cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.5123911.v1
title: Supplementary Material for: Voice Risk Factors in Kindergarten Teachers in Greece

description: <b><i>Objective:</i></b> The purpose of this study was to identify voice risk factors for female kindergarten teachers and nurses in Heraklion, Crete. <b><i>Patients and Methods:</i></b> A questionnaire consisting of voice use and lifestyle activities was given to 200 kindergarten teachers in Heraklion, Crete, of which 151 were returned (75.5%). A group of 89 nurses served as the control group. Both groups also completed the Greek version of the Voice Handicap Index (VHI-G). <b><i>Results:</i></b> Kindergarten teachers sing more often, speak loudly more often when they are at work and present with more infections of the upper respiratory tract compared to nurses. They talk less than 30 min per day on the phone, drink less alcohol and water and smoke less in comparison with nurses. The median VHI-G score for the kindergarten teachers was significantly higher than that for the nurses. <b><i>Conclusion:</i></b> The results suggest that there is a difference in the factors that may be responsible for the appearance of voice problems in kindergarten teachers and in nurses. For kindergarten teachers, the risk factors for voice disorders are primarily related to vocal load factors and for nurses appear to be lifestyle-related more than voice use alone.
DOI: 10.6084/m9.figshare.5123899
title: Supplementary Material for: Predictors of 1-Year Mortality at Hospital Admission for Acute Exacerbations of Chronic Obstructive Pulmonary Disease

description: <b><i>Background:</i></b> Acute exacerbations of chronic obstructive pulmonary disease (AE-COPD) are related to high mortality, especially in hospitalized patients. Predictors for severe outcomes are still not sufficiently defined. <b><i>Objectives:</i></b> To assess the mortality rate and identify potential determinants of mortality in a cohort of patients hospitalized for AE-COPD. <b><i>Methods:</i></b> A retrospective, observational cohort study including all consecutive patients admitted between January 1, 2009, and April 1, 2010, for AE-COPD. Potential predictors were assessed at initial presentation at the emergency room. The primary outcome was mortality during 1-year follow-up. Univariate and multivariate time-to-event analyses using Cox proportional hazard models were employed for statistical analysis. <b><i>Results:</i></b> A total of 260 patients were enrolled in this study. Mean age was 70.5 ± 10.8 years, 50.0% were male and 63.4% had severe COPD. The in-hospital mortality rate was 5.8% and the 1-year mortality rate was 27.7%. Independent risk factors for mortality were age [hazard ratio (HR) = 1.04; 95% confidence interval (CI) = 1.01–1.07], male sex (HR = 2.00; 95% CI = 1.15–3.48), prior hospitalization for AE-COPD in the last 2 years (HR = 2.56; 95% CI = 1.52–4.30), prior recorded congestive heart failure (HR = 1.75; 95% CI = 1.03–2.97), Paco<sub>2</sub> ≥6.0 kPa (HR = 2.90; 95% CI = 1.65–5.09) and urea ≥8.0 mmol/l (HR = 2.38; 95% CI = 1.42–3.99) at admission. <b><i>Conclusions:</i></b> Age, male sex, prior hospitalization for AE-COPD in the last 2 years, prior recorded congestive heart failure, hypercapnia and elevated levels of urea at hospital admission are independent predictors of mortality within the first year after admission.
DOI: 10.6084/m9.figshare.5123896
title: Supplementary Material for: Patent Foramen Ovale, Ischemic Stroke and Migraine: Systematic Review and Stratified Meta-Analysis of Association Studies

description: <b><i>Background:</i></b> Observational data have reported associations between patent foramen ovale (PFO), cryptogenic stroke and migraine. However, randomized trials of PFO closure do not demonstrate a clear benefit either because the underlying association is weaker than previously suggested or because the trials were underpowered. In order to resolve the apparent discrepancy between observational data and randomized trials, we investigated associations between (1) migraine and ischemic stroke, (2) PFO and ischemic stroke, and (3) PFO and migraine. <b><i>Methods:</i></b> Eligibility criteria were consistent; including all studies with specifically defined exposures and outcomes unrestricted by language. We focused on studies at lowest risk of bias by stratifying analyses based on methodological design and quantified associations using fixed-effects meta-analysis models. <b><i>Results:</i></b> We included 37 studies of 7,686 identified. Compared to reports in the literature as a whole, studies with population-based comparators showed weaker associations between migraine with aura and cryptogenic ischemic stroke in younger women (OR 1.4; 95% CI 0.9–2.0; 1 study), PFO and ischemic stroke (HR 1.6; 95 CI 1.0–2.5; 2 studies; OR 1.3; 95% CI 0.9–1.9; 3 studies), or PFO and migraine (OR 1.0; 95% CI 0.6–1.6; 1 study). It was not possible to look for interactions or effect modifiers. These results are limited by sources of bias within individual studies. <b><i>Conclusions:</i></b> The overall pairwise associations between PFO, cryptogenic ischemic stroke and migraine do not strongly suggest a causal role for PFO. Ongoing randomized trials of PFO closure may need larger numbers of participants to detect an overall beneficial effect.
DOI: 10.6084/m9.figshare.5123902
title: Supplementary Material for: Small Particle-Size Talc Is Associated with Poor Outcome and Increased Inflammation in Thoracoscopic Pleurodesis

description: <b><i>Rationale:</i></b> Talc is very effective for pleurodesis, but there is concern about complications, especially acute respiratory distress syndrome. <b><i>Objectives:</i></b> It was the aim of this study to investigate if talc with a high concentration of small particles induces greater production of cytokines, and if pleural tumor burden has any influence on the local production and spillover of cytokines to the systemic circulation and eventual complications. <b><i>Methods:</i></b> We investigated 227 consecutive patients with malignant effusion submitted to talc pleurodesis. One hundred and three patients received ‘small-particle talc' (ST; containing about 50% particles &lt;10 µm) and 124 received ‘large-particle talc' (with &lt;20% particles &lt;10 µm). Serial samples of both pleural fluid and blood were taken before and 3, 24, 48 and 72 h after thoracoscopy. Also, mesothelial cells were stimulated with both types of talc in vitro. <b><i>Measurements and Results:</i></b> Interleukin-8, tumor necrosis factor-α, vascular endothelial growth factor, basic fibroblast growth factor and thrombin-antithrombin complex were measured in all samples. Early death (&lt;7 days after talc) occurred in 8 of 103 patients in the ST and in 1 of 124 in the ‘large-particle talc' group (p = 0.007). Patients who received ST had significantly higher proinflammatory cytokines in pleural fluid and serum after talc application, and also in supernatants of the in vitro study. Pleural tumor burden correlated positively with proinflammatory cytokines in serum, suggesting that advanced tumor states induce stronger systemic reactions after talc application. <b><i>Conclusions:</i></b> ST provokes a strong inflammatory reaction in both pleural space and serum, which is associated with a higher rate of early deaths observed in patients receiving it.
DOI: 10.6084/m9.figshare.5123890
title: Supplementary Material for: Quantitative Proteomic Analyses of Cerebrospinal Fluid Using iTRAQ in a Primate Model of Iron Deficiency Anemia

description: Iron deficiency affects nearly 2 billion people worldwide, with pregnant women and young children being most severely impacted. Sustained anemia during the first year of life can cause cognitive, attention and motor deficits, which may persist despite iron supplementation. We conducted iTRAQ analyses on cerebrospinal fluid (CSF) from infant monkeys <i>(Macaca mulatta)</i> to identify differential protein expression associated with early iron deficiency. CSF was collected from 5 iron-sufficient and 8 iron-deficient anemic monkeys at weaning age (6–7 months) and again at 12–14 months. Despite consumption of iron-fortified food after weaning, which restored hematological indices into the normal range, expression of 5 proteins in the CSF remained altered. Most of the proteins identified are involved in neurite outgrowth, migration or synapse formation. The results reveal novel ways in which iron deficiency undermines brain growth and results in aberrant neuronal migration and connections. Taken together with gene expression data from rodent models of iron deficiency, we conclude that significant alterations in neuroconnectivity occur in the iron-deficient brain, which may persist even after resolution of the hematological anemia. The compromised brain infrastructure could account for observations of behavioral deficits in children during and after the period of anemia.
DOI: 10.6084/m9.figshare.5123893
title: Supplementary Material for: Attentional Bias Modification in Posttraumatic Stress Disorder: A Randomized Controlled Trial

description: <b><i>Background:</i></b> Attentional bias modification (ABM) is a new treatment for anxiety disorders. Three randomized controlled clinical trials have shown positive effects of ABM in social anxiety disorder and generalized anxiety disorder. This study investigated the efficacy of ABM in outpatients with chronic posttraumatic stress disorder (PTSD). <b><i>Methods:</i></b> Randomized controlled double-blind trial (n = 102). ABM and control treatment consisted of eight 20-min sessions over the course of 3 weeks. Symptoms and attentional bias were assessed before and after treatment and at 3-week follow-up. <b><i>Results:</i></b> ABM and the control treatment were equally effective in reducing the symptoms of PTSD. The effect sizes of the improvement (from before to after treatment) were 0.66 for ABM and 0.46 for the control treatment, which is comparable to the effect sizes of pill-placebos in pharmacotherapy trials of chronic PTSD. Both treatments did not affect attentional bias. The acceptability and tolerability of ABM was moderate. <b><i>Conclusions:</i></b> This version of ABM is not an effective treatment of PTSD.
DOI: 10.6084/m9.figshare.5123899.v1
title: Supplementary Material for: Predictors of 1-Year Mortality at Hospital Admission for Acute Exacerbations of Chronic Obstructive Pulmonary Disease

description: <b><i>Background:</i></b> Acute exacerbations of chronic obstructive pulmonary disease (AE-COPD) are related to high mortality, especially in hospitalized patients. Predictors for severe outcomes are still not sufficiently defined. <b><i>Objectives:</i></b> To assess the mortality rate and identify potential determinants of mortality in a cohort of patients hospitalized for AE-COPD. <b><i>Methods:</i></b> A retrospective, observational cohort study including all consecutive patients admitted between January 1, 2009, and April 1, 2010, for AE-COPD. Potential predictors were assessed at initial presentation at the emergency room. The primary outcome was mortality during 1-year follow-up. Univariate and multivariate time-to-event analyses using Cox proportional hazard models were employed for statistical analysis. <b><i>Results:</i></b> A total of 260 patients were enrolled in this study. Mean age was 70.5 ± 10.8 years, 50.0% were male and 63.4% had severe COPD. The in-hospital mortality rate was 5.8% and the 1-year mortality rate was 27.7%. Independent risk factors for mortality were age [hazard ratio (HR) = 1.04; 95% confidence interval (CI) = 1.01–1.07], male sex (HR = 2.00; 95% CI = 1.15–3.48), prior hospitalization for AE-COPD in the last 2 years (HR = 2.56; 95% CI = 1.52–4.30), prior recorded congestive heart failure (HR = 1.75; 95% CI = 1.03–2.97), Paco<sub>2</sub> ≥6.0 kPa (HR = 2.90; 95% CI = 1.65–5.09) and urea ≥8.0 mmol/l (HR = 2.38; 95% CI = 1.42–3.99) at admission. <b><i>Conclusions:</i></b> Age, male sex, prior hospitalization for AE-COPD in the last 2 years, prior recorded congestive heart failure, hypercapnia and elevated levels of urea at hospital admission are independent predictors of mortality within the first year after admission.
DOI: 10.6084/m9.figshare.5123902.v1
title: Supplementary Material for: Small Particle-Size Talc Is Associated with Poor Outcome and Increased Inflammation in Thoracoscopic Pleurodesis

description: <b><i>Rationale:</i></b> Talc is very effective for pleurodesis, but there is concern about complications, especially acute respiratory distress syndrome. <b><i>Objectives:</i></b> It was the aim of this study to investigate if talc with a high concentration of small particles induces greater production of cytokines, and if pleural tumor burden has any influence on the local production and spillover of cytokines to the systemic circulation and eventual complications. <b><i>Methods:</i></b> We investigated 227 consecutive patients with malignant effusion submitted to talc pleurodesis. One hundred and three patients received ‘small-particle talc' (ST; containing about 50% particles &lt;10 µm) and 124 received ‘large-particle talc' (with &lt;20% particles &lt;10 µm). Serial samples of both pleural fluid and blood were taken before and 3, 24, 48 and 72 h after thoracoscopy. Also, mesothelial cells were stimulated with both types of talc in vitro. <b><i>Measurements and Results:</i></b> Interleukin-8, tumor necrosis factor-α, vascular endothelial growth factor, basic fibroblast growth factor and thrombin-antithrombin complex were measured in all samples. Early death (&lt;7 days after talc) occurred in 8 of 103 patients in the ST and in 1 of 124 in the ‘large-particle talc' group (p = 0.007). Patients who received ST had significantly higher proinflammatory cytokines in pleural fluid and serum after talc application, and also in supernatants of the in vitro study. Pleural tumor burden correlated positively with proinflammatory cytokines in serum, suggesting that advanced tumor states induce stronger systemic reactions after talc application. <b><i>Conclusions:</i></b> ST provokes a strong inflammatory reaction in both pleural space and serum, which is associated with a higher rate of early deaths observed in patients receiving it.
DOI: 10.6084/m9.figshare.5123890.v1
title: Supplementary Material for: Quantitative Proteomic Analyses of Cerebrospinal Fluid Using iTRAQ in a Primate Model of Iron Deficiency Anemia

description: Iron deficiency affects nearly 2 billion people worldwide, with pregnant women and young children being most severely impacted. Sustained anemia during the first year of life can cause cognitive, attention and motor deficits, which may persist despite iron supplementation. We conducted iTRAQ analyses on cerebrospinal fluid (CSF) from infant monkeys <i>(Macaca mulatta)</i> to identify differential protein expression associated with early iron deficiency. CSF was collected from 5 iron-sufficient and 8 iron-deficient anemic monkeys at weaning age (6–7 months) and again at 12–14 months. Despite consumption of iron-fortified food after weaning, which restored hematological indices into the normal range, expression of 5 proteins in the CSF remained altered. Most of the proteins identified are involved in neurite outgrowth, migration or synapse formation. The results reveal novel ways in which iron deficiency undermines brain growth and results in aberrant neuronal migration and connections. Taken together with gene expression data from rodent models of iron deficiency, we conclude that significant alterations in neuroconnectivity occur in the iron-deficient brain, which may persist even after resolution of the hematological anemia. The compromised brain infrastructure could account for observations of behavioral deficits in children during and after the period of anemia.
DOI: 10.6084/m9.figshare.5123881
title: Supplementary Material for: Brain Natriuretic Peptide Is Associated with Worsening and Mortality in Acute Stroke Patients but Adds No Prognostic Value to Clinical Predictors of Outcome

description: <b><i>Background:</i></b> At the present time, the determination of the outcome of stroke patients is based on the analysis of clinical and neuroimaging data. The use of prognostic blood biomarkers could aid in decision-making processes, e.g. admitting patients to specialized stroke units. Although the prognostic role of natriuretic peptides has been studied in heart failure and coronary diseases, the value of brain natriuretic peptide (BNP) is less known within the field of strokes. <b><i>Objective:</i></b> We aimed to study the relationship between plasma levels of BNP and acute neurological worsening or mortality after stroke in a large cohort of patients (investigating both ischemic and hemorrhagic disease). <b><i>Methods:</i></b> Consecutive stroke patients (ischemic and hemorrhagic) admitted to the Stroke Unit of our University Hospital within 24 h of the onset of symptoms were included. Stroke severity was assessed according to the National Institutes of Health Stroke Scale (NIHSS) at admission and at discharge. Neurological worsening was defined as an increase of 4 or more points in the NIHSS score or death during the patient’s stay at the Stroke Unit. Blood samples were drawn upon admission to measure plasma levels of BNP (Biosite Inc., San Diego, Calif., USA). Statistical analysis was performed using SPSS 15.0 and R software. <b><i>Results:</i></b> Altogether, 896 patients were included in the study. BNP plasma levels were higher among patients who deteriorated the most over time (n = 112; 90.5 vs. 61.2 ng/l; p = 0.006) or died (n = 83; 118.2 vs. 60.9 ng/l; p &lt; 0.001). Multivariate logistic regression analysis indicated that plasma BNP level was an independent predictor of neurological worsening [BNP &gt;56.7 ng/l; odds ratio (OR) = 1.64; p = 0.04] and death after stroke (BNP &gt;65.3 ng/l; OR = 1.97; p = 0.034). Adding BNP level to other well-known clinical predictors of bad outcome did not significantly increase the predictive value. <b><i>Conclusions:</i></b> Plasma levels of BNP measured during the acute phase of stroke are associated both with early neurological worsening and mortality. However, this biological information does not supply prognostic information which would add to clinical variables, which limits its use as a biomarker. Further investigation and systematic reviews are needed to clarify the role of natriuretic peptides in stroke outcome.
DOI: 10.6084/m9.figshare.5123896.v1
title: Supplementary Material for: Patent Foramen Ovale, Ischemic Stroke and Migraine: Systematic Review and Stratified Meta-Analysis of Association Studies

description: <b><i>Background:</i></b> Observational data have reported associations between patent foramen ovale (PFO), cryptogenic stroke and migraine. However, randomized trials of PFO closure do not demonstrate a clear benefit either because the underlying association is weaker than previously suggested or because the trials were underpowered. In order to resolve the apparent discrepancy between observational data and randomized trials, we investigated associations between (1) migraine and ischemic stroke, (2) PFO and ischemic stroke, and (3) PFO and migraine. <b><i>Methods:</i></b> Eligibility criteria were consistent; including all studies with specifically defined exposures and outcomes unrestricted by language. We focused on studies at lowest risk of bias by stratifying analyses based on methodological design and quantified associations using fixed-effects meta-analysis models. <b><i>Results:</i></b> We included 37 studies of 7,686 identified. Compared to reports in the literature as a whole, studies with population-based comparators showed weaker associations between migraine with aura and cryptogenic ischemic stroke in younger women (OR 1.4; 95% CI 0.9–2.0; 1 study), PFO and ischemic stroke (HR 1.6; 95 CI 1.0–2.5; 2 studies; OR 1.3; 95% CI 0.9–1.9; 3 studies), or PFO and migraine (OR 1.0; 95% CI 0.6–1.6; 1 study). It was not possible to look for interactions or effect modifiers. These results are limited by sources of bias within individual studies. <b><i>Conclusions:</i></b> The overall pairwise associations between PFO, cryptogenic ischemic stroke and migraine do not strongly suggest a causal role for PFO. Ongoing randomized trials of PFO closure may need larger numbers of participants to detect an overall beneficial effect.
DOI: 10.6084/m9.figshare.5123878
title: Supplementary Material for: Effects of Repetitive Exposure to Pain and Morphine Treatment on the Neonatal Rat Brain

description: <b><i>Background:</i></b> Untreated exposure to pain in preterm neonates might damage the vulnerable premature brain and alter development. Pain treatment is limited because analgesic agents may also have adverse neurodevelopmental consequences in newborns. <b><i>Objective:</i></b> To study the effects of neonatal pain and morphine treatment on the developing brain in a neonatal rat model. <b><i>Methods:</i></b> Newborn rats were randomly assigned to: treatment with formalin injections (group 1), saline injections (group 2) and controls receiving no injections (group 3). Treatment was given on postnatal days 1–3 (model A), 1–5 (model B) and 10–12 (model C). Brains were studied histologically and protein expression was evaluated (protein kinase C epsilon and doublecortin). Effects of preemptive morphine treatment were studied in the same models (models A+M and B+M). <b><i>Results:</i></b> Formalin injections resulted in increased apoptotic scores in models A and B. Saline injections increased the number of degenerative cells only in model B. Morphine showed protective effects in formalin-treated animals of model A+M and saline-treated animals of model B+M only. In model C, no neurodegenerative effects were detected. The protein expression of doublecortin showed a pain-related upregulation in the thalamus region, whereas protein kinase C epsilon expression was upregulated in the cortex. <b><i>Conclusions:</i></b> Severe inflammatory pain and pain caused by repetitive injections in neonatal rats may cause major changes in the developing brain during the first week of life. Morphine may only protect the newborn brain against these changes in specific situations.
DOI: 10.6084/m9.figshare.5123884
title: Supplementary Material for: Twist Confers Chemoresistance to Anthracyclines in Bladder Cancer through Upregulating P-Glycoprotein

description: <b><i>Background:</i></b> The membrane transporter P-glycoprotein (P-gp) was found to mediate chemoresistance, which is one of the obstacles to effective chemotherapy in several types of human cancer. The transcription factor Twist, which has been reported to participate in cancer invasion and metastasis, also plays a vital role in the progression of chemoresistance. However, the effect of Twist on P-gp-related chemoresistance remains dubious. <b><i>Methods and Results:</i></b> We found that Twist can regulate the expression of P-gp and then confer resistance to anthracycline drugs in human bladder cancer cells. Firstly, Twist was found to be coexpressed with P-gp in human bladder cancer cells and tissues, which were associated with enhanced chemoresistance to anthracycline drugs. Secondly, knockdown of Twist by specific siRNA treatment significantly sensitized bladder cancer cells to anthracycline drugs via inhibiting P-gp expression. Bladder cancer cells that survived transient exposure to anthracycline drugs showed higher levels of P-gp expression and more nuclear localization of Twist than untreated cells. <b><i>Conclusion:</i></b> We report a novel mechanism of anthracycline chemoresistance in bladder cancer in which activated Twist mediates P-gp expression in addition to its antiapoptotic roles. Therapeutic strategies targeting Twist may improve the management of recurrent bladder cancer after chemotherapy.