cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.5241583.v1
title: Erratum: Regulation of Autophagy by High Glucose in Human Retinal Pigment Epithelium

description: <b><i>Background: </i></b>Autophagy is a self-degradative process that is important for balancing sources of energy at critical times in development and in response to nutrient stress. Retinal pigment epithelium (RPE) works as the outer blood retina barrier and is vulnerable to energy stress-induced injury. However, the effect of high glucose treatment on autophagy is still unclear in RPE. <b><i>Methods: </i></b>Transmission electron microscopy was used to detect the generation of autophagosome. Small interfering RNA (siRNA) and MTT was used to determine the effect of autophagy on cell viability. Western blots and immunohistochemistry were used to detect the expression pattern of autophagic markers, including LC3 and p62. <b><i>Results: </i></b>High glucose treatment results in a significant increase in the generation of autophagosome and altered expression of LC3 and p62. High glucose-induced autophagy is independent of mTOR signaling, but is mainly regulated via ROS-mediated ER stress signaling. <b><i>Conclusion: </i></b>In the scenario of high glucose-induced oxidative stress, autophagy may be required for the removal of damaged proteins, and provide a default mechanism to prevent high glucose-induced injury in RPE. © 2014 S. Karger AG, Basel
DOI: 10.6084/m9.figshare.5241568
title: Erratum: Outcome after Introduction of Complete Mesocolic Excision for Colon Cancer Is Similar for Open and Laparoscopic Surgical Treatments

description: <b><i>Background:</i></b> Complete mesocolic excision (CME) and a high (apical) vascular tie may improve oncologic outcome after surgery for colon cancer. Our primary aim was to emulate a previous national result of 73.8% overall survival (OS) with both the open and laparoscopic techniques. <b><i>Methods:</i></b> A prospective study of radical colon cancer was initiated in a Norwegian community teaching hospital in 2007 and comprised a consecutive group of 251 patients with TNM stages I-III that had surgery according to the CME principle. Oncological outcome was assessed as OS, disease-free survival (DFS) and cancer-specific survival (CSS), as well as time to recurrence (TTR), using Cox regression analysis. <b><i>Results:</i></b> In-hospital mortality was 3.6%, 2.3% for laparoscopic surgery and 4.9% for open management. Significantly more patients in the open CME group developed complications in the short term (p &lt; 0.001). Twelve or more lymph nodes were retrieved from 82.9% (208/251) of the specimens. Overall 3-year OS was 84.5%, DFS 77.4%, CSS 91.5% and TTR 86.8%. The surgical approach was not a significant predictor for any of the survival parameters. <b><i>Conclusions:</i></b> There was no survival difference between open and laparoscopic CME colonic resections, and the present OS improved from a previous OS from 2000.
DOI: 10.6084/m9.figshare.5241571
title: Erratum: Linkage of Type 2 Diabetes on Chromosome 9p24 in Mexican Americans: Additional Evidence from the Veterans Administration Genetic Epidemiology Study (VAGES)

description: <b><i>Objective:</i></b> Type 2 diabetes (T2DM) is a complex metabolic disease and is more prevalent in certain ethnic groups such as the Mexican Americans. The goal of our study was to perform a genome-wide linkage (GWL) analysis to localize T2DM susceptibility loci in Mexican Americans. <b><i>Methods:</i></b> We used the phenotypic and genotypic data from 1,122 Mexican-American individuals (307 families) who participated in the Veterans Administration Genetic Epidemiology Study (VAGES). GWL analysis was performed using the variance components approach. Data from 2 additional Mexican-American family studies, the San Antonio Family Heart Study (SAFHS) and the San Antonio Family Diabetes/Gallbladder Study (SAFDGS), were combined with the VAGES data to test for improved linkage evidence. <b><i>Results:</i></b> After adjusting for covariate effects, T2DM was found to be under significant genetic influences (h<sup>2</sup> = 0.62, p = 2.7 × 10<sup>-6</sup>). The strongest evidence for linkage of T2DM occurred between markers D9S1871 and D9S2169 on chromosome 9p24.2-p24.1 (LOD = 1.8). Given that we previously reported suggestive evidence for linkage of T2DM at this region also in SAFDGS, we found the significant and increased linkage evidence (LOD = 4.3, empirical p = 1.0 × 10<sup>-5</sup>, genome-wide p = 1.6 × 10<sup>-3</sup>) for T2DM at the same chromosomal region, when we performed a GWL analysis of the VAGES data combined with the SAFHS and SAFDGS data. <b><i>Conclusion:</i></b> Significant T2DM linkage evidence was found on chromosome 9p24 in Mexican Americans. Importantly, the chromosomal region of interest in this study overlaps with several recent genome-wide association studies involving T2DM-related traits. Given its overlap with such findings and our own initial T2DM association findings in the 9p24 chromosomal region, high throughput sequencing of the linked chromosomal region could identify the potential causal T2DM genes.
DOI: 10.6084/m9.figshare.5241562
title: Erratum: Staphylococcal Protein A, Panton-Valentine Leukocidin and Coagulase Aggravate the Bone Loss and Bone Destruction in Osteomyelitis

description: <b><i>Background/Aims: </i></b>Osteomyelitis is a debilitating infectious disease of the bone which is predominantly caused by <i>Staphylococcus aureus (S. aureus)</i>. The purpose of this study was to investigate the role of the <i>S. aureus </i>virulence factors, <i>i.e. </i>protein A (SpA), Panton-Valentine leukocidin (PVL) and coagulase (Coa) on osteomyelitis. <b><i>Methods: </i></b>The effect of SpA, PVL and Coa on osteoblasts was studied through the following aspects including osteoblast proliferation, apoptosis, bone formation, bone mineralization and RANK-L expression. <i>S. aureus </i>overexpressing PVL, SpA or Coa was constructed and used to study the role of PVL, SpA and Coa, respectively. <i>S. aureus </i>silencing PVL, SpA or Coa was also constructed and used for reversing verification. Osteoblast proliferation was detected by MTT tetrazolium dye reduction assay. Apoptosis was determined by Annexin V-FITC staining. The levels of pro-caspase 3, cleaved-caspase 3, pro-caspase 9 and cleaved-caspase 9 were detected by western blot. Bone formation markers including collagen I, osteopontin and osteocalcin were detected by real time RT-PCR. Alkaline phosphatase activity was measured by adding p-nitrophenyl phosphate as a phosphatase substrate. Von kossa stain and alizarin red stain were applied for determining phosphate and calcium deposition, respectively. The RANK-L expression was tested by ELISA. <b><i>Results: </i></b>PVL, SpA and Coa inhibited osteoblast proliferation, induced osteoblast apotosis, prohibited bone formation and mineralization and upregulated RANK-L expression. <b><i>Conclusions: </i></b>PVL, SpA and Coa play a critical role on bone loss and bone destruction of osteomyelitis.
DOI: 10.6084/m9.figshare.5241565
title: Erratum: Down-Regulation of MiR-30c Promotes the Invasion of Non-Small Cell Lung Cancer by Targeting MTA1

description: <b><i>Background: </i></b>The connection between microRNA expression and lung cancer development has been identified in recent literature. However, the mechanism of microRNA has been poorly elucidated in non-small-cell lung cancer (NSCLC). <b><i>Methods and Results: </i></b>Comparing with adjacent tissues (n=75), miR-30c has a lower expression in lung cancer specimens (n=75). The knockdown of miR-30c enhanced the invasion of A549 cells; meanwhile, the overexpression of miR-30c could reverse the effect of the knockdown of miR-30c <i>in vitro</i>. A luciferase assay revealed that miR-30c was directly bound to the 3‘-untranslated regions (3‘-UTR) of MTA1. QRT-PCR and western blot shows MTA1 was up-regulated in mRNA and protein levels. The effect taken on the invasion of NSCLC by overexpression of MTA1 works the same as down-regulated miR-30c. <b><i>Conclusion: </i></b>miR-30c may play a pivotal role in controlling lung cancer invasion through regulating MTA1in NSCLC.
DOI: 10.6084/m9.figshare.5241556
title: Erratum: Down Syndrome: Genes, Model Systems, and Progress towards Pharmacotherapies and Clinical Trials for Cognitive Deficits

description: Down syndrome (DS) is caused by an extra copy of all or part of the long arm of human chromosome 21 (HSA21). While the complete phenotype is both complex, involving most organs and organ systems, and variable in severity among individuals, intellectual disability (ID) is seen in all people with DS and may have the most significant impact on quality of life. Because the worldwide incidence of DS remains at approximately 1 in 1,000 live births, DS is the most common genetic cause of ID. In recent years, there have been important advances in our understanding of the functions of genes encoded by HSA21 and in the number and utility of in vitro and in vivo systems for modeling DS. Of particular importance, several pharmacological treatments have been shown to rescue learning and memory deficits in one mouse model of DS, the Ts65Dn. Because adult mice were used in the majority of these experiments, there is considerable interest in extending the studies to human clinical trials, and a number of trials have been completed, are in progress or are being planned. A recent conference brought together researchers with a diverse array of expertise and interests to discuss (1) the functions of HSA21 genes with relevance to ID in DS, (2) the utility of model systems including <i>Caenorhabditis elegans</i>, zebrafish and mouse, as well as human neural stem cells and induced pluripotent stems cells, for studies relevant to ID in DS, (3) outcome measures used in pharmacological treatment of mouse models of DS and (4) outcome measures suitable for clinical trials for cognition in adults and children with DS.
DOI: 10.6084/m9.figshare.5241571.v1
title: Erratum: Linkage of Type 2 Diabetes on Chromosome 9p24 in Mexican Americans: Additional Evidence from the Veterans Administration Genetic Epidemiology Study (VAGES)

description: <b><i>Objective:</i></b> Type 2 diabetes (T2DM) is a complex metabolic disease and is more prevalent in certain ethnic groups such as the Mexican Americans. The goal of our study was to perform a genome-wide linkage (GWL) analysis to localize T2DM susceptibility loci in Mexican Americans. <b><i>Methods:</i></b> We used the phenotypic and genotypic data from 1,122 Mexican-American individuals (307 families) who participated in the Veterans Administration Genetic Epidemiology Study (VAGES). GWL analysis was performed using the variance components approach. Data from 2 additional Mexican-American family studies, the San Antonio Family Heart Study (SAFHS) and the San Antonio Family Diabetes/Gallbladder Study (SAFDGS), were combined with the VAGES data to test for improved linkage evidence. <b><i>Results:</i></b> After adjusting for covariate effects, T2DM was found to be under significant genetic influences (h<sup>2</sup> = 0.62, p = 2.7 × 10<sup>-6</sup>). The strongest evidence for linkage of T2DM occurred between markers D9S1871 and D9S2169 on chromosome 9p24.2-p24.1 (LOD = 1.8). Given that we previously reported suggestive evidence for linkage of T2DM at this region also in SAFDGS, we found the significant and increased linkage evidence (LOD = 4.3, empirical p = 1.0 × 10<sup>-5</sup>, genome-wide p = 1.6 × 10<sup>-3</sup>) for T2DM at the same chromosomal region, when we performed a GWL analysis of the VAGES data combined with the SAFHS and SAFDGS data. <b><i>Conclusion:</i></b> Significant T2DM linkage evidence was found on chromosome 9p24 in Mexican Americans. Importantly, the chromosomal region of interest in this study overlaps with several recent genome-wide association studies involving T2DM-related traits. Given its overlap with such findings and our own initial T2DM association findings in the 9p24 chromosomal region, high throughput sequencing of the linked chromosomal region could identify the potential causal T2DM genes.
DOI: 10.17632/csng68c6z3.1
title: Dataset of The Attitude Of Mathematics Education Students Towards Learning Mathematics In Guilin, China

description: Dataset of The Attitude Of Mathematics Education Students Towards Learning Mathematics In Guilin, China
DOI: 10.6084/m9.figshare.5241568.v1
title: Erratum: Outcome after Introduction of Complete Mesocolic Excision for Colon Cancer Is Similar for Open and Laparoscopic Surgical Treatments

description: <b><i>Background:</i></b> Complete mesocolic excision (CME) and a high (apical) vascular tie may improve oncologic outcome after surgery for colon cancer. Our primary aim was to emulate a previous national result of 73.8% overall survival (OS) with both the open and laparoscopic techniques. <b><i>Methods:</i></b> A prospective study of radical colon cancer was initiated in a Norwegian community teaching hospital in 2007 and comprised a consecutive group of 251 patients with TNM stages I-III that had surgery according to the CME principle. Oncological outcome was assessed as OS, disease-free survival (DFS) and cancer-specific survival (CSS), as well as time to recurrence (TTR), using Cox regression analysis. <b><i>Results:</i></b> In-hospital mortality was 3.6%, 2.3% for laparoscopic surgery and 4.9% for open management. Significantly more patients in the open CME group developed complications in the short term (p &lt; 0.001). Twelve or more lymph nodes were retrieved from 82.9% (208/251) of the specimens. Overall 3-year OS was 84.5%, DFS 77.4%, CSS 91.5% and TTR 86.8%. The surgical approach was not a significant predictor for any of the survival parameters. <b><i>Conclusions:</i></b> There was no survival difference between open and laparoscopic CME colonic resections, and the present OS improved from a previous OS from 2000.
DOI: 10.6084/m9.figshare.5241544
title: Erratum: Safety, Tolerability and Pharmacokinetics of MCI-186 in Patients with Acute Ischemic Stroke: New Formulation and Dosing Regimen

description: <b><i>Background and Purpose:</i></b> MCI-186 (edaravone) is a free radical scavenger approved in Japan since 2001 for the treatment of patients with acute ischemic stroke within 24 h from the onset of symptoms. It was recommended by the Japanese Guidelines for the Management of Stroke 2004. Our aim was to investigate the safety, tolerability and pharmacokinetics of a new formulation and dose regimen (intravenous bolus plus infusion) of MCI-186 suitable for the treatment of acute ischemic stroke in Europe because the Japanese treatment protocol includes twice-a-day intravenous infusion of MCI-186 for a maximum of 14 days. Such a treatment protocol is not very practical in Europe, where hospital stay is much shorter in acute hospitals. <b><i>Methods:</i></b> In a double-blind, placebo-controlled randomized clinical trial we studied two dosing regimens, each in a cohort of 18 patients. Patients were randomized in a 2:1 ratio in both cohorts to receive MCI-186 or placebo. Review of safety and plasma concentration data from the first cohort (loading dose 0.08 mg/kg + 0.2 mg/kg/h infusion) preceded the second cohort (loading dose 0.16 mg/kg + 0.4 mg/kg/h infusion). Safety parameters included adverse events, severe adverse events, physical examinations, local reactions at infusion site, ECG, clinical chemistry and hematology, modified Total Neuropathy Score and CT scans. <b><i>Results:</i></b> Mean age and National Institutes of Health Stroke Scale (NIHSS) score on admission of patients in cohorts 1 and 2 and the placebo group were 64, 63, and 69 years and 5, 5, and 6, respectively. The number of treatment emergent adverse events that occurred was 109, most of which were transient, mild or moderate. Both doses of the new formulation and dosing regimen were well tolerated. After the initiation of the infusion, plasma concentrations of MCI-186 reached or exceeded prespecified target levels within 24 h in both MCI-186 cohorts, which were in the putative therapeutic range in humans. Geometric mean values of MCI-186 plasma concentration at the end of the infusion in cohorts 1 and 2 were 391 and 1,595 ng/ml, respectively. <b><i>Conclusions:</i></b> The primary objective of the present study, safety and tolerability of the new formulation and dosing regimen, was achieved. The new formula and both dosing regimens were well tolerated and achieved intended plasma concentrations suitable for larger safety studies before pivotal trials.
DOI: 10.6084/m9.figshare.5241547
title: Erratum: Niflumic Acid Reduces Histamine-Induced Interleukin-6 and -8 Expression in Human Conjunctival Epithelial Cells

description: <b><i>Background/Aims:</i></b> Histamine remains the main mediator of allergic conjunctivitis and induces interleukin (IL)-6 and IL-8 production in human conjunctival epithelial cells (HCEC). The purpose of the present study was to determine whether histamine induced IL-6 and IL-8 expression in HCEC, and to describe the relationship between human calcium-activated chloride channel (hCLCA) 1 activity and IL-6 and IL-8 expression. <b><i>Methods:</i></b> HCEC were isolated from human conjunctiva and cultured at an air-liquid interface. <i>IL-6</i> and <i>IL-8</i> mRNA expression was examined by real-time PCR, and IL-6 and IL-8 secretion was measured by ELISA after stimulation of HCEC with histamine. <b><i>Results:</i></b> Histamine upregulated <i>IL-6</i> and <i>IL-8</i> expression and IL-6 and IL-8 secretion in a dose-dependent manner in HCEC. Niflumic acid (NFA), an hCLCA blocker, reduced histamine-induced IL-6 and IL-8 expression. <b><i>Conclusion:</i></b> Histamine-induced IL-6 and IL-8 production could be attenuated by NFA, an hCLCA blocker.
DOI: 10.6084/m9.figshare.5241550
title: Erratum: Stress Impairs Synaptic Plasticity in Triple-Transgenic Alzheimer's Disease Mice: Rescue by Ryanodine

description: <b><i>Background:</i></b> A possible contributing factor to the development of cognitive deficits in Alzheimer's disease (AD) patients involves the exposure to early life stress. <b><i>Objective:</i></b> We explored the impact of stress on synaptic plasticity (long-term potentiation, LTP) of 6-month-old triple-transgenic mice (3×Tg-AD). <b><i>Methods:</i></b> 3×Tg-AD and control (NonTg) mice were exposed to three stressors at the age of 2 and 4 months. Excitatory postsynaptic potentials were recorded in the stratum radiatum of the CA1 region of hippocampal slices, in a two-pathway paradigm. <b><i>Results:</i></b> Slices taken from 3×Tg-AD mice exhibited significant deficits in LTP compared with NonTg slices. Early stress led to a further decrease in LTP in these mice, while it did not affect NonTg mice. LTP in 3×Tg-AD and stressed 3×Tg-AD mice was rescued by pre-exposure to 0.2 µM ryanodine. In an attempt to find a molecular correlate for the effects of stress in the 3×Tg-AD mice, we found that stressed mice have an altered ratio of Aβ42/40 both in the cortex and hippocampus. <b><i>Conclusions:</i></b> Stress experiences in young adults may accelerate the cognitive loss in AD mice, adding another dimension to the plethora of factors that lead to AD.
DOI: 10.6084/m9.figshare.5241541
title: Erratum: Role of the Cathelicidin-Related Antimicrobial Peptide in Inflammation and Mortality in a Mouse Model of Bacterial Meningitis

description: Antimicrobial peptides (AP) are important components of the innate immune system, yet little is known about their expression and function in the brain. Our previous work revealed upregulated gene expression of cathelicidin-related AP (CRAMP) following bacterial meningitis in primary rat glial cells as well as bactericidal activity against frequent meningitis-causing bacteria. However, the effect of cathelicidin expression on the progression of inflammation and mortality in bacterial meningitis remains unknown. Therefore, we used CRAMP-deficient mice to investigate the effect of CRAMP on bacterial growth, inflammatory responses and mortality in meningitis. Meningitis was induced by intracerebral injection of type 3 <i>Streptococcus pneumoniae</i>. The degree of inflammation was analyzed in various brain regions by means of immunohistochemistry and real-time RT-PCR. CRAMP deficiency led to a higher mortality rate that was associated with increased bacterial titers in the cerebellum, blood and spleen as well as decreased meningeal neutrophil infiltration. CRAMP-deficient mice displayed a higher degree of glial cell activation that was accompanied by a more pronounced proinflammatory response. Taken together, this work provides insight into the important role of CRAMP as part of the innate immune defense against pathogens in bacterial CNS infections. © 2013 S. Karger AG, Basel
DOI: 10.6084/m9.figshare.5241550.v1
title: Erratum: Stress Impairs Synaptic Plasticity in Triple-Transgenic Alzheimer's Disease Mice: Rescue by Ryanodine

description: <b><i>Background:</i></b> A possible contributing factor to the development of cognitive deficits in Alzheimer's disease (AD) patients involves the exposure to early life stress. <b><i>Objective:</i></b> We explored the impact of stress on synaptic plasticity (long-term potentiation, LTP) of 6-month-old triple-transgenic mice (3×Tg-AD). <b><i>Methods:</i></b> 3×Tg-AD and control (NonTg) mice were exposed to three stressors at the age of 2 and 4 months. Excitatory postsynaptic potentials were recorded in the stratum radiatum of the CA1 region of hippocampal slices, in a two-pathway paradigm. <b><i>Results:</i></b> Slices taken from 3×Tg-AD mice exhibited significant deficits in LTP compared with NonTg slices. Early stress led to a further decrease in LTP in these mice, while it did not affect NonTg mice. LTP in 3×Tg-AD and stressed 3×Tg-AD mice was rescued by pre-exposure to 0.2 µM ryanodine. In an attempt to find a molecular correlate for the effects of stress in the 3×Tg-AD mice, we found that stressed mice have an altered ratio of Aβ42/40 both in the cortex and hippocampus. <b><i>Conclusions:</i></b> Stress experiences in young adults may accelerate the cognitive loss in AD mice, adding another dimension to the plethora of factors that lead to AD.
DOI: 10.6084/m9.figshare.5241547.v1
title: Erratum: Niflumic Acid Reduces Histamine-Induced Interleukin-6 and -8 Expression in Human Conjunctival Epithelial Cells

description: <b><i>Background/Aims:</i></b> Histamine remains the main mediator of allergic conjunctivitis and induces interleukin (IL)-6 and IL-8 production in human conjunctival epithelial cells (HCEC). The purpose of the present study was to determine whether histamine induced IL-6 and IL-8 expression in HCEC, and to describe the relationship between human calcium-activated chloride channel (hCLCA) 1 activity and IL-6 and IL-8 expression. <b><i>Methods:</i></b> HCEC were isolated from human conjunctiva and cultured at an air-liquid interface. <i>IL-6</i> and <i>IL-8</i> mRNA expression was examined by real-time PCR, and IL-6 and IL-8 secretion was measured by ELISA after stimulation of HCEC with histamine. <b><i>Results:</i></b> Histamine upregulated <i>IL-6</i> and <i>IL-8</i> expression and IL-6 and IL-8 secretion in a dose-dependent manner in HCEC. Niflumic acid (NFA), an hCLCA blocker, reduced histamine-induced IL-6 and IL-8 expression. <b><i>Conclusion:</i></b> Histamine-induced IL-6 and IL-8 production could be attenuated by NFA, an hCLCA blocker.