cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.9958850
title: Poly-l-lactic acid scaffold incorporated chitosan-coated mesoporous silica nanoparticles as pH-sensitive composite for enhanced osteogenic differentiation of human adipose tissue stem cells by dexamethasone delivery

description: Nowadays, the development of drug-loaded electrospun organic-inorganic composite scaffolds for tissue engineering application is an attractive approach. In this study, a composite scaffold of Poly-l-lactic acid (PLLA) incorporated dexamethasone (Dexa) loaded Mesoporous Silica Nanoparticles (MSN) coated with Chitosan (CS) were fabricated by electrospinning for bone tissue engineering application. The MSN was prepared by precipitation method. After that, Dexamethasone (Dexa) was loaded into MSNs (MSN-Dexa). In the following, CS was coated over the prepared nanoparticles to form MSN-Dexa@CS and then, were mixed to PLLA solution to form MSN-Dexa@CS/PLLA composite for electrospinning. The surface morphology, hydrophilicity, tensile strength and the bioactivity of the scaffolds were characterized. The osteogenic proliferation and differentiation potential were evaluated by MTT assay and by measuring the basic osteogenic markers: the activity of the enzyme alkaline phosphatase and the level of calcium deposition. The composite scaffolds prepared here have conductive surface property and have a better osteogenic potential than pure PLLA scaffolds. Hence, the controlled release of nanoparticle containing Dexa from composite scaffold supported the osteogenesis and made the composite scaffolds ideal candidates for bone tissue engineering application and pH-sensitive delivery of drugs at the site of implantation in tissue regeneration.
DOI: 10.6084/m9.figshare.9958850.v1
title: Poly-l-lactic acid scaffold incorporated chitosan-coated mesoporous silica nanoparticles as pH-sensitive composite for enhanced osteogenic differentiation of human adipose tissue stem cells by dexamethasone delivery

description: Nowadays, the development of drug-loaded electrospun organic-inorganic composite scaffolds for tissue engineering application is an attractive approach. In this study, a composite scaffold of Poly-l-lactic acid (PLLA) incorporated dexamethasone (Dexa) loaded Mesoporous Silica Nanoparticles (MSN) coated with Chitosan (CS) were fabricated by electrospinning for bone tissue engineering application. The MSN was prepared by precipitation method. After that, Dexamethasone (Dexa) was loaded into MSNs (MSN-Dexa). In the following, CS was coated over the prepared nanoparticles to form MSN-Dexa@CS and then, were mixed to PLLA solution to form MSN-Dexa@CS/PLLA composite for electrospinning. The surface morphology, hydrophilicity, tensile strength and the bioactivity of the scaffolds were characterized. The osteogenic proliferation and differentiation potential were evaluated by MTT assay and by measuring the basic osteogenic markers: the activity of the enzyme alkaline phosphatase and the level of calcium deposition. The composite scaffolds prepared here have conductive surface property and have a better osteogenic potential than pure PLLA scaffolds. Hence, the controlled release of nanoparticle containing Dexa from composite scaffold supported the osteogenesis and made the composite scaffolds ideal candidates for bone tissue engineering application and pH-sensitive delivery of drugs at the site of implantation in tissue regeneration.
DOI: 10.13018/bmr28116
title: Sequence-specific Backbone Resonance Assignments of Human PrP(23-144) at pH 7.0
DOI: 10.13018/bmr28117
title: Heterogeneous ribonucleoprotein A18 RNA Recognition Motif
DOI: 10.6084/m9.figshare.9655397
title: Integrated metabolomics and 16S rRNA sequencing to investigate the regulation of Chinese yam on antibiotic-induced intestinal dysbiosis in rats

description: Antibiotics have saved hundreds of millions of patient’s lives, but there are also many side effects. This paper mainly studies the regulation of Chinese yam on antibiotic-induced gut dysbiosis in rats. Male Wistar rats were divided into three groups, normal control group, antibiotic group, and Chinese yam group. In the antibiotic group and the yam group, a rat model of intestinal dysfunction was established by intragastric administration of imipenem/cilastatin sodium (antibiotic) for 21 days. The yam group was also given yam decoction for intervention. The fecal samples of each group of rats were analyzed using an ultra-performance liquid chromatography quadrupole/time-of-flight mass spectrometry (UPLC-Q-TOF/MS) method to find potential biomarkers. The DNA in the feces was extracted, and analyzed using 16S rDNA method to find the differential flora. Spearman correlation analysis was performed on differential flora and differential metabolites to determine the main metabolic pathways of the host after intestinal flora dysregulation. The administration of antibiotics can lead to disorders of intestinal flora, decreased microbial diversity, and changes in host metabolic phenotype. Chinese yam can significantly improve the intestinal flora, making the host's metabolic phenotype tend toward normal. Long-term use of Imipenem/cilastatin sodium can cause disturbance of intestinal flora in normal rats. Chinese yam may regulate intestinal flora disorder and have potential prebiotic effects.
DOI: 10.6084/m9.figshare.9655397.v1
title: Integrated metabolomics and 16S rRNA sequencing to investigate the regulation of Chinese yam on antibiotic-induced intestinal dysbiosis in rats

description: Antibiotics have saved hundreds of millions of patient’s lives, but there are also many side effects. This paper mainly studies the regulation of Chinese yam on antibiotic-induced gut dysbiosis in rats. Male Wistar rats were divided into three groups, normal control group, antibiotic group, and Chinese yam group. In the antibiotic group and the yam group, a rat model of intestinal dysfunction was established by intragastric administration of imipenem/cilastatin sodium (antibiotic) for 21 days. The yam group was also given yam decoction for intervention. The fecal samples of each group of rats were analyzed using an ultra-performance liquid chromatography quadrupole/time-of-flight mass spectrometry (UPLC-Q-TOF/MS) method to find potential biomarkers. The DNA in the feces was extracted, and analyzed using 16S rDNA method to find the differential flora. Spearman correlation analysis was performed on differential flora and differential metabolites to determine the main metabolic pathways of the host after intestinal flora dysregulation. The administration of antibiotics can lead to disorders of intestinal flora, decreased microbial diversity, and changes in host metabolic phenotype. Chinese yam can significantly improve the intestinal flora, making the host's metabolic phenotype tend toward normal. Long-term use of Imipenem/cilastatin sodium can cause disturbance of intestinal flora in normal rats. Chinese yam may regulate intestinal flora disorder and have potential prebiotic effects.
DOI: 10.13018/bmr28118
title: 1H, 13C, 15N backbone and side-chain resonance assignment of Nostoc sp. C139A variant of the heme nitric oxide/oxygen binding (H-NOX) domain in complex with cinaciguat
DOI: 10.6084/m9.figshare.9916712
title: An integrated analysis of the circRNA–miRNA–mRNA network reveals novel insights into potential mechanisms of cell proliferation during liver regeneration

description: Cell proliferation constitutes the fundamental process and driving force behind regrowth during liver regeneration (LR). However, it remains unclear how competing endogenous RNA (ceRNA) networks affect hepatocyte proliferation and liver regeneration. Therefore, this study was designed to explore an LR-specific ceRNA network, which regulates cell proliferation. Based on the microarray data of mRNAs, and high-throughput sequencing data of miRNAs and circRNAs from regenerating livers, this study initially applied known 1484 LR associated mRNAs to perform GO analysis, and then selected 169 LR associated mRNAs involved in cell proliferation and the cell cycle. Subsequently, 188 interactive miRNA–mRNA pairs and 5206 circRNA–miRNA pairs, respectively, were predicted using bioinformatics methods. Next, in view of the differential expressions of these ceRNAs during LR, 26 miRNA–mRNA pairs and 71 circRNA–miRNA pairs were applied to generate a circRNA–miRNA–mRNA regulatory network, and only 14 triple interactive groups were obtained based on the predicted inverse interactions among ceRNAs. Finally, circ_19698/miR-423-5p axis was demonstrated to promote cell proliferation by modulating the expression of MYC, CCNA2, and CCND1 in rat BRL-3A cells. This study suggests a potential regulatory mechanism of cell proliferation in regenerating livers, as well as a novel pathway for modulating ceRNA networks to promote liver regeneration.
DOI: 10.6084/m9.figshare.9916712.v1
title: An integrated analysis of the circRNA–miRNA–mRNA network reveals novel insights into potential mechanisms of cell proliferation during liver regeneration

description: Cell proliferation constitutes the fundamental process and driving force behind regrowth during liver regeneration (LR). However, it remains unclear how competing endogenous RNA (ceRNA) networks affect hepatocyte proliferation and liver regeneration. Therefore, this study was designed to explore an LR-specific ceRNA network, which regulates cell proliferation. Based on the microarray data of mRNAs, and high-throughput sequencing data of miRNAs and circRNAs from regenerating livers, this study initially applied known 1484 LR associated mRNAs to perform GO analysis, and then selected 169 LR associated mRNAs involved in cell proliferation and the cell cycle. Subsequently, 188 interactive miRNA–mRNA pairs and 5206 circRNA–miRNA pairs, respectively, were predicted using bioinformatics methods. Next, in view of the differential expressions of these ceRNAs during LR, 26 miRNA–mRNA pairs and 71 circRNA–miRNA pairs were applied to generate a circRNA–miRNA–mRNA regulatory network, and only 14 triple interactive groups were obtained based on the predicted inverse interactions among ceRNAs. Finally, circ_19698/miR-423-5p axis was demonstrated to promote cell proliferation by modulating the expression of MYC, CCNA2, and CCND1 in rat BRL-3A cells. This study suggests a potential regulatory mechanism of cell proliferation in regenerating livers, as well as a novel pathway for modulating ceRNA networks to promote liver regeneration.
DOI: 10.13018/bmr28121
title: Assignment of first 249 residues of yeast eIF4G1
DOI: 10.6084/m9.figshare.8984126
title: The prognostic roles of cyclooxygenase-2 for patients with basal cell carcinoma

description: <i>Cyclooxygenase-2</i> (<i>Cox-2</i>) is critical for tumor invasion, angiogenesis, and poor prognosis in many human cancers. It was reported to be an abnormal expression in many human malignancies, including basal cell carcinoma (BCC). However, the prognostic significance of <i>cox-2</i> in BCC was still unclear. The aim of this study was to investigate the prognostic roles of <i>cox-2</i> for patients with BCC. We detected the expression of <i>cox-2</i> both at mRNA and protein level in tumor tissue and adjacent normal tissues from 180 patients with BCC by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot analysis, respectively. <i>Cox-2</i> expression was significantly increased in BCC tissues compared with the adjacent normal cohorts (<i>p</i> &lt; .001). Its expression was significantly associated with angiogenesis (<i>p</i> &lt; .001) and depth of invasion (<i>p</i> &lt; .001). Kaplan–Meier analysis suggested patients with high expression of <i>cox-2</i> had a shorter overall survival rate than those with low expression (log rank test, <i>p</i> &lt; .001). The expression of <i>cox-2</i> was up-regulated in BCC and it could be used as a bio-marker for the prognosis of BCC patients with a high risk of recurrence.
DOI: 10.6084/m9.figshare.9580493
title: Circular RNA ZFR accelerates non-small cell lung cancer progression by acting as a miR-101-3p sponge to enhance CUL4B expression

description: Non-small-cell lung carcinoma (NSCLC) is the most common type of lung cancer. Circular RNA ZFR (circZFR) is an identified circular RNA (circRNA) that is correlated with cancer progression. However, the role of circZFR in NSCLC remains unknown. In the present study, we aimed to investigate the function of circZFR in NSCLC and the underlying mechanism. The expression patterns of circZFR were determined using qRT-PCR in NSCLC samples and cell lines. The subcellular distribution of circZFR in NSCLC cells was analyzed by fluorescence <i>in situ</i> hybridization (FISH). Cell proliferation was examined utilizing the CCK-8 assay. Cell migration and invasion were evaluated using the Transwell assay. We used the bioinformatics software TargetScan and miRanda to predict circRNA–miRNA and miRNA–mRNA interactions. Our results showed that circZFR expressions were significantly upregulated in NSCLC tissues and cell lines. Knockdown of circZFR significantly inhibited the cell proliferation, migration and invasion of NSCLC cells <i>in vitro</i>. Furthermore, we demonstrated that circZFR acted as a sponge to absorb microRNA-101-3p (miR-101-3p) and promoted cullin 4B (CUL4B) expression. Collectively, our results demonstrated that circZFR exhibited a carcinogenic role by sponging miR-101-3p and regulating CUL4B expression in NSCLC. These findings provided evidence for understanding the role of circZFR in NSCLC tumourigenesis.
DOI: 10.6084/m9.figshare.9580493.v1
title: Circular RNA ZFR accelerates non-small cell lung cancer progression by acting as a miR-101-3p sponge to enhance CUL4B expression

description: Non-small-cell lung carcinoma (NSCLC) is the most common type of lung cancer. Circular RNA ZFR (circZFR) is an identified circular RNA (circRNA) that is correlated with cancer progression. However, the role of circZFR in NSCLC remains unknown. In the present study, we aimed to investigate the function of circZFR in NSCLC and the underlying mechanism. The expression patterns of circZFR were determined using qRT-PCR in NSCLC samples and cell lines. The subcellular distribution of circZFR in NSCLC cells was analyzed by fluorescence <i>in situ</i> hybridization (FISH). Cell proliferation was examined utilizing the CCK-8 assay. Cell migration and invasion were evaluated using the Transwell assay. We used the bioinformatics software TargetScan and miRanda to predict circRNA–miRNA and miRNA–mRNA interactions. Our results showed that circZFR expressions were significantly upregulated in NSCLC tissues and cell lines. Knockdown of circZFR significantly inhibited the cell proliferation, migration and invasion of NSCLC cells <i>in vitro</i>. Furthermore, we demonstrated that circZFR acted as a sponge to absorb microRNA-101-3p (miR-101-3p) and promoted cullin 4B (CUL4B) expression. Collectively, our results demonstrated that circZFR exhibited a carcinogenic role by sponging miR-101-3p and regulating CUL4B expression in NSCLC. These findings provided evidence for understanding the role of circZFR in NSCLC tumourigenesis.
DOI: 10.13018/bmr28122
title: 1H-13C-15N solid-state NMR assignment of a second conformation of HBV capsid
DOI: 10.6084/m9.figshare.8088503
title: Long non-coding RNA NEAT1 promotes steatosis via enhancement of estrogen receptor alpha-mediated AQP7 expression in HepG2 cells

description: Hepatic steatosis is one of the most important features of the pathogenesis for non-alcoholic fatty liver disease. Fat deposition in liver cells can influence hepatic lipogenesis along with other metabolic pathways and further lead to the irreversible liver cirrhosis and injury. However, the underlying mechanism of steatosis remains largely unexplored. Our previous study revealed that AQP7 played an important role in liver steatosis. In this study, we determined that the transcriptional level of AQP7 was up-regulated by estrogen receptor alpha (ERα) upon 17β-estradiol (E2) and oleic acids treated HepG2 cells. Furthermore, we identified long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) as a potential hallmark which was down-regulated in ERα silencing HepG2 cells by RNA-Seq. Finally, we validated that the 3’ terminal nucleotides of NEAT1 were contributed for the interaction with ERα to facilitate AQP7 transcription to suppress liver steatosis. Overall, our study gave evidence that NEAT1 played an important role in the activation of ERα to regulate AQP7-mediated hepatic steatosis.
DOI: 10.6084/m9.figshare.8088503.v1
title: Long non-coding RNA NEAT1 promotes steatosis via enhancement of estrogen receptor alpha-mediated AQP7 expression in HepG2 cells

description: Hepatic steatosis is one of the most important features of the pathogenesis for non-alcoholic fatty liver disease. Fat deposition in liver cells can influence hepatic lipogenesis along with other metabolic pathways and further lead to the irreversible liver cirrhosis and injury. However, the underlying mechanism of steatosis remains largely unexplored. Our previous study revealed that AQP7 played an important role in liver steatosis. In this study, we determined that the transcriptional level of AQP7 was up-regulated by estrogen receptor alpha (ERα) upon 17β-estradiol (E2) and oleic acids treated HepG2 cells. Furthermore, we identified long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) as a potential hallmark which was down-regulated in ERα silencing HepG2 cells by RNA-Seq. Finally, we validated that the 3’ terminal nucleotides of NEAT1 were contributed for the interaction with ERα to facilitate AQP7 transcription to suppress liver steatosis. Overall, our study gave evidence that NEAT1 played an important role in the activation of ERα to regulate AQP7-mediated hepatic steatosis.
DOI: 10.6084/m9.figshare.8984126.v1
title: The prognostic roles of cyclooxygenase-2 for patients with basal cell carcinoma

description: <i>Cyclooxygenase-2</i> (<i>Cox-2</i>) is critical for tumor invasion, angiogenesis, and poor prognosis in many human cancers. It was reported to be an abnormal expression in many human malignancies, including basal cell carcinoma (BCC). However, the prognostic significance of <i>cox-2</i> in BCC was still unclear. The aim of this study was to investigate the prognostic roles of <i>cox-2</i> for patients with BCC. We detected the expression of <i>cox-2</i> both at mRNA and protein level in tumor tissue and adjacent normal tissues from 180 patients with BCC by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot analysis, respectively. <i>Cox-2</i> expression was significantly increased in BCC tissues compared with the adjacent normal cohorts (<i>p</i> &lt; .001). Its expression was significantly associated with angiogenesis (<i>p</i> &lt; .001) and depth of invasion (<i>p</i> &lt; .001). Kaplan–Meier analysis suggested patients with high expression of <i>cox-2</i> had a shorter overall survival rate than those with low expression (log rank test, <i>p</i> &lt; .001). The expression of <i>cox-2</i> was up-regulated in BCC and it could be used as a bio-marker for the prognosis of BCC patients with a high risk of recurrence.
DOI: 10.6084/m9.figshare.9119924
title: Alkannin restrains oral squamous carcinoma cell growth, migration and invasion by regulating microRNA-9/RECK axis

description: Alkannin (ALK) has anti-inflammatory and anti-tumour activities. We tried to probe the underlying functions of ALK in oral squamous carcinoma (OSCC) cells growth, migration and invasion. OSCC cells viability was investigated after treatment with ALK. Then, BrdU, flow cytometry, Western blot and Transwell assays were executed to appraise proliferation, apoptosis, migration and invasion in OSCC cells with ALK stimulation. The biological functions of miR-9 were explored after miR-9 mimic/inhibitor transfection. The relevance of RECK and miR-9 was predicated by dual luciferase activity assay. JAK1/STAT3 and PI3K/AKT pathways were estimated by Western blot. Tumour formation <i>in vivo</i> was executed by xenograft tumours assay. We found that ALK restrained cell proliferation, facilitated apoptosis, repressed migration and invasion also interdicted JAK1/STAT3 and PI3K/AKT pathways in CAL-27 and SCC-9 cells. miR-9 expression was upgraded in OSCC tissues but decreased in OSCC cells along with ALK administration; meanwhile, overexpressed miR-9 inverted the influences of ALK in OSCC cells growth, migration and invasion. RECK was predicated as a novel target gene of miR-9, and overexpressed RECK hindered JAK1/STAT3 and PI3K/AKT pathways in OSCC cells. ALK prohibited tumour formation <i>in vivo</i>. In conclusion, ALK restrained OSCC cells growth, migration and invasion via adjusting miR-9/RECK axis.HighlightsALK restrains cell growth, migration and invasion in OSCC cells;miR-9 is enhanced in OSCC tissues but is repressed by ALK in OSCC cells;miR-9 inverts the repressive effect of ALK on CAL-27 and SCC-9 cells;RECK is a novel target of miR-9;ALK or RECK hinders JAK1/STAT3 and PI3K/AKT pathways in CAL-27 and SCC-9 cells;ALK prohibits tumour formation <i>in vivo</i>. ALK restrains cell growth, migration and invasion in OSCC cells; miR-9 is enhanced in OSCC tissues but is repressed by ALK in OSCC cells; miR-9 inverts the repressive effect of ALK on CAL-27 and SCC-9 cells; RECK is a novel target of miR-9; ALK or RECK hinders JAK1/STAT3 and PI3K/AKT pathways in CAL-27 and SCC-9 cells; ALK prohibits tumour formation <i>in vivo</i>.
DOI: 10.6084/m9.figshare.9119924.v1
title: Alkannin restrains oral squamous carcinoma cell growth, migration and invasion by regulating microRNA-9/RECK axis

description: Alkannin (ALK) has anti-inflammatory and anti-tumour activities. We tried to probe the underlying functions of ALK in oral squamous carcinoma (OSCC) cells growth, migration and invasion. OSCC cells viability was investigated after treatment with ALK. Then, BrdU, flow cytometry, Western blot and Transwell assays were executed to appraise proliferation, apoptosis, migration and invasion in OSCC cells with ALK stimulation. The biological functions of miR-9 were explored after miR-9 mimic/inhibitor transfection. The relevance of RECK and miR-9 was predicated by dual luciferase activity assay. JAK1/STAT3 and PI3K/AKT pathways were estimated by Western blot. Tumour formation <i>in vivo</i> was executed by xenograft tumours assay. We found that ALK restrained cell proliferation, facilitated apoptosis, repressed migration and invasion also interdicted JAK1/STAT3 and PI3K/AKT pathways in CAL-27 and SCC-9 cells. miR-9 expression was upgraded in OSCC tissues but decreased in OSCC cells along with ALK administration; meanwhile, overexpressed miR-9 inverted the influences of ALK in OSCC cells growth, migration and invasion. RECK was predicated as a novel target gene of miR-9, and overexpressed RECK hindered JAK1/STAT3 and PI3K/AKT pathways in OSCC cells. ALK prohibited tumour formation <i>in vivo</i>. In conclusion, ALK restrained OSCC cells growth, migration and invasion via adjusting miR-9/RECK axis.HighlightsALK restrains cell growth, migration and invasion in OSCC cells;miR-9 is enhanced in OSCC tissues but is repressed by ALK in OSCC cells;miR-9 inverts the repressive effect of ALK on CAL-27 and SCC-9 cells;RECK is a novel target of miR-9;ALK or RECK hinders JAK1/STAT3 and PI3K/AKT pathways in CAL-27 and SCC-9 cells;ALK prohibits tumour formation <i>in vivo</i>. ALK restrains cell growth, migration and invasion in OSCC cells; miR-9 is enhanced in OSCC tissues but is repressed by ALK in OSCC cells; miR-9 inverts the repressive effect of ALK on CAL-27 and SCC-9 cells; RECK is a novel target of miR-9; ALK or RECK hinders JAK1/STAT3 and PI3K/AKT pathways in CAL-27 and SCC-9 cells; ALK prohibits tumour formation <i>in vivo</i>.
DOI: 10.13018/bmr28123
title: Methionine sulfoxide-containing peptide for random coil chemical shifts at pH 2.3 and 7.4 (with Gly as succeeding residue)