cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.5281/zenodo.17734093
title: Electronic supplementary materials for Wei et al., (2026) The contingent advantage of photosymbiosis in coral evolution

description: Electronic supplementary materials for Wei et al., (2026) The contingent advantage of photosymbiosis in coral evolution.The electronic supplementary materials consist of three folders, including Data, Results and Scripts.All data and scripts for replicating the results in this manuscript are provided.
DOI: 10.15468/dl.xtnnjm
title: Occurrence Download

description: A dataset containing 10148 species occurrences available in GBIF matching the query:
{
 "and" : [
 "TaxonKey is Acritillas indica",
 "Year is one of (1985, 1986, 1987, 1988, 1989, 1990, 1991, 1992, 1993, 1994, 1995, 1996, 1997, 1998, 1999, 2000, 2001, 2002, 2003, 2004, 2005, 2006, 2007, 2008, 2009, 2010, 2011, 2012, 2013, 2014, 2015)",
 "HasGeospatialIssue is false",
 "HasCoordinate is true",
 "OccurrenceStatus is Present",
 "BasisOfRecord is Human Observation"
 ]
}

 The dataset includes 10148 records from 6 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0011557-251120083545085/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.7g2v3e
title: Occurrence Download

description: A dataset containing 164 species occurrences available in GBIF matching the query:
{
 "and" : [
 "CoordinateUncertaintyInMeters 0.0-12699.0",
 "Country is Spain",
 "HasCoordinate is true",
 "HasGeospatialIssue is false",
 "PublishingOrg is one of (0363cbd4-f666-455e-8e86-0bbddcf51950, 7b4f2f30-a456-11d9-8049-b8a03c50a862, ebda1cab-dda8-418b-8f25-df1e71ff5bc2, 8209258a-80e8-4094-aba2-a3febe5ed45b, cb202839-87c6-456a-821c-dc5b268a200f, 730cd32c-627f-44a8-9d93-fcfb23ade969, 6f3ccc65-0a54-4e65-ae7e-13b92d618e7c)",
 "TaxonKey is Senecio inaequidens"
 ]
}

 The dataset includes 164 records from 7 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0011558-251120083545085/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.ec4knb
title: Occurrence Download

description: A dataset containing 96535 species occurrences available in GBIF matching the query:
{
 "and" : [
 "Country is one of (China, Chinese Taipei)",
 "TaxonKey is Dicroglossidae"
 ]
}

 The dataset includes 96535 records from 68 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0011427-251120083545085/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.29039341
title: Application of bioinformatics techniques to discovery of mechanisms by which plasticizers promote acute myelogenous leukemia

description: This study aims to elucidate the potential roles of commonly used plasticizers, including Diethyl Phthalate (DEP), Dimethyl Phthalate (DMP), and Dioctyl Phthalate (DOP), in the pathogenesis of Acute Myeloid Leukemia (AML). The focus is to highlight the complex interactions between these environmental chemicals and key molecular pathways involved in tumorigenesis. We employed network toxicology and molecular docking techniques to analyze the interactions between plasticizers and key proteins associated with AML. Utilizing databases such as The Cancer Genome Atlas (TCGA), we divided selected key genes from AML bone marrow samples into two groups based on gene expression and compared their survival analyses. Enrichment analysis was conducted to identify the biological pathways associated with these genes. The enrichment analysis underscored the association between the plasticizer-targeted genes and essential pathways in AML development, indicating a broad impact of plasticizers on various cancers, including hematologic malignancies. Subsequent expression analysis using TCGA data for AML demonstrated that these genes have significant statistical relevance to the survival in AML, confirming their critical roles in tumor biology. This study provides evidence that exposure to plasticizers could influence the pathogenesis of AML through interactions with key proteins and signaling pathways. By utilizing network pharmacology and protein interaction analysis, our findings emphasize the potential risks associated with plasticizers. These results highlight the necessity for further epidemiological and clinical research to fully understand the impact of plasticizer exposure on AML risk, thereby informing future preventive and therapeutic strategies.
DOI: 10.6084/m9.figshare.29039341.v1
title: Application of bioinformatics techniques to discovery of mechanisms by which plasticizers promote acute myelogenous leukemia

description: This study aims to elucidate the potential roles of commonly used plasticizers, including Diethyl Phthalate (DEP), Dimethyl Phthalate (DMP), and Dioctyl Phthalate (DOP), in the pathogenesis of Acute Myeloid Leukemia (AML). The focus is to highlight the complex interactions between these environmental chemicals and key molecular pathways involved in tumorigenesis. We employed network toxicology and molecular docking techniques to analyze the interactions between plasticizers and key proteins associated with AML. Utilizing databases such as The Cancer Genome Atlas (TCGA), we divided selected key genes from AML bone marrow samples into two groups based on gene expression and compared their survival analyses. Enrichment analysis was conducted to identify the biological pathways associated with these genes. The enrichment analysis underscored the association between the plasticizer-targeted genes and essential pathways in AML development, indicating a broad impact of plasticizers on various cancers, including hematologic malignancies. Subsequent expression analysis using TCGA data for AML demonstrated that these genes have significant statistical relevance to the survival in AML, confirming their critical roles in tumor biology. This study provides evidence that exposure to plasticizers could influence the pathogenesis of AML through interactions with key proteins and signaling pathways. By utilizing network pharmacology and protein interaction analysis, our findings emphasize the potential risks associated with plasticizers. These results highlight the necessity for further epidemiological and clinical research to fully understand the impact of plasticizer exposure on AML risk, thereby informing future preventive and therapeutic strategies.
DOI: 10.6084/m9.figshare.28293830
title: Novel chlorinated oxime K870 protects rats against paraoxon poisoning better than obidoxime

description: The aim of this study was to determine the antidotal potential of the chlorinated oxime K870 compared to obidoxime, as a monotherapy and in combination with atropine, in paraoxon (POX)-poisoned rats. The treatment doses of oximes were chosen as 20% of their LD<sub>50</sub> values. The protective ratio (PR) of oxime K870 with atropine was significantly higher than that of obidoxime with atropine (68.8 and 125.0, respectively). In the biochemical part of the experiment POX subcutaneously (s.c.) (0.75% LD<sub>50</sub>) was administered and followed by oxime K870 or obidoxime i.m. 1 min later. Acetylcholinesterase (AChE) activity was determined spectrophotometrically in cerebrum, cerebellum, brainstem, diaphragm, and erythrocytes. Carboxylesterase activity was determined in plasma and liver. Both oximes successfully reactivated AChE in brain (cerebrum, cerebellum, and brainstem), diaphragm and erythrocytes, but the oxime K870 performed better than obidoxime. Both oximes reactivated carboxylesterase, obidoxime better in plasma and oxime K870 better in liver. In conclusion, the oxime K870, when co-administered with atropine, is a more effective antidote than the obidoxime-atropine combination in POX-poisoned rats.
DOI: 10.6084/m9.figshare.28293830.v1
title: Novel chlorinated oxime K870 protects rats against paraoxon poisoning better than obidoxime

description: The aim of this study was to determine the antidotal potential of the chlorinated oxime K870 compared to obidoxime, as a monotherapy and in combination with atropine, in paraoxon (POX)-poisoned rats. The treatment doses of oximes were chosen as 20% of their LD<sub>50</sub> values. The protective ratio (PR) of oxime K870 with atropine was significantly higher than that of obidoxime with atropine (68.8 and 125.0, respectively). In the biochemical part of the experiment POX subcutaneously (s.c.) (0.75% LD<sub>50</sub>) was administered and followed by oxime K870 or obidoxime i.m. 1 min later. Acetylcholinesterase (AChE) activity was determined spectrophotometrically in cerebrum, cerebellum, brainstem, diaphragm, and erythrocytes. Carboxylesterase activity was determined in plasma and liver. Both oximes successfully reactivated AChE in brain (cerebrum, cerebellum, and brainstem), diaphragm and erythrocytes, but the oxime K870 performed better than obidoxime. Both oximes reactivated carboxylesterase, obidoxime better in plasma and oxime K870 better in liver. In conclusion, the oxime K870, when co-administered with atropine, is a more effective antidote than the obidoxime-atropine combination in POX-poisoned rats.
DOI: 10.6084/m9.figshare.30400059
title: The protective effects of neferine against paracetamol-induced liver injury are associated with the activation of SIRT1/Nrf2/HO-1 signaling pathway and inhibition of NF-kappa B/TNF-alpha/iNOS/COX-II cascade

description: Drug-induced hepatotoxicity is a significant public health issue that influences the development of novel pharmaceutical therapies and the retraction of numerous promising medications from the market. Therefore, the current study investigated the potential hepato-protective benefits of NEF against hepatotoxicity caused by paracetamol (APAP) in mice and assessed its underlying mechanisms. Mice were divided randomly into six groups; control (received normal saline), NEF control, APAP, N-acetylcysteine (NAC; served as a standard treatment) + APAP, NEF (10 mg/kg) + APAP, and NEF (20 mg/kg) + APAP. The serum and hepatic tissues were collected for different biochemical, genetic, and histological assessments. APAP induced profound hepatic damage that was evident through all biochemical, histological, and molecular assessments. NEF pretreatment opposed the elevation of liver injury biomarkers and attenuated hepatic histological disruption. At the molecular level, NEF increased the hepatic level and protein expression of SIRT-1. NEF increased the hepatic mRNA and protein expression of Nrf2 and HO-1. NEF also decreased hepatic level of oxidative stress biomarker, MDA and increased the hepatic levels of antioxidants: GSH, GR, GST, TAC, and SOD, NEF also counteracted the activation of NF-κB and inhibited the upregulation of different inflammatory cytokines as TNF-α and interleukins- (IL-1β and IL-6). Furthermore, NEF pretreatment decreased the hepatic level and mRNA expression of COX-II and iNOS. NEF ameliorated APAP-induced liver injury in mice where the higher dose of NEF (20 mg/kg) was more effective than the lower (10 mg/kg) compared to NAC. This effect is association with upregulation of SIRT-1/Nrf2/HO-1 and interruption of NF-κB/cytokines/iNOS/COX-II signaling cascades. NEF ameliorated APAP-induced liver injury in mice.NEF increased SIRT-1 hepatic levels and protein expression.NEF increased the mRNA and protein expression of Nrf2 and HO-1.NEF decreased MDA and increased the antioxidants GSH, GR, GST, TAC, and SOD.NEF inhibited the upregulation of NF-κB, TNF-α, IL-1β, and IL-6.NEF pretreatment decreased mRNA expression of COX-II and iNOS. NEF ameliorated APAP-induced liver injury in mice. NEF increased SIRT-1 hepatic levels and protein expression. NEF increased the mRNA and protein expression of Nrf2 and HO-1. NEF decreased MDA and increased the antioxidants GSH, GR, GST, TAC, and SOD. NEF inhibited the upregulation of NF-κB, TNF-α, IL-1β, and IL-6. NEF pretreatment decreased mRNA expression of COX-II and iNOS.
DOI: 10.6084/m9.figshare.30400059.v1
title: The protective effects of neferine against paracetamol-induced liver injury are associated with the activation of SIRT1/Nrf2/HO-1 signaling pathway and inhibition of NF-kappa B/TNF-alpha/iNOS/COX-II cascade

description: Drug-induced hepatotoxicity is a significant public health issue that influences the development of novel pharmaceutical therapies and the retraction of numerous promising medications from the market. Therefore, the current study investigated the potential hepato-protective benefits of NEF against hepatotoxicity caused by paracetamol (APAP) in mice and assessed its underlying mechanisms. Mice were divided randomly into six groups; control (received normal saline), NEF control, APAP, N-acetylcysteine (NAC; served as a standard treatment) + APAP, NEF (10 mg/kg) + APAP, and NEF (20 mg/kg) + APAP. The serum and hepatic tissues were collected for different biochemical, genetic, and histological assessments. APAP induced profound hepatic damage that was evident through all biochemical, histological, and molecular assessments. NEF pretreatment opposed the elevation of liver injury biomarkers and attenuated hepatic histological disruption. At the molecular level, NEF increased the hepatic level and protein expression of SIRT-1. NEF increased the hepatic mRNA and protein expression of Nrf2 and HO-1. NEF also decreased hepatic level of oxidative stress biomarker, MDA and increased the hepatic levels of antioxidants: GSH, GR, GST, TAC, and SOD, NEF also counteracted the activation of NF-κB and inhibited the upregulation of different inflammatory cytokines as TNF-α and interleukins- (IL-1β and IL-6). Furthermore, NEF pretreatment decreased the hepatic level and mRNA expression of COX-II and iNOS. NEF ameliorated APAP-induced liver injury in mice where the higher dose of NEF (20 mg/kg) was more effective than the lower (10 mg/kg) compared to NAC. This effect is association with upregulation of SIRT-1/Nrf2/HO-1 and interruption of NF-κB/cytokines/iNOS/COX-II signaling cascades. NEF ameliorated APAP-induced liver injury in mice.NEF increased SIRT-1 hepatic levels and protein expression.NEF increased the mRNA and protein expression of Nrf2 and HO-1.NEF decreased MDA and increased the antioxidants GSH, GR, GST, TAC, and SOD.NEF inhibited the upregulation of NF-κB, TNF-α, IL-1β, and IL-6.NEF pretreatment decreased mRNA expression of COX-II and iNOS. NEF ameliorated APAP-induced liver injury in mice. NEF increased SIRT-1 hepatic levels and protein expression. NEF increased the mRNA and protein expression of Nrf2 and HO-1. NEF decreased MDA and increased the antioxidants GSH, GR, GST, TAC, and SOD. NEF inhibited the upregulation of NF-κB, TNF-α, IL-1β, and IL-6. NEF pretreatment decreased mRNA expression of COX-II and iNOS.
DOI: 10.6084/m9.figshare.29163646
title: The role of lncRNA H19/Hmox1 axis regulating ferroptosis in anthracycline-induced cardiotoxicity

description: This study investigates the molecular mechanisms underlying anthracyclines (ANT)-induced cardiotoxicity, with a specific focus on ferroptosis regulated by the long non-coding RNA (lncRNA) H19/heme oxygenase-1 (Hmox1) signaling axis. A retrospective analysis was performed on 50 breast cancer patients who developed ANT-associated cardiac dysfunction. Clinical assessments included measurements of left ventricular ejection fraction (LVEF) and serum markers, such as cardiac troponin I (cTnI), creatine kinase-MB (CK-MB), N-terminal pro-B-type natriuretic peptide (NT-proBNP), and serum iron levels. Serum analysis revealed a marked downregulation of lncRNA H19 and upregulation of Hmox1, both significantly correlated with impaired cardiac function and disrupted iron homeostasis. To further elucidate the mechanism, an Epirubicin (EPI)-induced injury model in HL-1 cardiomyocytes was established. EPI exposure led to suppression of lncRNA H19, upregulation of Hmox1, and induction of apoptosis and ferroptotic cell death. RNA-seq analysis identified potential downstream targets linking lncRNA H19 to iron metabolism via Hmox1 modulation. Functional assays demonstrated that overexpression of lncRNA H19 mitigated EPI-induced ferroptosis, while enforced expression of Hmox1 reversed these protective effects. Collectively, these findings identify the lncRNA H19/Hmox1 axis as a critical regulator of ferroptosis in ANT-induced cardiotoxicity and suggest it as a potential therapeutic target for mitigating cardiac injury in breast cancer patients undergoing anthracycline chemotherapy.
DOI: 10.6084/m9.figshare.29163646.v1
title: The role of lncRNA H19/Hmox1 axis regulating ferroptosis in anthracycline-induced cardiotoxicity

description: This study investigates the molecular mechanisms underlying anthracyclines (ANT)-induced cardiotoxicity, with a specific focus on ferroptosis regulated by the long non-coding RNA (lncRNA) H19/heme oxygenase-1 (Hmox1) signaling axis. A retrospective analysis was performed on 50 breast cancer patients who developed ANT-associated cardiac dysfunction. Clinical assessments included measurements of left ventricular ejection fraction (LVEF) and serum markers, such as cardiac troponin I (cTnI), creatine kinase-MB (CK-MB), N-terminal pro-B-type natriuretic peptide (NT-proBNP), and serum iron levels. Serum analysis revealed a marked downregulation of lncRNA H19 and upregulation of Hmox1, both significantly correlated with impaired cardiac function and disrupted iron homeostasis. To further elucidate the mechanism, an Epirubicin (EPI)-induced injury model in HL-1 cardiomyocytes was established. EPI exposure led to suppression of lncRNA H19, upregulation of Hmox1, and induction of apoptosis and ferroptotic cell death. RNA-seq analysis identified potential downstream targets linking lncRNA H19 to iron metabolism via Hmox1 modulation. Functional assays demonstrated that overexpression of lncRNA H19 mitigated EPI-induced ferroptosis, while enforced expression of Hmox1 reversed these protective effects. Collectively, these findings identify the lncRNA H19/Hmox1 axis as a critical regulator of ferroptosis in ANT-induced cardiotoxicity and suggest it as a potential therapeutic target for mitigating cardiac injury in breast cancer patients undergoing anthracycline chemotherapy.
DOI: 10.6084/m9.figshare.29061600
title: Toxicity study of compound honeysuckle moisturizing Chinese herbal extract by oral gavage for 13 weeks in sprague dawley rats

description: To assess the safety of oral compound honeysuckle moisturizing Chinese herbal extract for eczema treatment, Sprague-Dawley (SD) rats were oral administered three doses (20.8, 41.6, and 83.3 g/kg, based on raw materials) of the extract daily for 13 consecutive weeks. The study aimed to identify potential toxic reactions, mortality due to accumulation, and recovery after discontinuation. By observing these factors, we sought to determine the target organs of toxicity and establish nontoxic doses for SD rats. The results indicated that during the administration period and subsequent recovery period, there were no significant abnormalities in weight gain, food intake, hematology, blood biochemistry, or urine indicators. Additionally, histopathological analysis of major organs (heart, liver, lungs, kidneys, spleen, and brain) revealed no significant extract-related lesions. Moreover, no significant local toxic lesions were observed in the oral buccal and tongue mucosa. Finally, under the experimental conditions of this study, the preliminary nontoxic response dose of oral gavage compound honeysuckle moisturizing Chinese herbal extract administered to SD rats for 13 weeks was 83.3 g/kg/day (calculated as raw medicine).
DOI: 10.6084/m9.figshare.29061600.v1
title: Toxicity study of compound honeysuckle moisturizing Chinese herbal extract by oral gavage for 13 weeks in sprague dawley rats

description: To assess the safety of oral compound honeysuckle moisturizing Chinese herbal extract for eczema treatment, Sprague-Dawley (SD) rats were oral administered three doses (20.8, 41.6, and 83.3 g/kg, based on raw materials) of the extract daily for 13 consecutive weeks. The study aimed to identify potential toxic reactions, mortality due to accumulation, and recovery after discontinuation. By observing these factors, we sought to determine the target organs of toxicity and establish nontoxic doses for SD rats. The results indicated that during the administration period and subsequent recovery period, there were no significant abnormalities in weight gain, food intake, hematology, blood biochemistry, or urine indicators. Additionally, histopathological analysis of major organs (heart, liver, lungs, kidneys, spleen, and brain) revealed no significant extract-related lesions. Moreover, no significant local toxic lesions were observed in the oral buccal and tongue mucosa. Finally, under the experimental conditions of this study, the preliminary nontoxic response dose of oral gavage compound honeysuckle moisturizing Chinese herbal extract administered to SD rats for 13 weeks was 83.3 g/kg/day (calculated as raw medicine).
DOI: 10.15468/dl.g67r93
title: Occurrence Download

description: A dataset containing 9413 species occurrences available in GBIF matching the query:
{
 "and" : [
 "Country is Australia",
 "TaxonKey is Crocodylia",
 "Year 1985-2005"
 ]
}

 The dataset includes 9413 records from 21 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0011559-251120083545085/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.5281/zenodo.17726507
title: Influence of gut microbiota on chronic lymphocytic leukemia development and aggressiveness

description: Chronic lymphocytic leukemia (CLL) is highly heterogenous both clinically and biologically. Although genetic factors have been identified, several lines of evidence suggest a role for environmental factors in disease onset and progression. Diet is a recognized risk factor for various diseases including cancer and its relationship to the composition of the gut microbiome is well established. Taking advantage of the widely used Em-TCL1 transgenic model, we investigated the relationship between diet, gut microbiota and CLL development. We observed a progressive shift in the microbiome composition in animals fed with different diets and an acceleration of disease expansion associated with a specific diet and changes in the microbiome composition. Our data suggest a close link between diet, gut microbiota and CLL development and pave the way for detailed studies to be conducted in controlled cohorts of patients with CLL to elucidate the role of diet in disease incidence and evolution
DOI: 10.15468/dl.gfa73k
title: Occurrence Download

description: A dataset containing 102151 species occurrences available in GBIF matching the query:
{
 "and" : [
 "TaxonKey is one of (Apidae, Halictidae, Andrenidae, Megachilidae, Colletidae, Melittidae)",
 "Country is one of (Spain, Portugal)",
 "HasCoordinate is true",
 "HasGeospatialIssue is false",
 "BasisOfRecord is one of (Human Observation, Specimen)"
 ]
}

 The dataset includes 102151 records from 77 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0011543-251120083545085/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.bagayz
title: Occurrence Download

description: A dataset containing 129880 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is Amelanchier ovalis Medik."
 ]
}

 The dataset includes 129880 records from 651 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0002866-241007104925546/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.