cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.5309725.v1
title: Mask mitigates MAPT- and FUS-induced degeneration by enhancing autophagy through lysosomal acidification

description: Accumulation of intracellular misfolded or damaged proteins is associated with both normal aging and late-onset degenerative diseases. Two cellular clearance mechanisms, the ubiquitin-proteasome system (UPS) and the macroautophagy/autophagy-lysosomal pathway, work in concert to degrade harmful protein aggregates and maintain protein homeostasis. Here we show that Mask, an Ankyrin-repeat and KH-domain containing protein, plays a key role in promoting autophagy flux and mitigating degeneration caused by protein aggregation or impaired UPS function. In <i>Drosophila</i> eye models of human tauopathy or amyotrophic lateral sclerosis diseases, loss of Mask function enhanced, while gain of Mask function mitigated, eye degenerations induced by eye-specific expression of human pathogenic MAPT/TAU or FUS proteins. The fly larval muscle, a more accessible tissue, was then used to study the underlying molecular mechanisms in vivo. We found that Mask modulates the global abundance of K48- and K63-ubiquitinated proteins by regulating autophagy-lysosome-mediated degradation, but not UPS function. Indeed, upregulation of Mask compensated the partial loss of UPS function. We further demonstrate that Mask promotes autophagic flux by enhancing lysosomal function, and that Mask is necessary and sufficient for promoting the expression levels of the proton-pumping vacuolar (V)-type ATPases in a TFEB-independent manner. Moreover, the beneficial effects conferred by Mask expression on the UPS dysfunction and neurodegenerative models depend on intact autophagy-lysosomal pathway. Our findings highlight the importance of lysosome acidification in cellular surveillance mechanisms and establish a model for exploring strategies to mitigate neurodegeneration by boosting lysosomal function.
DOI: 10.6084/m9.figshare.5313484
title: Relating Dynamic Brain States to Dynamic Machine States: Human and Machine Solutions to the Speech Recognition Problem

description: There is widespread interest in the relationship between the neurobiological systems supporting human cognition and emerging computational systems capable of emulating these capacities. Human speech comprehension, poorly understood as a neurobiological process, is an important case in point. Automatic Speech Recognition (ASR) systems with near-human levels of performance are now available, which provide a computationally explicit solution for the recognition of words in continuous speech. This research aims to bridge the gap between speech recognition processes in humans and machines, using novel multivariate techniques to compare incremental ‘machine states’, generated as the ASR analysis progresses over time, to the incremental ‘brain states’, measured using combined electro- and magneto-encephalography (EMEG), generated as the same inputs are heard by human listeners. This direct comparison of dynamic human and machine internal states, as they respond to the same incrementally delivered sensory input, revealed a significant correspondence between neural response patterns in human superior temporal cortex and the structural properties of ASR-derived phonetic models. Spatially coherent patches in human temporal cortex responded selectively to individual phonetic features defined on the basis of machine-extracted regularities in the speech to lexicon mapping process. These results demonstrate the feasibility of relating human and ASR solutions to the problem of speech recognition, and suggest the potential for further studies relating complex neural computations in human speech comprehension to the rapidly evolving ASR systems that address the same problem domain.
DOI: 10.6084/m9.figshare.5313484.v1
title: Relating Dynamic Brain States to Dynamic Machine States: Human and Machine Solutions to the Speech Recognition Problem

description: There is widespread interest in the relationship between the neurobiological systems supporting human cognition and emerging computational systems capable of emulating these capacities. Human speech comprehension, poorly understood as a neurobiological process, is an important case in point. Automatic Speech Recognition (ASR) systems with near-human levels of performance are now available, which provide a computationally explicit solution for the recognition of words in continuous speech. This research aims to bridge the gap between speech recognition processes in humans and machines, using novel multivariate techniques to compare incremental ‘machine states’, generated as the ASR analysis progresses over time, to the incremental ‘brain states’, measured using combined electro- and magneto-encephalography (EMEG), generated as the same inputs are heard by human listeners. This direct comparison of dynamic human and machine internal states, as they respond to the same incrementally delivered sensory input, revealed a significant correspondence between neural response patterns in human superior temporal cortex and the structural properties of ASR-derived phonetic models. Spatially coherent patches in human temporal cortex responded selectively to individual phonetic features defined on the basis of machine-extracted regularities in the speech to lexicon mapping process. These results demonstrate the feasibility of relating human and ASR solutions to the problem of speech recognition, and suggest the potential for further studies relating complex neural computations in human speech comprehension to the rapidly evolving ASR systems that address the same problem domain.
DOI: 10.6084/m9.figshare.25467661
title: GaliciaNorthPortugal-Euroregion-University-Hospital_Inpatientdatabase

description: Efficient care management is key to the smooth running of any hospital, and also has a major economic and health impact on the population as a whole. One of the most important aspects of hospital care management and bed occupancy in the different departments is the quantitative and qualitative impact on the care that can be provided to patients.
In this work we will carry out an exhaustive analysis of the occupancy situation in the CHUS services with the highest number of admissions in recent years. The aim is to identify the critical points (both in terms of excess and limitation of existing beds) and to propose improvement actions where they are most needed. For this purpose, both spatial statistics and regression techniques will be used to model bed occupancy.
DOI: 10.6084/m9.figshare.25467661.v1
title: GaliciaNorthPortugal-Euroregion-University-Hospital_Inpatientdatabase

description: Efficient care management is key to the smooth running of any hospital, and also has a major economic and health impact on the population as a whole. One of the most important aspects of hospital care management and bed occupancy in the different departments is the quantitative and qualitative impact on the care that can be provided to patients.
In this work we will carry out an exhaustive analysis of the occupancy situation in the CHUS services with the highest number of admissions in recent years. The aim is to identify the critical points (both in terms of excess and limitation of existing beds) and to propose improvement actions where they are most needed. For this purpose, both spatial statistics and regression techniques will be used to model bed occupancy.
DOI: 10.6084/m9.figshare.5314822
title: Genomic history of the seventh pandemic of cholera in Africa

description: Africa was hit by cholera in 1970 and has since become the continent most affected by the seventh pandemic. We use high-resolution population-level genomic data to explain how cholera has spread consistently, and potentially predictably, across Africa between 1970 and 2014. We show that cholera was introduced at least 11 times, at two preferential foci — one in West Africa and the other in Eastern/Southern Africa — causing widespread epidemics lasting from a few years to almost 30 years. We also show that the last five introductions of cholera, all imported from Asia, involved multidrug-resistant Vibrio cholerae O1 lineages, resulting in the disappearance of antibiotic-susceptible isolates in Africa after 2000. The demonstration of the predictable nature of the introduction of a globally important multidrug-resistant infectious disease through stable transmission routes traversing Africa changes the paradigm for the control and prevention of this disease.<br><br>
DOI: 10.6084/m9.figshare.5314822.v1
title: Genomic history of the seventh pandemic of cholera in Africa

description: Africa was hit by cholera in 1970 and has since become the continent most affected by the seventh pandemic. We use high-resolution population-level genomic data to explain how cholera has spread consistently, and potentially predictably, across Africa between 1970 and 2014. We show that cholera was introduced at least 11 times, at two preferential foci — one in West Africa and the other in Eastern/Southern Africa — causing widespread epidemics lasting from a few years to almost 30 years. We also show that the last five introductions of cholera, all imported from Asia, involved multidrug-resistant Vibrio cholerae O1 lineages, resulting in the disappearance of antibiotic-susceptible isolates in Africa after 2000. The demonstration of the predictable nature of the introduction of a globally important multidrug-resistant infectious disease through stable transmission routes traversing Africa changes the paradigm for the control and prevention of this disease.<br><br>
DOI: 10.6084/m9.figshare.5314822.v2
title: Genomic history of the seventh pandemic of cholera in Africa

description: Africa was hit by cholera in 1970 and has since become the continent most affected by the seventh pandemic. We use high-resolution population-level genomic data to explain how cholera has spread consistently, and potentially predictably, across Africa between 1970 and 2014. We show that cholera was introduced at least 11 times, at two preferential foci — one in West Africa and the other in Eastern/Southern Africa — causing widespread epidemics lasting from a few years to almost 30 years. We also show that the last five introductions of cholera, all imported from Asia, involved multidrug-resistant Vibrio cholerae O1 lineages, resulting in the disappearance of antibiotic-susceptible isolates in Africa after 2000. The demonstration of the predictable nature of the introduction of a globally important multidrug-resistant infectious disease through stable transmission routes traversing Africa changes the paradigm for the control and prevention of this disease.<br><br>
DOI: 10.6084/m9.figshare.5314822.v3
title: Genomic history of the seventh pandemic of cholera in Africa

description: Africa was hit by cholera in 1970 and has since become the continent most affected by the seventh pandemic. We use high-resolution population-level genomic data to explain how cholera has spread consistently, and potentially predictably, across Africa between 1970 and 2014. We show that cholera was introduced at least 11 times, at two preferential foci — one in West Africa and the other in Eastern/Southern Africa — causing widespread epidemics lasting from a few years to almost 30 years. We also show that the last five introductions of cholera, all imported from Asia, involved multidrug-resistant Vibrio cholerae O1 lineages, resulting in the disappearance of antibiotic-susceptible isolates in Africa after 2000. The demonstration of the predictable nature of the introduction of a globally important multidrug-resistant infectious disease through stable transmission routes traversing Africa changes the paradigm for the control and prevention of this disease.<br><br>
DOI: 10.6084/m9.figshare.5318950
title: Evolutionary distinctiveness and conservation priority of the endangered <i>Najas ancistrocarpa</i> (Hydrocharitaceae)

description: Phylogeny is vitally important to evaluate evolutionary distinctiveness and conservation priorities of species. <i>Najas ancistrocarpa</i> is one of the rarest and least known East Asian species of the <i>c</i>. 30–40 species of the aquatic plant genus <i>Najas</i> (Hydrocharitaceae). We used a recently discovered collection of this nationally and regionally endangered species in Japan and East Asia to assess whether <i>N</i>. <i>ancistrocarpa</i> is a distinct species or an untypical form of other <i>Najas</i> species and to evaluate its conservation priority in a phylogenetic context. The sample set of our previous study, exploring worldwide phylogeny of the genus was used with <i>N. ancistrocarpa</i> to delimit species boundaries in <i>Najas</i> and obtain conservation priority scores, calculated by multiplying evolutionary distinctiveness and global extinction risks converted from Red List categories. We performed molecular phylogenetic analyses of plastid (ptDNA) and nuclear (ITS) DNA datasets, STACEY species delimitation analysis using the multilocus dataset and a measurement of conservation priority with Tuatara. <i>Najas ancistrocarpa</i> was consistently placed in ptDNA and ITS trees. Species delimitation analysis objectively assessed that <i>N</i>. <i>ancistrocarpa</i> is phylogenetically distinct. Phylogenetic conservation prioritization ranked <i>N</i>. <i>ancistrocarpa</i> the second highest priority species of the genus <i>Najas</i>. Overall, in terms of biodiversity conservation, <i>N</i>. <i>ancistrocarpa</i> represents an important <i>Najas</i> species in Japan and probably the world.
DOI: 10.6084/m9.figshare.5318950.v1
title: Evolutionary distinctiveness and conservation priority of the endangered <i>Najas ancistrocarpa</i> (Hydrocharitaceae)

description: Phylogeny is vitally important to evaluate evolutionary distinctiveness and conservation priorities of species. <i>Najas ancistrocarpa</i> is one of the rarest and least known East Asian species of the <i>c</i>. 30–40 species of the aquatic plant genus <i>Najas</i> (Hydrocharitaceae). We used a recently discovered collection of this nationally and regionally endangered species in Japan and East Asia to assess whether <i>N</i>. <i>ancistrocarpa</i> is a distinct species or an untypical form of other <i>Najas</i> species and to evaluate its conservation priority in a phylogenetic context. The sample set of our previous study, exploring worldwide phylogeny of the genus was used with <i>N. ancistrocarpa</i> to delimit species boundaries in <i>Najas</i> and obtain conservation priority scores, calculated by multiplying evolutionary distinctiveness and global extinction risks converted from Red List categories. We performed molecular phylogenetic analyses of plastid (ptDNA) and nuclear (ITS) DNA datasets, STACEY species delimitation analysis using the multilocus dataset and a measurement of conservation priority with Tuatara. <i>Najas ancistrocarpa</i> was consistently placed in ptDNA and ITS trees. Species delimitation analysis objectively assessed that <i>N</i>. <i>ancistrocarpa</i> is phylogenetically distinct. Phylogenetic conservation prioritization ranked <i>N</i>. <i>ancistrocarpa</i> the second highest priority species of the genus <i>Najas</i>. Overall, in terms of biodiversity conservation, <i>N</i>. <i>ancistrocarpa</i> represents an important <i>Najas</i> species in Japan and probably the world.
DOI: 10.6084/m9.figshare.5319478
title: MiR-541-5p regulates lung fibrosis by targeting cyclic nucleotide phosphodiesterase 1A

description: <b>Aim of the Study:</b> Idiopathic pulmonary fibrosis (IPF) is a lethal human disease with short survival time and few treatment options. In this study, we aim to demonstrate that cyclic nucleotide phosphodiesterase 1A (PDE1A), a Ca2+/calmodulin-stimulating PDE family member, plays a critical role in the induction of fibrosis and angiogenesis in the lung. <b>Materials and Methods:</b> To induce pulmonary damage, adult male SD rats were treated with bleomycin in a dose of 6 mg/kg body weight by a single intratracheal instillation. For in vivo silencing of PDE1A in rat lung, a nonspecific control siRNA or PDE1A-specific siRNA was used to treat rat through nasal instillation. Human normal pulmonary fibroblasts MRC-5 and hFL1 and rat lung fibroblasts were used as in vitro model. Immunohistochemistry and immunoflurescence staining were performed to detect PDE1A and α-SMA expression. Reverse transcription-qPCR was performed to detect microRNA and mRNA expression. In vitro wound healing assay was performed to detect pulmonary fibroblasts'mortality ability. <b>Results:</b> In vitro studies showed that PDE1A can stimulate lung fibroblasts to undergo myofibroblastic changes. This led to the identification of miR-541-5p as one of the miRNA candidates associated with bleomycin response. We found that miR-541-5p expression is downregulated in TGF-β-treated lung fibroblasts and the rat pulmonary fibrosis model. Overexpression of miR-541-5p in lung fibroblasts inhibited mortality of human lung fibroblasts. <b>Conclusions:</b> MiR-541-5p is a key effector in lung fibroblastsby by regulating PDE1A expression at protein translation level and its overexpression is protective against bleomycin-induced lung fibrosis.
DOI: 10.6084/m9.figshare.5319478.v1
title: MiR-541-5p regulates lung fibrosis by targeting cyclic nucleotide phosphodiesterase 1A

description: <b>Aim of the Study:</b> Idiopathic pulmonary fibrosis (IPF) is a lethal human disease with short survival time and few treatment options. In this study, we aim to demonstrate that cyclic nucleotide phosphodiesterase 1A (PDE1A), a Ca2+/calmodulin-stimulating PDE family member, plays a critical role in the induction of fibrosis and angiogenesis in the lung. <b>Materials and Methods:</b> To induce pulmonary damage, adult male SD rats were treated with bleomycin in a dose of 6 mg/kg body weight by a single intratracheal instillation. For in vivo silencing of PDE1A in rat lung, a nonspecific control siRNA or PDE1A-specific siRNA was used to treat rat through nasal instillation. Human normal pulmonary fibroblasts MRC-5 and hFL1 and rat lung fibroblasts were used as in vitro model. Immunohistochemistry and immunoflurescence staining were performed to detect PDE1A and α-SMA expression. Reverse transcription-qPCR was performed to detect microRNA and mRNA expression. In vitro wound healing assay was performed to detect pulmonary fibroblasts'mortality ability. <b>Results:</b> In vitro studies showed that PDE1A can stimulate lung fibroblasts to undergo myofibroblastic changes. This led to the identification of miR-541-5p as one of the miRNA candidates associated with bleomycin response. We found that miR-541-5p expression is downregulated in TGF-β-treated lung fibroblasts and the rat pulmonary fibrosis model. Overexpression of miR-541-5p in lung fibroblasts inhibited mortality of human lung fibroblasts. <b>Conclusions:</b> MiR-541-5p is a key effector in lung fibroblastsby by regulating PDE1A expression at protein translation level and its overexpression is protective against bleomycin-induced lung fibrosis.
DOI: 10.6084/m9.figshare.5319763
title: Clonality and distribution of clinical Ureaplasma isolates recovered from male patients and infertile couples in China

description: The manuscript was accepted by journal "PLoS ONE" under the title of "Clonality and distribution of clinical Ureaplasma isolates recovered from male patients and infertile couples in China", with a 
doi of 
10.1371/journal.pone.0183947. The uploaded file was the primary dataset 
of the distribution of <i>Ureaplasma </i>species, allele numbers, sequence types (STs), expanded sequence types (eSTs), and sub-groups in both male and female patients.
DOI: 10.6084/m9.figshare.5319763.v1
title: Clonality and distribution of clinical Ureaplasma isolates recovered from male patients and infertile couples in China

description: The manuscript was accepted by journal "PLoS ONE" under the title of "Clonality and distribution of clinical Ureaplasma isolates recovered from male patients and infertile couples in China", with a 
doi of 
10.1371/journal.pone.0183947. The uploaded file was the primary dataset 
of the distribution of <i>Ureaplasma </i>species, allele numbers, sequence types (STs), expanded sequence types (eSTs), and sub-groups in both male and female patients.
DOI: 10.6084/m9.figshare.5325322
title: BNIP3L/NIX-mediated mitophagy protects against ischemic brain injury independent of PARK2

description: Cerebral ischemia induces massive mitochondrial damage. These damaged mitochondria are cleared, thus attenuating brain injury, by mitophagy. Here, we identified the involvement of BNIP3L/NIX in cerebral ischemia-reperfusion (I-R)-induced mitophagy. <i>Bnip3l</i> knockout (<i>bnip3l</i><sup>−/−</sup>) impaired mitophagy and aggravated cerebral I-R injury in mice, which can be rescued by BNIP3L overexpression. The rescuing effects of BNIP3L overexpression can be observed in <i>park2</i><sup>−/−</sup> mice, which showed mitophagy deficiency after I-R. Interestingly, <i>bnip3l</i> and <i>park2</i> double-knockout mice showed a synergistic mitophagy deficiency with I-R treatment, which further highlighted the roles of BNIP3L-mediated mitophagy as being independent from PARK2. Further experiments indicated that phosphorylation of BNIP3L serine 81 is critical for BNIP3L-mediated mitophagy. Nonphosphorylatable mutant BNIP3L<sup>S81A</sup> failed to counteract both mitophagy impairment and neuroprotective effects in <i>bnip3l</i><sup>−/−</sup> mice. Our findings offer insights into mitochondrial quality control in ischemic stroke and bring forth the concept that BNIP3L could be a potential therapeutic target for ischemic stroke, beyond its accepted role in reticulocyte maturation.
DOI: 10.6084/m9.figshare.5325322.v1
title: BNIP3L/NIX-mediated mitophagy protects against ischemic brain injury independent of PARK2

description: Cerebral ischemia induces massive mitochondrial damage. These damaged mitochondria are cleared, thus attenuating brain injury, by mitophagy. Here, we identified the involvement of BNIP3L/NIX in cerebral ischemia-reperfusion (I-R)-induced mitophagy. <i>Bnip3l</i> knockout (<i>bnip3l</i><sup>−/−</sup>) impaired mitophagy and aggravated cerebral I-R injury in mice, which can be rescued by BNIP3L overexpression. The rescuing effects of BNIP3L overexpression can be observed in <i>park2</i><sup>−/−</sup> mice, which showed mitophagy deficiency after I-R. Interestingly, <i>bnip3l</i> and <i>park2</i> double-knockout mice showed a synergistic mitophagy deficiency with I-R treatment, which further highlighted the roles of BNIP3L-mediated mitophagy as being independent from PARK2. Further experiments indicated that phosphorylation of BNIP3L serine 81 is critical for BNIP3L-mediated mitophagy. Nonphosphorylatable mutant BNIP3L<sup>S81A</sup> failed to counteract both mitophagy impairment and neuroprotective effects in <i>bnip3l</i><sup>−/−</sup> mice. Our findings offer insights into mitochondrial quality control in ischemic stroke and bring forth the concept that BNIP3L could be a potential therapeutic target for ischemic stroke, beyond its accepted role in reticulocyte maturation.