cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.3413512.v2
title: original images of human and murine NETs induced by PMA and candida.zip

description: plos one microscopy part 2 <br>
DOI: 10.6084/m9.figshare.3413512.v1
title: PLOS One microscopy2.zip

description: microscopy
DOI: 10.6084/m9.figshare.3413398
title: Fructose intake during gestation and lactation differentially affects the expression of hippocampal neurosteroidogenic enzymes in rat offspring

description: Neurosteroids, steroidal hormones synthesized <i>de novo</i> from cholesterol within the brain, stimulate hippocampal functions such as neuron protection and synapse formation. Previously, we examined the effect of maternal fructose on the transcriptional regulation of neurosteroidogenic enzymes. We found that the mRNA expression level of the steroidogenic acute regulatory protein (StAR), peripheral benzodiazepine receptor (PBR), cytochrome P450(11β), 11β-hydroxysteroid dehydrogenase (HSD), and 17β-HSD was altered. However, we could not determine whether maternal fructose intake played a role in the gestation or lactation period because the dam rats were fed fructose solution during both periods. Thus, in this study, we analyzed the hippocampi of the offspring of dams fed fructose during the gestation or lactation period. Maternal fructose consumption during either the gestation or lactation period did not affect the mRNA levels of StAR, P450(17α), 11β-HSD-2, and 17β-HSD-1. PBR expression was down-regulated, even when rats consumed fructose during the lactation period only, while fructose consumption during gestation tended to activate the expression of P450(11β)-2. We found that maternal fructose intake during gestation and lactation differentially affected the expression of hippocampal neurosteroidogenic enzymes in the offspring.
DOI: 10.6084/m9.figshare.3413398.v1
title: Fructose intake during gestation and lactation differentially affects the expression of hippocampal neurosteroidogenic enzymes in rat offspring

description: Neurosteroids, steroidal hormones synthesized <i>de novo</i> from cholesterol within the brain, stimulate hippocampal functions such as neuron protection and synapse formation. Previously, we examined the effect of maternal fructose on the transcriptional regulation of neurosteroidogenic enzymes. We found that the mRNA expression level of the steroidogenic acute regulatory protein (StAR), peripheral benzodiazepine receptor (PBR), cytochrome P450(11β), 11β-hydroxysteroid dehydrogenase (HSD), and 17β-HSD was altered. However, we could not determine whether maternal fructose intake played a role in the gestation or lactation period because the dam rats were fed fructose solution during both periods. Thus, in this study, we analyzed the hippocampi of the offspring of dams fed fructose during the gestation or lactation period. Maternal fructose consumption during either the gestation or lactation period did not affect the mRNA levels of StAR, P450(17α), 11β-HSD-2, and 17β-HSD-1. PBR expression was down-regulated, even when rats consumed fructose during the lactation period only, while fructose consumption during gestation tended to activate the expression of P450(11β)-2. We found that maternal fructose intake during gestation and lactation differentially affected the expression of hippocampal neurosteroidogenic enzymes in the offspring.
DOI: 10.6084/m9.figshare.3413389
title: PGRMC1 participates in late events of bovine granulosa cells mitosis and oocyte meiosis

description: Progesterone Receptor Membrane Component 1 (PGRMC1) is expressed in both oocyte and ovarian somatic cells, where it is found in multiple cellular sub-compartments including the mitotic spindle apparatus. PGRMC1 localization in the maturing bovine oocytes mirrors its localization in mitotic cells, suggesting a possible common action in mitosis and meiosis. To test the hypothesis that altering PGRMC1 activity leads to similar defects in mitosis and meiosis, PGRMC1 function was perturbed in cultured bovine granulosa cells (bGC) and maturing oocytes and the effect on mitotic and meiotic progression assessed. RNA interference-mediated PGRMC1 silencing in bGC significantly reduced cell proliferation, with a concomitant increase in the percentage of cells arrested at G2/M phase, which is consistent with an arrested or prolonged M-phase. This observation was confirmed by time-lapse imaging that revealed defects in late karyokinesis. In agreement with a role during late mitotic events, a direct interaction between PGRMC1 and Aurora Kinase B (AURKB) was observed in the central spindle at of dividing cells. Similarly, treatment with the PGRMC1 inhibitor AG205 or PGRMC1 silencing in the oocyte impaired completion of meiosis I. Specifically the ability of the oocyte to extrude the first polar body was significantly impaired while meiotic figures aberration and chromatin scattering within the ooplasm increased. Finally, analysis of PGRMC1 and AURKB localization in AG205-treated oocytes confirmed an altered localization of both proteins when meiotic errors occur. The present findings demonstrate that PGRMC1 participates in late events of both mammalian mitosis and oocyte meiosis, consistent with PGRMC1's localization at the mid-zone and mid-body of the mitotic and meiotic spindle.
DOI: 10.6084/m9.figshare.3413389.v1
title: PGRMC1 participates in late events of bovine granulosa cells mitosis and oocyte meiosis

description: Progesterone Receptor Membrane Component 1 (PGRMC1) is expressed in both oocyte and ovarian somatic cells, where it is found in multiple cellular sub-compartments including the mitotic spindle apparatus. PGRMC1 localization in the maturing bovine oocytes mirrors its localization in mitotic cells, suggesting a possible common action in mitosis and meiosis. To test the hypothesis that altering PGRMC1 activity leads to similar defects in mitosis and meiosis, PGRMC1 function was perturbed in cultured bovine granulosa cells (bGC) and maturing oocytes and the effect on mitotic and meiotic progression assessed. RNA interference-mediated PGRMC1 silencing in bGC significantly reduced cell proliferation, with a concomitant increase in the percentage of cells arrested at G2/M phase, which is consistent with an arrested or prolonged M-phase. This observation was confirmed by time-lapse imaging that revealed defects in late karyokinesis. In agreement with a role during late mitotic events, a direct interaction between PGRMC1 and Aurora Kinase B (AURKB) was observed in the central spindle at of dividing cells. Similarly, treatment with the PGRMC1 inhibitor AG205 or PGRMC1 silencing in the oocyte impaired completion of meiosis I. Specifically the ability of the oocyte to extrude the first polar body was significantly impaired while meiotic figures aberration and chromatin scattering within the ooplasm increased. Finally, analysis of PGRMC1 and AURKB localization in AG205-treated oocytes confirmed an altered localization of both proteins when meiotic errors occur. The present findings demonstrate that PGRMC1 participates in late events of both mammalian mitosis and oocyte meiosis, consistent with PGRMC1's localization at the mid-zone and mid-body of the mitotic and meiotic spindle.
DOI: 10.6084/m9.figshare.3413386
title: FoxO1 antagonist suppresses autophagy and lipid droplet growth in adipocytes

description: Obesity and related metabolic disorders constitute one of the most pressing heath concerns worldwide. Increased adiposity is linked to autophagy upregulation in adipose tissues. However, it is unknown how autophagy is upregulated and contributes to aberrant adiposity. Here we show a FoxO1-autophagy-FSP27 axis that regulates adipogenesis and lipid droplet (LD) growth in adipocytes. Adipocyte differentiation was associated with upregulation of autophagy and fat specific protein 27 (FSP27), a key regulator of adipocyte maturation and expansion by promoting LD formation and growth. However, FoxO1 specific inhibitor AS1842856 potently suppressed autophagy, FSP27 expression, and adipocyte differentiation. In terminally differentiated adipocytes, AS1842856 significantly reduced FSP27 level and LD size, which was recapitulated by autophagy inhibitors (bafilomycin-A1 and leupeptin, BL). Similarly, AS1842856 and BL dampened autophagy activity and FSP27 expression in explant cultures of white adipose tissue. To our knowledge, this is the first study addressing FoxO1 in the regulation of adipose autophagy, shedding light on the mechanism of increased autophagy and adiposity in obese individuals. Given that adipogenesis and adipocyte expansion contribute to aberrant adiposity, targeting the FoxO1-autophagy-FSP27 axis may lead to new anti-obesity options.
DOI: 10.6084/m9.figshare.3413386.v1
title: FoxO1 antagonist suppresses autophagy and lipid droplet growth in adipocytes

description: Obesity and related metabolic disorders constitute one of the most pressing heath concerns worldwide. Increased adiposity is linked to autophagy upregulation in adipose tissues. However, it is unknown how autophagy is upregulated and contributes to aberrant adiposity. Here we show a FoxO1-autophagy-FSP27 axis that regulates adipogenesis and lipid droplet (LD) growth in adipocytes. Adipocyte differentiation was associated with upregulation of autophagy and fat specific protein 27 (FSP27), a key regulator of adipocyte maturation and expansion by promoting LD formation and growth. However, FoxO1 specific inhibitor AS1842856 potently suppressed autophagy, FSP27 expression, and adipocyte differentiation. In terminally differentiated adipocytes, AS1842856 significantly reduced FSP27 level and LD size, which was recapitulated by autophagy inhibitors (bafilomycin-A1 and leupeptin, BL). Similarly, AS1842856 and BL dampened autophagy activity and FSP27 expression in explant cultures of white adipose tissue. To our knowledge, this is the first study addressing FoxO1 in the regulation of adipose autophagy, shedding light on the mechanism of increased autophagy and adiposity in obese individuals. Given that adipogenesis and adipocyte expansion contribute to aberrant adiposity, targeting the FoxO1-autophagy-FSP27 axis may lead to new anti-obesity options.
DOI: 10.6084/m9.figshare.3413368
title: Minimum standards of clinical practice for physiotherapists working in critical care settings in Australia and New Zealand: A modified Delphi technique

description: <b><i>Objective:</i></b> Achieving competency in critical care in entry-level physiotherapy courses across Australia and New Zealand is not essential, and accredited training for qualified physiotherapists working in critical care units is lacking. As a result, practice standards and training may vary. The objective was to establish consensus-based minimum clinical practice standards for physiotherapists working in critical care settings in Australia and New Zealand. <b><i>Design:</i></b> A modified Delphi technique, which consisted of three rounds of questionnaires, was used to obtain consensus on items. <b><i>Setting:</i></b> Australian and New Zealand critical care settings. <b><i>Participants:</i></b> A panel (<i>n</i> = 61) was invited from a pool of eligible physiotherapists throughout Australia and New Zealand (<i>n</i> = 93). Eligibility criteria were defined <i>a-priori</i> on the basis of possession of expertise and experience in the practice and teaching of critical care physiotherapy clinical skills. <b><i>Main Outcome Measure:</i></b> Questionnaires were disseminated electronically (either via email, or SurveyMonkey<sup>®</sup>). Items were designated by participants as being ‘Essential/Unsure/Not Essential’. Consensus for inclusion was achieved when items were ranked ‘Essential’ by more than 70% of participants. <b><i>Results:</i></b> Fifty physiotherapists consented and participated in the initial Delphi round, of whom 45 (90%) completed all rounds. Consensus was reached on 199 (89%) items. The panel agreed that 132 (58%) items were ‘Essential’ items for inclusion in the final framework. <b><i>Conclusions:</i></b> This is the first study to develop a consensus framework of minimum standards of practice for physiotherapists working in critical care. The clinical utility of this framework now requires assessment.
DOI: 10.6084/m9.figshare.3413368.v1
title: Minimum standards of clinical practice for physiotherapists working in critical care settings in Australia and New Zealand: A modified Delphi technique

description: <b><i>Objective:</i></b> Achieving competency in critical care in entry-level physiotherapy courses across Australia and New Zealand is not essential, and accredited training for qualified physiotherapists working in critical care units is lacking. As a result, practice standards and training may vary. The objective was to establish consensus-based minimum clinical practice standards for physiotherapists working in critical care settings in Australia and New Zealand. <b><i>Design:</i></b> A modified Delphi technique, which consisted of three rounds of questionnaires, was used to obtain consensus on items. <b><i>Setting:</i></b> Australian and New Zealand critical care settings. <b><i>Participants:</i></b> A panel (<i>n</i> = 61) was invited from a pool of eligible physiotherapists throughout Australia and New Zealand (<i>n</i> = 93). Eligibility criteria were defined <i>a-priori</i> on the basis of possession of expertise and experience in the practice and teaching of critical care physiotherapy clinical skills. <b><i>Main Outcome Measure:</i></b> Questionnaires were disseminated electronically (either via email, or SurveyMonkey<sup>®</sup>). Items were designated by participants as being ‘Essential/Unsure/Not Essential’. Consensus for inclusion was achieved when items were ranked ‘Essential’ by more than 70% of participants. <b><i>Results:</i></b> Fifty physiotherapists consented and participated in the initial Delphi round, of whom 45 (90%) completed all rounds. Consensus was reached on 199 (89%) items. The panel agreed that 132 (58%) items were ‘Essential’ items for inclusion in the final framework. <b><i>Conclusions:</i></b> This is the first study to develop a consensus framework of minimum standards of practice for physiotherapists working in critical care. The clinical utility of this framework now requires assessment.
DOI: 10.6084/m9.figshare.3413044
title: Azadirachtin(A) distinctively modulates subdomain 2 of actin – novel mechanism to induce depolymerization revealed by molecular dynamics study

description: Azadirachtin(A) (AZA), a potential insecticide from neem, binds to actin and induces depolymerization in <i>Drosophila</i>. AZA binds to the pocket same as that of Latrunculin A (LAT), but LAT inhibits actin polymerization by stiffening the actin structure and affects the ADP–ATP exchange. The mechanism by which AZA induces actin depolymerization is not clearly understood. Therefore, different computational experiments were conducted to delineate the precise mechanism of AZA-induced actin depolymerization. Molecular dynamics studies showed that AZA strongly interacted with subdomain 2 and destabilized the interactions between subdomain 2 of one actin and subdomains 1 and 4 of the adjacent actin, causing the separation of actin subunits. The separation was observed between subdomain 3 of subunit n and subdomain 4 of subunit <i>n</i> + 2. However, the specific triggering point for the separation of the subunits was the destabilization of direct interactions between subdomain 2 of subunit n (Arg39, Val45, Gly46 and Arg62) and subdomain 4 of subunit <i>n</i> + 2 (Asp286, Ile287, Asp288, Ile289, Asp244 and Lys291). These results reveal a unique mechanism of an actin filament modulator that induces depolymerization. This mechanism of AZA can be used to design similar molecules against mammalian actins for cancer therapy.
DOI: 10.6084/m9.figshare.3413044.v1
title: Azadirachtin(A) distinctively modulates subdomain 2 of actin – novel mechanism to induce depolymerization revealed by molecular dynamics study

description: Azadirachtin(A) (AZA), a potential insecticide from neem, binds to actin and induces depolymerization in <i>Drosophila</i>. AZA binds to the pocket same as that of Latrunculin A (LAT), but LAT inhibits actin polymerization by stiffening the actin structure and affects the ADP–ATP exchange. The mechanism by which AZA induces actin depolymerization is not clearly understood. Therefore, different computational experiments were conducted to delineate the precise mechanism of AZA-induced actin depolymerization. Molecular dynamics studies showed that AZA strongly interacted with subdomain 2 and destabilized the interactions between subdomain 2 of one actin and subdomains 1 and 4 of the adjacent actin, causing the separation of actin subunits. The separation was observed between subdomain 3 of subunit n and subdomain 4 of subunit <i>n</i> + 2. However, the specific triggering point for the separation of the subunits was the destabilization of direct interactions between subdomain 2 of subunit n (Arg39, Val45, Gly46 and Arg62) and subdomain 4 of subunit <i>n</i> + 2 (Asp286, Ile287, Asp288, Ile289, Asp244 and Lys291). These results reveal a unique mechanism of an actin filament modulator that induces depolymerization. This mechanism of AZA can be used to design similar molecules against mammalian actins for cancer therapy.
DOI: 10.6084/m9.figshare.3413023
title: R script to obtain daily averages of ancillary water data (turbidity, specific conductivity, etc.)

description: We present the procedure to obtain daily averages of ancillary water data (e.g., turbidity and chlorophyll) that may be used to support the interpretation of the daily metabolic rate estimates. The Ancillary_DarilyAvg.R script needs to be executed as many times as the number of available ancillary water parameters (twice for our case). For the case of the SJR restoration reach, the data can be accessed by doing a query on the CDEC website indicating the sensor number (28 for chlorophyll, 27 for turbidity), the interval of the data (event or hourly), and the starting and ending dates of the period of interest. A comma separated value file is produced after the request, and each of these files will be the input to this R script.<br>Section 1 of the script sets up the working directory; the ancillary water data input file is read in section 2 and particular configuration parameters are specified in section 3. According to these parameters, a new table (‘table1’) with only the columns of interest is created in section 4; section 5 converts into NA’s all the cell values that report missing data (“m”) or errors (“-9998” or “-9997”). The actual daily averages are calculated in section 6 and stored in the variable ‘table4’. Section 7 deals with the transformation of the date column to an actual date format in order to identify whether or not there are missing days within the time series. The output of this section (dates and intervals between dates) as well as the daily averages contained in ‘table4’, are merged into a new variable ‘table5’. Finally, section 8 prints the output of this script as a tab separated text file.
DOI: 10.6084/m9.figshare.3413023.v1
title: R script to obtain daily averages of ancillary water data (turbidity, specific conductivity, etc.)

description: We present the procedure to obtain daily averages of ancillary water data (e.g., turbidity and chlorophyll) that may be used to support the interpretation of the daily metabolic rate estimates. The Ancillary_DarilyAvg.R script needs to be executed as many times as the number of available ancillary water parameters (twice for our case). For the case of the SJR restoration reach, the data can be accessed by doing a query on the CDEC website indicating the sensor number (28 for chlorophyll, 27 for turbidity), the interval of the data (event or hourly), and the starting and ending dates of the period of interest. A comma separated value file is produced after the request, and each of these files will be the input to this R script.<br>Section 1 of the script sets up the working directory; the ancillary water data input file is read in section 2 and particular configuration parameters are specified in section 3. According to these parameters, a new table (‘table1’) with only the columns of interest is created in section 4; section 5 converts into NA’s all the cell values that report missing data (“m”) or errors (“-9998” or “-9997”). The actual daily averages are calculated in section 6 and stored in the variable ‘table4’. Section 7 deals with the transformation of the date column to an actual date format in order to identify whether or not there are missing days within the time series. The output of this section (dates and intervals between dates) as well as the daily averages contained in ‘table4’, are merged into a new variable ‘table5’. Finally, section 8 prints the output of this script as a tab separated text file.
DOI: 10.6084/m9.figshare.3413014
title: Measuring the influence of nutrients and river water on the photosynthetic efficiency of <i>Didymosphenia geminata</i> using pulse amplitude modulated fluorometry

description: Over the past three decades the freshwater diatom <i>Didymosphenia geminata</i> (Lyngbye) M. Schmidt has expanded its range globally. In some rivers <i>D. geminata</i> has become invasive, forming expansive and thick polysaccharide-dominated mats. Techniques to maintain and study <i>D. geminata</i> in the laboratory are limited. In this study, a 96-well plate format assay using pulse amplitude modulated (PAM) fluorometry was developed to study <i>D. geminata</i> under controlled conditions. The PAM assay and morphological assessments were used to investigate the addition of sodium nitrate (NaNO<sub>3</sub>) to a previously developed <i>D. geminata-</i>specific growth medium (Didymo Medium; DM). Addition of low concentrations (ca. 0.003–0.018 µM) enhanced cell survival and health. Central-composite design (CCD) experiments coupled with response surface methodology were then used to investigate optimal concentrations of six key chemicals in DM (magnesium sulphate, calcium chloride, mono-potassium phosphate, sodium metasilicate pentahydrate, ferric sodium ethylenediaminetetraacetic acid (EDTA) and NaNO<sub>3</sub>). An optimised DM recipe is provided. The PAM assay was also used to analyse the influence of maintaining <i>D. geminata</i> cells in river waters sourced from locations with and without the diatom. A NaNO<sub>3</sub> spiking experiment was undertaken using water from one location. The maximum quantum yields of cells maintained in all river waters remained relatively constant and higher than those maintained in DM or Milli-Q water for the seven day test period. The results of the NaNO<sub>3</sub> river water spiking experiment provided contrasting results to the culture medium trials, with minimal impact on photosynthetic efficiency. These data, coupled with the results of the CCD experiment, suggest complex interactions among nutrients that have varying effects on <i>D. geminata</i> cell health. Together with microscopical observations, the 96-well plate PAM assay provides a useful tool for improving knowledge of <i>D. geminata</i> biology and growth requirements.