cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.4056504.v1
title: Supplementary Material for: Paricalcitol, Microvascular and Endothelial Function in Non-Diabetic Chronic Kidney Disease: A Randomized Trial

description: <br><strong><em>Background:</em></strong> Vitamin D deficiency, sympathetic activation and endothelial dysfunction are associated with increased cardiovascular risk in patients with chronic kidney disease (CKD). Studies have so far failed to establish the role of vitamin D and vitamin D receptor activator (VDRA) treatment in moderate CKD. This trial was designed to assess whether VDRA treatment can ameliorate sympathetic activation and macro- and microvascular dysfunction in non-diabetic patients with moderate CKD. <b><i>Methods:</i></b> We conducted a randomized controlled double-blind trial using placebo, 1 or 2 μg of paricalcitol, a VDRA, for 3 months. We assessed muscle sympathetic nerve activity (MSNA) by microneurography, pulse wave velocity (PWV) by tonometry, flow mediated vasodilatation (FMD) by brachial ultrasound, skin microcirculation assessed by iontophoresis and capillary blood velocity (CBV) by videophotometric capillaroscopy. <b><i>Results:</i></b> Thirty-six patients with a mean age of 65 years and mean estimated glomerular filtration rate of 40 ml/min/1.73 m<sup>2</sup> were included. We found a significant decline in endothelial function after 3 months, except in the group receiving 2 μg of paricalcitol. The higher dose (2 μg) seemed to attenuate the decline in microvascular endothelial function, assessed by iontophoresis of acetylcholine (p = 0.06 for all groups, p = 0.65 for the 2 μg group) and for FMD (p = 0.006 for all groups, p = 0.54 for the 2 μg group). We found a borderline significance (p = 0.05) for improved CBV in the treated groups. We found no significant changes between treatments in MSNA, PWV or albuminuria. <b><i>Conclusions:</i></b> Endothelial function declined significantly over 3 months in patients with moderate CKD, and this decline could be ameliorated by VDRA treatment (NCT01204528).
DOI: 10.6084/m9.figshare.4056510
title: Supplementary Material for: Common Genotypes of Long QT Syndrome in China and the Role of ECG Prediction

description: <br><strong><em>Objectives:</em></strong> Genetic testing, a gold standard for long QT syndrome (LQTS) diagnosis, is time-consuming and costly when all the 15 candidate genes are screened. Since genotype-specific ECG patterns are present in most LQT1-3 mutation carriers, we tested the utility of ECG-guided genotyping in a large cohort of Chinese LQTS patients. <b><i>Methods and Results:</i></b> We enrolled 230 patients (26 ± 17 years, 66% female) with a clinical diagnosis of LQTS. Genotypes were predicted as LQT1-3 based on the presence of ECG patterns typical for each genotype in 200 patients (85 LQT1, 110 LQT2 and 5 LQT3). Family-based genotype prediction was also conducted if gene-specific ECG patterns were found in other affected family members. Mutational screening identified 104 mutations (44% novel), i.e. 46 <i>KCNQ1,</i> 54 <i>KCNH2</i> and 4 <i>SCN5A </i>mutations. The overall predictive accuracy of ECG-guided genotyping was 79% (157/200) and 79% (67/85), 78% (86/110) and 80% (4/5) for LQT1, LQT2 and LQT3, respectively. The predictive accuracy was 98% (42/43) when family-based ECG assessment was performed. <b><i>Conclusions:</i></b> From this large-scale genotyping study, we found that LQT2 is the most common genotype among the Chinese. Family-based ECG-guided genotyping is highly accurate. ECG-guided genotyping is time- and cost-effective. We therefore recommend it as an optimal approach for the genetic diagnosis of LQTS.
DOI: 10.7910/dvn/v1rjpf/otxsfl
title: blc20151221_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4056498
title: Supplementary Material for: Intervention Associated Acute Kidney Injury and Long-Term Cardiovascular Outcomes

description: <br><strong><em>Background:</em></strong> Acute kidney injury (AKI) has been associated with all-cause short- and long-term mortality. However, its association with cardiovascular (CV) events remains unclear. We sought to investigate this in patients undergoing open (OAR) or endovascular (EVAR) abdominal aortic aneurysm repair, as they are likely to develop both AKI and CV morbidity. A meta-analysis was subsequently performed to confirm this in other CV-interventions. <b><i>Methods:</i></b> AKI-incidence was assessed in a multicentre-cohort of 1,068 patients undergoing EVAR (947 individuals) or OAR electively using the ‘Acute Kidney Injury Network' criteria. A composite-endpoint was used, consisting of non-fatal myocardial infarction (MI), stroke, vascular event, hospitalisation due to heart failure and CV death. A systematic literature review identified studies reporting AKI-incidence and CV events. Risk ratios (RRs) at 1 and 5 years were combined using meta-analysis. <b><i>Results:</i></b> During a median follow-up of 62 months (range 11-121), AKI was associated with CV events on adjusted (for CV risk-factors) analyses (Incidence 36% of EVAR, 32% of OAR patients; hazard ratio 1.73, 95% CI 1.06-3.39, p = 0.03) for the overall population. In the meta-analysis, 7 studies reported incidence of MI on 23,936 patients 1-year after coronary intervention (PCI) with a pooled RR of 1.76 (95% CI 1.45-2.83, p &lt; 0.001); at 2 years, 3 studies reported MI incidence on 17,773 patients after PCI with a pooled RR of 1.34 (95% CI 1.10-1.63, p = 0.003). MI-incidence was reported 5 years after cardiac surgery by 3 studies (33,701 patients) with a pooled RR of 1.60 (95% CI 1.43-1.81). <b><i>Conclusion:</i></b> AKI is associated with long-term CV events after surgery or endovascular intervention.
DOI: 10.7910/dvn/v1rjpf/dchrpm
title: blc20150415_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4056498.v1
title: Supplementary Material for: Intervention Associated Acute Kidney Injury and Long-Term Cardiovascular Outcomes

description: <br><strong><em>Background:</em></strong> Acute kidney injury (AKI) has been associated with all-cause short- and long-term mortality. However, its association with cardiovascular (CV) events remains unclear. We sought to investigate this in patients undergoing open (OAR) or endovascular (EVAR) abdominal aortic aneurysm repair, as they are likely to develop both AKI and CV morbidity. A meta-analysis was subsequently performed to confirm this in other CV-interventions. <b><i>Methods:</i></b> AKI-incidence was assessed in a multicentre-cohort of 1,068 patients undergoing EVAR (947 individuals) or OAR electively using the ‘Acute Kidney Injury Network' criteria. A composite-endpoint was used, consisting of non-fatal myocardial infarction (MI), stroke, vascular event, hospitalisation due to heart failure and CV death. A systematic literature review identified studies reporting AKI-incidence and CV events. Risk ratios (RRs) at 1 and 5 years were combined using meta-analysis. <b><i>Results:</i></b> During a median follow-up of 62 months (range 11-121), AKI was associated with CV events on adjusted (for CV risk-factors) analyses (Incidence 36% of EVAR, 32% of OAR patients; hazard ratio 1.73, 95% CI 1.06-3.39, p = 0.03) for the overall population. In the meta-analysis, 7 studies reported incidence of MI on 23,936 patients 1-year after coronary intervention (PCI) with a pooled RR of 1.76 (95% CI 1.45-2.83, p &lt; 0.001); at 2 years, 3 studies reported MI incidence on 17,773 patients after PCI with a pooled RR of 1.34 (95% CI 1.10-1.63, p = 0.003). MI-incidence was reported 5 years after cardiac surgery by 3 studies (33,701 patients) with a pooled RR of 1.60 (95% CI 1.43-1.81). <b><i>Conclusion:</i></b> AKI is associated with long-term CV events after surgery or endovascular intervention.
DOI: 10.7910/dvn/v1rjpf/xfqldl
title: blc20151116_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4056486
title: Supplementary Material for: Association Analysis of the Reticulon 1 Gene in End-Stage Kidney Disease

description: <br><strong><em>Background:</em></strong> The reticulon 1 gene <i>(RTN1)</i> encodes reticulons, endoplasmic reticulum stress proteins recently implicated in kidney disease progression. <b><i>Methods:</i></b><i>RTN1</i> single nucleotide polymorphisms (SNPs) were tested for association with type 2 diabetes (T2D)-associated end-stage kidney disease (ESKD) in African Americans (AAs) and European Americans (EAs), and AAs with non-diabetic ESKD. <i>RTN1</i> SNPs that were associated with T2D-ESKD in AA cases compared to non-nephropathy controls were identified from a discovery genome-wide association study (n = 1,797), then tested for replication in 1,847 additional AA T2D-ESKD cases and controls. <b><i>Results:</i></b> Three intronic <i>RTN1</i> variants were nominally associated with T2D-ESKD in both discovery and replication analyses: rs1952034, rs12431381 and rs12434215 (additive models); combined T2D-ESKD (discovery + replication) p values were 0.015-3.0 × 10<sup>-4</sup> (ORs 0.67-0.77; minor alleles protective). In addition, rs12434215 was weakly associated with T2D-ESKD in 557 EA T2D-ESKD cases contrasted with 753 EA non-nephropathy controls (p = 0.019; OR 0.69, dominant model). Nominal association extended to non-diabetic causes of ESKD in 1,459 additional AA cases (rs12431381 and rs12434215 p values 0.014-0.015; OR 0.77). An all-cause ESKD association analysis contrasted the 3,594 AA ESKD cases with 1,489 AA non-nephropathy controls and detected association with rs12434215 (p = 6.7 × 10<sup>-4</sup>, OR 0.73) and rs12431381 (p = 7.5 × 10<sup>-4</sup>, OR 0.75) in dominant models. Of the 3 SNPs, only rs12434215 was weakly associated with T2D per se when contrasting T2D non-nephropathy cases with non-diabetic controls (additive model p = 0.032 AAs; p = 0.048 EAs). <b><i>Conclusions:</i></b> These results suggest evidence of genetic association between common variants in <i>RTN1</i> and ESKD in AAs and EAs.
DOI: 10.6084/m9.figshare.4056483
title: Experimental data

description: Positions of pedestrians over time.<br>
DOI: 10.6084/m9.figshare.4056486.v1
title: Supplementary Material for: Association Analysis of the Reticulon 1 Gene in End-Stage Kidney Disease

description: <br><strong><em>Background:</em></strong> The reticulon 1 gene <i>(RTN1)</i> encodes reticulons, endoplasmic reticulum stress proteins recently implicated in kidney disease progression. <b><i>Methods:</i></b><i>RTN1</i> single nucleotide polymorphisms (SNPs) were tested for association with type 2 diabetes (T2D)-associated end-stage kidney disease (ESKD) in African Americans (AAs) and European Americans (EAs), and AAs with non-diabetic ESKD. <i>RTN1</i> SNPs that were associated with T2D-ESKD in AA cases compared to non-nephropathy controls were identified from a discovery genome-wide association study (n = 1,797), then tested for replication in 1,847 additional AA T2D-ESKD cases and controls. <b><i>Results:</i></b> Three intronic <i>RTN1</i> variants were nominally associated with T2D-ESKD in both discovery and replication analyses: rs1952034, rs12431381 and rs12434215 (additive models); combined T2D-ESKD (discovery + replication) p values were 0.015-3.0 × 10<sup>-4</sup> (ORs 0.67-0.77; minor alleles protective). In addition, rs12434215 was weakly associated with T2D-ESKD in 557 EA T2D-ESKD cases contrasted with 753 EA non-nephropathy controls (p = 0.019; OR 0.69, dominant model). Nominal association extended to non-diabetic causes of ESKD in 1,459 additional AA cases (rs12431381 and rs12434215 p values 0.014-0.015; OR 0.77). An all-cause ESKD association analysis contrasted the 3,594 AA ESKD cases with 1,489 AA non-nephropathy controls and detected association with rs12434215 (p = 6.7 × 10<sup>-4</sup>, OR 0.73) and rs12431381 (p = 7.5 × 10<sup>-4</sup>, OR 0.75) in dominant models. Of the 3 SNPs, only rs12434215 was weakly associated with T2D per se when contrasting T2D non-nephropathy cases with non-diabetic controls (additive model p = 0.032 AAs; p = 0.048 EAs). <b><i>Conclusions:</i></b> These results suggest evidence of genetic association between common variants in <i>RTN1</i> and ESKD in AAs and EAs.
DOI: 10.7910/dvn/v1rjpf/ypajvr
title: blc20150405_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4056483.v1
title: Experimental data

description: Positions of pedestrians over time.<br>
DOI: 10.7910/dvn/v1rjpf/ykcptj
title: blc20150504_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/cfgthq
title: blc20150226_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4056441
title: Relationship between cortical myeloarchitecture and electrophysiological networks

description: Supplementary Data to http://www.pnas.org/content/early/2016/11/07/1608587113.abstract.<br>Please find adjacency matrices for individual MEG frequency bands (AAL atlas regions) and a structural-covariance matrix of cortical myeloarchitecture measured using magnetisation transfer at 7T MRI. <br>For further information please contact Benjamin.Hunt@sickkids.ca
DOI: 10.7910/dvn/v1rjpf/ql5k3j
title: blc20150827_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/ijeyua
title: blc20151120_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/gmlfe1
title: blc20150802_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/xvcgtu
title: blc20150711_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/yzv8t3
title: blc20150402_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/gwmjt5
title: blc20150323_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/mzn4e4
title: blc20150306_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/f9l25h
title: blc20150209_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4056402
title: Estimating the size and number of autophagic bodies by electron microscopy

description: Much recent and ongoing research is focused on understanding the mechanisms and regulation of autophagy, a cellular self-degradation pathway with many links to human health. Although many assays exist to measure the total magnitude of autophagy, electron microscopy remains the tool of choice for the determination of the size and the number of autophagosomes formed in a given mutant or under given induction conditions. Here we present a detailed protocol for measuring autophagic bodies in the yeast <i>Saccharomyces cerevisiae</i> by electron microscopy. Furthermore, we present an improved mathematical method for estimating body size and a new method for estimating body number. Finally, we include a discussion of the merits and limitations of these methods and an example of their application to autophagic bodies formed in the <i>ume6∆</i> strain.
DOI: 10.6084/m9.figshare.4056402.v1
title: Estimating the size and number of autophagic bodies by electron microscopy

description: Much recent and ongoing research is focused on understanding the mechanisms and regulation of autophagy, a cellular self-degradation pathway with many links to human health. Although many assays exist to measure the total magnitude of autophagy, electron microscopy remains the tool of choice for the determination of the size and the number of autophagosomes formed in a given mutant or under given induction conditions. Here we present a detailed protocol for measuring autophagic bodies in the yeast <i>Saccharomyces cerevisiae</i> by electron microscopy. Furthermore, we present an improved mathematical method for estimating body size and a new method for estimating body number. Finally, we include a discussion of the merits and limitations of these methods and an example of their application to autophagic bodies formed in the <i>ume6∆</i> strain.
DOI: 10.7910/dvn/v1rjpf/t8sdhp
title: blc20150112_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4056399
title: The multifunctional autophagy pathway in the human malaria parasite, <i>Plasmodium falciparum</i>

description: Autophagy is a catabolic pathway typically induced by nutrient starvation to recycle amino acids, but can also function in removing damaged organelles. In addition, this pathway plays a key role in eukaryotic development. To date, not much is known about the role of autophagy in apicomplexan parasites and more specifically in the human malaria parasite <i>Plasmodium falciparum</i>. Comparative genomic analysis has uncovered some, but not all, orthologs of autophagy-related (<i>ATG</i>) genes in the malaria parasite genome. Here, using a genome-wide in silico analysis, we confirmed that <i>ATG</i> genes whose products are required for vesicle expansion and completion are present, while genes involved in induction of autophagy and cargo packaging are mostly absent. We subsequently focused on the molecular and cellular function of <i>P. falciparum</i> ATG8 (PfATG8), an autophagosome membrane marker and key component of the autophagy pathway, throughout the parasite asexual and sexual erythrocytic stages. In this context, we showed that PfATG8 has a distinct and atypical role in parasite development. PfATG8 localized in the apicoplast and in vesicles throughout the cytosol during parasite development. Immunofluorescence assays of PfATG8 in apicoplast-minus parasites suggest that PfATG8 is involved in apicoplast biogenesis. Furthermore, treatment of parasite cultures with bafilomycin A<sub>1</sub> and chloroquine, both lysosomotropic agents that inhibit autophagosome and lysosome fusion, resulted in dramatic morphological changes of the apicoplast, and parasite death. Furthermore, deep proteomic analysis of components associated with PfATG8 indicated that it may possibly be involved in ribophagy and piecemeal microautophagy of the nucleus. Collectively, our data revealed the importance and specificity of the autophagy pathway in the malaria parasite and offer potential novel therapeutic strategies.
DOI: 10.6084/m9.figshare.4056399.v1
title: The multifunctional autophagy pathway in the human malaria parasite, <i>Plasmodium falciparum</i>

description: Autophagy is a catabolic pathway typically induced by nutrient starvation to recycle amino acids, but can also function in removing damaged organelles. In addition, this pathway plays a key role in eukaryotic development. To date, not much is known about the role of autophagy in apicomplexan parasites and more specifically in the human malaria parasite <i>Plasmodium falciparum</i>. Comparative genomic analysis has uncovered some, but not all, orthologs of autophagy-related (<i>ATG</i>) genes in the malaria parasite genome. Here, using a genome-wide in silico analysis, we confirmed that <i>ATG</i> genes whose products are required for vesicle expansion and completion are present, while genes involved in induction of autophagy and cargo packaging are mostly absent. We subsequently focused on the molecular and cellular function of <i>P. falciparum</i> ATG8 (PfATG8), an autophagosome membrane marker and key component of the autophagy pathway, throughout the parasite asexual and sexual erythrocytic stages. In this context, we showed that PfATG8 has a distinct and atypical role in parasite development. PfATG8 localized in the apicoplast and in vesicles throughout the cytosol during parasite development. Immunofluorescence assays of PfATG8 in apicoplast-minus parasites suggest that PfATG8 is involved in apicoplast biogenesis. Furthermore, treatment of parasite cultures with bafilomycin A<sub>1</sub> and chloroquine, both lysosomotropic agents that inhibit autophagosome and lysosome fusion, resulted in dramatic morphological changes of the apicoplast, and parasite death. Furthermore, deep proteomic analysis of components associated with PfATG8 indicated that it may possibly be involved in ribophagy and piecemeal microautophagy of the nucleus. Collectively, our data revealed the importance and specificity of the autophagy pathway in the malaria parasite and offer potential novel therapeutic strategies.
DOI: 10.7910/dvn/v1rjpf/ghgiu6
title: blc20150427_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/ht2utj
title: blc20150530_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/jmx3os
title: blc20151103_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/bvhhce
title: blc20150703_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/usofvd
title: blc20150210_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/c1djo7
title: blc20150125_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4056345
title: Glory Hole cave (Yarrangobilly, Australia) drip water monitoring

description: This dataset is analysed and reported in the paper:<br><br>Coleborn, K., Rau, G. C., Cuthbert, M. O., Baker, A., and Navarre, O.: Solar forced diurnal regulation of cave drip rates via phreatophyte evapotranspiration, Hydrol. Earth Syst. Sci. Discuss., doi:10.5194/hess-2016-11, in review, 2016.
DOI: 10.7910/dvn/v1rjpf/irbht3
title: blc20150403_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/cltqgy
title: blc20150316_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4056345.v1
title: climate data

description: his dataset was monitored at Yarrangobilly caves in Australia. It has been analysed and published in "Solar-forced diurnal regulation of cave drip rates via phreatophyte evapotranspiration" in Hydrology and Earth System Sciences<br>
DOI: 10.7910/dvn/v1rjpf/wxulce
title: blc20150408_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/flgbbd
title: blc20150627_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4056345.v2
title: Yarrangobilly Caves drip water monitoring

description: This dataset is the one that's analysed and reported in the paper:<br><br>Coleborn, K., Rau, G. C., Cuthbert, M. O., Baker, A., and Navarre, O.: Solar forced diurnal regulation of cave drip rates via phreatophyte evapotranspiration, Hydrol. Earth Syst. Sci. Discuss., doi:10.5194/hess-2016-11, in review, 2016.
DOI: 10.6084/m9.figshare.4056345.v3
title: Yarrangobilly Caves drip water monitoring

description: This dataset is analysed and reported in the paper:<br><br>Coleborn, K., Rau, G. C., Cuthbert, M. O., Baker, A., and Navarre, O.: Solar forced diurnal regulation of cave drip rates via phreatophyte evapotranspiration, Hydrol. Earth Syst. Sci. Discuss., doi:10.5194/hess-2016-11, in review, 2016.
DOI: 10.7910/dvn/v1rjpf/awjdkk
title: blc20151106_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/jkpswu
title: blc20150114_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/smxrj4
title: blc20150928_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/dimwu7
title: blc20150913_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/oyrtis
title: blc20151113_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/gmnzgk
title: blc20150309_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/4h8ipi
title: blc20151013_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/hfy0ph
title: blc20150630_03.txt.gz

description: :unav