cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.5124955.v1
title: Supplementary Material for: Epidemiology of Traumatic Spinal Cord Injury in Developing Countries: A Systematic Review

description: <b><i>Background/Aims:</i></b> To describe the epidemiology of spinal cord injury (SCI) in the developing world. <b><i>Methods:</i></b> Developing countries were selected based on the definition proposed by the International Monetary Fund. A literature search was performed in July 2012 in Medline and Embase. Further article procurement was obtained via the reference lists of the identified articles, websites, and direct contact with the authors of the identified studies. We designed search strategies using the key words: SCI, epidemiology, incidence, and prevalence. According to the inclusion criteria, 64 studies from 28 countries were included. <b><i>Results:</i></b> The incidence of SCI in developing countries is 25.5/million/year (95% CI: 21.7-29.4/million/year) and ranges from 2.1 to 130.7/million/year. Males comprised 82.8% (95% CI: 80.3-85.2) of all SCIs with a mean age of 32.4 years (95% CI: 29.7-35.2). The two leading causes of SCI were found to be motor vehicle crashes (41.4%; 95% CI: 35.4-47.4) and falls (34.9%; 95% CI: 26.7-43.1). Complete SCIs were found to be more common than incomplete injuries (complete SCI: 56.5%; 95% CI: 47.6-65.3; incomplete SCI: 43.0%; 95% CI: 34.1-52.0). Similarly, paraplegia was found to be more common than tetraplegia (paraplegia: 58.7%; 95% CI: 51.5-66.0; tetraplegia: 40.6%; 95% CI: 33.3-48.0). <b><i>Conclusion:</i></b> Through an understanding of the epidemiology of SCI in developing countries, appropriate preventative strategies and resource allocation may decrease the incidence and improve the care of these injuries.
DOI: 10.6084/m9.figshare.5124958.v1
title: Supplementary Material for: Building a European Consensus on Minimum Quality Standards for Drug Treatment, Rehabilitation and Harm Reduction

description: <b><i>Background/Aims:</i></b> The Study on the Development of an EU Framework for Minimum Quality Standards and Benchmarks in Drug Demand Reduction (EQUS) has set up an inventory of quality standards and initiated a consensus-building process, aiming at establishing a set of European minimum quality standards (MQS) for treatment/rehabilitation and harm reduction in the field of drug abuse and dependence. <b><i>Methods:</i></b> Existing documents were collected by country-specific experts and integrated into a predefined framework of quality standards. Agreement, implementation status and expected implementation problems of the proposed standards were assessed by a survey of European stakeholders and the final lists of European MQS were established at a European conference. <b><i>Results:</i></b> Overall, 349 documents were identified as relevant. Major gaps were identified for ethical and legal standards, and for documents that provide grades of evidence for specific standards. A high level of acceptance was found for the treatment/rehabilitation MQS, while a somewhat lower level was found for the harm reduction MQS. The final lists of MQS were based on at least 80% of acceptance by European experts and stakeholders. <b><i>Conclusion:</i></b> A high consensus of European MQS for treatment/rehabilitation and harm reduction has been achieved. Further implementation and developmental steps are discussed.
DOI: 10.6084/m9.figshare.5124925
title: Supplementary Material for: Equity in Public Health: An Epigenetic Perspective

description: Evidence emerging from the study of epigenetics and epigenomics challenges notions of health by enhancing understanding of disease etiologies and improving awareness of new health risks. New paradigms arising from epigenetic and epigenomic research present challenging cases through which to debate theories of justice in health because they expand the concept of health and, controversially, place value on what was previously assumed to be ‘healthy' individual variance. Discoveries of the dynamic nature of the epigenome and its variable sensitivity towards change in numerous phenomena add further complexity to the assessment of health inequalities. Such evidence can cast doubt on perceptions of justice in health, which in turn raises questions over the suitability of actions taken in pursuit of equity. This article discusses how recent developments in epigenetics and epigenomics may impact upon assessments of equity in health. A review of literature discussing possible health risks associated with acquired yet heritable epigenetic variance is used to highlight the diversity of possible pathways through which health may be influenced. From this context, the consideration of health risk with respect to epigenetics, it is argued, demands a more inclusive concept of health when used in discussions of inequities.
DOI: 10.6084/m9.figshare.5124931
title: Supplementary Material for: Knockdown of PSMB7 Induces Autophagy in Cardiomyocyte Cultures: Possible Role in Endoplasmic Reticulum Stress

description: Proteasomal and autophagic pathways of protein degradation are two essential, endoplasmic reticulum (ER)-associated proteolytic systems involved in the ER stress response. The functional interaction between them has been shown by proteasome pharmacological inhibition. However, little data have been found concerning autophagy induction using an RNA interference approach due to the multisubunit composition of proteolytic systems. We suggested that silencing of single proteasome subunits can induce massive autophagy. <i>Psmb7</i>-specific small interference RNA added to isolated cardiomyocytes significantly affected mRNA expression of essential ER stress marker proteins, including DDIT3/CHOP and HSPA5/GRP78. mRNA expression of the key autophagy regulator MTOR was also increased. These findings were confirmed by single-cell reverse transcription real-time PCR on individual monodansylcadaverine (MDC)-labeled cardiomyocytes. RNA interference that decreased the levels of non-catalytic PSMB7 subunits of the proteasome had no influence on chymotrypsin- and trypsin-like activities, but significantly decreased peptidyl-glutamyl peptide-hydrolyzing activity. Immunohistochemical analysis showed increased levels of LC3-marked vacuoles in the cytoplasm of <i>Psmb7</i>-knockdown cells, and MDC staining showed significantly increased numbers of neonatal cardiomyocytes with autophagic vacuoles. After anoxia-reoxygenation, the number of cells with signs of autophagy after <i>Psmb7</i> gene silencing was higher. Our results indicate that <i>Psmb7</i> knockdown induces ER stress and autophagy in cardiomyocytes, which may be a useful approach to activate specific autophagy.
DOI: 10.6084/m9.figshare.5124919
title: Supplementary Material for: Tracking Chromosome Evolution in Southern African Gerbils Using Flow-Sorted Chromosome Paints

description: <i>Desmodillus</i> and <i>Gerbilliscus</i> (formerly <i>Tatera</i>) comprise a monophyletic group of gerbils (subfamily Gerbillinae) which last shared an ancestor approximately 8 million years ago; diploid chromosome number variation among the species ranges from 2n = 36 to 2n = 50. In an attempt to shed more light on chromosome evolution and speciation in these rodents, we compared the karyotypes of 7 species, representing 3 genera, based on homology data revealed by chromosome painting with probes derived from flow-sorted chromosomes of the hairy footed gerbil, <i>Gerbillurus paeba</i> (2n = 36). The fluorescent in situ hybridization data revealed remarkable genome conservation: these species share a high proportion of conserved chromosomes, and differences are due to 10 Robertsonian (Rb) rearrangements (3 autapomorphies, 3 synapomorphies and 4 hemiplasies/homoplasies). Our data suggest that chromosome evolution in <i>Desmodillus </i>occurred at a rate of ∼1.25 rearrangements per million years (Myr), and that the rate among <i>Gerbilliscus</i> over a time period spanning 8 Myr is also ∼1.25 rearrangements/Myr. The recently diverged <i>Gerbillurus (G. tytonis </i>and<i> G. paeba)</i> share an identical karyotype, while <i>Gerbilliscus kempi, G. afra</i> and <i>G. leucogaster</i> differ by 6 Rb rearrangements (a rate of ∼1 rearrangement/Myr). Thus, our data suggests a very slow rate of chromosomal evolution in Southern African gerbils.
DOI: 10.6084/m9.figshare.5125087.v9
title: Inferring the effects of sink strength on plant carbon balance processes from experimental measurements

description: This folder consists of existing dataset from the container volume experiment which was carried out at the Hawkesbury Forest Experiment site (33°37'S 150°44'E) in Richmond, NSW, Australia. The site and experimental setup have been explained in detail by Campany et al. (2017). <br>In brief, 20 weeks old Eucalyptus tereticornis seedlings in tube stock were chosen from a single local Cumberland plain cohort. Ten additional seedlings of similar age and growth were harvested to measure initial leaf area and dry mass of leaves, stems and roots. A total of 49 Eucalyptus tereticornis seedlings were grown in a range of container sizes (5 L to 35 L) in field conditions, using freely-rooted seedlings as a control for the container size treatments, with the goal to examine how the C balance of the plants are affected to belowground sink limitations. Six container sizes were used with each container experiment had a complete replicate set of six container volumes along with a free seedling. Similar notations are used here as Campany et al. (2017) for the treatments in different pots as 5 L, 10 L, 15 L, 20 L, 25 L and 35 L in respect of their pot sizes. The experiment tracked leaf-level gas exchange, leaf carbohydrate accumulation and seedling allometry over the course of 4 months for all 7 treatments.
DOI: 10.6084/m9.figshare.5124913
title: Supplementary Material for: Noonan Syndrome: Comparing Mutation-Positive with Mutation-Negative Dutch Patients

description: Noonan syndrome (NS) is an autosomal dominant disorder characterized by facial dysmorphisms, short stature and congenital heart defects. The disorder is genetically heterogeneous and shows clinical overlap with other RASopathies. These syndromes are caused by mutations in a variety of genes leading to dysregulation of the RAS-MAPK pathway: <i>PTPN11, KRAS, SOS1, RAF1, CBL, SHOC2, NRAS, BRAF, MAP2K1, MAP2K2, HRAS, NF1 and SPRED1.</i> In this study, we conduct a genotype-phenotype analysis of 33 patients with a clinical diagnosis of NS without a <i>PTPN11</i> mutation. Mutation analysis of the genes involved in RASopathies was performed, except for <i>NF1 and SPRED1.</i> In 14 (42%) NS patients, a mutation was found, 7 (21%) had a mutation in <i>SOS1</i>, 3 (9%) in <i>RAF1</i> and 1 (3%) in <i>KRAS</i>, <i>MAP2K2</i>, <i>BRAF</i> and <i>SHOC2</i> each. The phenotype of these mutation-positive cases corresponded to that described in the literature. In the cases with a <i>BRAF</i> and <i>MAP2K2</i> mutation, the diagnosis cardio-facio-cutaneous syndrome was made. The patient with the <i>SHOC2</i> mutation had features compatible with ‘Noonan-like syndrome with loose anagen hair'. Three major clinical features of NS - a typical face, short stature and a pulmonary valve stenosis - were less frequently present in the group without a mutation. Missense mutations in genes encoding proteins of the RAS-MAPK pathway cause NS. The 3 major clinical features of NS were less frequently present in the mutation-negative patients, which stresses the importance of the syndrome-specific symptoms of the face, heart and short stature in NS. However, all mutation-negative cases met the NS criteria, indicating that the involvement of novel genes is to be expected.
DOI: 10.6084/m9.figshare.5124907
title: Supplementary Material for: Impact of Humans on Long-Distance Communication Behaviour of Eastern Chimpanzees <b><i>(Pan troglodytes schweinfurthii)</i></b> in the Northern Democratic Republic of the Congo

description: We systematically recorded all long-distance chimpanzee vocalizations and tree drums over a 26-month study period in 13 forest regions in the Democratic Republic of the Congo. We found that the frequency of chimpanzee vocalizations and tree drums was considerably higher in the remote Gangu Forest than in other forest regions closer to human settlements and roads. We present evidence indicating that chimpanzees may reduce their levels of vocalizations in areas characterized by high levels of human hunting. The chimpanzees appear to have the behavioural flexibility necessary to modify their behaviour in areas where humans are a major threat. We discuss the possible consequences of this reduction in vocalization rate on the social system of the chimpanzees.
DOI: 10.6084/m9.figshare.5124919.v1
title: Supplementary Material for: Tracking Chromosome Evolution in Southern African Gerbils Using Flow-Sorted Chromosome Paints

description: <i>Desmodillus</i> and <i>Gerbilliscus</i> (formerly <i>Tatera</i>) comprise a monophyletic group of gerbils (subfamily Gerbillinae) which last shared an ancestor approximately 8 million years ago; diploid chromosome number variation among the species ranges from 2n = 36 to 2n = 50. In an attempt to shed more light on chromosome evolution and speciation in these rodents, we compared the karyotypes of 7 species, representing 3 genera, based on homology data revealed by chromosome painting with probes derived from flow-sorted chromosomes of the hairy footed gerbil, <i>Gerbillurus paeba</i> (2n = 36). The fluorescent in situ hybridization data revealed remarkable genome conservation: these species share a high proportion of conserved chromosomes, and differences are due to 10 Robertsonian (Rb) rearrangements (3 autapomorphies, 3 synapomorphies and 4 hemiplasies/homoplasies). Our data suggest that chromosome evolution in <i>Desmodillus </i>occurred at a rate of ∼1.25 rearrangements per million years (Myr), and that the rate among <i>Gerbilliscus</i> over a time period spanning 8 Myr is also ∼1.25 rearrangements/Myr. The recently diverged <i>Gerbillurus (G. tytonis </i>and<i> G. paeba)</i> share an identical karyotype, while <i>Gerbilliscus kempi, G. afra</i> and <i>G. leucogaster</i> differ by 6 Rb rearrangements (a rate of ∼1 rearrangement/Myr). Thus, our data suggests a very slow rate of chromosomal evolution in Southern African gerbils.
DOI: 10.6084/m9.figshare.5124901
title: Supplementary Material for: Differential Endothelial Coverage, Response to Injury and Neointimal Integration of CX3CR1/Smooth Muscle-Like Cells after Carotid or Femoral Arterial Injury

description: <b><i>Background:</i></b> Previously, we established the importance of the CX3CL1/CX3CR1 axis in the promotion of myeloid cell differentiation into neointimal smooth muscle-like cells (SMLC). <b><i>Methods:</i></b> In this study, acute (24 h) endothelial coverage and CX3CL1 expression as well as chronic (2 weeks) vascular remodeling was examined with respect to whether myeloid CX3CR1<sup>+</sup> SMLC number in the neointima differed between carotid and femoral artery wire injury. <b><i>Results and Conclusion:</i></b> Twenty-four hours after injury, CX3CL1 expression was significantly elevated in injured carotid compared to femoral arteries. In mice with CX3CR1 promoter-driven expression of green fluorescent protein, neointima formation was significantly greater (p &lt; 0.05) 2 weeks after injury in femoral versus carotid arteries as determined by the intima/media ratio. Although the percentage of F4/80/CX3CR1<sup>+</sup> cell integration was similar in both models, the carotid lesion had greater proportions of cells coexpressing CX3CR1 and both α-smooth muscle actin and calponin (p &lt; 0.05). Wire injury of carotid arteries was associated with greater CX3CL1 expression in the acute phase followed by greater CX3CR1 coexpressing SMLC content in later lesions as well as less neointima formation than in femoral arteries. This may, in part, explain the variability in lesion composition after carotid versus femoral wire injury.
DOI: 10.6084/m9.figshare.5124904
title: Supplementary Material for: Hyperuricemia Is an Independent Risk Factor for Mortality Only if Chronic Kidney Disease Is Present

description: <b><i>Background/Aims:</i></b> Hyperuricemia has been considered a risk factor for renal disease and cardiovascular disease. However, the potential contribution of hyperuricemia to mortality remains uncertain, and the results in the available literature vary according to kidney function. The aim of this study was to determine the association between hyperuricemia and mortality in patients undergoing percutaneous coronary intervention (PCI) across the interaction of kidney function. <b><i>Method:</i></b> We retrospectively reviewed patients who underwent PCI from 2003 to 2009. Propensity scores for hyperuricemia (&gt;7 mg/dl for males and &gt;6 mg/dl for females) were used to assemble a matched cohort of 693 pairs of patients with and without hyperuricemia for analysis from the 3,201 patients who fulfilled the inclusion criteria among the 4,842 patients who underwent PCI. <b><i>Results:</i></b> Of the 3,201 patients who underwent PCI and for whom data were available regarding their baseline serum uric acid level, 763 (23.8%) had hyperuricemia. The hyperuricemia-associated hazard ratios (HRs) [95% confidence intervals (CIs)] for all-cause mortality were 1.780 (1.270-2.495) in the unmatched cohort and 1.655 (1.109-2.468) in the matched cohort. The HRs (95% CI) for all-cause mortality among those with and without chronic kidney disease (CKD) were 2.080 (1.318-3.283) and 1.592 (0.778-3.256), respectively (p for interaction, 0.001). <b><i>Conclusions:</i></b> Hyperuricemia is an independent risk factor for all-cause mortality in those patients with CKD but not in those without CKD.
DOI: 10.6084/m9.figshare.5124895
title: Supplementary Material for: HIV-1 Nef Interacts with HCV Core, Recruits TRAF2, TRAF5 and TRAF6, and Stimulates HIV-1 Replication in Macrophages

description: Tumor necrosis factor receptor-associated factor (TRAF) signaling plays a central role in many biological activities, such as the regulation of immune and inflammatory responses and control of apoptosis, which are key events in the pathogenesis of the human immunodeficiency virus (HIV)-1 and the hepatitis C virus (HCV) infections. Here we show that TRAF2, TRAF5 and TRAF6 interact with the HIV-1 Nef protein, an immunomodulatory viral protein expressed and released by cells infected by the virus. We also found that TRAF2 and TRAF5 interact with the HCV Core protein. Interestingly, we observed that HIV-1 Nef interacts with HCV Core. The activation of TRAF (2, 5, 6) - mediated by HIV-1 Nef and HCV Core - enhanced the activation of the nuclear factor-kappa B (NF-κB) and increased HIV-1 replication in monocyte- derived macrophages (MDMs). The knockdown of TRAF2, TRAF5 and TRAF6 resulted in decreased NF-κB activation and reduced HIV-1 replication in MDMs. Our results reveal a mechanism by which the activation of the TRAF pathway by HIV-1 Nef and HCV Core favors the replication of HIV-1 in macrophages and could be a critical factor for optimal replication of HIV-1 in macrophages of HIV-HCV-coinfected patients.
DOI: 10.6084/m9.figshare.5124898
title: Supplementary Material for: CD300c is an Activating Receptor Expressed on Human Monocytes

description: Human CD300 molecules comprise a family of receptors that regulate many immune cell processes. They are mostly expressed on myeloid cells, although expression of two members, CD300a and CD300c, has also been described on lymphocytes. However, due to the lack of specific antibodies that distinguish between these two receptors, it has been difficult to determine the expression pattern and function of CD300a and CD300c in primary cells. Here, we have identified a specific monoclonal antibody, clone TX45, that recognizes only CD300c and show that within freshly isolated blood leukocytes, monocytes are the only cells that express CD300c on the cell surface. In vitro differentiation experiments revealed that CD300c is differentially expressed on different monocyte-derived cells, including macrophages and dendritic cells. Furthermore, TLR ligands LPS and flagellin dynamically regulate the expression of CD300c. Cross-linking of this receptor with clone TX45 monoclonal antibody induced calcium mobilization, upregulation of the costimulatory molecule CD86 and the production of inflammatory cytokines. Importantly, LPS-mediated production of inflammatory cytokines by monocytes was further enhanced if CD300c was simultaneously engaged by the agonist antibody. Altogether, our results show that human CD300c is an activating receptor expressed on monocytes and that it has a potential role in inflammatory responses.
DOI: 10.6084/m9.figshare.5125087.v10
title: Inferring the effects of sink strength on plant carbon balance processes from experimental measurements

description: This folder consists of existing dataset from the container volume experiment which was carried out at the Hawkesbury Forest Experiment site (33°37'S 150°44'E) in Richmond, NSW, Australia. The site and experimental setup have been explained in detail by Campany et al. (2017). <br>In brief, 20 weeks old Eucalyptus tereticornis seedlings in tube stock were chosen from a single local Cumberland plain cohort. Ten additional seedlings of similar age and growth were harvested to measure initial leaf area and dry mass of leaves, stems and roots. A total of 49 Eucalyptus tereticornis seedlings were grown in a range of container sizes (5 L to 35 L) in field conditions, using freely-rooted seedlings as a control for the container size treatments, with the goal to examine how the C balance of the plants are affected to belowground sink limitations. Six container sizes were used with each container experiment had a complete replicate set of six container volumes along with a free seedling. Similar notations are used here as Campany et al. (2017) for the treatments in different pots as 5 L, 10 L, 15 L, 20 L, 25 L and 35 L in respect of their pot sizes. The experiment tracked leaf-level gas exchange, leaf carbohydrate accumulation and seedling allometry over the course of 4 months for all 7 treatments.
DOI: 10.6084/m9.figshare.5124904.v1
title: Supplementary Material for: Hyperuricemia Is an Independent Risk Factor for Mortality Only if Chronic Kidney Disease Is Present

description: <b><i>Background/Aims:</i></b> Hyperuricemia has been considered a risk factor for renal disease and cardiovascular disease. However, the potential contribution of hyperuricemia to mortality remains uncertain, and the results in the available literature vary according to kidney function. The aim of this study was to determine the association between hyperuricemia and mortality in patients undergoing percutaneous coronary intervention (PCI) across the interaction of kidney function. <b><i>Method:</i></b> We retrospectively reviewed patients who underwent PCI from 2003 to 2009. Propensity scores for hyperuricemia (&gt;7 mg/dl for males and &gt;6 mg/dl for females) were used to assemble a matched cohort of 693 pairs of patients with and without hyperuricemia for analysis from the 3,201 patients who fulfilled the inclusion criteria among the 4,842 patients who underwent PCI. <b><i>Results:</i></b> Of the 3,201 patients who underwent PCI and for whom data were available regarding their baseline serum uric acid level, 763 (23.8%) had hyperuricemia. The hyperuricemia-associated hazard ratios (HRs) [95% confidence intervals (CIs)] for all-cause mortality were 1.780 (1.270-2.495) in the unmatched cohort and 1.655 (1.109-2.468) in the matched cohort. The HRs (95% CI) for all-cause mortality among those with and without chronic kidney disease (CKD) were 2.080 (1.318-3.283) and 1.592 (0.778-3.256), respectively (p for interaction, 0.001). <b><i>Conclusions:</i></b> Hyperuricemia is an independent risk factor for all-cause mortality in those patients with CKD but not in those without CKD.