cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.5469427.v1
title: Aetiology of stemphylium blight on lentil in Canada

description: Field isolates of <i>Stemphylium</i> spp. collected from lentil and nine other western Canadian crops were compared to the ex-type isolate of <i>Stemphylium botryosum</i> by morphology and by molecular phylogenetic analysis based on the internal transcribed spacer (ITS) and the <i>glyceraldehyde-3-phosphate dehydrogenase</i> gene regions. Sequence data of these genes for six other <i>Stemphylium</i> spp. obtained from GenBank were also included in the phylogenetic analysis. Morphology of colonies and morphometry of conidia agreed with previous descriptions of <i>S. botryosum</i>, but did not correlate with the clustering observed in the phylogenetic analysis. Sequence data revealed that <i>S. botryosum</i> is one of probably two <i>Stemphylium</i> spp. involved in the development of stemphylium blight on Canadian lentil, and is associated with other hosts such as faba bean, soybean, bean, pea, alfalfa, coriander, caraway and fenugreek. More than one validly described <i>Stemphylium</i> sp. was associated with the second cluster of isolates causing stemphylium blight, indicating that an extensive taxonomic review of the genus <i>Stemphylium</i> is required before this second stemphylium blight pathogen can be identified by name.
DOI: 10.6084/m9.figshare.5469343
title: REFSQ18-StudyResults

description: Study Results to our REFSQ18 paper
DOI: 10.6084/m9.figshare.5469325
title: Oxford Health NHS Foundation Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5469316
title: Gut microbiomes and reproductive isolation in Drosophila.

description: <b>In Drosophilids, the microbiome is reported as flexible and largely environmentally-determined. Therefore, RI would be transient and break down under dietary variation. In the absence of co-association between host and microbiome, there are also no advantages for the gut bacteria or host in effecting RI. To explore these puzzling effects and their mechanisms further, we repeated the tests for RI associated with diet-specific gut microbiomes in <i>D. melanogaster </i>found in Sharon et al 2011. Despite observing differences in the gut microbiomes in flies maintained on different diets, we found no evidence for diet-associated RI or for any role of gut bacteria, or for <i>L. plantarum </i>specifically<i>.</i> The results suggest that there is no general role for gut bacteria in driving the evolution of RI in this species and hence resolve this evolutionary riddle.</b>
DOI: 10.6084/m9.figshare.5469325.v1
title: Oxford Health NHS Foundation Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5469316.v1
title: Gut microbiomes and reproductive isolation in Drosophila.

description: <b>In Drosophilids, the microbiome is reported as flexible and largely environmentally-determined. Therefore, RI would be transient and break down under dietary variation. In the absence of co-association between host and microbiome, there are also no advantages for the gut bacteria or host in effecting RI. To explore these puzzling effects and their mechanisms further, we repeated the tests for RI associated with diet-specific gut microbiomes in <i>D. melanogaster </i>found in Sharon et al 2011. Despite observing differences in the gut microbiomes in flies maintained on different diets, we found no evidence for diet-associated RI or for any role of gut bacteria, or for <i>L. plantarum </i>specifically<i>.</i> The results suggest that there is no general role for gut bacteria in driving the evolution of RI in this species and hence resolve this evolutionary riddle.</b>
DOI: 10.6084/m9.figshare.5469292
title: GSBC2017 conference

description: poster for GSBC 2017 conference, China
DOI: 10.6084/m9.figshare.5469292.v1
title: GSBC2017 conference

description: poster for GSBC 2017 conference, China
DOI: 10.6084/m9.figshare.5469316.v2
title: Gut microbiomes and reproductive isolation in Drosophila.

description: <b>In Drosophilids, the microbiome is reported as flexible and largely environmentally-determined. Therefore, RI would be transient and break down under dietary variation. In the absence of co-association between host and microbiome, there are also no advantages for the gut bacteria or host in effecting RI. To explore these puzzling effects and their mechanisms further, we repeated the tests for RI associated with diet-specific gut microbiomes in <i>D. melanogaster </i>found in Sharon et al 2011. Despite observing differences in the gut microbiomes in flies maintained on different diets, we found no evidence for diet-associated RI or for any role of gut bacteria, or for <i>L. plantarum </i>specifically<i>.</i> The results suggest that there is no general role for gut bacteria in driving the evolution of RI in this species and hence resolve this evolutionary riddle.</b>
DOI: 10.6084/m9.figshare.5469142
title: Lazzaro_et_al_2017_All_data_DEF_prot.xlsx

description: Dataset used in: Lazzaro L, Mazza G, d'Errico G, Fabiani A, Giuliani C, Inghilesi AF., Lagomarsino A, Landi S, Lastrucci L, Pastorelli R, Roversi PF, Torrini G, Tricarico E, Foggi B [Accepted] How ecosystems change following invasion by Robinia pseudoacacia: insights from soil chemical properties and soil microbial, nematode, microarthropod and plant communities. Science of The Total Environment (in press).
DOI: 10.6084/m9.figshare.5469115
title: Supplementary Material for: Autosomal Dominant Polycystic Kidney Disease: Prevalence of Renal Neoplasias in Surgical Kidney Specimens

description: <b><i>Background:</i></b> The role of autosomal dominant polycystic kidney disease (ADPKD) as a risk factor for renal cell carcinoma (RCC) is still under discussion. Data on prevalence of RCC in ADPKD are limited, especially on a large population scale. The aim of this study was to analyze the prevalence of RCC in ADPKD kidneys and characterize the clinical features of this coincidence. <b><i>Methods:</i></b> Based on our histopathological registry for ADPKD and the Else Kröner-Fresenius Registry, we retrospectively reviewed malignant and benign renal lesions in patients with ADPKD who had undergone renal surgery from 1988 to 2011. <b><i>Results:</i></b> 240 ADPKD patients underwent 301 renal surgeries. Mean age at surgery was 54 years. Overall, 16 malignant and 11 benign lesions were analyzed in 301 kidneys (5.3%; 3.7%), meaning that 12/240 (5%; 1:20) patients presented with malignant renal lesions. 66.7% (8/12) of these patients had undergone dialysis prior to surgery. We found 10/16 (63%) papillary RCC, 5/16 (31%) clear cell RCC, and 1/16 (6%) papillary noninvasive urothelial cancer. Regarding all renal lesions, 6/17 (35.3%) patients had more than one histological finding in their kidneys. In 2 cases, metachronous metastases were removed. Mean follow-up was 66.7 months. <b><i>Conclusion:</i></b> Kidney-related prevalence of RCC in ADPKD kidneys was surprisingly high. Whether or not this is due to chronic dialysis or due to the underlying disease is still speculative. Like other cystic renal diseases with an increased risk for RCC, the attending physician should be aware of the malignant potential of ADPKD, especially with concomitant dialysis.
DOI: 10.6084/m9.figshare.5469142.v1
title: Lazzaro_et_al_2017_All_data_DEF_prot.xlsx

description: Dataset used in: Lazzaro L, Mazza G, d'Errico G, Fabiani A, Giuliani C, Inghilesi AF., Lagomarsino A, Landi S, Lastrucci L, Pastorelli R, Roversi PF, Torrini G, Tricarico E, Foggi B [Accepted] How ecosystems change following invasion by Robinia pseudoacacia: insights from soil chemical properties and soil microbial, nematode, microarthropod and plant communities. Science of The Total Environment (in press).
DOI: 10.6084/m9.figshare.5469028
title: Supplementary Material for: Association of Functional Kallikrein-1 Promoter Polymorphisms and Acute Kidney Injury: A Case-Control and Longitudinal Cohort Study

description: <b><i>Background:</i></b> Kallikrein-1 (KLK1) is a highly conserved serine protease that is expressed in the kidney and involved in blood pressure regulation. The activity of this enzyme is diminished in acute kidney injury (AKI). <b><i>Methods:</i></b> We first evaluated the potential role of functional multiallelic <i>KLK1</i> promoter gene polymorphisms in a case-control study of 481 subjects (214 hospitalized patients with AKI of mixed causes and 267 healthy subjects). The complex, multiallelic G/C-rich repeat region of the proximal <i>KLK1</i> promoter was determined by direct Sanger/capillary resequencing. <b><i>Results:</i></b> 16 alleles were identified in a complex, polymorphic G/C-rich region of the <i>KLK1</i> proximal promoter; 5 of these alleles (F, G, H, I, and K) were associated with development of AKI. Alleles I and G were classified as risk-alleles (unadjusted OR 1.86; 95% CI 1.23, 2.81; p = 0.003), whereas alleles F, H, and K were classified as protective-alleles (unadjusted OR 0.32; 95% CI 0.22, 0.46; p &lt; 0.001) according to their directional association with development of AKI. After adjustment for sex, race, preexisting chronic kidney disease and APACHE II score, the <i>KLK1</i> risk-allele (I or G) carrier state was associated with the composite of ≥2-fold increase in serum creatinine, oliguria, or dialysis requirement (adjusted OR 2.71; 95% CI 1.14, 6.44; p = 0.02). The <i>KLK1</i> risk-allele carrier state was also marginally associated with the composite of ≥2-fold increase in serum creatinine, oliguria, dialysis requirement, or in-hospital death (adjusted OR 2.33; 95% CI 0.98, 5.52; p = 0.06). <b><i>Conclusions:</i></b><i>KLK1</i> promoter polymorphisms are associated with development of AKI and adverse outcomes. Further studies are needed to validate these findings.
DOI: 10.6084/m9.figshare.5469028.v1
title: Supplementary Material for: Association of Functional Kallikrein-1 Promoter Polymorphisms and Acute Kidney Injury: A Case-Control and Longitudinal Cohort Study

description: <b><i>Background:</i></b> Kallikrein-1 (KLK1) is a highly conserved serine protease that is expressed in the kidney and involved in blood pressure regulation. The activity of this enzyme is diminished in acute kidney injury (AKI). <b><i>Methods:</i></b> We first evaluated the potential role of functional multiallelic <i>KLK1</i> promoter gene polymorphisms in a case-control study of 481 subjects (214 hospitalized patients with AKI of mixed causes and 267 healthy subjects). The complex, multiallelic G/C-rich repeat region of the proximal <i>KLK1</i> promoter was determined by direct Sanger/capillary resequencing. <b><i>Results:</i></b> 16 alleles were identified in a complex, polymorphic G/C-rich region of the <i>KLK1</i> proximal promoter; 5 of these alleles (F, G, H, I, and K) were associated with development of AKI. Alleles I and G were classified as risk-alleles (unadjusted OR 1.86; 95% CI 1.23, 2.81; p = 0.003), whereas alleles F, H, and K were classified as protective-alleles (unadjusted OR 0.32; 95% CI 0.22, 0.46; p &lt; 0.001) according to their directional association with development of AKI. After adjustment for sex, race, preexisting chronic kidney disease and APACHE II score, the <i>KLK1</i> risk-allele (I or G) carrier state was associated with the composite of ≥2-fold increase in serum creatinine, oliguria, or dialysis requirement (adjusted OR 2.71; 95% CI 1.14, 6.44; p = 0.02). The <i>KLK1</i> risk-allele carrier state was also marginally associated with the composite of ≥2-fold increase in serum creatinine, oliguria, dialysis requirement, or in-hospital death (adjusted OR 2.33; 95% CI 0.98, 5.52; p = 0.06). <b><i>Conclusions:</i></b><i>KLK1</i> promoter polymorphisms are associated with development of AKI and adverse outcomes. Further studies are needed to validate these findings.
DOI: 10.6084/m9.figshare.5468929
title: Nottinghamshire Healthcare NHS Foundation Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.<br>
DOI: 10.6084/m9.figshare.5468929.v1
title: Nottinghamshire Healthcare NHS Foundation Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.<br>
DOI: 10.6084/m9.figshare.5468866
title: Northumbria Healthcare NHS Foundation Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468821
title: Northern Lincolnshire and Goole NHS Foundation Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468830
title: Northumberland, Tyne and Wear NHS Foundation Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468821.v1
title: Northern Lincolnshire and Goole NHS Foundation Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468830.v1
title: Northumberland, Tyne and Wear NHS Foundation Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468866.v1
title: Northumbria Healthcare NHS Foundation Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468803
title: Northamptonshire Healthcare NHS Foundation Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468773
title: Northampton General Hospital NHS Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468809
title: Northern Devon Healthcare NHS Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468803.v1
title: Northamptonshire Healthcare NHS Foundation Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468773.v1
title: Northampton General Hospital NHS Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468809.v1
title: Northern Devon Healthcare NHS Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468728
title: North Tees and Hartlepool NHS Foundation Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468740
title: North West Ambulance Service NHS Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.<br>
DOI: 10.6084/m9.figshare.5468740.v1
title: North West Ambulance Service NHS Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.<br>
DOI: 10.6084/m9.figshare.5468698
title: North Essex Partnership University NHS Foundation Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468713
title: North Staffordshire Combined Healthcare NHS Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468716
title: Supplementary Material for: Cyclosporine-Induced Tubular Vacuolization: The Role of Bip/Grp78

description: Cyclosporine (CsA) nephrotoxicity shows characteristic tubular vacuolization (TV) which is endoplasmic reticulum (ER) in origin. However, the cellular events of CsA-induced TV and CsA-induced ER remained unclear. The aim of the present study was to study the nature of TV and the correlation to ER stress. Using proximal tubule NRK-52E cells in vitro and an in vivo model of acute CsA nephrotoxicity, we confirmed that CsA-induced TV was ER in origin and potentially reversible. Our results showed that CsA-induced ER stress and involved ER integrated stress response-related proteins (Bip/Grp78, ATF6, IRE1 and CHOP) but not cytoplasmic ER stress-related chaperones (HSP70, HSP40, HSP27, HSP90 and HSP60). Importantly, Bip/Grp78 was overexpressed on the membrane of TV and suppression of Bip/Grp78 blocked TV formation. In addition, suppression of Bip/Grp78-enhanced CsA-induced cell death and CsA-induced TV formation and Bip/Grp78 overexpression had a characteristic striped pattern in the tubulointerstitium. In summary, we demonstrate that CsA-induced TV was a potentially reversible process in which Bip/Grp78 overexpression is essential for TV formation. It is possible that Bip/Grp78 expression and TV formation may be involved in cellular defense mechanism against CsA nephrotoxicity.
DOI: 10.6084/m9.figshare.5468728.v1
title: North Tees and Hartlepool NHS Foundation Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468692
title: North East Ambulance Service NHS Foundation Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468695
title: North East London NHS Foundation Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468698.v1
title: North Essex Partnership University NHS Foundation Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468713.v1
title: North Staffordshire Combined Healthcare NHS Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468686
title: North Bristol NHS Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468692.v1
title: North East Ambulance Service NHS Foundation Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468674
title: Norfolk and Suffolk NHS Foundation Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468680
title: Supplementary Material for: Vitamin D Receptor Activators Upregulate and Rescue Podocalyxin Expression in High Glucose-Treated Human Podocytes

description: <b><i>Background:</i></b> Vitamin D is beneficial in human and experimental chronic kidney disease, the leading cause of which is diabetic nephropathy. Vitamin D through its receptor, VDR, provides renal protection in diabetic nephropathy, but limited data exist about its effect on podocytes. Renal podocytes form the main filtration barrier possessing a unique phenotype maintained by proteins including podocalyxin and nephrin, the expression of which is suppressed in pathological conditions. <b><i>Methods:</i></b> We used immortalized human podocytes (human glomerular epithelial cells, HGEC) to assess podocalyxin and nephrin expression after treatment with 1,25-dihydroxyvitamin D<sub>3</sub> (calcitriol) and its analogue paricalcitol. The involvement of VDR was investigated by silencing with hVDR-siRNA and ChIP analysis. <b><i>Results:</i></b> HGEC exhibit high glucose-mediated downregulation of podocalyxin and nephrin, loss of which has been linked with loss of the permselective renal barrier and proteinuria. Calcitriol and paricalcitol reversed high glucose-induced decrease of nephrin and significantly enhanced podocalyxin expression in podocytes cultured in high glucose. HGEC express VDR and retinoid X receptor (RXR). In the presence of calcitriol and paricalcitol, VDR expression was upregulated and VDR colocalized with RXR in the nucleus. VDR knockdown abolished the protective action of calcitriol and paricalcitol on podocalyxin expression indicating that podocalyxin activation of expression is partly mediated by VDR. Furthermore, VDR specifically regulates podocalyxin expression by bounding to a site upstream of the podocalyxin promoter. <b><i>Conclusion:</i></b> Vitamin D analogues maintain and, furthermore, re-activate the expression of specialized components of podocytes including podocalyxin, hence they provide protection against loss of the permselective renal barrier, with molecular mechanisms elucidated herein.
DOI: 10.6084/m9.figshare.5468686.v1
title: North Bristol NHS Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468695.v1
title: North East London NHS Foundation Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.
DOI: 10.6084/m9.figshare.5468665
title: Supplementary Material for: Fluorescence Imaging of Intracellular Calcium Signals in Intact Kidney Tissue

description: <b><i>Background:</i></b> Intracellular calcium (Ca<sup>2+</sup>) plays an important role in normal renal physiology and in the pathogenesis of various kidney diseases; however, the study of Ca<sup>2+</sup> signals in intact tissue has been limited by technical difficulties, including achieving adequate loading of Ca<sup>2+</sup>-sensitive fluorescent dyes. The kidney slice preparation represents a model whereby three-dimensional tissue architecture is preserved and structures in both the cortex and medulla can be imaged using confocal or multiphoton microscopy. <b><i>Methods:</i></b> Ca<sup>2+</sup>-sensitive dyes Rhod-2, Fura-red and Fluo-4 were loaded into tubular and vascular cells in rat kidney slices using a re-circulating perfusion system and real-time imaging of Ca<sup>2+</sup> signals was recorded by confocal microscopy. Kidney slices were also obtained from transgenic mice expressing the GCaMP2 Ca<sup>2+</sup>-sensor in their endothelial cells and real time Ca<sup>2+</sup> transients stimulated by physiological stimuli. <b><i>Results:</i></b> Wide spread loading of Ca<sup>2+</sup> indicators was achieved in the tubular and vascular structures of both the medulla and cortex. Real time Ca<sup>2+</sup> signals were successfully recorded in different intracellular compartments of both rat and mouse cortical and medullary tubules in response to physiological stimuli (ATP and angiotensin II). Glomerular Ca<sup>2+</sup> transients were similarly recorded in kidney slices taken from the transgenic mouse expressing the GCaMP2 Ca<sup>2+</sup>-sensor. <b><i>Conclusion:</i></b> We present new approaches that can be adopted to image cytosolic and mitochondrial Ca<sup>2+</sup> signals within various cell types in intact kidney tissue. Moreover, techniques described in this study can be used to facilitate future detailed investigations of intracellular Ca<sup>2+</sup> homeostasis in renal health and disease.
DOI: 10.6084/m9.figshare.5468674.v1
title: Norfolk and Suffolk NHS Foundation Trust

description: Response to our Freedom of Information Act request received from this NHS Trust.