cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.23586267
title: Knowing me, knowing you: a scoping review assessing the current field of social cognition in schizophrenia

description: Impaired social cognition (SC) occurs frequently in schizophrenia (SCZ), yet compared to autism spectrum disorder (ASD), the research on SC in SCZ is sparse and methodologically heterogeneous. To accurately assess between-group SC differences it is further necessary to establish the relationship between nonsocial cognition (NSC) and SC, particularly as this may not be identical across disorders. The present study aimed to map, index and assess the quality of research published between 2014–2021 investigating SC in SCZ, and to summarize existing limitations and recommendations for future research. Following <i>the PRISMA guidelines for scoping reviews</i> (PRISMA-ScR) fifteen (<i>n =</i> 15) case-control studies were identified and included across three electronic databases. Studies additionally utilizing ASD samples were included because of their clinical utility. Most studies reported significant SC impairments in SCZ relative to healthy controls (HC) with varying effect sizes. Significant differences between SCZ and ASD were not found in most studies including both samples. Weak-to-moderate correlations between SC and NSC were often found, although often only within patient samples. Across studies, SC tests were inconsistently described as measurements of "social cognition", "mentalization" and, most frequently and varyingly, “theory of mind”. Most studies lacked methodological transparency. Limitations related to sample sizes and test reliability were most frequently mentioned. The current research on SC in SCZ is limited by conceptual and methodological uncertainties. Future research should focus on ensuring clear and valid definitions of key terms, evaluating and clarifying SC outcome measures and further untangling the relationship between SC and NSC.
DOI: 10.6084/m9.figshare.23586267.v1
title: Knowing me, knowing you: a scoping review assessing the current field of social cognition in schizophrenia

description: Impaired social cognition (SC) occurs frequently in schizophrenia (SCZ), yet compared to autism spectrum disorder (ASD), the research on SC in SCZ is sparse and methodologically heterogeneous. To accurately assess between-group SC differences it is further necessary to establish the relationship between nonsocial cognition (NSC) and SC, particularly as this may not be identical across disorders. The present study aimed to map, index and assess the quality of research published between 2014–2021 investigating SC in SCZ, and to summarize existing limitations and recommendations for future research. Following <i>the PRISMA guidelines for scoping reviews</i> (PRISMA-ScR) fifteen (<i>n =</i> 15) case-control studies were identified and included across three electronic databases. Studies additionally utilizing ASD samples were included because of their clinical utility. Most studies reported significant SC impairments in SCZ relative to healthy controls (HC) with varying effect sizes. Significant differences between SCZ and ASD were not found in most studies including both samples. Weak-to-moderate correlations between SC and NSC were often found, although often only within patient samples. Across studies, SC tests were inconsistently described as measurements of "social cognition", "mentalization" and, most frequently and varyingly, “theory of mind”. Most studies lacked methodological transparency. Limitations related to sample sizes and test reliability were most frequently mentioned. The current research on SC in SCZ is limited by conceptual and methodological uncertainties. Future research should focus on ensuring clear and valid definitions of key terms, evaluating and clarifying SC outcome measures and further untangling the relationship between SC and NSC.
DOI: 10.6084/m9.figshare.23574858
title: Blood-borne extracellular vesicles of bacteria and intestinal cells in patients with psychotic disorders

description: Human cells and bacteria secrete extracellular vesicles (EV) which play a role in intercellular communication. EV from the host intestinal epithelium are involved in the regulation of bacterial gene expression and growth. Bacterial EV (bactEV) produced in the intestine can pass to various tissues where they deliver biomolecules to many kinds of cells, including neurons. Emerging data indicate that gut microbiota is altered in patients with psychotic disorders. We hypothesized that the amount and content of blood-borne EV from intestinal cells and bactEV in psychotic patients would differ from healthy controls. We analyzed for human intestinal proteins by proteomics, for bactEV by metaproteomic analysis, and by measuring the level of lipopolysaccharide (LPS) in blood-borne EV from patients with psychotic disorders (<i>n</i> = 25), tested twice, in the acute phase of psychosis and after improvement, with age- and sex-matched healthy controls (<i>n</i> = 25). Patients with psychotic disorders had lower LPS levels in their EV compared to healthy controls (<i>p</i> = .027). Metaproteome analyses confirmed LPS finding and identified Firmicute<i>s</i> and Bacteroidetes as dominating phyla. Total amounts of human intestine proteins in EV isolated from blood was lower in patients compared to controls (<i>p</i> = .02). Our results suggest that bactEV and host intestinal EV are decreased in patients with psychosis and that this topic is worthy of further investigation given potential pathophysiological implications. Possible mechanisms involve dysregulation of the gut microbiota by host EV, altered translocation of bactEV to systemic circulation where bactEV can interact with both the brain and the immune system.
DOI: 10.6084/m9.figshare.23574858.v1
title: Blood-borne extracellular vesicles of bacteria and intestinal cells in patients with psychotic disorders

description: Human cells and bacteria secrete extracellular vesicles (EV) which play a role in intercellular communication. EV from the host intestinal epithelium are involved in the regulation of bacterial gene expression and growth. Bacterial EV (bactEV) produced in the intestine can pass to various tissues where they deliver biomolecules to many kinds of cells, including neurons. Emerging data indicate that gut microbiota is altered in patients with psychotic disorders. We hypothesized that the amount and content of blood-borne EV from intestinal cells and bactEV in psychotic patients would differ from healthy controls. We analyzed for human intestinal proteins by proteomics, for bactEV by metaproteomic analysis, and by measuring the level of lipopolysaccharide (LPS) in blood-borne EV from patients with psychotic disorders (<i>n</i> = 25), tested twice, in the acute phase of psychosis and after improvement, with age- and sex-matched healthy controls (<i>n</i> = 25). Patients with psychotic disorders had lower LPS levels in their EV compared to healthy controls (<i>p</i> = .027). Metaproteome analyses confirmed LPS finding and identified Firmicute<i>s</i> and Bacteroidetes as dominating phyla. Total amounts of human intestine proteins in EV isolated from blood was lower in patients compared to controls (<i>p</i> = .02). Our results suggest that bactEV and host intestinal EV are decreased in patients with psychosis and that this topic is worthy of further investigation given potential pathophysiological implications. Possible mechanisms involve dysregulation of the gut microbiota by host EV, altered translocation of bactEV to systemic circulation where bactEV can interact with both the brain and the immune system.
DOI: 10.21335/nmdc-498394743
title: Physical and biogeochemical data collected by CTD in Masfjorden, Fensfjorden and Lurefjorden, Vestland, Norway during cruise KB2021605 in 24/2-2/3, 2021.

description: The files contain temperature, practical salinity, oxygen, and depth measurements binned into 1 db pressure bins, collected using a Seabird SBE 11plus V 5.2 CTD and post-processed with the Seasoft software package during cruise KB2021605 in February-March 2021. Data were collected in Masfjorden, Fensfjorden,Lurefjorden, the fjords around Osterøy and along the coast of in Vestland, Norway. Uncalibrated fluorescence, PAR, SPAR, and transmission data from the CTD are included, as are water sample data (Oxygen, Alkalinity, and Dissolved Inorganic Carbon) collected during the cruise. The cruise was organized as a part of the course GEOF232/337 run by the Geophysical Institute, University of Bergen. Data can be downloaded as one .nc file or three .txt file, where data in the .txt-files are separated into downcast (KB2021605_CTD.txt) and bottle (KB2021605_btl.txt) data and where meta-data are provided in KB2021605_meat-data.txt.
DOI: 10.6084/m9.figshare.24241474
title: Raw datas

description: Here are all the raw data for the manuscript "Reveals key role of IL6 in pelvic organ prolapse base on WGCNA and immune infiltration".
DOI: 10.6084/m9.figshare.24241474.v1
title: Raw datas

description: Here are all the raw data for the manuscript "Reveals key role of IL6 in pelvic organ prolapse base on WGCNA and immune infiltration".
DOI: 10.21335/nmdc-780098268
title: Physical and biogeochemical data collected by CTD in Masfjorden, Fensfjorden and Lurefjorden, Vestland, Norway during cruise KB2022605 in February, 2022.

description: The files contain temperature, practical salinity, oxygen, and depth measurements binned into 1 db pressure bins, collected using a Seabird SBE 11plus V 5.2 CTD and post-processed with the Seasoft software package during cruise KB2022605 in February 2022. Data were collected in Masfjorden, Fensfjorden, Lurefjorden and the fjords around Osterøy in Vestland, Norway. Uncalibrated fluorescence, PAR, SPAR, and transmission data from the CTD are included, as are water sample data (Oxygen, Alkalinity and Dissolved Inorganic Carbon) collected during the cruise. The cruise was organized as a part of the course GEOF232/337 run by the Geophysical Institute, University of Bergen. Data can be downloaded as one .nc file or three .txt file, where data in the .txt-files are separated into downcast (KB2022605_CTD.txt) and bottle (KB2022605_btl.txt) data and where meta-data are provided in KB2022605_meat-data.txt.
DOI: 10.6084/m9.figshare.24241522
title: Supplementary Material for: Proteomics to metabolomics: A new insight into the pathogenesis of hypertensive nephropathy

description: Abstract Background: Hypertensive nephropathy (HN) is a high burden disorder and a leading cause of end-stage renal disorder. In spite of huge investigations, the underlying mechanisms are yet largely unknown. Systems biology is a promising approach to provide a comprehensive insight towards this complex disorder. Methods: Protein expression profiles of kidney tubule and cortex sub-compartments were retrieved from the PRIDE database and the quality of the datasets were assessed using principal component analysis (PCA) and hierarchical clustering. Differentially expressed proteins (DEPs) were detected and their attributed metabolites were enriched and their interactions were assessed in multi-layer networks. Moreover, considering the DEPs and the predicted metabolites, key biomedical phenomena with a leading role in HN pathogenesis were proposed. Results: Amino acid and purine metabolisms are the most prominent alteration in kidney cortex whereas dysregulation of energy hemostasis is a key pathogenic mechanism in tubule. Besides, actin cytoskeleton disorganization is an enriched pathway in both anatomical areas. Conclusion: The proteomics profiles of kidney sub-compartments were analyzed using a top-down approach to infer the main pathogenic processes. The constructed holistic map of HN can be exploited to propose novel therapeutic strategies. Keywords: Hypertensive nephropathy, Proteomics, Metabolomics, Systems biology
DOI: 10.6084/m9.figshare.24241522.v1
title: Supplementary Material for: Proteomics to metabolomics: A new insight into the pathogenesis of hypertensive nephropathy

description: Abstract Background: Hypertensive nephropathy (HN) is a high burden disorder and a leading cause of end-stage renal disorder. In spite of huge investigations, the underlying mechanisms are yet largely unknown. Systems biology is a promising approach to provide a comprehensive insight towards this complex disorder. Methods: Protein expression profiles of kidney tubule and cortex sub-compartments were retrieved from the PRIDE database and the quality of the datasets were assessed using principal component analysis (PCA) and hierarchical clustering. Differentially expressed proteins (DEPs) were detected and their attributed metabolites were enriched and their interactions were assessed in multi-layer networks. Moreover, considering the DEPs and the predicted metabolites, key biomedical phenomena with a leading role in HN pathogenesis were proposed. Results: Amino acid and purine metabolisms are the most prominent alteration in kidney cortex whereas dysregulation of energy hemostasis is a key pathogenic mechanism in tubule. Besides, actin cytoskeleton disorganization is an enriched pathway in both anatomical areas. Conclusion: The proteomics profiles of kidney sub-compartments were analyzed using a top-down approach to infer the main pathogenic processes. The constructed holistic map of HN can be exploited to propose novel therapeutic strategies. Keywords: Hypertensive nephropathy, Proteomics, Metabolomics, Systems biology
DOI: 10.6084/m9.figshare.24241543
title: Supplementary Material for: Proteomics to metabolomics: A new insight into the pathogenesis of hypertensive nephropathy

description: Abstract Background: Hypertensive nephropathy (HN) is a high burden disorder and a leading cause of end-stage renal disorder. In spite of huge investigations, the underlying mechanisms are yet largely unknown. Systems biology is a promising approach to provide a comprehensive insight towards this complex disorder. Methods: Protein expression profiles of kidney tubule and cortex sub-compartments were retrieved from the PRIDE database and the quality of the datasets were assessed using principal component analysis (PCA) and hierarchical clustering. Differentially expressed proteins (DEPs) were detected and their attributed metabolites were enriched and their interactions were assessed in multi-layer networks. Moreover, considering the DEPs and the predicted metabolites, key biomedical phenomena with a leading role in HN pathogenesis were proposed. Results: Amino acid and purine metabolisms are the most prominent alteration in kidney cortex whereas dysregulation of energy hemostasis is a key pathogenic mechanism in tubule. Besides, actin cytoskeleton disorganization is an enriched pathway in both anatomical areas. Conclusion: The proteomics profiles of kidney sub-compartments were analyzed using a top-down approach to infer the main pathogenic processes. The constructed holistic map of HN can be exploited to propose novel therapeutic strategies. Keywords: Hypertensive nephropathy, Proteomics, Metabolomics, Systems biology
DOI: 10.6084/m9.figshare.24241543.v1
title: Supplementary Material for: Proteomics to metabolomics: A new insight into the pathogenesis of hypertensive nephropathy

description: Abstract Background: Hypertensive nephropathy (HN) is a high burden disorder and a leading cause of end-stage renal disorder. In spite of huge investigations, the underlying mechanisms are yet largely unknown. Systems biology is a promising approach to provide a comprehensive insight towards this complex disorder. Methods: Protein expression profiles of kidney tubule and cortex sub-compartments were retrieved from the PRIDE database and the quality of the datasets were assessed using principal component analysis (PCA) and hierarchical clustering. Differentially expressed proteins (DEPs) were detected and their attributed metabolites were enriched and their interactions were assessed in multi-layer networks. Moreover, considering the DEPs and the predicted metabolites, key biomedical phenomena with a leading role in HN pathogenesis were proposed. Results: Amino acid and purine metabolisms are the most prominent alteration in kidney cortex whereas dysregulation of energy hemostasis is a key pathogenic mechanism in tubule. Besides, actin cytoskeleton disorganization is an enriched pathway in both anatomical areas. Conclusion: The proteomics profiles of kidney sub-compartments were analyzed using a top-down approach to infer the main pathogenic processes. The constructed holistic map of HN can be exploited to propose novel therapeutic strategies. Keywords: Hypertensive nephropathy, Proteomics, Metabolomics, Systems biology
DOI: 10.6084/m9.figshare.24241561
title: Supplementary Material for: Assessment of micronuclei frequency in the peripheral blood of adult and pediatric patients receiving fractionated total body irradiation

description: The cytokinesis-block micronucleus (CBMN) assay is an established method for assessing chromosome damage in human peripheral blood lymphocytes resulting from exposure to genotoxic agents such as ionizing radiation. The objective of this study is to measure cytogenetic DNA damage and hematology parameters in vivo based on MN frequency in peripheral blood lymphocytes (PBLs) from adult and pediatric leukemia patients undergoing hematopoietic stem cell transplantation preceded by total body irradiation (TBI) as part of the conditioning regimen. CBMN assay cultures were prepared from fresh blood samples collected before and at 4- and 24- h after the start of TBI, corresponding to doses of 1.25 Gy and 3.75 Gy, respectively. For both age groups, there was a significant increase in MN yields with increasing dose (p &lt; 0.05) and dose-dependent decrease in the nuclear division index (NDI; p &lt; 0.0001). In the pre-radiotherapy samples, there was a significantly higher NDI measured in the pediatric cohort compared to the adult due to an increase in the percentage of tri- and quadra-nucleated cells scored. Complete blood counts with differential recorded before and after TBI at the 24 h time point, showed a rapid increase in neutrophil (p = 0.0001) and decrease in lymphocyte (p = 0.0006) counts, resulting in a highly elevated neutrophil-to-lymphocyte (NRL) ratio of 14.45 ± 1.85 after 3.75 Gy TBI (pre-exposure = 4.62 ± 0.49), indicating a strong systemic inflammatory response. Correlation of the hematological cell subset counts with cytogenetic damage, indicated that only the lymphocyte subset survival fraction (after-TBI compared with before-TBI) showed a negative correlation with increasing MN frequency from 0 to 1.25 Gy (r = -0.931; p = 0.007). Further, the data presented here indicate that the combination of CBMN assay endpoints (MN frequency and NDI values) and hematology parameters could be used to assess cytogenetic damage and early hematopoietic injury in the peripheral blood of leukemia patients, 24 h after TBI exposure
DOI: 10.6084/m9.figshare.24241561.v1
title: Supplementary Material for: Assessment of micronuclei frequency in the peripheral blood of adult and pediatric patients receiving fractionated total body irradiation

description: The cytokinesis-block micronucleus (CBMN) assay is an established method for assessing chromosome damage in human peripheral blood lymphocytes resulting from exposure to genotoxic agents such as ionizing radiation. The objective of this study is to measure cytogenetic DNA damage and hematology parameters in vivo based on MN frequency in peripheral blood lymphocytes (PBLs) from adult and pediatric leukemia patients undergoing hematopoietic stem cell transplantation preceded by total body irradiation (TBI) as part of the conditioning regimen. CBMN assay cultures were prepared from fresh blood samples collected before and at 4- and 24- h after the start of TBI, corresponding to doses of 1.25 Gy and 3.75 Gy, respectively. For both age groups, there was a significant increase in MN yields with increasing dose (p &lt; 0.05) and dose-dependent decrease in the nuclear division index (NDI; p &lt; 0.0001). In the pre-radiotherapy samples, there was a significantly higher NDI measured in the pediatric cohort compared to the adult due to an increase in the percentage of tri- and quadra-nucleated cells scored. Complete blood counts with differential recorded before and after TBI at the 24 h time point, showed a rapid increase in neutrophil (p = 0.0001) and decrease in lymphocyte (p = 0.0006) counts, resulting in a highly elevated neutrophil-to-lymphocyte (NRL) ratio of 14.45 ± 1.85 after 3.75 Gy TBI (pre-exposure = 4.62 ± 0.49), indicating a strong systemic inflammatory response. Correlation of the hematological cell subset counts with cytogenetic damage, indicated that only the lymphocyte subset survival fraction (after-TBI compared with before-TBI) showed a negative correlation with increasing MN frequency from 0 to 1.25 Gy (r = -0.931; p = 0.007). Further, the data presented here indicate that the combination of CBMN assay endpoints (MN frequency and NDI values) and hematology parameters could be used to assess cytogenetic damage and early hematopoietic injury in the peripheral blood of leukemia patients, 24 h after TBI exposure
DOI: 10.34740/kaggle/dsv/6607836
title: OnlineFree
DOI: 10.34740/kaggle/dsv/6607835
title: AutoXGB
DOI: 10.5281/zenodo.8405423
title: The dataset for water vapor research in margin of desert, arid and semi-arid area in northwestern China

description: The dataset for water vapor research in margin of desert, arid and semi-arid area in northwestern China
DOI: 10.5281/zenodo.8405422
title: The dataset for water vapor research in margin of desert, arid and semi-arid area in northwestern China

description: The dataset for water vapor research in margin of desert, arid and semi-arid area in northwestern China
DOI: 10.6084/m9.figshare.24241570
title: Supplementary Material for: Proteomics to metabolomics: A new insight into the pathogenesis of hypertensive nephropathy

description: Abstract Background: Hypertensive nephropathy (HN) is a high burden disorder and a leading cause of end-stage renal disorder. In spite of huge investigations, the underlying mechanisms are yet largely unknown. Systems biology is a promising approach to provide a comprehensive insight towards this complex disorder. Methods: Protein expression profiles of kidney tubule and cortex sub-compartments were retrieved from the PRIDE database and the quality of the datasets were assessed using principal component analysis (PCA) and hierarchical clustering. Differentially expressed proteins (DEPs) were detected and their attributed metabolites were enriched and their interactions were assessed in multi-layer networks. Moreover, considering the DEPs and the predicted metabolites, key biomedical phenomena with a leading role in HN pathogenesis were proposed. Results: Amino acid and purine metabolisms are the most prominent alteration in kidney cortex whereas dysregulation of energy hemostasis is a key pathogenic mechanism in tubule. Besides, actin cytoskeleton disorganization is an enriched pathway in both anatomical areas. Conclusion: The proteomics profiles of kidney sub-compartments were analyzed using a top-down approach to infer the main pathogenic processes. The constructed holistic map of HN can be exploited to propose novel therapeutic strategies. Keywords: Hypertensive nephropathy, Proteomics, Metabolomics, Systems biology