cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.5125381.v1
title: Supplementary Material for: Pilot Study Using Proteomics to Identify Predictive Biomarkers of Necrotizing Enterocolitis from Buccal Swabs in Very Low Birth Weight Infants

description: <b><i>Background:</i></b> Necrotizing enterocolitis (NEC) is a major cause of death and morbidity in very low birth weight infants. <b><i>Objective:</i></b> To identify biomarker(s) that would predict NEC using buccal swab samples utilizing a proteomic approach. <b><i>Methods:</i></b> Cumulative buccal swab samples derived from very low birth weight preterm infants (&lt;32 weeks' gestational age and &lt;1,250 g) at 1, 2 and 3 weeks prior to the development of NEC and matched controls were subjected to two-dimensional difference gel electrophoresis and LC-MS/MS analysis for proteomic protein discovery. After identification of 21 altered proteins, we chose 3 candidate proteins using a broad systems biologic analysis approach that suggested several altered cellular processes that could be associated with NEC. <b><i>Results:</i></b> Preliminary validation studies using Western blots on these samples and 10 additional NEC and 10 matched control buccal samples collected within 2 or 3 weeks before NEC diagnosis analysis showed lower interleukin-1 receptor antagonist. <b><i>Conclusion:</i></b> Our results suggest that interleukin-1 receptor antagonist is worthy of further studies to determine its utility in helping predict NEC.
DOI: 10.6084/m9.figshare.5125393.v1
title: Supplementary Material for: Chronic Kidney Disease Causes Disruption of Gastric and Small Intestinal Epithelial Tight Junction

description: <b><i>Background:</i></b> Integrity of the tight junction (TJ) which seals the gap between the epithelial cells of the gastrointestinal tract is critical in preventing the entry of the microbial toxins, antigens, and other harmful products in the subepithelial tissues and the internal milieu. By enabling the absorption of these products, impairment of the intestinal epithelial barrier leads to local and systemic inflammation. We have recently found depletion of the key protein constituents of colonic epithelial TJ in animals with chronic kidney disease (CKD). Postmortem studies have revealed the presence of inflammation throughout the gastrointestinal tract in uremic humans. This observation suggests that uremia may cause disruption of the epithelial barrier in all segments of the gastrointestinal tract including the stomach, jejunum, and ileum. The present study was undertaken to explore this possibility. <b><i>Methods:</i></b> Sprague-Dawley rats were randomized to CKD or control groups. The CKD group was subjected to 5/6 nephrectomy while the control group underwent a sham operation. The animals were observed for 10 weeks at which time they were euthanized and their stomachs, jejunums, and ileums were removed and processed for measurement of TJ proteins. <b><i>Results:</i></b> The CKD rats showed marked azotemia, systemic oxidative stress, and marked depletion of the key protein constituents of the epithelial TJ (claudin-1, occludin, and ZO1) in the stomach, jejunum, and ileum. <b><i>Conclusions:</i></b> The present study extends the earlier finding of uremia-induced disruption of colonic epithelial TJ by documenting the involvement of the stomach, jejunum, and ileum as well.
DOI: 10.6084/m9.figshare.5125372.v1
title: Supplementary Material for: Risk of Vascular Events after Nondisabling Small and Large Vessel Cerebral Ischemia

description: <b><i>Background:</i></b> Small- and large-vessel disease (SVD and LVD, respectively) might have a different pathogenesis and prognosis but the long-term risk of death and recurrent stroke appears to be similar in previous studies. In this study, we investigated the long-term vascular prognosis of patients with LVD and SVD in a large cohort of well-documented patients. <b><i>Methods:</i></b> We included 971 patients with transient ischemic attack (TIA) or nondisabling ischemic stroke of atherosclerotic origin referred to a university hospital in the Netherlands between 1994 and 2005 and followed them for the occurrence of vascular events or death. The primary outcome was a composite of stroke, myocardial infarction and vascular death, whichever happened first. Classification of SVD/LVD was primarily based on brain imaging. We used regression analyses to generate hazard ratios (HRs) with 95% confidence intervals (CIs). Sensitivity analyses were performed in subsets of the population, i.e. patients with subtype classification based on imaging, excluding TIA patients, first-ever stroke patients and LVD patients without a symptomatic carotid stenosis. <b><i>Results:</i></b> During a mean follow-up of 6.3 years, new vascular events occurred in 56 of 312 SVD patients (3.3%/year) and in 128 of 659 LVD patients (2.9%/year). These were ischemic strokes in 33 of the 56 events in SVD patients (2.0%/year) and 54 of the 128 events in LVD patients (1.2%/year). The corresponding age- and sex-adjusted HR for all new vascular events for LVD versus SVD was 0.76 (95% CI 0.56-1.05) for the total follow-up period. When this risk was split into early risk (&lt;1 year) and late risk (&gt;1 year), it was not significantly different for the 1-year risk of vascular events (HR 1.04, 95% CI 0.57-1.91); however, after 1 year of follow-up, LVD patients had fewer outcome events compared with SVD patients (HR 0.66, 95% CI 0.46-0.96). For ischemic strokes, the overall HR was 0.60 (95% CI 0.39-0.94). As with the primary outcome, here also the 1-year risk was not significantly different from &gt;1-year risk (HR 1.31, 95% CI 0.62-2.81, and HR 0.36, 95% CI 0.21-0.63, respectively). The sensitivity analyses showed virtually the same results. <b><i>Conclusion:</i></b> In patients with nondisabling cerebrovascular disease, we found, despite no differences at baseline in terms of vascular risk factors, a better long-term prognosis for patients with LVD for all vascular events, especially for recurrent strokes. Our observations support a different pathogenesis in SVD and LVD patients, and optimal prevention is indicated for patients with what was formerly regarded as ‘benign' SVD stroke.
DOI: 10.6084/m9.figshare.5125360
title: Supplementary Material for: <b><i>TFAP2B</i></b>-Dietary Protein and Glycemic Index Interactions and Weight Maintenance after Weight Loss in the DiOGenes Trial

description: <b><i>Background:</i></b><i>TFAP2B</i> rs987237 is associated with obesity and has shown interaction with the dietary fat-to-carbohydrate ratio, which has an effect on weight loss. We investigated interactions between rs987237 and protein-to-carbohydrate ratio or glycemic index (GI) in relation to weight maintenance after weight loss. <b><i>Methods:</i></b> This study included 742 obese individuals from 8 European countries who participated in the Diet, Obesity, and Genes (DiOGenes) trial, lost ≥8% of their initial body weight during an 8-week low-calorie diet and were randomized to one of 5 ad libitum diets with a fixed energy percentage from fat: either low-protein/low-GI, low-protein/high-GI, high-protein/low-GI, or high-protein/high-GI diets, or a control diet for a 6-month weight maintenance period. Using linear regression analyses and additive genetic models, we investigated main and dietary interaction effects of <i>TFAP2B</i> rs987237 in relation to weight maintenance. <b><i>Results:</i></b> In total, 468 completers of the trial were genotyped for rs987237. High-protein diets were beneficial for weight maintenance in the AA genotype group (67% of participants), but in the AG and GG groups no differences were observed for low- or high-protein diets. On the high-protein diet, carriers of the obesity risk allele (G allele) regained 1.84 kg (95% CI: 0.02; 3.67, p = 0.047) more body weight per risk allele than individuals on a low-protein diet. There was no interaction effect between rs987237 and GI on weight maintenance. <b><i>Conclusion:</i></b><i>TFAP2B</i> rs987237 and dietary protein/carbohydrate interacted to modify weight maintenance. Considering the carbohydrate proportion of the diet, the interaction was different from the previously reported rs987237-fat-to-carbohydrate ratio interaction for weight loss. Thus, <i>TFAP2B</i>-macronutrient interactions might diverge depending on the nutritional state.
DOI: 10.6084/m9.figshare.5125357
title: Supplementary Material for: Association of <b><i>HSD17B3</i></b> and <b><i>HSD3B1</i></b> Polymorphisms with Acne Vulgaris in Southwestern Han Chinese

description: Acne vulgaris is a very common skin disorder. Previous studies have indicated that genetic background factors play key roles in the onset of acne. Our previous investigation implicated several genes in the androgen metabolism pathway with acne vulgaris in the Han Chinese population. Thus, we further investigated genes and genetic variants that play important roles in this pathway for their relationship with the pathology of acne. In this study, a total of 610 subjects, including 403 acne patients and 207 healthy controls, were genotyped for 15 single-nucleotide polymorphisms in <i>HSD3B1</i> and <i>HSD17B3</i> genes. This study shows that rs6428829 in <i>HSD3B1</i> was associated with acne vulgaris in Han patients from Southwest China, even after adjusting for age and sex. The GG genotype was associated with an increased risk of acne vulgaris (p &lt; 0.05) and G allele carriers were associated with an increased risk of acne vulgaris (p &lt; 0.05). In addition, the haplotype AAT in <i>HSD3B1</i> significantly increased the risk of acne vulgaris in the case-control study (p &lt; 0.05). Furthermore, for another gene in this pathway, <i>HSD17B3</i>, the haplotype H8 was significantly associated with an increased risk of acne vulgaris. Based on these analyses, our study indicates that the cutaneous androgen metabolism-regulated genes <i>HSD3B1</i> and <i>HSD17B3</i> increase the susceptibility to acne vulgaris in Han Chinese from Southwest China.
DOI: 10.6084/m9.figshare.5125378.v1
title: Supplementary Material for: Effectiveness of Collaborative Stepped Care for Anxiety Disorders in Primary Care: A Pragmatic Cluster Randomised Controlled Trial

description: <b><i>Background:</i></b> Collaborative stepped care (CSC) may be an appropriate model to provide evidence-based treatment for anxiety disorders in primary care. <b><i>Methods:</i></b> In a<b> </b>cluster randomised controlled trial, the effectiveness of CSC compared to care as usual (CAU) for adults with panic disorder (PD) or generalised anxiety disorder (GAD) in primary care was evaluated. Thirty-one psychiatric nurses who provided their services to 43 primary care practices in the Netherlands were randomised to deliver CSC (16 psychiatric nurses, 23 practices) or CAU (15 psychiatric nurses, 20 practices). CSC was provided by the psychiatric nurses (care managers) in collaboration with the general practitioner and a consultant psychiatrist. The intervention consisted of 3 steps, namely guided self-help, cognitive behavioural therapy and antidepressants. Anxiety symptoms were measured with the Beck Anxiety Inventory (BAI) at baseline and after 3, 6, 9 and 12 months. <b><i>Results:</i></b> We recruited 180 patients with a DSM-IV diagnosis of PD or GAD, of whom 114 received CSC and 66 received usual primary care. On the BAI, CSC was<b> </b>superior to CAU [difference in gain scores from baseline to 3 months: -5.11, 95% confidence interval (CI) -8.28 to -1.94; 6 months: -4.65, 95% CI -7.93 to -1.38; 9 months: -5.67, 95% CI -8.97 to -2.36; 12 months: -6.84, 95% CI -10.13 to -3.55]. <b><i>Conclusions:</i></b> CSC, with guided self-help as a first step, was more effective than CAU for primary care patients with PD or GAD.
DOI: 10.6084/m9.figshare.5125354
title: Supplementary Material for: Effects of Phosphate Binder Therapy on Vascular Stiffness in Early-Stage Chronic Kidney Disease

description: <b><i>Background/Aims:</i></b> Cardiovascular disease (CVD) is increased in chronic kidney disease (CKD), and contributed to by the CKD-mineral bone disorder (CKD-MBD). CKD-MBD begins in early CKD and its vascular manifestations begin with vascular stiffness proceeding to increased carotid artery intima-media thickness (cIMT) and vascular calcification (VC). Phosphorus is associated with this progression and is considered a CVD risk factor in CKD. We hypothesized that modifying phosphorus balance with lanthanum carbonate (LaCO<sub>3</sub>) in early CKD would not produce hypophosphatemia and may affect vascular manifestations of CKD-MBD. <b><i>Methods:</i></b> We randomized 38 subjects with normophosphatemic stage 3 CKD to a fixed dose of LaCO<sub>3</sub> or matching placebo without adjusting dietary phosphorus in a 12-month randomized, double-blind, pilot and feasibility study. The primary outcome was the change in serum phosphorus. Secondary outcomes were changes in measures of phosphate homeostasis and vascular stiffness assessed by carotid-femoral pulse wave velocity (PWV), cIMT and VC over 12 months. <b><i>Results:</i></b> There were no statistically significant differences between LaCO<sub>3</sub> and placebo with respect to the change in serum phosphorus, urinary phosphorus, tubular reabsorption of phosphorus, PWV, cIMT, or VC. Biomarkers of the early CKD-MBD such as plasma fibroblast growth factor-23, Dickkopf-related protein 1 (DKK1), and sclerostin were increased 2- to 3-fold at baseline, but were not affected by LaCO<sub>3</sub>. <b><i>Conclusion</i></b>: Twelve months of LaCO<sub>3</sub> had no effect on serum phosphorus and did not alter phosphate homeostasis, PWV, cIMT, VC, or biomarkers of CKD-MBD.
DOI: 10.6084/m9.figshare.5125345
title: Supplementary Material for: Imaging Findings Associated with Cognitive Performance in Primary Lateral Sclerosis and Amyotrophic Lateral Sclerosis

description: <b><i>Introduction:</i></b> Executive dysfunction occurs in many patients with amyotrophic lateral sclerosis (ALS), but it has not been well studied in primary lateral sclerosis (PLS). The aims of this study were to (1) compare cognitive function in PLS to that in ALS patients, (2) explore the relationship between performance on specific cognitive tests and diffusion tensor imaging (DTI) metrics of white matter tracts and gray matter volumes, and (3) compare DTI metrics in patients with and without cognitive and behavioral changes. <b><i>Methods:</i></b> The Delis-Kaplan Executive Function System (D-KEFS), the Mattis Dementia Rating Scale (DRS-2), and other behavior and mood scales were administered to 25 ALS patients and 25 PLS patients. Seventeen of the PLS patients, 13 of the ALS patients, and 17 healthy controls underwent structural magnetic resonance imaging (MRI) and DTI. Atlas-based analysis using MRI Studio software was used to measure fractional anisotropy, and axial and radial diffusivity of selected white matter tracts. Voxel-based morphometry was used to assess gray matter volumes. The relationship between diffusion properties of selected association and commissural white matter and performance on executive function and memory tests was explored using a linear regression model. <b><i>Results:</i></b> More ALS than PLS patients had abnormal scores on the DRS-2. DRS-2 and D-KEFS scores were related to DTI metrics in several long association tracts and the callosum. Reduced gray matter volumes in motor and perirolandic areas were not associated with cognitive scores. <b><i>Conclusion:</i></b> The changes in diffusion metrics of white matter long association tracts suggest that the loss of integrity of the networks connecting fronto-temporal areas to parietal and occipital areas contributes to cognitive impairment.
DOI: 10.6084/m9.figshare.5125348
title: Supplementary Material for: Family History: Impact on Coronary Heart Disease Risk Assessment beyond Guideline-Defined Factors

description: <b><i>Objective:</i></b> Family history (FH) provides insights into the effects of shared genomic susceptibilities, environments and behaviors, making it a potentially valuable risk assessment tool for chronic diseases. We assessed whether coronary heart disease (CHD) risk assessment is improved when FH information is added to other clinical information recommended in guidelines. <b><i>Methods:</i></b> We applied logistic regression analyses to cross-sectional data originally obtained from a UK study of women who delivered a live-born infant between 1951 and 1970. We developed 3 models: Model 1 included only the covariates in a guideline applicable to the population, Model 2 added FH to Model 1, and Model 3 included a fuller range of risk factors. For each model, its ability to discriminate between study subjects with and those without CHD was evaluated and its impact on risk classification examined using the net reclassification index. <b><i>Results:</i></b> FH was an independent risk factor for CHD (odds ratio = 1.7, 95% confidence interval = 1.26-2.47) and improved discrimination beyond guideline-defined clinical factors (p &lt; 0.0006). However, the difference in the area under the curve of 2.8% and the extent of patient reclassification resulting from the inclusion of FH were small (p = 0.11). <b><i>Conclusion:</i></b> While FH were a significant independent risk factor for CHD, it added little to risk factors typically included in guidelines.
DOI: 10.6084/m9.figshare.5125354.v1
title: Supplementary Material for: Effects of Phosphate Binder Therapy on Vascular Stiffness in Early-Stage Chronic Kidney Disease

description: <b><i>Background/Aims:</i></b> Cardiovascular disease (CVD) is increased in chronic kidney disease (CKD), and contributed to by the CKD-mineral bone disorder (CKD-MBD). CKD-MBD begins in early CKD and its vascular manifestations begin with vascular stiffness proceeding to increased carotid artery intima-media thickness (cIMT) and vascular calcification (VC). Phosphorus is associated with this progression and is considered a CVD risk factor in CKD. We hypothesized that modifying phosphorus balance with lanthanum carbonate (LaCO<sub>3</sub>) in early CKD would not produce hypophosphatemia and may affect vascular manifestations of CKD-MBD. <b><i>Methods:</i></b> We randomized 38 subjects with normophosphatemic stage 3 CKD to a fixed dose of LaCO<sub>3</sub> or matching placebo without adjusting dietary phosphorus in a 12-month randomized, double-blind, pilot and feasibility study. The primary outcome was the change in serum phosphorus. Secondary outcomes were changes in measures of phosphate homeostasis and vascular stiffness assessed by carotid-femoral pulse wave velocity (PWV), cIMT and VC over 12 months. <b><i>Results:</i></b> There were no statistically significant differences between LaCO<sub>3</sub> and placebo with respect to the change in serum phosphorus, urinary phosphorus, tubular reabsorption of phosphorus, PWV, cIMT, or VC. Biomarkers of the early CKD-MBD such as plasma fibroblast growth factor-23, Dickkopf-related protein 1 (DKK1), and sclerostin were increased 2- to 3-fold at baseline, but were not affected by LaCO<sub>3</sub>. <b><i>Conclusion</i></b>: Twelve months of LaCO<sub>3</sub> had no effect on serum phosphorus and did not alter phosphate homeostasis, PWV, cIMT, VC, or biomarkers of CKD-MBD.
DOI: 10.6084/m9.figshare.5125360.v1
title: Supplementary Material for: <b><i>TFAP2B</i></b>-Dietary Protein and Glycemic Index Interactions and Weight Maintenance after Weight Loss in the DiOGenes Trial

description: <b><i>Background:</i></b><i>TFAP2B</i> rs987237 is associated with obesity and has shown interaction with the dietary fat-to-carbohydrate ratio, which has an effect on weight loss. We investigated interactions between rs987237 and protein-to-carbohydrate ratio or glycemic index (GI) in relation to weight maintenance after weight loss. <b><i>Methods:</i></b> This study included 742 obese individuals from 8 European countries who participated in the Diet, Obesity, and Genes (DiOGenes) trial, lost ≥8% of their initial body weight during an 8-week low-calorie diet and were randomized to one of 5 ad libitum diets with a fixed energy percentage from fat: either low-protein/low-GI, low-protein/high-GI, high-protein/low-GI, or high-protein/high-GI diets, or a control diet for a 6-month weight maintenance period. Using linear regression analyses and additive genetic models, we investigated main and dietary interaction effects of <i>TFAP2B</i> rs987237 in relation to weight maintenance. <b><i>Results:</i></b> In total, 468 completers of the trial were genotyped for rs987237. High-protein diets were beneficial for weight maintenance in the AA genotype group (67% of participants), but in the AG and GG groups no differences were observed for low- or high-protein diets. On the high-protein diet, carriers of the obesity risk allele (G allele) regained 1.84 kg (95% CI: 0.02; 3.67, p = 0.047) more body weight per risk allele than individuals on a low-protein diet. There was no interaction effect between rs987237 and GI on weight maintenance. <b><i>Conclusion:</i></b><i>TFAP2B</i> rs987237 and dietary protein/carbohydrate interacted to modify weight maintenance. Considering the carbohydrate proportion of the diet, the interaction was different from the previously reported rs987237-fat-to-carbohydrate ratio interaction for weight loss. Thus, <i>TFAP2B</i>-macronutrient interactions might diverge depending on the nutritional state.
DOI: 10.6084/m9.figshare.5125351
title: Supplementary Material for: Influence of Cochleostomy and Cochlear Implant Insertion on Drug Gradients following Intratympanic Application in Guinea Pigs

description: Locally applied drugs can protect residual hearing following cochlear implantation. The influence of cochlear implantation on drug levels in the scala tympani (ST) after round window application was investigated in guinea pigs using the marker trimethylphenylammonium (TMPA) measured in real time with TMPA-selective microelectrodes. TMPA concentration in the upper basal turn of the ST rapidly increased during implantation and then declined due to cerebrospinal fluid entering the ST at the cochlear aqueduct and exiting at the cochleostomy. The TMPA increase was found to be caused by the cochleostomy drilling if the burr tip partially entered the ST. TMPA distribution in the second turn was less affected by implantation procedures. These findings show that basal turn drug levels may be changed during implantation and the changes may need to be considered in the interpretation of therapeutic effects of drugs in conjunction with implantation.