cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.5125477
title: Supplementary Material for: Gene Expression Profiling in Peripheral White Blood Cells in Response to the Intake of Food with Different Glycemic Index Using a DNA Microarray

description: <b><i>Background/Aims:</i></b> Transcriptomics technology in human nutrition intervention studies would allow for genome-wide screening of the effects of nutrients. We observed the time course of gene expression changes in peripheral white blood cells (WBC) to elucidate the metabolic changes in the postprandial state that are a reflection and a marker of whole body metabolic changes. <b><i>Methods:</i></b> In a randomized crossover study, 7 healthy subjects consumed test meals of glucose (GL), white rice (WR) and rolled barley (BAR), each containing 75 g of available carbohydrate, and water (WAT). Blood glucose, insulin and nonesterified fatty acid concentrations, as well as the subjective levels of fullness and hunger were measured. Microarray analysis of the WBC and the real-time PCR were examined during 360 min after the intake of the test meals. <b><i>Results:</i></b> The number of genes that changed more than 1.5-fold and the expression patterns in the time course were different between the GL, the WR and the BAR groups. Several genes involved in glycolysis and fatty acid β-oxidation were markedly changed after the intake of the GL, the WR and the BAR; however, these genes did not change at any time point in the WAT. <b><i>Conclusions:</i></b> Gene expression profiling in the WBC can reflect food-related metabolic changes, even in the postprandial state.
DOI: 10.6084/m9.figshare.5125480.v1
title: Supplementary Material for: Analysis of Turner Syndrome Patients within the Jordanian Population, with a Focus on Four Patients with Y Chromosome Abnormalities

description: This study presents findings in Turner syndrome (TS) patients from the Jordanian population, with focus on 4 patients with Y chromosomal abnormalities. From 1989 to 2011, 504 patients with TS stigmata were referred to our institute for karyotyping, resulting in 142 positive TS cases. Of these, 62 (43.7%) had the typical 45,X karyotype and the remaining individuals (56.3%) were found to be mosaics. Fifteen TS patients (10.5%) carried a structural abnormality of the Y chromosome and presented with the mosaic 45,X/46,XY karyotype. From these, 4 TS cases were investigated further. Karyotyping revealed that 1 patient carried a small supernumerary marker chromosome, whereas cytogenetic and molecular analyses showed that 3 patients carried 2 copies of the <i>SRY </i>gene. Further analysis by <i>SRY</i> sequencing revealed no mutations within the gene. The analyzed patients were found to be phenotypically either females or males, depending on the predominance of the cell line carrying the Y chromosome. This study demonstrates the importance of detailed cytogenetic analysis (such as FISH) in TS patients, and it also emphasizes the need for molecular analysis (such as PCR and sequencing) when fragments of the Y chromosome are present.
DOI: 10.6084/m9.figshare.5125474
title: Supplementary Material for: Endothelial Dysfunction Occurs prior to Clinical Evidence of Polycystic Kidney Disease

description: <b><i>Objective:</i></b> Polycystic kidney disease (PKD), a monogenic disease with an autosomal dominant or an autosomal recessive form of inheritance (ARPKD), is the most common genetic cause of renal dysfunction and end-stage renal failure. In addition to the development of cysts, the autosomal form of PKD is associated with vascular endothelial dysfunction, a marker of vascular disease. Whether vascular endothelial dysfunction is also present in ARPKD, and its relationship with renal dysfunction remain to be determined. <b><i>Methods:</i></b> ARPKD rats (PCK model) and controls were studied at 6 and 10 weeks of age, and mean arterial pressure and renal function were measured. Aortic endothelial function was assessed using organ chamber techniques. Aortic endothelial cells (ECs) were isolated, characterized and their function studied. <b><i>Results:</i></b> Compared to controls, ARPKD animals had a decrease in the vasorelaxation to endothelium-dependent vasodilators, even prior to changes in mean arterial pressure or renal function. The abnormal vasoreactivity was corrected with L-arginine (a precursor of nitric oxide, NO), while the expression of endothelial NO synthase (eNOS) was unchanged. Furthermore, isolated ECs from 6-week-old ARPKD animals showed increased oxidative stress, with preserved eNOS expression and abnormal patterns of migration and angiogenic capacity (measured by the scratch and tube formation assays, respectively). <b><i>Conclusion:</i></b> ARPKD leads to impairments in aortic vascular function and ECs at an early stage, which can have significant functional consequences, potentially representing a novel therapeutic target in this disease.
DOI: 10.6084/m9.figshare.5125477.v1
title: Supplementary Material for: Gene Expression Profiling in Peripheral White Blood Cells in Response to the Intake of Food with Different Glycemic Index Using a DNA Microarray

description: <b><i>Background/Aims:</i></b> Transcriptomics technology in human nutrition intervention studies would allow for genome-wide screening of the effects of nutrients. We observed the time course of gene expression changes in peripheral white blood cells (WBC) to elucidate the metabolic changes in the postprandial state that are a reflection and a marker of whole body metabolic changes. <b><i>Methods:</i></b> In a randomized crossover study, 7 healthy subjects consumed test meals of glucose (GL), white rice (WR) and rolled barley (BAR), each containing 75 g of available carbohydrate, and water (WAT). Blood glucose, insulin and nonesterified fatty acid concentrations, as well as the subjective levels of fullness and hunger were measured. Microarray analysis of the WBC and the real-time PCR were examined during 360 min after the intake of the test meals. <b><i>Results:</i></b> The number of genes that changed more than 1.5-fold and the expression patterns in the time course were different between the GL, the WR and the BAR groups. Several genes involved in glycolysis and fatty acid β-oxidation were markedly changed after the intake of the GL, the WR and the BAR; however, these genes did not change at any time point in the WAT. <b><i>Conclusions:</i></b> Gene expression profiling in the WBC can reflect food-related metabolic changes, even in the postprandial state.
DOI: 10.6084/m9.figshare.5125468
title: Supplementary Material for: Live-Supervision: Vom Einwegspiegel zur videobasierten Online-Supervision

description: Live-Supervision ermöglicht dem Supervisor, Einblicke in eine laufende Therapiesitzung zu erhalten und in diese beratend einzugreifen. Die direkte Rückmeldung des Supervisors an den Supervisanden stellt dabei ein wichtiges Unterscheidungsmerkmal zu nachträglichen Supervisionsformen dar. In den letzten 60 Jahren wurden verschiedene Formen der Live-Supervision entwickelt, die im Rahmen dieser Arbeit in Hinblick auf ihre Praktikabilität, Akzeptanz und Effektivität diskutiert werden. Aufgrund der vielen Vorteile von videobasierter Live-Supervision («bug-in-the-eye», BITE) wird in dem aktuellen Beitrag ein besonderes Augenmerk auf diese neueste Entwicklung der Live-Supervision gelegt. Während einer BITE-Supervisionssitzung verfolgt der Supervisor die Therapie online über eine Videokamera und hat die Möglichkeit, über einen Monitor direkte Hinweise an den Therapeuten zu geben. Bei diesem Supervisionsformat ist es dem Supervisor möglich, die Supervision andernorts via Internet durchzuführen. In der vorliegenden Arbeit werden konkrete Hinweise für die Durchführung einer BITE-Supervisionssitzung gegeben. Zudem werden auf der Basis von 25 BITE-Sitzungen erste Ergebnisse einer Studie zur Akzeptanz dieses Verfahrens berichtet. Hierbei zeigte sich, dass die Akzeptanz von BITE-Supervision bei Therapeuten, Supervisoren und Patienten sehr hoch ist und diese als nützlich und hilfreich eingeschätzt wird. Abschließend wird diskutiert, auf welche Weise BITE-Supervision in die Psychotherapieausbildung integriert werden könnte.
DOI: 10.6084/m9.figshare.5125483.v1
title: Supplementary Material for: Transcriptional Repressor HipB Regulates the Multiple Promoters in <b><i>Escherichia coli</i></b>

description: HipB is a DNA-binding protein in <i>Escherichia coli</i> and negatively regulates its own promoter by binding to the palindromic sequences [TATCCN<sub>8</sub>GGATA (N represents any nucleotides)] on the <i>hipBA</i> promoter. For such sequences, bioinformatic analysis revealed that there are a total of 39 palindromic sequences (TATCCN<sub>(x)</sub>GGATA: N is any nucleotides and x is the number of nucleotides from 1 to 30) in the promoter regions of 33 genes on the <i>E. coli</i> genome. Notably, <i>eutH</i> and <i>fadH</i> have two and three TATCCN<sub>(x)</sub>GGATA palindromic sequences located in their promoters, respectively. Another significant finding was that a palindromic sequence was also identified in the promoter region of <i>hipAB</i> locus, known to be involved in the RelA-dependent persister cell formation in bacteria. Here, we demonstrated that HipB binds to the palindromic structures in the <i>eutH</i>,<i> fadH</i>, as well as the <i>relA</i> promoter regions and represses their expressions. We further demonstrated that HipA enhances the repression of the <i>relA</i> promoter activity by HipB. This effect was not observed with D291A HipA mutant which was previously shown to lack an ability to interact with HipB, indicating that HipA enhances the HipB's repressor activity through direct interaction with HipB.
DOI: 10.6084/m9.figshare.5125462
title: Supplementary Material for: Circulating Leptin Concentrations in Patients with Chronic Obstructive Pulmonary Disease: A Systematic Review and Meta-Analysis

description: <b><i>Background:</i></b> Weight loss is a clinically important risk factor indicating a poor prognosis in chronic obstructive pulmonary disease (COPD). Leptin is an important regulator of food intake and energy expenditure. <b><i>Objectives:</i></b> To conduct a meta-analysis to determine whether the level of leptin is related to the disease status of COPD. <b><i>Methods:</i></b> Studies published before December 2012 were identified by searching PubMed, Embase and the Cochrane Database. Observational studies comparing circulating leptin levels between COPD patients and healthy controls were included. Data were independently extracted by two investigators and analyzed using Stata 12.0 software. <b><i>Results:</i></b> Ten articles were included in the meta-analysis. Circulating leptin levels were correlated with the body mass index (BMI) as well as percent fat mass in stable COPD patients. The correlation coefficient tended to be weaker during exacerbation. A positive correlation between leptin and tumor necrosis factor (TNF)-α levels was found in COPD exacerbations, while it disappeared in patients with stable disease. Most studies indicated that circulating leptin levels in stable COPD patients were not significantly different from those in healthy controls when adjusted for gender and BMI, whilst leptin levels tended to elevate in exacerbation groups. <b><i>Conclusions:</i></b> The normal regulatory mechanism of leptin is maintained in stable COPD patients despite weight loss. The additional correlation between leptin and TNF-α during exacerbations may support the closer association of leptin with changes in nutritional parameters and suggests its valuable role in the evaluation of systemic inflammatory responses in COPD patients during exacerbation, which merits further study.
DOI: 10.6084/m9.figshare.5125465
title: Supplementary Material for: Endothelial Nitric Oxide Synthase Phosphorylation at Threonine 495 and Mitochondrial Reactive Oxygen Species Formation in Response to a High H<sub>2</sub>O<sub>2</sub> Concentration

description: <b><i>Background:</i></b> Hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) is produced in vessels during ischemia/reperfusion and during inflammation, both leading to vascular dysfunction. We investigated cellular pathways involved in endothelial nitric oxide synthase (eNOS) phosphorylation at Threonine 495 (Thr<sup>495</sup>) in human umbilical vein endothelial cells (HUVECs) exposed to H<sub>2</sub>O<sub>2</sub>. <b><i>Methods:</i></b> HUVECs were exposed to 400 μM H<sub>2</sub>O<sub>2</sub> for 30 min. Phosphorylation at Thr<sup>495</sup> was assessed by Western blotting and reactive oxygen species (ROS) monitored by flow cytometry. Protein kinase C (PKC) pathways were investigated by pretreatment with PKC-β inhibitor ruboxistaurin or pan-PKC inhibitor GF109203X. In addition, we investigated ROCK and ERK pathways by MEKK1/2 inhibitor U0126 and ROCK inhibitor Y27632. <b><i>Results:</i></b> H<sub>2</sub>O<sub>2</sub> increased eNOS phosphorylation at Thr<sup>495</sup> (to 176% vs. control (100%), p &lt; 0.001) along with increased mitochondrial ROS formation (from 19.7 to 45.3%, p &lt; 0.01). This rise in phosphorylation could be prevented by U0126 and Y27632 in a dose-dependent manner, but did not result in lowered mitochondrial ROS formation. Conversely, addition of the antioxidant N-acetyl-L-cysteine only prevented mitochondrial ROS formation but did not prevent phosphorylation of eNOS Thr<sup>495</sup>. <b><i>Conclusion:</i></b> H<sub>2</sub>O<sub>2</sub>-mediated phosphorylation of eNOS Thr<sup>495</sup> is mediated by ROCK and ERK activity, but not by PKC, and is uncoupled from mitochondrial ROS signaling. Furthermore, ERK inhibition increased mitochondrial ROS formation.
DOI: 10.6084/m9.figshare.5125471
title: Supplementary Material for: Palmitic Acid Increases Medial Calcification by Inducing Oxidative Stress

description: <b><i>Background:</i></b> Aortic medial calcification is a cellular-regulated process leading to arterial stiffness. Although epidemiological studies have suggested an association between the saturation of fatty acids (FA) and arterial stiffness, there is no evidence that saturated FA can induce arterial calcification. This study investigated the capacity of palmitic acid (PA) to induce medial calcification and the signaling pathway(s) implicated in this process. <b><i>Methods:</i></b> Rat aortic segments and vascular smooth muscle cells (VSMC) were exposed to calcification medium supplemented with PA. In vivo, rats were treated with warfarin to induce calcification and fed a PA-enriched diet. <b><i>Results:</i></b> In vitro and ex vivo, palmitate increases calcification and ROS production. Palmitate increases extracellular-signal-regulated kinase (ERK1/2) phosphorylation and osteogenic gene expression. Inhibition of NADPH oxidase with apocynin or an siRNA prevents these effects. ERK1/2 inhibition attenuates the amplification of osteogenic gene expression and calcification induced by palmitate. In vivo, a PA-enriched diet amplified medial calcification and pulse wave velocity (PWV). These effects are mediated by ROS production as indicated by the inhibition of calcification and PWV normalization in rats concomitantly treated with apocynin. <b><i>Conclusion:</i></b> ROS induction by palmitate leads to ERK1/2 phosphorylation and subsequently induces the osteogenic differentiation of VSMC.
DOI: 10.6084/m9.figshare.5125459
title: Supplementary Material for: hCLCA1 DNA Vaccine Suppresses Cell Hyperplasia and Mucin Expression of Goblet Cells in vitro

description: <b><i>Background:</i></b> Excessive airway mucus secretion is a remarkable trait of asthma. Mucus overproduction mainly resulted from an increase in goblet cell numbers, which causes considerable damage to health. However, effective therapeutic treatments are still lacking for mucus hypersecretion. Human calcium-activated chloride channel 1 (hCLCA1) has been identified to be predominantly responsible for mucus hypersecretion. <b><i>Objectives:</i></b> In this study, we investigated the effects of an hCLCA1 DNA vaccine on the control of mucus production and goblet cell proliferation using an in vitro model goblet cell line (NCI-H292). <b><i>Methods:</i></b> The effect of the hCLCA1 DNA vaccine on cell viability and proliferative activity of NCI-H292/hCLCA1 was analyzed by electron microscopy, MTT assay, and flow cytometry. Expression of mucins and MUC5AC, a major member of the mucin gene family in airway goblet cells, was assessed under hCLCA1 DNA vaccine challenges by periodic acid-Schiff staining, quantitative real-time PCR and Western blot, respectively, and the expression profile of granulocyte-macrophage colony-stimulating factor (GM-CSF), a critical cytokine in airway inflammation, was also examined by real-time PCR and immunocytochemistry. <b><i>Results:</i></b> Results showed that hCLCA1 overexpression caused high cell proliferation and mucin expression, whereas the hCLCA1 DNA vaccine could effectively reverse these abnormal effects. In addition, GM-CSF expression was highly induced by hCLCA1 overexpression and efficiently suppressed by hCLCA1 DNA vaccine. <b><i>Conclusions:</i></b> These results illustrate that the hCLCA1 DNA vaccine effectively inhibits cell hyperplasia and mucin gene expression of goblet cells, suggesting that the hCLCA1 DNA vaccine has potential value in the treatment of human asthma.
DOI: 10.6084/m9.figshare.5125462.v1
title: Supplementary Material for: Circulating Leptin Concentrations in Patients with Chronic Obstructive Pulmonary Disease: A Systematic Review and Meta-Analysis

description: <b><i>Background:</i></b> Weight loss is a clinically important risk factor indicating a poor prognosis in chronic obstructive pulmonary disease (COPD). Leptin is an important regulator of food intake and energy expenditure. <b><i>Objectives:</i></b> To conduct a meta-analysis to determine whether the level of leptin is related to the disease status of COPD. <b><i>Methods:</i></b> Studies published before December 2012 were identified by searching PubMed, Embase and the Cochrane Database. Observational studies comparing circulating leptin levels between COPD patients and healthy controls were included. Data were independently extracted by two investigators and analyzed using Stata 12.0 software. <b><i>Results:</i></b> Ten articles were included in the meta-analysis. Circulating leptin levels were correlated with the body mass index (BMI) as well as percent fat mass in stable COPD patients. The correlation coefficient tended to be weaker during exacerbation. A positive correlation between leptin and tumor necrosis factor (TNF)-α levels was found in COPD exacerbations, while it disappeared in patients with stable disease. Most studies indicated that circulating leptin levels in stable COPD patients were not significantly different from those in healthy controls when adjusted for gender and BMI, whilst leptin levels tended to elevate in exacerbation groups. <b><i>Conclusions:</i></b> The normal regulatory mechanism of leptin is maintained in stable COPD patients despite weight loss. The additional correlation between leptin and TNF-α during exacerbations may support the closer association of leptin with changes in nutritional parameters and suggests its valuable role in the evaluation of systemic inflammatory responses in COPD patients during exacerbation, which merits further study.
DOI: 10.6084/m9.figshare.5125465.v1
title: Supplementary Material for: Endothelial Nitric Oxide Synthase Phosphorylation at Threonine 495 and Mitochondrial Reactive Oxygen Species Formation in Response to a High H<sub>2</sub>O<sub>2</sub> Concentration

description: <b><i>Background:</i></b> Hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) is produced in vessels during ischemia/reperfusion and during inflammation, both leading to vascular dysfunction. We investigated cellular pathways involved in endothelial nitric oxide synthase (eNOS) phosphorylation at Threonine 495 (Thr<sup>495</sup>) in human umbilical vein endothelial cells (HUVECs) exposed to H<sub>2</sub>O<sub>2</sub>. <b><i>Methods:</i></b> HUVECs were exposed to 400 μM H<sub>2</sub>O<sub>2</sub> for 30 min. Phosphorylation at Thr<sup>495</sup> was assessed by Western blotting and reactive oxygen species (ROS) monitored by flow cytometry. Protein kinase C (PKC) pathways were investigated by pretreatment with PKC-β inhibitor ruboxistaurin or pan-PKC inhibitor GF109203X. In addition, we investigated ROCK and ERK pathways by MEKK1/2 inhibitor U0126 and ROCK inhibitor Y27632. <b><i>Results:</i></b> H<sub>2</sub>O<sub>2</sub> increased eNOS phosphorylation at Thr<sup>495</sup> (to 176% vs. control (100%), p &lt; 0.001) along with increased mitochondrial ROS formation (from 19.7 to 45.3%, p &lt; 0.01). This rise in phosphorylation could be prevented by U0126 and Y27632 in a dose-dependent manner, but did not result in lowered mitochondrial ROS formation. Conversely, addition of the antioxidant N-acetyl-L-cysteine only prevented mitochondrial ROS formation but did not prevent phosphorylation of eNOS Thr<sup>495</sup>. <b><i>Conclusion:</i></b> H<sub>2</sub>O<sub>2</sub>-mediated phosphorylation of eNOS Thr<sup>495</sup> is mediated by ROCK and ERK activity, but not by PKC, and is uncoupled from mitochondrial ROS signaling. Furthermore, ERK inhibition increased mitochondrial ROS formation.
DOI: 10.6084/m9.figshare.5125453
title: Supplementary Material for: Clinical, Dermoscopic and Histopathological Features of Eccrine Poroid Neoplasms

description: <b><i>Background:</i></b> Eccrine poroma (EP) belongs to the group of benign adnexal tumors, but cases of eccrine porocarcinoma (EPC) arising on long-standing and untreated EP suggest a certain risk of malignant transformation. <b><i>Objectives:</i></b> To describe the clinical, dermoscopic and histopathologic features associated with different extremes in the spectrum of eccrine poroid neoplasms and to review the according literature. <b><i>Methods:</i></b> A retrospective analysis of patient characteristics and morphologic features associated with EP, EPC in situ and invasive porocarcinoma patients who attended two skin lesion clinics in Italy and Turkey between 2010 and 2011. <b><i>Results:</i></b> A total of 4 cases including 1 EP, 1 EPC in situ and 2 cases of invasive EPC in 4 patients were analyzed. Recent changes including bleeding, ulceration and sudden enlargement of a pre-existing lesion were associated with malignant transformation. Dermoscopically, polymorphous vessels consisting of coiled, hairpin and linear vessels were seen at all stages of progression. Histopathological findings of EPC in situ were limited to the epidermal component and were evident only at higher magnification. <b><i>Conclusions:</i></b> Clinicians and pathologists should carefully evaluate EPs with a recent history of change and erosion in order to avoid overlooking the potential development of EPC.