cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.5432779
title: Gradually morphing a thematic map series based on cellular automata

description: Maps are often animated to help users make comparisons and comprehend trends. However, large and complex differences between sequential maps can inhibit users from doing so. This paper proposes a morphing technique to highlight trends without manual intervention. Changes between sequential maps are considered as the diffusion processes of expanding classes, with these processes simulated by cellular automata. A skeleton extraction technique is introduced to handle special cases. Experimental results demonstrate that the proposed morphing technique can reveal obvious trends between dramatically changed maps. The potential application of the proposed morphing technique in sequential spatial data (e.g. remote-sensing images) is discussed.
DOI: 10.6084/m9.figshare.5432779.v2
title: Gradually morphing a thematic map series based on cellular automata

description: Maps are often animated to help users make comparisons and comprehend trends. However, large and complex differences between sequential maps can inhibit users from doing so. This paper proposes a morphing technique to highlight trends without manual intervention. Changes between sequential maps are considered as the diffusion processes of expanding classes, with these processes simulated by cellular automata. A skeleton extraction technique is introduced to handle special cases. Experimental results demonstrate that the proposed morphing technique can reveal obvious trends between dramatically changed maps. The potential application of the proposed morphing technique in sequential spatial data (e.g. remote-sensing images) is discussed.
DOI: 10.6084/m9.figshare.5432779.v1
title: Gradually morphing a thematic map series based on cellular automata

description: Maps are often animated to help users make comparisons and comprehend trends. However, large and complex differences between sequential maps can inhibit users from doing so. This paper proposes a morphing technique to highlight trends without manual intervention. Changes between sequential maps are considered as the diffusion processes of expanding classes, with these processes simulated by cellular automata. A skeleton extraction technique is introduced to handle special cases. Experimental results demonstrate that the proposed morphing technique can reveal obvious trends between dramatically changed maps. The potential application of the proposed morphing technique in sequential spatial data (e.g. remote-sensing images) is discussed.
DOI: 10.6084/m9.figshare.5445826
title: A workflow of massive identification and application of intron markers using snakes as a model

description: NEXUS alignments for phylogenetic analyses and the candidate
database of our newly-developed intron markers (nucleotide sequence of the1,273
marker candidates)<br>
DOI: 10.6084/m9.figshare.5445826.v1
title: A workflow of massive identification and application of intron markers using snakes as a model

description: NEXUS alignments for phylogenetic analyses and the candidate
database of our newly-developed intron markers (nucleotide sequence of the1,273
marker candidates)<br>
DOI: 10.6084/m9.figshare.5450779
title: Remarkable increases of α1-antichymotrypsin in brain tissues of rodents during prion infection

description: α1-Antichymotrypsin (α1-ACT) belongs to a kind of acute-phase inflammatory protein. Recently, such protein has been proved exist in the amyloid deposits which is the hallmark of Alzheimer's disease, but limitedly reported in prion disease. To estimate the change of α1-ACT during prion infection, the levels of α1-ACT in the brain tissues of scrapie agents 263K-, 139A- and ME7-infected rodents were analyzed, respectively. Results shown that α1-ACT levels were significantly increased in the brain tissues of the three kinds of scrapie-infected rodents, displaying a time-dependent manner during prion infection. Immunohistochemistry assays revealed the increased α1-ACT mainly accumulated in some cerebral regions of rodents infected with prion, such as cortex, thalamus and cerebellum. Immunofluorescent assays illustrated ubiquitously localization of α1-ACT with GFAP positive astrocytes, Iba1-positive microglia and NeuN-positive neurons. Moreover, double-stained immunofluorescent assays and immunohistochemistry assays using series of brain slices demonstrated close morphological colocalization of α1-ACT signals with that of PrP and PrP<sup>Sc</sup> in the brain slices of 263K-infected hamster. However, co-immunoprecipitation does not identify any detectable molecular interaction between the endogenous α1-ACT and PrP either in the brain homogenates of 263K-infected hamsters or in the lysates of prion-infected cultured cells. Our data here imply that brain α1-ACT is increased abnormally in various scrapie-infected rodent models. Direct molecular interaction between α1-ACT and PrP seems not to be essential for the morphological colocalization of those two proteins in the brain tissues of prion infection.
DOI: 10.6084/m9.figshare.5450779.v1
title: Remarkable increases of α1-antichymotrypsin in brain tissues of rodents during prion infection

description: α1-Antichymotrypsin (α1-ACT) belongs to a kind of acute-phase inflammatory protein. Recently, such protein has been proved exist in the amyloid deposits which is the hallmark of Alzheimer's disease, but limitedly reported in prion disease. To estimate the change of α1-ACT during prion infection, the levels of α1-ACT in the brain tissues of scrapie agents 263K-, 139A- and ME7-infected rodents were analyzed, respectively. Results shown that α1-ACT levels were significantly increased in the brain tissues of the three kinds of scrapie-infected rodents, displaying a time-dependent manner during prion infection. Immunohistochemistry assays revealed the increased α1-ACT mainly accumulated in some cerebral regions of rodents infected with prion, such as cortex, thalamus and cerebellum. Immunofluorescent assays illustrated ubiquitously localization of α1-ACT with GFAP positive astrocytes, Iba1-positive microglia and NeuN-positive neurons. Moreover, double-stained immunofluorescent assays and immunohistochemistry assays using series of brain slices demonstrated close morphological colocalization of α1-ACT signals with that of PrP and PrP<sup>Sc</sup> in the brain slices of 263K-infected hamster. However, co-immunoprecipitation does not identify any detectable molecular interaction between the endogenous α1-ACT and PrP either in the brain homogenates of 263K-infected hamsters or in the lysates of prion-infected cultured cells. Our data here imply that brain α1-ACT is increased abnormally in various scrapie-infected rodent models. Direct molecular interaction between α1-ACT and PrP seems not to be essential for the morphological colocalization of those two proteins in the brain tissues of prion infection.
DOI: 10.6084/m9.figshare.5454598
title: P2016050386-B1-4_results.zip

description: In our study,
melon transcriptome sequencing was used to identify key genes controlling the
differentiation of callus into embryogenic callus. The overall gene expression
levels were higher, photosynthesis-related
gene expression was increased and the pathways related to metabolic
processes and secondary metabolite biosynthesis were activated in the
embryogenic callus compared with the non-embryogenic callus. Therefore, the genes associated with
these pathways may be closely related to the control of melon callus
differentiation into embryogenic callus.<b></b>
DOI: 10.6084/m9.figshare.5454598.v1
title: P2016050386-B1-4_results.zip

description: In our study,
melon transcriptome sequencing was used to identify key genes controlling the
differentiation of callus into embryogenic callus. The overall gene expression
levels were higher, photosynthesis-related
gene expression was increased and the pathways related to metabolic
processes and secondary metabolite biosynthesis were activated in the
embryogenic callus compared with the non-embryogenic callus. Therefore, the genes associated with
these pathways may be closely related to the control of melon callus
differentiation into embryogenic callus.<b></b>
DOI: 10.6084/m9.figshare.5454961
title: Characterization of an <i>Alteromonas</i> long-type ulvan lyase involved in the degradation of ulvan extracted from <i>Ulva ohnoi</i>

description: Ulvan is a sulfated polysaccharide found in the cell wall of the green algae <i>Ulva</i>. We first isolated several ulvan-utilizing <i>Alteromonas</i> sp. from the feces of small marine animals. The strain with the highest ulvan-degrading activity, KUL17, was analyzed further. We identified a 55-kDa ulvan-degrading protein secreted by this strain and cloned the gene encoding for it. The deduced amino acid sequence indicated that the enzyme belongs to polysaccharide lyase family 24 and thus the protein was named ulvan lyase. The predicted molecular mass of this enzyme is 110 kDa, which is different from that of the identified protein. By deletion analysis, the catalytic domain was proven to be located on the N-terminal half of the protein. KUL17 contains two ulvan lyases, one long and one short, but the secreted and cleaved long ulvan lyase was demonstrated to be the major enzyme for ulvan degradation. (A) Domain structure of UllA<sub>KUL17</sub> and plasmids containing UllA<sub>KUL17</sub><i>.</i> (B) CBB R-250 staining of 10% SDS-PAGE gel. (C) Activity staining with ulvan-containing agarose gel.
DOI: 10.6084/m9.figshare.5454961.v1
title: Characterization of an <i>Alteromonas</i> long-type ulvan lyase involved in the degradation of ulvan extracted from <i>Ulva ohnoi</i>

description: Ulvan is a sulfated polysaccharide found in the cell wall of the green algae <i>Ulva</i>. We first isolated several ulvan-utilizing <i>Alteromonas</i> sp. from the feces of small marine animals. The strain with the highest ulvan-degrading activity, KUL17, was analyzed further. We identified a 55-kDa ulvan-degrading protein secreted by this strain and cloned the gene encoding for it. The deduced amino acid sequence indicated that the enzyme belongs to polysaccharide lyase family 24 and thus the protein was named ulvan lyase. The predicted molecular mass of this enzyme is 110 kDa, which is different from that of the identified protein. By deletion analysis, the catalytic domain was proven to be located on the N-terminal half of the protein. KUL17 contains two ulvan lyases, one long and one short, but the secreted and cleaved long ulvan lyase was demonstrated to be the major enzyme for ulvan degradation. (A) Domain structure of UllA<sub>KUL17</sub> and plasmids containing UllA<sub>KUL17</sub><i>.</i> (B) CBB R-250 staining of 10% SDS-PAGE gel. (C) Activity staining with ulvan-containing agarose gel.
DOI: 10.6084/m9.figshare.5455165.v1
title: A systematic review of pharmacoeconomic guidelines

description: <b>Objective:</b> To review, summarize, and analyze both similarities and differences of pharmacoeconomic (PE) guidelines, to enable researchers to access their characteristics and the current state of PE guidelines; furthermore, to learn which methodological issues still remain contested and to promote the methodological development of PE guidelines. <b>Materials and methods:</b> The authors performed a search for PE guidelines using PubMed, the Cochrane library database, and the websites of the International Society for Pharmacoeconomics and Outcomes Research. Information of each guideline was extracted using a pre-designed extraction template, which included 22 aspects; the guidelines were summarized in the forms of charts, and their characteristics have been described. <b>Results:</b> A total of 40 PE guidelines were studied. The most common methodological issues include the types of analysis, sources for effectiveness, use of quality-adjusted life-years (QALYs) to measure outcomes, and use of incremental cost effectiveness ratios to present results. The majority of the guidelines preferred a cost utility analysis with outcomes expressed in terms of QALYs. Most of the guidelines preferred meta-analysis or meta-analysis of the randomized controlled trials, and required a systematic review of all evidence. Issues that varied most in the guidelines were the choice of the comparator, recommended costs to be included, methods related to indirect cost calculations, methods of sensitivity analysis, and discounting rate. <b>Conclusion:</b> A comparison of these guidelines revealed that a number of differences exist among them in several key aspects, and some critical methodological issues still exist, for which no best solution is available. Furthermore, efforts need to be made to develop harmonious methods for the PE, and to improve the transferability of the outcomes of PE evaluations.
DOI: 10.6084/m9.figshare.5457220
title: Training and testing data used in the paper "An equation-of-state-meter of QCD transition from deep learning"

description: Training and testing data to identify the QCD transition using deep learning and traditional machine learning.<br>1. training_data.csv, testing_iebevishnu.csv, testing_ipglasma.csv<br>There are 723 entries in each row. The first row is the description of the data. The 0th entry in each row is the event id, the entries from 1 to 720 are the pion density distribution at mid-rapidity -- rho(pt, phi) at 15 different pt bins and 48 different azimuthal angle phi bins with phi as the inner loop. The 721st entry is the equation of state type (0 or 1). The 722 entry is extra information of each event.<br>2. training_observables.csv, test_iebe_observables.csv, test_ipglasma_observables.csv <br>There are 87 entries in each row. The first row is the header which describes the data of the following rows. In the following rows, the first entry is the event id, the second entry is the equation of state type (0 or 1), the remaining entries are 85 observables computed from raw spectra, which will be used in various traditional classifiers in machine learning toolbox.<br>The meaning of these entries and the Monte Carlo model used to generate these data can be found in the paper,http://inspirehep.net/record/1503189<br><br><br>
DOI: 10.6084/m9.figshare.5458165
title: Ptyctolepis brachynotus gen. et sp. nov. IVPP V23386: CT scan data and surface files of a new sarcopterygian from Early Devonian of South China

description: X-ray computed microtomography scanning for these specimens was performed at IVPP, Chinese Academy of Sciences (CAS), Beijing, China, using a 225 kV microCT. After scanning, data were segmented in Mimics (biomedical.materialise.com/mimics; Materialise, Leuven, Belgium). Surface meshes were then exported into and imaged in Blender (blender.org; Stitching Blender Foundation, Amsterdam, the Netherlands).<br>High-resolution micro computed tomography (μCT) of three-dimensionally preserved skulls illuminates internal cranial anatomy of lobe-finned fishes, and provides evidence for the stepwise evolution of key sarcopterygian features, but also lend additional weight to the idea of a sudden and explosive episode of sarcopterygian evolution in the late Silurian and Early Devonian of China. <br>Article abstract: Recent discoveries of psarolepids, putative stem sarcopterygians from the late Silurian and Early Devonian of South China, have increased our knowledge of the morphology and initial diversification of osteichthyans while highlighting incongruities in character evolution in the largest group of jawed vertebrates. Character-rich endocrania are incompletely preserved for these taxa, limiting a detailed understanding of complex internal morphology and evolutionary changes in the head skeleton. We report a new sarcopterygian (Ptyctolepis brachynotus gen. et sp. nov.) from the Pragian (Early Devonian) of South China, which preserves the only example of a completely ossified otoccipital division of the braincase in a stem sarcopterygian. The skull roof bears vermiculate ridged ornamentation, with middle and posterior pit-lines lying close to the midline. The paired hyomandibular facets sit dorsal to the jugular canal, representing a hitherto unobserved combination of derived and primitive character states. The suite of characters in this new taxon prompts a reassessment of early osteichthyan evolution, including the phylogenetic placement of psarolepids, which we suggest might branch from the osteichthyan—rather than sarcopterygian—stem.
DOI: 10.6084/m9.figshare.5459632
title: Aberrant alterations of the expressions and <i>S</i>-nitrosylation of calmodulin and the downstream factors in the brains of the rodents during scrapie infection

description: The aberrant alterations of calmodulin (CaM) and its downstream substrates have been reported in some neurodegenerative diseases, but rarely described in prion disease. In this study, the potential changes of Ca<sup>2+</sup>/CaM and its associated agents in the brains of scrapie agent 263K-infected hamsters and the prion infected cell line SMB-S15 were evaluated by various methodologies. We found that the level of CaM in the brains of 263K-infected hamsters started to increase at early stage and maintained at high level till terminal stage. The increased CaM mainly accumulated in the regions of cortex, thalamus and cerebellum of 263K-infected hamsters and well localization of CaM with NeuN positive cells. However, the related kinases such as total and phosphorylated forms of CaMKII and CaMKIV, as well as the downstream proteins such as CREB and BDNF in the brain of 263K-infected hamsters were decreased. Further analysis showed a remarkable increase of <i>S</i>-nitrosylated (SNO) form of CaM in the brains of 263K-infected hamsters. Dynamic analysis of <i>S</i>-nitrosylated CaM showed the SNO form of CaM abnormally increases in a time-dependent manner during prion infection. Compared with that of the normal partner cell line SMB-PS, the CaM level in SMB-S15 cells was increased, meanwhile, the downstream proteins, such as CaMKII, p-CaMKII, CREB, as well as BDNF, were also increased, especially in the nucleic fraction. No SNO-CaM was detected in the cell lines SMB-S15 and SMB-PS. Our data indicate an aberrant increase of CaM during prion infection <i>in vivo</i> and <i>in vitro</i>.
DOI: 10.6084/m9.figshare.5459632.v1
title: Aberrant alterations of the expressions and <i>S</i>-nitrosylation of calmodulin and the downstream factors in the brains of the rodents during scrapie infection

description: The aberrant alterations of calmodulin (CaM) and its downstream substrates have been reported in some neurodegenerative diseases, but rarely described in prion disease. In this study, the potential changes of Ca<sup>2+</sup>/CaM and its associated agents in the brains of scrapie agent 263K-infected hamsters and the prion infected cell line SMB-S15 were evaluated by various methodologies. We found that the level of CaM in the brains of 263K-infected hamsters started to increase at early stage and maintained at high level till terminal stage. The increased CaM mainly accumulated in the regions of cortex, thalamus and cerebellum of 263K-infected hamsters and well localization of CaM with NeuN positive cells. However, the related kinases such as total and phosphorylated forms of CaMKII and CaMKIV, as well as the downstream proteins such as CREB and BDNF in the brain of 263K-infected hamsters were decreased. Further analysis showed a remarkable increase of <i>S</i>-nitrosylated (SNO) form of CaM in the brains of 263K-infected hamsters. Dynamic analysis of <i>S</i>-nitrosylated CaM showed the SNO form of CaM abnormally increases in a time-dependent manner during prion infection. Compared with that of the normal partner cell line SMB-PS, the CaM level in SMB-S15 cells was increased, meanwhile, the downstream proteins, such as CaMKII, p-CaMKII, CREB, as well as BDNF, were also increased, especially in the nucleic fraction. No SNO-CaM was detected in the cell lines SMB-S15 and SMB-PS. Our data indicate an aberrant increase of CaM during prion infection <i>in vivo</i> and <i>in vitro</i>.
DOI: 10.6084/m9.figshare.5459656
title: Autophagy protects auditory hair cells against neomycin-induced damage

description: Aminoglycosides are toxic to sensory hair cells (HCs). Macroautophagy/autophagy is an essential and highly conserved self-digestion pathway that plays important roles in the maintenance of cellular function and viability under stress. However, the role of autophagy in aminoglycoside-induced HC injury is unknown. Here, we first found that autophagy activity was significantly increased, including enhanced autophagosome-lysosome fusion, in both cochlear HCs and HEI-OC-1 cells after neomycin or gentamicin injury, suggesting that autophagy might be correlated with aminoglycoside-induced cell death. We then used rapamycin, an autophagy activator, to increase the autophagy activity and found that the ROS levels, apoptosis, and cell death were significantly decreased after neomycin or gentamicin injury. In contrast, treatment with the autophagy inhibitor 3-methyladenine (3-MA) or knockdown of autophagy-related (ATG) proteins resulted in reduced autophagy activity and significantly increased ROS levels, apoptosis, and cell death after neomycin or gentamicin injury. Finally, after neomycin injury, the antioxidant N-acetylcysteine could successfully prevent the increased apoptosis and HC loss induced by 3-MA treatment or ATG knockdown, suggesting that autophagy protects against neomycin-induced HC damage by inhibiting oxidative stress. We also found that the dysfunctional mitochondria were not eliminated by selective autophagy (mitophagy) in HEI-OC-1 cells after neomycin treatment, suggesting that autophagy might not directly target the damaged mitochondria for degradation. This study demonstrates that moderate ROS levels can promote autophagy to recycle damaged cellular constituents and maintain cellular homeostasis, while the induction of autophagy can inhibit apoptosis and protect the HCs by suppressing ROS accumulation after aminoglycoside injury.
DOI: 10.6084/m9.figshare.5459656.v1
title: Autophagy protects auditory hair cells against neomycin-induced damage

description: Aminoglycosides are toxic to sensory hair cells (HCs). Macroautophagy/autophagy is an essential and highly conserved self-digestion pathway that plays important roles in the maintenance of cellular function and viability under stress. However, the role of autophagy in aminoglycoside-induced HC injury is unknown. Here, we first found that autophagy activity was significantly increased, including enhanced autophagosome-lysosome fusion, in both cochlear HCs and HEI-OC-1 cells after neomycin or gentamicin injury, suggesting that autophagy might be correlated with aminoglycoside-induced cell death. We then used rapamycin, an autophagy activator, to increase the autophagy activity and found that the ROS levels, apoptosis, and cell death were significantly decreased after neomycin or gentamicin injury. In contrast, treatment with the autophagy inhibitor 3-methyladenine (3-MA) or knockdown of autophagy-related (ATG) proteins resulted in reduced autophagy activity and significantly increased ROS levels, apoptosis, and cell death after neomycin or gentamicin injury. Finally, after neomycin injury, the antioxidant N-acetylcysteine could successfully prevent the increased apoptosis and HC loss induced by 3-MA treatment or ATG knockdown, suggesting that autophagy protects against neomycin-induced HC damage by inhibiting oxidative stress. We also found that the dysfunctional mitochondria were not eliminated by selective autophagy (mitophagy) in HEI-OC-1 cells after neomycin treatment, suggesting that autophagy might not directly target the damaged mitochondria for degradation. This study demonstrates that moderate ROS levels can promote autophagy to recycle damaged cellular constituents and maintain cellular homeostasis, while the induction of autophagy can inhibit apoptosis and protect the HCs by suppressing ROS accumulation after aminoglycoside injury.