cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.4542694.v1
title: Supplementary Material for: Antipathy of Trichoderma against Sclerotium rolfsii Sacc.: Evaluation of Cell Wall-Degrading Enzymatic Activities and Molecular Diversity Analysis of Antagonists

description: The fungus <i>Trichoderma</i> is a teleomorph of the <i>Hypocrea</i> genus and associated with biological control of plant diseases. The microscopic, biochemical, and molecular characterization of <i>Trichoderma </i>was carried out and evaluated for in vitro antagonistic activity against the fungal pathogen <i>Sclerotium rolfsii</i> causing stem rot disease in groundnut. In total, 11 isolates of <i>Trichoderma</i> were examined for antagonism at 6 and 12 days after inoculation (DAI). Out of 11, <i>T. virens </i>NBAII Tvs12 evidenced the highest (87.91%) growth inhibition of the test pathogen followed by <i>T. koningii</i> MTCC 796 (67.03%), <i>T. viride </i>NBAII Tv23 (63.74%), and <i>T. harzianum </i>NBAII Th1 (60.44%). Strong mycoparasitism was observed in the best antagonist Tvs12 strain during 6-12 DAI. The specific activity of cell wall-degrading enzymes - chitinase and β-1,3-glucanase - was positively correlated with growth inhibition of the test pathogen. In total, 18 simple sequence repeat (SSR) polymorphisms were reported to amplify 202 alleles across 11 <i>Trichoderma </i>isolates. The average polymorphism information content for SSR markers was found to be 0.80. The best antagonist Tvs 12 was identified with 7 unique SSR alleles amplified by 5 SSR markers. Clustering patterns of 11 <i>Trichoderma </i>strains showed the best antagonist <i>T. virens</i> NBAII Tvs 12 outgrouped with a minimum 3% similarity from the rest of <i>Trichoderma.</i>
DOI: 10.6084/m9.figshare.4542709.v2
title: Toward a Smell-aware Bug Prediction Model

description: Code smells are symptoms of poor design and implementation choices. Previous studies empirically assessed the impact of smells on code quality and clearly indicate their negative impact on maintainability, including a higher bug-proneness of components affected by code smells. In this paper, we capture previous findings on bug-proneness to build a specialized bug prediction model for smelly classes. Specifically, we evaluate the contribution of a measure of the severity of code smells (i.e., code smell intensity) by adding it to existing bug prediction models based on both product and process metrics, and comparing the results of the new model against the baseline models. Results indicate that the accuracy of a bug prediction model increases by adding the code smell intensity as predictor. We also compare the results achieved by the proposed model with the ones of an alternative technique which considers metrics about the history of code smells in files, finding that our model works generally better. However, we observed interesting complementarities between the set of buggy and smelly classes correctly classified by the two models. By evaluating the actual information gain provided by the intensity index with respect to the other metrics in the model, we found that the intensity index is a relevant feature for both product and process metrics-based models. At the same time, the metric counting the average number of code smells in previous versions of a class considered by the alternative model is also able to reduce the entropy of the model. On the basis of this result, we devise and evaluate a smell-aware combined bug prediction model that included product, process, and smell-related features. We demonstrate how such model classifies bug-prone code components with an F-Measure at least 13% higher than the existing state-of-the-art models.
DOI: 10.6084/m9.figshare.4542616
title: Supplementary Material for: Three Novel Pathogenic Mutations in KATP Channel Genes and Somatic Imprinting Alterations of the 11p15 Region in Pancreatic Tissue in Patients with Congenital Hyperinsulinism

description: <b><i>Background/Aims:</i></b> This study was performed to investigate the molecular pathology underlying focal and diffuse congenital hyperinsulinism (CHI). <b><i>Methods:</i></b> The <i>ABCC8</i> and <i>KCNJ11</i> genes were analyzed in 3 patients with focal CHI and in 1 patient with diffuse CHI. Immunohistochemistry, real-time PCR, methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA) and microsatellite marker analyses of the 11p15 region were performed on both normal tissues and adenomatous hyperplasia lesions. <b><i>Results:</i></b> The 3 patients with focal CHI harbored paternally inherited <i>ABCC8</i> or <i>KCNJ11</i> mutations. Compound heterozygous <i>ABCC8</i> mutations were identified in the patient with diffuse CHI. In the 3 patients with focal CHI, homozygous <i>ABCC8</i> or <i>KCNJ11</i> mutations were identified within the lesions. MLPA and real-time PCR revealed the presence of two copies of 11p15. MS-MLPA and microsatellite analyses demonstrated abnormal imprinting patterns and focal loss of maternal 11p13-15 within the lesions. In contrast, parental heterozygosity was preserved in the normal tissue. In the patient with diffuse CHI, the two <i>ABCC8</i> mutations were conserved, and imprinting patterns at 11p15 were normal. <b><i>Conclusions:</i></b> The epigenetic alteration at the 11p15 region plays a central role in developing focal CHI by paternally derived mutations of the K<sub>ATP</sub> channel and maternal allelic loss at this region. MS-MLPA and microsatellite analyses are useful to investigate the molecular etiology of CHI.
DOI: 10.6084/m9.figshare.4542607
title: Supplementary Material for: Evaluation of Methods for the Estimation of Threshold Concentrations by the Skin Prick Test

description: <b><i>Background:</i></b> The allergen dose-response curve is flat; thus, small changes in wheal size reflect large differences in skin sensitivity. The sensitivity as measured by provocation tests is given by the threshold concentration that causes symptoms and/or objective signs. The threshold concentrations differ by several magnitudes between the most and the least sensitive individuals clinically allergic to the same allergen. Variation in technique can be minimized by relating allergen responses to that to histamine. The aim here is to present and validate simple methods for estimation of the skin sensitivity given as the concentration inducing a wheal of the same size as that with the positive reference, 10 mg/ml of histamine HCl, in the same patient. <b><i>Methods:</i></b> Data from previously reported trials on the biological equilibration of allergen extracts were used to document a method to calculate the concentration of allergen required to induce a wheal of the same size as that with 10 mg/ml of histamine dihydrochloride in the same patient, and to validate the methods using the parallel line bioassay as the gold standard. <b><i>Results:</i></b> The validated methods correlated well with the results obtained using the gold standard method and provide results of skin prick testing based on threshold concentrations of allergen. <b><i>Conclusions:</i></b> The validated methods reduce the error of differences in testing techniques and make it possible to report skin sensitivity at threshold concentrations. A simple method to be used in clinical practice and a method suitable to describe changes in skin reactivity over time or during treatment are proposed.
DOI: 10.6084/m9.figshare.4542616.v1
title: Supplementary Material for: Three Novel Pathogenic Mutations in KATP Channel Genes and Somatic Imprinting Alterations of the 11p15 Region in Pancreatic Tissue in Patients with Congenital Hyperinsulinism

description: <b><i>Background/Aims:</i></b> This study was performed to investigate the molecular pathology underlying focal and diffuse congenital hyperinsulinism (CHI). <b><i>Methods:</i></b> The <i>ABCC8</i> and <i>KCNJ11</i> genes were analyzed in 3 patients with focal CHI and in 1 patient with diffuse CHI. Immunohistochemistry, real-time PCR, methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA) and microsatellite marker analyses of the 11p15 region were performed on both normal tissues and adenomatous hyperplasia lesions. <b><i>Results:</i></b> The 3 patients with focal CHI harbored paternally inherited <i>ABCC8</i> or <i>KCNJ11</i> mutations. Compound heterozygous <i>ABCC8</i> mutations were identified in the patient with diffuse CHI. In the 3 patients with focal CHI, homozygous <i>ABCC8</i> or <i>KCNJ11</i> mutations were identified within the lesions. MLPA and real-time PCR revealed the presence of two copies of 11p15. MS-MLPA and microsatellite analyses demonstrated abnormal imprinting patterns and focal loss of maternal 11p13-15 within the lesions. In contrast, parental heterozygosity was preserved in the normal tissue. In the patient with diffuse CHI, the two <i>ABCC8</i> mutations were conserved, and imprinting patterns at 11p15 were normal. <b><i>Conclusions:</i></b> The epigenetic alteration at the 11p15 region plays a central role in developing focal CHI by paternally derived mutations of the K<sub>ATP</sub> channel and maternal allelic loss at this region. MS-MLPA and microsatellite analyses are useful to investigate the molecular etiology of CHI.
DOI: 10.6084/m9.figshare.4542604
title: Supplementary Material for: One-Year Mortality Rates in US Children with End-Stage Renal Disease

description: <b><i>Background/Aims:</i></b> Few published data describe survival rates for pediatric end-stage renal disease (ESRD) patients. We aimed to describe one-year mortality rates for US pediatric ESRD patients over a 15-year period. <b><i>Methods:</i></b> In this retrospective cohort study, we used the US Renal Data System database to identify period-prevalent cohorts of patients aged younger than 19 for each year during the period 1995-2010. Yearly cohorts averaged approximately 1,200 maintenance dialysis patients (60% hemodialysis, 40% peritoneal dialysis) and 1,100 transplant recipients. Patients were followed for up to 1 year and censored at change in modality, loss to follow-up, or death. We calculated the unadjusted model-based mortality rates per time at risk, within each cohort year, by treatment modality (hemodialysis, peritoneal dialysis, transplant) and patient characteristics; percentage of deaths by cause; and overall adjusted odds of mortality by characteristics and modality. <b><i>Results:</i></b> Approximately 50% of patients were in the age group 15-18, 55% were male, and 45% were female. The most common causes of ESRD were congenital/reflux/obstructive causes (55%) and glomerulonephritis (30%). One-year mortality rates showed evidence of a decrease in the number of peritoneal dialysis patients (6.03 per 100 patient-years, 1995; 2.43, 2010; p = 0.0263). Mortality rates for transplant recipients (average 0.68 per 100 patient-years) were consistently lower than the rates for all dialysis patients (average 4.36 per 100 patient-years). <b><i>Conclusions:</i></b> One-year mortality rates differ by treatment modality in pediatric ESRD patients.
DOI: 10.6084/m9.figshare.4542604.v1
title: Supplementary Material for: One-Year Mortality Rates in US Children with End-Stage Renal Disease

description: <b><i>Background/Aims:</i></b> Few published data describe survival rates for pediatric end-stage renal disease (ESRD) patients. We aimed to describe one-year mortality rates for US pediatric ESRD patients over a 15-year period. <b><i>Methods:</i></b> In this retrospective cohort study, we used the US Renal Data System database to identify period-prevalent cohorts of patients aged younger than 19 for each year during the period 1995-2010. Yearly cohorts averaged approximately 1,200 maintenance dialysis patients (60% hemodialysis, 40% peritoneal dialysis) and 1,100 transplant recipients. Patients were followed for up to 1 year and censored at change in modality, loss to follow-up, or death. We calculated the unadjusted model-based mortality rates per time at risk, within each cohort year, by treatment modality (hemodialysis, peritoneal dialysis, transplant) and patient characteristics; percentage of deaths by cause; and overall adjusted odds of mortality by characteristics and modality. <b><i>Results:</i></b> Approximately 50% of patients were in the age group 15-18, 55% were male, and 45% were female. The most common causes of ESRD were congenital/reflux/obstructive causes (55%) and glomerulonephritis (30%). One-year mortality rates showed evidence of a decrease in the number of peritoneal dialysis patients (6.03 per 100 patient-years, 1995; 2.43, 2010; p = 0.0263). Mortality rates for transplant recipients (average 0.68 per 100 patient-years) were consistently lower than the rates for all dialysis patients (average 4.36 per 100 patient-years). <b><i>Conclusions:</i></b> One-year mortality rates differ by treatment modality in pediatric ESRD patients.
DOI: 10.6084/m9.figshare.4542607.v1
title: Supplementary Material for: Evaluation of Methods for the Estimation of Threshold Concentrations by the Skin Prick Test

description: <b><i>Background:</i></b> The allergen dose-response curve is flat; thus, small changes in wheal size reflect large differences in skin sensitivity. The sensitivity as measured by provocation tests is given by the threshold concentration that causes symptoms and/or objective signs. The threshold concentrations differ by several magnitudes between the most and the least sensitive individuals clinically allergic to the same allergen. Variation in technique can be minimized by relating allergen responses to that to histamine. The aim here is to present and validate simple methods for estimation of the skin sensitivity given as the concentration inducing a wheal of the same size as that with the positive reference, 10 mg/ml of histamine HCl, in the same patient. <b><i>Methods:</i></b> Data from previously reported trials on the biological equilibration of allergen extracts were used to document a method to calculate the concentration of allergen required to induce a wheal of the same size as that with 10 mg/ml of histamine dihydrochloride in the same patient, and to validate the methods using the parallel line bioassay as the gold standard. <b><i>Results:</i></b> The validated methods correlated well with the results obtained using the gold standard method and provide results of skin prick testing based on threshold concentrations of allergen. <b><i>Conclusions:</i></b> The validated methods reduce the error of differences in testing techniques and make it possible to report skin sensitivity at threshold concentrations. A simple method to be used in clinical practice and a method suitable to describe changes in skin reactivity over time or during treatment are proposed.
DOI: 10.6084/m9.figshare.4542598
title: Supplementary Material for: Canadian Administrative Health Data Can Identify Patients with Myasthenia Gravis

description: <b><i>Introduction:</i></b> Incidence and prevalence estimates for myasthenia gravis (MG) have varied widely, and the ability of administrative health data (AHD) records to accurately identify cases of MG is yet to be ascertained. The goal of the current study was to validate an algorithm to identify patients with MG in Ontario, Canada using AHD - thereby enabling future disease surveillance. <b><i>Methods:</i></b> A reference standard population was established using automated key word searching within EMRALD (Electronic Medical Record Administrative data Linked Database) and chart review of potential cases. AHD algorithms were generated and tested against the reference standard. The data was used to calculate MG prevalence rates. <b><i>Results:</i></b> There were 123,997 eligible adult patients, and 49 patients had definite MG (forming the reference standard). An algorithm requiring: (1 hospital discharge abstract with MG listed as a reason for hospitalization or a comorbid condition), or (5 outpatient MG visits and 1 relevant diagnostic test, within 1 year), or (3 pyridostigmine prescriptions, within 1 year) identified MG with sensitivity = 81.6%, specificity = 100%, positive predictive value = 80.0% and negative predictive value = 100%. The population prevalence within our cohort was 0.04%. <b><i>Conclusions:</i></b> This novel validation method demonstrates the feasibility of using administrative health data to identify patients with myasthenia gravis among the Ontario population.
DOI: 10.6084/m9.figshare.4542589
title: Supplementary Material for: The Interleukin-13 Receptor-α1 Chain Is Essential for Induction of the Alternative Macrophage Activation Pathway by IL-13 but Not IL-4

description: Macrophages coexpress both the interleukin (IL)-2Rγ chain (γ<sub>c</sub>) and IL-13Rα1. These receptor chains can heterodimerize with IL-4Rα to form type I or type II IL-4 receptor complexes, respectively. We used macrophages derived from <i>Il2rg</i> and <i>Il13ra1</i> knockout (KO) mice to evaluate the requirements for these receptor chains for induction of the alternative macrophage activation (AMA) pathway by IL-4 and IL-13. Absence of γ<sub>c</sub> significantly decreased activation of STAT6 by IL-4 but not IL-13. However, although activation of STAT6 by IL-4 was markedly reduced in γ<sub>c</sub> KO macrophages, it was not abolished, indicating that IL-4 can still signal through type II IL-4 receptors via the IL-13Rα1 chain. IL-13 failed to activate STAT6 in macrophages derived from <i>Il13ra1</i> KO mice; however, these cells remained fully responsive to IL-4. The inability of IL-13 but not IL-4 to signal in <i>Il13ra1</i><sup>-/-</sup> macrophages correlated with the inability of IL-13 but not IL-4 to induce expression of genes such as <i>Arg1</i>,<i> Retnla </i>and<i> Ccl11</i> that are characteristically expressed by alternatively activated macrophages. In addition, IL-13 but not IL-4 failed to induce membrane fusion and giant cell formation by <i>Il13ra1</i> KO macrophages. These findings demonstrate that the IL-13Rα1 chain is essential for induction of the AMA pathway by IL-13 but not IL-4.
DOI: 10.6084/m9.figshare.4542598.v1
title: Supplementary Material for: Canadian Administrative Health Data Can Identify Patients with Myasthenia Gravis

description: <b><i>Introduction:</i></b> Incidence and prevalence estimates for myasthenia gravis (MG) have varied widely, and the ability of administrative health data (AHD) records to accurately identify cases of MG is yet to be ascertained. The goal of the current study was to validate an algorithm to identify patients with MG in Ontario, Canada using AHD - thereby enabling future disease surveillance. <b><i>Methods:</i></b> A reference standard population was established using automated key word searching within EMRALD (Electronic Medical Record Administrative data Linked Database) and chart review of potential cases. AHD algorithms were generated and tested against the reference standard. The data was used to calculate MG prevalence rates. <b><i>Results:</i></b> There were 123,997 eligible adult patients, and 49 patients had definite MG (forming the reference standard). An algorithm requiring: (1 hospital discharge abstract with MG listed as a reason for hospitalization or a comorbid condition), or (5 outpatient MG visits and 1 relevant diagnostic test, within 1 year), or (3 pyridostigmine prescriptions, within 1 year) identified MG with sensitivity = 81.6%, specificity = 100%, positive predictive value = 80.0% and negative predictive value = 100%. The population prevalence within our cohort was 0.04%. <b><i>Conclusions:</i></b> This novel validation method demonstrates the feasibility of using administrative health data to identify patients with myasthenia gravis among the Ontario population.
DOI: 10.6084/m9.figshare.4542709
title: Toward a Smell-aware Bug Prediction Model

description: Code smells are symptoms of poor design and implementation choices. Previous studies empirically assessed the impact of smells on code quality and clearly indicate their negative impact on maintainability, including a higher bug-proneness of components affected by code smells. In this paper, we capture previous findings on bug-proneness to build a specialized bug prediction model for smelly classes. Specifically, we evaluate the contribution of a measure of the severity of code smells (i.e., code smell intensity) by adding it to existing bug prediction models based on both product and process metrics, and comparing the results of the new model against the baseline models. Results indicate that the accuracy of a bug prediction model increases by adding the code smell intensity as predictor. We also compare the results achieved by the proposed model with the ones of an alternative technique which considers metrics about the history of code smells in files, finding that our model works generally better. However, we observed interesting complementarities between the set of buggy and smelly classes correctly classified by the two models. By evaluating the actual information gain provided by the intensity index with respect to the other metrics in the model, we found that the intensity index is a relevant feature for both product and process metrics-based models. At the same time, the metric counting the average number of code smells in previous versions of a class considered by the alternative model is also able to reduce the entropy of the model. On the basis of this result, we devise and evaluate a smell-aware combined bug prediction model that included product, process, and smell-related features. We demonstrate how such model classifies bug-prone code components with an F-Measure at least 13% higher than the existing state-of-the-art models.
DOI: 10.6084/m9.figshare.4542589.v1
title: Supplementary Material for: The Interleukin-13 Receptor-α1 Chain Is Essential for Induction of the Alternative Macrophage Activation Pathway by IL-13 but Not IL-4

description: Macrophages coexpress both the interleukin (IL)-2Rγ chain (γ<sub>c</sub>) and IL-13Rα1. These receptor chains can heterodimerize with IL-4Rα to form type I or type II IL-4 receptor complexes, respectively. We used macrophages derived from <i>Il2rg</i> and <i>Il13ra1</i> knockout (KO) mice to evaluate the requirements for these receptor chains for induction of the alternative macrophage activation (AMA) pathway by IL-4 and IL-13. Absence of γ<sub>c</sub> significantly decreased activation of STAT6 by IL-4 but not IL-13. However, although activation of STAT6 by IL-4 was markedly reduced in γ<sub>c</sub> KO macrophages, it was not abolished, indicating that IL-4 can still signal through type II IL-4 receptors via the IL-13Rα1 chain. IL-13 failed to activate STAT6 in macrophages derived from <i>Il13ra1</i> KO mice; however, these cells remained fully responsive to IL-4. The inability of IL-13 but not IL-4 to signal in <i>Il13ra1</i><sup>-/-</sup> macrophages correlated with the inability of IL-13 but not IL-4 to induce expression of genes such as <i>Arg1</i>,<i> Retnla </i>and<i> Ccl11</i> that are characteristically expressed by alternatively activated macrophages. In addition, IL-13 but not IL-4 failed to induce membrane fusion and giant cell formation by <i>Il13ra1</i> KO macrophages. These findings demonstrate that the IL-13Rα1 chain is essential for induction of the AMA pathway by IL-13 but not IL-4.