cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.11816532.v1
title: Assemblies

description: Hybrid asseblies of 45 clinical Enterobacteriacae isolates from bloodstream infections of patients in Oxfordshire 2008-2018
DOI: 10.6084/m9.figshare.11816577.v4
title: 3D_mapping_data.zip from Three-dimensional digital mapping of ecosystems: a new era in spatial ecology

description: Ecological processes occur over multiple spatial, temporal and thematic scales in three-dimensional (3D) ecosystems. Characterizing and monitoring change in 3D structure at multiple scales is challenging within the practical constraints of conventional ecological tools. Remote sensing from satellites and crewed aircraft has revolutionized broad-scale spatial ecology, but fine-scale patterns and processes operating at sub-metre resolution have remained understudied over continuous extents. We introduce two high-resolution remote sensing tools for rapid and accurate 3D mapping in ecology—terrestrial laser scanning and structure-from-motion photogrammetry. These technologies are likely to become standard sampling tools for mapping and monitoring 3D ecosystem structure across currently under-sampled scales. We present practical guidance in the use of the tools and address barriers to widespread adoption, including testing the accuracy of structure-from-motion models for ecologists. We aim to highlight a new era in spatial ecology that uses high-resolution remote sensing to interrogate 3D digital ecosystems.
DOI: 10.6084/m9.figshare.11816412
title: Updated tree files

description: Updated tree files for two gene families: EPF and ERECTA
DOI: 10.6084/m9.figshare.11816403
title: Land plant phylogeny treefile

description: Raw newick treefile of land plant phylogeny
DOI: 10.6084/m9.figshare.11816406
title: Radiation effects on <i>Toxoplasma</i> antigens: different immune responses of irradiated intact tachyzoites or soluble antigens in experimental mice models

description: <b>Purpose:</b> Purpose: Protein irradiation causes aggregation, chain breakage, and oxidation, enhancing its uptake by antigen-presenting cells. To evaluate if irradiated proteins participate on the protection, we studied the immune response induced in mice immunized with irradiated soluble extracts of <i>T. gondii</i> tachyzoites (STag) or irradiated intact <i>T. gondii</i> RH tachyzoites (RH<sup>0.25 kGy</sup>). <b>Material and Methods:</b> Soluble extracts of <i>Toxoplasma gondii</i> tachyzoites (STag) were irradiated at different dose by Cobalt-60 source. By polyacrylamide gel electrophoresis (SDS-Page) we evaluated the effects on primary structures of protein STags induced by irradiation. By Enzyme-linked Immunosorbent Assay (ELISA) we evaluated the difference between humoral immune response induced by irradiated STag or RH tachyzoites in immunized mice from the detection of specific immunoglobulin G (IgG) antibodies in the serum of immunized mice. From challenge with viable RH strain of <i>T. gondii</i> we evaluated the protection induced in the immunized animals. By cytometry we performed the phenotyping of T and B lymphocytes in the peripheral blood of the immunized animals. <b>Results:</b> Irradiation dose of 1.5 kGy induced minimal changes in most proteins, without affecting their antigenicity or immunogenicity. Immunization showed saturation at the dose of 10 µg/mice, with worst response at higher doses. STag irradiated at 1.5 kGy (STag<sup>1.5 kGy</sup>) induced higher survival and protection similar to <i>T. gondii</i> RH strain irradiated at 0.25 kGy (RH<sup>0.25 kGy</sup>), with higher serum levels of high affinity IgG compared to STag native. Blood immune memory cells of mice immunized with STag<sup>1.5 kGy</sup> had higher proportions of CD19<sup>+</sup> (cluster of differentiation 19) and CD4<sup>+</sup> (cluster of differentiation 14) cells, whereas mice RH<sup>0.25 kGy</sup> had high proportion of memory CD8<sup>+</sup> (cluster of differentiation 8) cells. <b>Conclusions:</b> Our data suggest that major histocompatibility complex type I (MHCI) pathway, appears seem to be used by RH<sup>0.25 kGy</sup> to generate cytotoxic cells while STag1.5 kGy uses a major histocompatibility complex type II (MHCII) pathway for B-cell memory, but both induce sufficient immune response for protection in mice without any adjuvant. Irradiation of soluble protein extracts enhances their immune response, allowing similar protection against <i>T. gondii</i> in mice as compared to irradiated intact parasites.
DOI: 10.6084/m9.figshare.11816406.v1
title: Radiation effects on <i>Toxoplasma</i> antigens: different immune responses of irradiated intact tachyzoites or soluble antigens in experimental mice models

description: <b>Purpose:</b> Purpose: Protein irradiation causes aggregation, chain breakage, and oxidation, enhancing its uptake by antigen-presenting cells. To evaluate if irradiated proteins participate on the protection, we studied the immune response induced in mice immunized with irradiated soluble extracts of <i>T. gondii</i> tachyzoites (STag) or irradiated intact <i>T. gondii</i> RH tachyzoites (RH<sup>0.25 kGy</sup>). <b>Material and Methods:</b> Soluble extracts of <i>Toxoplasma gondii</i> tachyzoites (STag) were irradiated at different dose by Cobalt-60 source. By polyacrylamide gel electrophoresis (SDS-Page) we evaluated the effects on primary structures of protein STags induced by irradiation. By Enzyme-linked Immunosorbent Assay (ELISA) we evaluated the difference between humoral immune response induced by irradiated STag or RH tachyzoites in immunized mice from the detection of specific immunoglobulin G (IgG) antibodies in the serum of immunized mice. From challenge with viable RH strain of <i>T. gondii</i> we evaluated the protection induced in the immunized animals. By cytometry we performed the phenotyping of T and B lymphocytes in the peripheral blood of the immunized animals. <b>Results:</b> Irradiation dose of 1.5 kGy induced minimal changes in most proteins, without affecting their antigenicity or immunogenicity. Immunization showed saturation at the dose of 10 µg/mice, with worst response at higher doses. STag irradiated at 1.5 kGy (STag<sup>1.5 kGy</sup>) induced higher survival and protection similar to <i>T. gondii</i> RH strain irradiated at 0.25 kGy (RH<sup>0.25 kGy</sup>), with higher serum levels of high affinity IgG compared to STag native. Blood immune memory cells of mice immunized with STag<sup>1.5 kGy</sup> had higher proportions of CD19<sup>+</sup> (cluster of differentiation 19) and CD4<sup>+</sup> (cluster of differentiation 14) cells, whereas mice RH<sup>0.25 kGy</sup> had high proportion of memory CD8<sup>+</sup> (cluster of differentiation 8) cells. <b>Conclusions:</b> Our data suggest that major histocompatibility complex type I (MHCI) pathway, appears seem to be used by RH<sup>0.25 kGy</sup> to generate cytotoxic cells while STag1.5 kGy uses a major histocompatibility complex type II (MHCII) pathway for B-cell memory, but both induce sufficient immune response for protection in mice without any adjuvant. Irradiation of soluble protein extracts enhances their immune response, allowing similar protection against <i>T. gondii</i> in mice as compared to irradiated intact parasites.
DOI: 10.6084/m9.figshare.11816403.v1
title: Untitled Item

description: Raw newick treefile of land plant phylogeny
DOI: 10.6084/m9.figshare.11816358
title: Scientific Advisory Board Committee IFKAD

description: Bashar Malkawi, member, Scientific Advisory Board Committee IFKAD
DOI: 10.6084/m9.figshare.11816358.v1
title: Scientific Advisory Board Committee IFKAD

description: Bashar Malkawi, member, Scientific Advisory Board Committee IFKAD
DOI: 10.6084/m9.figshare.11816325
title: Characterizing and understanding body weight patterns in patients treated with pregabalin

description: We examined patterns of weight change among patients treated with pregabalin for up to 1 year. Patients with ≥1 pre-treatment weight measurement, ≥2 measurements in Period 1 (day 2–56), and ≥2 during Period 2 (day 57–356) were identified from pooled data of 106 studies including 43,525 patients. Seven patterns were developed and used for exploratory ‘change point’ analyses (day on-treatment when weight-change trend changed from initial trajectory) and to assess patterns of weight change by baseline weight/body mass index (BMI). A total of 3187 patients (from 41 studies) were eligible. 98.9% of patients were described by three of the seven patterns. The majority of patients (2607/3187 [81.8%]) remained within ±7% of baseline weight (‘Pattern 4’). Fewer patients (463/3187 [14.5%]) were ‘delayed weight gainers’ (exceeded 7% weight gain in Period 2 but not Period 1 [‘Pattern 6’]), fewer still (82/3187 [2.6%]) were ‘early weight gainers’ (exceeded ≥7% baseline weight in Period 1 and remained above 7% or continued to gain weight in Period 2 [‘Pattern 7’]). Overall weight gainers (Patterns 6, 7) experienced 1-year weight gain (median [% change]) of +6.20 kg [+9.12%] and 5.46 kg [+13.9%] vs. 2.22 kg [+2.10%] for non-weight gainers (Pattern 4). Average baseline weight/BMI was lower for weight gainers (Patterns 6, 7) versus other patterns. Early weight gainers (Pattern 7) had change point day at day 40 versus day 54 for Pattern 4 and day 69 for Pattern 6. Use of concomitant medications and influence of comorbid conditions on weight should be considered as inherent variables when interpreting the study. The majority of patients treated with pregabalin (150–600 mg/day) for 1 year maintained weight within ±7% baseline weight. One in six patients gained ≥7% weight from baseline, and generally exceeded 7%, 2–12 months after treatment onset.
DOI: 10.6084/m9.figshare.11816325.v1
title: Characterizing and understanding body weight patterns in patients treated with pregabalin

description: We examined patterns of weight change among patients treated with pregabalin for up to 1 year. Patients with ≥1 pre-treatment weight measurement, ≥2 measurements in Period 1 (day 2–56), and ≥2 during Period 2 (day 57–356) were identified from pooled data of 106 studies including 43,525 patients. Seven patterns were developed and used for exploratory ‘change point’ analyses (day on-treatment when weight-change trend changed from initial trajectory) and to assess patterns of weight change by baseline weight/body mass index (BMI). A total of 3187 patients (from 41 studies) were eligible. 98.9% of patients were described by three of the seven patterns. The majority of patients (2607/3187 [81.8%]) remained within ±7% of baseline weight (‘Pattern 4’). Fewer patients (463/3187 [14.5%]) were ‘delayed weight gainers’ (exceeded 7% weight gain in Period 2 but not Period 1 [‘Pattern 6’]), fewer still (82/3187 [2.6%]) were ‘early weight gainers’ (exceeded ≥7% baseline weight in Period 1 and remained above 7% or continued to gain weight in Period 2 [‘Pattern 7’]). Overall weight gainers (Patterns 6, 7) experienced 1-year weight gain (median [% change]) of +6.20 kg [+9.12%] and 5.46 kg [+13.9%] vs. 2.22 kg [+2.10%] for non-weight gainers (Pattern 4). Average baseline weight/BMI was lower for weight gainers (Patterns 6, 7) versus other patterns. Early weight gainers (Pattern 7) had change point day at day 40 versus day 54 for Pattern 4 and day 69 for Pattern 6. Use of concomitant medications and influence of comorbid conditions on weight should be considered as inherent variables when interpreting the study. The majority of patients treated with pregabalin (150–600 mg/day) for 1 year maintained weight within ±7% baseline weight. One in six patients gained ≥7% weight from baseline, and generally exceeded 7%, 2–12 months after treatment onset.
DOI: 10.6084/m9.figshare.11815905
title: Misconnecting the dots: altered mitochondrial protein-protein interactions and their role in neurodegenerative disorders

description: <b>Introduction</b>: Mitochondria (mt) are protein-protein interaction (PPI) hubs in the cell where mt-localized and associated proteins interact in a fashion critical for cell fitness. Altered mtPPIs are linked to neurodegenerative disorders (NDs) and drivers of pathological associations to mediate ND progression. Mapping altered mtPPIs will reveal how mt dysfunction is linked to NDs. <b>Areas covered</b>: This review discusses how database sources reflect on the number of mt protein or interaction predictions, and serves as an update on mtPPIs in mt dynamics and homeostasis. Emphasis is given to mRNA expression profiles for mt proteins in human tissues, cellular models relevant to NDs, and altered mtPPIs in NDs such as Parkinson’s disease (PD), Amyotrophic lateral sclerosis (ALS) and Alzheimer’s disease (AD). <b>Expert opinion</b>: We highlight the scarcity of biomarkers to improve diagnostic accuracy and tracking of ND progression, obstacles in recapitulating NDs using human cellular models to underpin the pathophysiological mechanisms of disease, and the shortage of mt protein interactome reference database(s) of neuronal cells. These bottlenecks are addressed by improvements in induced pluripotent stem cell creation and culturing, patient-derived 3D brain organoids to recapitulate structural arrangements of the brain, and cell sorting to elucidate mt proteome disparities between cell types.
DOI: 10.6084/m9.figshare.11815905.v1
title: Misconnecting the dots: altered mitochondrial protein-protein interactions and their role in neurodegenerative disorders

description: <b>Introduction</b>: Mitochondria (mt) are protein-protein interaction (PPI) hubs in the cell where mt-localized and associated proteins interact in a fashion critical for cell fitness. Altered mtPPIs are linked to neurodegenerative disorders (NDs) and drivers of pathological associations to mediate ND progression. Mapping altered mtPPIs will reveal how mt dysfunction is linked to NDs. <b>Areas covered</b>: This review discusses how database sources reflect on the number of mt protein or interaction predictions, and serves as an update on mtPPIs in mt dynamics and homeostasis. Emphasis is given to mRNA expression profiles for mt proteins in human tissues, cellular models relevant to NDs, and altered mtPPIs in NDs such as Parkinson’s disease (PD), Amyotrophic lateral sclerosis (ALS) and Alzheimer’s disease (AD). <b>Expert opinion</b>: We highlight the scarcity of biomarkers to improve diagnostic accuracy and tracking of ND progression, obstacles in recapitulating NDs using human cellular models to underpin the pathophysiological mechanisms of disease, and the shortage of mt protein interactome reference database(s) of neuronal cells. These bottlenecks are addressed by improvements in induced pluripotent stem cell creation and culturing, patient-derived 3D brain organoids to recapitulate structural arrangements of the brain, and cell sorting to elucidate mt proteome disparities between cell types.
DOI: 10.6084/m9.figshare.11815920
title: Where to with treatment for ADHD?

description: Where to with treatment for ADHD?
DOI: 10.6084/m9.figshare.11815920.v1
title: Where to with treatment for ADHD?

description: Where to with treatment for ADHD?
DOI: 10.6084/m9.figshare.11815899
title: Long-term safety of naproxen and esomeprazole magnesium fixed-dose combination: phase III study in patients at risk for NSAID-associated gastric ulcers

description: To evaluate long-term safety of enteric-coated naproxen 500 mg and immediate-release esomeprazole magnesium 20 mg fixed-dose combination (FDC) in patients at risk of NSAID-associated upper gastrointestinal (UGI) ulcers. In this open-label, multicenter, phase III study, <i>Helicobacter pylori</i>-negative patients aged ≥50 years or 18–49 years with history of uncomplicated ulcer within the past 5 years, who had osteoarthritis, rheumatoid arthritis, or other condition requiring daily NSAIDs for ≥12 months received naproxen/esomeprazole twice daily for 12 months. NCT00527904. Adverse events (AEs), vital signs, physical examination, and laboratory tests. Subgroup analyses included age and low-dose aspirin (LDA) use. Predefined NSAID-associated UGI and cardiovascular AEs were analyzed. Of 239 patients treated (safety population), 135 completed ≥348 treatment days (12-month completers). AE incidence was approximately 70%; dyspepsia, constipation, upper respiratory tract infection, nausea, back pain, and contusion were most frequent (≥5% patients, either population). Treatment-related AEs occurred in 28.0% and 23.7% of patients in the safety and 12-month completer populations, respectively; 18.8% of patients withdrew due to AEs (safety population). Few serious AEs and no deaths occurred. In the safety population, AE incidence was 71.4% and 76.9% in patients aged &lt;65 years (<i>n</i> = 161) and ≥65 years (<i>n</i> = 78), respectively, and 67.6% and 75.8% in LDA users (<i>n</i> = 74) and non-users (<i>n</i> = 165), respectively. Predefined UGI and cardiovascular AEs were observed in 18.8% and 6.3% of patients, respectively, in the safety population, and 16.3% and 5.2%, respectively, in 12-month completers. Dyspepsia and hypertension were most common. Additional assessments showed no unexpected findings. Based on these outcome measures, long-term treatment with FDC naproxen/esomeprazole is not associated with any new safety issues, including predefined UGI and cardiovascular AEs, in patients requiring NSAID therapy who are at risk of UGI complications.
DOI: 10.6084/m9.figshare.11815890
title: Pharmacotherapy of low back pain: targeting nociceptive and neuropathic pain components

description: To review pharmacological management of chronic low back pain (LBP), with respect to management of nociceptive and neuropathic components. Studies were identified by a PubMed search of English-language papers from the last 10 years, with additional hand searches of relevant reviews. Paracetamol, non-steroidal anti-inflammatory drugs and cyclo-oxygenase-2 inhibitors target the nociceptive component of chronic LBP, and do not affect neuropathic pain mechanisms. Antidepressants target the neuropathic component of chronic LBP; however, conflicting efficacy results have been reported. Opioids target both nociceptive and to a lesser extent neuropathic pain. They are effective in chronic LBP, but many patients require higher doses or combination treatment. The long-term efficacy of opioids in chronic LBP has been questioned because of the absence of high-quality data and concerns regarding tolerability and dependence. The topical preparation lidocaine 5% plaster, indicated in post-herpetic neuralgia, is effective in localized neuropathic pain in patients with chronic LBP. Pregabalin is ineffective as monotherapy for chronic LBP but is effective when combined with celecoxib or opioids. Muscle relaxant monotherapy is ineffective in chronic LBP. Combination therapy is often necessary in patients with chronic LBP, in order to manage both nociceptive and neuropathic pain components. Chronic LBP often comprises both nociceptive and neuropathic components, therefore a multimodal and individualized treatment approach is necessary. Combining drugs with different mechanisms of action (e.g. an agent with µ-receptor activity plus an agent of a different class) represents a rational approach to management of chronic LBP with both nociceptive and neuropathic components.
DOI: 10.6084/m9.figshare.11815899.v1
title: Long-term safety of naproxen and esomeprazole magnesium fixed-dose combination: phase III study in patients at risk for NSAID-associated gastric ulcers

description: To evaluate long-term safety of enteric-coated naproxen 500 mg and immediate-release esomeprazole magnesium 20 mg fixed-dose combination (FDC) in patients at risk of NSAID-associated upper gastrointestinal (UGI) ulcers. In this open-label, multicenter, phase III study, <i>Helicobacter pylori</i>-negative patients aged ≥50 years or 18–49 years with history of uncomplicated ulcer within the past 5 years, who had osteoarthritis, rheumatoid arthritis, or other condition requiring daily NSAIDs for ≥12 months received naproxen/esomeprazole twice daily for 12 months. NCT00527904. Adverse events (AEs), vital signs, physical examination, and laboratory tests. Subgroup analyses included age and low-dose aspirin (LDA) use. Predefined NSAID-associated UGI and cardiovascular AEs were analyzed. Of 239 patients treated (safety population), 135 completed ≥348 treatment days (12-month completers). AE incidence was approximately 70%; dyspepsia, constipation, upper respiratory tract infection, nausea, back pain, and contusion were most frequent (≥5% patients, either population). Treatment-related AEs occurred in 28.0% and 23.7% of patients in the safety and 12-month completer populations, respectively; 18.8% of patients withdrew due to AEs (safety population). Few serious AEs and no deaths occurred. In the safety population, AE incidence was 71.4% and 76.9% in patients aged &lt;65 years (<i>n</i> = 161) and ≥65 years (<i>n</i> = 78), respectively, and 67.6% and 75.8% in LDA users (<i>n</i> = 74) and non-users (<i>n</i> = 165), respectively. Predefined UGI and cardiovascular AEs were observed in 18.8% and 6.3% of patients, respectively, in the safety population, and 16.3% and 5.2%, respectively, in 12-month completers. Dyspepsia and hypertension were most common. Additional assessments showed no unexpected findings. Based on these outcome measures, long-term treatment with FDC naproxen/esomeprazole is not associated with any new safety issues, including predefined UGI and cardiovascular AEs, in patients requiring NSAID therapy who are at risk of UGI complications.
DOI: 10.6084/m9.figshare.11815890.v1
title: Pharmacotherapy of low back pain: targeting nociceptive and neuropathic pain components

description: To review pharmacological management of chronic low back pain (LBP), with respect to management of nociceptive and neuropathic components. Studies were identified by a PubMed search of English-language papers from the last 10 years, with additional hand searches of relevant reviews. Paracetamol, non-steroidal anti-inflammatory drugs and cyclo-oxygenase-2 inhibitors target the nociceptive component of chronic LBP, and do not affect neuropathic pain mechanisms. Antidepressants target the neuropathic component of chronic LBP; however, conflicting efficacy results have been reported. Opioids target both nociceptive and to a lesser extent neuropathic pain. They are effective in chronic LBP, but many patients require higher doses or combination treatment. The long-term efficacy of opioids in chronic LBP has been questioned because of the absence of high-quality data and concerns regarding tolerability and dependence. The topical preparation lidocaine 5% plaster, indicated in post-herpetic neuralgia, is effective in localized neuropathic pain in patients with chronic LBP. Pregabalin is ineffective as monotherapy for chronic LBP but is effective when combined with celecoxib or opioids. Muscle relaxant monotherapy is ineffective in chronic LBP. Combination therapy is often necessary in patients with chronic LBP, in order to manage both nociceptive and neuropathic pain components. Chronic LBP often comprises both nociceptive and neuropathic components, therefore a multimodal and individualized treatment approach is necessary. Combining drugs with different mechanisms of action (e.g. an agent with µ-receptor activity plus an agent of a different class) represents a rational approach to management of chronic LBP with both nociceptive and neuropathic components.