Can AI-generated art stimulate the sustainability of intangible cultural heritage? A quantitative research on cultural and creative products of New Year Prints generated by AI.

The transformation of social development modes has led to profound changes in the pattern of intangible cultural heritage, while simultaneously posing significant challenges to its preservation. The rapid development of artificial intelligence (AI) technology has brought new development opportunities in various research fields. This study intends, by constructing and evaluating a theoretical model, to investigate whether AI-generated cultural and creative products can promote the sustainability of intangible cultural heritage. The central focus of this research is to measure the effectiveness of AI technologies in promoting the sustainability of intangible cultural heritage. The context of the research design is rooted in the attention, interest, search, action, and share (AISAS) model, incorporating theories of perceived value and cultural identity, to forecast the long-term viability of AI-generated cultural and creative products in the promotion of intangible cultural heritage. This research was conducted in Tianjin, China and carried out using quantitative methods, a questionnaire survey, and the accidental sampling method, taking a sample of 291 participants for analysis. The results show that 1) the attraction of and interest and participation in AI-generated Yangliuqing New Year Print cultural and creative products have a positive effect on perceived value; 2) the purchase and sharing of these products have a positive impact on cultural identity; 3) the perceived value has a positive impact on cultural identity; and 4) cultural identity has a positive impact on the sustainability of intangible cultural heritage. This study contributes to the theoretical development and practical application of the AISAS model and offers valuable insights into the future development trajectory of intangible cultural heritage, thereby promoting its sustainability. The limitations of this study are its small sample size and geographical restrictions. In future studies, the sample size will be expanded and will include more regions for data analysis.

Dielectrophoresis-assisted removal of Cd and Cu heavy metal ions by using Chlorella microalgae.

A novel dielectrophoresis (DEP)-assisted device for the bioremediation of heavy metal ions by using Chlorella microalgae is presented in this paper. To generate the DEP forces, pairs of electrode mesh were inserted in the DEP-assisted device. By applying DC electric field via the electrodes, the inhomogeneous electric field gradient is induced and the strongest non-uniform electric field exists near the mesh cross-corner. After the adsorption of Cd and Cu heavy metal ions by Chlorella, the Chlorella chain were trapped along the vicinity of the electrode mesh. Then, the effects of Chlorella concentration on the adsorption of heavy metal ions, and the applied voltage and electrode mesh size on the removal of Chlorella are conducted. In the co-existing Cd and Cu solutions, the individual adsorption ratio of Cd and Cu reaches as high as approximately 96% and 98%, respectively, showing excellent bioremediation capability of multiple heavy metal ions in wastewater. By adjusting the applied electric voltage and the mesh size, the Chlorella adsorbed with Cd and Cu are captured by negative DC-DEP effects and the removal ratio of Chlorella reach an average of 97%, providing a method for the removal of multiple heavy metal ions in wastewater by using Chlorella microalgae.

Tunable magnetophoretic method for distinguishing and separating wear debris particles in an Fe-PDMS-based microfluidic chip.

Wear debris analysis provides an early warning of mechanical transmission system aging and wear fault diagnosis, which has been widely used in machine health monitoring. The ability to detect and distinguish the ferromagnetic and nonmagnetic debris in oil is becoming an effective way to assess the health status of machinery. In this work, an Fe-poly(dimethylsiloxane) (PDMS)-based magnetophoretic method for the continuous separation of ferromagnetic iron particles by diameter and the isolation of ferromagnetic particles and nonmagnetic particles with similar diameter by type is developed. The particles experience magnetophoretic effects when passing through the vicinity of the Fe-PDMS where the strongest gradient of the magnetic fields exists. By choosing a relatively short distance between the magnet and the sidewall of the horizontal main channel and the length of Fe-PDMS with controlled particles flow rate, the diameter-dependent separation of ferromagnetic iron particles, that is, smaller than 7 µm, in the range of 8-12 µm, and larger than 14 µm, and the isolation of ferromagnetic iron particles and nonmagnetic aluminum particles based on opposite magnetophoretic behaviors by types are demonstrated, providing a potential method for the detection of wear debris particles with a high sensitivity and resolution and the diagnostic of mechanical system.

DC-Dielectrophoretic Manipulation and Isolation of Microplastic Particle-Treated Microalgae Cells in Asymmetric-Orifice-Based Microfluidic Chip.

A novel direct-current dielectrophoretic (DC-DEP) method is proposed for the manipulation and isolation of microplastic particle (MP)-treated microalgae cells according to their dielectric properties in a microfluidic chip. The lateral migration and trajectory of the microalgae cells were investigated. To induce stronger DC-DEP effects, a non-homogeneous electric-field gradient was generated by applying the DC electric voltages through triple pairs of asymmetric orifices with three small orifices and one large orifice located on the opposite microchannel wall across the whole channel, leading to the enhanced magnitude of the non-uniform electric-field gradient and effective dielectrophoretic area. The effects of the applied voltage, the polystyrene (PS) adsorption coverage, and thickness on the DC-DEP behaviors and migration were numerically investigated, and it was found that the effect of the PS adsorption thickness of the Chlorella cells on the DC-DEP behaviors can be neglected, but the effect on their trajectory shifts cannot. In this way, the separation of 3 µm and 6 µm Chlorella coated with 100% PS particles and the isolation of the Chlorella cells from those coated with various coverages and thicknesses of PS particles was successfully achieved, providing a promising method for the isolation of microalgae cells and the removal of undesired cells from a target suspension.

Combination of anlotinib and gemcitabine promotes the G0/G1 cell cycle arrest and apoptosis of intrahepatic cholangiocarcinoma in vitro.

BACKGROUND: Intrahepatic cholangiocarcinoma (ICC) is a malignant carcinoma with high rate of mortality. The current treatment is ineffective with poor survival time. Therefore, there is an urgent need for effective therapeutic drug regimens. The multi-target tyrosine kinase inhibitor (TKI) anlotinib has been approved for treating non-small cell lung cancer (NSCLC); however, the combined therapeutic regimen of anlotinib for ICC has not been investigated yet. This study aims to investigate the inhibitory effect of anlotinib and the mechanism of gemcitabine combination for ICC treatment. METHODS: Two ICC cell lines, HCCC-9810 and RBE cells, were used in this study. Cell Counting Kit-8 (CCK-8) was used to study the cell viability, and flow cytometry (FCM) was used to evaluate the apoptosis and cell cycle arrest. Compusyn software was used to calculate the combination index (CI) of anlotinib and gemcitabine. The protein expression rate of cleaved PARP/PARP and cleaved caspase-3/caspase-3 was detected by Western blotting. RESULTS: Our result showed that the anlotinib and gemcitabine combination significantly inhibits the growth of ICC cell lines. Compusyn software results showed that the combination regimen had an anti-tumor synergistic effect. FCM results showed that it promoted apoptosis. Moreover, it increased the protein expression rate of cleaved PARP/PARP and cleaved caspase-3/caspase-3. Finally, we found a synergistic anti-tumor effect by increasing G0/G1 cell cycle arrest. CONCLUSION: The combination of anlotinib and gemcitabine can increase the anti-tumor effect and may be a potential therapeutic drug regimen in a clinical setting.

Reverse engineering a predictive signature characterized by proliferation, DNA damage, and immune escape from stage I lung adenocarcinoma recurrence.

Identifying early-stage cancer patients at risk for progression is a major goal of biomarker research. This report describes a novel 19-gene signature (19-GCS) that predicts stage I lung adenocarcinoma (LAC) recurrence and response to therapy and performs comparably in pancreatic adenocarcinoma (PAC), which shares LAC molecular traits. Kaplan-Meier, Cox regression, and cross-validation analyses were used to build the signature from training, test, and validation sets comprising 831 stage I LAC transcriptomes from multiple independent data sets. A statistical analysis was performed using the R language. Pathway and gene set enrichment were used to identify underlying mechanisms. 19-GCS strongly predicts overall survival and recurrence-free survival in stage I LAC (P=0.002 and P<0.001, respectively) and in stage I-II PAC (P<0.0001 and P<0.0005, respectively). A multivariate cox regression analysis demonstrated the independence of 19-GCS from significant clinical factors. Pathway analyses revealed that 19-GCS high-risk LAC and PAC tumors are characterized by increased proliferation, enhanced stemness, DNA repair deficiency, and compromised MHC class I and II antigen presentation along with decreased immune infiltration. Importantly, high-risk LAC patients do not appear to benefit from adjuvant cisplatin while PAC patients derive additional benefit from FOLFIRINOX compared with gemcitabine-based regimens. When validated prospectively, this proof-of-concept biomarker may contribute to tailoring treatment, recurrence reduction, and survival improvements in early-stage lung and pancreatic cancers.

Cosmc overexpression enhances malignancies in human colon cancer.

Cosmc is known as a T-synthase-specific molecular chaperone that plays a crucial role in the process of O-glycosylation. Cosmc dysfunction leads to inactive T-synthase and results in aberrant O-glycosylation, which is associated with various tumour malignancies. However, it is unclear whether Cosmc has some other functions beyond its involvement in O-glycosylation. In this study, we aimed to investigate the functional role of Cosmc in human colorectal cancer (CRC). We first assessed the expression levels of Cosmc in human CRC specimens and then forcedly expressed Cosmc in human CRC cell lines (HCT116, SW480) to examine its impact on cellular behaviours. The mechanisms for aberrant expression of Cosmc in CRC tissues and the altered behaviours of tumour cells were explored. It showed that the mRNA and protein levels of Cosmc were markedly elevated in human CRC specimens relative to normal colorectal tissues. The occurrence of endoplasmic reticulum (ER) stress may largely contribute to the increased Cosmc expression in cancer tissue and cells. Cosmc overexpression in CRC cells significantly promoted cell migration and invasion, which could be attributed to the activation of the epithelial-mesenchymal transition (EMT) pathway rather than aberrant O-glycosylation. These data indicate that Cosmc expression was elevated in human CRC possibly caused by ER stress, which further enhanced malignancies through the activation of EMT but independently of aberrant O-glycosylation.

Disruption of Core 1-mediated O-glycosylation oppositely regulates CD44 expression in human colon cancer cells and tumor-derived exosomes.

Aberrant O-glycosylation truncates O-glycans and is known to be closely associated with colorectal cancer (CRC), a major gastrointestinal tumor. CD44 is one of the highly post-transcriptionally modified O-glycoproteins participating in a series of physiological and pathobiological processes. In this research, we aimed to investigate whether CD44 expression in cells and exosomes can be influenced by disruption of Core 1-mediated O-glycosylation. Exosomes derived from LS174T and LSC human colon cancer cell lines were isolated from cell culture supernatant and pulled down using tetraspanin-specific antibody CD63 immunoaffinity magnetic beads. Identifications have been performed via transmission electron microscopy (TEM) and flow cytometry. CD63 immunoaffinity-purified exosomes are examined for CD44 expression by flow cytometric analyses. The percentages of CD44 in exosomes derived from abnormally O-glycosylated cells are significantly higher compared with those derived from normal ones, however, which is surprisingly contrary to the cellular expression levels of CD44. The secretion of truncated glycoproteins to the extracellular environment via microvesicles may be most likely its underlying mechanism. CD44 in exosomes might be a potential biomarker of aberrant O-glycosylation. This is the first study indicating that aberrant O-glycosylation can affect expression or delivery of O-glycoproteins via exosomes, which provides us some new sights in therapeutic strategies for human colon cancer.

DCLK1 Plays a Metastatic-Promoting Role in Human Breast Cancer Cells.

BACKGROUND: Doublecortin-like kinase 1 (DCLK1) has been universally identified as a cancer stem cell (CSC) marker and is found to be overexpressed in many types of cancers including breast cancer. However, there is little data regarding the functional role of DCLK1 in breast cancer metastasis. In the present study, we sought to investigate whether and how DCLK1 plays a metastatic-promoting role in human breast cancer cells. METHODS: We used Crispr/Cas9 technology to knock out DCLK1 in breast cancer cell line BT474, which basically possesses DCLK1 at a higher level, and stably overexpressed DCLK1 in another breast cancer cell line, T47D, that basically expresses DCLK1 at a lower level. We further analyzed the alterations of metastatic characteristics and the underlying mechanisms in these cells. RESULTS: It was shown that, compared with the corresponding control cells, DCLK1 overexpression led to an increase in metastatic behaviors including enhanced migration and invasion of T47D cells. By contrast, forced depletion of DCLK1 drastically inhibited these metastatic characteristics in BT474 cells. Mechanistically, the epithelial-mesenchymal transition (EMT) program, which is critical for cancer metastasis, was prominently activated in DCLK1-overexpressing cancer cells, evidenced by a decrease in an epithelial marker ZO-1 and an enhancement in several mesenchymal markers including ZEB1 and Vimentin. In addition, DCLK1 overexpression induced the ERK MAPK pathway, which resultantly enhanced the expression of MT1-MMP that is also involved in cancer metastasis. Knockout of DCLK1 could reverse these events, further supporting a metastatic-promoting role for DCLK1. CONCLUSIONS: Collectively, our data suggested that DCLK1 overexpression may be responsible for the increased metastatic features in breast cancer cells. Targeting DCLK1 may become a therapeutic option for breast cancer metastasis.

Aberrant O-glycosylation contributes to tumorigenesis in human colorectal cancer.

Aberrant O-glycosylation is frequently observed in colorectal cancer (CRC) patients, but it is unclear if it contributes intrinsically to tumorigenesis. Here, we investigated the biological consequences of aberrant O-glycosylation in CRC. We first detected the expression profile of Tn antigen in a serial of human CRC tissues and then explored the genetic and biosynthetic mechanisms. Moreover, we used a human CRC cell line (LS174T), which express Tn antigen, to assess whether aberrant O-glycosylation can directly promote oncogenic properties. It showed that Tn antigen was detected in around 86% human primary and metastatic CRC tissues. Bio-functional investigations showed that T-synthase and Cosmc were both impaired in cancer tissues. A further analysis detected an occurrence of hypermethylation of Cosmc gene, which possibly caused its loss-of-function and a consequent inactive T-synthase. Transfection of LS174T cells with WT Cosmc restored mature O-glycosylation, which subsequently down-regulated cancer cell proliferation, migration and apoptotic-resistant ability. Significantly, the expression of MUC2, a heavily O-glycosylated glycoprotein that plays an essential role in intestinal function, was uniformly reduced in human CRC tissues as well as in LS174T cells. These data suggest that aberrant O-glycosylation contributes to the development of CRC through direct induction of oncogenic properties in cancer cells.

T-Synthase Deficiency Enhances Oncogenic Features in Human Colorectal Cancer Cells via Activation of Epithelial-Mesenchymal Transition.

BACKGROUND: Immature truncated O-glycans such as Tn antigen are frequently detected in human colorectal cancer (CRC); however, the precise pathological consequences of Tn antigen expression on CRC are unknown. T-synthase is the key enzyme required for biosynthesis of mature O-glycans. Here we investigated the functional roles of Tn antigen expression mediated by T-synthase deficiency in CRC cells. METHODS: To knock out T-synthase, we used CRISPR-Cas9 technology to target C1GALT1, the gene encoding T-synthase, in a CRC cell line (HCT116). Deletion of T-synthase was confirmed by western blotting, and expression of Tn antigen was determined by flow cytometry in HCT116 cells. We then assessed the biological effects of T-synthase deficiency on oncogenic behaviors in HCT116 cells. Furthermore, we analyzed the mechanistic role of T-synthase deficiency in cancer cells by determining the epithelial-mesenchymal transition (EMT) pathway. RESULTS: We showed that forced knockout of T-synthase in HCT116 cells significantly induced Tn antigen expression, which represented the occurrence of aberrant O-glycosylation. Loss of T-synthase significantly enhanced cell proliferation and adhesion, as well as migration and invasiveness in culture. More importantly, we demonstrated that T-synthase deficiency directly induced classical EMT characteristics in cancer cells. E-cadherin, a typical epithelial cell marker, was markedly decreased in T-synthase knockout HCT 116 cells, accompanied by an enhanced expression of mesenchymal markers including snail and fibronectin (FN). CONCLUSIONS: These findings indicate that T-synthase deficiency in CRC cells not only is responsible for aberrant O-glycosylation, but also triggers the molecular process of EMT pathway, which may translate to increased invasiveness and metastasis in cancers.

Correlation of Tn antigen expression with mucins in Chinese patients with colorectal cancer.

Objective: Tn antigen expression, indicative of aberrant O-glycosylation, is frequently observed in human colorectal cancer (CRC) and is proposed to play key roles in tumorigenesis and cancer progression. Tn antigen appears to produce global effects on O-glycosylation of proteins, particularly on mucins. However, the association between expression of Tn antigen and mucins in CRC remains unclear. Here, we investigated the expression profile of Tn antigen as well as MUC1, MUC2, and MUC4 in a series of human CRC tissues, with the aim of determining whether the Tn antigen has an influence on mucins in the development of CRC. Methods: Expression and localization of Tn antigen, MUC1, MUC2, and MUC4 were determined by multiplex immunohistochemical staining in formalin-fixed, paraffin-embedded colonic sections from Chinese patients with primary CRC. Results: The data show that 65 of 78 (83.3%) patients with CRC were found to express Tn antigen, which was most often stained in the apical cell membranes, mucin droplets, and cytoplasm of the cancer tissues. No Tn antigen was detected in normal colonic tissues. Correspondingly, there were altered patterns in the expression of mucins. Compared with normal colonic tissues that were absent of Tn staining, MUC1 and MUC4 showed an up-regulated and diffuse expression pattern in cancer tissues that expressed Tn antigen, whereas MUC2 expression was significantly decreased in Tn-positive cancer tissues. Conclusions: These results indicate that Tn antigen expression is closely associated with altered expression of mucins in human CRC. Tn antigen may promote development of CRC through affecting the associated mucins expression.

DCLK1 is up-regulated and associated with metastasis and prognosis in colorectal cancer.

PURPOSE: Metastasis is a primary cause of colorectal cancer (CRC)-related death, and cancer stem cells (CSCs) are thought to be majorly responsible for initiating metastatic behaviors. Doublecortin-like kinase 1 (DCLK1) was recently discovered to be a marker for gastrointestinal CSCs. Here, we aimed to explore whether DCLK1 is associated with CRC metastasis through clinical and in vitro investigations. METHODS: The expression levels of DCLK1 mRNA and protein in human CRC tissues were analyzed through quantitative RT-PCR and immunohistochemistry staining, respectively. Human CRC cell line SW480 was selected to explore the effect of DCLK1 overexpression on cell migration and invasion. Besides, the associations between DCLK1 and epithelial-mesenchymal transition (EMT) were determined. RESULTS: Compared to normal colorectal tissues, DCLK1 expression was significantly up-regulated in human CRC tissues and correlated well with high lymphatic metastasis and poor prognosis in patients. DCLK1 expression was inversely associated with overall survival in CRC patients. Overexpression of DCLK1 in SW480 cells markedly promoted cell migration and invasion. Furthermore, we validated that DCLK1 could facilitate EMT in cancer cells by up-regulation of the mesenchymal markers Vimentin and ZEB1 and down-regulation of the epithelial marker E-cadherin in SW480 cells. CONCLUSIONS: DCLK1 up-regulation may play a contributory role in CRC metastasis and poor prognosis via activation of EMT. DCLK1 may serve as an independent predictor for CRC prognosis.