cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.3380119
title: Combination chemotherapy with 5-fluorouracil and dacarbazine in advanced medullary thyroid cancer, a possible alternative?

description: Combination chemotherapy with 5-fluorouracil and dacarbazine in advanced medullary thyroid cancer, a possible alternative?
DOI: 10.6084/m9.figshare.3380119.v1
title: Combination chemotherapy with 5-fluorouracil and dacarbazine in advanced medullary thyroid cancer, a possible alternative?

description: Combination chemotherapy with 5-fluorouracil and dacarbazine in advanced medullary thyroid cancer, a possible alternative?
DOI: 10.6084/m9.figshare.3380116
title: 2016 Philippine vice-presidential elections precinct-level data

description: This dataset contains clustered precinct-level data about the 2016 Philippine vice-presidential elections scraped from the official electoral commission (COMELEC) website, pilipinaselectionresults2016.com. The script used for scraping data is at https://github.com/ianalis/scraper2016 but the data for clustered precinct 67060001 was manually added because it did not follow the assumption of the script (it only transmitted results for VP, party lists and vice governor). The transmission timestamp is based on raw data, as of 12 May 2016 15:45, made available by NAMFREL (http://www.elections.org.ph/2016/results/raw-data.php). This dataset is recent as of 26 May 2016 18:00 UTC.<br><br>The fields contained in this dataset are:<br>* region<br>* province<br>* municipality<br>* barangay<br>* clustered_precinct<br>* cayetano<br>* escudero<br>* honasan<br>* marcos<br>* robredo<br>* trillanes<br>* registered_voters<br>* ballots_cast<br>* precincts<br>* polling_center<br>* timestamp<br><br>This dataset contains data from 90642 clustered precincts. However, the source website notes that there were 90655 election returns (ERs) received out of the 93754 ERs expected. The citizens' arms NAMFREL and PPCRV both expect data to come from 94276 clustered precincts. The discrepancies in the numbers of received and expected ERs are still unresolved.<br>
DOI: 10.6084/m9.figshare.3379993
title: Outcomes and healthcare resource utilization associated with medically attended hypoglycemia in older patients with type 2 diabetes initiating basal insulin in a US managed care setting

description: <b>Objective:</b> To assess health outcomes and the economic burden of hypoglycemia in older patients with type 2 diabetes initiating basal insulin (BI). <b>Research design and methods:</b> Medicare Advantage claims data were extracted for patients with type 2 diabetes initiating BI and patients were stratified into two groups: those with medically attended hypoglycemia during the first year of BI treatment (HG group) and those without (non-HG group). Main outcome measures were hospitalization, mortality, healthcare utilization and costs 1 year before and 1 year after BI initiation. <b>Results:</b> Of 31,035 patients included (mean age 72 years [SD 9.2]), 3066 (9.9%; HG group) experienced hypoglycemia during 1 year post-BI initiation. After adjustment for demographic, comorbidity and medication history, hypoglycemia was associated with risk of hospitalization (HR 1.59; 95% CI: 1.53–1.65) and death (HR 1.50; 95% CI: 1.40–1.60). Healthcare utilization was higher pre-index and showed greater increases post-BI initiation in the HG vs. the non-HG group. Per-patient healthcare costs were substantially higher for the HG group than the non-HG group, both pre-index ($54,057 vs. $30,249, respectively) and post-BI initiation ($75,398 vs. $27,753, respectively). <b>Conclusions:</b> Based on available claims data, hypoglycemia during the first year of BI treatment is associated with risk of hospitalization or death in older people, increasing healthcare utilization and costs. Due to the observational nature of this study, causality cannot be attributed, and further prospective studies into the effect of hypoglycemia on health outcomes in this population are warranted.
DOI: 10.6084/m9.figshare.3379993.v2
title: Outcomes and healthcare resource utilization associated with medically attended hypoglycemia in older patients with type 2 diabetes initiating basal insulin in a US managed care setting

description: <b>Objective:</b> To assess health outcomes and the economic burden of hypoglycemia in older patients with type 2 diabetes initiating basal insulin (BI). <b>Research design and methods:</b> Medicare Advantage claims data were extracted for patients with type 2 diabetes initiating BI and patients were stratified into two groups: those with medically attended hypoglycemia during the first year of BI treatment (HG group) and those without (non-HG group). Main outcome measures were hospitalization, mortality, healthcare utilization and costs 1 year before and 1 year after BI initiation. <b>Results:</b> Of 31,035 patients included (mean age 72 years [SD 9.2]), 3066 (9.9%; HG group) experienced hypoglycemia during 1 year post-BI initiation. After adjustment for demographic, comorbidity and medication history, hypoglycemia was associated with risk of hospitalization (HR 1.59; 95% CI: 1.53–1.65) and death (HR 1.50; 95% CI: 1.40–1.60). Healthcare utilization was higher pre-index and showed greater increases post-BI initiation in the HG vs. the non-HG group. Per-patient healthcare costs were substantially higher for the HG group than the non-HG group, both pre-index ($54,057 vs. $30,249, respectively) and post-BI initiation ($75,398 vs. $27,753, respectively). <b>Conclusions:</b> Based on available claims data, hypoglycemia during the first year of BI treatment is associated with risk of hospitalization or death in older people, increasing healthcare utilization and costs. Due to the observational nature of this study, causality cannot be attributed, and further prospective studies into the effect of hypoglycemia on health outcomes in this population are warranted.
DOI: 10.6084/m9.figshare.3379993.v1
title: Outcomes and Healthcare Resource Utilisation Associated with Medically Attended Hypoglycaemia in Older Patients with Type 2 Diabetes Initiating Basal Insulin in a US Managed Care Setting

description: <b>Objective:</b> To assess health outcomes and the economic burden of hypoglycaemia in older patients with type 2 diabetes initiating basal insulin (BI). <b>Research design and methods:</b> Medicare Advantage claims data were extracted for patients with type 2 diabetes initiating BI and patients were stratified into two groups: those with medically attended hypoglycaemia during the first year of BI treatment (HG group) and those without (non-HG group). Main outcome measures were hospitalisation, mortality, healthcare utilisation and costs 1 year before and 1 year after BI initiation. <b>Results:</b> Of 31,035 patients included (mean age 72 years [SD 9.2]), 3,066 (9.9%; HG group) experienced hypoglycaemia during 1 year post-BI initiation. After adjustment for demographic, comorbidity and medication history, hypoglycaemia was associated with risk of hospitalisation (HR 1.59; 95% CI: 1.53–1.65) and death (HR 1.50; 95% CI: 1.40–1.60). Healthcare utilisation was higher pre-index and showed greater increases post-BI initiation in the HG <i>vs</i> the non-HG group. Per-patient healthcare costs were substantially higher for the HG group than the non-HG group, both pre-index ($54,057 <i>vs</i> $30,249, respectively) and post-BI initiation ($75,398 <i>vs</i> $27,753, respectively). <b>Conclusions:</b> Based on available claims data, hypoglycaemia during the first year of BI treatment is associated with risk of hospitalisation or death in older people, increasing healthcare utilisation and costs. Due to the observational nature of this study, causality cannot be attributed, and further prospective studies into the effect of hypoglycaemia on health outcomes in this population are warranted.
DOI: 10.6084/m9.figshare.3379444
title: myutil-win

description: Simple utility R library for windows os.
DOI: 10.6084/m9.figshare.3379444.v2
title: myutil-win

description: Simple utility R library for windows os.
DOI: 10.6084/m9.figshare.3379444.v1
title: myutil-win

description: Simple utility R library for windows os.
DOI: 10.6084/m9.figshare.3378811
title: MMTool-win

description: Simple R library utility tool for multiple myeloma gene expression data analysis.
DOI: 10.6084/m9.figshare.3378811.v1
title: MMTool-win

description: Simple R library utility tool for multiple myeloma gene expression data analysis.
DOI: 10.6084/m9.figshare.3378811.v2
title: MMTool-win

description: Simple R library utility tool for multiple myeloma gene expression data analysis.
DOI: 10.6084/m9.figshare.3378811.v3
title: MMTool-win

description: Simple R library utility tool for multiple myeloma gene expression data analysis.
DOI: 10.6084/m9.figshare.3378091
title: MMTool

description: Simple R library tool for multiple myeloma gene expression data analysis.
DOI: 10.6084/m9.figshare.3378091.v1
title: MMTool

description: Simple R library tool for multiple myeloma gene expression data analysis.
DOI: 10.6084/m9.figshare.3378091.v2
title: MMTool

description: Simple R library tool for multiple myeloma gene expression data analysis.
DOI: 10.6084/m9.figshare.3378091.v3
title: MMTool

description: Simple R library tool for multiple myeloma gene expression data analysis.
DOI: 10.6084/m9.figshare.3376393
title: Database Snapshot, October 29, 2015

description: Database snapshot for the Neotoma Paleoecological Database, October 29, 2015. The Neotoma Database is available online through http://netomadb.org
DOI: 10.6084/m9.figshare.3376393.v1
title: Database Snapshot, October 29, 2015

description: Database snapshot for the Neotoma Paleoecological Database, October 29, 2015. The Neotoma Database is available online through http://netomadb.org
DOI: 10.6084/m9.figshare.3376390
title: Spermiotoxicity of nickel nanoparticles in the marine invertebrate <i>Ciona intestinalis</i> (ascidians)

description: Nickel nanoparticles (Ni NPs) are increasingly used in modern industries as catalysts, sensors, and in electronic applications. Due to this large use, their inputs into marine environment have significantly increased; however, the potential ecotoxicological effects in marine environment have so far received little attention. In particular, little is known on the impact of NPs on gamete quality of marine organisms and on the consequences on fertility potential. The present study examines, for the first time, the impact of Ni NPs exposure on sperm quality of the marine invertebrate <i>Ciona intestinalis</i> (ascidian). Several parameters related with sperm status such as plasma membrane lipid peroxidation, mitochondrial membrane potential (MMP), intracellular pH, DNA integrity, and fertilizing ability were assessed as toxicity end points after exposure to different Ni NPs concentrations. Ni NPs generate oxidative stress that in turn induces lipid peroxidation and DNA fragmentation, and alters MMP and sperm morphology. Furthermore, sperm exposure to Ni NPs affects their fertilizing ability and causes developmental anomalies in the offspring. All together, these results reveal a spermiotoxicity of Ni NPs in ascidians suggesting that the application of these NPs should be carefully assessed as to their potential toxic effects on the health of marine organisms that, in turn, may influence the ecological system. This study shows that ascidian sperm represent a suitable and sensitive tool for the investigation of the toxicity of NPs entered into marine environment, for defining the mechanisms of toxic action and for the environmental monitoring purpose.
DOI: 10.6084/m9.figshare.3376267
title: Targeting by AutophaGy proteins (TAG): Targeting of IFNG-inducible GTPases to membranes by the LC3 conjugation system of autophagy

description: LC3 has been used as a marker to locate autophagosomes. However, it is also well established that LC3 can localize on various membranous structures other than autophagosomes. We recently demonstrated that the LC3 conjugation system (ATG7, ATG3, and ATG12–ATG5-ATG16L1) is required to target LC3 and IFNG (interferon, gamma)-inducible GTPases to the parasitophorus vacuole membrane (PVM) of a protist parasite <i>Toxoplasma gondii</i> and consequently for IFNG to control <i>T. gondii</i> infection. Here we show that not only LC3, but also its homologs (GABARAP, GABARAPL1, and GABARAPL2) localize on the PVM of <i>T. gondii</i> in a conjugation-dependent manner. Knockout/knockdown of all LC3 homologs led to a significant reduction in targeting of the IFNG-inducible GTPases to the PVM of <i>T. gondii</i> and the IFNG-mediated control of <i>T. gondii</i> infection. Furthermore, when we relocated the ATG12–ATG5-ATG16L1 complex, which specifies the conjugation site of LC3 homologs, to alternative target membranes, the IFNG-inducible GTPases were targeted to the new target membranes rather than the PVM of <i>T. gondii</i>. These data suggest that the localization of LC3 homologs onto a membrane by the LC3 conjugation system is necessary and sufficient for targeting of the IFNG-inducible GTPases to the membrane, implying Targeting by AutophaGy proteins (TAG). Our data further suggest that the conjugation of ubiquitin-like LC3 homologs to the phospholipids of membranes may change the destiny of the membranes beyond degradation through lysosomal fusion, as the conjugation of ubiquitin to proteins changes the destiny of the proteins beyond proteasomal degradation.
DOI: 10.6084/m9.figshare.3376267.v1
title: Targeting by AutophaGy proteins (TAG): Targeting of IFNG-inducible GTPases to membranes by the LC3 conjugation system of autophagy

description: LC3 has been used as a marker to locate autophagosomes. However, it is also well established that LC3 can localize on various membranous structures other than autophagosomes. We recently demonstrated that the LC3 conjugation system (ATG7, ATG3, and ATG12–ATG5-ATG16L1) is required to target LC3 and IFNG (interferon, gamma)-inducible GTPases to the parasitophorus vacuole membrane (PVM) of a protist parasite <i>Toxoplasma gondii</i> and consequently for IFNG to control <i>T. gondii</i> infection. Here we show that not only LC3, but also its homologs (GABARAP, GABARAPL1, and GABARAPL2) localize on the PVM of <i>T. gondii</i> in a conjugation-dependent manner. Knockout/knockdown of all LC3 homologs led to a significant reduction in targeting of the IFNG-inducible GTPases to the PVM of <i>T. gondii</i> and the IFNG-mediated control of <i>T. gondii</i> infection. Furthermore, when we relocated the ATG12–ATG5-ATG16L1 complex, which specifies the conjugation site of LC3 homologs, to alternative target membranes, the IFNG-inducible GTPases were targeted to the new target membranes rather than the PVM of <i>T. gondii</i>. These data suggest that the localization of LC3 homologs onto a membrane by the LC3 conjugation system is necessary and sufficient for targeting of the IFNG-inducible GTPases to the membrane, implying Targeting by AutophaGy proteins (TAG). Our data further suggest that the conjugation of ubiquitin-like LC3 homologs to the phospholipids of membranes may change the destiny of the membranes beyond degradation through lysosomal fusion, as the conjugation of ubiquitin to proteins changes the destiny of the proteins beyond proteasomal degradation.
DOI: 10.6084/m9.figshare.3376264.v2
title: TFEB and TFE3 cooperate in the regulation of the innate immune response in activated macrophages

description: The activation of transcription factors is critical to ensure an effective defense against pathogens. In this study we identify a critical and complementary role of the transcription factors TFEB and TFE3 in innate immune response. By using a combination of chromatin immunoprecipitation, CRISPR-Cas9-mediated genome-editing technology, and in vivo models, we determined that TFEB and TFE3 collaborate with each other in activated macrophages and microglia to promote efficient autophagy induction, increased lysosomal biogenesis, and transcriptional upregulation of numerous proinflammatory cytokines. Furthermore, secretion of key mediators of the inflammatory response (CSF2, IL1B, IL2, and IL27), macrophage differentiation (CSF1), and macrophage infiltration and migration to sites of inflammation (CCL2) was significantly reduced in TFEB and TFE3 deficient cells. These new insights provide us with a deeper understanding of the transcriptional regulation of the innate immune response.
DOI: 10.6084/m9.figshare.3376264.v1
title: TFEB and TFE3 Cooperate in the Regulation of the Innate Immune Response in Activated Macrophages

description: The activation of transcription factors is critical to ensure an effective defense against pathogens. In this study we identify a critical and complementary role of the transcription factors TFEB and TFE3 in innate immune response. By using a combination of chromatin immunoprecipitation, CRISPR-Cas9-mediated genome-editing technology, and <i>in vivo</i> models, we determined that TFEB and TFE3 collaborate with each other in activated macrophages and microglia to promote efficient autophagy induction, increased lysosomal biogenesis, and transcriptional upregulation of numerous proinflammatory cytokines. Furthermore, secretion of key mediators of the inflammatory response (CSF2, IL1B, IL2, and IL27), macrophage differentiation (CSF1), and macrophage infiltration and migration to sites of inflammation (CCL2) was significantly reduced in TFEB and TFE3 deficient cells. These new insights provide us with a deeper understanding of the transcriptional regulation of the innate immune response.
DOI: 10.6084/m9.figshare.3376258.v2
title: Essential control of mitochondrial morphology and function by chaperone-mediated autophagy through degradation of PARK7

description: As a selective degradation system, chaperone-mediated autophagy (CMA) is essential for maintaining cellular homeostasis and survival under stress conditions. Increasing evidence points to an important role for the dysfunction of CMA in the pathogenesis of Parkinson disease (PD). However, the mechanisms by which CMA regulates neuronal survival under stress and its role in neurodegenerative diseases are not fully understood. <i>PARK7/DJ-1</i> is an autosomal recessive familial PD gene. PARK7 plays a critical role in antioxidative response and its dysfunction leads to mitochondrial defects. In the current study, we showed that CMA mediated the lysosome-dependent degradation of PARK7. Importantly, CMA preferentially removed the oxidatively damaged nonfunctional PARK7 protein. Furthermore, CMA protected cells from mitochondrial toxin MPP<sup>+</sup>-induced changes in mitochondrial morphology and function, and increased cell viability. These protective effects were lost under PARK7-deficiency conditions. Conversely, overexpression of PARK7 significantly attenuated the mitochondrial dysfunction and cell death exacerbated by blocking CMA under oxidative stress. Thus, our findings reveal a mechanism by which CMA protects mitochondrial function by degrading nonfunctional PARK7 and maintaining its homeostasis, and dysregulation of this pathway may contribute to the neuronal stress and death in PD pathogenesis.
DOI: 10.6084/m9.figshare.3376258.v1
title: Essential Control of Mitochondrial Morphology and Function by Chaperone-mediated Autophagy through Degradation of PARK7

description: As a selective degradation system, chaperone-mediated autophagy (CMA) is essential for maintaining cellular homeostasis and survival under stress conditions. Increasing evidence points to an important role for the dysfunction of CMA in the pathogenesis of Parkinson disease (PD). However, the mechanisms by which CMA regulates neuronal survival under stress and its role in neurodegenerative diseases are not fully understood. <i>PARK7/DJ-1</i> is an autosomal recessive familial PD gene. PARK7 plays a critical role in antioxidative response and its dysfunction leads to mitochondrial defects. In the current study, we showed that CMA mediated the lysosome-dependent degradation of PARK7. Importantly, CMA preferentially removed the oxidatively damaged nonfunctional PARK7 protein. Furthermore, CMA protected cells from mitochondrial toxin MPP<sup>+</sup>-induced changes in mitochondrial morphology and function, and increased cell viability. These protective effects were lost under PARK7-deficiency conditions. Conversely, overexpression of PARK7 significantly attenuated the mitochondrial dysfunction and cell death exacerbated by blocking CMA under oxidative stress. Thus, our findings reveal a mechanism by which CMA protects mitochondrial function by degrading nonfunctional PARK7 and maintaining its homeostasis, and dysregulation of this pathway may contribute to the neuronal stress and death in PD pathogenesis.
DOI: 10.6084/m9.figshare.3376252
title: TP53INP2/DOR, a mediator of cell autophagy, promotes rDNA transcription via facilitating the assembly of the POLR1/RNA polymerase I preinitiation complex at rDNA promoters

description: Cells control their metabolism through modulating the anabolic and catabolic pathways. TP53INP2/DOR (tumor protein p53 inducible nuclear protein 2), participates in cell catabolism by serving as a promoter of autophagy. Here we uncover a novel function of TP53INP2 in protein synthesis, a major biosynthetic and energy-consuming anabolic process. TP53INP2 localizes to the nucleolus through its nucleolar localization signal (NoLS) located at the C-terminal domain. Chromatin immunoprecipitation (ChIP) assays detected an association of TP53INP2 with the ribosomal DNA (rDNA), when exclusion of TP53INP2 from the nucleolus repressed rDNA promoter activity and the production of ribosomal RNA (rRNA) and proteins. The removal of TP53INP2 also impaired the association of the POLR1/RNA polymerase I preinitiation complex (PIC) with rDNA. Further, TP53INP2 interacts directly with POLR1 PIC, and is required for the assembly of the complex. These data indicate that TP53INP2 promotes ribosome biogenesis through facilitating rRNA synthesis at the nucleolus, suggesting a dual role of TP53INP2 in cell metabolism, assisting anabolism on the nucleolus, and stimulating catabolism off the nucleolus.
DOI: 10.6084/m9.figshare.3376252.v2
title: TP53INP2/DOR, a mediator of cell autophagy, promotes rDNA transcription via facilitating the assembly of the POLR1/RNA polymerase I preinitiation complex at rDNA promoters

description: Cells control their metabolism through modulating the anabolic and catabolic pathways. TP53INP2/DOR (tumor protein p53 inducible nuclear protein 2), participates in cell catabolism by serving as a promoter of autophagy. Here we uncover a novel function of TP53INP2 in protein synthesis, a major biosynthetic and energy-consuming anabolic process. TP53INP2 localizes to the nucleolus through its nucleolar localization signal (NoLS) located at the C-terminal domain. Chromatin immunoprecipitation (ChIP) assays detected an association of TP53INP2 with the ribosomal DNA (rDNA), when exclusion of TP53INP2 from the nucleolus repressed rDNA promoter activity and the production of ribosomal RNA (rRNA) and proteins. The removal of TP53INP2 also impaired the association of the POLR1/RNA polymerase I preinitiation complex (PIC) with rDNA. Further, TP53INP2 interacts directly with POLR1 PIC, and is required for the assembly of the complex. These data indicate that TP53INP2 promotes ribosome biogenesis through facilitating rRNA synthesis at the nucleolus, suggesting a dual role of TP53INP2 in cell metabolism, assisting anabolism on the nucleolus, and stimulating catabolism off the nucleolus.