cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1569108
title: Induction of <i>VEGFA</i> mRNA translation by CoCl<sub>2</sub> mediated by HuR

description: Vascular endothelial growth factor (VEGF) A is a master regulator of neovascularization and angiogenesis. VEGFA is potently induced by hypoxia and by pathological conditions including diabetic retinopathy and tumorigenesis. Fine-tuning of VEGFA expression by different stimuli is important for maintaining tissue vascularization and organ homeostasis. Here, we tested the effect of the hypoxia mimetic cobalt chloride (CoCl<sub>2</sub>) on VEGFA expression in human cervical carcinoma HeLa cells. We found that CoCl<sub>2</sub> increased the levels of <i>VEGFA</i> mRNA and VEGFA protein without affecting <i>VEGFA</i> mRNA stability. Biotin pulldown analysis to capture the RNA-binding proteins (RBPs) bound to <i>VEGFA</i> mRNA followed by mass spectrometry analysis revealed that the RBP HuR [human antigen R, a member of the embryonic lethal abnormal vision (ELAV) family of proteins], interacts with <i>VEGFA</i> mRNA. <i>VEGFA</i> mRNA-tagging experiments showed that exposure to CoCl<sub>2</sub> increases the interaction of HuR with <i>VEGFA</i> mRNA and promoted the colocalization of HuR and the distal part of the <i>VEGFA</i> 3′-untranslated region (UTR) in the cytoplasm. We propose that under hypoxia-like conditions, HuR enhances <i>VEGFA</i> mRNA translation.
DOI: 10.6084/m9.figshare.1569106
title: Extreme mitogenomic divergence between two syntopic specimens of <i>Arremon aurantiirostris</i> (Aves: Emberizidae) in central Panama suggests possible cryptic species

description: We report the complete mitochondrial genome of two specimens of Orange-billed Sparrow <i>Arremon aurantiirostris </i>from Colón Province, in central Panama. The two specimens were collected on the same day, and at the same locality; however, they showed substantial divergence (6.3% average pairwise divergence among coding genes). A survey of ND2 sequence variation across Panama suggests that this divergence is the result of geographic differentiation and secondary contact. This high level of mitochondrial divergence among co-occurring individuals raises the possibility of multiple biological species in Orange-billed Sparrows. Our results are yet another demonstration that much remains to be discovered regarding avian biodiversity in Panama and throughout the Neotropics.
DOI: 10.6084/m9.figshare.1569106.v1
title: Extreme mitogenomic divergence between two syntopic specimens of <i>Arremon aurantiirostris</i> (Aves: Emberizidae) in central Panama suggests possible cryptic species

description: We report the complete mitochondrial genome of two specimens of Orange-billed Sparrow <i>Arremon aurantiirostris </i>from Colón Province, in central Panama. The two specimens were collected on the same day, and at the same locality; however, they showed substantial divergence (6.3% average pairwise divergence among coding genes). A survey of ND2 sequence variation across Panama suggests that this divergence is the result of geographic differentiation and secondary contact. This high level of mitochondrial divergence among co-occurring individuals raises the possibility of multiple biological species in Orange-billed Sparrows. Our results are yet another demonstration that much remains to be discovered regarding avian biodiversity in Panama and throughout the Neotropics.
DOI: 10.6084/m9.figshare.1569108.v2
title: Induction of <i>VEGFA</i> mRNA translation by CoCl<sub>2</sub> mediated by HuR

description: Vascular endothelial growth factor (VEGF) A is a master regulator of neovascularization and angiogenesis. VEGFA is potently induced by hypoxia and by pathological conditions including diabetic retinopathy and tumorigenesis. Fine-tuning of VEGFA expression by different stimuli is important for maintaining tissue vascularization and organ homeostasis. Here, we tested the effect of the hypoxia mimetic cobalt chloride (CoCl<sub>2</sub>) on VEGFA expression in human cervical carcinoma HeLa cells. We found that CoCl<sub>2</sub> increased the levels of <i>VEGFA</i> mRNA and VEGFA protein without affecting <i>VEGFA</i> mRNA stability. Biotin pulldown analysis to capture the RNA-binding proteins (RBPs) bound to <i>VEGFA</i> mRNA followed by mass spectrometry analysis revealed that the RBP HuR [human antigen R, a member of the embryonic lethal abnormal vision (ELAV) family of proteins], interacts with <i>VEGFA</i> mRNA. <i>VEGFA</i> mRNA-tagging experiments showed that exposure to CoCl<sub>2</sub> increases the interaction of HuR with <i>VEGFA</i> mRNA and promoted the colocalization of HuR and the distal part of the <i>VEGFA</i> 3′-untranslated region (UTR) in the cytoplasm. We propose that under hypoxia-like conditions, HuR enhances <i>VEGFA</i> mRNA translation.
DOI: 10.6084/m9.figshare.1569108.v3
title: Induction of <i>VEGFA</i> mRNA translation by CoCl<sub>2</sub> mediated by HuR

description: Vascular endothelial growth factor (VEGF) A is a master regulator of neovascularization and angiogenesis. VEGFA is potently induced by hypoxia and by pathological conditions including diabetic retinopathy and tumorigenesis. Fine-tuning of VEGFA expression by different stimuli is important for maintaining tissue vascularization and organ homeostasis. Here, we tested the effect of the hypoxia mimetic cobalt chloride (CoCl<sub>2</sub>) on VEGFA expression in human cervical carcinoma HeLa cells. We found that CoCl<sub>2</sub> increased the levels of <i>VEGFA</i> mRNA and VEGFA protein without affecting <i>VEGFA</i> mRNA stability. Biotin pulldown analysis to capture the RNA-binding proteins (RBPs) bound to <i>VEGFA</i> mRNA followed by mass spectrometry analysis revealed that the RBP HuR [human antigen R, a member of the embryonic lethal abnormal vision (ELAV) family of proteins], interacts with <i>VEGFA</i> mRNA. <i>VEGFA</i> mRNA-tagging experiments showed that exposure to CoCl<sub>2</sub> increases the interaction of HuR with <i>VEGFA</i> mRNA and promoted the colocalization of HuR and the distal part of the <i>VEGFA</i> 3′-untranslated region (UTR) in the cytoplasm. We propose that under hypoxia-like conditions, HuR enhances <i>VEGFA</i> mRNA translation.
DOI: 10.6084/m9.figshare.1569108.v4
title: Induction of <i>VEGFA</i> mRNA translation by CoCl<sub>2</sub> mediated by HuR

description: Vascular endothelial growth factor (VEGF) A is a master regulator of neovascularization and angiogenesis. VEGFA is potently induced by hypoxia and by pathological conditions including diabetic retinopathy and tumorigenesis. Fine-tuning of VEGFA expression by different stimuli is important for maintaining tissue vascularization and organ homeostasis. Here, we tested the effect of the hypoxia mimetic cobalt chloride (CoCl<sub>2</sub>) on VEGFA expression in human cervical carcinoma HeLa cells. We found that CoCl<sub>2</sub> increased the levels of <i>VEGFA</i> mRNA and VEGFA protein without affecting <i>VEGFA</i> mRNA stability. Biotin pulldown analysis to capture the RNA-binding proteins (RBPs) bound to <i>VEGFA</i> mRNA followed by mass spectrometry analysis revealed that the RBP HuR [human antigen R, a member of the embryonic lethal abnormal vision (ELAV) family of proteins], interacts with <i>VEGFA</i> mRNA. <i>VEGFA</i> mRNA-tagging experiments showed that exposure to CoCl<sub>2</sub> increases the interaction of HuR with <i>VEGFA</i> mRNA and promoted the colocalization of HuR and the distal part of the <i>VEGFA</i> 3′-untranslated region (UTR) in the cytoplasm. We propose that under hypoxia-like conditions, HuR enhances <i>VEGFA</i> mRNA translation.
DOI: 10.6084/m9.figshare.1569108.v5
title: Induction of <i>VEGFA</i> mRNA translation by CoCl<sub>2</sub> mediated by HuR

description: Vascular endothelial growth factor (VEGF) A is a master regulator of neovascularization and angiogenesis. VEGFA is potently induced by hypoxia and by pathological conditions including diabetic retinopathy and tumorigenesis. Fine-tuning of VEGFA expression by different stimuli is important for maintaining tissue vascularization and organ homeostasis. Here, we tested the effect of the hypoxia mimetic cobalt chloride (CoCl<sub>2</sub>) on VEGFA expression in human cervical carcinoma HeLa cells. We found that CoCl<sub>2</sub> increased the levels of <i>VEGFA</i> mRNA and VEGFA protein without affecting <i>VEGFA</i> mRNA stability. Biotin pulldown analysis to capture the RNA-binding proteins (RBPs) bound to <i>VEGFA</i> mRNA followed by mass spectrometry analysis revealed that the RBP HuR [human antigen R, a member of the embryonic lethal abnormal vision (ELAV) family of proteins], interacts with <i>VEGFA</i> mRNA. <i>VEGFA</i> mRNA-tagging experiments showed that exposure to CoCl<sub>2</sub> increases the interaction of HuR with <i>VEGFA</i> mRNA and promoted the colocalization of HuR and the distal part of the <i>VEGFA</i> 3′-untranslated region (UTR) in the cytoplasm. We propose that under hypoxia-like conditions, HuR enhances <i>VEGFA</i> mRNA translation.
DOI: 10.6084/m9.figshare.1569108.v6
title: Induction of <i>VEGFA</i> mRNA translation by CoCl<sub>2</sub> mediated by HuR

description: Vascular endothelial growth factor (VEGF) A is a master regulator of neovascularization and angiogenesis. VEGFA is potently induced by hypoxia and by pathological conditions including diabetic retinopathy and tumorigenesis. Fine-tuning of VEGFA expression by different stimuli is important for maintaining tissue vascularization and organ homeostasis. Here, we tested the effect of the hypoxia mimetic cobalt chloride (CoCl<sub>2</sub>) on VEGFA expression in human cervical carcinoma HeLa cells. We found that CoCl<sub>2</sub> increased the levels of <i>VEGFA</i> mRNA and VEGFA protein without affecting <i>VEGFA</i> mRNA stability. Biotin pulldown analysis to capture the RNA-binding proteins (RBPs) bound to <i>VEGFA</i> mRNA followed by mass spectrometry analysis revealed that the RBP HuR [human antigen R, a member of the embryonic lethal abnormal vision (ELAV) family of proteins], interacts with <i>VEGFA</i> mRNA. <i>VEGFA</i> mRNA-tagging experiments showed that exposure to CoCl<sub>2</sub> increases the interaction of HuR with <i>VEGFA</i> mRNA and promoted the colocalization of HuR and the distal part of the <i>VEGFA</i> 3′-untranslated region (UTR) in the cytoplasm. We propose that under hypoxia-like conditions, HuR enhances <i>VEGFA</i> mRNA translation.
DOI: 10.6084/m9.figshare.1569108.v7
title: Induction of <i>VEGFA</i> mRNA translation by CoCl<sub>2</sub> mediated by HuR

description: Vascular endothelial growth factor (VEGF) A is a master regulator of neovascularization and angiogenesis. VEGFA is potently induced by hypoxia and by pathological conditions including diabetic retinopathy and tumorigenesis. Fine-tuning of VEGFA expression by different stimuli is important for maintaining tissue vascularization and organ homeostasis. Here, we tested the effect of the hypoxia mimetic cobalt chloride (CoCl<sub>2</sub>) on VEGFA expression in human cervical carcinoma HeLa cells. We found that CoCl<sub>2</sub> increased the levels of <i>VEGFA</i> mRNA and VEGFA protein without affecting <i>VEGFA</i> mRNA stability. Biotin pulldown analysis to capture the RNA-binding proteins (RBPs) bound to <i>VEGFA</i> mRNA followed by mass spectrometry analysis revealed that the RBP HuR [human antigen R, a member of the embryonic lethal abnormal vision (ELAV) family of proteins], interacts with <i>VEGFA</i> mRNA. <i>VEGFA</i> mRNA-tagging experiments showed that exposure to CoCl<sub>2</sub> increases the interaction of HuR with <i>VEGFA</i> mRNA and promoted the colocalization of HuR and the distal part of the <i>VEGFA</i> 3′-untranslated region (UTR) in the cytoplasm. We propose that under hypoxia-like conditions, HuR enhances <i>VEGFA</i> mRNA translation.
DOI: 10.6084/m9.figshare.1569057
title: A Microbial Arsenic Cycle in Sediments of an Acidic Mine Impoundment: Herman Pit, Clear Lake, California

description: The involvement of prokaryotes in the redox reactions of arsenic occurring between its +5 [arsenate; As(V)] and +3 [arsenite; As(III)] oxidation states has been well established. Most research to date has focused upon circum-neutral pH environments (e.g., freshwater or estuarine sediments) or arsenic-rich “extreme” environments like hot springs and soda lakes. In contrast, relatively little work has been conducted in acidic environments. With this in mind we conducted experiments with sediments taken from the Herman Pit, an acid mine drainage impoundment of a former mercury (cinnabar) mine. Due to the large adsorptive capacity of the abundant Fe(III)-rich minerals, we were unable to initially detect in solution either As(V) or As(III) added to the aqueous phase of live sediment slurries or autoclaved controls, although the former consumed added electron donors (i.e., lactate, acetate, hydrogen), while the latter did not. This prompted us to conduct further experiments with diluted slurries using the live materials from the first incubation as inoculum. In these experiments we observed reduction of As(V) to As(III) under anoxic conditions and reduction rates were enhanced by addition of electron donors. We also observed oxidation of As(III) to As(V) in oxic slurries as well as in anoxic slurries amended with nitrate. We noted an acid-tolerant trend for sediment slurries in the cases of As(III) oxidation (aerobic and anaerobic) as well as for anaerobic As(V) reduction. These observations indicate the presence of a viable microbial arsenic redox cycle in the sediments of this extreme environment, a result reinforced by the successful amplification of arsenic functional genes (<i>aioA</i>, and <i>arrA</i>) from these materials.
DOI: 10.6084/m9.figshare.1569057.v2
title: A Microbial Arsenic Cycle in Sediments of an Acidic Mine Impoundment: Herman Pit, Clear Lake, California

description: The involvement of prokaryotes in the redox reactions of arsenic occurring between its +5 [arsenate; As(V)] and +3 [arsenite; As(III)] oxidation states has been well established. Most research to date has focused upon circum-neutral pH environments (e.g., freshwater or estuarine sediments) or arsenic-rich “extreme” environments like hot springs and soda lakes. In contrast, relatively little work has been conducted in acidic environments. With this in mind we conducted experiments with sediments taken from the Herman Pit, an acid mine drainage impoundment of a former mercury (cinnabar) mine. Due to the large adsorptive capacity of the abundant Fe(III)-rich minerals, we were unable to initially detect in solution either As(V) or As(III) added to the aqueous phase of live sediment slurries or autoclaved controls, although the former consumed added electron donors (i.e., lactate, acetate, hydrogen), while the latter did not. This prompted us to conduct further experiments with diluted slurries using the live materials from the first incubation as inoculum. In these experiments we observed reduction of As(V) to As(III) under anoxic conditions and reduction rates were enhanced by addition of electron donors. We also observed oxidation of As(III) to As(V) in oxic slurries as well as in anoxic slurries amended with nitrate. We noted an acid-tolerant trend for sediment slurries in the cases of As(III) oxidation (aerobic and anaerobic) as well as for anaerobic As(V) reduction. These observations indicate the presence of a viable microbial arsenic redox cycle in the sediments of this extreme environment, a result reinforced by the successful amplification of arsenic functional genes (<i>aioA</i>, and <i>arrA</i>) from these materials.
DOI: 10.6084/m9.figshare.1569057.v1
title: A microbial arsenic cycle in sediments of an acidic mine impoundment: Herman Pit, Clear Lake, California.

description: The involvement of prokaryotes in the redox reactions of arsenic occurring between its +5 [arsenate; As(V)] and + 3 [arsenite; As(III)] oxidation states has been well established. Most research to date has focused upon circum-neutral pH environments (e.g., freshwater or estuarine sediments) or arsenic-rich “extreme” environments like hot springs and soda lakes. In contrast, relatively little work has been conducted in acidic environments. With this in mind we conducted experiments with sediments taken from the Herman Pit, an acid mine drainage impoundment of a former mercury (cinnabar) mine. Owing to the large adsorptive capacity of the abundant Fe(III)-rich minerals, we were unable to initially detect in solution either As(V) or As(III) added to the aqueous phase of live sediment slurries or autoclaved controls, although the former consumed added electron donors (i.e., lactate, acetate, hydrogen) while the latter did not. This prompted us to conduct further experiments with diluted slurries using the live materials from the first incubation as inoculum. In these experiments we observed reduction of As(V) to As(III) under anoxic conditions and reduction rates were enhanced by addition of electron donors. We also observed oxidation of As(III) to As(V) in oxic slurries as well as in anoxic slurries amended with nitrate. We noted an acid-tolerant trend for sediment slurries in the cases of As(III) oxidation (aerobic and anaerobic) as well as for anaerobic As(V) reduction. These observations indicate the presence of a viable microbial arsenic redox cycle in the sediments of this extreme environment, a result reinforced by the successful amplification of arsenic functional genes (<i>aioA</i>, and <i>arrA</i>) from these materials.
DOI: 10.6084/m9.figshare.1569047
title: Atypical expression of circadian clock genes in denervated mouse skeletal muscle

description: The central circadian clock in the suprachiasmatic nucleus of the hypothalamus synchronizes peripheral clocks through neural and humoral signals in most mammalian tissues. Here, we analyzed the effects of unilateral sciatic denervation on the expression of circadian clock- and clock-controlled genes in the gastrocnemius muscles of mice twice per day on days 0, 3, 7, 9, 11 and 14 after denervation and six times on each of days 7 and 28 after denervation to assess the regulation mechanism of the circadian clock in skeletal muscle. Sciatic denervation did not affect systemic circadian rhythms since core body temperature (Day 7), corticosterone secretion (Days 7 and 28), and hepatic clock gene expression remained intact (Days 7 and 28). Expression levels of most circadian clock-related genes such as <i>Arntl, Per1, Rora, Nr1d1</i> and <i>Dbp</i> were reduced in accordance with the extent of muscle atrophy, although circadian <i>Per2</i> expression was significantly augmented (Day 28). Cosinor analysis revealed that the circadian expression of <i>Arntl</i> (Days 7 and 28) and <i>Dbp</i> (Day 28) was phase advanced in denervated muscle. The mRNA expression of <i>Clock</i> was significantly increased in denervated muscle on Day 3 when the severe atrophy was absent, and it was not affected by atrophic progression for 28 days. Sciatic denervation did not affect the expression of these genes in the contralateral muscle (Days 7 and 28), suggesting that humoral changes were not involved in denervation-induced muscle clock disruption. We then analyzed genome-wide gene expression using microarrays to determine the effects of disrupting the molecular clock in muscle on circadian rhythms at Day 7. Among 478 circadian genes, 313 lost rhythmicity in the denervated muscles. These denervation-sensitive genes included the lipid metabolism-related genes, <i>Nrip1, Bbs1, Ptgis, Acot1, Scd2, Hpgd, Insig1, Dhcr24, Ldlr</i> and <i>Mboat1</i>. Our findings revealed that sciatic denervation disrupts the circadian expression of clock and clock-controlled genes either directly or indirectly via muscle atrophy in the gastrocnemius muscles of mice in a gene-specific manner.
DOI: 10.6084/m9.figshare.1569047.v1
title: Atypical expression of circadian clock genes in denervated mouse skeletal muscle

description: The central circadian clock in the suprachiasmatic nucleus of the hypothalamus synchronizes peripheral clocks through neural and humoral signals in most mammalian tissues. Here, we analyzed the effects of unilateral sciatic denervation on the expression of circadian clock- and clock-controlled genes in the gastrocnemius muscles of mice twice per day on days 0, 3, 7, 9, 11 and 14 after denervation and six times on each of days 7 and 28 after denervation to assess the regulation mechanism of the circadian clock in skeletal muscle. Sciatic denervation did not affect systemic circadian rhythms since core body temperature (Day 7), corticosterone secretion (Days 7 and 28), and hepatic clock gene expression remained intact (Days 7 and 28). Expression levels of most circadian clock-related genes such as <i>Arntl, Per1, Rora, Nr1d1</i> and <i>Dbp</i> were reduced in accordance with the extent of muscle atrophy, although circadian <i>Per2</i> expression was significantly augmented (Day 28). Cosinor analysis revealed that the circadian expression of <i>Arntl</i> (Days 7 and 28) and <i>Dbp</i> (Day 28) was phase advanced in denervated muscle. The mRNA expression of <i>Clock</i> was significantly increased in denervated muscle on Day 3 when the severe atrophy was absent, and it was not affected by atrophic progression for 28 days. Sciatic denervation did not affect the expression of these genes in the contralateral muscle (Days 7 and 28), suggesting that humoral changes were not involved in denervation-induced muscle clock disruption. We then analyzed genome-wide gene expression using microarrays to determine the effects of disrupting the molecular clock in muscle on circadian rhythms at Day 7. Among 478 circadian genes, 313 lost rhythmicity in the denervated muscles. These denervation-sensitive genes included the lipid metabolism-related genes, <i>Nrip1, Bbs1, Ptgis, Acot1, Scd2, Hpgd, Insig1, Dhcr24, Ldlr</i> and <i>Mboat1</i>. Our findings revealed that sciatic denervation disrupts the circadian expression of clock and clock-controlled genes either directly or indirectly via muscle atrophy in the gastrocnemius muscles of mice in a gene-specific manner.
DOI: 10.6084/m9.figshare.1569020
title: Adaptive radiotherapy for locally advanced non-small cell lung cancer, can we predict when and for whom?

description: ABSTRACT<b>Background.</b> Adaptive radiotherapy (ART) could be a tool to reduce toxicity and to facilitate dose escalation in stage III NSCLC. Our aim was to identify the most appropriate time and potential benefit of ART.<b>Material and methods.</b> We analyzed volume reduction and dosimetric consequences of 41 patients who were treated with concurrent (cCRT) (n = 21) or sequential (sCRT) chemoradiotherapy to a median dose of 70 Gy, 2 Gy/F. At every treatment fraction a cone-beam CT (CBCT) was performed. The gross tumor volume (GTV-T) was adapted (exclusion of lymph nodes) to create the GTV-T-F1. Every fifth fraction (F5–F30), the GTV-T-F1 was adapted on the CBCT to create a GTV-T-Fx. Dose volume histograms were recalculated for every GTV-T-Fx, enabling to create lookup tables to predict the theoretical dosimetric advantage on common lung dose constraints.<b>Results.</b> The average GTV reduction was 42.1% (range 4.0–69.3%); 50.1% and 33.7% for the cCRT and sCRT patients, respectively. A linear relationship between GTV-T-F1 volume and absolute volume decrease was found for both groups. The mean V5, V20, V30 and mean lung dose increased by 0.8, 3.1, 5.2 and 3.4%, respectively. A larger increase (p &lt; 0.05) was observed for peripheral tumors and cCRT. Lookup tables were generated.<b>Conclusion.</b> ART offers the most beneficial dosimetric effects when performed around fraction 15, especially for patients with a large initial GTV-T treated by cCRT.