cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.29110005
title: The causal relationship between circulating metabolites and gestational hypertension, pre-eclampsia, eclampsia: A bidirectional two-sample Mendelian randomization study

description: Gestational hypertension, pre-eclampsia, and eclampsia pose significant risks to maternal and fetal health, yet their underlying causes remain unclear. This study investigates the associations between 233 metabolites and these conditions. We analyzed data from the Genome-Wide Association Studies (GWAS) database for gestational hypertension, pre-eclampsia, and eclampsia. The bidirectional two-sample MR analysis examined causal relationships using inverse variance weighting as the primary method, supplemented by MR-Egger, weighted median, simple mode, and weighted mode. Sensitivity analyses assessed robustness, heterogeneity, and horizontal pleiotropy. In the forward Mendelian randomization analysis, a reduction in citrate levels (OR = 0.906, 95% CI = 0.829–0.990, <i>p</i> = .029) is associated with an increased risk of gestational hypertension. The ratio of conjugated linoleic acid to total fatty acids (OR = 1.172, 95% CI = 1.026–1.339, <i>p</i> = .019) is associated with an increased risk of gestational hypertension. The ratio of conjugated linoleic acid to total fatty acids (OR = 1.288, 95% CI = 1.064–1.560, <i>p</i> = .009) is associated with an increased risk of preeclampsia and eclampsia. The phospholipids to total lipids ratio in large HDL (OR = 1.227, 95% CI = 1.120–1.344, <i>p</i> = 9.91 × 10^-6) is associated with an increased risk of preeclampsia and eclampsia. The total cholesterol to total lipids ratio in chylomicrons and extremely large VLDL (OR = 0.884, 95% CI = 0.789–0.990, <i>p</i> = .033) is associated with an increased risk of preeclampsia and eclampsia. In the reverse Mendelian randomization analysis, the occurrence of gestational hypertension is associated with a reduction in Cholesteryl esters to total lipids ratio in very large VLDL (OR = 0.987, 95% CI = 0.975–0.999, <i>p</i> = .044). The occurrence of preeclampsia and eclampsia is associated with a reduction in total choline levels (OR = 0.989, 95% CI = 0.979–0.998, <i>p</i> = .029), and with a reduction in total phosphoglycerides levels (OR = 0.988, 95% CI = 0.978–0.997, <i>p</i> = .012). Sensitivity analysis did not detect significant heterogeneity or pleiotropy. This research elucidates the causal links between specific metabolites and gestational hypertension, pre-eclampsia, and eclampsia, potentially informing new clinical approaches for diagnosis and treatment.
DOI: 10.6084/m9.figshare.29110005.v1
title: The causal relationship between circulating metabolites and gestational hypertension, pre-eclampsia, eclampsia: A bidirectional two-sample Mendelian randomization study

description: Gestational hypertension, pre-eclampsia, and eclampsia pose significant risks to maternal and fetal health, yet their underlying causes remain unclear. This study investigates the associations between 233 metabolites and these conditions. We analyzed data from the Genome-Wide Association Studies (GWAS) database for gestational hypertension, pre-eclampsia, and eclampsia. The bidirectional two-sample MR analysis examined causal relationships using inverse variance weighting as the primary method, supplemented by MR-Egger, weighted median, simple mode, and weighted mode. Sensitivity analyses assessed robustness, heterogeneity, and horizontal pleiotropy. In the forward Mendelian randomization analysis, a reduction in citrate levels (OR = 0.906, 95% CI = 0.829–0.990, <i>p</i> = .029) is associated with an increased risk of gestational hypertension. The ratio of conjugated linoleic acid to total fatty acids (OR = 1.172, 95% CI = 1.026–1.339, <i>p</i> = .019) is associated with an increased risk of gestational hypertension. The ratio of conjugated linoleic acid to total fatty acids (OR = 1.288, 95% CI = 1.064–1.560, <i>p</i> = .009) is associated with an increased risk of preeclampsia and eclampsia. The phospholipids to total lipids ratio in large HDL (OR = 1.227, 95% CI = 1.120–1.344, <i>p</i> = 9.91 × 10^-6) is associated with an increased risk of preeclampsia and eclampsia. The total cholesterol to total lipids ratio in chylomicrons and extremely large VLDL (OR = 0.884, 95% CI = 0.789–0.990, <i>p</i> = .033) is associated with an increased risk of preeclampsia and eclampsia. In the reverse Mendelian randomization analysis, the occurrence of gestational hypertension is associated with a reduction in Cholesteryl esters to total lipids ratio in very large VLDL (OR = 0.987, 95% CI = 0.975–0.999, <i>p</i> = .044). The occurrence of preeclampsia and eclampsia is associated with a reduction in total choline levels (OR = 0.989, 95% CI = 0.979–0.998, <i>p</i> = .029), and with a reduction in total phosphoglycerides levels (OR = 0.988, 95% CI = 0.978–0.997, <i>p</i> = .012). Sensitivity analysis did not detect significant heterogeneity or pleiotropy. This research elucidates the causal links between specific metabolites and gestational hypertension, pre-eclampsia, and eclampsia, potentially informing new clinical approaches for diagnosis and treatment.
DOI: 10.3535/4vw-k5q-0w7
title: Leucoma salicis (Linnaeus, 1758)

description: Digital Specimen for the physical specimen hosted at Finnish Museum of Natural History.
DOI: 10.6084/m9.figshare.28263895
title: Effect of oral potassium supplementation on urinary potassium excretion and its diagnostic value for primary aldosteronism

description: We aimed to: (1) explore the effect of oral potassium supplementation on urinary potassium excretion, and (2) evaluate the value of urinary potassium-related indicators in distinguishing primary aldosteronism (PA) from non-PA patients. A prospective study of 20 patients with hypertension and hypokalemia caused by renal potassium loss between November 2023 and April 2024 was conducted. Demographic features, 24-hour urine collection before and after potassium supplementation were all collected. The patients had a mean age of 49.38 years and 70% were male. Following a median potassium supplement dose of 8.50 g, serum potassium increased from 3.25 to 3.90 mmol/L (<i>p</i> &lt; .001), and 24-hour urinary potassium (24 h UK) rose from 41.40 to 59.75 mmol/24 h (<i>p</i> = .004). After supplementation, 20% of patients had decreased 24 h UK, while 25%, 25%, and 40% showed increases of 0–10, 10–20, and &gt; 20 mmol/24 h. Urinary-to-serum potassium ratio (USR) decreased in 40% of patients, while it increased by 0–5, 5–10, and &gt; 10 L/24 h in 25%, 25%, and 10% of patients, respectively. Both 24 h UK and USR after repletion predicted PA with moderate-to-high accuracy (AUC = 0.808 for both). The optimal cutoff of 24 h UK and USR after supplementation were 51 mmol/24 h and 17.43 L/24 h. The AUC for 24 h USR and 24 h UK before repletion in predicting PA were 0.788 and 0.652, respectively. Urinary potassium does not increase proportionally with serum potassium levels or the oral potassium dose, showing individual variability. Post-supplementation urinary potassium has greater diagnostic value for distinguishing PA than pre-supplementation indicators.
DOI: 10.6084/m9.figshare.28263895.v1
title: Effect of oral potassium supplementation on urinary potassium excretion and its diagnostic value for primary aldosteronism

description: We aimed to: (1) explore the effect of oral potassium supplementation on urinary potassium excretion, and (2) evaluate the value of urinary potassium-related indicators in distinguishing primary aldosteronism (PA) from non-PA patients. A prospective study of 20 patients with hypertension and hypokalemia caused by renal potassium loss between November 2023 and April 2024 was conducted. Demographic features, 24-hour urine collection before and after potassium supplementation were all collected. The patients had a mean age of 49.38 years and 70% were male. Following a median potassium supplement dose of 8.50 g, serum potassium increased from 3.25 to 3.90 mmol/L (<i>p</i> &lt; .001), and 24-hour urinary potassium (24 h UK) rose from 41.40 to 59.75 mmol/24 h (<i>p</i> = .004). After supplementation, 20% of patients had decreased 24 h UK, while 25%, 25%, and 40% showed increases of 0–10, 10–20, and &gt; 20 mmol/24 h. Urinary-to-serum potassium ratio (USR) decreased in 40% of patients, while it increased by 0–5, 5–10, and &gt; 10 L/24 h in 25%, 25%, and 10% of patients, respectively. Both 24 h UK and USR after repletion predicted PA with moderate-to-high accuracy (AUC = 0.808 for both). The optimal cutoff of 24 h UK and USR after supplementation were 51 mmol/24 h and 17.43 L/24 h. The AUC for 24 h USR and 24 h UK before repletion in predicting PA were 0.788 and 0.652, respectively. Urinary potassium does not increase proportionally with serum potassium levels or the oral potassium dose, showing individual variability. Post-supplementation urinary potassium has greater diagnostic value for distinguishing PA than pre-supplementation indicators.
DOI: 10.6084/m9.figshare.30231311
title: Association of different diet quality scores with cardiovascular disease mortality risk in hypertension treatment group

description: This study investigated the association between several dietary quality scores—including the healthy eating index-2015(HEI-2015), dietary inflammatory index (DII), and dietary approaches to stop hypertension (DASH)—and the risk of cardiovascular disease(CVD) mortality in hypertension treatment group. Data were obtained from 11,310 participants in the the U.S. Centers for Disease Control and Prevention's National Health and Nutrition Examination Survey (1999-2016). Diet quality scores were calculated based on the type and quantity of food and beverages consumed by participants in the past 24 h. CVD mortality was defined as deaths from heart or cerebrovascular disease (ICD-10). We used cox proportional hazards regression to assess the association between diet quality scores and CVD mortality. During an average follow-up period of 109 months, 1324 deaths from CVD were confirmed. HEI−2015 and DII showed statistically significant negative association (HR, 0.9404 (95% CI = 0.8846, 0.9998), <i>p</i> = 0.0491) and positive correlation (HR, 1.0514 (95% CI = 1.0055, 1.0995), <i>p</i> = 0.0278) with CVD mortality. DASH showed no statistically significant negative correlation with CVD mortality (HR, 0.9639 (95% CI = 0.9215, 1.0083), <i>p</i> = 0.1096). However, trend tests for all three diet quality scores were significant (<i>p </i>&lt; 0.05). The HEI-2015 and DASH dietary patterns reduce the risk of CVD mortality in the hypertension treatment group. In contrast, the DII dietary pattern increases the risk of CVD mortality in such patients.
DOI: 10.6084/m9.figshare.30691845
title: Identification of endoplasmic reticulum stress-associated signatures of human pulmonary arterial hypertension: A bioinformatic analysis

description: Pulmonary arterial hypertension (PAH) is a group of complex vasculopathies characterized by increased pulmonary arterial pressure and subsequent pulmonary vascular remodeling. However, the underlying pathogenesis of PAH has not been fully elucidated. In the present study, we employed bioinformatics technology to investigate the pathogenesis of PAH. Microarray datasets related to PAH were retrieved from the Gene Expression Omnibus database to screen for ER stress-related genes (ERSRGs) between normal control and PAH samples. The differentially expressed genes (DEGs) were analyzed for functional enrichment and protein‒protein interaction (PPI) networks. DEG-related miRNAs and transcriptional factor (TF) were predicted to construct the miRNA-TF-hub gene network. The diagnostic accuracy of the hub genes was assessed via receiver operating characteristic (ROC) curve analysis. The relative abundances of different types of immune cells were determined via immune infiltration analysis. The screening detected 20 ERSRGs between normal and PAH samples, nine of which (HIF1A, BCL2L1, TLR4, HMOX1, VCAM1, EGR1, MAPK8, LCN2, and CEBPB) were further identified as hub genes via the PPI network. To construct a regulatory network analysis of the Hub genes, 57 miRNAs and 35 TFs were subsequently predicted. There was a significant difference in the infiltration of 17 types of immune cells between the two groups. These results suggest that the nine hub genes might play crucial roles in the development of PAH. These findings might provide new therapeutic targets for PAH or potential biomarkers for its diagnosis.
DOI: 10.6084/m9.figshare.30691845.v1
title: Identification of endoplasmic reticulum stress-associated signatures of human pulmonary arterial hypertension: A bioinformatic analysis

description: Pulmonary arterial hypertension (PAH) is a group of complex vasculopathies characterized by increased pulmonary arterial pressure and subsequent pulmonary vascular remodeling. However, the underlying pathogenesis of PAH has not been fully elucidated. In the present study, we employed bioinformatics technology to investigate the pathogenesis of PAH. Microarray datasets related to PAH were retrieved from the Gene Expression Omnibus database to screen for ER stress-related genes (ERSRGs) between normal control and PAH samples. The differentially expressed genes (DEGs) were analyzed for functional enrichment and protein‒protein interaction (PPI) networks. DEG-related miRNAs and transcriptional factor (TF) were predicted to construct the miRNA-TF-hub gene network. The diagnostic accuracy of the hub genes was assessed via receiver operating characteristic (ROC) curve analysis. The relative abundances of different types of immune cells were determined via immune infiltration analysis. The screening detected 20 ERSRGs between normal and PAH samples, nine of which (HIF1A, BCL2L1, TLR4, HMOX1, VCAM1, EGR1, MAPK8, LCN2, and CEBPB) were further identified as hub genes via the PPI network. To construct a regulatory network analysis of the Hub genes, 57 miRNAs and 35 TFs were subsequently predicted. There was a significant difference in the infiltration of 17 types of immune cells between the two groups. These results suggest that the nine hub genes might play crucial roles in the development of PAH. These findings might provide new therapeutic targets for PAH or potential biomarkers for its diagnosis.
DOI: 10.6084/m9.figshare.28740407.v1
title: Lycopene attenuates trimethylamine-N-oxide-induced senescence in endothelial progenitor cells via the AMPK/SIRT1 pathway

description: Aging-related diseases, which are associated with the senescence of endothelial progenitor cells (EPCs), are consistently accompanied by elevated levels of circulating trimethylamine-N-oxide (TMAO), a marker predictive of poor prognosis. Lycopene (Lyc) deficiency has been demonstrated to be linked to these age-related diseases. The AMPK/SIRT1 pathway plays a pivotal role in cellular senescence. In this study, we hypothesize that lycopene could mitigate TMAO-induced EPCs senescence, with involvement of the AMPK/SIRT1 pathway. EPCs were subjected to treatment with TMAO, Lyc, small interfering RNA targeting AMP-activated protein kinase (siAMPK), or sirtin-1 (siSIRT1). The biological functions of EPCs were evaluated through, CCK-8, transwell and tube formation assays, while their senescence was assessed via SA-β-gal activity assay and Western blotting. ROS generation was measured using dichlorodihydrofluorescein diacetate staining. TMAO-induced suppression of EPCs’ functionality was alleviated by Lyc, but this effect was reversed by siAMPK and siSIRT1. TMAO increased SA-β-gal-positive cell number and ROS production, while reducing the expression of AMPK and SIRT1. These effects were attenuated by Lyc. However, the protective effects were diminished by siAMPK and siSIRT1. In conclusion, Lyc ameliorates TMAO-induced EPCs senescence through the AMPK/SIRT1 pathway.
DOI: 10.6084/m9.figshare.30231311.v1
title: Association of different diet quality scores with cardiovascular disease mortality risk in hypertension treatment group

description: This study investigated the association between several dietary quality scores—including the healthy eating index-2015(HEI-2015), dietary inflammatory index (DII), and dietary approaches to stop hypertension (DASH)—and the risk of cardiovascular disease(CVD) mortality in hypertension treatment group. Data were obtained from 11,310 participants in the the U.S. Centers for Disease Control and Prevention's National Health and Nutrition Examination Survey (1999-2016). Diet quality scores were calculated based on the type and quantity of food and beverages consumed by participants in the past 24 h. CVD mortality was defined as deaths from heart or cerebrovascular disease (ICD-10). We used cox proportional hazards regression to assess the association between diet quality scores and CVD mortality. During an average follow-up period of 109 months, 1324 deaths from CVD were confirmed. HEI−2015 and DII showed statistically significant negative association (HR, 0.9404 (95% CI = 0.8846, 0.9998), <i>p</i> = 0.0491) and positive correlation (HR, 1.0514 (95% CI = 1.0055, 1.0995), <i>p</i> = 0.0278) with CVD mortality. DASH showed no statistically significant negative correlation with CVD mortality (HR, 0.9639 (95% CI = 0.9215, 1.0083), <i>p</i> = 0.1096). However, trend tests for all three diet quality scores were significant (<i>p </i>&lt; 0.05). The HEI-2015 and DASH dietary patterns reduce the risk of CVD mortality in the hypertension treatment group. In contrast, the DII dietary pattern increases the risk of CVD mortality in such patients.
DOI: 10.3535/jcn-w5z-pzv
title: Brachionycha nubeculosa Esper, 1785

description: Digital Specimen for the physical specimen hosted at Finnish Museum of Natural History.
DOI: 10.3535/qt6-dzj-ky1
title: Xanthia (Cirrhia) Hübner, 1816

description: Digital Specimen for the physical specimen hosted at Finnish Museum of Natural History.
DOI: 10.6084/m9.figshare.28740407
title: Lycopene attenuates trimethylamine-N-oxide-induced senescence in endothelial progenitor cells via the AMPK/SIRT1 pathway

description: Aging-related diseases, which are associated with the senescence of endothelial progenitor cells (EPCs), are consistently accompanied by elevated levels of circulating trimethylamine-N-oxide (TMAO), a marker predictive of poor prognosis. Lycopene (Lyc) deficiency has been demonstrated to be linked to these age-related diseases. The AMPK/SIRT1 pathway plays a pivotal role in cellular senescence. In this study, we hypothesize that lycopene could mitigate TMAO-induced EPCs senescence, with involvement of the AMPK/SIRT1 pathway. EPCs were subjected to treatment with TMAO, Lyc, small interfering RNA targeting AMP-activated protein kinase (siAMPK), or sirtin-1 (siSIRT1). The biological functions of EPCs were evaluated through, CCK-8, transwell and tube formation assays, while their senescence was assessed via SA-β-gal activity assay and Western blotting. ROS generation was measured using dichlorodihydrofluorescein diacetate staining. TMAO-induced suppression of EPCs’ functionality was alleviated by Lyc, but this effect was reversed by siAMPK and siSIRT1. TMAO increased SA-β-gal-positive cell number and ROS production, while reducing the expression of AMPK and SIRT1. These effects were attenuated by Lyc. However, the protective effects were diminished by siAMPK and siSIRT1. In conclusion, Lyc ameliorates TMAO-induced EPCs senescence through the AMPK/SIRT1 pathway.
DOI: 10.3535/9xl-83d-5nq
title: Diaphora mendica (Clerck, 1759)

description: Digital Specimen for the physical specimen hosted at Finnish Museum of Natural History.
DOI: 10.6084/m9.figshare.28485535
title: High-salt diets provoke phosphorus absorption from the small intestine in mice

description: Recent studies indicate that tenapanor, an inhibitor of sodium/proton exchanger-3 (NHE3), diminishes intestinal phosphorus (Pi) absorption. Given NHE3’s pivotal role in sodium (Na+) metabolism, there is a suspected functional link between Na+ and Pi metabolism. High-salt diets (HSD) have been demonstrated to disrupt calcium (Ca2+) metabolism. Since Ca2+ and Pi share analogous metabolic pathways, it is yet to be determined whether HSD also impacts Pi metabolism. Male C57 mice were randomly assigned to three groups: a standard diet group, HSD groups for 1 week (HSD-1w) and 4 weeks (HSD-4w). Throughout the study, dietary intake and water consumption were monitored using metabolic cages, and urine and feces were collected. Blood pressure was measured using a noninvasive tail vein sphygmomanometer. Upon completion of the intervention, mice were euthanized under anesthesia for blood collection, and intestinal and renal tissues were harvested for molecular analysis. Although plasma Pi levels were comparable between HSD groups and the control group, HSD groups exhibited increased urinary Pi excretion and decreased fecal Pi excretion. The HSD-4w group displayed elevated parathyroid hormone levels, reduced fibroblast growth factor 23 levels, and higher renal Cyp27b1 mRNA expression. The expression of sodium-dependent phosphate transporter 2b (Npt2b) and NHE3 was elevated in the intestine of HSD mice. HSD disrupts Pi metabolism by enhancing urinary Pi excretion and altering hormonal levels. The decrease in fecal Pi excretion, coupled with the upregulation of intestinal Pi transporter expression, suggests that HSD promotes intestinal Pi absorption in mice.
DOI: 10.6084/m9.figshare.28485535.v1
title: High-salt diets provoke phosphorus absorption from the small intestine in mice

description: Recent studies indicate that tenapanor, an inhibitor of sodium/proton exchanger-3 (NHE3), diminishes intestinal phosphorus (Pi) absorption. Given NHE3’s pivotal role in sodium (Na+) metabolism, there is a suspected functional link between Na+ and Pi metabolism. High-salt diets (HSD) have been demonstrated to disrupt calcium (Ca2+) metabolism. Since Ca2+ and Pi share analogous metabolic pathways, it is yet to be determined whether HSD also impacts Pi metabolism. Male C57 mice were randomly assigned to three groups: a standard diet group, HSD groups for 1 week (HSD-1w) and 4 weeks (HSD-4w). Throughout the study, dietary intake and water consumption were monitored using metabolic cages, and urine and feces were collected. Blood pressure was measured using a noninvasive tail vein sphygmomanometer. Upon completion of the intervention, mice were euthanized under anesthesia for blood collection, and intestinal and renal tissues were harvested for molecular analysis. Although plasma Pi levels were comparable between HSD groups and the control group, HSD groups exhibited increased urinary Pi excretion and decreased fecal Pi excretion. The HSD-4w group displayed elevated parathyroid hormone levels, reduced fibroblast growth factor 23 levels, and higher renal Cyp27b1 mRNA expression. The expression of sodium-dependent phosphate transporter 2b (Npt2b) and NHE3 was elevated in the intestine of HSD mice. HSD disrupts Pi metabolism by enhancing urinary Pi excretion and altering hormonal levels. The decrease in fecal Pi excretion, coupled with the upregulation of intestinal Pi transporter expression, suggests that HSD promotes intestinal Pi absorption in mice.
DOI: 10.3535/pzs-zzz-r39
title: Ochropacha duplaris (Linnaeus, 1761)

description: Digital Specimen for the physical specimen hosted at Finnish Museum of Natural History.
DOI: 10.3535/z4t-n73-w0m
title: Katha depressa (Esper, 1786)

description: Digital Specimen for the physical specimen hosted at Finnish Museum of Natural History.