cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.25471189.v1
title: RAD-Loci_LE

description: Hybridization between two divergente lineages of weevils
DOI: 10.6084/m9.figshare.25469959.v1
title: chimeric_crosslinks_Ago2IP_miR181a/b-1-KO_minus.bed

description: Chimeric crosslinks of Ago2 in mouse thymocytes, from miR181-eCLIP experiment in Verheyden & Klostermann et al 2024. Merge of all 3 replicates, crosslinks from minus strand.
DOI: 10.6084/m9.figshare.24225457.v2
title: N2 fixation in the (sub)tropical western North Pacific.xlsx

description: <i>The dataset includes high-density observations of N</i><sub><em>2</em></sub><i> fixation rates in the (sub)tropical western North Pacific and the associated environmental parameters.</i>
DOI: 10.6069/pd43-2q47
title: Analysis of N-Glycosylation for SARS-CoV-2 expressed receptor-binding domain VOCs and membrane protein with LC-MS.

description: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can infect human cells by first attaching to the ACE-2 receptor via its receptor-binding domain (RBD) in the spike protein. We investigated the influence of N-glycosylation sites of the RBD and the membrane (M) protein on IgG antibody binding in serum samples from patients infected with the original SARS-CoV-2 strain in Germany. The N-glycosylation sites Asn331, Asn334, Asn343, Asn370 and Asn381 of   RBDs of the wildtype, alpha, beta, gamma, kappa, and omicron BA.1 variants expressed in HEK293T and HEK293S GnTI- cells , as well as Asn5 for the M-protein were analyzed with tandem mass spectrometry for N-glycosylation.
DOI: 10.5281/zenodo.8052099
title: Frozen Nextstrain Lithuania Timetree

description: Frozen tunetree dataset from Nextstrain.


https://nextstrain.org/groups/neherlab/ncov/lithuania timetree data range from 2019-12-16 to 2023-05-15.


As of download data was updated on 2023-05-22
DOI: 10.5281/zenodo.8052100
title: Frozen Nextstrain Lithuania Timetree

description: Frozen tunetree dataset from Nextstrain.


https://nextstrain.org/groups/neherlab/ncov/lithuania timetree data range from 2019-12-16 to 2023-05-15.


As of download data was updated on 2023-05-22
DOI: 10.6084/m9.figshare.20080880
title: circFCHO2 promotes gastric cancer progression by activating the JAK1/STAT3 pathway via sponging miR-194-5p

description: circFCHO2 has been revealed to be overexpressed in gastric cancer (GC) patients. This article identified the function of circFCHO2 on GC progression. The expression of circFCHO2, miR-194-5p and JAK1 in 30 GC patients and cells was monitored by quantitative reverse transcription-polymerase chain reaction. circFCHO2 localization in GC cells was monitored by RNA fluorescence in situ hybridization. Cell counting kit-8 assay, 5-ethynyl-2-deoxyuridine staining, transwell experiment, tube formation and sphere formation experiments were applied to detect GC cell proliferation, invasion, angiogenesis and cancer stem cell characteristics. Dual-luciferase reporter gene assay, RNA pull down assay and RNA immunoprecipitation experiment were utilized to research the binding between two genes. In vivo tumorigenesis and lung metastasis were studied using nude mice. Immunohistochemistry and hematoxylin–eosin staining were conducted. Protein expression was assessed by Western blot. Serum exosomes of GC patients and healthy participants were isolated. circFCHO2 up-modulation in GC patients was related to poor outcome. circFCHO2 was located in the cytoplasm of GC cells. circFCHO2 silencing weakened the proliferation, invasion, angiogenesis and stem cell characteristics of GC cells. miR-194-5p knockdown counteracted this effect. circFCHO2 activated the JAK1/STAT3 pathway by sponging miR-194-5p. miR-194-5p overexpression attenuated the malignant phenotypes of GC cells. JAK1 overexpression abrogated this effect. circFCHO2 silencing weakened GC cells growth and lung metastasis in vivo. circFCHO2 was up-modulated in serum exosomes of GC patients. circFCHO2 was an oncogene in GC by activating the JAK1/STAT3 pathway via sponging miR-194-5p. circFCHO2 might be a novel target and diagnostic marker for GC.
DOI: 10.6084/m9.figshare.20080880.v1
title: circFCHO2 promotes gastric cancer progression by activating the JAK1/STAT3 pathway via sponging miR-194-5p

description: circFCHO2 has been revealed to be overexpressed in gastric cancer (GC) patients. This article identified the function of circFCHO2 on GC progression. The expression of circFCHO2, miR-194-5p and JAK1 in 30 GC patients and cells was monitored by quantitative reverse transcription-polymerase chain reaction. circFCHO2 localization in GC cells was monitored by RNA fluorescence in situ hybridization. Cell counting kit-8 assay, 5-ethynyl-2-deoxyuridine staining, transwell experiment, tube formation and sphere formation experiments were applied to detect GC cell proliferation, invasion, angiogenesis and cancer stem cell characteristics. Dual-luciferase reporter gene assay, RNA pull down assay and RNA immunoprecipitation experiment were utilized to research the binding between two genes. In vivo tumorigenesis and lung metastasis were studied using nude mice. Immunohistochemistry and hematoxylin–eosin staining were conducted. Protein expression was assessed by Western blot. Serum exosomes of GC patients and healthy participants were isolated. circFCHO2 up-modulation in GC patients was related to poor outcome. circFCHO2 was located in the cytoplasm of GC cells. circFCHO2 silencing weakened the proliferation, invasion, angiogenesis and stem cell characteristics of GC cells. miR-194-5p knockdown counteracted this effect. circFCHO2 activated the JAK1/STAT3 pathway by sponging miR-194-5p. miR-194-5p overexpression attenuated the malignant phenotypes of GC cells. JAK1 overexpression abrogated this effect. circFCHO2 silencing weakened GC cells growth and lung metastasis in vivo. circFCHO2 was up-modulated in serum exosomes of GC patients. circFCHO2 was an oncogene in GC by activating the JAK1/STAT3 pathway via sponging miR-194-5p. circFCHO2 might be a novel target and diagnostic marker for GC.
DOI: 10.6084/m9.figshare.20106366
title: Substance P promotes the progression of bronchial asthma through activating the PI3K/AKT/NF-κB pathway mediated cellular inflammation and pyroptotic cell death in bronchial epithelial cells

description: NOD-like receptor family pyrin domain containing three (NLRP3) inflammasome-mediated pyroptotic cell death and inflammation contribute to the pathogenesis of bronchial asthma, and it is reported that Substance P (SP) plays important role in the process, however, the detailed molecular mechanisms by which SP participates in the aggravation of bronchial asthma have not been fully studied. Here, our clinical data showed that SP and its receptor Neurokinin-1 receptor (NK1R) were significantly elevated in the plasma and peripheral blood mononuclear cell (PBMC) collected from patients with bronchial asthma, and further pre-clinical experiments evidenced that SP suppressed cell viability, accelerated lactate dehydrogenase (LDH) release, and upregulated ASC, Caspase-1, NLRP3, IL-1β and IL-18 to promote pyroptotic cell death and cellular inflammation in the human bronchial epithelial cells and asthmatic mice models <i>in vitro</i> and <i>in vivo</i>. Interestingly, SP-induced pyroptotic cell death was reversed by NK1R inhibitor L732138. Then, we uncovered the underlying mechanisms, and found that SP activated the downstream PI3K/AKT/NF-κB signal pathway in a NK1R-dependent manner, and blockage of this pathway by both PI3K inhibitor (LY294002) and NF-κB inhibitor (MG132) reversed SP-induced pyroptotic cell death and recovered cell viability in bronchial epithelial cells. Collectively, we concluded that SP interacted with its receptor NK1R to activate the PI3K/AKT/NF-κB pathway, which further triggered NLRP3-mediated pyroptotic cell death in the bronchial epithelial cells, resulting in the aggravation of bronchial asthma.
DOI: 10.6084/m9.figshare.20106366.v3
title: Substance P promotes the progression of bronchial asthma through activating the PI3K/AKT/NF-κB pathway mediated cellular inflammation and pyroptotic cell death in bronchial epithelial cells

description: NOD-like receptor family pyrin domain containing three (NLRP3) inflammasome-mediated pyroptotic cell death and inflammation contribute to the pathogenesis of bronchial asthma, and it is reported that Substance P (SP) plays important role in the process, however, the detailed molecular mechanisms by which SP participates in the aggravation of bronchial asthma have not been fully studied. Here, our clinical data showed that SP and its receptor Neurokinin-1 receptor (NK1R) were significantly elevated in the plasma and peripheral blood mononuclear cell (PBMC) collected from patients with bronchial asthma, and further pre-clinical experiments evidenced that SP suppressed cell viability, accelerated lactate dehydrogenase (LDH) release, and upregulated ASC, Caspase-1, NLRP3, IL-1β and IL-18 to promote pyroptotic cell death and cellular inflammation in the human bronchial epithelial cells and asthmatic mice models <i>in vitro</i> and <i>in vivo</i>. Interestingly, SP-induced pyroptotic cell death was reversed by NK1R inhibitor L732138. Then, we uncovered the underlying mechanisms, and found that SP activated the downstream PI3K/AKT/NF-κB signal pathway in a NK1R-dependent manner, and blockage of this pathway by both PI3K inhibitor (LY294002) and NF-κB inhibitor (MG132) reversed SP-induced pyroptotic cell death and recovered cell viability in bronchial epithelial cells. Collectively, we concluded that SP interacted with its receptor NK1R to activate the PI3K/AKT/NF-κB pathway, which further triggered NLRP3-mediated pyroptotic cell death in the bronchial epithelial cells, resulting in the aggravation of bronchial asthma.
DOI: 10.6084/m9.figshare.20281874
title: Comparing the mitochondrial signatures in ESCs and iPSCs and their neural derivations

description: Embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs) have distinct origins: ESCs are derived from pre-implanted embryos while iPSCs are reprogrammed somatic cells. Both have their own characteristics and lineage specificity, and both are valuable tools for studying human neurological development and disease. Thus far, few studies have analyzed how differences between stem cell types influence mitochondrial function and mitochondrial DNA (mtDNA) homeostasis during differentiation into neural and glial lineages. In this study, we compared mitochondrial function and mtDNA replication in human ESCs and iPSCs at three different stages − pluripotent, neural progenitor and astrocyte. We found that while ESCs and iPSCs have a similar mitochondrial signature, neural and astrocyte derivations manifested differences. At the neural stem cell (NSC) stage, iPSC-NSCs displayed decreased ATP production and a reduction in mitochondrial respiratory chain (MRC) complex IV expression compared to ESC-NSCs. IPSC-astrocytes showed increased mitochondrial activity including elevated ATP production, MRC complex IV expression, mtDNA copy number and mitochondrial biogenesis relative to those derived from ESCs. These findings show that while ESCs and iPSCs are similar at the pluripotent stage, differences in mitochondrial function may develop during differentiation and must be taken into account when extrapolating results from different cell types. <b>Abbreviation:</b> BSA: Bovine serum albumin; DCFDA: 2′,7′‐dichlorodihydrofluorescein diacetate; DCX: Doublecortin; EAAT-1: Excitatory amino acid transporter 1; ESCs: Embryonic stem cells; GFAP: Glial fibrillary acidic protein; GS: Glutamine synthetase; iPSCs: Induced pluripotent stem cells; LC3B: Microtubule-associated protein 1 light chain 3β; LC-MS: Liquid chromatography-mass spectrometry; mito-ROS: Mitochondrial ROS; MMP: Mitochondrial membrane potential; MRC: Mitochondrial respiratory chain; mtDNA: Mitochondrial DNA; MTDR: MitoTracker Deep Red; MTG: MitoTracker Green; NSCs: Neural stem cells; PDL: Poly-D-lysine; PFA: Paraformaldehyde; PGC-1α: PPAR-γ coactivator-1 alpha; PPAR-γ: Peroxisome proliferator-activated receptor-gamma; p-SIRT1: Phosphorylated sirtuin 1; p-ULK1: Phosphorylated unc-51 like autophagy activating kinase 1; qPCR: Quantitative PCR; RT: Room temperature; RT-qPCR: Quantitative reverse transcription PCR; SEM: Standard error of the mean; TFAM: Mitochondrial transcription factor A; TMRE: Tetramethylrhodamine ethyl ester; TOMM20: Translocase of outer mitochondrial membrane 20
DOI: 10.6084/m9.figshare.20106366.v2
title: Substance P promotes the progression of bronchial asthma through activating the PI3K/AKT/NF-κB pathway mediated cellular inflammation and pyroptotic cell death in bronchial epithelial cells

description: NOD-like receptor family pyrin domain containing three (NLRP3) inflammasome-mediated pyroptotic cell death and inflammation contribute to the pathogenesis of bronchial asthma, and it is reported that Substance P (SP) plays important role in the process, however, the detailed molecular mechanisms by which SP participates in the aggravation of bronchial asthma have not been fully studied. Here, our clinical data showed that SP and its receptor Neurokinin-1 receptor (NK1R) were significantly elevated in the plasma and peripheral blood mononuclear cell (PBMC) collected from patients with bronchial asthma, and further pre-clinical experiments evidenced that SP suppressed cell viability, accelerated lactate dehydrogenase (LDH) release, and upregulated ASC, Caspase-1, NLRP3, IL-1β and IL-18 to promote pyroptotic cell death and cellular inflammation in the human bronchial epithelial cells and asthmatic mice models <i>in vitro</i> and <i>in vivo</i>. Interestingly, SP-induced pyroptotic cell death was reversed by NK1R inhibitor L732138. Then, we uncovered the underlying mechanisms, and found that SP activated the downstream PI3K/AKT/NF-κB signal pathway in a NK1R-dependent manner, and blockage of this pathway by both PI3K inhibitor (LY294002) and NF-κB inhibitor (MG132) reversed SP-induced pyroptotic cell death and recovered cell viability in bronchial epithelial cells. Collectively, we concluded that SP interacted with its receptor NK1R to activate the PI3K/AKT/NF-κB pathway, which further triggered NLRP3-mediated pyroptotic cell death in the bronchial epithelial cells, resulting in the aggravation of bronchial asthma.
DOI: 10.6084/m9.figshare.20281874.v1
title: Comparing the mitochondrial signatures in ESCs and iPSCs and their neural derivations

description: Embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs) have distinct origins: ESCs are derived from pre-implanted embryos while iPSCs are reprogrammed somatic cells. Both have their own characteristics and lineage specificity, and both are valuable tools for studying human neurological development and disease. Thus far, few studies have analyzed how differences between stem cell types influence mitochondrial function and mitochondrial DNA (mtDNA) homeostasis during differentiation into neural and glial lineages. In this study, we compared mitochondrial function and mtDNA replication in human ESCs and iPSCs at three different stages − pluripotent, neural progenitor and astrocyte. We found that while ESCs and iPSCs have a similar mitochondrial signature, neural and astrocyte derivations manifested differences. At the neural stem cell (NSC) stage, iPSC-NSCs displayed decreased ATP production and a reduction in mitochondrial respiratory chain (MRC) complex IV expression compared to ESC-NSCs. IPSC-astrocytes showed increased mitochondrial activity including elevated ATP production, MRC complex IV expression, mtDNA copy number and mitochondrial biogenesis relative to those derived from ESCs. These findings show that while ESCs and iPSCs are similar at the pluripotent stage, differences in mitochondrial function may develop during differentiation and must be taken into account when extrapolating results from different cell types. <b>Abbreviation:</b> BSA: Bovine serum albumin; DCFDA: 2′,7′‐dichlorodihydrofluorescein diacetate; DCX: Doublecortin; EAAT-1: Excitatory amino acid transporter 1; ESCs: Embryonic stem cells; GFAP: Glial fibrillary acidic protein; GS: Glutamine synthetase; iPSCs: Induced pluripotent stem cells; LC3B: Microtubule-associated protein 1 light chain 3β; LC-MS: Liquid chromatography-mass spectrometry; mito-ROS: Mitochondrial ROS; MMP: Mitochondrial membrane potential; MRC: Mitochondrial respiratory chain; mtDNA: Mitochondrial DNA; MTDR: MitoTracker Deep Red; MTG: MitoTracker Green; NSCs: Neural stem cells; PDL: Poly-D-lysine; PFA: Paraformaldehyde; PGC-1α: PPAR-γ coactivator-1 alpha; PPAR-γ: Peroxisome proliferator-activated receptor-gamma; p-SIRT1: Phosphorylated sirtuin 1; p-ULK1: Phosphorylated unc-51 like autophagy activating kinase 1; qPCR: Quantitative PCR; RT: Room temperature; RT-qPCR: Quantitative reverse transcription PCR; SEM: Standard error of the mean; TFAM: Mitochondrial transcription factor A; TMRE: Tetramethylrhodamine ethyl ester; TOMM20: Translocase of outer mitochondrial membrane 20
DOI: 10.6084/m9.figshare.25470001
title: RNA-seq raw data

description: RNA-sequence raw data
DOI: 10.17043/miocene-temperature-portal-3
title: Miocene temperature portal
DOI: 10.6084/m9.figshare.25471414
title: Figshare Table 2 Contribution of SIG-III Initiatives to Member Engagement.pdf

description: The study identifies factors influencing professional associations’ member engagement using the “information practices” approach. In this autoethnography study, the experiences, epiphanies, and the frequency counts of 11 information practices of six SIG-III officers and volunteers when planning and implementing 184 activities of eight initiatives online from 2020 to 2023 helped us identify 99 factors that influence member engagement. Using thematic analysis, we classify these factors into 18 clusters and three groups, namely, management-centric, sharing-centric, and benefits for members. Eight tables representing eight SIG-III initiatives with detailed activities from the Information Practice lens are presented in the attached file. Operational definitions of the information practices are presented.
DOI: 10.6084/m9.figshare.25471414.v1
title: Figshare Table 2 Contribution of SIG-III Initiatives to Member Engagement.pdf

description: The study identifies factors influencing professional associations’ member engagement using the “information practices” approach. In this autoethnography study, the experiences, epiphanies, and the frequency counts of 11 information practices of six SIG-III officers and volunteers when planning and implementing 184 activities of eight initiatives online from 2020 to 2023 helped us identify 99 factors that influence member engagement. Using thematic analysis, we classify these factors into 18 clusters and three groups, namely, management-centric, sharing-centric, and benefits for members. Eight tables representing eight SIG-III initiatives with detailed activities from the Information Practice lens are presented in the attached file. Operational definitions of the information practices are presented.
DOI: 10.5281/zenodo.10868442
title: 1-km high resolution model outputs using the WRF and WRF-Hydro model Raw data from the manuscipt "Process-based Atmosphere-Hydrology-Malaria Modeling: Performance for Spatio-temporal Malaria Transmission Dynamics in Sub-Saharan Africa "

description: Here we provide the model outputs from the numerical climate model WRF (Weather Research and Forecasting) and its hydrological coupled model WRF-Hydro for the Health and Demographic Surveillance Systems (HDSS) site regions of Nouna in Burkina Faso. Model results are used for investigating the influence of surface hydrology representation, environmental and climate-sensitive driver factors on malaria incidence.The experiments use the following model configuration: 1km horizontal resolution with 200*200 grid points, WSM6 microphysics, ACM2 PBL, and RRTM & Dudhia radiation scheme. WRF uses the Noah LSM, and WRF-Hydro uses the Noah LSM with enhanced lateral hydrological description (https://ral.ucar.edu/projects/wrf_hydro/overview). These simulations were conducted in the Karlsruhe Steinbuch Centre for Computing (SCC) Horeka.

Model outputs are provided in daily step (originally derived from the hourly output). Filename with "wrf-hydro_pr_2000-2020_d02-1km.nc" provides Precipitation,n mm/day"wrf-hydro_tas_2000-2020_d02-1km.nc" provides mean temperature in Celsius, "wrf-hydro_tasmax_2000-2020_d02-1km.nc" provides maximum temperature in Celsius, "wrf-hydro_tasmin_2000-2020_d02-1km.nc" provides minmum temperature in Celsius, "wrf-hydro_dtr_2000-2020_d02-1km.nc" provides diurnal temperature ranges in Celius, "wrf-hydro_rh_2000-2020_d02-1km.nc" provides relative humudity in % and "wrf-hydro_sw_2000-2020_d02-1km.nc" provides the surface hydrology.
DOI: 10.5517/ccdc.csd.cc23n0xq
title: CCDC 1955663: Experimental Crystal Structure Determination

description: Related Article: Kanishka Sikligar, Steven Paul Kelley, Durgesh Wagle, Piyuni Ishtaweera, Gary A Baker, Jerry L. Atwood|2023|Chemical Science|14|9063|doi:10.1039/D3SC01629C
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5517/ccdc.csd.cc27jgy6
title: CCDC 2071418: Experimental Crystal Structure Determination

description: Related Article: Kanishka Sikligar, Steven Paul Kelley, Durgesh Wagle, Piyuni Ishtaweera, Gary A Baker, Jerry L. Atwood|2023|Chemical Science|14|9063|doi:10.1039/D3SC01629C
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5517/ccdc.csd.cc2ch0yv
title: CCDC 2189187: Experimental Crystal Structure Determination

description: Related Article: Ian J. S. Fairlamb, Jan Lang, Aleš Růžička, Miloš Sedlák, Jiří Váňa
|2023|Organometallics|42|2197|doi:10.1021/acs.organomet.3c00178
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5517/ccdc.csd.cc2d3y1j
title: CCDC 2208317: Experimental Crystal Structure Determination

description: Related Article: Alejandro Suárez-Lustres, Nuria Martínez-Yáñez, Álvaro Velasco-Rubio, Jesús A. Varela, Carlos Saá|2023|Org.Lett.|25|794|doi:10.1021/acs.orglett.2c04300
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5517/ccdc.csd.cc2d3y2k
title: CCDC 2208318: Experimental Crystal Structure Determination

description: Related Article: Alejandro Suárez-Lustres, Nuria Martínez-Yáñez, Álvaro Velasco-Rubio, Jesús A. Varela, Carlos Saá|2023|Org.Lett.|25|794|doi:10.1021/acs.orglett.2c04300
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.