cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.14290825
title: Effects of purine nucleotide administration on purine nucleotide metabolism in brains of heroin-dependent rats

description: ABSTRACT Heroin is known to enhance catabolism and inhibit anabolism of purine nucleotides, leading to purine nucleotide deficiencies in rat brains. Here, we determined the effect of exogenous purine nucleotide administration on purine nucleotide metabolism in the brains of heroin-dependent rats. Heroin was administrated in increasing doses for 9 consecutive days to induce addiction, and the biochemical changes associated with heroin and purine nucleotide administration were compared among the treated groups. HPLC was performed to detect the absolute concentrations of purine nucleotides in the rat brain cortices. The enzymatic activities of adenosine deaminase (ADA) and xanthine oxidase (XO) in the treated rat cortices were analyzed, and qRT-PCR was performed to determine the relative expression of ADA, XO, adenine phosphoribosyl transferase (APRT), hypoxanthine-guaninephosphoribosyl transferase (HGPRT), and adenosine kinase (AK). Heroin increased the enzymatic activity of ADA and XO, and up-regulated the transcription of ADA and XO. Alternatively, heroin decreased the transcription of AK, APRT, and HGPRT in the rat cortices. Furthermore, purine nucleotide administration alleviated the effect of heroin on purine nucleotide content, activity of essential purine nucleotide metabolic enzymes, and transcript levels of these genes. Our findings therefore represent a novel, putative approach to the treatment of heroin addiction.
DOI: 10.6084/m9.figshare.14290825.v1
title: Effects of purine nucleotide administration on purine nucleotide metabolism in brains of heroin-dependent rats

description: ABSTRACT Heroin is known to enhance catabolism and inhibit anabolism of purine nucleotides, leading to purine nucleotide deficiencies in rat brains. Here, we determined the effect of exogenous purine nucleotide administration on purine nucleotide metabolism in the brains of heroin-dependent rats. Heroin was administrated in increasing doses for 9 consecutive days to induce addiction, and the biochemical changes associated with heroin and purine nucleotide administration were compared among the treated groups. HPLC was performed to detect the absolute concentrations of purine nucleotides in the rat brain cortices. The enzymatic activities of adenosine deaminase (ADA) and xanthine oxidase (XO) in the treated rat cortices were analyzed, and qRT-PCR was performed to determine the relative expression of ADA, XO, adenine phosphoribosyl transferase (APRT), hypoxanthine-guaninephosphoribosyl transferase (HGPRT), and adenosine kinase (AK). Heroin increased the enzymatic activity of ADA and XO, and up-regulated the transcription of ADA and XO. Alternatively, heroin decreased the transcription of AK, APRT, and HGPRT in the rat cortices. Furthermore, purine nucleotide administration alleviated the effect of heroin on purine nucleotide content, activity of essential purine nucleotide metabolic enzymes, and transcript levels of these genes. Our findings therefore represent a novel, putative approach to the treatment of heroin addiction.
DOI: 10.6084/m9.figshare.16912199.v1
title: Effect and Mechanism of BDNF/TrkB Signaling on Vestibular Compensation

description: Brain-derived neurotrophic factor (BDNF) regulates neuronal plasticity by targeting the tyrosine kinase B receptor (TrkB) receptor, but limited researches concentrate on the role of BDNF/TrkB signaling in vestibular compensation. In this study, rats with unilateral vestibular dysfunction were established by unilateral labyrinthectomy (UL) and infusion with siBDNF or 7, 8-Dihydroxyflavone (7,8-DHF, a TrkB receptor agonist). The behavioral scores of rats with vestibular deficits were determined and the rotarod test was performed after UL. BDNF and TrkB levels after UL were determined by western blot and quantitative reverse transcription PCR (qRT-PCR). 5-bromo-2ʹ-deoxyuridine (BrdU)-positive cells (newly generated cells) and GAD67-positive cells (GABAergic neurons) were identified by immunohistochemistry. Glial fibrillary acidic protein (GFAP) (astrocyte marker)-positive cells were identified and GABA type A receptor (GABA<sub>A</sub>R) expression was detected by immunofluorescence. We found that after UL, BDNF and TrkB levels were up-regulated with a maximum value at 4 h, and then progressively down-regulated during 4 h~7 d. Blocking BDNF/TrkB signaling inhibited the recovery from vestibular deficits, decreased the numbers of newly generated cells and astrocytes in medial vestibular nucleus (MVN), inferior vestibular nerve (IVN), superior vestibular nerve (SVN) and lateral vestibular nucleus (LVN), and disrupted the balances of GABAergic neurons and GABA<sub>A</sub>R expressions in the left (lesioned) side and right (intact) side of MVN, whereas activation of BDNF/TrkB signaling caused opposite results. The current study indicated that BDNF/TrkB signaling avails vestibular compensation, depending on the number of newly generated cells and astrocytes, the rebalance of GABAergic neurons, and GABA<sub>A</sub>R expression in bilateral MVN.
DOI: 10.6084/m9.figshare.16912033
title: FAIM regulates autophagy through glutaminolysis in lung adenocarcinoma

description: Altered glutamine metabolism is an important aspect of cancer metabolic reprogramming. The GLS isoform GAC (glutaminase C), the rate-limiting enzyme in glutaminolysis, plays a vital role in cancer initiation and progression. Our previous studies demonstrated that phosphorylation of GAC was essential for its high enzymatic activity. However, the molecular mechanisms for GAC in maintaining its high enzymatic activity and protein stability still need to be further clarified. FAIM/FAIM1 (Fas apoptotic inhibitory molecule) is known as an important anti-apoptotic protein, but little is known about its function in tumorigenesis. Here, we found that knocking down FAIM induced macroautophagy/autophagy through suppressing the activation of the MTOR pathway in lung adenocarcinoma. Further studies demonstrated that FAIM could promote the tetramer formation of GAC through increasing PRKCE/PKCε-mediated phosphorylation. What’s more, FAIM also stabilized GAC through sequestering GAC from degradation by protease ClpXP. These effects increased the production of α-ketoglutarate, leading to the activation of MTOR. Besides, FAIM also promoted the association of ULK1 and MTOR and this further suppressed autophagy induction. These findings discovered new functions of FAIM and elucidated an important molecular mechanism for GAC in maintaining its high enzymatic activity and protein stability.
DOI: 10.6084/m9.figshare.19533870.v1
title: Additional file 1 of Genome-wide identification and expression of SAUR gene family in peanut (Arachis hypogaea L.) and functional identification of AhSAUR3 in drought tolerance

description: Additional file 1.
DOI: 10.6084/m9.figshare.20581095.v1
title: Additional file 5 of A pan-Zea genome map for enhancing maize improvement

description: Additional file 5: Tables S4. Pan Zea gene features.
DOI: 10.6084/m9.figshare.14290741.v1
title: Studies on the formation and synthetic mechanism of related substance G in potassium clavulanate production

description: The objective of this study was to investigate the formation and synthetic mechanism of related substance G in potassium clavulanate production. The impurity in the potassium clavulanate final product, with a retention time of 13.5 min, was confirmed as related substance G by high performance liquid chromatography-mass spectrometry/mass spectrometry. Related substance G analysis during the production of clavulanic acid showed that this impurity could be synthesized during fermentation, and the amount increased with the fermentation time. Studies on its synthetic mechanism showed that L-tyrosine and succinic acid were the precursors for biosynthesis of related substance G in vivo. The reaction was deduced to be catalyzed by an enzyme. The enzyme was a type of extracellular enzyme present in the fermentation supernatant.
DOI: 10.6084/m9.figshare.16912196.v1
title: Essential meiotic structure-specific endonuclease1 (<i>EME1</i>) promotes malignant features in gastric cancer cells via the Akt/GSK3B/CCND1 pathway

description: DNA damage plays a key role in various biological processes involved in malignant disease, the role of the DNA damage repair gene <i>EME1</i> (essential meiotic structure-specific endonuclease 1) in gastric cancer (GC) development is unknown. This work aimed to investigate expression and role of <i>EME1</i> in tumorigenesis. Quantitative real-time polymerase chain reaction (qRT-PCR), immunoblot, cell viability and dual-luciferase reporter assays, RNAi and gene transfection, and immunofluorescent staining were performed to assess <i>EME1</i> regulation in GC tumorigenesis. Further, mouse xenografts were established for <i>in vivo</i> mechanistic studies. <i>EME1</i> was found to be upregulated in both gastric cancer cells and clinically obtained tumors. Additionally, <i>EME1</i> levels were strongly associated with the differentiation level of GC and lymph node metastasis. <i>In vivo</i> and <i>in vitro</i> knockdown of <i>EME1</i> markedly suppressed the proliferative, migratory, and invasive abilities of GC cells and enhanced apoptotic cell death and cell cycle arrest rates. Mechanistically, <i>EME1</i> modulated Akt/GSK3B/CCND1 signaling. <i>MYB</i> may also have contributed to <i>EME1</i>-dependent gastric carcinogenesis. Elevated <i>EME1</i> expressions may enhance the proliferative and metastatic abilities of GC cells, thereby acting as a tumor-promoting factor via Akt. These findings reveal that <i>EME1</i> is an important biomarker for GC prognosis and treatment in humans. <b>Abbreviations</b>: Essential meiotic structure-specific endonuclease 1 (<i>EME1</i>); MYB proto-oncogene (<i>MYB</i>); Cell counting kit-8 (CCK-8); 4,6-diamimo-2-phenyl indole (DAPI); Quantitative real-time PCR (qRT-PCR); Gastric cancer (GC); Immunofluorescence (IF); Small interfering RNA (siRNA); Small hairpin RNA (shRNA); Alpha serine threonine-protein kinase (Akt); Glycogen synthase kinase 3 beta (GSK3B); Cyclin D1 (CCND1); Glyceraldehyde-3-phosphate dehydrogenase (GAPDH); Disease-free survival (DFS); Overall survival (OS); Negative controls (NC); American Joint Committee on Cancer (AJCC); Coding sequence (CDS); Lymph node metastasis (LNM); Tris-Buffered Saline-Tween-20 (TBST); Horseradish Peroxidase (HRP); Electrochemiluminescence (ECL); Polyvinylidene Fluoride (PVDF); Excision repair cross complementation group 1 (ERCC1).
DOI: 10.25413/sun.24331114
title: Ship Motion Measurements and Human Responses Captured on the SA Agulhas II - Winter Cruise 2022

description: This dataset contains digitised human responses related to motion sickness recorded by participants on the SA Agulhas II during SCALE Winter Cruise of 2022 using paper-based questionnaire booklets, called daily diaries, and a mobile application, called Mariner 4.0.Additionally, this dataset contains ship motion measured by accelerometers in a specific array that enables the computation of z-oriented acceleration at points of interest on board beyond the array measurement locations. Acceleration measurements in the dataset are stored in 5-minute batches with a 10 Hz sample rate at the locations and orientations detailed in the associated readme file in the data collection. This dataset is a down-sampled subset of acceleration measurements sampled at 2048 Hz during the SCALE Winter Cruise of 2022.Lastly, this dataset contains Motion Sickness Dose Values computed from ship motion measurements at each near-field communication tag installed shipboard, as detailed by position vectors in the supporting documentation.Note: A Readme file is included to guide dataset navigation and understanding.
DOI: 10.6084/m9.figshare.19533345
title: MM-associated circular RNA downregulates microRNA-19a through methylation to suppress proliferation of pancreatic adenocarcinoma cells

description: Opposite roles of circular RNA MM-associated circular RNA (circ-MYBL2) have been observed in different malignancies, and its role in pancreatic adenocarcinoma (PA) is unknown. Our preliminary sequencing data revealed its inverse correlation with microRNA-19a (miR-19a). This study was performed to explore the role of circ-MYBL2 in PA and its crosstalk with miR-19a. The accumulation of circ-MYBL2 and miR-19a in PA was detected by RT-qPCR. Participation of circ-MYBL2 in the regulation of miR-19a and its RNA gene methylation was studied with an overexpression assay, followed by RT-qPCR and MSP analyses. The role of miR-19a and circ-MYBL2 in PA cell proliferation and movement was evaluated using the BrdU assay and the Transwell assay, respectively. Downregulation of circ-MYBL2 and upregulation of miR-19a were observed in PA. In PA cells, circ-MYBL2 decreased the accumulation of miR-19a but increased its RNA gene methylation. Overexpression of circ-MYBL2 decreased PA cell proliferation and movement, while overexpression of miR-19a showed an opposite effect. In addition, circ-MYBL2 suppressed the role of miR-19a in cell proliferation, migration, and invasion. In conclusion, circ-MYBL2 was downregulated in PA and it downregulated miR-19a through methylation to suppress PA cell proliferation.
DOI: 10.6084/m9.figshare.19533345.v1
title: MM-associated circular RNA downregulates microRNA-19a through methylation to suppress proliferation of pancreatic adenocarcinoma cells

description: Opposite roles of circular RNA MM-associated circular RNA (circ-MYBL2) have been observed in different malignancies, and its role in pancreatic adenocarcinoma (PA) is unknown. Our preliminary sequencing data revealed its inverse correlation with microRNA-19a (miR-19a). This study was performed to explore the role of circ-MYBL2 in PA and its crosstalk with miR-19a. The accumulation of circ-MYBL2 and miR-19a in PA was detected by RT-qPCR. Participation of circ-MYBL2 in the regulation of miR-19a and its RNA gene methylation was studied with an overexpression assay, followed by RT-qPCR and MSP analyses. The role of miR-19a and circ-MYBL2 in PA cell proliferation and movement was evaluated using the BrdU assay and the Transwell assay, respectively. Downregulation of circ-MYBL2 and upregulation of miR-19a were observed in PA. In PA cells, circ-MYBL2 decreased the accumulation of miR-19a but increased its RNA gene methylation. Overexpression of circ-MYBL2 decreased PA cell proliferation and movement, while overexpression of miR-19a showed an opposite effect. In addition, circ-MYBL2 suppressed the role of miR-19a in cell proliferation, migration, and invasion. In conclusion, circ-MYBL2 was downregulated in PA and it downregulated miR-19a through methylation to suppress PA cell proliferation.
DOI: 10.6084/m9.figshare.20057408.v1
title: Additional file 3 of Development and validation of a novel mitophagy-related gene prognostic signature for glioblastoma multiforme

description: Additional file 3.
DOI: 10.25413/sun.24331114.v1
title: Ship Motion Measurements and Human Responses Captured on the SA Agulhas II - Winter Cruise 2022

description: This dataset contains digitised human responses related to motion sickness recorded by participants on the SA Agulhas II during SCALE Winter Cruise of 2022 using paper-based questionnaire booklets, called daily diaries, and a mobile application, called Mariner 4.0.Additionally, this dataset contains ship motion measured by accelerometers in a specific array that enables the computation of z-oriented acceleration at points of interest on board beyond the array measurement locations. Acceleration measurements in the dataset are stored in 5-minute batches with a 10 Hz sample rate at the locations and orientations detailed in the associated readme file in the data collection. This dataset is a down-sampled subset of acceleration measurements sampled at 2048 Hz during the SCALE Winter Cruise of 2022.Lastly, this dataset contains Motion Sickness Dose Values computed from ship motion measurements at each near-field communication tag installed shipboard, as detailed by position vectors in the supporting documentation.Note: A Readme file is included to guide dataset navigation and understanding.
DOI: 10.6084/m9.figshare.19533876
title: Additional file 2 of Genome-wide identification and expression of SAUR gene family in peanut (Arachis hypogaea L.) and functional identification of AhSAUR3 in drought tolerance

description: Additional file 2.
DOI: 10.6084/m9.figshare.19533879.v1
title: Additional file 3 of Genome-wide identification and expression of SAUR gene family in peanut (Arachis hypogaea L.) and functional identification of AhSAUR3 in drought tolerance

description: Additional file 3.
DOI: 10.6084/m9.figshare.20579637
title: Additional file 2 of Integrated single-cell RNA-seq and DNA methylation reveal the effects of air pollution in patients with recurrent spontaneous abortion

description: Additional file 2: Table 2. Total of DMR between patients with RSA and controls detected through RRBS.
DOI: 10.6084/m9.figshare.16912033.v1
title: FAIM regulates autophagy through glutaminolysis in lung adenocarcinoma

description: Altered glutamine metabolism is an important aspect of cancer metabolic reprogramming. The GLS isoform GAC (glutaminase C), the rate-limiting enzyme in glutaminolysis, plays a vital role in cancer initiation and progression. Our previous studies demonstrated that phosphorylation of GAC was essential for its high enzymatic activity. However, the molecular mechanisms for GAC in maintaining its high enzymatic activity and protein stability still need to be further clarified. FAIM/FAIM1 (Fas apoptotic inhibitory molecule) is known as an important anti-apoptotic protein, but little is known about its function in tumorigenesis. Here, we found that knocking down FAIM induced macroautophagy/autophagy through suppressing the activation of the MTOR pathway in lung adenocarcinoma. Further studies demonstrated that FAIM could promote the tetramer formation of GAC through increasing PRKCE/PKCε-mediated phosphorylation. What’s more, FAIM also stabilized GAC through sequestering GAC from degradation by protease ClpXP. These effects increased the production of α-ketoglutarate, leading to the activation of MTOR. Besides, FAIM also promoted the association of ULK1 and MTOR and this further suppressed autophagy induction. These findings discovered new functions of FAIM and elucidated an important molecular mechanism for GAC in maintaining its high enzymatic activity and protein stability.
DOI: 10.6084/m9.figshare.19533876.v1
title: Additional file 2 of Genome-wide identification and expression of SAUR gene family in peanut (Arachis hypogaea L.) and functional identification of AhSAUR3 in drought tolerance

description: Additional file 2.
DOI: 10.6084/m9.figshare.19533879
title: Additional file 3 of Genome-wide identification and expression of SAUR gene family in peanut (Arachis hypogaea L.) and functional identification of AhSAUR3 in drought tolerance

description: Additional file 3.
DOI: 10.6084/m9.figshare.14291418
title: LncRNA NORAD engages in psoriasis by binding to miR-26a to regulate keratinocyte proliferation

description: Psoriasis is a chronic, inflammatory skin disease. It was reported that lncRNA Non-coding RNA-activated by DNA damage (NORAD) has potential regulatory effects on skin diseases. Our previous studies found that lncRNA NORAD was highly expressed and its potential target miR-26a was down-regulated in psoriasis model mice. Here, we aimed to investigate the role of NORAD in the development of psoriasis. IL-22/LPS (interleukin-22/lipopolysaccharide)-stimulated HaCaT (human immortalized keratinocytes) cell model and imiquimod-induced mouse model were established. Keratin 6 (K6), Keratin 16 (K16), Keratin 17 (K17), and Cell division cycle 6 (CDC6) levels were detected by western blot. Cell activity was detected by CCK-8, MTT, and EdU assays. Quantitative real-time PCR was performed to examine the levels of NORAD, miR-26a, CDC6, K6, K16, and K17. Haematoxylin-eosin staining was applied to observe the degree of skin thickening and hyperplasia. Fluorescence <i>in situ</i> hybridization detects the location of NORAD. RNA immunoprecipitation, RNA pull-down, and Luciferase test were performed to detect the interaction between NORAD and miR-26a. In IL-22/LPS-stimulated HaCaT cells, NORAD, CDC6, and keratinocyte proliferation-related proteins (K6, K16, and K17) were up-regulated and miR-26a was down-regulated. Cell survival and proliferation were also increased. However, the results were reversed after interference with NORAD. Also, <i>in vitro</i> experiments revealed that NORAD negatively regulated miR-26a. In IL-22/LPS-stimulated HaCaT cells and skin of imiquimod-induced mice, we found that lower NORAD resulted in an increase of miR-26a and a decrease of CDC6, further decreased levels of keratinocyte proliferation-related proteins (K6, K16, and K17).
DOI: 10.6084/m9.figshare.14290866
title: Exploring the shared genes of hypertension, diabetes and hyperlipidemia based on microarray

description: Given their relationship with metabolic syndrome and systematic inflammatory diseases, the pathogenesis of hypertension, hyperglycemia, and hyperlipidemia is closely related. To explore the common genes among these three conditions, spontaneous hypertensive rats (SHR), spontaneous diabetic Goto-Kakizaki rats (GK) and hyperlipidemia rats (HMR) were reared for experiments. Gene array was used to identify the genes of SHR, GK and HMR compared with normal Wistar rats using TBtools software. First, real-time PCR was applied to verify these genes, and Cytoscape software was used to construct networks based on the National Center for Biotechnology Information (NCBI) database. Second, Kyoto Encyclopedia of Genes and Genomes (KEGG) database analysis was performed to classify the genes. Visualization and Integrated Discovery (DAVID) database and Gene Ontology database were used to explore the biological function. Finally, Onto-tools Pathway Express was used to analyze the pathways of shared genes. Importantly, upregulated common genes, such as Bad, Orm1, Arntl and Zbtb7a, were used to construct a network of 150 genes, while downregulated genes, such as Mif and Gpx1, formed a network of 29 genes. Interestingly, the networks were involved in various pathways, such as insulin signal pathway, endometrial cancer pathway, circadian rhythm pathway, and pancreatic cancer pathway. We discovered common genes of SHR, GK and HMR compared with normal Wistar rats, and the association of these genes together with biological function were preliminarily revealed.