cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.30900259.v1
title: Gait differences after ACL reconstruction versus healthy controls: a three-level meta-analysis of kinematics, kinetics, and spatiotemporal parameters

description: This meta-analysis was designed to evaluate whether individuals following ACL reconstruction exhibit normalized gait biomechanics when compared to healthy controls. This review was conducted across five databases: PubMed, Embase, The Cochrane Library, Web of Science and EBSCOhost-SportDiscus, yielding a total of 5,251 records, with 21 qualified studies (52 independent samples from 861 participants; based on available data, the mean age was 26.5 ± 4.3 years and 51.3% were female) eligible for quantitative synthesis following rigorous screening. A three-level meta-analysis model was implemented to address effect size dependencies. Six gait parameters were analyzed, including kinematic variables (peak knee flexion and extension angles during stance), kinetic variables (peak external knee flexion and extension moments during stance) and spatiotemporal variables (stride length and walking speed). Among the six gait parameters that were analyzed, only the peak knee extension angle during stance (<i>k</i> = 9, <i>d</i> = 0.83, 95% CI: 0.26–1.40, I<sup>2</sup> = 77.53%, <i>p</i> = 0.01) showed a significant difference between ACL reconstruction patients and healthy controls. However, peak knee flexion angle, peak external knee flexion and extension moments during stance, stride length and walking speed were not significantly different between groups (<i>p</i> &gt; 0.05). Meta-regression identified a significant time-dependent improvement only for knee extension angle (<i>F</i> = 5.656, <i>p</i> = 0.049), while postoperative duration had no significant effect on other outcomes. This meta-analysis shows that the majority of gait parameters during stance, including peak knee flexion angle, external knee flexion and extension moments, stride length and walking speed, do not differ significantly between individuals with ACL reconstruction and healthy controls. Only peak knee extension angle remained impaired, though it showed signs of improvement over time. Persistent knee extension deficits emphasize the need for targeted quadriceps and knee control training as a key focus for long-term ACLR rehabilitation. Most stance-phase gait parameters normalize after anterior cruciate ligament surgery.Knee extension angle remains impaired but improves gradually with recovery time.Long-term rehabilitation should target knee extension control to restore function. Most stance-phase gait parameters normalize after anterior cruciate ligament surgery. Knee extension angle remains impaired but improves gradually with recovery time. Long-term rehabilitation should target knee extension control to restore function.
DOI: 10.6084/m9.figshare.28682877
title: The burden of diseases attributable to high body mass index in Asia from 1990 - 2019: results from the global burden of disease study 2019

description: Our study aimed to report the burden of diseases attributable to high body mass index (BMI) in Asia from 1990 to 2019. Utilizing data from the Global Burden of Disease (GBD) Study 2019, we calculated disability-adjusted life years (DALYs) and deaths, with trends quantified by the estimated annual percentage change (EAPC). We also made projections for selected countries and estimated the relationship between the Sociodemographic Index (SDI) and high BMI-related disease burden. From 1990 to 2019, high BMI-related diseases observed significant increases in the absolute number of deaths and DALYs, with EAPCs of 4.62 and 4.69, respectively, while the age-standardized rates of both deaths and DALYs also showed upward trends, with EAPCs of 1.39 and 1.80. Cardiovascular diseases, diabetes and kidney diseases, and neoplasms were the major contributors to the high BMI-related burden. The burden of high BMI-related diseases generally tended to be greater among males and older age groups. Predictions for selected countries indicated a continued rise in the number of deaths and DALYs for high BMI-related diseases, with a stabilization in the age-standardized rate. There was no significant association between SDI levels and the burden of high BMI-related diseases in Asia (coefficient=0.13, <i>p</i> = 0.39). The burden of high BMI-related diseases, a major public health issue, was increasing in Asia. To address this problem, coordinated action by governments, civil society and other key stakeholders should be taken to enhance awareness of the risks associated with high BMI and effectively reduce its impact.
DOI: 10.6084/m9.figshare.28682877.v1
title: The burden of diseases attributable to high body mass index in Asia from 1990 - 2019: results from the global burden of disease study 2019

description: Our study aimed to report the burden of diseases attributable to high body mass index (BMI) in Asia from 1990 to 2019. Utilizing data from the Global Burden of Disease (GBD) Study 2019, we calculated disability-adjusted life years (DALYs) and deaths, with trends quantified by the estimated annual percentage change (EAPC). We also made projections for selected countries and estimated the relationship between the Sociodemographic Index (SDI) and high BMI-related disease burden. From 1990 to 2019, high BMI-related diseases observed significant increases in the absolute number of deaths and DALYs, with EAPCs of 4.62 and 4.69, respectively, while the age-standardized rates of both deaths and DALYs also showed upward trends, with EAPCs of 1.39 and 1.80. Cardiovascular diseases, diabetes and kidney diseases, and neoplasms were the major contributors to the high BMI-related burden. The burden of high BMI-related diseases generally tended to be greater among males and older age groups. Predictions for selected countries indicated a continued rise in the number of deaths and DALYs for high BMI-related diseases, with a stabilization in the age-standardized rate. There was no significant association between SDI levels and the burden of high BMI-related diseases in Asia (coefficient=0.13, <i>p</i> = 0.39). The burden of high BMI-related diseases, a major public health issue, was increasing in Asia. To address this problem, coordinated action by governments, civil society and other key stakeholders should be taken to enhance awareness of the risks associated with high BMI and effectively reduce its impact.
DOI: 10.6084/m9.figshare.28043434
title: Characteristics, outcomes and the necessity of continued guideline-directed medical therapy in patients with heart failure with improved ejection fraction

description: Much remains to be learned about patients with heart failure with improved ejection fraction (HFimpEF). This study sheds light on the characteristics and clinical outcomes of HFimpEF patients, including the consequences of halting guideline-directed medical therapy (GDMT). This retrospective study was conducted on patients diagnosed with heart failure with reduced ejection fraction (HFrEF) who underwent a second echocardiogram at least 6 months apart between January 2009 and February 2023. The primary outcomes were major adverse cardiovascular events (MACEs), including all-cause mortality and heart failure hospitalization. The second outcome was recurrent HFrEF. Of 4,560 HFrEF patients were included, 3,289 (72.1%) achieved HFimpEF within a median follow-up period of 3.4 years (IQR: 1.8 − 5.9 years). Among these HFimpEF patients, recurrent HFrEF was observed in 941 (28.6%) patients during a median follow-up period of 2.3 years (IQR: 0.8–4.6 years). The proportion of patients who halted GDMT was 70.4%, 53.2%, 59.8% and 63.8% for MRA, beta-blockers, ACEI/ARB/ARNI and SGLT-2 inhibitors. Multivariable Cox analysis revealed ischemic heart disease, chronic kidney disease, coronary heart disease, lower left ventricular ejection fraction, larger left ventricular diastolic dimension and non-use GDMT are associated with recurrent HFrEF. Individuals without GDMT use exhibited lower chances of persistently recovering ejection fraction and high risks of MACEs compared to those who continue use. HFimpEF is a common condition across all clinical follow-ups. Prevalent discontinuation of GDMT medications may contribute significantly to recurrent HFrEF, placing patients at a higher risk for poor prognosis.
DOI: 10.6084/m9.figshare.28043434.v1
title: Characteristics, outcomes and the necessity of continued guideline-directed medical therapy in patients with heart failure with improved ejection fraction

description: Much remains to be learned about patients with heart failure with improved ejection fraction (HFimpEF). This study sheds light on the characteristics and clinical outcomes of HFimpEF patients, including the consequences of halting guideline-directed medical therapy (GDMT). This retrospective study was conducted on patients diagnosed with heart failure with reduced ejection fraction (HFrEF) who underwent a second echocardiogram at least 6 months apart between January 2009 and February 2023. The primary outcomes were major adverse cardiovascular events (MACEs), including all-cause mortality and heart failure hospitalization. The second outcome was recurrent HFrEF. Of 4,560 HFrEF patients were included, 3,289 (72.1%) achieved HFimpEF within a median follow-up period of 3.4 years (IQR: 1.8 − 5.9 years). Among these HFimpEF patients, recurrent HFrEF was observed in 941 (28.6%) patients during a median follow-up period of 2.3 years (IQR: 0.8–4.6 years). The proportion of patients who halted GDMT was 70.4%, 53.2%, 59.8% and 63.8% for MRA, beta-blockers, ACEI/ARB/ARNI and SGLT-2 inhibitors. Multivariable Cox analysis revealed ischemic heart disease, chronic kidney disease, coronary heart disease, lower left ventricular ejection fraction, larger left ventricular diastolic dimension and non-use GDMT are associated with recurrent HFrEF. Individuals without GDMT use exhibited lower chances of persistently recovering ejection fraction and high risks of MACEs compared to those who continue use. HFimpEF is a common condition across all clinical follow-ups. Prevalent discontinuation of GDMT medications may contribute significantly to recurrent HFrEF, placing patients at a higher risk for poor prognosis.
DOI: 10.6084/m9.figshare.29715859
title: A controlled comparative study of the effects of methotrexate and pharmacogenetic factors on arterial blood pressure and arterial stiffness in patients with rheumatoid arthritis

description: Observational studies have shown that methotrexate, a conventional synthetic disease-modifying antirheumatic drug (csDMARD), is associated with lower arterial blood pressure (BP) and may reduce cardiovascular risk in rheumatoid arthritis (RA). However, it remains unclear whether a cause-and-effect relationship exists between the use of methotrexate and blood pressure reduction. We conducted a controlled comparative study of treatment-naïve newly diagnosed RA patients commenced on subcutaneous methotrexate (Group 1, <i>n</i> = 31, age 57 ± 15 years, 65% females, Disease Activity Score-28 – C-reactive protein, DAS28-CRP = 4.7 ± 1.2) or the DMARD comparator sulfasalazine (Group 2, <i>n</i> = 31, 54 ± 17 years, 61% females, DAS28-CRP = 5.0 ± 0.8). Clinic systolic (SBP, primary study endpoint) and diastolic BP (DBP) and augmentation index (AIx, a marker of arterial stiffness) were measured at baseline and after one and six months of treatment (ClinicalTrials.gov: NCT03254589). After six months, compared to Group 2, Group 1 patients had significantly lower SBP (−7.4 mmHg, 95% CI −14.0 to −0.8, <i>p</i> = 0.03). By contrast, there were no significant between-group differences in DBP (<i>p</i> = 0.18), AIx (<i>p</i> = 0.85), or DAS28-CRP (<i>p</i> = 0.16). A significant effect of single nucleotide polymorphisms (SNPs) rs1801133 (methyl tetrahydrofolate reductase) and rs2231142 (ATP-binding cassette subfamily G member 2) on BP changes during methotrexate treatment was observed. This is the first comparative study showing that methotrexate significantly reduces SBP in RA. This effect did not coincide with significant changes in arterial stiffness or disease activity. Further research is warranted to investigate the mechanisms underpinning the SBP-lowering effects of methotrexate, the role of specific SNPs, and whether such effects may account for reduced cardiovascular risk in patients with RA.
DOI: 10.6084/m9.figshare.29715859.v1
title: A controlled comparative study of the effects of methotrexate and pharmacogenetic factors on arterial blood pressure and arterial stiffness in patients with rheumatoid arthritis

description: Observational studies have shown that methotrexate, a conventional synthetic disease-modifying antirheumatic drug (csDMARD), is associated with lower arterial blood pressure (BP) and may reduce cardiovascular risk in rheumatoid arthritis (RA). However, it remains unclear whether a cause-and-effect relationship exists between the use of methotrexate and blood pressure reduction. We conducted a controlled comparative study of treatment-naïve newly diagnosed RA patients commenced on subcutaneous methotrexate (Group 1, <i>n</i> = 31, age 57 ± 15 years, 65% females, Disease Activity Score-28 – C-reactive protein, DAS28-CRP = 4.7 ± 1.2) or the DMARD comparator sulfasalazine (Group 2, <i>n</i> = 31, 54 ± 17 years, 61% females, DAS28-CRP = 5.0 ± 0.8). Clinic systolic (SBP, primary study endpoint) and diastolic BP (DBP) and augmentation index (AIx, a marker of arterial stiffness) were measured at baseline and after one and six months of treatment (ClinicalTrials.gov: NCT03254589). After six months, compared to Group 2, Group 1 patients had significantly lower SBP (−7.4 mmHg, 95% CI −14.0 to −0.8, <i>p</i> = 0.03). By contrast, there were no significant between-group differences in DBP (<i>p</i> = 0.18), AIx (<i>p</i> = 0.85), or DAS28-CRP (<i>p</i> = 0.16). A significant effect of single nucleotide polymorphisms (SNPs) rs1801133 (methyl tetrahydrofolate reductase) and rs2231142 (ATP-binding cassette subfamily G member 2) on BP changes during methotrexate treatment was observed. This is the first comparative study showing that methotrexate significantly reduces SBP in RA. This effect did not coincide with significant changes in arterial stiffness or disease activity. Further research is warranted to investigate the mechanisms underpinning the SBP-lowering effects of methotrexate, the role of specific SNPs, and whether such effects may account for reduced cardiovascular risk in patients with RA.
DOI: 10.6084/m9.figshare.28129523
title: Sleep features and the risk of type 2 diabetes mellitus: a systematic review and meta-analysis

description: This study aimed to assess the associations between multidimensional sleep features and type 2 diabetes mellitus (T2DM). We conducted a systematic search across the PubMed, Embase, Web of Science, and Scopus databases for observational studies examining the association between nighttime sleep duration, nighttime sleep quality, sleep chronotype, and daytime napping with type 2 diabetes mellitus (T2DM), up to October 1, 2024. If <i>I</i><sup>2</sup> &lt; 50%, a combined analysis was performed based on a fixed-effects model, and vice versa, using a random-effects model. Our analysis revealed that a nighttime sleep duration of less than 7 h (odds ratio [<i>OR</i>] = 1.18; 95% <i>CI</i> = 1.13, 1.23) or more than 8 h (<i>OR</i> = 1.13; 95% <i>CI</i> = 1.09, 1.18) significantly increased the risk of T2DM. Additionally, poor sleep quality (<i>OR</i> = 1.50; 95% <i>CI</i> = 1.30, 1.72) and evening chronotype (<i>OR</i> = 1.59; 95% <i>CI</i> = 1.18, 2.13) were associated with a notably greater risk of developing T2DM. Daytime napping lasting more than 30 min augments the risk of T2DM by 7-20%. Interactively, the incidence of T2DM was most significantly elevated among individuals with poor sleep quality and nighttime sleep duration of more than 8 h (<i>OR</i> = 2.15; 95% <i>CI</i> = 1.19, 3.91). A U-shaped relationship was observed between sleep duration and type 2 diabetes mellitus (T2DM), with the lowest risk occurring at a sleep duration of 7 to 8 h. Additionally, poor sleep quality, evening chronotypes, and daytime napping exceeding 30 min emerged as potential risk factors for T2DM. These high-risk sleep characteristics interacted with one another, amplifying the overall risk of developing the disease.
DOI: 10.6084/m9.figshare.28129523.v1
title: Sleep features and the risk of type 2 diabetes mellitus: a systematic review and meta-analysis

description: This study aimed to assess the associations between multidimensional sleep features and type 2 diabetes mellitus (T2DM). We conducted a systematic search across the PubMed, Embase, Web of Science, and Scopus databases for observational studies examining the association between nighttime sleep duration, nighttime sleep quality, sleep chronotype, and daytime napping with type 2 diabetes mellitus (T2DM), up to October 1, 2024. If <i>I</i><sup>2</sup> &lt; 50%, a combined analysis was performed based on a fixed-effects model, and vice versa, using a random-effects model. Our analysis revealed that a nighttime sleep duration of less than 7 h (odds ratio [<i>OR</i>] = 1.18; 95% <i>CI</i> = 1.13, 1.23) or more than 8 h (<i>OR</i> = 1.13; 95% <i>CI</i> = 1.09, 1.18) significantly increased the risk of T2DM. Additionally, poor sleep quality (<i>OR</i> = 1.50; 95% <i>CI</i> = 1.30, 1.72) and evening chronotype (<i>OR</i> = 1.59; 95% <i>CI</i> = 1.18, 2.13) were associated with a notably greater risk of developing T2DM. Daytime napping lasting more than 30 min augments the risk of T2DM by 7-20%. Interactively, the incidence of T2DM was most significantly elevated among individuals with poor sleep quality and nighttime sleep duration of more than 8 h (<i>OR</i> = 2.15; 95% <i>CI</i> = 1.19, 3.91). A U-shaped relationship was observed between sleep duration and type 2 diabetes mellitus (T2DM), with the lowest risk occurring at a sleep duration of 7 to 8 h. Additionally, poor sleep quality, evening chronotypes, and daytime napping exceeding 30 min emerged as potential risk factors for T2DM. These high-risk sleep characteristics interacted with one another, amplifying the overall risk of developing the disease.
DOI: 10.6084/m9.figshare.28586915
title: Identification and mechanism analysis of biomarkers related to butyrate metabolism in COVID-19 patients

description: Butyrate may inhibit SARS-CoV-2 replication and affect the development of COVID-19. However, there have been no systematic comprehensive analyses of the role of butyrate metabolism-related genes (BMRGs) in COVID-19. We performed differential expression analysis of BMRGs in the brain, liver and pancreas of COVID-19 patients and controls in GSE157852 and GSE151803. The differentially expressed genes (DEGs) and module genes between COVID-19 patients and healthy controls in GSE171110 were screened through ‘limma’ and ‘WGANA’ R package, respectively, followed by an intersection with BMRGs via ‘ggvenn’ R package. Six machine learning algorithms were employed to determine the best model for identifying biomarkers, and receiver operating characteristic (ROC) curves were plotted to evaluate the diagnostic value of the biomarkers in COVID-19. Moreover, the differences in immune-infiltrating cells between the COVID-19 and control groups were compared using CIBERSORT. The differences in immune cells and expression levels of biomarkers in immune cells among different tissues were analysed using GSE171668. The BMRGs were the most different in the brain between the COVID-19 and control groups, including 21 upregulated and 16 downregulated genes. Five important common BMRGs were screened as biomarkers for COVID-19 using XGBoost, namely CCNB1, CCNA2, BRCA1, HBB and HSPA5, with increased diagnostic performance. Enrichment analysis revealed that these five genes were related to the cell cycle, cell proliferation and cell senescence. The infiltrating abundance of 12 immune cells was different between the COVID-19 and control groups. Finally, the expression levels of HSPA5, BRCA1 and HBB were higher in annotated cells than in CCNB1 and CCNA2, and there were four different types of immune cells in the liver, heart, lungs and kidneys. These five genes may be potential biomarkers of butyrate metabolism in COVID-19 patients. These findings provide a direction for further studies on the molecular mechanisms underlying COVID-19.
DOI: 10.6084/m9.figshare.28586915.v1
title: Identification and mechanism analysis of biomarkers related to butyrate metabolism in COVID-19 patients

description: Butyrate may inhibit SARS-CoV-2 replication and affect the development of COVID-19. However, there have been no systematic comprehensive analyses of the role of butyrate metabolism-related genes (BMRGs) in COVID-19. We performed differential expression analysis of BMRGs in the brain, liver and pancreas of COVID-19 patients and controls in GSE157852 and GSE151803. The differentially expressed genes (DEGs) and module genes between COVID-19 patients and healthy controls in GSE171110 were screened through ‘limma’ and ‘WGANA’ R package, respectively, followed by an intersection with BMRGs via ‘ggvenn’ R package. Six machine learning algorithms were employed to determine the best model for identifying biomarkers, and receiver operating characteristic (ROC) curves were plotted to evaluate the diagnostic value of the biomarkers in COVID-19. Moreover, the differences in immune-infiltrating cells between the COVID-19 and control groups were compared using CIBERSORT. The differences in immune cells and expression levels of biomarkers in immune cells among different tissues were analysed using GSE171668. The BMRGs were the most different in the brain between the COVID-19 and control groups, including 21 upregulated and 16 downregulated genes. Five important common BMRGs were screened as biomarkers for COVID-19 using XGBoost, namely CCNB1, CCNA2, BRCA1, HBB and HSPA5, with increased diagnostic performance. Enrichment analysis revealed that these five genes were related to the cell cycle, cell proliferation and cell senescence. The infiltrating abundance of 12 immune cells was different between the COVID-19 and control groups. Finally, the expression levels of HSPA5, BRCA1 and HBB were higher in annotated cells than in CCNB1 and CCNA2, and there were four different types of immune cells in the liver, heart, lungs and kidneys. These five genes may be potential biomarkers of butyrate metabolism in COVID-19 patients. These findings provide a direction for further studies on the molecular mechanisms underlying COVID-19.
DOI: 10.6084/m9.figshare.29500538
title: Evaluated anatomical variations in children by sacrococcygeal ultrasonography as a new tool: a report from a Chinese tertiary hospital

description: Anatomical variations in the sacrococcygeal region can lead to complications such as accidental dural puncture during caudal block. This study aimed to determine the prevalence of sacrococcygeal anatomical variations using ultrasonography and to evaluate the necessity of ultrasound guidance in sacral block procedures. Ultrasound findings of sacrococcygeal anatomy were validated against magnetic resonance imaging (MRI). A detailed ultrasound protocol was subsequently applied to assess sacrococcygeal anatomy in pediatric patients. Ultrasound and MRI demonstrated strong concordance in evaluating sacrococcygeal anatomy. The most common anatomical variation was a low-lying dural sac (16.2%), followed by incomplete sacral cornua (4.9%). The dural sac termination level was inversely associated with age (odds ratio: 0.996, 95% CI: 0.945–0.987; <i>p</i> &lt; 0.001). Other variations included abnormal coccyx curvature (4.3%), sacral skewness (3.8%), and sacral hiatus atresia (1.1%), with no pathological abnormalities detected. Comprehensive ultrasound scanning effectively identifies anatomical variations in the sacrococcygeal region of pediatric patients, which are highly prevalent. Routine preprocedural ultrasound examinations and ultrasound guidance during caudal block procedures are strongly recommended to enhance safety and accuracy.