cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.22721983
title: Ansai peasant paintings: inheritance of chinese primitive culture and primitive philosophy

description: Abstract: Chinese primitive philosophy, as the unity of cosmological ontology, epistemology and methodology of the Chinese philosophical system, is a complete and mature philosophical system formed in the late primitive society as early as before the Xia, Shang and Zhou Dynasties. It is also the unity of the concept of Yin and Yang and constant life that is sublimated from the human-beings’ basic cultural consciousness: life consciousness and reproduction consciousness. The Chinese primitive culture, from the painted pottery culture 7,000 years ago to today, from the underground archaeological culture to the group culture on the ground, is a plastic art based on the concept of viewing objects and taking images. It is a broad concept of fine arts that determines the philosophical view, artistic view, emotional temperament, psychological quality and national spirit of the Chinese nation. The most primitive culture and primitive philosophy in China have been preserved with extremely rich and complete historical remains in the group’s cultural and social life. It is for this reason that China is the only country with an ancient history of civilization that has not experienced a cultural break. The primitive culture and philosophical system of China, as the philosophical basis and main connotation of ethnic group culture, are completely accumulated in the ethnic groups’ social life. Folk art, which has accumulated the hundreds of millions of working masses’ wisdom in China, is the mother of the Chinese national culture and art that has been inherited from primitive society until today with distinct national and regional characteristics. It is a long-standing cultural form with the longest history, the widest mass participation, the most distinct regional characteristics and the richest cultural connotation in the Chinese national cultural form. The rapid development of the times makes the traditional folk customs and folk arts, which are generally deposited in the rural areas of China, become precarious. As a result, the research advantages of the unique human culture and the original culture of China will cease to exist. Therefore, it is an urgent historical task to make use of this advantage to study the original culture of China and the philosophical genes of the Chinese nation. Protection is imminent, and inheritance is the historical mission, which highlights the deeper significance of studying primitive culture and primitive philosophy in modern society.
DOI: 10.6084/m9.figshare.6993458.v1
title: Transcriptome analysis of <i>Lilium Oriental</i> × <i>Trumpet</i> hybrid roots reveals auxin-related genes and stress-related genes involved in picloram-induced somatic embryogenesis induction

description: Highly efficient somatic embryogenesis (SE) initiation systems are crucial for the clonal propagation and genetic transformation of <i>Lilium Oriental</i> × <i>Trumpet</i> hybrid. To elucidate the underlying mechanism of SE induction, we conducted <i>de novo</i> transcriptome sequencing of the roots at four different times in relation to SE initiation (0 days, control; 20 days, embryogenic callus induction (ECI) 1; 40 days, ECI2; 55 days, ECI3). A total of 4621, 7582, and 7427 differentially expressed genes (DEGs) were identified from the ECI1 vs. control, ECI2 vs. control, and ECI3 vs. control comparisons, respectively. The gene-enrichment analysis revealed 54 significant DEGs. Further analysis showed that the transcript levels of the auxin-related genes <i>ARF9/15/16</i>, the abscisic acid-related (ABA-related) genes <i>PYL4/9</i>, and stress-related transcription factors, including <i>WRKY26, MYB36, NAC100, bHLH2</i>/<i>5</i>/<i>18</i>/<i>112</i>, and <i>HSP90</i>, were increased at the ECI1 stage. <i>ABI5 </i>can influence the expression of stress-responsive genes as an ABA signalling regulator. The upregulated <i>ABI5 </i>could be caused by the increased <i>ARF9/15/16, PYL4/9, WRKY26, MYB36, NAC100, bHLH2</i>/<i>5</i>/<i>18</i>/<i>112</i>, and <i>HSP90 </i>at the ECI2 and ECI3 stages to regulate the ECI. These genes had the most abundant transcripts among the DEGs, indicating that auxin and stress-related signalling pathways are involved in SE initiation of <i>Lilium</i> spp.
DOI: 10.6084/m9.figshare.20101050
title: Long non-coding RNA X-inactive specific transcript suppresses the progression of hepatocellular carcinoma through microRNA-221-3p-targeted regulation of O6-methylguanine-DNA methyltransferase

description: MicroRNA-221-3p (miR-221-3p) is an important regulator involved in the progression and prognosis of various cancers. In this study, we aimed to investigate the diagnostic and prognostic value of miR-221-3p expression along with long non-coding RNA X–inactive specific transcript (XIST), which was identified as its upstream regulator in hepatocellular carcinoma (HCC) by bioinformatics analysis, and further validated by RNA immunoprecipitation (RIP) and dual-luciferase reporter assays. Their expression was measured in tumor tissues and corresponding non-tumor tissues by quantitative real-time PCR (qRT-PCR), which revealed that XIST was weakly expressed in HCC cells and tumors, while miR-221-3p was overexpressed. Complete knockdown of XIST enhanced HCC cell proliferation and migration and inhibited apoptosis, as observed by MTT, transwell, and flow cytometry experiments, respectively. Animal studies validated that XIST knockdown induces tumor growth <i>in vivo</i>. In contrast, upregulation of XIST in HCC cells suppressed their proliferation and migration, stimulated apoptosis, and retarded the growth rate of tumors <i>in vivo</i>. These effects were partially reversed by upregulating miR-221-3p expression. Furthermore, we demonstrated that O<sup>6</sup>-methylguanine-DNA methyltransferase (MGMT) is a downstream target of miR-221-3p. It was weakly expressed in HCC cells and tumors and showed a negative correlation with miR-221-3p. Forced MGMT expression repressed proliferation and migration and enhanced apoptosis in HCC cells. Nevertheless, these anti-tumor effects induced by MGMT overexpression could be abolished by miR-221-3p upregulation. Collectively, our findings reveal that XIST blocks the development of HCC through miR-221-3p-targeted regulation of MGMT. This reveals a new mechanism involved in the development of HCC.
DOI: 10.5281/zenodo.10652997
title: Secondary metabolite discovery with Galaxy - GTN material

description: GTN material for the Tutorial: Secondary metabolite discovery with Galaxy
DOI: 10.5281/zenodo.10652998
title: Secondary metabolite discovery with Galaxy - GTN material

description: GTN material for the Tutorial: Secondary metabolite discovery with Galaxy
DOI: 10.6084/m9.figshare.20625109
title: Additional file 1 of Prevalence of dyslipidemia, treatment rate and its control among patients with type 2 diabetes mellitus in Northwest China: a cross-sectional study

description: Additional file 1.
DOI: 10.6084/m9.figshare.14936109
title: Additional file 2 of Full-length transcriptome analysis reveals the mechanism of acupuncture at PC6 improves cardiac function in myocardial ischemia model

description: Additional file 2: Table S2. The differentially expressed genes in PC6 group compared to MI group.
DOI: 10.6084/m9.figshare.20625109.v1
title: Additional file 1 of Prevalence of dyslipidemia, treatment rate and its control among patients with type 2 diabetes mellitus in Northwest China: a cross-sectional study

description: Additional file 1.
DOI: 10.6084/m9.figshare.20101073
title: DEAD-box helicase 56 functions as an oncogene promote cell proliferation and invasion in gastric cancer via the FOXO1/p21 Cip1/c-Myc signaling pathway

description: DEAD-box helicase (DDX) family exerts a critical effect on cancer initiation and progression through alternative splicing, transcription and ribosome biogenesis. Increasing evidence has demonstrated that DEAD-box helicase 56 (DDX56) is over-expressed in several cancers, which plays an oncogenic role. Till the present, the impact of DDX56 on gastric cancer (GC) remains unclear. We conducted high-throughput sequencing (RNA-seq) to demonstrate aberrant DDX56 levels within 10 GC and matched non-carcinoma tissue samples. DDX56 levels were detected through qRT‐PCR, western blotting (WB) and immunochemical staining in GC patients. We conducted gain- and loss-of-function studies to examine DDX56’s biological role in GC development. In vitro, we carried out 5‑Ethynyl‑2‑deoxyuridine (EdU), scratch, Transwell, and flow cytometry (FCM) assays for detecting GC cell growth, invasion, migration and apoptosis. Additionally, gene set enrichment analysis (GSEA), WB assay, and Encyclopedia of RNA Interactomes (ENCORI) were carried out for analyzing DDX56-regulated downstream genes and signaling pathways. In vivo, tumor xenograft experiment was performed for investigating how DDX56 affected GC development within BALB/c nude mice. Functionally, DDX56 knockdown arrested cell cycle at G1 phase, invasion and migration of AGS and MKN28 cells, and enhanced their apoptosis. Ectopic DDX56 expression enhanced the cell growth, migration and invasion, and inhibited apoptosis. Knockdown of DDX56 suppressed GC growth in the tumor models of BALB/c nude mice. Mechanistically, DDX56 post-transcriptionally suppressed FOXO1/p21 Cip1 protein expression, which could activate its downstream cyclin E1/CDK2/c-Myc signaling pathways. This sheds lights on the GC pathogenic mechanism and offers a potential anti-cancer therapeutic target.
DOI: 10.6084/m9.figshare.20101073.v1
title: DEAD-box helicase 56 functions as an oncogene promote cell proliferation and invasion in gastric cancer via the FOXO1/p21 Cip1/c-Myc signaling pathway

description: DEAD-box helicase (DDX) family exerts a critical effect on cancer initiation and progression through alternative splicing, transcription and ribosome biogenesis. Increasing evidence has demonstrated that DEAD-box helicase 56 (DDX56) is over-expressed in several cancers, which plays an oncogenic role. Till the present, the impact of DDX56 on gastric cancer (GC) remains unclear. We conducted high-throughput sequencing (RNA-seq) to demonstrate aberrant DDX56 levels within 10 GC and matched non-carcinoma tissue samples. DDX56 levels were detected through qRT‐PCR, western blotting (WB) and immunochemical staining in GC patients. We conducted gain- and loss-of-function studies to examine DDX56’s biological role in GC development. In vitro, we carried out 5‑Ethynyl‑2‑deoxyuridine (EdU), scratch, Transwell, and flow cytometry (FCM) assays for detecting GC cell growth, invasion, migration and apoptosis. Additionally, gene set enrichment analysis (GSEA), WB assay, and Encyclopedia of RNA Interactomes (ENCORI) were carried out for analyzing DDX56-regulated downstream genes and signaling pathways. In vivo, tumor xenograft experiment was performed for investigating how DDX56 affected GC development within BALB/c nude mice. Functionally, DDX56 knockdown arrested cell cycle at G1 phase, invasion and migration of AGS and MKN28 cells, and enhanced their apoptosis. Ectopic DDX56 expression enhanced the cell growth, migration and invasion, and inhibited apoptosis. Knockdown of DDX56 suppressed GC growth in the tumor models of BALB/c nude mice. Mechanistically, DDX56 post-transcriptionally suppressed FOXO1/p21 Cip1 protein expression, which could activate its downstream cyclin E1/CDK2/c-Myc signaling pathways. This sheds lights on the GC pathogenic mechanism and offers a potential anti-cancer therapeutic target.
DOI: 10.6084/m9.figshare.20101097.v1
title: Circ_0092012 knockdown restrains non-small cell lung cancer progression by inhibiting cell malignant phenotype and immune escape through microRNA-635/programmed death ligand 1 axis

description: Circular RNAs have been reported to play roles in non-small cell lung cancer (NSCLC) progression. Herein, this work aimed to investigate the potential value of circ_0092012 in NSCLC progression. Levels of genes and proteins were detected using quantitative reverse transcription-polymerase chain reaction and Western blot, respectively. The growth, malignant phenotypes and immune escape in NSCLC were investigated. The binding between microRNA (miR)-635 and circ_0092012 or programmed death ligand 1 (PDL1) was verified. Circ_0092012 was highly expressed in NSCLC. Circ_0092012 deficiency suppressed NSCLC cell proliferation, invasion and migration, moreover, as well as was able to inhibit the apoptosis of CD8 + T cells and induce higher interferon-γ and tumor necrosis factor-α levels when co-cultured with peripheral blood mononuclear cells. Mechanistically, circ_0092012 sponged miR-635, which targeted PDL1. Further rescue experiments suggested that the anticancer effects of circ_0092012 knockdown were reversed by miR-635 inhibition. Additionally, miR-635 re-expression suppressed NSCLC cell malignant phenotypes mentioned above and immune escape, which were attenuated by PDL1 overexpression. Moreover, circ_0092012 deletion retarded NSCLC growth <i>in vivo</i>. In all, circ_0092012 knockdown suppressed NSCLC cell oncogenic phenotypes and immune escape by miR-635/PDL1 axis.
DOI: 10.6084/m9.figshare.20101050.v1
title: Long non-coding RNA X-inactive specific transcript suppresses the progression of hepatocellular carcinoma through microRNA-221-3p-targeted regulation of O6-methylguanine-DNA methyltransferase

description: MicroRNA-221-3p (miR-221-3p) is an important regulator involved in the progression and prognosis of various cancers. In this study, we aimed to investigate the diagnostic and prognostic value of miR-221-3p expression along with long non-coding RNA X–inactive specific transcript (XIST), which was identified as its upstream regulator in hepatocellular carcinoma (HCC) by bioinformatics analysis, and further validated by RNA immunoprecipitation (RIP) and dual-luciferase reporter assays. Their expression was measured in tumor tissues and corresponding non-tumor tissues by quantitative real-time PCR (qRT-PCR), which revealed that XIST was weakly expressed in HCC cells and tumors, while miR-221-3p was overexpressed. Complete knockdown of XIST enhanced HCC cell proliferation and migration and inhibited apoptosis, as observed by MTT, transwell, and flow cytometry experiments, respectively. Animal studies validated that XIST knockdown induces tumor growth <i>in vivo</i>. In contrast, upregulation of XIST in HCC cells suppressed their proliferation and migration, stimulated apoptosis, and retarded the growth rate of tumors <i>in vivo</i>. These effects were partially reversed by upregulating miR-221-3p expression. Furthermore, we demonstrated that O<sup>6</sup>-methylguanine-DNA methyltransferase (MGMT) is a downstream target of miR-221-3p. It was weakly expressed in HCC cells and tumors and showed a negative correlation with miR-221-3p. Forced MGMT expression repressed proliferation and migration and enhanced apoptosis in HCC cells. Nevertheless, these anti-tumor effects induced by MGMT overexpression could be abolished by miR-221-3p upregulation. Collectively, our findings reveal that XIST blocks the development of HCC through miR-221-3p-targeted regulation of MGMT. This reveals a new mechanism involved in the development of HCC.
DOI: 10.6084/m9.figshare.12757435.v1
title: Additional file 4 of Establishment and characterization of breast cancer organoids from a patient with mammary Paget’s disease

description: Additional file 4: Data S2. The somatic mutations of the organoids.
DOI: 10.6084/m9.figshare.20101231
title: Petrogenesis of Cretaceous felsic volcanic rocks in Zhejiang province, China: insights from zircon U-Pb age and Lu-Hf isotopes

description: Late Mesozoic felsic volcanic rocks are mostly distributed in the Zhejiang, Fujian, and Guangdong provinces, southeastern China, with an outcrop area of &gt;100,000 km<sup>2</sup>. Although many studies have been published, however, the petrogenesis and tectonic background of these felsic volcanic rocks have remained controversial. Here, we present nineteen new SHRIMP U-Pb zircon ages and Lu-Hf isotopes of the felsic volcanic rocks from southeastern Zhejiang Province. The studied samples have zircon U-Pb ages range from 134 to 89 Ma and become younger towards the coastal zone. A group of zircons with U-Pb ages of 120–110 Ma have been documented, which argue against the proposed magmatic quiescence of 120–110 Ma in the study area. Together with all the published data, our zircon U-Pb mapping has shown that the lower volcanic series (140–120 Ma) are all distributed in the inland of Zhejiang Province, whereas the upper volcanic series (120–90 Ma) are mostly exposed in the coastal zone. Furthermore, nine felsic volcanic samples from Yandangshan area show negative correlation between the zircon ɛHf(t) values and the volcanic ages, which suggests the increased juvenile components in the source region with time. Our zircon Lu-Hf isotope mapping does not show a clearly trend towards the coastal zone. The variation of zircon Lu-Hf isotopes among felsic volcanic rocks were most likely attribute to the different degrees of juvenile contribution. Based on our new results, a episodic roll-back of the Palaeo-Pacific plate model can well explain the petrogenesis of the felsic volcanic rocks. There is no evidence supporting the scenario that a large volume of felsic magma erupted at a short interval of 3–10 Ma. Therefore, at least in Zhejiang Province, the Cretaceous felsic volcanic rocks cannot be considered as a part of a Silicic Large Igneous Province.
DOI: 10.6084/m9.figshare.20101109.v1
title: Ginsenoside Rg3 and sorafenib combination therapy relieves the hepatocellular carcinomaprogression through regulating the HK2-mediated glycolysis and PI3K/Akt signaling pathway

description: Hepatocellular carcinoma (HCC) is the most common pathological type of primary hepatic carcinoma. This study investigated the effects of ginsenoside Rg3 (Rg3) and sorafenib (SFN) combination therapy on HCC progression. The HCC-related data were obtained from TCGA database, and the data of HK2 mRNA, clinicopathological features, and survival outcomes were extracted using R Programming 4.0. The human hepatoma cell lines HepG2 and Bel7404 were used. Cell viability was tested using the MTT assay. Glucose consumption and lactate levels of HCC cells were detected using the corresponding kits. Western blotting was used to determine the protein expression of HK2, PI3K, and Akt. HK2 was overexpressed in patients with HCC. Compared with patients with overexpressed HK2, those with low levels of HK2 achieved a longer survival time. In addition, the Rg3 and SFN combination therapy significantly reduced cell viability, glucose consumption, lactate levels, and protein expression of HK2, PI3K, and Akt in HCC cells. Additionally, the Rg3 and SFN combination therapy exhibited a better effect than the single drug group. Inhibition of the PI3K/Akt signaling pathway or exogenous lactate intervention reversed the effects of Rg3 and SFN combination therapy in HCC cells. In conclusion, Rg3 has a synergistic effect on the sensitivity of HepG2 and Bel7404 hepatoma cells to SFN, which is related to HK2-mediated glycolysis and the PI3K/Akt signaling pathway.
DOI: 10.6084/m9.figshare.20101231.v1
title: Petrogenesis of Cretaceous felsic volcanic rocks in Zhejiang province, China: insights from zircon U-Pb age and Lu-Hf isotopes

description: Late Mesozoic felsic volcanic rocks are mostly distributed in the Zhejiang, Fujian, and Guangdong provinces, southeastern China, with an outcrop area of &gt;100,000 km<sup>2</sup>. Although many studies have been published, however, the petrogenesis and tectonic background of these felsic volcanic rocks have remained controversial. Here, we present nineteen new SHRIMP U-Pb zircon ages and Lu-Hf isotopes of the felsic volcanic rocks from southeastern Zhejiang Province. The studied samples have zircon U-Pb ages range from 134 to 89 Ma and become younger towards the coastal zone. A group of zircons with U-Pb ages of 120–110 Ma have been documented, which argue against the proposed magmatic quiescence of 120–110 Ma in the study area. Together with all the published data, our zircon U-Pb mapping has shown that the lower volcanic series (140–120 Ma) are all distributed in the inland of Zhejiang Province, whereas the upper volcanic series (120–90 Ma) are mostly exposed in the coastal zone. Furthermore, nine felsic volcanic samples from Yandangshan area show negative correlation between the zircon ɛHf(t) values and the volcanic ages, which suggests the increased juvenile components in the source region with time. Our zircon Lu-Hf isotope mapping does not show a clearly trend towards the coastal zone. The variation of zircon Lu-Hf isotopes among felsic volcanic rocks were most likely attribute to the different degrees of juvenile contribution. Based on our new results, a episodic roll-back of the Palaeo-Pacific plate model can well explain the petrogenesis of the felsic volcanic rocks. There is no evidence supporting the scenario that a large volume of felsic magma erupted at a short interval of 3–10 Ma. Therefore, at least in Zhejiang Province, the Cretaceous felsic volcanic rocks cannot be considered as a part of a Silicic Large Igneous Province.
DOI: 10.6084/m9.figshare.4896848
title: Modeling the firm's response to research & development tax credit policies

description: In this article, we develop a microeconomic model of normative firm behavior under the incentive of a research and development (R&D) tax credit. The model is based on the well-known concept of a two-factor learning model in which R&D expenditures and manufacturing capacity expansion are the principle determinants of cost reduction in a new technology product. We distinguish between the behavior of start-up firms and ongoing firms and study the potential impacts of progressively larger R&D tax credits. We find highly significant differences in the potential impact of the credit on start-up firms versus ongoing firms. We also find that the credit can significantly impact optimal product pricing of the technology when introduced into the marketplace. We examine the implications of this latter fact on the overall social cost of the R&D tax credit.
DOI: 10.6084/m9.figshare.20101097
title: Circ_0092012 knockdown restrains non-small cell lung cancer progression by inhibiting cell malignant phenotype and immune escape through microRNA-635/programmed death ligand 1 axis

description: Circular RNAs have been reported to play roles in non-small cell lung cancer (NSCLC) progression. Herein, this work aimed to investigate the potential value of circ_0092012 in NSCLC progression. Levels of genes and proteins were detected using quantitative reverse transcription-polymerase chain reaction and Western blot, respectively. The growth, malignant phenotypes and immune escape in NSCLC were investigated. The binding between microRNA (miR)-635 and circ_0092012 or programmed death ligand 1 (PDL1) was verified. Circ_0092012 was highly expressed in NSCLC. Circ_0092012 deficiency suppressed NSCLC cell proliferation, invasion and migration, moreover, as well as was able to inhibit the apoptosis of CD8 + T cells and induce higher interferon-γ and tumor necrosis factor-α levels when co-cultured with peripheral blood mononuclear cells. Mechanistically, circ_0092012 sponged miR-635, which targeted PDL1. Further rescue experiments suggested that the anticancer effects of circ_0092012 knockdown were reversed by miR-635 inhibition. Additionally, miR-635 re-expression suppressed NSCLC cell malignant phenotypes mentioned above and immune escape, which were attenuated by PDL1 overexpression. Moreover, circ_0092012 deletion retarded NSCLC growth <i>in vivo</i>. In all, circ_0092012 knockdown suppressed NSCLC cell oncogenic phenotypes and immune escape by miR-635/PDL1 axis.
DOI: 10.6084/m9.figshare.20097938
title: Additional file 3 of Tumor and peritumor radiomics analysis based on contrast-enhanced CT for predicting early and late recurrence of hepatocellular carcinoma after liver resection

description: Additional file 3.