cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.25931715.v1
title: Early prediction of acute gallstone pancreatitis severity: a novel machine learning model based on CT features and open access online prediction platform

description: Early diagnosis of acute gallstone pancreatitis severity (GSP) is challenging in clinical practice. We aimed to investigate the efficacy of CT features and radiomics for the early prediction of acute GSP severity. We retrospectively recruited GSP patients who underwent CT imaging within 48 h of admission from tertiary referral centre. Radiomics and CT features were extracted from CT scans. The clinical and CT features were selected by the random forest algorithm to develop the ML GSP model for the identification of severity of GSP (mild or severe), and its predictive efficacy was compared with radiomics model. The predictive performance was assessed by the area under operating characteristic curve. Calibration curve and decision curve analysis were performed to demonstrate the classification performance and clinical efficacy. Furthermore, we built a web-based open access GSP severity calculator. The study was registered with ClinicalTrials.gov (NCT05498961). A total of 301 patients were enrolled. They were randomly assigned into the training (<i>n</i> = 210) and validation (<i>n</i> = 91) cohorts at a ratio of 7:3. The random forest algorithm identified the level of calcium ions, WBC count, urea level, combined cholecystitis, gallbladder wall thickening, gallstones, and hydrothorax as the seven predictive factors for severity of GSP. In the validation cohort, the areas under the curve for the radiomics model and ML GSP model were 0.841 (0.757–0.926) and 0.914 (0.851–0.978), respectively. The calibration plot shows that the ML GSP model has good consistency between the prediction probability and the observation probability. Decision curve analysis showed that the ML GSP model had high clinical utility. We built the ML GSP model based on clinical and CT image features and distributed it as a free web-based calculator. Our results indicated that the ML GSP model is useful for predicting the severity of GSP. ML GSP model based on machine learning has good severity discrimination in both training and validation cohorts (0.916 (0.872–0.958), 0.914 (0.851–0.978), respectively).We built an online user-friendly platform for the ML GSP model to help clinicians better identify the severity of GSP. ML GSP model based on machine learning has good severity discrimination in both training and validation cohorts (0.916 (0.872–0.958), 0.914 (0.851–0.978), respectively). We built an online user-friendly platform for the ML GSP model to help clinicians better identify the severity of GSP.
DOI: 10.6084/m9.figshare.27934044.v1
title: 123

description: Transparency materials will be uploaded if our paper passes the minor revision stage.
DOI: 10.6084/m9.figshare.27951795
title: FOXG1 interaction with SATB2 promotes autophagy to alleviate neuroinflammation and mechanical abnormal pain in rats with lumbar disc herniation

description: Most patients with lumbar disc herniation can be relieved or cured by surgical or non-surgical treatment; however, postoperative persistent radiculopathy is common. This study demonstrates the regulation of autophagy by the FOXG1/SATB2 axis in lumbar disc herniation (LDH). Rat dorsal root neurons were induced with TNF-α <i>in vitro</i>. Sprague Dawley (SD) rats were used to construct the LDH rat model, which was treated with <i>L. paracasei S16</i> or oe-FOXG1. Paw withdrawal threshold or latency assay (PWT/L) was performed. Peripheral blood samples were collected and analysed using ELISA and miRNAseq. RT-qPCR was used to analyse the expression of FOXG1, LC3B, Beclin1, p62, and SATB2. TUNEL staining and flow cytometry were used to analyse apoptosis. The expression of Cyclin D1, PCNA, Ki67, FOXG1, SATB2, and autophagy proteins was measured using western blotting. TNF-α induced low expression of FOXG1 and SATB2 in dorsal root ganglion (DRG) neurons of rats. TNF-α induced an increase in p62 protein and a decrease in LC3II/I and Beclin-1 proteins in neurons, which were blocked by oe-FOXG1. oe-FOXG1 suppressed inflammation and apoptosis in TNF-α-induced DRG neurons and LDH rats and promoted the expression of Cyclin D1, PCNA, and Ki67. Many miRNAs were increased in the peripheral blood of LDH rats, but decreased after <i>L. paracasei S16</i> intervention. <i>L. paracasei S16</i> affects miR-31a-5p and SATB2 expression. Dual luciferase reporter gene assay confirmed that miR-31a-5p bound to SATB2. Co-IP analysis confirmed the interaction between FOXG1 and SATB2. Silencing of SATB2 inhibited the beneficial effects of oe-FOXG1 in TNF-α-induced dorsal root ganglion neurons. Animal experiments further demonstrated that oe-FOXG1 improved LDH disease characteristics by downregulating PWT, PWL, inflammation, and apoptosis levels and upregulating SATB2-autophagy levels. MiR-31a-5p/SATB2 is involved in the treatment of <i>L. paracasei S16</i> in LDH rats. Overexpression of FOXG1 promotes autophagy through SATB2 to improve LDH levels This provides a new approach for the treatment of LDH.
DOI: 10.6084/m9.figshare.27889277.v1
title: Association between tumor markers elevation and poor functional outcomes after acute ischemic stroke: a longitudinal stroke center-based study

description: Previous studies revealed that the elevation of serum tumor markers (TMs) can serve as a prognostic indicator for diseases other than cancer, but little is known about its association with acute ischemic stroke (AIS). Based on a series of molecular markers and gene pathways shared in both stroke and cancer, we aimed to investigate whether the elevation of TMs could predict clinical outcomes after AIS. Patients diagnosed with AIS were enrolled and classified into the elevated TMs group and the non-elevated TMs group according to whether any TMs were elevated or not. Then they were followed up 6 months to assess clinical outcomes. Poor functional outcomes were defined as modified Rankin Scale (mRS) &gt; 2 points. 289 AIS patients were finally enrolled, of which 197 (68.2%) were classified as the elevated TMs group. Patients in the elevated TMs group were more likely (OR = 2.384; <i>p</i> =<b> </b>0.005) to have poor functional outcomes at follow-up than those in the non-elevated TMs group. However, no specific TM was significantly more elevated than the other TMs in the patients with poor functional outcome. The combination of TMs was more sensitive than individual TM in terms of prognosis prediction. Furthermore, rather than the number of elevated items, whether any TM was elevated or not was the most appropriate discriminator for functional outcomes after AIS. Elevation of TMs may indicate poor functional outcomes after AIS. Consequently, AIS patients with elevated TMs required close clinical monitoring and intensified treatment.
DOI: 10.6084/m9.figshare.27289595
title: Establishment and validation of the prognostic risk model based on the anoikis-related genes in esophageal squamous cell carcinoma

description: Esophageal squamous cell carcinoma (ESCC) is a malignant condition in humans. Anoikis-related genes (ARGs) are crucial to cancer progression. Therefore, more studies on the relationship between ARGs and ESCC are warranted. The study acquired ESCC-related transcriptome data from TCGA. Differentially expressed ARGs (DE-ARGs) were obtained by differential analysis and candidates were filtered out by survival analysis. Prognostic genes were determined by Cox and LASSO regression. A risk model was constructed based on prognostic gene expressions. An immune infiltration study was done to explain how these genes contribute to ESCC development. The IC50 test was adopted to assess the clinical response of chemotherapy drugs. Single cell analysis was performed on the GSE145370 dataset. Moreover, the prognostic gene expressions were detected by qRT-PCR. 53 DE-ARGs were screened and four candidate genes including PBK, LAMC2, TNFSF10 and KL were obtained. Cox and LASSO regression identified the two prognostic genes, TNFSF10 and PBK. Immuno-infiltration analysis revealed positive associations of PBK with Macrophages M0 cells, and TNFSF10 with Macrophages M1 cells. The IC50 values of predicted drugs, in the case of Tozasertib 1096 and WIKI4 1940, were significantly variant between risk groups. Single cell analysis revealed that TNFSF10 and PBK levels were higher in epithelial cells than in other cells. The prognostic genes expression results by qRT-PCR were compatible with the dataset analysis. The study established an ARG prognosis model of ESCC. It provided a reference for the research of ARGs in ESCC.
DOI: 10.6084/m9.figshare.27289595.v1
title: Establishment and validation of the prognostic risk model based on the anoikis-related genes in esophageal squamous cell carcinoma

description: Esophageal squamous cell carcinoma (ESCC) is a malignant condition in humans. Anoikis-related genes (ARGs) are crucial to cancer progression. Therefore, more studies on the relationship between ARGs and ESCC are warranted. The study acquired ESCC-related transcriptome data from TCGA. Differentially expressed ARGs (DE-ARGs) were obtained by differential analysis and candidates were filtered out by survival analysis. Prognostic genes were determined by Cox and LASSO regression. A risk model was constructed based on prognostic gene expressions. An immune infiltration study was done to explain how these genes contribute to ESCC development. The IC50 test was adopted to assess the clinical response of chemotherapy drugs. Single cell analysis was performed on the GSE145370 dataset. Moreover, the prognostic gene expressions were detected by qRT-PCR. 53 DE-ARGs were screened and four candidate genes including PBK, LAMC2, TNFSF10 and KL were obtained. Cox and LASSO regression identified the two prognostic genes, TNFSF10 and PBK. Immuno-infiltration analysis revealed positive associations of PBK with Macrophages M0 cells, and TNFSF10 with Macrophages M1 cells. The IC50 values of predicted drugs, in the case of Tozasertib 1096 and WIKI4 1940, were significantly variant between risk groups. Single cell analysis revealed that TNFSF10 and PBK levels were higher in epithelial cells than in other cells. The prognostic genes expression results by qRT-PCR were compatible with the dataset analysis. The study established an ARG prognosis model of ESCC. It provided a reference for the research of ARGs in ESCC.
DOI: 10.6084/m9.figshare.27889277
title: Association between tumor markers elevation and poor functional outcomes after acute ischemic stroke: a longitudinal stroke center-based study

description: Previous studies revealed that the elevation of serum tumor markers (TMs) can serve as a prognostic indicator for diseases other than cancer, but little is known about its association with acute ischemic stroke (AIS). Based on a series of molecular markers and gene pathways shared in both stroke and cancer, we aimed to investigate whether the elevation of TMs could predict clinical outcomes after AIS. Patients diagnosed with AIS were enrolled and classified into the elevated TMs group and the non-elevated TMs group according to whether any TMs were elevated or not. Then they were followed up 6 months to assess clinical outcomes. Poor functional outcomes were defined as modified Rankin Scale (mRS) &gt; 2 points. 289 AIS patients were finally enrolled, of which 197 (68.2%) were classified as the elevated TMs group. Patients in the elevated TMs group were more likely (OR = 2.384; <i>p</i> =<b> </b>0.005) to have poor functional outcomes at follow-up than those in the non-elevated TMs group. However, no specific TM was significantly more elevated than the other TMs in the patients with poor functional outcome. The combination of TMs was more sensitive than individual TM in terms of prognosis prediction. Furthermore, rather than the number of elevated items, whether any TM was elevated or not was the most appropriate discriminator for functional outcomes after AIS. Elevation of TMs may indicate poor functional outcomes after AIS. Consequently, AIS patients with elevated TMs required close clinical monitoring and intensified treatment.
DOI: 10.6084/m9.figshare.27826749.v1
title: A meta-analysis of the prognostic significance of CDKN deletions in acute lymphoblastic leukaemia

description: B-cell acute lymphoblastic leukaemia (B-ALL) and T-cell acute lymphoblastic leukaemia (T-ALL) are both types of acute lymphoblastic leukaemia (ALL), which is a cancer of the blood and bone marrow characterized by the rapid proliferation of immature lymphocytes. In ALL, CDKN gene deletions have been extensively studied regarding their prognostic significance. The purpose of this meta-analysis is to determine whether there is a consistent relationship between CDKN gene variations and the incidence of lymphocytic leukaemia. The following databases contain relevant studies published between inception and 25 October 2023: PubMed, EMBASE, the Cochrane library and Web of Science were comprehensively searched. Based on the random-effects or fixed-effects model, the hazard ratio (HR) and its 95% confidence interval (95% CI) were pooled. A subgroup analysis and sensitivity analysis were also conducted. We estimated publication bias using a funnel plot. This meta-analysis included 19 studies containing 1333 patients. Among included studies, 12 studies only reported B-ALL, four studies included patients with T-ALL and B-ALL, and three studies reported T-ALL. A deletion of the CDKN gene was found to be an adverse indicator of both EFS (HR = 1.83, 95% CI: 1.03–2.62), DFS (HR = 1.49, 95% CI 1.23–1.77), RFS (HR = 1.34, 95% CI 0.96–1.73) and OS (HR = 1.39, 95% CI 1.19–1.58). Single-arm emphasized the greater influence on OS. The subgroup analysis based on the CDKN2A, CDKN2A/b and different ALL subtypes further strengthen the validity of the findings. Our meta-analysis revealed that CDKN gene deletions (including CDKN 2A/B, CDKN 2A) serve as adverse prognostic indicators for T-ALL/B-ALL patients. Acute lymphoblastic leukaemia is a complex hematologic malignancy, requiring precise risk stratification to tailor treatment regimens for individual patients.Due to their prognostic significance in acute lymphoblastic leukaemia (ALL), CDKN gene deletions have been the subject of extensive research.Based on the results of this meta-analysis, CDKN gene deletions are potential adverse prognostic indicators for T-cell acute lymphoblastic leukaemia (T-ALL)/B-cell acute lymphoblastic leukaemia (B-ALL) patients. Acute lymphoblastic leukaemia is a complex hematologic malignancy, requiring precise risk stratification to tailor treatment regimens for individual patients. Due to their prognostic significance in acute lymphoblastic leukaemia (ALL), CDKN gene deletions have been the subject of extensive research. Based on the results of this meta-analysis, CDKN gene deletions are potential adverse prognostic indicators for T-cell acute lymphoblastic leukaemia (T-ALL)/B-cell acute lymphoblastic leukaemia (B-ALL) patients.
DOI: 10.6084/m9.figshare.27826749
title: A meta-analysis of the prognostic significance of CDKN deletions in acute lymphoblastic leukaemia

description: B-cell acute lymphoblastic leukaemia (B-ALL) and T-cell acute lymphoblastic leukaemia (T-ALL) are both types of acute lymphoblastic leukaemia (ALL), which is a cancer of the blood and bone marrow characterized by the rapid proliferation of immature lymphocytes. In ALL, CDKN gene deletions have been extensively studied regarding their prognostic significance. The purpose of this meta-analysis is to determine whether there is a consistent relationship between CDKN gene variations and the incidence of lymphocytic leukaemia. The following databases contain relevant studies published between inception and 25 October 2023: PubMed, EMBASE, the Cochrane library and Web of Science were comprehensively searched. Based on the random-effects or fixed-effects model, the hazard ratio (HR) and its 95% confidence interval (95% CI) were pooled. A subgroup analysis and sensitivity analysis were also conducted. We estimated publication bias using a funnel plot. This meta-analysis included 19 studies containing 1333 patients. Among included studies, 12 studies only reported B-ALL, four studies included patients with T-ALL and B-ALL, and three studies reported T-ALL. A deletion of the CDKN gene was found to be an adverse indicator of both EFS (HR = 1.83, 95% CI: 1.03–2.62), DFS (HR = 1.49, 95% CI 1.23–1.77), RFS (HR = 1.34, 95% CI 0.96–1.73) and OS (HR = 1.39, 95% CI 1.19–1.58). Single-arm emphasized the greater influence on OS. The subgroup analysis based on the CDKN2A, CDKN2A/b and different ALL subtypes further strengthen the validity of the findings. Our meta-analysis revealed that CDKN gene deletions (including CDKN 2A/B, CDKN 2A) serve as adverse prognostic indicators for T-ALL/B-ALL patients. Acute lymphoblastic leukaemia is a complex hematologic malignancy, requiring precise risk stratification to tailor treatment regimens for individual patients.Due to their prognostic significance in acute lymphoblastic leukaemia (ALL), CDKN gene deletions have been the subject of extensive research.Based on the results of this meta-analysis, CDKN gene deletions are potential adverse prognostic indicators for T-cell acute lymphoblastic leukaemia (T-ALL)/B-cell acute lymphoblastic leukaemia (B-ALL) patients. Acute lymphoblastic leukaemia is a complex hematologic malignancy, requiring precise risk stratification to tailor treatment regimens for individual patients. Due to their prognostic significance in acute lymphoblastic leukaemia (ALL), CDKN gene deletions have been the subject of extensive research. Based on the results of this meta-analysis, CDKN gene deletions are potential adverse prognostic indicators for T-cell acute lymphoblastic leukaemia (T-ALL)/B-cell acute lymphoblastic leukaemia (B-ALL) patients.
DOI: 10.6084/m9.figshare.25599604
title: Cohabiting with ulcerative colitis patients decreases differences of gut microbiome between healthy individuals and the patients

description: <b>Background:</b> Ulcerative colitis (UC), which is characterized by chronic relapsing inflammation of the colon, results from a complex interaction of factors involving the host, environment, and microbiome. The present study aimed to investigate the gut microbial composition and metabolic variations in patients with UC and their spouses. <b>Materials and Methods:</b> Fecal samples were collected from 13 healthy spouses and couples with UC. 16S rRNA gene amplicon sequencing and metagenomics sequencing were used to analyze gut microbiota composition, pathways, gene expression, and enzyme activity, followed by the Kyoto Encyclopedia of Genes and Genomes. <b>Results:</b> We found that the microbiome diversity of couples with UC decreased, especially that of UC patients. Bacterial composition, such as Firmicutes, was altered between UC patients and healthy controls, but was not significantly different between UC patients and their spouses. This has also been observed in pathways, such as metabolism, genetic information processing, organismal systems, and human diseases. However, the genes and enzymes of spouses with UC were not significantly different from those of healthy individuals. Furthermore, the presence of <i>Faecalibacterium</i> correlated with oxidative phosphorylation, starch and sucrose metabolism, amino sugar and nucleotide sugar metabolism, and the bacterial secretion system, showed a marked decline in the UC group compared with their spouses, but did not vary between healthy couples. <b>Conclusion</b>: Our study revealed that cohabitation with UC patients decreased differences in the gut microbiome between healthy individuals and patients. Not only was the composition and diversity of the microbiota diminished, but active pathways also showed some decline. Furthermore, Firmicutes, <i>Faecalibacterium,</i> and the four related pathways may be associated with the pathological state of the host rather than with human behavior.
DOI: 10.6084/m9.figshare.25599604.v1
title: Cohabiting with ulcerative colitis patients decreases differences of gut microbiome between healthy individuals and the patients

description: <b>Background:</b> Ulcerative colitis (UC), which is characterized by chronic relapsing inflammation of the colon, results from a complex interaction of factors involving the host, environment, and microbiome. The present study aimed to investigate the gut microbial composition and metabolic variations in patients with UC and their spouses. <b>Materials and Methods:</b> Fecal samples were collected from 13 healthy spouses and couples with UC. 16S rRNA gene amplicon sequencing and metagenomics sequencing were used to analyze gut microbiota composition, pathways, gene expression, and enzyme activity, followed by the Kyoto Encyclopedia of Genes and Genomes. <b>Results:</b> We found that the microbiome diversity of couples with UC decreased, especially that of UC patients. Bacterial composition, such as Firmicutes, was altered between UC patients and healthy controls, but was not significantly different between UC patients and their spouses. This has also been observed in pathways, such as metabolism, genetic information processing, organismal systems, and human diseases. However, the genes and enzymes of spouses with UC were not significantly different from those of healthy individuals. Furthermore, the presence of <i>Faecalibacterium</i> correlated with oxidative phosphorylation, starch and sucrose metabolism, amino sugar and nucleotide sugar metabolism, and the bacterial secretion system, showed a marked decline in the UC group compared with their spouses, but did not vary between healthy couples. <b>Conclusion</b>: Our study revealed that cohabitation with UC patients decreased differences in the gut microbiome between healthy individuals and patients. Not only was the composition and diversity of the microbiota diminished, but active pathways also showed some decline. Furthermore, Firmicutes, <i>Faecalibacterium,</i> and the four related pathways may be associated with the pathological state of the host rather than with human behavior.
DOI: 10.6084/m9.figshare.26893598
title: Assessment of <i>LINC-PINT</i> genetic polymorphisms and esophageal squamous cell carcinoma risk in the Hainan Han population

description: Esophageal squamous cell carcinoma (ESCC) is a malignant tumor with high incidence and mortality rates worldwide. This study aimed to investigate the correlation between <i>LINC-PINT</i> polymorphisms and ESCC risk in the Hainan Han population. A total of 391 patients with ESCC and 452 healthy controls were enrolled to evaluate the effect of <i>LINC-PINT</i> SNPs (single nucleotide polymorphisms) on ESCC susceptibility. Associations were evaluated by calculating odds ratios (OR) and 95% confidence intervals (CIs). Multifactor dimensionality reduction analysis was performed to explore the association between SNP-SNP interactions and ESCC susceptibility. We further determined the correlation between clinical indicators and SNP in patients with ESCC. Our study showed that rs157916 (OR 0.63, <i>p</i> = 0.011) and rs157928 (OR 0.80, <i>p</i> = 0.021) were associated with a decreased risk of ESCC. Stratified analysis indicated that rs157916 could decrease the risk of ESCC in people aged &gt;64 years, in males, and non-drinkers (OR 0.58, <i>p</i> = 0.042; OR 0.58, <i>p</i> = 0.010; OR 0.62, <i>p</i> = 0.025, respectively). Rs16873842 was related to a decreased risk of ESCC in males (OR 0.70, <i>p</i> = 0.015). Rs7801029 was associated with ESCC risk in females (OR 0.39, <i>p</i> = 0.033) and non-drinkers (OR 0.68, <i>p</i> = 0.040). Rs7781295 decreased the ESCC risk in smokers (OR 0.58, <i>p</i> = 0.046) and drinkers (OR 0.58, <i>p</i> = 0.046). In addition, rs157928 played a protective role in ESCC risk in females (OR 0.39, <i>p</i> = 0.033) and non-smokers (OR 0.32, <i>p</i> = 0.006). Additionally, the best predictive model for ESCC was a combination of rs157916, rs16873842, rs7801029, rs7781295, rs28662387, and rs157928. Our study revealed that <i>LINC-PINT</i> polymorphisms were associated with ESCC risk.