cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.5281/zenodo.10656412
title: Rotational electron diffraction patterns of mono/tripeptoids and organic semiconductor materials

description: Rotational electron diffraction patterns of mono/tripeptoids and organic semiconductor materials, Ph-BTBT-C10 and anit-BTBTT-C6. Collected with a JEOL CRYO ARM 300 electron microscope operated at an accelerating voltage of 300kV at RIKEN, SPring-8 Center. The data for monopeptoid were recorded on a TVIPS XF416 detector, while those for the other compounds were recorded on a DirectElectron DE64 detector.
DOI: 10.6084/m9.figshare.19794310
title: FAM198B promotes colorectal cancer progression by regulating the polarization of tumor-associated macrophages via the SMAD2 signaling pathway

description: Colorectal cancer (CRC) is one of the most common malignant tumors. Tumor-associated macrophages (TAMs) promote the progression of CRC, but the mechanism is not completely clear. The present study aimed to reveal the expression and function of FAM198B in TAMs, and the role of FAM198B in mediating macrophage polarization in CRC. The role of FAM198B in macrophage activity, cell cycle, and angiogenesis was evaluated by CCK-8 assay, flow cytometry, and vasculogenic mimicry assay. The effects of FAM198B on macrophage polarization were determined by flow cytometry. The function of FAM198B-mediated macrophage polarization on CRC progression was evaluated by transwell assays. Bioinformatic analyses and rescue assays were performed to identify biological functions and signaling pathways involved in FAM198B regulation of macrophage polarization. Increased FAM198B expression in TAMs is negatively associated with poor CRC prognosis. Functional assays showed that FAM198B promotes M2 macrophage polarization, which leads to CRC cell proliferation, migration, and invasion. Mechanistically, FAM198B regulates the M2 polarization of macrophages by targeting SMAD2, identifying the SMAD2 pathway as a mechanism by which FAM198B promotes CRC progression through regulating macrophage polarization. These findings provide a possible molecular mechanism for FAM198B in TAMs in CRC and suggest that FAM198B may be a novel therapeutic target in CRC.
DOI: 10.6084/m9.figshare.19794310.v1
title: FAM198B promotes colorectal cancer progression by regulating the polarization of tumor-associated macrophages via the SMAD2 signaling pathway

description: Colorectal cancer (CRC) is one of the most common malignant tumors. Tumor-associated macrophages (TAMs) promote the progression of CRC, but the mechanism is not completely clear. The present study aimed to reveal the expression and function of FAM198B in TAMs, and the role of FAM198B in mediating macrophage polarization in CRC. The role of FAM198B in macrophage activity, cell cycle, and angiogenesis was evaluated by CCK-8 assay, flow cytometry, and vasculogenic mimicry assay. The effects of FAM198B on macrophage polarization were determined by flow cytometry. The function of FAM198B-mediated macrophage polarization on CRC progression was evaluated by transwell assays. Bioinformatic analyses and rescue assays were performed to identify biological functions and signaling pathways involved in FAM198B regulation of macrophage polarization. Increased FAM198B expression in TAMs is negatively associated with poor CRC prognosis. Functional assays showed that FAM198B promotes M2 macrophage polarization, which leads to CRC cell proliferation, migration, and invasion. Mechanistically, FAM198B regulates the M2 polarization of macrophages by targeting SMAD2, identifying the SMAD2 pathway as a mechanism by which FAM198B promotes CRC progression through regulating macrophage polarization. These findings provide a possible molecular mechanism for FAM198B in TAMs in CRC and suggest that FAM198B may be a novel therapeutic target in CRC.
DOI: 10.14473/csda/l1ii3j/clxdyf
title: kf_data_bez_diakritiky_w1_chps_cz_v1.1_ENG_FIN.tab

description: Data
DOI: 10.14473/csda/l1ii3j/gc3pw3
title: D04_CHPSEN101.pdf

description: Questionnaire_04 - Time use diary (Child 10-17)
DOI: 10.14473/csda/l1ii3j/qbad90
title: D05_CHPSEN101.pdf

description: Questionnaire_05 - Time use diary (Adult respondent - 18 year or older)
DOI: 10.6084/m9.figshare.12978572
title: Additional file 2 of Genome-wide identification and expression patterns analysis of the RPD3/HDA1 gene family in cotton

description: Additional file 2: Table S2. Location of Hist_deacetyl domain in cotton RPD3 proteins.
DOI: 10.6084/m9.figshare.12978572.v1
title: Additional file 2 of Genome-wide identification and expression patterns analysis of the RPD3/HDA1 gene family in cotton

description: Additional file 2: Table S2. Location of Hist_deacetyl domain in cotton RPD3 proteins.
DOI: 10.6084/m9.figshare.12978584
title: Additional file 6 of Genome-wide identification and expression patterns analysis of the RPD3/HDA1 gene family in cotton

description: Additional file 6: Table S5. Ka/Ks ratios and occurrence times of segmentally duplicated RPD3 gene pairs of three cotton species. When Ks was equal to 0, Ka/Ks ratios was marked as Ka&gt; &gt; Ks.
DOI: 10.6084/m9.figshare.12978584.v1
title: Additional file 6 of Genome-wide identification and expression patterns analysis of the RPD3/HDA1 gene family in cotton

description: Additional file 6: Table S5. Ka/Ks ratios and occurrence times of segmentally duplicated RPD3 gene pairs of three cotton species. When Ks was equal to 0, Ka/Ks ratios was marked as Ka&gt; &gt; Ks.
DOI: 10.6084/m9.figshare.12978587
title: Additional file 7 of Genome-wide identification and expression patterns analysis of the RPD3/HDA1 gene family in cotton

description: Additional file 7: Table S6. Cis-acting elements in the promoters of GhRPD3 genes.
DOI: 10.6084/m9.figshare.12978587.v1
title: Additional file 7 of Genome-wide identification and expression patterns analysis of the RPD3/HDA1 gene family in cotton

description: Additional file 7: Table S6. Cis-acting elements in the promoters of GhRPD3 genes.
DOI: 10.6084/m9.figshare.11405718
title: MOESM13 of Maternal milk and fecal microbes guide the spatiotemporal development of mucosa-associated microbiota and barrier function in the porcine neonatal gut

description: Additional file 13: Table S6. Contrasts for MUC1, MUC2 and pBD1 expression analyzed within each intestinal segment.
DOI: 10.6084/m9.figshare.11405718.v1
title: MOESM13 of Maternal milk and fecal microbes guide the spatiotemporal development of mucosa-associated microbiota and barrier function in the porcine neonatal gut

description: Additional file 13: Table S6. Contrasts for MUC1, MUC2 and pBD1 expression analyzed within each intestinal segment.
DOI: 10.6084/m9.figshare.12978593
title: Additional file 9 of Genome-wide identification and expression patterns analysis of the RPD3/HDA1 gene family in cotton

description: Additional file 9: Table S7. The FPKM value of GhRPD3 genes in different tissues and under four different abiotic stresses.
DOI: 10.6084/m9.figshare.11405727
title: MOESM14 of Maternal milk and fecal microbes guide the spatiotemporal development of mucosa-associated microbiota and barrier function in the porcine neonatal gut

description: Additional file 14: Table S7. Correlation of the relative abundance of OTUs and expression of genes involved in the development of intestinal barrier function.
DOI: 10.6084/m9.figshare.11405727.v1
title: MOESM14 of Maternal milk and fecal microbes guide the spatiotemporal development of mucosa-associated microbiota and barrier function in the porcine neonatal gut

description: Additional file 14: Table S7. Correlation of the relative abundance of OTUs and expression of genes involved in the development of intestinal barrier function.
DOI: 10.6084/m9.figshare.12978593.v1
title: Additional file 9 of Genome-wide identification and expression patterns analysis of the RPD3/HDA1 gene family in cotton

description: Additional file 9: Table S7. The FPKM value of GhRPD3 genes in different tissues and under four different abiotic stresses.
DOI: 10.6084/m9.figshare.25256791
title: Network training database and experimental data.mat

description: Network training database and experimental data for neural network training
DOI: 10.6084/m9.figshare.25256791.v1
title: Network training database and experimental data.mat

description: Network training database and experimental data for neural network training
DOI: 10.15468/mfwmxb
title: Freshwater fish records at The University of the South Pacific

description: Freshwater biodiversity in the Oceania region is not well studied and underreported. The preserved specimens of freshwater fish at The University of the South Pacific (Suva, Fiji) are documented in this dataset and is a work in progress. No coordinates have been included as the sites need to be georeferenced. This is a long term goal. The records in this dataset were mobilised from a catalouge prepared by Lekima Copeland, one of the few freshwater ichthyologist's from Fiji. Data mobilisation and publication followed the guidelines provided by GBIF. Taxonomic names were verified using the OpenRefine script developed by SIB-Colombia for Taxonomic Validation with WORMS's API, available on GitHub.
DOI: 10.25403/upresearchdata.25215059
title: Statistical shape model (SSM) black South African faces based on from facial landmarks on a CT and CBCT scan population

description: The research developed normative reference values of black South African faces for various inter-landmark distances, and derived a statistical shape model (SSM) of 3D facial shape variation which can be applied to estimate missing soft tissue segments on simulated defective faces, such as for facial prosthetics. The research was conducted on 235 computed tomography and cone beam computed tomography scans.1) SSM_BlackSA: The statistical shape model containing the shape variation of a black South African adult population is provided as a matlab output file2) Defect estimation accuracy: an excel file containing the root mean square errors for estimating defect reconstruction accuracy for various facial defects, including for the full nose, partial nose, orbit, cheek, lips, bi-ortibal and two types of composite defects (small and large)3) Intra and interobserver distances: this excel provides data of 2 observers that each manually calculated inter-landmark distances for 20 clinically relevant distances on the face. Each observer had 3 sets of landmarks.4) Landmark_coordinates: This excel supplies the x,y,z coordinates of 24 facial landmarks of 235 sample faces.5) Manual_interlandmark_distances: this excel gives the calculated inter-landmark measurements of 20 clinically relevant distances calculated from manually placed landmarks on the face. This information was used to determine the population norms.6) Samples_list: an excel with the samples used in this research with basic demographic information such as sex, age and modality7) SSM_Graphic: a figure showing the visual representation of the SSM provided as a matlab file. This figure indicates the modes of variation most responsible for variation, as well as the multinormal distribution of variation
DOI: 10.25403/upresearchdata.25215059.v1
title: Statistical shape model (SSM) black South African faces based on from facial landmarks on a CT and CBCT scan population

description: The research developed normative reference values of black South African faces for various inter-landmark distances, and derived a statistical shape model (SSM) of 3D facial shape variation which can be applied to estimate missing soft tissue segments on simulated defective faces, such as for facial prosthetics. The research was conducted on 235 computed tomography and cone beam computed tomography scans.1) SSM_BlackSA: The statistical shape model containing the shape variation of a black South African adult population is provided as a matlab output file2) Defect estimation accuracy: an excel file containing the root mean square errors for estimating defect reconstruction accuracy for various facial defects, including for the full nose, partial nose, orbit, cheek, lips, bi-ortibal and two types of composite defects (small and large)3) Intra and interobserver distances: this excel provides data of 2 observers that each manually calculated inter-landmark distances for 20 clinically relevant distances on the face. Each observer had 3 sets of landmarks.4) Landmark_coordinates: This excel supplies the x,y,z coordinates of 24 facial landmarks of 235 sample faces.5) Manual_interlandmark_distances: this excel gives the calculated inter-landmark measurements of 20 clinically relevant distances calculated from manually placed landmarks on the face. This information was used to determine the population norms.6) Samples_list: an excel with the samples used in this research with basic demographic information such as sex, age and modality7) SSM_Graphic: a figure showing the visual representation of the SSM provided as a matlab file. This figure indicates the modes of variation most responsible for variation, as well as the multinormal distribution of variation
DOI: 10.5281/zenodo.10686680
title: PV plant simulation

description: simulation of annual power production
DOI: 10.5281/zenodo.10686681
title: PV plant simulation

description: simulation of annual power production
DOI: 10.6084/m9.figshare.24982822
title: Rapid and reliable testing for clinically actionable EGFR mutations in non-small cell lung cancer using the Idylla<sup>TM</sup> platform: a real-world two-center experience in Greece

description: Limited information exists on epidermal growth factor receptor <i>(EGFR)</i> molecular epidemiology in Greece. Next-generation sequencing (NGS) is the recommended method for <i>EGFR</i> genotyping in NSCLC. The Idylla Biocartis platform is a fully automated system for actionable <i>EGFR</i> mutation detection. We describe the prevalence of EGFR mutations in NSCLC patients in two high-volume clinical centers in Greece and compare key methods used for their determination. Eight hundred and fifty-seven FFPE samples from NSCLC patients were tested for EGFR mutations at University of Crete (UoC; <i>n</i> = 324) and at Evangelismos Hospital, Athens (Evangelismos; <i>n</i> = 503). The prevalence of <i>EGFR</i> mutations was 11.1% in the whole cohort (11.5% in non-squamous). The detection rate was 11.0% by NGS, 9.8% by Sanger and 11.3% by Idylla for the whole cohort (12.0% in non-squamous). The agreement between Idylla and Sanger was 93.2%. A targetable <i>EGFR</i> mutation was detected in 10.0% using tissue NGS alone, and in 16.0% using concurrent Idylla ct<i>EGFR</i> testing. The frequency of <i>EGFR</i> mutations was as expected for a Caucasian population. The Idylla <i>EGFR</i> test performance is comparable to reference methods and with a shorter TAT. Adding a concurrent plasma Idylla test to tissue NGS testing increases the detection rate of <i>EGFR</i> mutations in NSCLC.
DOI: 10.6084/m9.figshare.25041968.v1
title: Optimization of time interval for the measurement of plasma lipids for cardiovascular disease risk assessment

description: Lipid testing for atherosclerotic cardiovascular disease (ASCVD) risk is often performed every 4–6 years, but we hypothesized that the optimum time interval may vary depending on baseline risk. Using lipid values and other risk factors from the National Health and Nutrition Examination Survey (NHANES) (<i>n</i> = 9,704), we calculated a 10-year risk score with the pooled-cohort equations. Future risk scores were predicted by increasing age and projecting systolic blood pressure (SBP) and lipid changes, using the mean-percentile age group change in NHANES for SBP (<i>n</i> = 17,329) and the Lifelines Cohort study for lipids (<i>n</i> = 133,540). The crossing of high and intermediate-risk thresholds were calculated by time to determine optimum intervals for lipid testing. Time to crossing risk thresholds depends on baseline risk, but the mean increase in the risk score plateaus at 1% per year for those with a baseline 10-year risk greater than 15%. Based on these findings, we recommend the following maximum time intervals for lipid testing: baseline risk &lt; 15%: 5-years, 16%: 4-years, 17%: 3-years, 18%: 2-years, and 19%: ≤1-year. Testing patients for lipids who have a higher baseline risk more often could identify high-risk patients sooner, allowing for earlier and more effective therapeutic intervention.
DOI: 10.6084/m9.figshare.25189089
title: Polymerase Spiral Reaction (PSR) as a point-of-care diagnostic assay: A systematic review

description: The current systematic review aimed to collect and analyze the comprehensive evidence regarding Polymerase Spiral Reaction (PSR) and to estimate its diagnostic performance and usefulness as a point-of-care (PoC) assay. Literature was retrieved systematically from 2015 to 2023 from PubMed and Scopus. Studies were screened and selected against pre-determined inclusion and exclusion criteria. Quality assessment and risk of bias were critiqued using QUADAS-2. A systematic, qualitative narrative synthesis was employed to synthesize the data.  11 studies were selected for the systematic review, testing diseases in humans utilizing PSR. Only 2 studies clinically validated the test with a sample size &gt; 150. 5 studies were of poor quality; 3 studies were of moderate quality and 3 studies were deemed to be of high quality. 3 studies quantified the diagnostic throughput and reported clinical sensitivity and specificity of PSR approaching to be &gt; 92% and ~ 100%, respectively. Polymerase spiral reaction promises to be an optimistic isothermal assay; however, a huge research gap can be attributed to the lack of statistical and clinical evidence to validate the assay. Adequate research, focused on optimization, coupled with statistical and clinical validation, can help in estimating its true diagnostic potential and applicability. A detailed protocol of this review is registered and available in Prospero (registration number CRD42023406265).
DOI: 10.6084/m9.figshare.25189089.v2
title: Polymerase Spiral Reaction (PSR) as a point-of-care diagnostic assay: A systematic review

description: The current systematic review aimed to collect and analyze the comprehensive evidence regarding Polymerase Spiral Reaction (PSR) and to estimate its diagnostic performance and usefulness as a point-of-care (PoC) assay. Literature was retrieved systematically from 2015 to 2023 from PubMed and Scopus. Studies were screened and selected against pre-determined inclusion and exclusion criteria. Quality assessment and risk of bias were critiqued using QUADAS-2. A systematic, qualitative narrative synthesis was employed to synthesize the data.  11 studies were selected for the systematic review, testing diseases in humans utilizing PSR. Only 2 studies clinically validated the test with a sample size &gt; 150. 5 studies were of poor quality; 3 studies were of moderate quality and 3 studies were deemed to be of high quality. 3 studies quantified the diagnostic throughput and reported clinical sensitivity and specificity of PSR approaching to be &gt; 92% and ~ 100%, respectively. Polymerase spiral reaction promises to be an optimistic isothermal assay; however, a huge research gap can be attributed to the lack of statistical and clinical evidence to validate the assay. Adequate research, focused on optimization, coupled with statistical and clinical validation, can help in estimating its true diagnostic potential and applicability. A detailed protocol of this review is registered and available in Prospero (registration number CRD42023406265).
DOI: 10.6084/m9.figshare.24982822.v1
title: Rapid and reliable testing for clinically actionable EGFR mutations in non-small cell lung cancer using the Idylla<sup>TM</sup> platform: a real-world two-center experience in Greece

description: Limited information exists on epidermal growth factor receptor <i>(EGFR)</i> molecular epidemiology in Greece. Next-generation sequencing (NGS) is the recommended method for <i>EGFR</i> genotyping in NSCLC. The Idylla Biocartis platform is a fully automated system for actionable <i>EGFR</i> mutation detection. We describe the prevalence of EGFR mutations in NSCLC patients in two high-volume clinical centers in Greece and compare key methods used for their determination. Eight hundred and fifty-seven FFPE samples from NSCLC patients were tested for EGFR mutations at University of Crete (UoC; <i>n</i> = 324) and at Evangelismos Hospital, Athens (Evangelismos; <i>n</i> = 503). The prevalence of <i>EGFR</i> mutations was 11.1% in the whole cohort (11.5% in non-squamous). The detection rate was 11.0% by NGS, 9.8% by Sanger and 11.3% by Idylla for the whole cohort (12.0% in non-squamous). The agreement between Idylla and Sanger was 93.2%. A targetable <i>EGFR</i> mutation was detected in 10.0% using tissue NGS alone, and in 16.0% using concurrent Idylla ct<i>EGFR</i> testing. The frequency of <i>EGFR</i> mutations was as expected for a Caucasian population. The Idylla <i>EGFR</i> test performance is comparable to reference methods and with a shorter TAT. Adding a concurrent plasma Idylla test to tissue NGS testing increases the detection rate of <i>EGFR</i> mutations in NSCLC.
DOI: 10.6084/m9.figshare.25041968
title: Optimization of time interval for the measurement of plasma lipids for cardiovascular disease risk assessment

description: Lipid testing for atherosclerotic cardiovascular disease (ASCVD) risk is often performed every 4–6 years, but we hypothesized that the optimum time interval may vary depending on baseline risk. Using lipid values and other risk factors from the National Health and Nutrition Examination Survey (NHANES) (<i>n</i> = 9,704), we calculated a 10-year risk score with the pooled-cohort equations. Future risk scores were predicted by increasing age and projecting systolic blood pressure (SBP) and lipid changes, using the mean-percentile age group change in NHANES for SBP (<i>n</i> = 17,329) and the Lifelines Cohort study for lipids (<i>n</i> = 133,540). The crossing of high and intermediate-risk thresholds were calculated by time to determine optimum intervals for lipid testing. Time to crossing risk thresholds depends on baseline risk, but the mean increase in the risk score plateaus at 1% per year for those with a baseline 10-year risk greater than 15%. Based on these findings, we recommend the following maximum time intervals for lipid testing: baseline risk &lt; 15%: 5-years, 16%: 4-years, 17%: 3-years, 18%: 2-years, and 19%: ≤1-year. Testing patients for lipids who have a higher baseline risk more often could identify high-risk patients sooner, allowing for earlier and more effective therapeutic intervention.