cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.5281/zenodo.8222954
title: An infoveillance analysis of public interest, national data and wastewater monitoring in Wales, UK

description: Infoveillance, wastewater and national data.R - The R script used for the analyses and figures present in the manuscript. R functions: flattenCorrMatrix.R -A function for correlation analysis cormtest.R - A function for correlation analysis Data files: Medical data.csv - Data extracted from the UK government portal for COVID-19 cases, deaths and vaccinations South Wales qPCR data.csv - qPCR data for different South Wales sites on each date, with ‘signal’ denoting the signal of SARS-CoV-2 detection in wastewater samples Wales GT data.csv - Google Trends relative search volume data extracted directly from Google Trends for the region of Wales
DOI: 10.5281/zenodo.8231989
title: An infoveillance analysis of public interest, national data and wastewater monitoring in Wales, UK

description: Infoveillance, wastewater and national data.R - The R script used for the analyses and figures present in the manuscript. R functions: flattenCorrMatrix.R -A function for correlation analysis cormtest.R - A function for correlation analysis Data files: Medical data.csv - Data extracted from the UK government portal for COVID-19 cases, deaths and vaccinations South Wales qPCR data.csv - qPCR data for different South Wales sites on each date, with ‘signal’ denoting the signal of SARS-CoV-2 detection in wastewater samples Wales GT data.csv - Google Trends relative search volume data extracted directly from Google Trends for the region of Wales
DOI: 10.25442/hku.23798622
title: Supporting data for "Ecological and adaptive physiological responses of seagrasses to heavy metal pollution in highly urbanized areas"

description: This project aims to use molecular approaches to assess and monitor the ecological impacts of heavy metal pollution in populations of seagrasses in Hong Kong. Through a combination of metagenomics and transcriptomics analysis, this project provides important information about the health of local populations of seagrasses, their resilience and responses to heavy metal pollution, as well as the ecological impacts on the structure and function of seagrass-associated biodiversity.
DOI: 10.25442/hku.23798622.v1
title: Supporting data for "Ecological and adaptive physiological responses of seagrasses to heavy metal pollution in highly urbanized areas"

description: This project aims to use molecular approaches to assess and monitor the ecological impacts of heavy metal pollution in populations of seagrasses in Hong Kong. Through a combination of metagenomics and transcriptomics analysis, this project provides important information about the health of local populations of seagrasses, their resilience and responses to heavy metal pollution, as well as the ecological impacts on the structure and function of seagrass-associated biodiversity.
DOI: 10.25442/hku.23806962
title: Support data for ''Some Innovative Studies on Stability Analysis, Landslide Mechanism and Stabilization Measure of Soil Slopes''

description: The dataset is the suppot data for thesis ''Support data for ''Some Innovative Studies on Stability Analysis, Landslide Mechanism and Stabilization Measure of Soil Slopes''. It including three files.<b>''Support data_Fold1_Slope stability analysis model''</b><b> </b>includes the generated files of Slope/W for slope stability analysis. The files includes the information about the slope models and the results of the slope stability analysis. <b>'' Support data_Fold2_flume test video''</b><b> </b> includes videos of the flume tests about landslide triggered by pressurized pore-gas or its combination with water. <b>''Support data_Fold3_UCS test data''</b><b> </b>includes results of the uniaxial compressive tests of cement-stabilized soil specimens.
DOI: 10.25442/hku.23806962.v1
title: Support data for ''Some Innovative Studies on Stability Analysis, Landslide Mechanism and Stabilization Measure of Soil Slopes''

description: The dataset is the suppot data for thesis ''Support data for ''Some Innovative Studies on Stability Analysis, Landslide Mechanism and Stabilization Measure of Soil Slopes''. It including three files.<b>''Support data_Fold1_Slope stability analysis model''</b><b> </b>includes the generated files of Slope/W for slope stability analysis. The files includes the information about the slope models and the results of the slope stability analysis. <b>'' Support data_Fold2_flume test video''</b><b> </b> includes videos of the flume tests about landslide triggered by pressurized pore-gas or its combination with water. <b>''Support data_Fold3_UCS test data''</b><b> </b>includes results of the uniaxial compressive tests of cement-stabilized soil specimens.
DOI: 10.25442/hku.23807343
title: Supporting data for "Exosomes specifically regulate immune cells to enhance anti-tumor effects"

description: Primary liver cancer—the sixth most prevalent malignant tumor and the third highest cause of cancer-related deaths globally—is typically diagnosed at an advanced stage when treatment options are scarce. This makes the development of innovative treatments crucial. Tumor-associated macrophages (TAMs), which are abundant within the hepatocellular carcinoma (HCC) tumor microenvironment, play a pivotal role in tumor progression. Reprogramming the tumor-promoting M2-like TAMs into the M1 phenotype could restore anti-tumor immunity and initiate therapeutic effects.<br>Exosomes are naturally occurring nanovesicles with diverse physiological functions, and they hold potential as drug delivery platforms. Modifying these exosomes to target TAMs offers a novel approach to liver cancer treatment. In this research, a parental cell-based exosome engineering method was utilized to design targeted peptides, leveraging unique proteins or receptors on human and mouse M2 macrophages. These peptides were fused to the N-terminus of exosomal membrane protein Lamp2b, enabling the display of the targeting moiety on the exosome surface. A dual luciferase reporter system validated the targeting ability of engineered exosomes towards different cells.<br>After confirming the clinical relevance of Galectin 9 or CD36-positive M2 macrophages in HCC, two pairs of gRNAs for the human and mouse LGALS9 or CD36 genes were designed. The gRNAs were used to establish a CRISPR-Cas9 gene knockout system, which was then integrated into targeted exosomes for therapeutic exploration. Galectin 9, a galectin that binds β-galactoside, and CD36, a transmembrane glycoprotein receptor, were both found to have significant effects on macrophage polarization and HCC tumor growth.<br>Our research validated that these engineered exosomes could target human or murine M2 macrophages both in vitro and in vivo. Using the orthotopic liver implant mouse model, it was discovered that engineered exosomes significantly diminished M2 macrophage-induced tumor growth. Thus, our study suggests that engineered exosomes can enhance anti-tumor activity by reprogramming TAMs, offering fresh insights into the development of HCC therapeutic strategies.
DOI: 10.25442/hku.23807343.v1
title: Supporting data for "Exosomes specifically regulate immune cells to enhance anti-tumor effects"

description: Primary liver cancer—the sixth most prevalent malignant tumor and the third highest cause of cancer-related deaths globally—is typically diagnosed at an advanced stage when treatment options are scarce. This makes the development of innovative treatments crucial. Tumor-associated macrophages (TAMs), which are abundant within the hepatocellular carcinoma (HCC) tumor microenvironment, play a pivotal role in tumor progression. Reprogramming the tumor-promoting M2-like TAMs into the M1 phenotype could restore anti-tumor immunity and initiate therapeutic effects.<br>Exosomes are naturally occurring nanovesicles with diverse physiological functions, and they hold potential as drug delivery platforms. Modifying these exosomes to target TAMs offers a novel approach to liver cancer treatment. In this research, a parental cell-based exosome engineering method was utilized to design targeted peptides, leveraging unique proteins or receptors on human and mouse M2 macrophages. These peptides were fused to the N-terminus of exosomal membrane protein Lamp2b, enabling the display of the targeting moiety on the exosome surface. A dual luciferase reporter system validated the targeting ability of engineered exosomes towards different cells.<br>After confirming the clinical relevance of Galectin 9 or CD36-positive M2 macrophages in HCC, two pairs of gRNAs for the human and mouse LGALS9 or CD36 genes were designed. The gRNAs were used to establish a CRISPR-Cas9 gene knockout system, which was then integrated into targeted exosomes for therapeutic exploration. Galectin 9, a galectin that binds β-galactoside, and CD36, a transmembrane glycoprotein receptor, were both found to have significant effects on macrophage polarization and HCC tumor growth.<br>Our research validated that these engineered exosomes could target human or murine M2 macrophages both in vitro and in vivo. Using the orthotopic liver implant mouse model, it was discovered that engineered exosomes significantly diminished M2 macrophage-induced tumor growth. Thus, our study suggests that engineered exosomes can enhance anti-tumor activity by reprogramming TAMs, offering fresh insights into the development of HCC therapeutic strategies.
DOI: 10.25442/hku.23808564
title: Supporting Data for '<b>Kinase Library Screen identified VRK3 as a Novel DNA Damage Factor</b>'

description: Data from the CRISPR library screen enabled us to isolate the target protein in this research. Using live-cell imaging, we were able to validate the involvement of the hits from the CRISPR library screening. Laser microirradiation experiments coupled with live-cell imaging to study the temporal accumulation kinetics of targets that participate in DNA damage repair. We also utilized several DNA damage markers in immunofluorescence staining upon DNA damage induction. The interactions between the target protein and DNA damage factors were also explored using co-immunoprecipitation and pull-down assays, as shown in the western blot data.
DOI: 10.25442/hku.23808564.v1
title: Supporting Data for '<b>Kinase Library Screen identified VRK3 as a Novel DNA Damage Factor</b>'

description: Data from the CRISPR library screen enabled us to isolate the target protein in this research. Using live-cell imaging, we were able to validate the involvement of the hits from the CRISPR library screening. Laser microirradiation experiments coupled with live-cell imaging to study the temporal accumulation kinetics of targets that participate in DNA damage repair. We also utilized several DNA damage markers in immunofluorescence staining upon DNA damage induction. The interactions between the target protein and DNA damage factors were also explored using co-immunoprecipitation and pull-down assays, as shown in the western blot data.
DOI: 10.25442/hku.23812965
title: Supporting Data for the association of autonomy, competence and relatedness with L2 reading engagement in teacher-directed and student-directed reading contexts

description: The data consisted of quantitative survey data and checklist ratings, qualitative interview and stimulated recall data. The data were collected in order to investigate participants' perceptions of the influence of the need for autonomy, competence and relatedness on their L2 behavioral, emotional and cognitive engagement in the self-directed and teacher-directed context respectively.
DOI: 10.25442/hku.23812965.v1
title: Supporting Data for the association of autonomy, competence and relatedness with L2 reading engagement in teacher-directed and student-directed reading contexts

description: The data consisted of quantitative survey data and checklist ratings, qualitative interview and stimulated recall data. The data were collected in order to investigate participants' perceptions of the influence of the need for autonomy, competence and relatedness on their L2 behavioral, emotional and cognitive engagement in the self-directed and teacher-directed context respectively.
DOI: 10.25442/hku.23819010
title: Supporting data for thesis entitled "Distinct vestibular neuron subtypes contribute to navigation and motor coordination"

description: This dataset comprises research studies exploring the intricate networks and functional roles of various neuron types in the brain. The studies focus on molecular, connectivity, and electrophysiological properties of specific neuron populations, such as somatostatin (SST) and parvalbumin (PV) neurons in different brain regions. These investigations shed light on the contribution of these neurons to complex behaviors, including sensory processing, cognitive functions, and motor coordination. By analyzing the molecular profiles, connectivity patterns, and electrophysiological characteristics of these neurons, we gain insights into their specific roles in neural circuitry and their implications for behavior. These findings have important implications for understanding brain function and potential therapeutic interventions for neurological and neuropsychiatric disorders.
DOI: 10.25442/hku.23819010.v1
title: Supporting data for thesis entitled "Distinct vestibular neuron subtypes contribute to navigation and motor coordination"

description: This dataset comprises research studies exploring the intricate networks and functional roles of various neuron types in the brain. The studies focus on molecular, connectivity, and electrophysiological properties of specific neuron populations, such as somatostatin (SST) and parvalbumin (PV) neurons in different brain regions. These investigations shed light on the contribution of these neurons to complex behaviors, including sensory processing, cognitive functions, and motor coordination. By analyzing the molecular profiles, connectivity patterns, and electrophysiological characteristics of these neurons, we gain insights into their specific roles in neural circuitry and their implications for behavior. These findings have important implications for understanding brain function and potential therapeutic interventions for neurological and neuropsychiatric disorders.
DOI: 10.25442/hku.23821407
title: Supporting data for “SYNTHESIS AND CHARACTERIZATION OF METAL−ORGANIC FRAMEWORKS SUPPORTED COPPER CATALYSTS AND THEIR APPLICATIONS IN PHOTOCATALYTIC ORGANIC TRANSFORMATIONS”

description: This dataset is used for the purpose of PhD thesis submission. The theis is about the preparation and characterization of some photocatalysts. So the dataste is divided into four parts, which is corresponding to the section of research data of the thesis. In each section, some figures are displayed. It gives a detaied characterization and optical performance test for the catalyst in each charpter.<br>
DOI: 10.25442/hku.23821407.v1
title: Supporting data for “SYNTHESIS AND CHARACTERIZATION OF METAL−ORGANIC FRAMEWORKS SUPPORTED COPPER CATALYSTS AND THEIR APPLICATIONS IN PHOTOCATALYTIC ORGANIC TRANSFORMATIONS”

description: This dataset is used for the purpose of PhD thesis submission. The theis is about the preparation and characterization of some photocatalysts. So the dataste is divided into four parts, which is corresponding to the section of research data of the thesis. In each section, some figures are displayed. It gives a detaied characterization and optical performance test for the catalyst in each charpter.<br>
DOI: 10.6084/m9.figshare.23918262
title: Supplementary Material for: Childhood-onset Refractory Hypertension Results from Neurofibromatosis type 1 Caused by a Splicing NF1 mutation

description: Background: Neurofibromatosis type 1 (NF-1) is caused by mutations in the NF1 gene that encodes neurofibromin, a negative regulator of RAS proto-oncogene. Approximately one-third of the reported pathogenic mutations in NF1 are splicing mutations, but most consequences are unclear. The objective of this study was to identify the pathogenicity of splicing mutation in a Chinese family with NF-1 and determine the effects of the pre-mRNA splicing mutation by in vitro functional analysis. Methods: Next-generation sequencing was used to screen candidate mutations. We performed a minigene splicing assay to determine the effect of the splicing mutation on NF1 expression and three-dimensional structure models of neurofibromin were generated using SWISS-MODEL and PROCHECK method, respectively. Results: A pathogenic splicing mutation c.479+1G&gt;C in NF1 was found in the proband characterized by childhood-onset refractory hypertension. In vitro analysis demonstrated that c.479+1G&gt;C mutation caused skipping of exon 4, leading to a Glutamine to Valine substitution at position 97 in neurofibromin and an open reading frame shift terminating at codon 108. Protein modelling showed that several major domains were missing in the truncated neurofibromin protein. Conclusion: The splicing mutation c.479+1G&gt;C identified in a Chinese patient with NF-1 and childhood-onset refractory hypertension caused skipping of exon 4 and a truncated protein. Our findings offered new evidence for the molecular diagnosis of NF-1.
DOI: 10.6084/m9.figshare.23918262.v1
title: Supplementary Material for: Childhood-onset Refractory Hypertension Results from Neurofibromatosis type 1 Caused by a Splicing NF1 mutation

description: Background: Neurofibromatosis type 1 (NF-1) is caused by mutations in the NF1 gene that encodes neurofibromin, a negative regulator of RAS proto-oncogene. Approximately one-third of the reported pathogenic mutations in NF1 are splicing mutations, but most consequences are unclear. The objective of this study was to identify the pathogenicity of splicing mutation in a Chinese family with NF-1 and determine the effects of the pre-mRNA splicing mutation by in vitro functional analysis. Methods: Next-generation sequencing was used to screen candidate mutations. We performed a minigene splicing assay to determine the effect of the splicing mutation on NF1 expression and three-dimensional structure models of neurofibromin were generated using SWISS-MODEL and PROCHECK method, respectively. Results: A pathogenic splicing mutation c.479+1G&gt;C in NF1 was found in the proband characterized by childhood-onset refractory hypertension. In vitro analysis demonstrated that c.479+1G&gt;C mutation caused skipping of exon 4, leading to a Glutamine to Valine substitution at position 97 in neurofibromin and an open reading frame shift terminating at codon 108. Protein modelling showed that several major domains were missing in the truncated neurofibromin protein. Conclusion: The splicing mutation c.479+1G&gt;C identified in a Chinese patient with NF-1 and childhood-onset refractory hypertension caused skipping of exon 4 and a truncated protein. Our findings offered new evidence for the molecular diagnosis of NF-1.
DOI: 10.6084/m9.figshare.23918268
title: Supplementary Material for: Childhood-onset Refractory Hypertension Results from Neurofibromatosis type 1 Caused by a Splicing NF1 mutation

description: Background: Neurofibromatosis type 1 (NF-1) is caused by mutations in the NF1 gene that encodes neurofibromin, a negative regulator of RAS proto-oncogene. Approximately one-third of the reported pathogenic mutations in NF1 are splicing mutations, but most consequences are unclear. The objective of this study was to identify the pathogenicity of splicing mutation in a Chinese family with NF-1 and determine the effects of the pre-mRNA splicing mutation by in vitro functional analysis. Methods: Next-generation sequencing was used to screen candidate mutations. We performed a minigene splicing assay to determine the effect of the splicing mutation on NF1 expression and three-dimensional structure models of neurofibromin were generated using SWISS-MODEL and PROCHECK method, respectively. Results: A pathogenic splicing mutation c.479+1G&gt;C in NF1 was found in the proband characterized by childhood-onset refractory hypertension. In vitro analysis demonstrated that c.479+1G&gt;C mutation caused skipping of exon 4, leading to a Glutamine to Valine substitution at position 97 in neurofibromin and an open reading frame shift terminating at codon 108. Protein modelling showed that several major domains were missing in the truncated neurofibromin protein. Conclusion: The splicing mutation c.479+1G&gt;C identified in a Chinese patient with NF-1 and childhood-onset refractory hypertension caused skipping of exon 4 and a truncated protein. Our findings offered new evidence for the molecular diagnosis of NF-1.
DOI: 10.6084/m9.figshare.23918268.v1
title: Supplementary Material for: Childhood-onset Refractory Hypertension Results from Neurofibromatosis type 1 Caused by a Splicing NF1 mutation

description: Background: Neurofibromatosis type 1 (NF-1) is caused by mutations in the NF1 gene that encodes neurofibromin, a negative regulator of RAS proto-oncogene. Approximately one-third of the reported pathogenic mutations in NF1 are splicing mutations, but most consequences are unclear. The objective of this study was to identify the pathogenicity of splicing mutation in a Chinese family with NF-1 and determine the effects of the pre-mRNA splicing mutation by in vitro functional analysis. Methods: Next-generation sequencing was used to screen candidate mutations. We performed a minigene splicing assay to determine the effect of the splicing mutation on NF1 expression and three-dimensional structure models of neurofibromin were generated using SWISS-MODEL and PROCHECK method, respectively. Results: A pathogenic splicing mutation c.479+1G&gt;C in NF1 was found in the proband characterized by childhood-onset refractory hypertension. In vitro analysis demonstrated that c.479+1G&gt;C mutation caused skipping of exon 4, leading to a Glutamine to Valine substitution at position 97 in neurofibromin and an open reading frame shift terminating at codon 108. Protein modelling showed that several major domains were missing in the truncated neurofibromin protein. Conclusion: The splicing mutation c.479+1G&gt;C identified in a Chinese patient with NF-1 and childhood-onset refractory hypertension caused skipping of exon 4 and a truncated protein. Our findings offered new evidence for the molecular diagnosis of NF-1.
DOI: 10.3886/e193214
title: ASEAN as network governance: An alternative lens to evaluate policymaking and performance

description: This project offers a new perspective of ASEAN as network governance (NG) at its core, with a hierarchical organisational structure as its front (hybrid organisation). The works on network forms of organisation and policy network theory (PNT) were used for the analysis.
description: This is bibliographic data showing the sources where the information was derived for the articles and provides links to ASEAN and other sources should researchers be interested to use the data for their work.
DOI: 10.3886/e193214v1
title: ASEAN as network governance: An alternative lens to evaluate policymaking and performance

description: This project offers a new perspective of ASEAN as network governance (NG) at its core, with a hierarchical organisational structure as its front (hybrid organisation). The works on network forms of organisation and policy network theory (PNT) were used for the analysis.
description: This is bibliographic data showing the sources where the information was derived for the articles and provides links to ASEAN and other sources should researchers be interested to use the data for their work.