to predict mutation status of isocitrate dehydrogenase 1 (IDH1). Methods A total of 596 patients with gliomas confirmed by postoperative pathology in The First Affiliated Hospital with Nanjing Medical University from January 2011 to June 2021 were enrolled, including 72 insular gliomas, 213 frontal gliomas, 165 temporal gliomas, 76 parietal gliomas, 28 and 29 midline gliomas. All patients were examined by MRI, fifteen glioma⁃related features were selected from the visually accessible rembrandt images (VASARI), including enhancement quality, enhancement proportion, non⁃enhancement proportion, necrosis proportion, edema proportion, cyst, thickness of enhanced margin, definition of the enhanced margin, hemorrhage, diffusion, deep white matter involvement, deep ventricle involvement, midline cross, T2⁃FLAIR mismatch, maximum diameter of tumor. Univariate and multivariate Logistic regression analysis were used to screen the predictive factors related to IDH1⁃mutant in insular glioma. The receiver operating characteristic (ROC) curve was plotted and area under the curve (AUC), sensitivity and specificity were calculated to evaluate the predictive power of MRI features for IDH1⁃mutant glioma. Results IDH1 mutation rate was higher in insular and frontal gliomas (P＜0.01, for all). WHO grade Ⅱ had the highest IDH1 mutation rate (P=0.008, 0.000), and grade Ⅳ had the lowest mutation rate (P=0.000). The IDH1 mutation rate in low⁃expression Ki⁃67 gliomas was higher than that in high⁃expression gliomas (P=0.000). Logistic regression analysis showed that weak enhancement (OR=35.671, 95%CI: 2.805-453.600; P=0.006), non⁃enhancement (OR=75.453, 95%CI: 2.881-1872.759; P=0.009), unlimited diffusion (OR=10.573, 95%CI: 1.043-107.175; P=0.046), no deep ventricle involvement (OR=187.601, 95%CI: 2.269-15507.607; P=0.020), T2⁃FLAIR mismatch (OR=47.536, 95%CI: 2.838-796.097; P=0.007) were independent predictive factors for IDH1 mutation in insular glioma. The AUC of enhancement degree, diffusion, deep ventricle involvement and T2⁃FLAIR mismatch for the diagnosis of IDH1⁃mutant glioma were 0.846 (95%CI: 0.748-0.944, P=0.000), 0.730 (95%CI: 0.609-0.850, P=0.001), 0.708 (95%CI: 0.584-0.833, P=0.003) and 0.745 (95%CI: 0.627-0.864, P=0.000). The combination of the 4 groups had the highest diagnostic efficacy, and the AUC was 0.961 (95%CI: 0.923-0.999, P=0.000). Conclusions Low grade insular glioma has a high IDH1 mutation rate. MRI features of weak enhancement and non⁃enhancement, unlimited diffusion, non deep ventricle involvement and T2⁃FLAIR mismatch contribute to noninvasive prediction of IDH1⁃mutant insular glioma.

Background: Distinguishing between tumor recurrence and pseudoprogression (PsP) in high-grade glioma postoperatively is challenging. This study aims to enhance this differentiation using a combination of intratumoral and peritumoral radiomics. Purpose: To assess the effectiveness of intratumoral and peritumoral radiomics in improving the differentiation between high-grade glioma recurrence and pseudoprogression after surgery. Material and Methods: A total of 109 cases were randomly divided into training and validation sets, with 1316 features extracted from intratumoral and peritumoral volumes of interest (VOIs) on conventional magnetic resonance imaging (MRI) and apparent diffusion coefficient (ADC) maps. Feature selection was performed using the mRMR algorithm, resulting in intratumoral (100 features), peritumoral (100 features), and combined (200 features) subsets. Optimal features were then selected using PCC and RFE algorithms and modeled using LR, SVM, and LDA classifiers. Diagnostic performance was compared using area under the receiver operating characteristic curve (AUC), evaluated in the validation set. A nomogram was established using radscores from intratumoral, peritumoral, and combined models. Results: The combined model, utilizing 14 optimal features (8 peritumoral, 6 intratumoral) and LR as the best classifier, outperformed the single intratumoral and peritumoral models. In the training set, the AUC values for the combined model, intratumoral model, and peritumoral model were 0.938, 0.921, and 0.847, respectively; in the validation set, the AUC values were 0.841, 0.755, and 0.705. The nomogram model demonstrated AUCs of 0.960 (training set) and 0.850 (validation set). Conclusion: The combination of intratumoral and peritumoral radiomics is effective in distinguishing high-grade glioma recurrence from pseudoprogression after surgery. [ABSTRACT FROM AUTHOR]

BackgroundGastric cancer (GC) is ranked as the third leading cause of cancer-related mortality worldwide. 1,2,3,4,6-Pentagalloyl-β-D-glucose (β-PGG) has various pharmacological activities and has been shown to suppress cancer development. However, the mechanism by which β-PGG inhibits gastric cancer has not been elucidated.ObjectiveThis study explored the potential targets and mechanism of β-PGG in GC using the network pharmacology approach combined with in-vitro experiments.MethodsThe PharmMapper software was used to predict the potential targets of β-PGG, and GC-related genes were identified on the GeneCards database. PPI analysis of common genes was performed using the STRING database. The potential regulatory mechanism of β-PGG in GC was explored through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. The binding ability of key genes and target proteins was verified by molecular docking. The effects of β-PGG on genes and proteins were evaluated using the CCK-8 assay, cell cycle analysis, apoptosis assay, real-time fluorescence quantification polymerase chain reaction (qRT-PCR), and Western blotting.ResultsEight hub genes involved in cell cycle progression and apoptosis were identified. Cancer-related signaling pathways were identified using the Cytoscape tool. Some of those genes were significantly enriched in the p53 signaling pathway. The CCK-8 assay showed that β-PGG inhibited the proliferation of GC cells. Cell cycle and apoptosis experiments revealed that β-PGG induced cell cycle arrest and apoptosis of gastric cancer cells. qRT-PCR and Western blot analysis showed that β-PGG inhibited β-PGG cells by modulating the p53 signaling pathway.ConclusionIn the present study, the targets and mechanism of β-PGG in gastric cancer were explored. The results indicate that β-PGG can be used to develop treatments for GC.

BackgroundTrapa bispinosa Roxb. is grown worldwide as an important aquatic cash crop. Current research on Trapa bispinosa primarily focuses on the separation and identification of active ingredients, as well as the inhibitory effect on tumors; however, research on the molecular mechanism of secondary metabolite accumulation is rather limited. Consequently, an integrative analysis of transcriptome and metabolome is required to identify the key metabolic pathways, and key genes, and to explain the molecular mechanism of Trapa bispinosa.ResultsThe biosynthesis pathways of phenolics in Trapa bispinosa were examined through transcriptome and metabolome analyses. Transcriptome analysis yielded 42.76 million clean reads representing 81,417 unigenes with an average length of 1,752 bp. KEGG pathway analysis revealed that 1,623 unigenes, including 88 candidate unigenes related to phenolics biosynthesis, were up-regulated in Trapa bispinosa shell (FR) when compared to leaves (LF), root (RT), and stem (ST). The FR vs. LF group had the highest number of specific genes involved in phenylpropanoid, flavonoid, flavone, and flavonol biosynthesis pathways compared to all other comparison groups. In addition, RNA sequencing revealed 18,709 SSRs spanning 14,820 unigenes and 4,387 unigenes encoding transcription factors. Metabolome analysis identified 793 metabolites, including 136 flavonoids and 31 phenylpropane compounds. In the FR group compared to the LF group, there were 202 differentially accumulated metabolites (DAMs). The combined transcriptome and metabolome analyses indicated a significant correlation between 1,050 differentially expressed genes (DEGs) and 62 DAMs. This view proposes a schematic of flavonoid biosynthesis in the FR vs. LF group, providing evidence for the differences in genes and metabolites between FR and LF.ConclusionIn this study, through de novo transcriptome assembly and metabolome analysis, several DEGs and DAMs were identified, which were subsequently used to build flavonoid biosynthesis pathways and a correlation network. The findings pave the way for future research into the molecular mechanisms and functional characterization of Trapa bispinosa candidate genes for phenolics biosynthesis.

Objective To study the clinical outcome of short segment percutaneous pedicle screw(PPS) combined with unilateral percutaneous vertebroplasty(PVP) for Kümmell disease stage Ⅲ without neurological symptoms. Methods Retrospective analysis of 11 patients with Kümmell disease stage Ⅲ hospitalized in the department of spine surgery of Luoyang Orthopedic-Traumatological Hospital of Henan Province from May 2018 to August 2019(5 males and 6 females),who were received posterior short-segment percutaneous pedicle screw fixation combined with unilateral percutaneous vertebroplasty. The mean age was 72.2 years old, with an average disease course of 5.5 months. All the patients had osteoporosis. The lesion segments included T11, T12 and L1. According to the follow up results,including the operation time,blood loss,the volume of injected bone cement,kyphosis Cobb angle,Oswesay disability index(ODI),height restoration of the vertebral, the incidence of adjacent vertebral fracture and stability of implant were assessed. Results The operations were successfully performed on the 11 patients, and all the patients were followed up for 12 to 15 months, average (14.27±1.01) months. Compared with preoperation, the observational targets (ODI, VAS score, Cobb angle and the height of anterior edge of injured vertebra) in last follow-up and a week after surgery were improved significantly(P＜0.05). Two cases had slight displacement of internal fixation during the follow-up, and 1 case had cement leakage without symptom to the disc during operation. Conclusions Short segment percutaneous pedicle screw fixation combined with unilateral percutaneous vertebroplasty is safe and effective for treatment of Kümmell disease stage Ⅲ without neurological symptoms, alleviate clinical symptoms and reduce the complication of long-term bed rest.

The electrochemical CO2 reduction reaction (CO2RR) holds significant promise in advancing carbon neutrality. Developing catalysts for the electrochemical CO2RR to multi-carbon (C2+) products (e.g., C2H4) under industrial-level current density is urgently needed and pivotal. Herein, we report the Cu2O nanoparticles doped with interstitial carbon atoms (denoted as C-Cu2O NPs) for the conversion of CO2 to C2+ products. The interstitial carbon promotes the C-Cu2O NPs to possess abundant unsaturated Cu–O bonds, leading to a high-density Cuδ+ (0 < δ <1) species. The obtained C-Cu2O NPs exhibited significant Faradic efficiency (FE) of C2+ products approaching 76.9% and a partial current density reaching 615.2 mA·cm−2 under an industrial-level current density of 800 mA·cm−2. Furthermore, the efficient electrosynthesis of C2H4 achieved an FE of 57.4% with a partial current density of 459.2 mA·cm−2. In situ electrochemical attenuated total reflection Fourier transform infrared spectroscopy and in situ Raman spectroscopy analyses revealed that C-Cu2O NPs stabilized the intermediate *CO and facilitated C–C coupling, leading to increased selectivity towards C2+ products. [ABSTRACT FROM AUTHOR]

The efficiency of proton exchange membrane water electrolysis (PEM-WE) for hydrogen production is heavily dependent on the noble metal iridium-based catalysts. However, the scarcity of iridium limits the large-scale application of PEM-WE. To address this issue, it is promising to select an appropriate support because it not only enhances the utilization efficiency of noble metals but also improves mass transport under high current. Herein, we supported amorphous IrOx nanosheets onto the hollow TiO2 sphere (denoted as IrOx), which demonstrated excellent performance in acidic electrolytic water splitting. Specifically, the annealed IrOx catalyst at 150 °C in air exhibited a mass activity of 1347.5 A·gIr−1, which is much higher than that of commercial IrO2 of 12.33 A·gIr−1 at the overpotential of 300 mV for oxygen evolution reaction (OER). Meanwhile, the annealed IrOx exhibited good stability for 600 h operating at 10 mA·cm−2. Moreover, when using IrOx and annealed IrOx catalysts for water splitting, a cell voltage as low as 1.485 V can be achieved at 10 mA·cm−2. The cell can continuously operate for 200 h with negligible degradation of performance. [ABSTRACT FROM AUTHOR]

Parkinson’s disease (PD) is a common neurodegenerative disease characterized pathologically by dopaminergic neuron loss and the formation of Lewy bodies, which are enriched with aggregated α-synuclein (α-syn). PD currently has no cure, but therapeutic strategies are available to alleviate symptoms. Early diagnosis can greatly improve therapeutic interventions, but the clinical diagnosis of PD remains challenging and depends mainly on clinical features and imaging tests. Efficient and specific biomarkers are crucial for the diagnosis, monitoring, and evaluation of PD. Here, we reviewed the biomarkers of PD in different tissues and biofluids, along with the current clinical biochemical detection methods. We found that the sensitivity and specificity of single biomarkers are limited, and selecting appropriate indicators for combined detection can improve the diagnostic accuracy of PD. [ABSTRACT FROM AUTHOR]