cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.17134117.v1
title: Prevalence and risk factors of active tuberculosis in patients with rheumatic diseases: a multi-center, cross-sectional study in China

description: Evidence of active tuberculosis (ATB) in patients with rheumatic diseases are research priorities but limited data from China have been reported. Research targeting patients not taking anti-TNF biologics are especially insufficient. We aimed to investigate the prevalence and risk factors of ATB in this at-risk population. We conducted a tertiary hospital-based, multi-center, cross-sectional study by using stratified multi-stage cluster sampling strategy to screen ATB in patients with rheumatic diseases. We estimated the prevalence of ATB in patients with rheumatic diseases and identified risk factors among those who were not taking anti-TNF biologic. A total of 13,550 eligible patients were enrolled, and the result showed the standardized prevalence of ATB according to the composition ratio of various types of rheumatic disease was 882/100000 (95% confidence interval (CI): 706-1057). Multivariable logistic regression analysis in patients not taking anti-TNF biologics showed that the independent risk factors of ATB were having systemic lupus erythematosus (SLE) (OR=2.722, 95% CI: 1.437-5.159, <i>p</i>=0.002), having Behcet’s disease (BD) (OR= 5.261, 95% CI: 2.071-13.365, <i>p</i>&lt;0.001), taking azathioprine(AZA) within the past two years (OR=2.095, 95% CI: 0.986-4.450, <i>p</i>=0.054), exposing to glucocorticoids ≥30mg/d for more than four weeks within the past two years (OR=2.031, 95% CI: 1.247-3.309, <i>p</i>=0.004) and having evidences of previous TB (OR= 6.185, 95% CI: 3.487-10.969, <i>p</i>&lt;0.001). The prevalence of ATB was higher in patients with rheumatic diseases compared to the general population. Patients with SLE or BD, prolonged exposure to moderate to high dose of glucocorticoids and previous TB were independent risk factors for ATB.
DOI: 10.6084/m9.figshare.6124289
title: Crosstalk between lysine methylation and phosphorylation of ATG16L1 dictates the apoptosis of hypoxia/reoxygenation-induced cardiomyocytes

description: Post-translational modifications of autophagy-related (<i>ATG</i>) genes are necessary to modulate their functions. However, ATG protein methylation and its physiological role have not yet been elucidated. The methylation of non-histone proteins by SETD7, a SET domain-containing lysine methyltransferase, is a novel regulatory mechanism to control cell protein function in response to various cellular stresses. Here we present evidence that the precise activity of ATG16L1 protein in hypoxia/reoxygenation (H/R)-treated cardiomyocytes is regulated by a balanced methylation and phosphorylation switch. We first show that H/R promotes autophagy and decreases SETD7 expression, whereas autophagy inhibition by 3-MA increases SETD7 level in cardiomyocytes, implying a tight correlation between autophagy and SETD7. Then we demonstrate that SETD7 methylates ATG16L1 at lysine 151 while KDM1A/LSD1 (lysine demethylase 1A) removes this methyl mark. Furthermore, we validate that this methylation at lysine 151 impairs the binding of ATG16L1 to the ATG12–ATG5 conjugate, leading to inhibition of autophagy and increased apoptosis in H/R-treated cardiomyocytes. However, the cardiomyocytes with shRNA-knocked down SETD7 or inhibition of SETD7 activity by a small molecule chemical, display increased autophagy and decreased apoptosis following H/R treatment. Additionally, methylation at lysine 151 inhibits phosphorylation of ATG16L1 at S139 by CSNK2 which was previously shown to be critical for autophagy maintenance, and <i>vice versa</i>. Together, our findings define a novel modification of ATG16L1 and highlight the importance of an ATG16L1 phosphorylation-methylation switch in determining the fate of H/R-treated cardiomyocytes.
DOI: 10.6084/m9.figshare.6124289.v1
title: Crosstalk between lysine methylation and phosphorylation of ATG16L1 dictates the apoptosis of hypoxia/reoxygenation-induced cardiomyocytes

description: Post-translational modifications of autophagy-related (<i>ATG</i>) genes are necessary to modulate their functions. However, ATG protein methylation and its physiological role have not yet been elucidated. The methylation of non-histone proteins by SETD7, a SET domain-containing lysine methyltransferase, is a novel regulatory mechanism to control cell protein function in response to various cellular stresses. Here we present evidence that the precise activity of ATG16L1 protein in hypoxia/reoxygenation (H/R)-treated cardiomyocytes is regulated by a balanced methylation and phosphorylation switch. We first show that H/R promotes autophagy and decreases SETD7 expression, whereas autophagy inhibition by 3-MA increases SETD7 level in cardiomyocytes, implying a tight correlation between autophagy and SETD7. Then we demonstrate that SETD7 methylates ATG16L1 at lysine 151 while KDM1A/LSD1 (lysine demethylase 1A) removes this methyl mark. Furthermore, we validate that this methylation at lysine 151 impairs the binding of ATG16L1 to the ATG12–ATG5 conjugate, leading to inhibition of autophagy and increased apoptosis in H/R-treated cardiomyocytes. However, the cardiomyocytes with shRNA-knocked down SETD7 or inhibition of SETD7 activity by a small molecule chemical, display increased autophagy and decreased apoptosis following H/R treatment. Additionally, methylation at lysine 151 inhibits phosphorylation of ATG16L1 at S139 by CSNK2 which was previously shown to be critical for autophagy maintenance, and <i>vice versa</i>. Together, our findings define a novel modification of ATG16L1 and highlight the importance of an ATG16L1 phosphorylation-methylation switch in determining the fate of H/R-treated cardiomyocytes.
DOI: 10.6084/m9.figshare.17134636.v1
title: Identification and in vitro validation of prognostic lncRNA signature in head and neck squamous cell carcinoma

description: Long non-coding RNAs (lncRNAs) are promising cancer prognostic markers. However, the clinical significance of lncRNA signatures in evaluating overall survival (OS) outcomes of head and neck squamous cell carcinoma (HNSCC) has not been explored. This study aimed to assess the significance of lncRNA in HNSCC and to develop a lncRNA signature related to OS in HNSCC. LncRNA expression matrices were retrieved from the Cancer Genome Atlas (TCGA) data. Least Absolute Shrinkage and Selection of the Operator (LASSO), univariate and multivariate Cox regression were used for establishing a prognostic model. In vitro experiments were carried out to demonstrate the biological role of lncRNA. A prognosis model based on 7 DElncRNAs was finally established.The patients were then divided into high-risk and low-risk groups. Relative to the low-risk group, overall survival times for patients in the high-risk group were significantly low (P=2.466e−07). Risk score remained an independent prognostic factor in univariate (HR=1.329, 95%CI=1.239−1.425, p &lt; 0.001) and multivariate (HR=1.279, 95%CI=1.184−1.382, p &lt; 0.001) Cox regression analyses. The area under the curve (AUC) of the signature was as high as 0.78. Expressions of FOXD2-AS1  in tumor tissues were elevated, and significantly correlated with OS (P=0.008). FOXD2-AS1 silencing then significantly reduced HNSCC cell proliferation, invasion, and migration. In conclusion, a lncRNA signature was established for HNSCC prognostic prediction and FOXD2-AS1 was identified as an HNSCC oncogene.
DOI: 10.6084/m9.figshare.12940149
title: Additional file 1 of A Cyclophilin OsCYP20–2 Interacts with OsSYF2 to Regulate Grain Length by Pre-mRNA Splicing

description: Additional file 1: Supplemental Table S1. Primers used in this study.
DOI: 10.6084/m9.figshare.16610037
title: Aggravating effect of obstructive sleep apnoea on left ventricular remodelling and function disorder in patients with type 2 diabetes mellitus: a case-control study by 3D speckle tracking echocardiography

description: The purpose of this study was to evaluate the early alterations of left ventricular (LV) structure and function in type 2 diabetes mellitus (T2DM) patients with or without obstructive sleep apnoea (OSA) using 3 D speckle tracking echocardiography (3DSTE). Eighty T2DM patients with preserved LVEF were included, half of whom had OSA as co-morbidity. Forty age- and sex-matched controls were also enrolled. LV structure and function were evaluated by conventional echocardiography and 3DSTE. LV global longitudinal strain (GLS), global circumferential strain (GCS), global area strain (GAS), and global radial strain (GRS) were all measured by 3DSTE. Four geometric patterns (normal geometry, concentric remodelling, concentric and eccentric hypertrophy) occupied significantly different proportions within the three groups (<i>p</i> = .014). LV remodelling made up higher shares in two T2DM groups than in the controls, whereas LV hypertrophy appeared most frequently in the patients with T2DM and OSA. The patients with T2DM alone had significantly lower GLS and GCS than the controls (both <i>p</i> &lt; .01). The patients with T2DM and OSA had significantly lower GLS, GCS, GAS, and GRS than the controls and the patients with T2DM alone (all <i>p</i> &lt; .01). Fasting plasma glucose (FPG), OSA and BMI had negative impacts on all and part of the strain values in T2DM patients. The T2DM patients with moderate-to-severe OSA showed significantly lower GLS, GCS, GAS, and GRS than those with mild OSA (all <i>p</i> &lt; .05). The 3DSTE plus conventional echocardiography could detect the sub-clinical LV alterations in T2DM patients with or without OSA.
DOI: 10.6084/m9.figshare.16610037.v1
title: Aggravating effect of obstructive sleep apnoea on left ventricular remodelling and function disorder in patients with type 2 diabetes mellitus: a case-control study by 3D speckle tracking echocardiography

description: The purpose of this study was to evaluate the early alterations of left ventricular (LV) structure and function in type 2 diabetes mellitus (T2DM) patients with or without obstructive sleep apnoea (OSA) using 3 D speckle tracking echocardiography (3DSTE). Eighty T2DM patients with preserved LVEF were included, half of whom had OSA as co-morbidity. Forty age- and sex-matched controls were also enrolled. LV structure and function were evaluated by conventional echocardiography and 3DSTE. LV global longitudinal strain (GLS), global circumferential strain (GCS), global area strain (GAS), and global radial strain (GRS) were all measured by 3DSTE. Four geometric patterns (normal geometry, concentric remodelling, concentric and eccentric hypertrophy) occupied significantly different proportions within the three groups (<i>p</i> = .014). LV remodelling made up higher shares in two T2DM groups than in the controls, whereas LV hypertrophy appeared most frequently in the patients with T2DM and OSA. The patients with T2DM alone had significantly lower GLS and GCS than the controls (both <i>p</i> &lt; .01). The patients with T2DM and OSA had significantly lower GLS, GCS, GAS, and GRS than the controls and the patients with T2DM alone (all <i>p</i> &lt; .01). Fasting plasma glucose (FPG), OSA and BMI had negative impacts on all and part of the strain values in T2DM patients. The T2DM patients with moderate-to-severe OSA showed significantly lower GLS, GCS, GAS, and GRS than those with mild OSA (all <i>p</i> &lt; .05). The 3DSTE plus conventional echocardiography could detect the sub-clinical LV alterations in T2DM patients with or without OSA.
DOI: 10.6084/m9.figshare.12940149.v1
title: Additional file 1 of A Cyclophilin OsCYP20–2 Interacts with OsSYF2 to Regulate Grain Length by Pre-mRNA Splicing

description: Additional file 1: Supplemental Table S1. Primers used in this study.
DOI: 10.6084/m9.figshare.12940527.v1
title: Additional file 1 of Genome-wide identification, phylogeny and expression analysis of the SPL gene family in wheat

description: Additional file 1: Table S1. Characteristic features of the SPL gene family identified in wheat. Table S2. Primers used for qRT-PCR. Table S3. Ka/Ks ratios and estimated divergence time for duplicated TaSPL gene pairs. Table S4. Ka/Ks ratios and estimated divergence time for orthologous TaSPL genes between wheat and rice. Table S5. Ka/Ks ratios and estimated divergence time for orthologous TaSPL genes between wheat and maize. Table S6. Ka/Ks ratios and estimated divergence time for orthologous TaSPL genes between wheat and A. tauschii. Table S7. Ka/Ks ratios and estimated divergence time for orthologous TaSPL genes between wheat and B. distachyon. Table S8. GO annotations of TaSPL proteins. Table S9. The protein-protein interaction between TaSPLs and other proteins in wheat. Table S10. Cis-elements contained in the TaSPL genes promoter region. Figure S1. Cis-regulatory elements in the promoter region of TaSPL genes.
DOI: 10.6084/m9.figshare.16608986
title: Additional file 2 of Integrated analysis of lncRNA and mRNA in liver of Megalobrama amblycephala post Aeromonas hydrophila infection

description: Additional file 2: Supplementary Table 2. Correlation of repeated samples.
DOI: 10.6084/m9.figshare.16610486.v2
title: Lychee seed polyphenol protects blood–retinal barrier by increasing tight joint proteins and inhibiting the activation of TLR4/MYD88/NF-κB-mediated NLRP3 inflammasome

description: Emerging evidence indicates that blood–retinal barrier (BRB) damage is the main cause of diabetic retinopathy (DR), and the downregulation of tight proteins (TJs) located between endothelial cells and the activation of NLRP3 inflammasome-mediated inflammation in Müller cells result in BRB injury. In this study, we aimed to study the protective effect of lychee seed polyphenol (LSP) on BRB integrity and the mechanism of action. By establishing a cellular model of BRB injury by using high glucose (HG)-induced hRECs or co-culture system of hRECs with MIO-M1 cells, we found that LSP significantly maintained the integrity of monolayer of hRECs as revealed by the decreased PD40 permeability and increased TJs, including ZO-1, Occludin, and Claudin 5. In addition, LSP inhibited the NLRP3 inflammasome activation and the levels of inflammatory cytokines via the TLR4/MYD88/NF-κB pathway. Collectively, this study provides valuable insight into the utilization of LSP in the treatment of DR.
DOI: 10.6084/m9.figshare.12940527
title: Additional file 1 of Genome-wide identification, phylogeny and expression analysis of the SPL gene family in wheat

description: Additional file 1: Table S1. Characteristic features of the SPL gene family identified in wheat. Table S2. Primers used for qRT-PCR. Table S3. Ka/Ks ratios and estimated divergence time for duplicated TaSPL gene pairs. Table S4. Ka/Ks ratios and estimated divergence time for orthologous TaSPL genes between wheat and rice. Table S5. Ka/Ks ratios and estimated divergence time for orthologous TaSPL genes between wheat and maize. Table S6. Ka/Ks ratios and estimated divergence time for orthologous TaSPL genes between wheat and A. tauschii. Table S7. Ka/Ks ratios and estimated divergence time for orthologous TaSPL genes between wheat and B. distachyon. Table S8. GO annotations of TaSPL proteins. Table S9. The protein-protein interaction between TaSPLs and other proteins in wheat. Table S10. Cis-elements contained in the TaSPL genes promoter region. Figure S1. Cis-regulatory elements in the promoter region of TaSPL genes.
DOI: 10.6084/m9.figshare.24998973.v1
title: Pharmacokinetics, metabolism, excretion and safety of iruplinalkib (WX-0593), a Novel ALK Inhibitor, in healthy subjects: a phase I human radiolabeled Mass balance study

description: Iruplinalkib is a novel anaplastic lymphoma kinase (ALK) inhibitor for the treatment of ALK-positive crizotinib-resistant NSCLC. A single oral dose of 120 mg/3.7 MBq [<sup>14</sup>C]iruplinalkib was administered to healthy subjects. Blood, urine and fecal samples were collected and analyzed for iruplinalkib and its metabolites. The safety of iruplinalkib was also assessed. Iruplinalkib was absorbed quickly and eliminated slowly from plasma, with a T<sub>max</sub> of 1.5 h and t<sub>1/2</sub> of 28.6 h. About 88.85% of iruplinalkib was excreted at 312 h, including 20.23% in urine and 68.63% in feces. Seventeen metabolites of iruplinalkib were identified, and M3b (demethylation), M7 (cysteine conjugation), M11 (oxidative dehydrogenation and cysteine conjugation of M3b) and M12 (oxidative dehydrogenation and cysteine conjugation) were considered the prominent metabolites in humans. Iruplinalkib-related compounds were found to be covalently bound to proteins, accounting for 7.70% in plasma and 17.96% in feces, which suggested chemically reactive metabolites were formed. There were no serious adverse events observed in the study. Iruplinalkib was widely metabolized and excreted mainly through feces in humans. Unchanged iruplinalkib, cysteine conjugates and covalent protein binding products were the main drug-related compounds in circulation. Iruplinalkib was well tolerated at the study dose. The trial is registered at ClinicalTrials.gov (Identifier: Anonymized).
DOI: 10.6084/m9.figshare.8222018
title: Additional file 4: of A family of auxin conjugate hydrolases from Solanum lycopersicum and analysis of their roles in flower pedicel abscission

description: The raw data of GC-MS IAA content. (XLSX 10 kb)
DOI: 10.6084/m9.figshare.17134637.v1
title: Hsa_circ_0001879 promotes the progression of atherosclerosis by regulating the proliferation and migration of oxidation of low density lipoprotein (ox-LDL)-induced vascular endothelial cells via the miR-6873-5p-HDAC9 axis

description: Atherosclerosis (AS) is a typical vascular disease. Emerging evidence has shown that circRNAs play key roles in the progression of AS, but the potential function and underlying mechanism of hsa_circ_0001879 remains unknown. We detected the expression level of hsa_circ_0001879 was determined by qRT-PCR, and the proliferation rate and migration ability of HUVECs were measured by CCK-8 assay and Transwell assay, respectively. Proliferative markers and epithelium mesenchymal transition (EMT) markers were measured through immunoblotting. A dual luciferase activity assay was performed to detect the interaction between circRNAs, miRNAs, and mRNAs. Hsa_circ_0001879 was upregulated in AS patients. Hsa_circ_0001879 inhibited the proliferation and migration ability of Human umbilical vein endothelial cells (HUVECs). Hsa_circ_0001879 directly bound to miR-6873-5p and acted as a sponge. miR-6873-5p-induced HDAC9 mRNA degradation was inhibited by hsa_circ_0001879. Hsa_circ_0001879 decreased the proliferation and migration of HUVECs by inhibiting miR-6873-5p-induced HDAC9 degradation.
DOI: 10.6084/m9.figshare.17134640
title: Effects of SPARCL1 on the proliferation and differentiation of sheep preadipocytes

description: Important candidate genes that regulate lipid metabolism have the potential to increase the content of intramuscular fat (IMF) and improve meat quality. <i>Secreted protein acidic and rich in cysteine like 1</i>(<i>SPARCL1</i>) is a secreted glycoprotein with important physiological functions and is involved in the proliferation and differentiation of various cells. However, the role of the <i>SPARCL1</i> gene in sheep preadipocytes and its regulatory mechanism is still unclear. In this study, we explored the effect of <i>SPARCL1</i> on the proliferation and differentiation of sheep preadipocytes. The results showed that the expression level of the <i>SPARCL1</i> gene is higher in fat tissue than in other tissues, and the gene was significantly increased on the 6<sup>th</sup> day of preadipocyte differentiation. In the preadipocyte proliferation stage, interference of <i>SPARCL1</i> gene reduced cell viability and increased cell apoptosis. In preadipocyte differentiation stage, <i>SPARCL1</i> overexpression significantly inhibited lipid droplets accumulation and triglyceride content by increasing <i>Wnt10b, Fzd8, IL6</i>, and <i>β-catenin</i> and inhibiting <i>PPARγ, C/EBPα, LPL</i>, and <i>IGF1</i> genes expression, whereas <i>SPARCL1</i> deficiency significantly promoted cell differentiation by inhibiting <i>β-catenin</i> and increasing <i>GSK3β, PPARγ, C/EBPα</i>, and <i>LPL</i>. The results of this study suggest that <i>SPARCL1</i> plays a negative role during preadipocyte differentiation and may become a novel target for regulating preadipocyte differentiation and improving IMF. <b>Abbreviations:</b><b>IMF</b>: Intramuscular fat <b><i>SPARCL1</i></b>: Secreted protein acidic and rich in cysteine like 1 <b><i>PPARγ</i></b>: Peroxisome proliferator-activated receptor γ <b><i>C/EBPα</i></b>: CCAAT/enhancer-binding protein-α <b><i>LPL</i></b>: Lipoprotein lipase <b><i>IGF1</i></b>: Insulin-like growth factor 1 <b><i>Wnt10b</i></b>: Wnt family member 10B <b><i>Fzd8</i></b>: Frizzled class receptor 8 <b>IL6</b>: Interleukin 6 <b><i>β-catenin</i></b>: Catenin beta interacting protein 1 <b><i>GSK3β</i></b>: Glycogen synthase kinase 3 beta <b><i>LRP5/6</i></b>: Low-density lipoprotein receptor-related protein 5/6
DOI: 10.6084/m9.figshare.8222018.v1
title: Additional file 4: of A family of auxin conjugate hydrolases from Solanum lycopersicum and analysis of their roles in flower pedicel abscission

description: The raw data of GC-MS IAA content. (XLSX 10 kb)
DOI: 10.6084/m9.figshare.20278988
title: Additional file 6 of Eimeria falciformis secretes extracellular vesicles to modulate proinflammatory response during interaction with mouse intestinal epithelial cells

description: Additional file 6: Mass spectrometry data set for identified proteins.
DOI: 10.6084/m9.figshare.17134640.v1
title: Effects of SPARCL1 on the proliferation and differentiation of sheep preadipocytes

description: Important candidate genes that regulate lipid metabolism have the potential to increase the content of intramuscular fat (IMF) and improve meat quality. <i>Secreted protein acidic and rich in cysteine like 1</i>(<i>SPARCL1</i>) is a secreted glycoprotein with important physiological functions and is involved in the proliferation and differentiation of various cells. However, the role of the <i>SPARCL1</i> gene in sheep preadipocytes and its regulatory mechanism is still unclear. In this study, we explored the effect of <i>SPARCL1</i> on the proliferation and differentiation of sheep preadipocytes. The results showed that the expression level of the <i>SPARCL1</i> gene is higher in fat tissue than in other tissues, and the gene was significantly increased on the 6<sup>th</sup> day of preadipocyte differentiation. In the preadipocyte proliferation stage, interference of <i>SPARCL1</i> gene reduced cell viability and increased cell apoptosis. In preadipocyte differentiation stage, <i>SPARCL1</i> overexpression significantly inhibited lipid droplets accumulation and triglyceride content by increasing <i>Wnt10b, Fzd8, IL6</i>, and <i>β-catenin</i> and inhibiting <i>PPARγ, C/EBPα, LPL</i>, and <i>IGF1</i> genes expression, whereas <i>SPARCL1</i> deficiency significantly promoted cell differentiation by inhibiting <i>β-catenin</i> and increasing <i>GSK3β, PPARγ, C/EBPα</i>, and <i>LPL</i>. The results of this study suggest that <i>SPARCL1</i> plays a negative role during preadipocyte differentiation and may become a novel target for regulating preadipocyte differentiation and improving IMF. <b>Abbreviations:</b><b>IMF</b>: Intramuscular fat <b><i>SPARCL1</i></b>: Secreted protein acidic and rich in cysteine like 1 <b><i>PPARγ</i></b>: Peroxisome proliferator-activated receptor γ <b><i>C/EBPα</i></b>: CCAAT/enhancer-binding protein-α <b><i>LPL</i></b>: Lipoprotein lipase <b><i>IGF1</i></b>: Insulin-like growth factor 1 <b><i>Wnt10b</i></b>: Wnt family member 10B <b><i>Fzd8</i></b>: Frizzled class receptor 8 <b>IL6</b>: Interleukin 6 <b><i>β-catenin</i></b>: Catenin beta interacting protein 1 <b><i>GSK3β</i></b>: Glycogen synthase kinase 3 beta <b><i>LRP5/6</i></b>: Low-density lipoprotein receptor-related protein 5/6