cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.5281/zenodo.3939717
title: IODP Expedition 362, Hole U1480G - Well Logging Data

description: Logging data are measurements of physical properties of the formation surrounding a borehole, acquired in situ after completion of coring (wireline logging) or during drilling (Logging-While-Drilling, LWD). The range of data (resistivity, gamma radiation, velocity, density, borehole images,…) in any hole depends on the scientific objectives and operational constraints.
description: IODP Expedition 362: Sumatra Seismogenic Zone
DOI: 10.15468/ufcgtw
title: A new species of Loneura Navás and taxonomic update of L. boliviana Williner and L. meridionalis García Aldrete (Psocodea: Psocomorpha: Ptiloneuridae)

description: This dataset contains the digitized treatments in Plazi based on the original journal article Cutrim, Marcelo, Neto, Alberto Moreira Da Silva, García Aldrete, Alfonso N., Rafael, José Albertino (2021): A new species of Loneura Navás and taxonomic update of L. boliviana Williner and L. meridionalis García Aldrete (Psocodea: Psocomorpha: Ptiloneuridae). Zootaxa 4969 (1): 135-148, DOI: https://doi.org/10.11646/zootaxa.4969.1.7
DOI: 10.6084/m9.figshare.5120851.v1
title: Anti-acetylcholinesterase activity and antioxidant properties of extracts and fractions of <i>Carpolobia lutea</i>

description: <b>Context:</b> There is an unmet need to discover new treatments for Alzheimer’s disease. This study determined the anti-acetylcholinesterase (AChE) activity, DPPH free radical scavenging and antioxidant properties of <i>Carpolobia lutea</i> G. Don (Polygalaceae). <b>Objective:</b> The objective of this study is to quantify <i>C. lutea</i> anti-AChE, DPPH free radical scavenging, and antioxidant activities and cell cytotoxicity. <b>Materials and methods:</b> Plant stem, leaves and roots were subjected to sequential solvent extractions, and screened for anti-AChE activity across a concentration range of 0.02–200 μg/mL. Plant DPPH radical scavenging activity, reducing power, and total phenolic and flavonoid contents were determined, and cytotoxicity evaluated using human hepatocytes. <b>Results:</b><i>Carpolobia lutea</i> exhibited concentration-dependent anti-AChE activity. The most potent inhibitory activity for the stem was the crude ethanol extract and hexane stem fraction oil (IC<sub>50</sub> = 140 μg/mL); for the leaves, the chloroform leaf fraction (IC<sub>50</sub> = 60 μg/mL); and for roots, the methanol, ethyl acetate and aqueous root fractions (IC<sub>50</sub> = 0.3–3 μg/mL). Dose-dependent free radical scavenging activity and reducing power were observed with increasing stem, leaf or root concentration. Total phenolic contents were the highest in the stem: ∼632 mg gallic acid equivalents/g for a hexane stem fraction oil. Total flavonoid content was the highest in the leaves: ∼297 mg quercetin equivalents/g for a chloroform leaf fraction. At 1 μg/mL, only the crude ethanol extract oil was significantly cytotoxic to hepatocytes. <b>Discussion and conclusions:</b><i>Carpolobia lutea</i> possesses anti-AChE activity and beneficial antioxidant capacity indicative of its potential development as a treatment of Alzheimer’s and other diseases characterized by a cholinergic deficit.
DOI: 10.6084/m9.figshare.3806598.v1
title: Fruit vinegars attenuate cardiac injury via anti-inflammatory and anti-adiposity actions in high-fat diet-induced obese rats

description: <b>Context:</b> Fruit vinegars (FVs) are used in Mediterranean folk medicine for their hypolipidemic and weight-reducing properties. <b>Objective:</b> To investigate the preventive effects of three types of FV, commonly available in Algeria, namely prickly pear [<i>Opuntia ficus-indica</i> (L.) Mill (Cectaceae)], pomegranate [<i>Punica granatum</i> L. (Punicaceae)], and apple [<i>Malus domestica</i> Borkh. (Rosaceae)], against obesity-induced cardiomyopathy and its underlying mechanisms. <b>Materials and methods:</b> Seventy-two male Wistar rats were equally divided into 12 groups. The first group served as normal control (distilled water, 7 mL/kg bw), and the remaining groups were respectively treated with distilled water (7 mL/kg bw), acetic acid (0.5% w/v, 7 mL/kg bw) and vinegars of pomegranate, apple or prickly pear (at doses of 3.5, 7 and 14 mL/kg bw, acetic acid content as mentioned above) along with a high-fat diet (HFD). The effects of the oral administration of FV for 18 weeks on the body and visceral adipose tissue (VAT) weights, plasma inflammatory and cardiac enzymes biomarkers, and in heart tissue were evaluated. <b>Results:</b> Vinegars treatments significantly (<i>p</i> <b>Discussion and conclusion:</b> These findings suggest that pomegranate, apple and prickly pear vinegars may prevent HFD-induced obesity and obesity-related cardiac complications, and that this prevention may result from the potent anti-inflammatory and anti-adiposity properties of these vinegars.
DOI: 10.5255/ukda-sn-854753
title: N - 2 Repetition Cost Using a Truncated Trial Procedure in a Single-registration and Double-registration Design, 2018-2019

description: Backward inhibition has been posited to aid our ability to switch between tasks by counteracting the tendency to repeat a recently performed task. Evidence suggests that backward inhibition might be triggered during task-preparation, prior to performance, yet so far it has not been detected following trials involving task-preparation but no task-performance (Schuch & Koch, 2003 and Philipp, Jolicoeur, Falkenstein & Koch, 2007). However, those previous studies deployed a nogo method that might have prevented preparation-driven effects from being detected, due to the nogo signal wiping the effects of task processing (Lenartowicz, Yeung, & Cohen, 2011). To avoid the need for a nogo signal, we truncated trial n – 1 following task-preparation and used the n – 2 repetition cost (ABA versus CBA trial sequences) to measure the effect of returning to a previous task. In the cue-only abstract cues experiment we used abstract cues in an attempt to increase the size of any potential n – 2 repetition cost triggered by preparation on the preceding trial. In the double-registration cue-only experiment, responses were required to cues as well as to targets, to enable us to know that participants did some form of preparation on the truncated trials. In both experiments, the existence of an n – 2 repetition cost following truncated trials would constitute evidence that backward inhibition can be triggered task-preparation.
DOI: 10.5281/zenodo.4811884
title: ANANSE GRN references

description: Gene Ontology and expression correlation GRN references. See ANANSE manuscript for details: https://www.biorxiv.org/content/10.1101/2020.06.05.135798v2
DOI: 10.5281/zenodo.4811883
title: ANANSE GRN references

description: Gene Ontology and expression correlation GRN references. See ANANSE manuscript for details: https://www.biorxiv.org/content/10.1101/2020.06.05.135798v2
DOI: 10.6084/m9.figshare.11513178
title: High spatiotemporal resolution mapping of global urban change from 1985 to 2015

description: This dataset includes three parts:<br>(1) The mapped global annual urban dynamics (GAUD) and green recovery from 1985 to 2015 at a 30-m resolution. This part of data is organized by 10-degree grids (totally 224).Shapefiles of 10-degree grids can be found in "grids_world.zip".Urban expansion data is packaged in "urban_grid_i.zip" (i ranges from 0 to 223). Green recovery data is packaged in "green_grid_0-223.zip".Their format is GeoTiff, and for each pixel, values from 1985 to 2015 demonstrate the urbanized or green recovery year, while 0 means no data.<br>(2) The interpreted samples of urban extent in 1985 and 2015, and urbanized year during 1985 and 2015. This part of data is for examining the accuracies of our data fusion and temporal segmentation approach. Interpreted urban extent is packaged in "Ref_tif_clip_1985.rar" and "Ref_tif_clip_2015.rar".Its format is GeoTiff, and for each pixel, value 1 means urban areas, while 0 means non-urban areas.Valid samples of urbanized year can be found in "validation_urbanized_year.xls".<br>(3) A demo of NUACI calculation and urbanized years dectection can be found at link:https://code.earthengine.google.com/1c901129fa8c9d81b292824e8fb4ff1c<br>22.05.2021:Solved the problem of stripe after image mosaic (grid 138)<br><br>
DOI: 10.6084/m9.figshare.14089017.v3
title: Mouse models for hereditary spastic paraplegia uncover a role of PI4K2A in autophagic lysosome reformation

description: Hereditary spastic paraplegia (HSP) denotes genetically heterogeneous disorders characterized by leg spasticity due to degeneration of corticospinal axons. SPG11 and SPG15 have a similar clinical course and together are the most prevalent autosomal recessive HSP entity. The respective proteins play a role for macroautophagy/autophagy and autophagic lysosome reformation (ALR). Here, we report that <i>spg11</i> and <i>zfyve26</i> KO mice developed motor impairments within the same course of time. This correlated with enhanced accumulation of autofluorescent material in neurons and progressive neuron loss. In agreement with defective ALR, tubulation events were diminished in starved KO mouse embryonic fibroblasts (MEFs) and lysosomes decreased in neurons of KO brain sections. Confirming that both proteins act in the same molecular pathway, the pathologies were not aggravated upon simultaneous disruption of both. We further show that PI4K2A (phosphatidylinositol 4-kinase type 2 alpha), which phosphorylates phosphatidylinositol to phosphatidylinositol-4-phosphate (PtdIns4P), accumulated in autofluorescent deposits isolated from KO but not WT brains. Elevated PI4K2A abundance was already found at autolysosomes of neurons of presymptomatic KO mice. Immunolabelings further suggested higher levels of PtdIns4P at LAMP1-positive structures in starved KO MEFs. An increased association with LAMP1-positive structures was also observed for clathrin and DNM2/dynamin 2, which are important effectors of ALR recruited by phospholipids. Because PI4K2A overexpression impaired ALR, while its knockdown increased tubulation, we conclude that PI4K2A modulates phosphoinositide levels at autolysosomes and thus the recruitment of downstream effectors of ALR. Therefore, PI4K2A may play an important role in the pathogenesis of SPG11 and SPG15. <b>Abbreviations</b>: ALR: autophagic lysosome reformation; AP-5: adaptor protein complex 5; BFP: blue fluorescent protein; dKO: double knockout; EBSS: Earle’s balanced salt solution; FBA: foot base angle; GFP: green fluorescent protein; HSP: hereditary spastic paraplegia; KO: knockout; LAMP1: lysosomal-associated membrane protein 1; MAP1LC3B/LC3: microtubule-associated protein 1 light chain 3 beta; MEF: mouse embryonic fibroblast; SQSTM1/p62: sequestosome 1; PI4K2A: phosphatidylinositol 4-kinase type 2 alpha; PtdIns3P: phosphatidylinositol-3-phosphate; PtdIns4P: phosphatidylinositol-4-phosphate; RFP: red fluorescent protein; SPG: spastic paraplegia gene; TGN: trans-Golgi network; WT: wild type
DOI: 10.6084/m9.figshare.14089017.v2
title: Mouse models for hereditary spastic paraplegia uncover a role of PI4K2A in autophagic lysosome reformation

description: Hereditary spastic paraplegia (HSP) denotes genetically heterogeneous disorders characterized by leg spasticity due to degeneration of corticospinal axons. SPG11 and SPG15 have a similar clinical course and together are the most prevalent autosomal recessive HSP entity. The respective proteins play a role for macroautophagy/autophagy and autophagic lysosome reformation (ALR). Here, we report that <i>spg11</i> and <i>zfyve26</i> KO mice developed motor impairments within the same course of time. This correlated with enhanced accumulation of autofluorescent material in neurons and progressive neuron loss. In agreement with defective ALR, tubulation events were diminished in starved KO mouse embryonic fibroblasts (MEFs) and lysosomes decreased in neurons of KO brain sections. Confirming that both proteins act in the same molecular pathway, the pathologies were not aggravated upon simultaneous disruption of both. We further show that PI4K2A (phosphatidylinositol 4-kinase type 2 alpha), which phosphorylates phosphatidylinositol to phosphatidylinositol-4-phosphate (PtdIns4P), accumulated in autofluorescent deposits isolated from KO but not WT brains. Elevated PI4K2A abundance was already found at autolysosomes of neurons of presymptomatic KO mice. Immunolabelings further suggested higher levels of PtdIns4P at LAMP1-positive structures in starved KO MEFs. An increased association with LAMP1-positive structures was also observed for clathrin and DNM2/dynamin 2, which are important effectors of ALR recruited by phospholipids. Because PI4K2A overexpression impaired ALR, while its knockdown increased tubulation, we conclude that PI4K2A modulates phosphoinositide levels at autolysosomes and thus the recruitment of downstream effectors of ALR. Therefore, PI4K2A may play an important role in the pathogenesis of SPG11 and SPG15. <b>Abbreviations</b>: ALR: autophagic lysosome reformation; AP-5: adaptor protein complex 5; BFP: blue fluorescent protein; dKO: double knockout; EBSS: Earle’s balanced salt solution; FBA: foot base angle; GFP: green fluorescent protein; HSP: hereditary spastic paraplegia; KO: knockout; LAMP1: lysosomal-associated membrane protein 1; MAP1LC3B/LC3: microtubule-associated protein 1 light chain 3 beta; MEF: mouse embryonic fibroblast; SQSTM1/p62: sequestosome 1; PI4K2A: phosphatidylinositol 4-kinase type 2 alpha; PtdIns3P: phosphatidylinositol-3-phosphate; PtdIns4P: phosphatidylinositol-4-phosphate; RFP: red fluorescent protein; SPG: spastic paraplegia gene; TGN: trans-Golgi network; WT: wild type
DOI: 10.6084/m9.figshare.14676504.v3
title: Item Matrix for Evaluating the External Evaluation of Primary Health Care.docx

description: MIND / AE / PMAQ-AB has 06 dimensions, 24 subdimensions and 38 items. It presents an adequacy of the theoretical bases - guided by the dimensions proposed in the Centers for Disease Control and Prevention (CDC) framework and by the rules and criteria of the Joint Committee on Standards for Educational Evaluation (JCSEE) to the theoretical assumptions and the design of an External Assessment of Attention Primary to Health. For MIND / AE / PMAQ-AB, we maintained the proposed dimensions with their respective standards and criteria, systematizing them in items.
DOI: 10.6084/m9.figshare.12851384.v1
title: RETREG1/FAM134B mediated autophagosomal degradation of AMFR/GP78 and OPA1 —a dual organellar turnover mechanism

description: Turnover of cellular organelles, including endoplasmic reticulum (ER) and mitochondria, is orchestrated by an efficient cellular surveillance system. We have identified a mechanism for dual regulation of ER and mitochondria under stress. It is known that AMFR, an ER E3 ligase and ER-<i>a</i>ssociated <i>d</i>egradation (ERAD) regulator, degrades outer mitochondrial membrane (OMM) proteins, MFNs (mitofusins), via the proteasome and triggers mitophagy. We show that destabilized mitochondria are almost devoid of the OMM and generate “mitoplasts”. This brings the inner mitochondrial membrane (IMM) in the proximity of the ER. When AMFR levels are high and the mitochondria are stressed, the reticulophagy regulatory protein RETREG1 participates in the formation of the mitophagophore by interacting with OPA1. Interestingly, OPA1 and other IMM proteins exhibit similar RETREG1-dependent autophagosomal degradation as AMFR, unlike most of the OMM proteins. The “mitoplasts” generated are degraded by reticulo-mito-phagy – simultaneously affecting dual organelle turnover.
DOI: 10.15468/dxpk7m
title: New species and a new record of Entomobryinae (Collembola, Entomobryomorpha) from Amurskaya Region (the Far East of Russia)

description: This dataset contains the digitized treatments in Plazi based on the original journal article Baquero, Enrique, Potapov, Mikhail, Jordana, Rafael (2021): New species and a new record of Entomobryinae (Collembola, Entomobryomorpha) from Amurskaya Region (the Far East of Russia). Zootaxa 4969 (1): 119-134, DOI: https://doi.org/10.11646/zootaxa.4969.1.6
DOI: 10.18430/m37mhv
title: X-ray diffraction data for the crystal Structure of Cysteine desulfurase NifS from Legionella pneumophila Philadelphia 1 in complex with pyridoxal 5'-phosphate (7MHV)
DOI: 10.6084/m9.figshare.1460859
title: Intramembrane protease PARL defines a negative regulator of PINK1- and PARK2/Parkin-dependent mitophagy

description: Mutations in PINK1 and PARK2/Parkin are a main risk factor for familial Parkinson disease. While the physiological mechanism of their activation is unclear, these proteins have been shown in tissue culture cells to serve as a key trigger for autophagy of depolarized mitochondria. Here we show that ablation of the mitochondrial rhomboid protease PARL leads to retrograde translocation of an intermembrane space-bridging PINK1 import intermediate. Subsequently, it is rerouted to the outer membrane in order to recruit PARK2, which phenocopies mitophagy induction by uncoupling agents. Consistent with a role of this retrograde translocation mechanism in neurodegenerative disease, we show that pathogenic PINK1 mutants which are not cleaved by PARL affect PINK1 kinase activity and the ability to induce PARK2-mediated mitophagy. Altogether we suggest that PARL is an important intrinsic player in mitochondrial quality control, a system substantially impaired in Parkinson disease as indicated by reduced removal of damaged mitochondria in affected patients.
DOI: 10.6084/m9.figshare.1460859.v5
title: Intramembrane protease PARL defines a negative regulator of PINK1- and PARK2/Parkin-dependent mitophagy

description: Mutations in PINK1 and PARK2/Parkin are a main risk factor for familial Parkinson disease. While the physiological mechanism of their activation is unclear, these proteins have been shown in tissue culture cells to serve as a key trigger for autophagy of depolarized mitochondria. Here we show that ablation of the mitochondrial rhomboid protease PARL leads to retrograde translocation of an intermembrane space-bridging PINK1 import intermediate. Subsequently, it is rerouted to the outer membrane in order to recruit PARK2, which phenocopies mitophagy induction by uncoupling agents. Consistent with a role of this retrograde translocation mechanism in neurodegenerative disease, we show that pathogenic PINK1 mutants which are not cleaved by PARL affect PINK1 kinase activity and the ability to induce PARK2-mediated mitophagy. Altogether we suggest that PARL is an important intrinsic player in mitochondrial quality control, a system substantially impaired in Parkinson disease as indicated by reduced removal of damaged mitochondria in affected patients.
DOI: 10.6084/m9.figshare.1460859.v4
title: Intramembrane protease PARL defines a negative regulator of PINK1- and PARK2/Parkin-dependent mitophagy

description: Mutations in PINK1 and PARK2/Parkin are a main risk factor for familial Parkinson disease. While the physiological mechanism of their activation is unclear, these proteins have been shown in tissue culture cells to serve as a key trigger for autophagy of depolarized mitochondria. Here we show that ablation of the mitochondrial rhomboid protease PARL leads to retrograde translocation of an intermembrane space-bridging PINK1 import intermediate. Subsequently, it is rerouted to the outer membrane in order to recruit PARK2, which phenocopies mitophagy induction by uncoupling agents. Consistent with a role of this retrograde translocation mechanism in neurodegenerative disease, we show that pathogenic PINK1 mutants which are not cleaved by PARL affect PINK1 kinase activity and the ability to induce PARK2-mediated mitophagy. Altogether we suggest that PARL is an important intrinsic player in mitochondrial quality control, a system substantially impaired in Parkinson disease as indicated by reduced removal of damaged mitochondria in affected patients.
DOI: 10.6084/m9.figshare.1493046
title: Long-term live imaging reveals cytosolic immune responses of host hepatocytes against <i>Plasmodium</i> infection and parasite escape mechanisms

description: <i>Plasmodium</i> parasites are transmitted by <i>Anopheles</i> mosquitoes to the mammalian host and actively infect hepatocytes after passive transport in the bloodstream to the liver. In their target host hepatocyte, parasites reside within a parasitophorous vacuole (PV). In the present study it was shown that the parasitophorous vacuole membrane (PVM) can be targeted by autophagy marker proteins LC3, ubiquitin, and SQSTM1/p62 as well as by lysosomes in a process resembling selective autophagy. The dynamics of autophagy marker proteins in individual <i>Plasmodium berghei</i>-infected hepatocytes were followed by live imaging throughout the entire development of the parasite in the liver. Although the host cell very efficiently recognized the invading parasite in its vacuole, the majority of parasites survived this initial attack. Successful parasite development correlated with the gradual loss of all analyzed autophagy marker proteins and associated lysosomes from the PVM. However, other autophagic events like nonselective canonical autophagy in the host cell continued. This was indicated as LC3, although not labeling the PVM anymore, still localized to autophagosomes in the infected host cell. It appears that growing parasites even benefit from this form of nonselective host cell autophagy as an additional source of nutrients, as in host cells deficient for autophagy, parasite growth was retarded and could partly be rescued by the supply of additional amino acid in the medium. Importantly, mouse infections with <i>P. berghei</i> sporozoites confirmed LC3 dynamics, the positive effect of autophagy activation on parasite growth, and negative effects upon autophagy inhibition.
DOI: 10.6084/m9.figshare.1501108.v5
title: The marine n-3 PUFA DHA evokes cytoprotection against oxidative stress and protein misfolding by inducing autophagy and NFE2L2 in human retinal pigment epithelial cells

description: Accumulation and aggregation of misfolded proteins is a hallmark of several diseases collectively known as proteinopathies. Autophagy has a cytoprotective role in diseases associated with protein aggregates. Age-related macular degeneration (AMD) is the most common neurodegenerative eye disease that evokes blindness in elderly. AMD is characterized by degeneration of retinal pigment epithelial (RPE) cells and leads to loss of photoreceptor cells and central vision. The initial phase associates with accumulation of intracellular lipofuscin and extracellular deposits called drusen. Epidemiological studies have suggested an inverse correlation between dietary intake of marine n-3 polyunsaturated fatty acids (PUFAs) and the risk of developing neurodegenerative diseases, including AMD. However, the disease-preventive mechanism(s) mobilized by n-3 PUFAs is not completely understood. In human retinal pigment epithelial cells we find that physiologically relevant doses of the n-3 PUFA docosahexaenoic acid (DHA) induce a transient increase in cellular reactive oxygen species (ROS) levels that activates the oxidative stress response regulator NFE2L2/NRF2 (nuclear factor, erythroid derived 2, like 2). Simultaneously, there is a transient increase in intracellular protein aggregates containing SQSTM1/p62 (sequestosome 1) and an increase in autophagy. Pretreatment with DHA rescues the cells from cell cycle arrest induced by misfolded proteins or oxidative stress. Cells with a downregulated oxidative stress response, or autophagy, respond with reduced cell growth and survival after DHA supplementation. These results suggest that DHA both induces endogenous antioxidants and mobilizes selective autophagy of misfolded proteins. Both mechanisms could be relevant to reduce the risk of developing aggregate-associate diseases such as AMD.