cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.15468/dl.uupil5
title: Occurrence Download

description: A dataset containing 9796 species occurrences available in GBIF matching the query:
{
 "and" : [
 {
 "or" : [
 "TaxonKey is Brassicogethes aeneus (Fabricius, 1775)",
 "TaxonKey is Braula coeca Nitzsch, 1818",
 "TaxonKey is Brevipalpus californicus (Banks, 1904)",
 "TaxonKey is Brevipalpus obovatus Donnadieu, 1875"
 ]
 },
 "HasCoordinate is true",
 "HasGeospatialIssue is false"
 ]
}

 The dataset includes 9796 records from 150 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0011622-180508205500799/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.6084/m9.figshare.24960139.v1
title: CXC chemokine receptor 7 ameliorates renal fibrosis by inhibiting β-catenin signaling and epithelial-to-mesenchymal transition in tubular epithelial cells

description: Renal fibrosis is a common feature of various chronic kidney diseases. However, the underlying mechanism remains poorly understood. The CXC chemokine receptor (CXCR) family plays a role in renal fibrosis; however, the detailed mechanisms have not been elucidated. In this study, we investigated the potential role of CXCR7 in mediating renal fibrosis. CXCR7 expression is decreased in unilateral ischemia–reperfusion injury (UIRI) and unilateral ureteral obstruction mouse models. Furthermore, CXCR7 was specifically expressed primarily in the Lotus Tetragonolobus Lectin-expressing segment of tubules, was slightly expressed in the peanut agglutinin-expressing segment, and was barely expressed in the Dolichos biflorus agglutinin-expressing segment. Administration of pFlag-CXCR7, an overexpression plasmid for CXCR7, significantly inhibited the activation of β-catenin signaling and protected against the progression of epithelial-to-mesenchymal transition (EMT) and renal fibrosis in a UIRI mouse model. Using cultured HKC-8 cells, we found that CXCR7 significantly downregulated the expression of active β-catenin and fibrosis-related markers, including fibronectin, Collagen I, and α-SMA. Furthermore, CXCR7 significantly attenuated TGF-β1-induced changes in β-catenin signaling, EMT and fibrosis. These results suggest that CXCR7 plays a crucial role in inhibiting the activation of β-catenin signaling and the progression of EMT and renal fibrosis. Thus, CXCR7 could be a novel therapeutic target for renal fibrosis.
DOI: 10.6084/m9.figshare.24960139
title: CXC chemokine receptor 7 ameliorates renal fibrosis by inhibiting β-catenin signaling and epithelial-to-mesenchymal transition in tubular epithelial cells

description: Renal fibrosis is a common feature of various chronic kidney diseases. However, the underlying mechanism remains poorly understood. The CXC chemokine receptor (CXCR) family plays a role in renal fibrosis; however, the detailed mechanisms have not been elucidated. In this study, we investigated the potential role of CXCR7 in mediating renal fibrosis. CXCR7 expression is decreased in unilateral ischemia–reperfusion injury (UIRI) and unilateral ureteral obstruction mouse models. Furthermore, CXCR7 was specifically expressed primarily in the Lotus Tetragonolobus Lectin-expressing segment of tubules, was slightly expressed in the peanut agglutinin-expressing segment, and was barely expressed in the Dolichos biflorus agglutinin-expressing segment. Administration of pFlag-CXCR7, an overexpression plasmid for CXCR7, significantly inhibited the activation of β-catenin signaling and protected against the progression of epithelial-to-mesenchymal transition (EMT) and renal fibrosis in a UIRI mouse model. Using cultured HKC-8 cells, we found that CXCR7 significantly downregulated the expression of active β-catenin and fibrosis-related markers, including fibronectin, Collagen I, and α-SMA. Furthermore, CXCR7 significantly attenuated TGF-β1-induced changes in β-catenin signaling, EMT and fibrosis. These results suggest that CXCR7 plays a crucial role in inhibiting the activation of β-catenin signaling and the progression of EMT and renal fibrosis. Thus, CXCR7 could be a novel therapeutic target for renal fibrosis.
DOI: 10.6084/m9.figshare.25391025
title: Gut microbiota in the association between obesity and kidney function decline: a metagenomics-based study in a rat model

description: Obesity can induce dysbiosis in the gut microbiota and is considered a separate risk factor for kidney function decline. Nonetheless, the precise function of intestinal microorganisms in facilitating the connection between obesity and kidney function decline remains uncertain. Hence, the objective of this study was to investigate the alterations in the gut microbiota composition that take place during obesity and their correlations with renal function utilizing a rat model. For 20 weeks, 25 Sprague–Dawley rats were fed either a high-fat diet (HFD) or a normal-fat normal diet (ND). Physiological indices, peripheral plasma, kidney tissue, and colon contents were collected for comparison between groups. Metagenomic analysis of intestinal flora was performed. The HFD group demonstrated significantly increased levels of creatinine and urea nitrogen in the peripheral blood. Additionally, the HFD rats exhibited a significantly larger glomerular diameter compared to the ND group, accompanied by the presence of glomerulosclerosis, tubular vacuolar transformation, and other pathological changes in certain glomeruli. Metagenomics analysis revealed a notable rise in the prevalence of the Firmicutes phylum within the HFD group, primarily comprising the <i>Rumenococcus</i> genus. Functional analysis indicated that the gut microbiota in the HFD group primarily correlated with infectious diseases, signal transduction, and signaling molecules and interactions. This study provides evidence that the consumption of a HFD induces modifications in the composition and functionality of the gut microbiome in rats, which may serve as a potential mechanism underlying the relationship between obesity and the progression of kidney function decline.
DOI: 10.6084/m9.figshare.25391025.v1
title: Gut microbiota in the association between obesity and kidney function decline: a metagenomics-based study in a rat model

description: Obesity can induce dysbiosis in the gut microbiota and is considered a separate risk factor for kidney function decline. Nonetheless, the precise function of intestinal microorganisms in facilitating the connection between obesity and kidney function decline remains uncertain. Hence, the objective of this study was to investigate the alterations in the gut microbiota composition that take place during obesity and their correlations with renal function utilizing a rat model. For 20 weeks, 25 Sprague–Dawley rats were fed either a high-fat diet (HFD) or a normal-fat normal diet (ND). Physiological indices, peripheral plasma, kidney tissue, and colon contents were collected for comparison between groups. Metagenomic analysis of intestinal flora was performed. The HFD group demonstrated significantly increased levels of creatinine and urea nitrogen in the peripheral blood. Additionally, the HFD rats exhibited a significantly larger glomerular diameter compared to the ND group, accompanied by the presence of glomerulosclerosis, tubular vacuolar transformation, and other pathological changes in certain glomeruli. Metagenomics analysis revealed a notable rise in the prevalence of the Firmicutes phylum within the HFD group, primarily comprising the <i>Rumenococcus</i> genus. Functional analysis indicated that the gut microbiota in the HFD group primarily correlated with infectious diseases, signal transduction, and signaling molecules and interactions. This study provides evidence that the consumption of a HFD induces modifications in the composition and functionality of the gut microbiome in rats, which may serve as a potential mechanism underlying the relationship between obesity and the progression of kidney function decline.
DOI: 10.17632/bstzgj6yvy
title: A Review of the Effect of Different Exercise Types on Medication Craving in Patients with Substance Use Disorders-Based on a Dose-Response Relationship Perspective

description: BACKGROUND: Exercise interventions can significantly reduce medication cravings and improve the physical and mental health of patients with substance use disorders (SUDs), but finding the optimal type and dose of exercise to maximize the benefits of SUDs requires in-depth investigation.
METHODS: A literature search of randomized controlled trials on the effects of exercise interventions on SUDs' medication cravings over the past 20 years (2005-2025) was conducted through electronic databases such as PubMed, Web of Science, CNKI, and EMBASE.Thirty papers were obtained based on inclusion and exclusion criteria, involving 1717 patients (male=1258, female=459) and processed using network meta-analysis.
CONCLUSION: Aerobic exercise is the best form of exercise to improve medication craving in SUDs, in which the exercise dose showed low dose effectiveness and effect plateau characteristics for SUDs improvement, and the total intervention dose was kept at 180 METs-min/week as optimal, i.e., close to moderate-intensity, three-times-weekly and 60-minute-per-per-exercise aerobic exercise.
DOI: 10.17632/bstzgj6yvy.1
title: A Review of the Effect of Different Exercise Types on Medication Craving in Patients with Substance Use Disorders-Based on a Dose-Response Relationship Perspective

description: BACKGROUND: Exercise interventions can significantly reduce medication cravings and improve the physical and mental health of patients with substance use disorders (SUDs), but finding the optimal type and dose of exercise to maximize the benefits of SUDs requires in-depth investigation.
METHODS: A literature search of randomized controlled trials on the effects of exercise interventions on SUDs' medication cravings over the past 20 years (2005-2025) was conducted through electronic databases such as PubMed, Web of Science, CNKI, and EMBASE.Thirty papers were obtained based on inclusion and exclusion criteria, involving 1717 patients (male=1258, female=459) and processed using network meta-analysis.
CONCLUSION: Aerobic exercise is the best form of exercise to improve medication craving in SUDs, in which the exercise dose showed low dose effectiveness and effect plateau characteristics for SUDs improvement, and the total intervention dose was kept at 180 METs-min/week as optimal, i.e., close to moderate-intensity, three-times-weekly and 60-minute-per-per-exercise aerobic exercise.
DOI: 10.6084/m9.figshare.25205397
title: Current perspectives and trends of the research on hypertensive nephropathy: a bibliometric analysis from 2000 to 2023

description: Hypertensive nephropathy continues to be a major cause of end-stage renal disease and poses a significant global health burden. Despite the staggering development of research in hypertensive nephropathy, scientists and clinicians can only seek out useful information through articles and reviews, it remains a hurdle for them to quickly track the trend in this field. This study uses the bibliometric method to identify the evolutionary development and recent hotspots of hypertensive nephropathy. The Web of Science Core Collection database was used to extract publications on hypertensive nephropathy from January 2000 to November 2023. CiteSpace was used to capture the patterns and trends from multi-perspectives, including countries/regions, institutions, keywords, and references. In total, 557 publications on hypertensive nephropathy were eligible for inclusion. China (<i>n </i>= 208, 37.34%) was the most influential contributor among all the countries. Veterans Health Administration (<i>n </i>= 19, 3.41%) was found to be the most productive institution. Keyword bursting till now are renal fibrosis, outcomes, and mechanisms which are predicted to be the potential frontiers and hotspots in the future. The top seven references were listed, and their burst strength was shown. A comprehensive overview of the current status and research frontiers of hypertensive nephropathy has been provided through the bibliometric perspective. Recent advancements and challenges in hypertensive nephropathy have been discussed. These findings can offer informative instructions for researchers and scholars.
DOI: 10.6084/m9.figshare.25205397.v1
title: Current perspectives and trends of the research on hypertensive nephropathy: a bibliometric analysis from 2000 to 2023

description: Hypertensive nephropathy continues to be a major cause of end-stage renal disease and poses a significant global health burden. Despite the staggering development of research in hypertensive nephropathy, scientists and clinicians can only seek out useful information through articles and reviews, it remains a hurdle for them to quickly track the trend in this field. This study uses the bibliometric method to identify the evolutionary development and recent hotspots of hypertensive nephropathy. The Web of Science Core Collection database was used to extract publications on hypertensive nephropathy from January 2000 to November 2023. CiteSpace was used to capture the patterns and trends from multi-perspectives, including countries/regions, institutions, keywords, and references. In total, 557 publications on hypertensive nephropathy were eligible for inclusion. China (<i>n </i>= 208, 37.34%) was the most influential contributor among all the countries. Veterans Health Administration (<i>n </i>= 19, 3.41%) was found to be the most productive institution. Keyword bursting till now are renal fibrosis, outcomes, and mechanisms which are predicted to be the potential frontiers and hotspots in the future. The top seven references were listed, and their burst strength was shown. A comprehensive overview of the current status and research frontiers of hypertensive nephropathy has been provided through the bibliometric perspective. Recent advancements and challenges in hypertensive nephropathy have been discussed. These findings can offer informative instructions for researchers and scholars.
DOI: 10.6084/m9.figshare.25205521
title: Cardiovascular and renal safety outcomes of hypoxia-inducible factor prolyl-hydroxylase inhibitor roxadustat for anemia patients with chronic kidney disease: a systematic review and meta-analysis

description: This systematic review and meta-analysis were conducted to evaluate the cardiac and kidney-related adverse effects of roxadustat for the treatment of anemia in CKD patients. 18 trials with a total of 8806 participants were identified for analysis. We employed a fixed-effects model for analysis. The pooled result revealed no significant difference in the risk of occurrence of cardiac disorders when comparing CKD patients receiving roxadustat with the placebo (RR = 1.049; CI [0.918 to 1.200]) or ESA (RR = 1.066; CI [0.919 to 1.235]), in both dialysis-dependent (DD) (RR = 1.094; CI [0.925 to 1.293]) or non-dialysis-dependent (NDD) (RR = 1.036; CI [0.916 to 1.171]) CKD patients. No significant difference was observed in the risk of kidney-related adverse events when comparing roxadustat with the placebo (RR = 1.088; CI [0.980 to 1.209]) or ESA (RR = 0.968; CI [0.831 to 1.152]), in DD (RR = 2.649; CI [0.201 to 34.981]) or NDD (RR = 1.053; CI [0.965 to 1.149]) CKD patients. A high risk of hyperkalemia was observed in the roxadustat group in DD (RR = 0.939; CI [0.898 to 0.981]). Incidence of hypertension was higher in the roxadustat for NDD patients (RR = 1.198; CI [1.042 to 1.377]), or compared to the placebo (RR = 1.374; CI [1.153 to 1.638]). In summary, the risk of cardiac or kidney-related events observed in the roxadustat was not significantly increase whether in DD or NDD patients. However, attention must be paid to the occurrence of hyperkalemia for DD patients and hypertension in NDD patients using roxadustat.
DOI: 10.6084/m9.figshare.25205521.v1
title: Cardiovascular and renal safety outcomes of hypoxia-inducible factor prolyl-hydroxylase inhibitor roxadustat for anemia patients with chronic kidney disease: a systematic review and meta-analysis

description: This systematic review and meta-analysis were conducted to evaluate the cardiac and kidney-related adverse effects of roxadustat for the treatment of anemia in CKD patients. 18 trials with a total of 8806 participants were identified for analysis. We employed a fixed-effects model for analysis. The pooled result revealed no significant difference in the risk of occurrence of cardiac disorders when comparing CKD patients receiving roxadustat with the placebo (RR = 1.049; CI [0.918 to 1.200]) or ESA (RR = 1.066; CI [0.919 to 1.235]), in both dialysis-dependent (DD) (RR = 1.094; CI [0.925 to 1.293]) or non-dialysis-dependent (NDD) (RR = 1.036; CI [0.916 to 1.171]) CKD patients. No significant difference was observed in the risk of kidney-related adverse events when comparing roxadustat with the placebo (RR = 1.088; CI [0.980 to 1.209]) or ESA (RR = 0.968; CI [0.831 to 1.152]), in DD (RR = 2.649; CI [0.201 to 34.981]) or NDD (RR = 1.053; CI [0.965 to 1.149]) CKD patients. A high risk of hyperkalemia was observed in the roxadustat group in DD (RR = 0.939; CI [0.898 to 0.981]). Incidence of hypertension was higher in the roxadustat for NDD patients (RR = 1.198; CI [1.042 to 1.377]), or compared to the placebo (RR = 1.374; CI [1.153 to 1.638]). In summary, the risk of cardiac or kidney-related events observed in the roxadustat was not significantly increase whether in DD or NDD patients. However, attention must be paid to the occurrence of hyperkalemia for DD patients and hypertension in NDD patients using roxadustat.
DOI: 10.6084/m9.figshare.25699906
title: Iguratimod prevents renal fibrosis in unilateral ureteral obstruction model mice by suppressing M2 macrophage infiltration and macrophage–myofibroblast transition

description: Iguratimod is a novel synthetic, small-molecule immunosuppressive agent used to treat rheumatoid arthritis. Through ongoing exploration of its role and mechanisms of action, iguratimod has been observed to have antifibrotic effects in the lung and skin; however, its effect on renal fibrosis remains unknown. This study aimed to investigate whether iguratimod could affect renal fibrosis progression. Three different concentrations of iguratimod (30 mg/kg/day, 10 mg/kg/day, and 3 mg/kg/day) were used to intervene in unilateral ureteral obstruction (UUO) model mice. Iguratimod at 10 mg/kg/day was observed to be effective in slowing UUO-mediated renal fibrosis. In addition, stimulating bone marrow-derived macrophages with IL-4 and/or iguratimod, or with TGF-β and iguratimod or SRC inhibitors <i>in vitro</i>, suggested that iguratimod mitigates the progression of renal fibrosis in UUO mice, at least in part, by inhibiting the IL-4/STAT6 signaling pathway to attenuate renal M2 macrophage infiltration, as well as by impeding SRC activation to reduce macrophage–myofibroblast transition. These findings reveal the potential of iguratimod as a treatment for renal disease.
DOI: 10.6084/m9.figshare.25699906.v1
title: Iguratimod prevents renal fibrosis in unilateral ureteral obstruction model mice by suppressing M2 macrophage infiltration and macrophage–myofibroblast transition

description: Iguratimod is a novel synthetic, small-molecule immunosuppressive agent used to treat rheumatoid arthritis. Through ongoing exploration of its role and mechanisms of action, iguratimod has been observed to have antifibrotic effects in the lung and skin; however, its effect on renal fibrosis remains unknown. This study aimed to investigate whether iguratimod could affect renal fibrosis progression. Three different concentrations of iguratimod (30 mg/kg/day, 10 mg/kg/day, and 3 mg/kg/day) were used to intervene in unilateral ureteral obstruction (UUO) model mice. Iguratimod at 10 mg/kg/day was observed to be effective in slowing UUO-mediated renal fibrosis. In addition, stimulating bone marrow-derived macrophages with IL-4 and/or iguratimod, or with TGF-β and iguratimod or SRC inhibitors <i>in vitro</i>, suggested that iguratimod mitigates the progression of renal fibrosis in UUO mice, at least in part, by inhibiting the IL-4/STAT6 signaling pathway to attenuate renal M2 macrophage infiltration, as well as by impeding SRC activation to reduce macrophage–myofibroblast transition. These findings reveal the potential of iguratimod as a treatment for renal disease.
DOI: 10.6084/m9.figshare.24947428
title: A Mendelian randomization study: physical activities and chronic kidney disease

description: Increasing evidence has shown that physical activity is related to a lower risk of chronic kidney disease (CKD), thus indicating a potential target for prevention. However, the causality is not clear; specifically, physical activity may protect against CKD, and CKD may lead to a reduction in physical activity. Our study examined the potential bidirectional relationship between physical activity and CKD by using a genetically informed method. Genome-wide association studies from the UK Biobank baseline data were used for physical activity phenotypes and included 460,376 participants. For kidney function (estimated Glomerular Filtration Rate (eGFR) and CKD, with eGFR &lt; 60 mL/min/1.73 m<sup>2</sup>), CKDGen Consortium data were used, which included 480,698 CKD participants of European ancestry. Mendelian randomization (MR) analysis was used to determine the causal relationship between physical activities and kidney function. Two-sample MR genetically predicted that heavy DIY (do it yourself) (e.g., weeding, lawn mowing, carpentry, and digging) decreased the risk of CKD (odds ratio [OR] = 0.287, 95% CI = 0.117–0.705, <i>p</i> = 0.0065) and improved the level of eGFR (β = 0.036, 95% CI = 0.005–0.067, <i>p</i> = 0.021). The bidirectional MR showed no reverse causality. It is worth noting that other physical activities, such as walking for pleasure, strenuous sports, light DIY (e.g., pruning and watering the lawn), and other exercises (e.g., swimming, cycling, keeping fit, and bowling), were not significantly correlated with CKD and eGFR. This study used genetic data to provide reliable and robust causal evidence that heavy physical activity (e.g., weeding, lawn mowing, carpentry, and digging) can protect kidney function and further lower the risk of CKD.
DOI: 10.6084/m9.figshare.24947428.v1
title: A Mendelian randomization study: physical activities and chronic kidney disease

description: Increasing evidence has shown that physical activity is related to a lower risk of chronic kidney disease (CKD), thus indicating a potential target for prevention. However, the causality is not clear; specifically, physical activity may protect against CKD, and CKD may lead to a reduction in physical activity. Our study examined the potential bidirectional relationship between physical activity and CKD by using a genetically informed method. Genome-wide association studies from the UK Biobank baseline data were used for physical activity phenotypes and included 460,376 participants. For kidney function (estimated Glomerular Filtration Rate (eGFR) and CKD, with eGFR &lt; 60 mL/min/1.73 m<sup>2</sup>), CKDGen Consortium data were used, which included 480,698 CKD participants of European ancestry. Mendelian randomization (MR) analysis was used to determine the causal relationship between physical activities and kidney function. Two-sample MR genetically predicted that heavy DIY (do it yourself) (e.g., weeding, lawn mowing, carpentry, and digging) decreased the risk of CKD (odds ratio [OR] = 0.287, 95% CI = 0.117–0.705, <i>p</i> = 0.0065) and improved the level of eGFR (β = 0.036, 95% CI = 0.005–0.067, <i>p</i> = 0.021). The bidirectional MR showed no reverse causality. It is worth noting that other physical activities, such as walking for pleasure, strenuous sports, light DIY (e.g., pruning and watering the lawn), and other exercises (e.g., swimming, cycling, keeping fit, and bowling), were not significantly correlated with CKD and eGFR. This study used genetic data to provide reliable and robust causal evidence that heavy physical activity (e.g., weeding, lawn mowing, carpentry, and digging) can protect kidney function and further lower the risk of CKD.