cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.23590333
title: Vascular, valvular and kidney calcification manifested in mouse models of adenine-induced chronic kidney disease

description: Ectopic calcification (EC) involves multiple organ systems in chronic kidney disease (CKD). Previous CKD-animal models primarily focused on a certain histological abnormality but did not show the correlation with calcified development among various tissues. This study compared calcified deposition in various tissues during CKD progression in mice. Male 8-week-old C57BL/6J mice were randomly allocated to the seven groups: a basic, adenine, high-phosphorus, or adenine and high-phosphorus diet for 12–16 weeks (Ctl16, A12, P16, or AP16, respectively); an adenine diet for 4–6 weeks; and a high-phosphorus or adenine and high-phosphorus diet for 10–12 weeks (A6 + P10, A4 + P12, or A4 + AP12, respectively). Compared to the Ctl16 mice, the P16 mice only displayed a slight abnormality in serum calcium and phosphorus; the A12 mice had the most serious kidney impairment; the A4 + P12 and A6 + P10 mice had similar conditions of CKD, mineral abnormalities, and mild calcification in the kidney and aortic valves; the A4 + AP12 and AP16 groups had severe kidney impairment, mineral abnormalities and calcification in the kidneys, aortic valves and aortas. Furthermore, calcium-phosphate particles were deposited not only in the tubulointerstitial compartment but in the glomerular and tubular basement membrane. The elemental composition of EC in various tissues matched the calcification of human cardiovascular tissue as determined by energy dispersive spectroscopy. The severity of CKD was unparalleled with the progression of mineral metabolism disorder and EC. Calcification was closely related in different tissues and observed in the glomerular and tubular basement membranes. Previous CKD-animal models primarily focused on a certain histological abnormality but lacked investigations of the interplay of EC in various tissues. This study compared calcified deposition in several tissues during CKD progression in mice, which was closely related. The severity of CKD was unparalleled with the development of ectopic calcification. Glomerular and tubular basement membrane calcification was detected in CKD mice, which has been considered extremely rare in clinical.
DOI: 10.6084/m9.figshare.23756815
title: Acute kidney injury in patients with cancer receiving anti-PD-1/PD-L1 antibodies: incidence, risk factors, and prognosis

description: Anti-PD-1/PD-L1 antibodies are widely used in anti-cancer therapy. While they have improved cancer prognoses, immune-related adverse events, which can cause acute kidney injury (AKI), cannot be ignored. The purpose of this retrospective cohort study was to assess the incidence, risk factors, and prognosis of AKI associated with anti-PD-1/PD-L1 antibodies. Patients who received anti-PD-1/PD-L1 antibody treatment at our hospital between January 2018 and December 2022 were enrolled. Clinical information, combined medications, concomitant diseases, tumor types, and laboratory indicators were collected from patient records, and the incidence of AKI was determined. The risk factors for AKI were assessed using univariate and multivariate logistic regression analyses. Overall, 1418 patients were enrolled. The median follow-up time was 112 days and 92 (6.5%) developed AKI. The median time from the initial anti-PD-1/PD-L1 antibody treatment to AKI was 99.85 days. Head and neck cancer and combined use of diuretics, non-steroidal anti-inflammatory drugs (NSAIDs), lower hemoglobin level, and other types of chemotherapeutic drugs were independent risk factors for AKI. The complete recovery, partial recovery, non-recovery, and unknown AKI rates were 7.6%, 28.3%, 52.2%, and 11.9%, respectively. Kidney biopsies were performed on two patients with AKI and pathology confirmed diagnosis of acute tubulointerstitial nephritis. In this cohort, AKI was not uncommon in patients treated with anti-PD-1/PD-L1 antibodies; therefore, it is necessary to monitor renal function and identify AKI early, especially in patients with head and neck tumors. Improving anemia and minimizing the use of diuretics, NSAIDs, and chemotherapeutics may reduce AKI.
DOI: 10.6084/m9.figshare.23756815.v1
title: Acute kidney injury in patients with cancer receiving anti-PD-1/PD-L1 antibodies: incidence, risk factors, and prognosis

description: Anti-PD-1/PD-L1 antibodies are widely used in anti-cancer therapy. While they have improved cancer prognoses, immune-related adverse events, which can cause acute kidney injury (AKI), cannot be ignored. The purpose of this retrospective cohort study was to assess the incidence, risk factors, and prognosis of AKI associated with anti-PD-1/PD-L1 antibodies. Patients who received anti-PD-1/PD-L1 antibody treatment at our hospital between January 2018 and December 2022 were enrolled. Clinical information, combined medications, concomitant diseases, tumor types, and laboratory indicators were collected from patient records, and the incidence of AKI was determined. The risk factors for AKI were assessed using univariate and multivariate logistic regression analyses. Overall, 1418 patients were enrolled. The median follow-up time was 112 days and 92 (6.5%) developed AKI. The median time from the initial anti-PD-1/PD-L1 antibody treatment to AKI was 99.85 days. Head and neck cancer and combined use of diuretics, non-steroidal anti-inflammatory drugs (NSAIDs), lower hemoglobin level, and other types of chemotherapeutic drugs were independent risk factors for AKI. The complete recovery, partial recovery, non-recovery, and unknown AKI rates were 7.6%, 28.3%, 52.2%, and 11.9%, respectively. Kidney biopsies were performed on two patients with AKI and pathology confirmed diagnosis of acute tubulointerstitial nephritis. In this cohort, AKI was not uncommon in patients treated with anti-PD-1/PD-L1 antibodies; therefore, it is necessary to monitor renal function and identify AKI early, especially in patients with head and neck tumors. Improving anemia and minimizing the use of diuretics, NSAIDs, and chemotherapeutics may reduce AKI.
DOI: 10.6084/m9.figshare.22746441
title: Association of serum thymosin β4 with malnutrition-inflammation-atherosclerosis syndrome in peritoneal dialysis patients: a cross-sectional study

description: Malnutrition-inflammation-atherosclerosis (MIA) syndrome may worsen the prognosis of peritoneal dialysis (PD) patients. Serum thymosin β4 (sTβ4) protects against inflammation, fibrosis and cardiac dysfunction. The present study aimed to characterize the association between sTβ4 and MIA syndrome as well as to investigate the potential of regulating sTβ4 to improve the prognosis of PD patients. We performed a cross-sectional, single-center pilot study involving 76 PD patients. Demographic characteristics, clinical characteristics, nutritional profiles, inflammatory mediators, atherosclerosis-related factors and sTβ4 levels were collected and subjected to association analysis for sTβ4 and MIA syndrome. sTβ4 levels did not significantly vary with sex or primary disease in PD patients. Ages and PD features did not vary between patients with different levels of sTβ4. PD patients with higher levels of sTβ4 had significantly higher levels of nutritional indicators, including subjective global nutritional assessment (SGA) (<i>p</i> &lt; 0.001) and serum albumin (ALB) (<i>p</i> &lt; 0.001) but lower levels of inflammatory and atherosclerotic indicators, including serum C reaction protein (CRP) (<i>p</i> = 0.009), the right common carotid artery (RCCA) intimal thickness (<i>p</i> &lt; 0.001) and the left common carotid artery (LCCA) intimal thickness (<i>p</i> = 0.02). Correlation analysis showed that sTβ4 was positively associated with SGA (<i>p</i> &lt; 0.001) and serum ALB (<i>p</i> &lt; 0.001) but negatively associated with CRP (<i>p</i> = 0.020), RCCA intimal thickness (<i>p</i> &lt; 0.001) and LCCA intimal thickness (<i>p</i> = 0.033). In multiple adjusted models, the prevalence of MIA syndrome was significantly decreased in PD patients with increased levels of sTβ4 when patients without MIA syndrome were compared to those with all indicators of MIA syndrome (OR = 0.996, 95% CI 0.993–0.999, <i>p</i> = 0.003) or those with at least one indicator of MIA syndrome (OR = 0.997, 95% CI 0.995–0.998, <i>p</i> &lt; 0.001). The sTβ4 level decreases in PD patients with MIA syndrome. The prevalence of MIA syndrome decreases significantly as the level of sTβ4 increases in PD patients.
DOI: 10.6084/m9.figshare.22746441.v1
title: Association of serum thymosin β4 with malnutrition-inflammation-atherosclerosis syndrome in peritoneal dialysis patients: a cross-sectional study

description: Malnutrition-inflammation-atherosclerosis (MIA) syndrome may worsen the prognosis of peritoneal dialysis (PD) patients. Serum thymosin β4 (sTβ4) protects against inflammation, fibrosis and cardiac dysfunction. The present study aimed to characterize the association between sTβ4 and MIA syndrome as well as to investigate the potential of regulating sTβ4 to improve the prognosis of PD patients. We performed a cross-sectional, single-center pilot study involving 76 PD patients. Demographic characteristics, clinical characteristics, nutritional profiles, inflammatory mediators, atherosclerosis-related factors and sTβ4 levels were collected and subjected to association analysis for sTβ4 and MIA syndrome. sTβ4 levels did not significantly vary with sex or primary disease in PD patients. Ages and PD features did not vary between patients with different levels of sTβ4. PD patients with higher levels of sTβ4 had significantly higher levels of nutritional indicators, including subjective global nutritional assessment (SGA) (<i>p</i> &lt; 0.001) and serum albumin (ALB) (<i>p</i> &lt; 0.001) but lower levels of inflammatory and atherosclerotic indicators, including serum C reaction protein (CRP) (<i>p</i> = 0.009), the right common carotid artery (RCCA) intimal thickness (<i>p</i> &lt; 0.001) and the left common carotid artery (LCCA) intimal thickness (<i>p</i> = 0.02). Correlation analysis showed that sTβ4 was positively associated with SGA (<i>p</i> &lt; 0.001) and serum ALB (<i>p</i> &lt; 0.001) but negatively associated with CRP (<i>p</i> = 0.020), RCCA intimal thickness (<i>p</i> &lt; 0.001) and LCCA intimal thickness (<i>p</i> = 0.033). In multiple adjusted models, the prevalence of MIA syndrome was significantly decreased in PD patients with increased levels of sTβ4 when patients without MIA syndrome were compared to those with all indicators of MIA syndrome (OR = 0.996, 95% CI 0.993–0.999, <i>p</i> = 0.003) or those with at least one indicator of MIA syndrome (OR = 0.997, 95% CI 0.995–0.998, <i>p</i> &lt; 0.001). The sTβ4 level decreases in PD patients with MIA syndrome. The prevalence of MIA syndrome decreases significantly as the level of sTβ4 increases in PD patients.
DOI: 10.21233/vmbw-q443
title: LDDsite3113 ostracode surface sample dataset

description: Raw data for the LDDsite3113 ostracode surface sample dataset submitted to the Neotoma Paleoecology Database. Data is available through the landing page in JSON format. The landing page referenced by the DOI also contains links to publications and a map-based viewer for the dataset. The Neotoma Paleoecology Database maintains a homepage at https://www.neotomadb.org.
DOI: 10.6084/m9.figshare.22109591
title: Bone marrow mesenchymal stem cell-derived exosomal miR-30e-5p ameliorates high-glucose induced renal proximal tubular cell pyroptosis by inhibiting ELAVL1

description: The rapid increase in the prevalence of diabetes has resulted in more cases of diabetic kidney disease (DKD). Treatment with bone marrow mesenchymal stem cells (BMSCs) may represent an alternative strategy to manage DKD. HK-2 cells were treated with 30 mM high glucose (HG). Bone marrow MSC-derived exosomes (BMSC-exos) were isolated and internalized into HK-2 cells. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide (MTT) and lactate dehydrogenase (LDH) assays were used to measure viability and cytotoxicity. The secretion of IL-1β and IL-18 was measured by ELISA. Pyroptosis was assessed by flow cytometry. Quantitative RT-PCR was used to measure the levels of miR-30e-5p, ELAV like RNA binding protein 1 (ELAVL1), IL-1β, and IL-18. The expression of ELAVL1 and pyroptosis-associated cytokine proteins was determined by western blot analysis. A dual-luciferase reporter gene assay was conducted to confirm the relationship between miR-30e-5p and ELAVL1. BMSC-exos decreased LDH, IL-1β, and IL-18 secretion and inhibited the expression of the pyroptosis-related factors (IL-1β, caspase-1, GSDMD-N, and NLRP3) in HG-induced HK-2 cells. Moreover, miR-30e-5p depletion derived from BMSC-exos promoted HK-2 cell pyroptosis. Besides, miR-30e-5p over-expression or ELVAL1 knockdown could directly inhibit pyroptosis. ELAVL1 was a target of miR-30e-5p and knocking down ELAVL1 reversed the effect of miR-30e-5p inhibition in BMSC-exos-treated HK-2 cells. BMSC-derived exosomal miR-30e-5p inhibits caspase-1-mediated pyroptosis by targeting ELAVL1 in HG-induced HK-2 cells, which might provide a new strategy for treating DKD.
DOI: 10.6084/m9.figshare.22109591.v1
title: Bone marrow mesenchymal stem cell-derived exosomal miR-30e-5p ameliorates high-glucose induced renal proximal tubular cell pyroptosis by inhibiting ELAVL1

description: The rapid increase in the prevalence of diabetes has resulted in more cases of diabetic kidney disease (DKD). Treatment with bone marrow mesenchymal stem cells (BMSCs) may represent an alternative strategy to manage DKD. HK-2 cells were treated with 30 mM high glucose (HG). Bone marrow MSC-derived exosomes (BMSC-exos) were isolated and internalized into HK-2 cells. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide (MTT) and lactate dehydrogenase (LDH) assays were used to measure viability and cytotoxicity. The secretion of IL-1β and IL-18 was measured by ELISA. Pyroptosis was assessed by flow cytometry. Quantitative RT-PCR was used to measure the levels of miR-30e-5p, ELAV like RNA binding protein 1 (ELAVL1), IL-1β, and IL-18. The expression of ELAVL1 and pyroptosis-associated cytokine proteins was determined by western blot analysis. A dual-luciferase reporter gene assay was conducted to confirm the relationship between miR-30e-5p and ELAVL1. BMSC-exos decreased LDH, IL-1β, and IL-18 secretion and inhibited the expression of the pyroptosis-related factors (IL-1β, caspase-1, GSDMD-N, and NLRP3) in HG-induced HK-2 cells. Moreover, miR-30e-5p depletion derived from BMSC-exos promoted HK-2 cell pyroptosis. Besides, miR-30e-5p over-expression or ELVAL1 knockdown could directly inhibit pyroptosis. ELAVL1 was a target of miR-30e-5p and knocking down ELAVL1 reversed the effect of miR-30e-5p inhibition in BMSC-exos-treated HK-2 cells. BMSC-derived exosomal miR-30e-5p inhibits caspase-1-mediated pyroptosis by targeting ELAVL1 in HG-induced HK-2 cells, which might provide a new strategy for treating DKD.
DOI: 10.6084/m9.figshare.22820749
title: Association of circulating proprotein convertase subtilisin/kexin type 9 concentration with coagulation abnormalities in patients with primary membranous nephropathy

description: The aims of the study were to explore the potential associations between plasma proprotein convertase subtilisin/kexin type 9 (PCSK9) and coagulation indexes in patients with primary membranous nephropathy (PMN). A total of 87 patients diagnosed with PMN were enrolled in our study. 30 healthy participants were recruited to match PMN participants. Plasma PCSK9 concentrations were tested by enzyme-linked immunosorbent assay (ELISA). Correlations between PCSK9 and coagulation abnormalities in patients with PMN were analyzed using univariate and multiple linear regression analysis. Plasma PCSK9 levels in patients with PMN were significantly higher than that in healthy controls [232.0 (143.5, 359.5) ng/mL <i>vs</i>. 166.8 (129.7, 199.7) ng/mL; <i>p</i> = 0.001]. Plasma levels of PCSK9 were positively correlated with factor VIII, factor IX, factor XI, log-transformed tissue factor, protein C and protein S (<i>r</i> = 0.267, <i>p</i> = 0.013; <i>r</i> = 0.496, <i>p</i> &lt; 0.001; <i>r</i> = 0.217, <i>p</i> = 0.045; <i>r</i> = 0.584, <i>p</i> &lt; 0.001; <i>r</i> = 0.372, <i>p</i> = 0.001; <i>r</i> = 0.282, <i>p</i> = 0.011). In multiple linear regression analysis, PCSK9 concentration was independently and positively correlated with factor VIII, factor IX, and tissue factor (β = 0.186, <i>p</i> = 0.047; β = 0.325, <i>p</i> = 0.001; β = 0.531, <i>p</i> &lt; 0.001; respectively). PCSK9 concentration was independently and negatively correlated with PT (β= −0.343, <i>p</i> = 0.011). Plasma PCSK9 levels had good positive correlations with procoagulant clotting factors and negative correlations with PT in PMN, which might provide novel information with regard to PCSK9 and hypercoagulability in PMN.
DOI: 10.6084/m9.figshare.22261782
title: Effect of aromatherapy on quality of life in maintenance hemodialysis patients: a systematic review and meta-analysis

description: Aromatherapy has been used for patients on maintenance hemodialysis (MHD), but the outcomes are still controversial. Thus, we conducted this study to systematically evaluate the effect of aromatherapy on the quality of life of patients on MHD. We searched the PubMed, Embays, Scopus, Web of Science, and CNKI databases for randomized controlled trials that evaluated the use of aromatherapy in dialysis patients and reported at least one outcome of interest. Twenty-two relevant studies were included in the meta-analysis. The meta-analysis revealed that aromatherapy significantly increased subjective sleep quality (a lower score indicates better sleep quality) [standardized mean difference (SMD) = −1.52, 95% CI (−2.38, −0.67), <i>p</i> &lt; 0.01] and reduced fatigue [SMD = −1.14, 95% CI (−1.95, −0.33), <i>p</i> = 0.01], anxiety [SMD = −1.38, 95% CI (−2.09, −0.67), <i>p</i> &lt; 0.01], symptoms of restless legs syndrome [RLS; SMD = −1.71, 95% CI (−2.09, −1.33), <i>p</i> &lt; 0.01], and arteriovenous fistula puncture pain [SMD= −1.56, 95% CI (−2.60, −0.52), <i>p</i> &lt; 0.01]. Aromatherapy may be used as a novel complementary and alternative therapy to improve sleep quality and reduce fatigue, anxiety, symptoms of RLS, and arteriovenous fistula puncture pain in patients on MHD.
DOI: 10.6084/m9.figshare.22261782.v1
title: Effect of aromatherapy on quality of life in maintenance hemodialysis patients: a systematic review and meta-analysis

description: Aromatherapy has been used for patients on maintenance hemodialysis (MHD), but the outcomes are still controversial. Thus, we conducted this study to systematically evaluate the effect of aromatherapy on the quality of life of patients on MHD. We searched the PubMed, Embays, Scopus, Web of Science, and CNKI databases for randomized controlled trials that evaluated the use of aromatherapy in dialysis patients and reported at least one outcome of interest. Twenty-two relevant studies were included in the meta-analysis. The meta-analysis revealed that aromatherapy significantly increased subjective sleep quality (a lower score indicates better sleep quality) [standardized mean difference (SMD) = −1.52, 95% CI (−2.38, −0.67), <i>p</i> &lt; 0.01] and reduced fatigue [SMD = −1.14, 95% CI (−1.95, −0.33), <i>p</i> = 0.01], anxiety [SMD = −1.38, 95% CI (−2.09, −0.67), <i>p</i> &lt; 0.01], symptoms of restless legs syndrome [RLS; SMD = −1.71, 95% CI (−2.09, −1.33), <i>p</i> &lt; 0.01], and arteriovenous fistula puncture pain [SMD= −1.56, 95% CI (−2.60, −0.52), <i>p</i> &lt; 0.01]. Aromatherapy may be used as a novel complementary and alternative therapy to improve sleep quality and reduce fatigue, anxiety, symptoms of RLS, and arteriovenous fistula puncture pain in patients on MHD.
DOI: 10.6084/m9.figshare.22820749.v1
title: Association of circulating proprotein convertase subtilisin/kexin type 9 concentration with coagulation abnormalities in patients with primary membranous nephropathy

description: The aims of the study were to explore the potential associations between plasma proprotein convertase subtilisin/kexin type 9 (PCSK9) and coagulation indexes in patients with primary membranous nephropathy (PMN). A total of 87 patients diagnosed with PMN were enrolled in our study. 30 healthy participants were recruited to match PMN participants. Plasma PCSK9 concentrations were tested by enzyme-linked immunosorbent assay (ELISA). Correlations between PCSK9 and coagulation abnormalities in patients with PMN were analyzed using univariate and multiple linear regression analysis. Plasma PCSK9 levels in patients with PMN were significantly higher than that in healthy controls [232.0 (143.5, 359.5) ng/mL <i>vs</i>. 166.8 (129.7, 199.7) ng/mL; <i>p</i> = 0.001]. Plasma levels of PCSK9 were positively correlated with factor VIII, factor IX, factor XI, log-transformed tissue factor, protein C and protein S (<i>r</i> = 0.267, <i>p</i> = 0.013; <i>r</i> = 0.496, <i>p</i> &lt; 0.001; <i>r</i> = 0.217, <i>p</i> = 0.045; <i>r</i> = 0.584, <i>p</i> &lt; 0.001; <i>r</i> = 0.372, <i>p</i> = 0.001; <i>r</i> = 0.282, <i>p</i> = 0.011). In multiple linear regression analysis, PCSK9 concentration was independently and positively correlated with factor VIII, factor IX, and tissue factor (β = 0.186, <i>p</i> = 0.047; β = 0.325, <i>p</i> = 0.001; β = 0.531, <i>p</i> &lt; 0.001; respectively). PCSK9 concentration was independently and negatively correlated with PT (β= −0.343, <i>p</i> = 0.011). Plasma PCSK9 levels had good positive correlations with procoagulant clotting factors and negative correlations with PT in PMN, which might provide novel information with regard to PCSK9 and hypercoagulability in PMN.
DOI: 10.5281/zenodo.15364370
title: Wind data

description: Wind data used to validate Gauhati University ST radar against Radiosonde observation
DOI: 10.5281/zenodo.15364371
title: Wind data

description: Wind data used to validate Gauhati University ST radar against Radiosonde observation
DOI: 10.6084/m9.figshare.22226895
title: Serum sclerostin in vascular calcification in CKD: a meta-analysis

description: Vascular calcification (VC) is recognized as a predictor of all-cause and CVD mortality in chronic kidney disease (CKD). VC in CKD is possibly associated with serum sclerostin. The study systematically investigated the role of serum sclerostin in VC in CKD. Following the Preferred Reporting Items for Systematic Review and Meta-Analysis Protocols, a systematic search was performed of the PubMed, Cochrane Library, and EMBASE databases from inception to 11 November 2022, to identify relevant eligible studies. The data were retrieved, analyzed, and summarized. The hazard ratios (HRs) and odds ratios (ORs) with their corresponding confidence intervals (CIs) were derived and pooled. Thirteen reports (3125 patients) met the inclusion criteria and were included. Sclerostin was associated with the presence of VC (pooled OR = 2.75, 95%CI = 1.81–4.19, <i>p</i> &lt; 0.01) and all-cause mortality (pooled HR = 1.22, 95%CI = 1.19–1.25, <i>p</i> &lt; 0.01) among patients with CKD, but with a decreased risk of cardiovascular events (HR = 0.98, 95%CI = 0.97–1.00, <i>p</i> = 0.02). This meta-analysis suggests that serum sclerostin is associated with VC and all-cause mortality among patients with CKD.