cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.30231168.v1
title: Prevalence of fibromyalgia in asthma and its impact on asthma control: a case-control study

description: Asthma and fibromyalgia are chronic conditions that significantly impair quality of life and share common inflammatory and neurophysiological mechanisms. This study aimed to investigate the prevalence of fibromyalgia in asthma patients and examine its impact on asthma control. In this case-control study, 120 patients diagnosed with asthma and 120 age- and sex-matched healthy controls were enrolled. Fibromyalgia was diagnosed based on the 2016 revised ACR criteria using the Widespread Pain Index (WPI) and Symptom Severity Scale (SSS). Asthma control was assessed using the Asthma Control Test (ACT). The relationship between fibromyalgia and asthma control was analyzed using independent t-tests, chi-square tests, logistic regression, and ROC analysis. The prevalence of fibromyalgia in the asthma group was 16.7% compared to 3.3% in controls (<i>p</i> &lt; 0.001). Asthma patients with fibromyalgia had significantly lower ACT scores than those without (18.2 ± 2.9 vs. 20.1 ± 2.4; <i>p</i> = 0.004). The proportion of patients with uncontrolled asthma was higher among those with fibromyalgia (60% vs. 35%). Logistic regression showed that fibromyalgia was associated with increased odds of uncontrolled asthma (OR = 2.16), although this was not statistically significant (<i>p</i> = 0.103). ACT scores showed no significant correlation with WPI or SSS. ROC analysis revealed that the ACT score had no discriminatory power in identifying fibromyalgia (AUC = 0.50). Fibromyalgia is a common comorbidity in asthma patients and may adversely affect perceived asthma control. However, the ACT score alone may not be a reliable indicator of fibromyalgia presence, suggesting the need for multidimensional assessment tools in routine asthma care.
DOI: 10.6084/m9.figshare.28681501
title: Clinical outcomes and therapeutic modalities in older Chinese patients with MCL: a multi-center real-world retrospective study

description: Mantle cell lymphoma (MCL), an uncommon lymphoma subtype, is clinically characterized by its heterogenous behavior. Established prediction system including several clinical and biological parameters can help in determining the aggressiveness of MCL in younger patients. However, there are limited parameters on predicting the clinical outcome of older patients. The present study was performed to identify the prognostic factors and optimal treatment modalities in older Chinese MCL patients. Patients (age ≥ 65 yrs) with MCL from 19 comprehensive hospitals in China were included. Clinical characteristics, therapeutic strategies, progression-free survival (PFS) and overall survival (OS) time of these patients were collected. Totally, 259 eligible patients were enrolled. The median age of patients was 69 years (range, 65–88). The median of PFS and OS were 29 months (95%CI: 26–37) and 76 months (95%CI: 61–96) months, respectively. Multivariate regression analysis determined that ECOG score ≥ 2, high MIPI score and absence of maintenance treatment were independently associated with poorer PFS of MCL patients; while ECOG score ≥ 2 and absence of maintenance treatment were independently correlated with a poorer OS. Patients with MCL who received BTKi-containing regimens or maintenance therapy showed significantly longer PFS and OS than those who did not receive these therapies. Maintenance treatment can improve the survival rate of older patients with MCL regardless of TP53 status. ECOG ≥ 2, high MIPI score, and absence of maintenance therapy were associated with poorer survival outcomes for older Chinese MCL patients. Maintenance therapy and BTKi-containing regimens have been shown to increase the survival rate of older Chinese MCL patients.
DOI: 10.6084/m9.figshare.28681501.v1
title: Clinical outcomes and therapeutic modalities in older Chinese patients with MCL: a multi-center real-world retrospective study

description: Mantle cell lymphoma (MCL), an uncommon lymphoma subtype, is clinically characterized by its heterogenous behavior. Established prediction system including several clinical and biological parameters can help in determining the aggressiveness of MCL in younger patients. However, there are limited parameters on predicting the clinical outcome of older patients. The present study was performed to identify the prognostic factors and optimal treatment modalities in older Chinese MCL patients. Patients (age ≥ 65 yrs) with MCL from 19 comprehensive hospitals in China were included. Clinical characteristics, therapeutic strategies, progression-free survival (PFS) and overall survival (OS) time of these patients were collected. Totally, 259 eligible patients were enrolled. The median age of patients was 69 years (range, 65–88). The median of PFS and OS were 29 months (95%CI: 26–37) and 76 months (95%CI: 61–96) months, respectively. Multivariate regression analysis determined that ECOG score ≥ 2, high MIPI score and absence of maintenance treatment were independently associated with poorer PFS of MCL patients; while ECOG score ≥ 2 and absence of maintenance treatment were independently correlated with a poorer OS. Patients with MCL who received BTKi-containing regimens or maintenance therapy showed significantly longer PFS and OS than those who did not receive these therapies. Maintenance treatment can improve the survival rate of older patients with MCL regardless of TP53 status. ECOG ≥ 2, high MIPI score, and absence of maintenance therapy were associated with poorer survival outcomes for older Chinese MCL patients. Maintenance therapy and BTKi-containing regimens have been shown to increase the survival rate of older Chinese MCL patients.
DOI: 10.6084/m9.figshare.30819512
title: Predictive value of motor-evoked potentials for upper limb functional outcomes in acute ischemic stroke

description: Stroke remains a leading cause of acquired physical disability globally, with upper limb motor impairment significantly affecting independence and quality of life. Currently, objective neurophysiological biomarkers are not routinely incorporated into stroke care. This study aimed to investigate the predictive value of MEPs for upper limb outcomes in acute ischemic stroke. This prospective cohort study included 133 adults experiencing their first acute ischemic stroke. Within 10 days of onset, participants underwent Motor-evoked potential (MEP) testing via transcranial magnetic stimulation (TMS) and were categorized as MEP+ (with preserved responses) or MEP– (with absent responses). Outcome measures included the Fugl-Meyer Assessment (FMA), Barthel Index, and modified Rankin Scale (mRS), assessed at baseline and 90 days. Logistic regression models adjusted for age and baseline stroke severity were used to determine the independent predictive value of MEP status. Among 133 patients (mean age 63.6 ± 12.2 years; 57.9% male), those with preserved MEPs (57.1%) demonstrated significantly better motor and functional outcomes at 90 days. MEP+ patients had higher FMA scores (61.0 ± 9.5 vs. 33.5 ± 25.5), Barthel Index scores (80.3 ± 25.0 vs. 57.7 ± 30.0), and greater odds of achieving minimal disability (mRS ≤ 1: 52.6% vs. 17.5%; all <i>p</i> &lt; 0.001). Proportional recovery was also significantly higher in the MEP+ group for both the FMA and the Barthel Index (both <i>p</i> &lt; 0.001). Early MEP assessment is a valuable prognostic tool for upper-limb stroke recovery, supporting its routine incorporation into clinical practice.
DOI: 10.6084/m9.figshare.30819512.v1
title: Predictive value of motor-evoked potentials for upper limb functional outcomes in acute ischemic stroke

description: Stroke remains a leading cause of acquired physical disability globally, with upper limb motor impairment significantly affecting independence and quality of life. Currently, objective neurophysiological biomarkers are not routinely incorporated into stroke care. This study aimed to investigate the predictive value of MEPs for upper limb outcomes in acute ischemic stroke. This prospective cohort study included 133 adults experiencing their first acute ischemic stroke. Within 10 days of onset, participants underwent Motor-evoked potential (MEP) testing via transcranial magnetic stimulation (TMS) and were categorized as MEP+ (with preserved responses) or MEP– (with absent responses). Outcome measures included the Fugl-Meyer Assessment (FMA), Barthel Index, and modified Rankin Scale (mRS), assessed at baseline and 90 days. Logistic regression models adjusted for age and baseline stroke severity were used to determine the independent predictive value of MEP status. Among 133 patients (mean age 63.6 ± 12.2 years; 57.9% male), those with preserved MEPs (57.1%) demonstrated significantly better motor and functional outcomes at 90 days. MEP+ patients had higher FMA scores (61.0 ± 9.5 vs. 33.5 ± 25.5), Barthel Index scores (80.3 ± 25.0 vs. 57.7 ± 30.0), and greater odds of achieving minimal disability (mRS ≤ 1: 52.6% vs. 17.5%; all <i>p</i> &lt; 0.001). Proportional recovery was also significantly higher in the MEP+ group for both the FMA and the Barthel Index (both <i>p</i> &lt; 0.001). Early MEP assessment is a valuable prognostic tool for upper-limb stroke recovery, supporting its routine incorporation into clinical practice.
DOI: 10.6084/m9.figshare.28776430
title: ITGA3–MET interaction promotes papillary thyroid cancer progression via ERK and PI3K/AKT pathways

description: Studies have examined the role of integrin α3 (ITGA3) in papillary thyroid carcinoma (PTC). However, the functional and molecular mechanism by which ITGA3 is involved in the progression of PTC remains poorly understood. To investigate the role of ITGA3 in PTC, raw PTC transcriptome data underwent comprehensive bioinformatics analyses, including differential expression, co-expression network, and enrichment analyses. ITGA3 expression was validated <i>via</i> immunohistochemistry and western blotting in PTC tissues. Cell functional assays and xenograft models assessed PTC cell behaviour. The potential mechanisms of ITGA3 were elucidated using bioinformatics analyses, western blotting, co-immunoprecipitation, and immunofluorescence. Finally, integration of ITGA3 expression with clinical parameters enabled nomogram construction for precise prediction of cervical lymph node metastasis (CLNM) in PTC. ITGA3 was upregulated in PTC and associated strongly with CLNM (79.5% <i>vs.</i> 53.84%, <i>p</i> = 0.016). ITGA3 expression enhanced PTC proliferation and migration <i>in vitro</i> and <i>in vivo via</i> cooperating with the MET protein tyrosine kinase, followed by phosphorylation of MET at Tyr1234/1235, and activation of ERK and PI3K/AKT signaling pathways. Furthermore, upregulation ITGA3 reduced phosphorylation at FAK-Tyr397 and Src-Tyr416 in PTC cells. Finally, a nomogram combining ITGA3 expression and clinical parameters for predicting CLNM was constructed and validated, achieving a ROC curve AUC of 0.719, suggesting potential application for PTC diagnosis. ITGA3 promotes PTC cell proliferation and migration by cooperating with MET to activate MET-ERK and MET-PI3K-AKT signalling. ITGA3-MET cooperation may serve as a potential therapeutic target.
DOI: 10.6084/m9.figshare.28776430.v1
title: ITGA3–MET interaction promotes papillary thyroid cancer progression via ERK and PI3K/AKT pathways

description: Studies have examined the role of integrin α3 (ITGA3) in papillary thyroid carcinoma (PTC). However, the functional and molecular mechanism by which ITGA3 is involved in the progression of PTC remains poorly understood. To investigate the role of ITGA3 in PTC, raw PTC transcriptome data underwent comprehensive bioinformatics analyses, including differential expression, co-expression network, and enrichment analyses. ITGA3 expression was validated <i>via</i> immunohistochemistry and western blotting in PTC tissues. Cell functional assays and xenograft models assessed PTC cell behaviour. The potential mechanisms of ITGA3 were elucidated using bioinformatics analyses, western blotting, co-immunoprecipitation, and immunofluorescence. Finally, integration of ITGA3 expression with clinical parameters enabled nomogram construction for precise prediction of cervical lymph node metastasis (CLNM) in PTC. ITGA3 was upregulated in PTC and associated strongly with CLNM (79.5% <i>vs.</i> 53.84%, <i>p</i> = 0.016). ITGA3 expression enhanced PTC proliferation and migration <i>in vitro</i> and <i>in vivo via</i> cooperating with the MET protein tyrosine kinase, followed by phosphorylation of MET at Tyr1234/1235, and activation of ERK and PI3K/AKT signaling pathways. Furthermore, upregulation ITGA3 reduced phosphorylation at FAK-Tyr397 and Src-Tyr416 in PTC cells. Finally, a nomogram combining ITGA3 expression and clinical parameters for predicting CLNM was constructed and validated, achieving a ROC curve AUC of 0.719, suggesting potential application for PTC diagnosis. ITGA3 promotes PTC cell proliferation and migration by cooperating with MET to activate MET-ERK and MET-PI3K-AKT signalling. ITGA3-MET cooperation may serve as a potential therapeutic target.
DOI: 10.6084/m9.figshare.30257480
title: The role of the transcription factor KLF16 in metabolic dysfunction associated fatty liver disease: regulatory linkages between lipid deposition and the expression of ATF4

description: The escalating prevalence of metabolic dysfunction-associated fatty liver disease (MAFLD) poses a significant global health burden. MAFLD is characterized by abnormal lipid accumulation in liver parenchymal cells and activation of endoplasmic reticulum stress. However, the effect of Krüppel-like factor 16(KLF16) on glycolipid metabolism has been limited. We investigated whether KLF16 could alleviate MAFLD through endoplasmic reticulum stress. HepG2 and mouse primary hepatocytes were treated with oleic acid (OA) to model MAFLD <i>in vitro</i>. siRNA was used to downregulate KLF16 expression in cells. C57/BL6J mice were fed a high-fat diet to model MAFLD <i>in vivo</i>, and AAV8 was used to regulate KLF16 and ATF4 expression. Western-blot, RT-qPCR, oil red O staining, and dual-luciferase reporter assays were used to explore the underlying mechanisms in MAFLD. T-test and ANOVA were used to compare the differences among groups. KLF16 expression was upregulated in MAFLD models. KLF16 downregulation aggravates lipid deposition in liver cells. The expression of ATF4 protein was downregulated in MAFLD models with KLF16 knockdown. KLF16 transcriptionally regulates ATF4 expression through two binding sites. ATF4 overexpression alleviates lipid deposition exacerbated by KLF16 knockdown in mice. In the face of abnormal lipid deposition in MAFLD, liver cells can play a spontaneous protective role by upregulating KLF16, which can promote the expression of ATF4 at the transcriptional level, further affecting downstream lipid metabolism-related genes. KLF16 may serve as a promising target gene to improve the progression or prognosis of MAFLD.
DOI: 10.6084/m9.figshare.30257480.v1
title: The role of the transcription factor KLF16 in metabolic dysfunction associated fatty liver disease: regulatory linkages between lipid deposition and the expression of ATF4

description: The escalating prevalence of metabolic dysfunction-associated fatty liver disease (MAFLD) poses a significant global health burden. MAFLD is characterized by abnormal lipid accumulation in liver parenchymal cells and activation of endoplasmic reticulum stress. However, the effect of Krüppel-like factor 16(KLF16) on glycolipid metabolism has been limited. We investigated whether KLF16 could alleviate MAFLD through endoplasmic reticulum stress. HepG2 and mouse primary hepatocytes were treated with oleic acid (OA) to model MAFLD <i>in vitro</i>. siRNA was used to downregulate KLF16 expression in cells. C57/BL6J mice were fed a high-fat diet to model MAFLD <i>in vivo</i>, and AAV8 was used to regulate KLF16 and ATF4 expression. Western-blot, RT-qPCR, oil red O staining, and dual-luciferase reporter assays were used to explore the underlying mechanisms in MAFLD. T-test and ANOVA were used to compare the differences among groups. KLF16 expression was upregulated in MAFLD models. KLF16 downregulation aggravates lipid deposition in liver cells. The expression of ATF4 protein was downregulated in MAFLD models with KLF16 knockdown. KLF16 transcriptionally regulates ATF4 expression through two binding sites. ATF4 overexpression alleviates lipid deposition exacerbated by KLF16 knockdown in mice. In the face of abnormal lipid deposition in MAFLD, liver cells can play a spontaneous protective role by upregulating KLF16, which can promote the expression of ATF4 at the transcriptional level, further affecting downstream lipid metabolism-related genes. KLF16 may serve as a promising target gene to improve the progression or prognosis of MAFLD.
DOI: 10.6084/m9.figshare.29554295
title: The association between cerebral small vessel disease and unfavorable hematoma morphology in primary intracerebral hemorrhage

description: To study the association between cerebral small vessel diseases (CSVD) and unfavorable hematoma morphology in primary intracerebral hemorrhage (ICH). Patients with primary ICH who were admitted to West China Hospital of Sichuan University from March 2012 to January 2021 were consecutively included. The unfavorable hematoma morphology included any hypodensity, any irregularity, black hole, blend sign, Barras shape score ≥3, Barras density score ≥3, immature hematoma and combined Barras total score (CBTS) ≥4. The combined hematoma morphology score (CHMS) was evaluated by allocating 1 point for the presence of each of the mentioned unfavorable hematoma morphology. Multivariable binary logistic and ordinal regressions, together with unsupervised machine learning, were used to determine the association between CSVD and unfavorable hematoma morphology features. Univariable analysis showed that older age and hypertension were associated with white matter hyperintensities (WMH) presence. Regarding hematoma morphology, Barras density score ≥3, CBTS ≥4 and higher CHMS were associated with WMH absence (all <i>p</i> &lt; 0.05). Multivariable regression indicated that lower WMH presence were significantly associated with both CBTS ≥4 and higher CHMS after correcting for confounders. Futhermore, we employed unsupervised machine learning using K-means algorithm to cluster patients into different groups according to CSVD burden, and the results showed that cluster with higher CSVD burden was less likely to be associated with unfavorable hematoma morphology such as black hole and higher CHMS after correcting for confounders. Lower CSVD burden might be associated with higher incidence of unfavorable hematoma morphology features, such as CTBS ≥4 and higher CHMS.
DOI: 10.6084/m9.figshare.29554295.v1
title: The association between cerebral small vessel disease and unfavorable hematoma morphology in primary intracerebral hemorrhage

description: To study the association between cerebral small vessel diseases (CSVD) and unfavorable hematoma morphology in primary intracerebral hemorrhage (ICH). Patients with primary ICH who were admitted to West China Hospital of Sichuan University from March 2012 to January 2021 were consecutively included. The unfavorable hematoma morphology included any hypodensity, any irregularity, black hole, blend sign, Barras shape score ≥3, Barras density score ≥3, immature hematoma and combined Barras total score (CBTS) ≥4. The combined hematoma morphology score (CHMS) was evaluated by allocating 1 point for the presence of each of the mentioned unfavorable hematoma morphology. Multivariable binary logistic and ordinal regressions, together with unsupervised machine learning, were used to determine the association between CSVD and unfavorable hematoma morphology features. Univariable analysis showed that older age and hypertension were associated with white matter hyperintensities (WMH) presence. Regarding hematoma morphology, Barras density score ≥3, CBTS ≥4 and higher CHMS were associated with WMH absence (all <i>p</i> &lt; 0.05). Multivariable regression indicated that lower WMH presence were significantly associated with both CBTS ≥4 and higher CHMS after correcting for confounders. Futhermore, we employed unsupervised machine learning using K-means algorithm to cluster patients into different groups according to CSVD burden, and the results showed that cluster with higher CSVD burden was less likely to be associated with unfavorable hematoma morphology such as black hole and higher CHMS after correcting for confounders. Lower CSVD burden might be associated with higher incidence of unfavorable hematoma morphology features, such as CTBS ≥4 and higher CHMS.
DOI: 10.6084/m9.figshare.30231061
title: Global, regional, and national burden and trends of idiopathic epilepsy among children and adolescents from 1990 to 2021: insights from the global burden of disease study 2021

description: Idiopathic epilepsy (IE) is a severe chronic disease that poses a serious threat to the life and health of patients. Based on the Global Burden of Disease (GBD) 2021 database, we analyzed the global, regional, and national burdens and trends of IE in children and adolescents (aged 0–19 years). Utilizing the GBD 2021 data, we analyzed the prevalence, incidence, disability-adjusted life years (DALYs), and mortality of IE across 204 countries and regions globally. The regions were stratified according to the Socio-demographic Index (SDI). Time trends were assessed using the estimated annual percentage change (EAPC). Over a 32-year period, global IE prevalence and incidence cases increased by 19% and 29%, while DALYs and death cases declined by 9% and 20%, respectively. Prevalence, DALYs, and death rates decreased annually, except for incidence rates, which rose. Low-middle SDI regions showed the highest disease burden, while high SDI regions experienced the greatest increase in prevalence rates. By age, the 10–19 age group had the highest growth in prevalence and incidence rates, while the &lt;5 age group showed the largest decline in DALYs and death rates. The total number of IE cases increased, while DALYs and mortality rates decreased, reflecting the improvement of global medical interventions. The disease burden remains high in low SDI regions, and it is necessary to optimize prevention and control strategies according to the characteristics of different regions, ages, and genders.
DOI: 10.6084/m9.figshare.30231061.v1
title: Global, regional, and national burden and trends of idiopathic epilepsy among children and adolescents from 1990 to 2021: insights from the global burden of disease study 2021

description: Idiopathic epilepsy (IE) is a severe chronic disease that poses a serious threat to the life and health of patients. Based on the Global Burden of Disease (GBD) 2021 database, we analyzed the global, regional, and national burdens and trends of IE in children and adolescents (aged 0–19 years). Utilizing the GBD 2021 data, we analyzed the prevalence, incidence, disability-adjusted life years (DALYs), and mortality of IE across 204 countries and regions globally. The regions were stratified according to the Socio-demographic Index (SDI). Time trends were assessed using the estimated annual percentage change (EAPC). Over a 32-year period, global IE prevalence and incidence cases increased by 19% and 29%, while DALYs and death cases declined by 9% and 20%, respectively. Prevalence, DALYs, and death rates decreased annually, except for incidence rates, which rose. Low-middle SDI regions showed the highest disease burden, while high SDI regions experienced the greatest increase in prevalence rates. By age, the 10–19 age group had the highest growth in prevalence and incidence rates, while the &lt;5 age group showed the largest decline in DALYs and death rates. The total number of IE cases increased, while DALYs and mortality rates decreased, reflecting the improvement of global medical interventions. The disease burden remains high in low SDI regions, and it is necessary to optimize prevention and control strategies according to the characteristics of different regions, ages, and genders.