cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.30231153.v1
title: Pathological protection and molecular regulation of cystatin B in Nile tilapia (<i>Oreochromis niloticus</i>) bacterial disease

description: Cystatin B (CSTB) is an endogenous cysteine protease inhibitor that plays a critical role in the modulation of numerous biological processes, involving immune responses, apoptosis, and inflammation in mammals. However, its immunological functions in teleost, particularly Nile tilapia (<i>Oreochromis niloticus</i>) remain unclear. In the present study, the <i>CSTB</i> was cloned and characterized from Nile tilapia (<i>On-CSTB</i>) and its role in bacterial infection was revealed. The On-CSTB open reading frame is 300 bp encoding 99 amino acids that contains a conserved cystatin domain. Multiple sequence alignment analysis revealed that On-CSTB share over 75% identity with fish lineages, and 45% identity with mammals. qPCR analysis showed that <i>On-CSTB</i> is widely expressed across various tissues and highly expressed in blood cells and intestines and can be significantly inducted by <i>Streptococcus agalactiae</i> (<i>S. agalactiae</i>) and <i>Aeromonas hydrophila</i> (<i>A. hydrophila</i>). In vivo experiments demonstrated that On-CSTB protein could suppress inflammation while participating in the MyD88/NF-κB signaling pathway and inflammasome activation, affecting apoptosis and pyroptosis processes. Moreover, On-CSTB contributed to enhanced tissue integrity and alleviated pathological damage. These findings collectively highlight On-CSTB as a crucial immunomodulator that contributes to host defense and tissue protection in fish. The present study offers novel perspectives on the immunomodulatory role of CSTB in tilapia, providing a basis for disease resistance strategies in aquaculture.
DOI: 10.6084/m9.figshare.28761869
title: <i>Staphylococcus aureus</i> β-hemolysin impairs oxygen transport without causing hemolysis

description: <i>Staphylococcus aureus</i> (<i>S. aureus</i>) infection can lead to the occurrence of hypoxia, however, the underlying mechanisms have not been fully elucidated. β-hemolysin (Hlb) induced hemolysis of red blood cells (RBCs) requires a temperature transition from “hot” to “cold,” a phenomenon not observed under physiological conditions. In this study, we discovered that RBCs treated with Hlb exhibited a high level of intracellular Ca<sup>2+</sup> and underwent a shape transformation from biconcave discoid to spherical, which was contingent upon the degradation of sphingomyelin of the cell membrane and led to impaired oxygen transport. The increase in intracellular Ca<sup>2+</sup> levels induced by Hlb was dependent on the activation of the ion channel N-methyl-D-aspartate receptor. Furthermore, we found that Hlb-induced Ca<sup>2+</sup> influx increased the cytoplasmic pH and subsequently attenuated the oxygen release from RBCs, which were also observed in both <i>hlb</i> transgenic mice and a murine model with <i>S. aureus</i> challenge. Our findings reveal a novel role for Hlb as sphingomyelinase in impairing RBC function under non-lytic conditions, shedding light on the mechanism behind hypoxia associated with <i>S. aureus</i> infection.
DOI: 10.6084/m9.figshare.28761869.v1
title: <i>Staphylococcus aureus</i> β-hemolysin impairs oxygen transport without causing hemolysis

description: <i>Staphylococcus aureus</i> (<i>S. aureus</i>) infection can lead to the occurrence of hypoxia, however, the underlying mechanisms have not been fully elucidated. β-hemolysin (Hlb) induced hemolysis of red blood cells (RBCs) requires a temperature transition from “hot” to “cold,” a phenomenon not observed under physiological conditions. In this study, we discovered that RBCs treated with Hlb exhibited a high level of intracellular Ca<sup>2+</sup> and underwent a shape transformation from biconcave discoid to spherical, which was contingent upon the degradation of sphingomyelin of the cell membrane and led to impaired oxygen transport. The increase in intracellular Ca<sup>2+</sup> levels induced by Hlb was dependent on the activation of the ion channel N-methyl-D-aspartate receptor. Furthermore, we found that Hlb-induced Ca<sup>2+</sup> influx increased the cytoplasmic pH and subsequently attenuated the oxygen release from RBCs, which were also observed in both <i>hlb</i> transgenic mice and a murine model with <i>S. aureus</i> challenge. Our findings reveal a novel role for Hlb as sphingomyelinase in impairing RBC function under non-lytic conditions, shedding light on the mechanism behind hypoxia associated with <i>S. aureus</i> infection.
DOI: 10.6084/m9.figshare.29062740
title: A RACK1 family protein regulates pathogenicity of <i>Peronophythora litchii</i> by acting as a scaffold for MAPK signal modules

description: Litchi downy blight caused by <i>Peronophythora litchii</i> is the most destructive disease of litchi (<i>Litchi chinensis</i>). RACK1 (Receptor for activated C kinase 1) is a group of scaffold proteins, mainly involved in the regulation of various signaling pathways by interacting with signal transduction proteins and affecting the activity of these proteins. In this study, a RACK1 homologue identified in <i>P. litchii</i>, and named PlRACK1. The protein was found to interact with the mitogen-activated protein kinases, PlMAPK1 and PlMAPK2. CRISPR/Cas9-mediated genome editing technology was used to knock out <i>PlRACK1</i>, and we found that it was involved in mycelial growth, cell wall integrity, ROS metabolism, laccase activity, and pathogenicity of <i>P. litchii</i>. PlMAPK1 interacted with RACK1, and they jointly regulated sporangiophore branching of <i>P</i>. <i>litchii</i>. Transcriptome analysis showed that <i>P</i>. <i>litchii</i> MAPK Phosphatase 1 (PlMKP1) and beta-glucoside (PlBglX) were regulated by PlRACK1, both of which were also required for the pathogenicity of <i>P</i>. <i>litchii</i>. As well, PlMKP1 also interacted with PlMAPK1 and PlMAPK2. These results provide insights into the direct interactions between RACK1, MAPKs, and MKP, and their functions in growth, development, and pathogenesis in a plant pathogenic oomycete. PlRACK1 played a critical role in response to ROS and pathogenesis of <i>P</i>. <i>litchii</i>.PlMAPK1 interacted with PlRACK1, and they jointly regulated sporangiophore branching.PlMKP1 interacted with PlMAPK1/PlMAPK2 and was involved in pathogenesis.PlBglX, identified by transcriptome analysis of PlRACK1 mutant, is a virulence factor. PlRACK1 played a critical role in response to ROS and pathogenesis of <i>P</i>. <i>litchii</i>. PlMAPK1 interacted with PlRACK1, and they jointly regulated sporangiophore branching. PlMKP1 interacted with PlMAPK1/PlMAPK2 and was involved in pathogenesis. PlBglX, identified by transcriptome analysis of PlRACK1 mutant, is a virulence factor.
DOI: 10.6084/m9.figshare.29062740.v1
title: A RACK1 family protein regulates pathogenicity of <i>Peronophythora litchii</i> by acting as a scaffold for MAPK signal modules

description: Litchi downy blight caused by <i>Peronophythora litchii</i> is the most destructive disease of litchi (<i>Litchi chinensis</i>). RACK1 (Receptor for activated C kinase 1) is a group of scaffold proteins, mainly involved in the regulation of various signaling pathways by interacting with signal transduction proteins and affecting the activity of these proteins. In this study, a RACK1 homologue identified in <i>P. litchii</i>, and named PlRACK1. The protein was found to interact with the mitogen-activated protein kinases, PlMAPK1 and PlMAPK2. CRISPR/Cas9-mediated genome editing technology was used to knock out <i>PlRACK1</i>, and we found that it was involved in mycelial growth, cell wall integrity, ROS metabolism, laccase activity, and pathogenicity of <i>P. litchii</i>. PlMAPK1 interacted with RACK1, and they jointly regulated sporangiophore branching of <i>P</i>. <i>litchii</i>. Transcriptome analysis showed that <i>P</i>. <i>litchii</i> MAPK Phosphatase 1 (PlMKP1) and beta-glucoside (PlBglX) were regulated by PlRACK1, both of which were also required for the pathogenicity of <i>P</i>. <i>litchii</i>. As well, PlMKP1 also interacted with PlMAPK1 and PlMAPK2. These results provide insights into the direct interactions between RACK1, MAPKs, and MKP, and their functions in growth, development, and pathogenesis in a plant pathogenic oomycete. PlRACK1 played a critical role in response to ROS and pathogenesis of <i>P</i>. <i>litchii</i>.PlMAPK1 interacted with PlRACK1, and they jointly regulated sporangiophore branching.PlMKP1 interacted with PlMAPK1/PlMAPK2 and was involved in pathogenesis.PlBglX, identified by transcriptome analysis of PlRACK1 mutant, is a virulence factor. PlRACK1 played a critical role in response to ROS and pathogenesis of <i>P</i>. <i>litchii</i>. PlMAPK1 interacted with PlRACK1, and they jointly regulated sporangiophore branching. PlMKP1 interacted with PlMAPK1/PlMAPK2 and was involved in pathogenesis. PlBglX, identified by transcriptome analysis of PlRACK1 mutant, is a virulence factor.
DOI: 10.6084/m9.figshare.30200472
title: Isolation and comprehensive characterization of bovine parvovirus 1 from diarrheic calves in Northeast China: Insights into evolution and biology

description: Bovine parvovirus (BPV) is among the pathogens associated with respiratory, digestive, and reproductive disorders in cattle, contributing to significant economic losses in the global cattle industry. To investigate the prevalence and genetic variability of BPV in diarrheic cattle, 14 BPV strains were isolated from 673 bovine diarrhea samples (2017–2022, Northeast China) using BT cells. Notably, the DQ7498 strain exhibited the highest proliferation efficiency (titer reaching 10<sup>8.12</sup>TCID<sub>50</sub>/mL). Sensitive cell detection assays showed isolated strains stably serially passaged only in BT and bovine lung cells. Electron microscopy revealed that all isolates as non-enveloped icosahedrons structures (approximately 25 nm in diameter), consistent with parvovirus morphology. Complete coding sequence (CDS) and phylogenetic analysis revealed that the 14 isolates strains were closely related to BPV1 reference strains (DQ335247, NC001540), with high genetic identity (96.5%-99%). Recombination analysis identified genomic recombination events in four strains (JL108, JL60, DQ7706 and DQ7728), suggesting DQ8186 and ZD0510, or earlier unisolated strains, as potential parental strains. Amino acid sequence analysis revealed multiple coding mutations among the 14 isolates. Although antigenic epitope mutations (A362T and N399D) were identified in VP2, they did not induce significant conformational changes. Physicochemical characterization demonstrated that the virus exhibited sensitivity to chloroform and loses its infectivity after chloroform treatment, which is inconsistent with previous research reports. This study reports the first isolation of 14 BPV1 strains in Northeast China, revealing BPV1 genetic evolution, antigenic variation, and the first documented recombination events among regional strains, providing new insights into the molecular evolution of BPV1 and disease control.
DOI: 10.6084/m9.figshare.30200472.v1
title: Isolation and comprehensive characterization of bovine parvovirus 1 from diarrheic calves in Northeast China: Insights into evolution and biology

description: Bovine parvovirus (BPV) is among the pathogens associated with respiratory, digestive, and reproductive disorders in cattle, contributing to significant economic losses in the global cattle industry. To investigate the prevalence and genetic variability of BPV in diarrheic cattle, 14 BPV strains were isolated from 673 bovine diarrhea samples (2017–2022, Northeast China) using BT cells. Notably, the DQ7498 strain exhibited the highest proliferation efficiency (titer reaching 10<sup>8.12</sup>TCID<sub>50</sub>/mL). Sensitive cell detection assays showed isolated strains stably serially passaged only in BT and bovine lung cells. Electron microscopy revealed that all isolates as non-enveloped icosahedrons structures (approximately 25 nm in diameter), consistent with parvovirus morphology. Complete coding sequence (CDS) and phylogenetic analysis revealed that the 14 isolates strains were closely related to BPV1 reference strains (DQ335247, NC001540), with high genetic identity (96.5%-99%). Recombination analysis identified genomic recombination events in four strains (JL108, JL60, DQ7706 and DQ7728), suggesting DQ8186 and ZD0510, or earlier unisolated strains, as potential parental strains. Amino acid sequence analysis revealed multiple coding mutations among the 14 isolates. Although antigenic epitope mutations (A362T and N399D) were identified in VP2, they did not induce significant conformational changes. Physicochemical characterization demonstrated that the virus exhibited sensitivity to chloroform and loses its infectivity after chloroform treatment, which is inconsistent with previous research reports. This study reports the first isolation of 14 BPV1 strains in Northeast China, revealing BPV1 genetic evolution, antigenic variation, and the first documented recombination events among regional strains, providing new insights into the molecular evolution of BPV1 and disease control.
DOI: 10.6084/m9.figshare.28209245
title: Structural and functional analysis reveals the catalytic mechanism and substrate binding mode of the broad-spectrum endolysin Ply2741

description: The emergence of antibiotic-resistant bacteria has attracted interest in the field of endolysins. Here, we analyzed the diversity of <i>Streptococcus</i> endolysins and identified a new endolysin, Ply2741, that exhibited broad-spectrum bactericidal activity. Our results demonstrated that Ply2741 could effectively eradicate multidrug-resistant gram-positive pathogens <i>in vitro</i> and <i>in vivo</i>. Structural analysis revealed that the bactericidal activity of Ply2741 depends on the classic “Cys-His-Asn” catalytic triad. Site-directed mutagenesis results further identified that the conserved residue Gln29, located near the catalytic triad, also contributes to the lytic activity of Ply2741. Furthermore, the key residues (R189 and W250) in the Ply2741 cell wall binding domain (CBD) responsible for binding to peptidoglycan were revealed by molecular docking and fluorescence-activated cell sorting (FACS) analysis. Ply2741 demonstrates a broad lytic spectrum, with significant bactericidal activity against <i>Enterococcus</i>, <i>Staphylococcu</i>s, <i>and Streptococcus</i> and species. To the best of our knowledge, we found that residue Gln29 participated in the lytic activity of endolysin for the first time. Additionally, we systematically elucidate the binding mode and key residues of the Ply2741CBD. This study proposes Ply2741 as a potential antibiotic substitute and provides a structural basis for the modification and design of endolysins.
DOI: 10.6084/m9.figshare.28209245.v1
title: Structural and functional analysis reveals the catalytic mechanism and substrate binding mode of the broad-spectrum endolysin Ply2741

description: The emergence of antibiotic-resistant bacteria has attracted interest in the field of endolysins. Here, we analyzed the diversity of <i>Streptococcus</i> endolysins and identified a new endolysin, Ply2741, that exhibited broad-spectrum bactericidal activity. Our results demonstrated that Ply2741 could effectively eradicate multidrug-resistant gram-positive pathogens <i>in vitro</i> and <i>in vivo</i>. Structural analysis revealed that the bactericidal activity of Ply2741 depends on the classic “Cys-His-Asn” catalytic triad. Site-directed mutagenesis results further identified that the conserved residue Gln29, located near the catalytic triad, also contributes to the lytic activity of Ply2741. Furthermore, the key residues (R189 and W250) in the Ply2741 cell wall binding domain (CBD) responsible for binding to peptidoglycan were revealed by molecular docking and fluorescence-activated cell sorting (FACS) analysis. Ply2741 demonstrates a broad lytic spectrum, with significant bactericidal activity against <i>Enterococcus</i>, <i>Staphylococcu</i>s, <i>and Streptococcus</i> and species. To the best of our knowledge, we found that residue Gln29 participated in the lytic activity of endolysin for the first time. Additionally, we systematically elucidate the binding mode and key residues of the Ply2741CBD. This study proposes Ply2741 as a potential antibiotic substitute and provides a structural basis for the modification and design of endolysins.
DOI: 10.6084/m9.figshare.30556725
title: Unraveling the immunosuppressive role of Elastase B produced by cystic fibrosis isolates of <i>Pseudomonas aeruginosa</i> in an organotypic 3D lung epithelial cell model

description: <i>Pseudomonas aeruginosa</i> chronically infects the lungs of people with cystic fibrosis (pwCF), where it produces a broad range of proteases that impact host immunity and inflammation. While some studies suggest these enzymes induce inflammation and may contribute to the excessive inflammatory response in pwCF, others indicate that they degrade cytokines and suppress the immune response. Here, we investigate the role of <i>P. aeruginosa</i> proteases in CF lung inflammation by culturing clinical isolates under physiologically relevant conditions and studying the inflammatory response in an organotypic 3D lung cell culture model. Exposure to supernatants from isolates with proteolytic activity led to cytokine degradation and reduced cytokine release in the 3D model. To identify the specific protease(s) responsible, we performed a proteomics analysis on the supernatants of the isolates with and without proteolytic activity. In total, 79 proteases were identified in the supernatants, with extracellular proteases among the most differentially expressed in the proteolytically active isolate group. Metalloprotease Elastase B (LasB) exhibited the highest level of differential expression. Therefore, we determined the contribution of LasB to the observed reduction in cytokine levels by utilizing <i>P. aeruginosa lasB</i> knockout mutants. Compared to the <i>lasB</i> mutant, the wild-type strain significantly decreased inflammation by degrading MCP-1, IL-1β, GM-CSF, and IL-8. While this study brings to light a key role for LasB, our findings demonstrate that immunomodulation by <i>P. aeruginosa</i> most likely involves the combined action of multiple proteases. This study provides a foundation for future research into protease-mediated immune evasion during chronic infection.
DOI: 10.6084/m9.figshare.30734627
title: Negative regulation of reassortant canine influenza virus replication and key site identification in porcine and ferret bronchial epithelial cell lines

description: The segmented nature and high mutability of the influenza virus RNA genome facilitate rapid mutation and reassortment, allowing the virus to breach host barriers and migrate between different species, potentially leading to unpredictable influenza outbreaks. With dogs emerging as new natural hosts for influenza virus, vigilant surveillance and scientific prevention strategies are imperative. Here, based on our previous isolation of 21 strains, which are reassortments of the canine influenza virus (CIV) H3N2 (KR/07) with gene segments from the influenza A pandemic (H1N1) 2009 virus strain (CA/09), the replication kinetics of these reassortants in immortalized mammalian respiratory epithelial cell lines from swine and ferret named hTERT-PBECs and hTERT-FBECs, alongside induced changes in cytokine expression, were investigated. Reverse genetics was utilized to generate the reassortment H3N2 canine influenza rKR/07-PB2/NP, which contains the PB2 and NP segments from CA/09. The viral titer of rKR/07-PB2/NP was significantly lower than those of the parental viruses KR/07 and CA/09. In addition, rKR/07-PB2/NP notably decreased expression levels of interleukin-1β (IL-1β) and interleukin-10 (IL-10) in both immortal cells, particularly in hTERT-PBECs. Our findings not only contribute to the understanding and exploring cross-species transmission mechanisms of influenza virus, but also provide new ideas for prevention and treatment of CIV.
DOI: 10.6084/m9.figshare.30734627.v1
title: Negative regulation of reassortant canine influenza virus replication and key site identification in porcine and ferret bronchial epithelial cell lines

description: The segmented nature and high mutability of the influenza virus RNA genome facilitate rapid mutation and reassortment, allowing the virus to breach host barriers and migrate between different species, potentially leading to unpredictable influenza outbreaks. With dogs emerging as new natural hosts for influenza virus, vigilant surveillance and scientific prevention strategies are imperative. Here, based on our previous isolation of 21 strains, which are reassortments of the canine influenza virus (CIV) H3N2 (KR/07) with gene segments from the influenza A pandemic (H1N1) 2009 virus strain (CA/09), the replication kinetics of these reassortants in immortalized mammalian respiratory epithelial cell lines from swine and ferret named hTERT-PBECs and hTERT-FBECs, alongside induced changes in cytokine expression, were investigated. Reverse genetics was utilized to generate the reassortment H3N2 canine influenza rKR/07-PB2/NP, which contains the PB2 and NP segments from CA/09. The viral titer of rKR/07-PB2/NP was significantly lower than those of the parental viruses KR/07 and CA/09. In addition, rKR/07-PB2/NP notably decreased expression levels of interleukin-1β (IL-1β) and interleukin-10 (IL-10) in both immortal cells, particularly in hTERT-PBECs. Our findings not only contribute to the understanding and exploring cross-species transmission mechanisms of influenza virus, but also provide new ideas for prevention and treatment of CIV.
DOI: 10.15468/dl.x3yqud
title: Occurrence Download

description: A dataset containing 31 species occurrences available in GBIF matching the query:
{
 "and" : [
 "OccurrenceStatus is Present",
 "TaxonKey is Molossus alvarezi González-Ruiz, Ramírez-Pulido & Arroyo-Cabrales, 2011"
 ]
}

 The dataset includes 31 records from 7 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0003942-250426092105405/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.j3gvjz
title: Occurrence Download

description: A dataset containing 27 species occurrences available in GBIF matching the query:
{
 "and" : [
 "Country is China",
 "TaxonKey is Rhododendron tsariense Cowan"
 ]
}

 The dataset includes 27 records from 6 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0001356-250424135625364/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.17632/cwzd57w23j
title: Soil nitrogen pools

description: Soil nitrogen pools
DOI: 10.17632/cwzd57w23j.1
title: Soil nitrogen pools

description: Soil nitrogen pools
DOI: 10.15468/dl.9ygnvn
title: Occurrence Download

description: A dataset containing 1440 species occurrences available in GBIF matching the query:
{
 "and" : [
 "Country is China",
 "TaxonKey is Rhododendron pachytrichum Franch."
 ]
}

 The dataset includes 1440 records from 18 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0001358-250424135625364/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.17632/gdf933sdfk.1
title: EFFECT OF DEVELOPED EXERCISE PROTOCOL FOR POSTMENOPAUSAL FEMALES

description: Menopause, occurring around age 50, leads to a drop in estrogen, causing symptoms like hot flashes, mood swings, cognitive decline, and autonomic dysfunction. These changes affect quality of life and daily functioning. Hormone therapy helps but carries health risks, making non-drug options important. Exercise shows promise in easing symptoms, but few studies address cognitive, autonomic, and vasomotor issues together. This study aims to test a multidimensional exercise protocol to improve overall well-being in postmenopausal women.