cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.12050814
title: Additional file 7 of Whole genome resequencing reveals an association of ABCC4 variants with preaxial polydactyly in pigs

description: Additional file 7: TableS6. The highly differentiated regions based on INDELs between PPD affected and normal pigs. Chr: Chromosome; Win_Start: Window’s Start; Win_End: Window’s End; N_SNPs: Number of INDELs.
DOI: 10.6084/m9.figshare.12050814.v1
title: Additional file 7 of Whole genome resequencing reveals an association of ABCC4 variants with preaxial polydactyly in pigs

description: Additional file 7: TableS6. The highly differentiated regions based on INDELs between PPD affected and normal pigs. Chr: Chromosome; Win_Start: Window’s Start; Win_End: Window’s End; N_SNPs: Number of INDELs.
DOI: 10.6084/m9.figshare.12050805
title: Additional file 4 of Whole genome resequencing reveals an association of ABCC4 variants with preaxial polydactyly in pigs

description: Additional file 4: Table S4. The highly differentiated windows based on whole-genome SNPs. Chr: Chromosome; Win_Start: Window’s Start; Win_End: Window’s End; N_SNPs: Number of SNPs.
DOI: 10.6084/m9.figshare.12050808.v1
title: Additional file 5 of Whole genome resequencing reveals an association of ABCC4 variants with preaxial polydactyly in pigs

description: Additional file 5: Table S5. The highly differentiated SNPs within the highly differentiated windows. The bold italic highlighted rows (*) represent the SNPs which identified in association test and for DAF analysis.
DOI: 10.6084/m9.figshare.12050799
title: Additional file 3 of Whole genome resequencing reveals an association of ABCC4 variants with preaxial polydactyly in pigs

description: Additional file 3: Table S3. The highly remarkable regions (XP-EHH &gt; 2) with annotation.
DOI: 10.6084/m9.figshare.12050799.v1
title: Additional file 3 of Whole genome resequencing reveals an association of ABCC4 variants with preaxial polydactyly in pigs

description: Additional file 3: Table S3. The highly remarkable regions (XP-EHH &gt; 2) with annotation.
DOI: 10.6084/m9.figshare.12050805.v1
title: Additional file 4 of Whole genome resequencing reveals an association of ABCC4 variants with preaxial polydactyly in pigs

description: Additional file 4: Table S4. The highly differentiated windows based on whole-genome SNPs. Chr: Chromosome; Win_Start: Window’s Start; Win_End: Window’s End; N_SNPs: Number of SNPs.
DOI: 10.6084/m9.figshare.12050787
title: Additional file 1 of Whole genome resequencing reveals an association of ABCC4 variants with preaxial polydactyly in pigs

description: Additional file 1: Table S1. Information of all samples and their genome resequencing data characteristics.
DOI: 10.6084/m9.figshare.12050793
title: Additional file 2 of Whole genome resequencing reveals an association of ABCC4 variants with preaxial polydactyly in pigs

description: Additional file 2: Table S2. Distribution and annotation of SNPs identified in this study. ENCODE indicate that the SNPs which were located in the homologous sequences of human counterparts have ENCODE annotations; Motif indicates that the SNPs which were located in the homologous sequences of transcription factor DNA-binding motifs of human counterparts; UTR, untranslated regions; CDS, coding sequence.
DOI: 10.5281/zenodo.10851311
title: Rapid and Accurate Identification of Stem Cell Differentiation Stages via SERS and Convolutional Neural Networks

description: Monitoring the transition of cell states during induced pluripotent stem cell (iPSC) differentiation is crucial for clinical medicine and basic research. However, both identification category and prediction accuracy need further improvement. Here, we propose a method combining Surface-Enhanced Raman spectroscopy (SERS) with convolutional neural networks (CNN) to precisely identify and distinguish cell states during stem cell differentiation. First, mitochondria-targeted probes were synthesized by combining AuNRs and mitochondrial localization signal (MLS) peptides to obtain effective and stable SERS spectra signals at various stages of cell differentiation. Then, the SERS spectra served as input datasets, and their distinctive features were learned and distinguished by CNN. As a result, rapid and accurate identification of six different cell states, including the embryoid body (EB) stage, was successfully achieved throughout the stem cell differentiation process with an impressive prediction accuracy of 98.5%. Furthermore, the impact of different spectral feature peaks on the identification results was investigated, which provides a valuable reference for selecting appropriate spectral bands to identify cell states. This is also beneficial for shortening the spectral acquisition region to enhance spectral acquisition speed. These results suggest the potential for SERS-CNN models in quality monitoring of stem cells, advancing the practical applications of stem cells.
description: The data file is located at" \pythonProject\123\DATE".Among them, G600-1800-6.csv is a 6-categorical data set, and G600-1800-12.csv is a 12-categorical data set
DOI: 10.5281/zenodo.10851312
title: Rapid and Accurate Identification of Stem Cell Differentiation Stages via SERS and Convolutional Neural Networks

description: Monitoring the transition of cell states during induced pluripotent stem cell (iPSC) differentiation is crucial for clinical medicine and basic research. However, both identification category and prediction accuracy need further improvement. Here, we propose a method combining Surface-Enhanced Raman spectroscopy (SERS) with convolutional neural networks (CNN) to precisely identify and distinguish cell states during stem cell differentiation. First, mitochondria-targeted probes were synthesized by combining AuNRs and mitochondrial localization signal (MLS) peptides to obtain effective and stable SERS spectra signals at various stages of cell differentiation. Then, the SERS spectra served as input datasets, and their distinctive features were learned and distinguished by CNN. As a result, rapid and accurate identification of six different cell states, including the embryoid body (EB) stage, was successfully achieved throughout the stem cell differentiation process with an impressive prediction accuracy of 98.5%. Furthermore, the impact of different spectral feature peaks on the identification results was investigated, which provides a valuable reference for selecting appropriate spectral bands to identify cell states. This is also beneficial for shortening the spectral acquisition region to enhance spectral acquisition speed. These results suggest the potential for SERS-CNN models in quality monitoring of stem cells, advancing the practical applications of stem cells.
description: The data file is located at" \pythonProject\123\DATE".Among them, G600-1800-6.csv is a 6-categorical data set, and G600-1800-12.csv is a 12-categorical data set
DOI: 10.6084/m9.figshare.25459051
title: Supplementary Material for: Does the diagnostic Accuracy and Rates of face-to-face visits occurring shortly after an asynchronized Tele-dermatology consultations justify its implementation: An 18-month Cohort Study

description: Introduction: 
In 2019, Maccabi Health Services (MHS), rolled out the store-and-forward “Dermadetect” teledermatology consultation (TC) application. Study goal was to analyze MHS records of TCs (August 2019-February 2021) for the rate and reasons for face to face consultations (FTFC) occurring shortly after a TC with emphasis on FTFCs resulting in a different diagnosis for the same indication. 
Methods: 
The records of FTFCs held up shortly after TCs were reviewed and classified into cases marked as unsuited for tele-dermatology, cases which the indication differed and cases with the same indication which were analyzed for concordance of diagnoses. 
Results:
Dermadetect was used by 12815 MHS beneficiaries. In 30% of cases, a following FTFC occurred within the subsequent 5 months and 901 of them occurred in the subsequent 2 weeks and were analyzed: Thirty percent were not suited for tele-dermatology, 15% were held for a different indication and 55% occurred for same indication. The diagnosis concordance between the TC and recurrent FTFC for the same indication was 97.4%, with full concordance at 68.1% and partial concordance at 29.3%.Overall, 13 patients (1.4%) of the 901 patients using the application only once had a subsequent FTFC within 2 weeks and received a different diagnosis than the one given in the TC.
Conclusions:
When considering the implementation of store and forward TC's, a 30% rate of a following FTFC's during the next 5 months should be considered when planning the reimbursement model. Diagnosis discordance may be disregarded due its low rates.
DOI: 10.6084/m9.figshare.25459051.v1
title: Supplementary Material for: Does the diagnostic Accuracy and Rates of face-to-face visits occurring shortly after an asynchronized Tele-dermatology consultations justify its implementation: An 18-month Cohort Study

description: Introduction: 
In 2019, Maccabi Health Services (MHS), rolled out the store-and-forward “Dermadetect” teledermatology consultation (TC) application. Study goal was to analyze MHS records of TCs (August 2019-February 2021) for the rate and reasons for face to face consultations (FTFC) occurring shortly after a TC with emphasis on FTFCs resulting in a different diagnosis for the same indication. 
Methods: 
The records of FTFCs held up shortly after TCs were reviewed and classified into cases marked as unsuited for tele-dermatology, cases which the indication differed and cases with the same indication which were analyzed for concordance of diagnoses. 
Results:
Dermadetect was used by 12815 MHS beneficiaries. In 30% of cases, a following FTFC occurred within the subsequent 5 months and 901 of them occurred in the subsequent 2 weeks and were analyzed: Thirty percent were not suited for tele-dermatology, 15% were held for a different indication and 55% occurred for same indication. The diagnosis concordance between the TC and recurrent FTFC for the same indication was 97.4%, with full concordance at 68.1% and partial concordance at 29.3%.Overall, 13 patients (1.4%) of the 901 patients using the application only once had a subsequent FTFC within 2 weeks and received a different diagnosis than the one given in the TC.
Conclusions:
When considering the implementation of store and forward TC's, a 30% rate of a following FTFC's during the next 5 months should be considered when planning the reimbursement model. Diagnosis discordance may be disregarded due its low rates.
DOI: 10.6084/m9.figshare.6886586
title: Functional convergence of <i>gliP</i> and <i>aspf1</i> in <i>Aspergillus fumigatus</i> pathogenicity

description: Gliotoxin contributes to the virulence of the fungus <i>Aspergillus fumigatus</i> in non-neutropenic mice that are immunosuppressed with corticosteroids. To investigate how the absence of gliotoxin affects both the fungus and the host, we used a nanoString nCounter to analyze their transcriptional responses during pulmonary infection of a non-neutropenic host with a gliotoxin-deficient Δ<i>gliP</i> mutant. We found that the Δ<i>gliP</i> mutation led to increased expression of <i>aspf1</i>, which specifies a secreted ribotoxin. Prior studies have shown that <i>aspf1</i>, like <i>gliP</i>, is not required for virulence in a neutropenic infection model, but its role in a non-neutropenic infection model has not been fully investigated. To investigate the functional significance of this up-regulation of <i>aspf1</i>, a Δ<i>aspf1</i> single mutant and a Δ<i>aspf1</i> Δ<i>gliP</i> double mutant were constructed. Both Δ<i>aspf1</i> and Δ<i>gliP</i> single mutants had reduced lethality in non-neutropenic mice, and a Δ<i>aspf1</i> Δ<i>gliP</i> double mutant had a greater reduction in lethality than either single mutant. Analysis of mice infected with these mutants indicated that the presence of <i>gliP</i> is associated with massive apoptosis of leukocytes at the foci of infection and inhibition of chemokine production. Also, the combination of <i>gliP</i> and <i>aspf1</i> is associated with suppression of CXCL1 chemokine expression. Thus, <i>aspf1</i> contributes to <i>A. fumigatus</i> pathogenicity in non-neutropenic mice and its up-regulation in the Δ<i>gliP</i> mutant may partially compensate for the absence of gliotoxin. <b>Abbreviations</b>:PAS: periodic acid-Schiff; PBS: phosphate buffered saline; ROS: reactive oxygen species; TUNEL: terminal deoxynucleotidyl transferase dUTP nick-end labeling
DOI: 10.6084/m9.figshare.6886586.v2
title: Functional convergence of <i>gliP</i> and <i>aspf1</i> in <i>Aspergillus fumigatus</i> pathogenicity

description: Gliotoxin contributes to the virulence of the fungus <i>Aspergillus fumigatus</i> in non-neutropenic mice that are immunosuppressed with corticosteroids. To investigate how the absence of gliotoxin affects both the fungus and the host, we used a nanoString nCounter to analyze their transcriptional responses during pulmonary infection of a non-neutropenic host with a gliotoxin-deficient Δ<i>gliP</i> mutant. We found that the Δ<i>gliP</i> mutation led to increased expression of <i>aspf1</i>, which specifies a secreted ribotoxin. Prior studies have shown that <i>aspf1</i>, like <i>gliP</i>, is not required for virulence in a neutropenic infection model, but its role in a non-neutropenic infection model has not been fully investigated. To investigate the functional significance of this up-regulation of <i>aspf1</i>, a Δ<i>aspf1</i> single mutant and a Δ<i>aspf1</i> Δ<i>gliP</i> double mutant were constructed. Both Δ<i>aspf1</i> and Δ<i>gliP</i> single mutants had reduced lethality in non-neutropenic mice, and a Δ<i>aspf1</i> Δ<i>gliP</i> double mutant had a greater reduction in lethality than either single mutant. Analysis of mice infected with these mutants indicated that the presence of <i>gliP</i> is associated with massive apoptosis of leukocytes at the foci of infection and inhibition of chemokine production. Also, the combination of <i>gliP</i> and <i>aspf1</i> is associated with suppression of CXCL1 chemokine expression. Thus, <i>aspf1</i> contributes to <i>A. fumigatus</i> pathogenicity in non-neutropenic mice and its up-regulation in the Δ<i>gliP</i> mutant may partially compensate for the absence of gliotoxin. <b>Abbreviations</b>:PAS: periodic acid-Schiff; PBS: phosphate buffered saline; ROS: reactive oxygen species; TUNEL: terminal deoxynucleotidyl transferase dUTP nick-end labeling
DOI: 10.6084/m9.figshare.6886586.v1
title: Functional convergence of <i>gliP</i> and <i>aspf1</i> in <i>Aspergillus fumigatus</i> pathogenicity

description: Gliotoxin contributes to the virulence of the fungus <i>Aspergillus fumigatus</i> in non-neutropenic mice that are immunosuppressed with corticosteroids. To investigate how the absence of gliotoxin affects both the fungus and the host, we used a nanoString nCounter to analyze their transcriptional responses during pulmonary infection of a non-neutropenic host with a gliotoxin-deficient Δ<i>gliP</i> mutant. We found that the Δ<i>gliP</i> mutation led to increased expression of <i>aspf1</i>, which specifies a secreted ribotoxin. Prior studies have shown that <i>aspf1</i>, like <i>gliP</i>, is not required for virulence in a neutropenic infection model, but its role in a non-neutropenic infection model has not been fully investigated. To investigate the functional significance of this up-regulation of <i>aspf1</i>, a Δ<i>aspf1</i> single mutant and a Δ<i>aspf1</i> Δ<i>gliP</i> double mutant were constructed. Both Δ<i>aspf1</i> and Δ<i>gliP</i> single mutants had reduced lethality in non-neutropenic mice, and a Δ<i>aspf1</i> Δ<i>gliP</i> double mutant had a greater reduction in lethality than either single mutant. Analysis of mice infected with these mutants indicated that the presence of <i>gliP</i> is associated with massive apoptosis of leukocytes at the foci of infection and inhibition of chemokine production. Also, the combination of <i>gliP</i> and <i>aspf1</i> is associated with suppression of CXCL1 chemokine expression. Thus, <i>aspf1</i> contributes to <i>A. fumigatus</i> pathogenicity in non-neutropenic mice and its up-regulation in the Δ<i>gliP</i> mutant may partially compensate for the absence of gliotoxin. <b>Abbreviations</b>:PAS: periodic acid-Schiff; PBS: phosphate buffered saline; ROS: reactive oxygen species; TUNEL: terminal deoxynucleotidyl transferase dUTP nick-end labeling
DOI: 10.6084/m9.figshare.6886571
title: IgM cleavage by <i>Streptococcus suis</i> reduces IgM bound to the bacterial surface and is a novel complement evasion mechanism

description: <i>Streptococcus suis</i> (<i>S. suis</i>) causes meningitis, arthritis and endocarditis in piglets. The aim of this study was to characterize the IgM degrading enzyme of <i>S. suis</i> (Ide<i><sub>Ssuis</sub></i>) and to investigate the role of IgM cleavage in evasion of the classical complement pathway and pathogenesis. Targeted mutagenesis of a cysteine in the putative active center of Ide<i><sub>Ssuis</sub></i> abrogated IgM cleavage completely. In contrast to wt rIde<i><sub>Ssuis</sub></i>, point mutated rIde<i><sub>Ssuis</sub></i>_C195S did not reduce complement-mediated hemolysis indicating that complement inhibition by rIde<i><sub>Ssuis</sub></i> depends on the IgM proteolytic activity. A <i>S. suis</i> mutant expressing Ide<i><sub>Ssuis</sub></i>_C195S did not reduce IgM labeling, whereas the wt and complemented mutant showed less IgM F(ab’)2 and IgM Fc antigen on the surface. IgM cleavage increased survival of <i>S. suis</i> in porcine blood <i>ex vivo</i> and mediated complement evasion as demonstrated by blood survival and C3 deposition assays including the comparative addition of rIde<i><sub>Ssuis</sub></i> and rIde<i><sub>Ssuis</sub></i>_C195S. However, experimental infection of piglets disclosed no significant differences in virulence between <i>S. suis</i> wt and isogenic mutants without IgM cleavage activity. This work revealed for the first time <i>in vivo</i> labeling of <i>S. suis</i> with IgM in the cerebrospinal fluid of piglets with meningitis. In conclusion, this study classifies Ide<i><sub>Ssuis</sub></i> as a cysteine protease and emphasizes the role of IgM cleavage for bacterial survival in porcine blood and complement evasion though IgM cleavage is not crucial for the pathogenesis of serotype 2 meningitis.
DOI: 10.6084/m9.figshare.6886571.v2
title: IgM cleavage by <i>Streptococcus suis</i> reduces IgM bound to the bacterial surface and is a novel complement evasion mechanism

description: <i>Streptococcus suis</i> (<i>S. suis</i>) causes meningitis, arthritis and endocarditis in piglets. The aim of this study was to characterize the IgM degrading enzyme of <i>S. suis</i> (Ide<i><sub>Ssuis</sub></i>) and to investigate the role of IgM cleavage in evasion of the classical complement pathway and pathogenesis. Targeted mutagenesis of a cysteine in the putative active center of Ide<i><sub>Ssuis</sub></i> abrogated IgM cleavage completely. In contrast to wt rIde<i><sub>Ssuis</sub></i>, point mutated rIde<i><sub>Ssuis</sub></i>_C195S did not reduce complement-mediated hemolysis indicating that complement inhibition by rIde<i><sub>Ssuis</sub></i> depends on the IgM proteolytic activity. A <i>S. suis</i> mutant expressing Ide<i><sub>Ssuis</sub></i>_C195S did not reduce IgM labeling, whereas the wt and complemented mutant showed less IgM F(ab’)2 and IgM Fc antigen on the surface. IgM cleavage increased survival of <i>S. suis</i> in porcine blood <i>ex vivo</i> and mediated complement evasion as demonstrated by blood survival and C3 deposition assays including the comparative addition of rIde<i><sub>Ssuis</sub></i> and rIde<i><sub>Ssuis</sub></i>_C195S. However, experimental infection of piglets disclosed no significant differences in virulence between <i>S. suis</i> wt and isogenic mutants without IgM cleavage activity. This work revealed for the first time <i>in vivo</i> labeling of <i>S. suis</i> with IgM in the cerebrospinal fluid of piglets with meningitis. In conclusion, this study classifies Ide<i><sub>Ssuis</sub></i> as a cysteine protease and emphasizes the role of IgM cleavage for bacterial survival in porcine blood and complement evasion though IgM cleavage is not crucial for the pathogenesis of serotype 2 meningitis.
DOI: 10.6084/m9.figshare.6886571.v1
title: IgM cleavage by <i>Streptococcus suis</i> reduces IgM bound to the bacterial surface and is a novel complement evasion mechanism

description: <i>Streptococcus suis</i> (<i>S. suis</i>) causes meningitis, arthritis and endocarditis in piglets. The aim of this study was to characterize the IgM degrading enzyme of <i>S. suis</i> (Ide<i><sub>Ssuis</sub></i>) and to investigate the role of IgM cleavage in evasion of the classical complement pathway and pathogenesis. Targeted mutagenesis of a cysteine in the putative active center of Ide<i><sub>Ssuis</sub></i> abrogated IgM cleavage completely. In contrast to wt rIde<i><sub>Ssuis</sub></i>, point mutated rIde<i><sub>Ssuis</sub></i>_C195S did not reduce complement-mediated hemolysis indicating that complement inhibition by rIde<i><sub>Ssuis</sub></i> depends on the IgM proteolytic activity. A <i>S. suis</i> mutant expressing Ide<i><sub>Ssuis</sub></i>_C195S did not reduce IgM labeling, whereas the wt and complemented mutant showed less IgM F(ab’)2 and IgM Fc antigen on the surface. IgM cleavage increased survival of <i>S. suis</i> in porcine blood <i>ex vivo</i> and mediated complement evasion as demonstrated by blood survival and C3 deposition assays including the comparative addition of rIde<i><sub>Ssuis</sub></i> and rIde<i><sub>Ssuis</sub></i>_C195S. However, experimental infection of piglets disclosed no significant differences in virulence between <i>S. suis</i> wt and isogenic mutants without IgM cleavage activity. This work revealed for the first time <i>in vivo</i> labeling of <i>S. suis</i> with IgM in the cerebrospinal fluid of piglets with meningitis. In conclusion, this study classifies Ide<i><sub>Ssuis</sub></i> as a cysteine protease and emphasizes the role of IgM cleavage for bacterial survival in porcine blood and complement evasion though IgM cleavage is not crucial for the pathogenesis of serotype 2 meningitis.
DOI: 10.6084/m9.figshare.6887360.v3
title: Spontaneous point mutations in the capsule synthesis locus leading to structural and functional changes of the capsule in serogroup A meningococcal populations

description: Whole genome sequencing analysis of 100 <i>Neisseria meningitidis</i> serogroup A isolates has revealed that the <i>csaABCD-ctrABCD-ctrEF</i> capsule polysaccharide synthesis locus represents a spontaneous point mutation hotspot. Structural and functional properties of the capsule of 11 carriage and two disease isolates with non-synonymous point mutations or stop codons in capsule synthesis genes were analyzed for their capsular polysaccharide expression, recognition by antibodies and sensitivity to bactericidal killing. Eight of eleven carriage isolates presenting capsule locus mutations expressed no or reduced amounts of capsule. One isolate with a stop codon in the O-acetyltransferase gene expressed non-O-acetylated polysaccharide, and was not recognized by anti-capsule antibodies. Capsule and O-acetylation deficient mutants were resistant to complement deposition and killing mediated by anti-capsular antibodies, but not by anti-lipopolysaccharide antibodies. Two capsule polymerase mutants, one carriage and one case isolate, showed capsule over-expression and increased resistance against bactericidal activity of both capsule- and lipopolysaccharide-specific antibodies. Meningococci have developed multiple strategies for changing capsule expression and structure, which is relevant both for colonization and virulence. Here we show that point mutations in the capsule synthesis genes substantially contribute to the repertoire of genetic mechanisms in natural populations leading to variability in capsule expression.