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11,869 results for “metabolic”

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dryad36/100

Body and wing morphology, flight metabolic rates, and wingbeat frequencies for 13 stingless bee species

<p><span>Understanding the effect of body size on flight costs is critical for development of models of aerodynamics and animal energetics. Prior scaling studies that have shown that flight costs scale hypometrically have focused primarily on larger (&gt; 100 mg) insects and birds, but most flying species are smaller. We studied the flight physiology of thirteen stingless bee species over a large range of body sizes (1-115 mg). Metabolic rate during hovering scaled hypermetrically (scaling slope = 2.11). Larger bees had warm thoraxes while small bees were nearly ecothermic; however, even controlling for body temperature variation, flight metabolic rate scaled hypermetrically across this clade. Despite having a lower mass-specific metabolic rate during flight, smaller bees could carry the same proportional load. Wingbeat frequency did not vary with body size, in contrast to most studies that find wingbeat frequency increases as body size decreases. Smaller stingless bees have greater relative wing surface area which may help them reduce the energy requirements needed to fly. Further, we hypothesize that the relatively larger heads of smaller species may change their body pitch in flight. Synthesizing across all flying insects, we demonstrate that the scaling of flight metabolic rate changes from hypermetric to hypometric at approximately 58 mg body mass with hypermetic scaling below (slope=1.2) and hypometric scaling (slope=0.67) above 58 mg in body mass. The reduced cost of flight likely provides selective advantages for the evolution of small body size in insects. The biphasic scaling of flight metabolic rates and wingbeat frequencies in insects supports the hypothesis that the scaling of metabolic rate is closely related to the power requirements of locomotion and cycle frequencies.</span></p>

opencc-zeroJul 2022View details →
dryad36/100

A simple method reveals minimum time required to quantify steady-rate metabolism and net cost of transport for human walking

<p>The U-shaped net cost of transport (COT) curve of walking has helped scientists understand the biomechanical basis that underlies energy minimization during walking. However, to produce an individual's net COT curve, data must be analyzed during periods of steady-rate metabolism. Traditionally, studies analyze the last few minutes of a 6–10 min trial, assuming that steady-rate metabolism has been achieved. Yet, it is possible that an individual achieves steady rates of metabolism much earlier. However, there is no consensus on how to objectively quantify steady-rate metabolism across a range of walking speeds. Therefore, we developed a simple slope method to determine the minimum time needed for humans to achieve steady rates of metabolism across slow to fast walking speeds.We hypothesized that a shorter time window could be used to produce a net COT curve that is comparable to the net COT curve created using traditional methods. We analyzed metabolic data from 21 subjects who completed several 7 min walking trials ranging from 0.50 to 2.00 m s−1. We partitioned the metabolic data for each trial into moving 1, 2 and 3 min intervals and calculated their slopes. We statistically compared these slope values with values derived from the last 3 min of the 7 min trial, our 'gold' standard comparison. We found that a minimum of 2 min is required to achieve steady-rate metabolism and that data from 2–4 min yields a net COT curve that is not statistically different from the one derived from experimental protocols that are generally accepted in the field.</p>

opencc-zeroAug 2022View details →
dryad36/100

Scaling of metabolic rate in hibernators: Translation of literature data: For a comment to Nespolo et al. (2022)

<p>This spreadsheet provides a translation of data from the literature for the manuscript: Do bears hibernate in the woods? Comment on 'Why bears hibernate? Redefining the scaling energetics of hibernation', and includes both the background data for Figure 1 which is presented in the manuscript.</p> <p>Full reference for article it is commented on: Nespolo, R. F., Mejias, C., and Bozinovic, F. Why bears hibernate? Redefining the scaling energetics of hibernation. Proc. R. Soc. B. 2022; 289(1973):20220456. We have made corrections to the data in the original article's Table S1, and translated empirical BMR data from literature instead of calculating a regression line from White, C.R. &amp; Seymour, R.S. (2003). This changes the body mass where regression lines for Log (DDE<sub>HIB</sub>) and Log(BMR) cross, and thus where no savings from hibernation can be expected, from 75 kg to over 2,250 kg and shows that bears hibernate to save energy.</p>

opencc-zeroAug 2022View details →
zenodo36/100

Source data for "Ca2+ channels couple spiking to mitochondrial metabolism in substantia nigra dopaminergic neurons"

<p><strong>Fig.1Aa-c.tif</strong></p> <p>2PLSM images (Fura-2 filled neuron) used for the reconstruction in Fig.1A</p> <p>&nbsp;</p> <p><strong>Fig1CDJ.xlsx</strong></p> <p>Numerical data for the charts in Fig. 1C, Fig.1D, Fig.1J</p> <p>&nbsp;</p> <p><strong>Fig.1F_GCEPIA1er.tif</strong></p> <p>Confocal image (green channel, G-CEPIA1er) for Fig. 1F</p> <p>&nbsp;</p> <p><strong>Fig.1F_TH.tif</strong></p> <p>Confocal image (blue channel, anti-TH immunostaining) for Fig. 1F</p> <p>&nbsp;</p> <p><strong>Fig.1G_GCEPIA1er.tif</strong></p> <p>Confocal image (green channel, G-CEPIA1er) for Fig. 1G</p> <p>&nbsp;</p> <p><strong>Fig.1G_CRT.tif</strong></p> <p>Confocal image (magenta channel, anti-CRT immunostaining) for Fig. 1G</p> <p>&nbsp;</p> <p><strong>Fig.1H_GCEPIA1er.tif</strong></p> <p>Confocal image (green channel, G-CEPIA1er) for Fig. 1H</p> <p>&nbsp;</p> <p><strong>Fig.1H_TH.tif</strong></p> <p>Confocal image (blue channel, anti-TH immunostaining) for Fig. 1H</p> <p>&nbsp;</p> <p><strong>Fig. 2B_mitoGCaMP6.tif</strong></p> <p>Confocal image (green channel, mito-GCaMP6) for Fig. 2B</p> <p>&nbsp;</p> <p><strong>Fig.2B_TH.tif</strong></p> <p>Confocal image (blue channel, anti-TH immunostaining) for Fig. 2B</p> <p>&nbsp;</p> <p><strong>Fig. 2C_mitoGCaMP6.tif</strong></p> <p>Confocal image (green channel, mito-GCaMP6) for Fig. 2C</p> <p>&nbsp;</p> <p><strong>Fig.2C_COXIV.tif</strong></p> <p>Confocal image (magenta channel, anti-COXIV immunostaining) for Fig. 2C</p> <p>&nbsp;</p> <p><strong>Fig. 2D_mitoGCaMP6.tif</strong></p> <p>Confocal image (green channel, mito-GCaMP6) for Fig. 2D</p> <p>&nbsp;</p> <p><strong>Fig.2D_TH.tif</strong></p> <p>Confocal image (blue channel, anti-TH immunostaining) for Fig. 2D</p> <p>&nbsp;</p> <p><strong>Fig.2FGJL.xlsx</strong></p> <p>Numerical data for the charts in Fig. 2F, Fig.2G, Fig.2J, Fig.2L</p> <p>&nbsp;</p> <p><strong>Fig.3BDE.xlsx</strong></p> <p>Numerical data for the charts in Fig. 3B, Fig.3D, Fig.3E</p> <p>&nbsp;</p> <p><strong>Fig.3C_Alexa.tif</strong></p> <p>MAX Projection of z-stack of 2PLSM images (magenta channel, Alexa 594 dye) used to generate Fig.3C top panel</p> <p>&nbsp;</p> <p><strong>Fig.3C_mitoGCaMP6.tif</strong></p> <p>MAX Projection of&nbsp;z-stack of 2PLSM images (green channel, mito-GCaMP6) used to generate Fig.3C top panel</p> <p>&nbsp;</p> <p><strong>Fig.3C_inset_dendritic_mitoGCaMP6.tif</strong></p> <p>2PLSM image (green channel, mito-GCaMP6) for Fig.3C bottom left panel</p> <p>&nbsp;</p> <p><strong>Fig.3C_inset_soma_mitoGCaMP6.tif</strong></p> <p>2PLSM image (green channel, mito-GCaMP6) for Fig.3C bottom right panel</p> <p>&nbsp;</p> <p><strong>Fig. 4A_PercevalHR.tif</strong></p> <p>Confocal image (green channel, PercevalHR) for Fig.4A</p> <p>&nbsp;</p> <p><strong>Fig.4A_TH.tif</strong></p> <p>Confocal image (blue channel, anti-TH immunostaining) for Fig.4A</p> <p>&nbsp;</p> <p><strong>Fig. 4B_PercevalHR.tif</strong></p> <p>Confocal image (green channel, PercevalHR) for Fig.4B</p> <p>&nbsp;</p> <p><strong>Fig.4B_TH.tif</strong></p> <p>Confocal image (blue channel, anti-TH immunostaining) for Fig.4B</p> <p>&nbsp;</p> <p><strong>Fig.4G.xlsx</strong></p> <p>Numerical data for the charts in Fig.4G</p> <p>&nbsp;</p> <p><strong>Fig.5BDFHI.xlsx</strong></p> <p>Numerical data for the charts in Fig.5B, Fig.5D, Fig.5F, Fig.5H, Fig.5I</p> <p>&nbsp;</p> <p><strong>Fig.6ADEFJKLN.xlsx</strong></p> <p>Numerical data for the charts in Fig.6A, Fig.6D, Fig.6E, Fig.6F, Fig.6J, Fig.6K, Fig.6L, Fig.6N</p> <p>&nbsp;</p> <p><strong>Fig.6H_mitoroGFP.tif</strong></p> <p>2PLSM image (green channel, mito-roGFP) for Fig.6H</p> <p>&nbsp;</p> <p><strong>Fig.6M_MCU-KO.tif</strong></p> <p>Combined EM micrographs used to generate Fig. 6M right side</p> <p>&nbsp;</p> <p><strong>Fig.6M_wildtype.tif</strong></p> <p>Combined EM micrographs used to generate Fig. 6M left side</p> <p>&nbsp;</p> <p><strong>Fig.7CEFG.xlsx</strong></p> <p>Numerical data for the charts in Fig.7C, Fig.7E, Fig.7F, Fig.7G</p> <p>&nbsp;</p> <p><strong>Fig.8CEHJK.xlsx</strong></p> <p>Numerical data for the charts in Fig.8C, Fig.8E, Fig.8H, Fig.8J, Fig.8K</p> <p>&nbsp;</p> <p><strong>Fig.S1A_bottom.tif</strong></p> <p>2PLSM image (green channel, G-CEPIA1er) for Fig.S1A bottom panel (low Ca2+)</p> <p>&nbsp;</p> <p><strong>Fig.S1A_top.tif</strong></p> <p>2PLSM image (green channel, G-CEPIA1er) for Fig.S1A top panel (high Ca2+)</p> <p>&nbsp;</p> <p><strong>Fig.S1B.xlsx</strong></p> <p>Numerical data for the chart in Fig.S1B</p> <p>&nbsp;</p> <p><strong>Fig.S2A_baseline.tif</strong></p> <p>2PLSM image (green channel, mito-GCaMP6) for Fig.S2A middle panel (baseline)</p> <p>&nbsp;</p> <p><strong>Fig.S2A_MAX.tif</strong></p> <p>2PLSM image (green channel, mito-GCaMP6) for Fig.S2A top panel (high Ca2+)</p> <p>&nbsp;</p> <p><strong>Fig.S2A_min.tif</strong></p> <p>2PLSM image (green channel, mito-GCaMP6) for Fig.S2A bottom panel (low Ca2+)</p> <p>&nbsp;</p> <p><strong>Fig.S2C_baseline.tif</strong></p> <p>2PLSM image (green channel, mito-GCaMP6) for Fig.S2C middle panel (baseline)</p> <p>&nbsp;</p> <p><strong>Fig.S2C_MAX.tif</strong></p> <p>2PLSM image (green channel, mito-GCaMP6) for Fig.S2C top panel (high Ca2+)</p> <p>&nbsp;</p> <p><strong>Fig.S2C_min.tif</strong></p> <p>2PLSM image (green channel, mito-GCaMP6) for Fig.S2C bottom panel (low Ca2+)</p> <p>&nbsp;</p> <p><strong>Fig.S2E_baseline.tif</strong></p> <p>2PLSM image (green channel, mito-GCaMP6) for Fig.S2E bottom left panel (baseline)</p> <p>&nbsp;</p> <p><strong>Fig.S2E_end.tif</strong></p> <p>2PLSM image (green channel, mito-GCaMP6) for Fig.S2E bottom right panel</p> <p>&nbsp;</p> <p><strong>Fig.S2E_peak.tif</strong></p> <p>2PLSM image (green channel, mito-GCaMP6) for Fig.S2E bottom center panel</p> <p>&nbsp;</p> <p><strong>Fig.S2F.xlsx</strong></p> <p>Numerical data for the chart in Fig.S2F</p> <p>&nbsp;</p> <p><strong>Fig.S3ABC.xlsx</strong></p> <p>Numerical data for the charts in Fig.S3A, Fig.S3B, Fig.S3C</p> <p>&nbsp;</p> <p><strong>Fig.S4CD.xlsx</strong></p> <p>Numerical data for the charts in Fig.S4C, Fig.S4D</p> <p>&nbsp;</p> <p><strong>Fig.S5ABC.xlsx</strong></p> <p>Numerical data for the charts in Fig.S5A, Fig.S5B, Fig.S5C</p> <p>&nbsp;</p> <p><strong>Fig.S7A.tif</strong></p> <p>2PLSM image (green channel, GCaMP6) for Fig.S7A</p> <p>&nbsp;</p> <p><strong>Fig.S7CEFGH.xlsx</strong></p> <p>Numerical data for the charts in Fig.S7C, Fig.S7E, Fig.S7F, Fig.S7G, Fig.S7H</p> <p>&nbsp;</p> <p><strong>Fig.S8ABCDEF.xlsx</strong></p> <p>Numerical data for the charts in Fig.S8A, Fig.S8B, Fig.S8C, Fig.S8D, Fig.S8E, Fig.S8F</p> <p>&nbsp;</p> <p><strong>Fig.S9AHIJK.xlsx</strong></p> <p>Numerical data for the charts in Fig.S9A, Fig.S9H, Fig.S9I, Fig.S9J, Fig.S9K</p> <p>&nbsp;</p> <p><strong>Fig.S9B_wildtype_DLStr.tif</strong></p> <p>Confocal image of dorso-laterateral striatum in wildtype mouse (red channel, anti-TH immunostaining) for Fig.S9B</p> <p>&nbsp;</p> <p><strong>Fig.S9C_MCU-KO_DLStr.tif</strong></p> <p>Confocal image of dorso-laterateral striatum in MCU-KO mouse (red channel, anti-TH immunostaining) for Fig.S9C</p> <p>&nbsp;</p> <p><strong>Fig.S9D_wildtype_SN.tif</strong></p> <p>Confocal image of midbrain in wildtype mouse (red channel, anti-TH immunostaining) for Fig.S9D</p> <p>&nbsp;</p> <p><strong>Fig.S9E_MCU-KO_SN.tif</strong></p> <p>Confocal image of midbrain in MCU-KO mouse (red channel, anti-TH immunostaining) for Fig.S9E</p> <p>&nbsp;</p> <p><strong>Fig.S9F_wildtype_openfield.png</strong></p> <p>Open field path tracked for wildtype mouse for Fig.S9F</p> <p>&nbsp;</p> <p><strong>Fig.S9G_MCU-KO_openfield.png</strong></p> <p>Open field path tracked for MCU-KO mouse for Fig.S9G</p> <p>&nbsp;</p> <p><strong>Fig.S10A.xlsx</strong></p> <p>Numerical data for the charts in Fig.S10A</p>

opencc-by-4.0Aug 2022View details →
zenodo36/100

Dataset related to article "'Understanding fibrosis pathogenesis via modelling macrophage-fibroblast interplay in immune-metabolic context"

<p>This record contains raw data related to article &ldquo; &#39;Understanding fibrosis pathogenesis via modelling macrophage-fibroblast interplay in immune-metabolic context&quot;</p> <p>Abstract not avaible at the moment</p>

opencc-by-4.0Sep 2021View details →
zenodo36/100

Transcriptional and metabolic changes in Candida albicans during yeast-to-hypha transition

<p>In this study hypha-associated transcriptional and metabolic changes were investigated in the opportunistich human pathogen <em>Candida albicans</em>. Three different strains were investigated the SC5314 wildtype and two filamentation-affected mutant strains <em>cph1</em>&Delta;<em>efg1</em>&Delta; and <em>hgc1</em>&Delta;. Three different hypha-inducing conditions were compared with two respective yeast conditions: SD minimal medium with 10% human serum or N-acetylglucosamin vs. SD minimal medium, and M199 pH7.4 vs. M199 pH4. Sampling time points were 0, 90 and 240 min. ON cultures were prepared in SD and re-inoculated in SD and grown to early log-phase prior to the experiment. Cells were collected, washed and used to inoculate the test medium at OD0.3. All cultures were generally maintained at 37&deg;C. Obtained samples were submitted for transcriptional profiling (RNA-Seq with 10 million reads per sample and 150 bp paired-ends) and metabolomics.</p> <p>Media list:</p> <p>SD: 2% glucose, 0.17% YNB without amino acids, 0.5% ammonium sulfate, pH 4.5</p> <p>HS - SD with 10 vol% human serum (Male, AB negative)</p> <p>GlcNAc - 2% <em>N</em>-acetylglucosamine, 0.17% YNB without amino acids, 0.5% ammonium sulfate, pH 4.5</p> <p>Medium 199 with Earle&#39;s salts and L-Glu&nbsp; buffered to either pH 4 or 7.4 by addition of 1/5 volume of 0.1&nbsp;M citric acid and 0.2&nbsp;M Na<sub>2</sub>HPO<sub>4</sub> buffer</p>

opencc-by-4.0Aug 2022View details →
dryad36/100

Feeding foliar nano-selenium biofortified Panax notoginseng could reduce the occurrence of glycolipid metabolism disorder in mice caused by high-fat diets

<p><span>Nano-selenium (nano-Se) has been extensively explored as a biostimulant for improving the quality of grain crops. However, there are few reports about the effect on the medicinal components of Chinese herbal medicine cultured with nano-Se. Here, we sprayed nano-Se during the cultivation of </span><span><em>Panax notoginseng</em> (SePN), and measured the changes of medicinal components compared with conventional <em>Panax notoginseng</em> (PN). Furthermore, we identified a more pronounced effect of SePN on reducing obesity in animals compared with PN. By measuring antioxidant capacity, histopathology, gene expression related to glycolipid metabolism, and gut microbiota composition, we propose a potential mechanism for SePN to improve animal health.</span><span> Compared with the control groups, foliar spraying of nano-Se increased saponins content (Rb2, Rb3, Rc, F2, Rb2, and Rf) in the roots of <em>Panax notoginseng</em>, and the content of Rb2 increased by 3.9 times in particular. Interestingly, animal studies indicated that taking selenium-rich <em>Panax notoginseng</em> (SePN) can further ameliorate liver antioxidation (SOD, MDA, and GSH) and enzyme activities involved in glycolipid metabolism (ATGL and PFK). It also relieved inflammation and regulated the expression of genes (<em>MCAD</em>, <em>PPAR-α</em>, and <em>PCSK9</em>) related to fatty acid oxidation.</span> <span>The abundance ratio of Firmicutes/Bacteroides and beneficial bacteria abundance (<em>Bifidobacterium</em>, <em>Butyricimonas</em>, and <em>Parasutterella</em>) in gut microbiota were improved relative to the control. In summary, the application of nano-Se on PN may</span> <span>effectively raise the content of <em>Panax notoginseng</em> saponins (PNS) and immensely lower the risk of metabolic disorders of glycolipids.</span></p>

opencc-zeroAug 2022View details →
dryad36/100

Thallium(I) exposure perturbs the gut microbiota and metabolic profile as well as the regional immune function of C57BL/6 J mice

<p><span>Intestinal microbes</span><span> regulate the development of diseases induced by environmental exposure. Thallium (Tl) is a highly toxic heavy metal</span><span>, </span><span>and its toxicity is rarely discussed in relation to gut microbes. Herein, we showed that Tl(I) exposure (10 ppm for two weeks) affected the alpha diversity of bacteria in </span><span>the ileum, colon, and </span><span>feces, but had little effect on the beta diversity of bacteria through 16S rRNA sequencing. LEfSe analysis revealed that Tl(I) exposure changed the abundance of intestinal microbiota along the digestive tract. Cecum metabolomic detection and analysis showed that Tl(I) exposure altered the abundance and composition of metabolites. In addition, the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis revealed that Tl(I) exposure impaired amino acid, lipid, purine metabolism, and G protein-coupled receptor signalling pathways. A consistency test revealed a strong correlation, and a Pearson's correlation analysis showed an extensive interaction, between microorganisms and metabolites. Analysis of the intestinal immunity revealed that Tl(I) exposure suppressed the immune responses, which also had regional differences. These results identify the perturbation of the intestinal microenvironment by Tl exposure and provide a new explanation for Tl toxicity.</span></p>

opencc-zeroSep 2022View details →
dryad36/100

Pace-of-life syndrome: linking personality, metabolism and colour ornamentation in male guppies

<p>Within populations, there commonly exists consistent among-individual differences in behaviour. As a potential mechanism maintaining this variation, the pace-of-life-syndrome (POLS) hypothesis posits that consistent differences in the behaviour of individuals (i.e. 'personality') are intercorrelated and have coevolved with consistent individual differences in metabolism and life-history traits. Here, using adult male guppies, <em>Poecilia reticulata</em>, we tested under laboratory conditions (1) whether behavioural and metabolic traits vary consistently among individuals over time (≤ 7 days) and (2) the POLS prediction that repeatable behavioural traits should be intercorrelated with each other and with repeatable metabolic rate at the among-individual level. Furthermore, based on indicator models of sexual selection, we expected that sexually selected male colour ornamentation would predict individual personality and metabolic rate. We repeatedly assayed three behavioural traits (sociability, boldness, exploration) and three metabolic traits (resting metabolic rate, maximal metabolic rate, aerobic scope) in a set of males that varied in body size and colour ornamentation. All behavioural trait measures were repeatable, consistent with individual personality. Of the three metabolic traits, only resting metabolic rate (RMR) was repeatable. Behavioural trait measures were significantly intercorrelated and thus integrated in a behavioural syndrome. More 'proactive' males were bolder, more exploratory and more sociable than 'reactive' ones. However, contrary to the POLS hypothesis, <span>RMR</span>was not significantly correlated with any of the behavioural trait measures, suggesting that consistent individual differences in RMR do not drive or support differences in personality, or vice versa. Male colour ornamentation did not covary with behaviour or RMR and thus does not appear to be a reliable predictor of either behavioural or metabolic phenotypes. We therefore did not find any compelling support for the POLS hypothesis, suggesting that <span>individual differences in metabolism do not underlie the evolution and maintenance of among-individual  behavioural variation in our study population.</span></p>

opencc-zeroSep 2022View details →
zenodo36/100

Functional and metabolic alteration of gut microbiota in children with new-onset type 1 diabetes

<p>Worldwide T1D incidence has been steadily increasing annually over the past 30 years. The etiology of T1D is multifactorial, consisting of genetic susceptibility and environmental factors, including gut microbiota alterations. The comprehensive profiling of functional and metabolic dysbiosis of gut microbiota in T1D is lacking. To decipher the T1D-associated functional features of gut dysbiosis, we performed integrative metagenomic and metabolomic analyses in pediatric patients with new-onset T1D.</p>

opencc-by-4.0Sep 2022View details →
zenodo36/100

Decoding the metabolic response of Escherichia coli for sensing trace heavy metals in water

<p>As: Raman spectra from E. coli lysate sample after exposing&nbsp;to As in DI water</p> <p>Cr:&nbsp;Raman spectra from E. coli lysate sample after exposing&nbsp;to Cr in DI water</p> <p>As_TapWater:&nbsp;Raman spectra from E. coli lysate sample after exposing&nbsp;to As in tap&nbsp;water</p> <p>WasteWater_FineTune_Dataset: Raman spectra from E. coli lysate sample after exposing&nbsp;to As in waste&nbsp;water</p> <p>WasteWater &#39;Unknow&#39; Dataset:&nbsp;Raman spectra from E. coli lysate sample after exposing&nbsp;to&nbsp;waste&nbsp;water</p>

opencc-by-4.0Sep 2022View details →
zenodo36/100

Metabolic syndrome severity score and associated cardiovascular risk in postmenopausal women of Bangladesh

<p>This data help to construct metabolic syndrome severity score and seek its association with absolute cardiovascular risk.</p>

opencc-by-4.0Sep 2022View details →
zenodo36/100

KidDO progress presentation 2022: Metabolic Targets for Therapeutic Intervention in Kidney Disease

<p>This is a recorded talk with head of the KidDO project - Robert Fenton -&nbsp;where he presents the latest project progress.</p> <p>The talk was given at one of ODIN&#39;s (the Open Discovery Innovation Network) Knowledge Sharing Events in May 2022.</p> <p>&nbsp;</p> <p>&nbsp;</p>

opencc-by-4.0May 2022View details →
zenodo36/100

The frequent occurrence and metabolic versatility of Marinifilaceae bacteria involved in organic matter mineralization as a key member in global deep sea

<p>Transfer of animal and plant detritus of both terrestrial and marine origins to the deep sea occurs on the global scale. Microorganisms play an important role in mineralizing them therein, yet to identify <em>in situ</em>. To observe key bacteria involved, we conducted long-term <em>in situ</em> incubation and found the family <em>Marinifilaceae </em>occurred as one of the most predominant bacteria thriving on the new inputs of plant and animal biomasses in the deep sea of both marginal and oceanic areas. This taxa is diverse and ubiquitous in marine environments. A total of 11 MAGs belonging to MF were retrieved from metagenomic data and diverged into four subgroups based on the phylogenomic tree. We described the metabolic features and <em>in situ</em> metabolizing activities of different MF subgroups via the metagenomic and metatranscriptomic data. One representative subgroup MF-2 dominated plant detritus-enriched cultures and specialized in polysaccharide degradation and lignin oxidation. Intriguingly, they encode nitrogen fixation pathway to compensate for the shortage of nitrogen sources inside the plant detritus. In contrast, those dominating the animal tissue-supported microbiomes were more diverse and formed three subgroups, which distinguished themselves from MF-2 in carbon and nitrogen metabolisms. Despite these metabolic divergences of MF lineages, they harbored anaerobic processes for energy&nbsp;conservation via organic fermentation, anaerobic respiration via iron and manganese reduction, and/or dimethyl sulfoxide reduction. These results highlight the role of <em>Marinifilaceae</em> bacteria neglected before in organic matter mineralizing in marine environments coupling carbon and nitrogen cycling with metals and other elements.</p>

opencc-by-4.0Sep 2022View details →
dryad36/100

Oxygen availability regulates the quality of soil dissolved organic matter by mediating microbial metabolism and iron oxidation

<p>Dissolved organic matter (DOM) plays a vital role in biogeochemical processes and in determining the responses of soil organic matter (SOM) to global change. Although the quantity of soil DOM has been inventoried across diverse spatio-temporal scales, the underlying mechanisms accounting for variability in DOM dynamics remain unclear, especially in upland ecosystems. Here, a gradient of SOM storage across twelve croplands in northeast China was used to understand links between DOM dynamics, microbial metabolism, and abiotic conditions. We assessed the composition, biodegradability and key biodegradable components of DOM. In addition, SOM and mineral-associated organic matter (MAOM) composition, soil enzyme activities, oxygen availability, soil texture, iron (Fe), Fe-bound organic matter and nutrient concentrations were quantified to clarify the drivers of DOM quality (composition and biodegradability). The proportion of biodegradable DOM increased exponentially with decreasing initial DOM concentration due to larger fractions of depolymerized DOM that was rich in small-molecular phenols and proteinaceous components. Unexpectedly, the composition of DOM was decoupled from that of SOM or MAOM, but significantly related to enzymatic properties. These results indicate that microbial metabolism exhibited a dominant role in DOM generation. As DOM concentration declined, increased soil oxygen availability regulated DOM composition and enhanced its biodegradability mainly through mediating microbial metabolism and Fe oxidation. The oxygen-induced oxidation of Fe(II) to Fe(III) removed complex DOM compounds with large molecular weight. Moreover, increased oxygen availability stimulated oxidase-catalyzed depolymerization of aromatic substances, and promoted production of protein-like DOM components due to lower enzymatic C/N acquisition ratio. As global changes in temperature and moisture will have large impacts on soil oxygen availability, the role of oxygen in regulating DOM dynamics highlights the importance of integrating soil oxygen supply with microbial metabolism and Fe redox status to improve model predictions of soil carbon under climate change.</p>

opencc-zeroOct 2022View details →
dryad36/100

Plant secondary metabolic responses to global climate change: A meta-analysis in medicinal and aromatic plants

<p><span>Plant secondary metabolites (SMs) play crucial roles in plant-environment interactions and contribute greatly to human health. Global climate changes are expected to dramatically affect plant secondary metabolism, yet a systematic understanding of such influences is still lacking. Here, we employed medicinal and aromatic plants (MAAPs) as model plant taxa and performed a meta-analysis from 360 publications using 1828 paired observations to assess the responses of different SMs levels and the accompanying plant traits to elevated carbon dioxide (eCO<sub>2</sub>), elevated temperature (eT), elevated nitrogen deposition (eN), and decreased precipitation (dP). The overall results showed that phenolic and terpenoid levels generally respond positively to eCO<sub>2</sub> but negatively to eN, while the total alkaloid concentration was increased remarkably by eN. By contrast, dP promotes the levels of all SMs, while eT exclusively exerts a positive influence on the levels of phenolic compounds. Further analysis highlighted the dependence of SM responses on different moderators such as plant functional types, climate change levels or exposure durations, mean annual temperature and mean annual precipitation. Moreover, plant phenolic and terpenoid responses to climate changes could be attributed to the variations in C/N ratio and total soluble sugar levels, while the <em>trade-off</em> supposition contributed to SM responses to climate changes other than eCO<sub>2</sub>. Taken together, our results predicted the distinctive SM responses to diverse climate changes in MAAPs, and allowed us to define potential moderators responsible for these variations. Further, linking SM responses to C-N metabolism and growth-defence balance provided biological understandings in terms of plant secondary metabolic regulation.</span></p>

opencc-zeroOct 2022View details →
zenodo36/100

Connecting signaling and metabolic pathways in EGF receptor-mediated oncogenesis of glioblastoma

<p>This repository contains signalling to metabolic pathways interconnecting (S-M) protein-protein interaction (PPI) paths. The repository consists of two file:</p> <p><a href="https://zenodo.org/api/files/61dbb365-104e-4c41-ad0a-79f4c657bbee/S-M_paths_z-score_greater_equal_1.txt">S-M_paths_z-score_greater_equal_1.txt </a>: It contains all the S-M paths having z-score &gt;= 1.</p> <p><a href="https://zenodo.org/api/files/61dbb365-104e-4c41-ad0a-79f4c657bbee/S-M_paths_z-score_greater_equal_3.txt">S-M_paths_z-score_greater_equal_3.txt </a>: It contains all the S-M paths having z-score &gt;=3</p>

opencc-by-4.0May 2019View details →
zenodo36/100

Using a whole-body 31P birdcage transmit coil and 16-element receive array for human cardiac metabolic imaging at 7T

<p>The uploaded data relate to the PLoS ONE manuscript of Valkovič et al. entitled "Using a whole-body 31P birdcage transmit coil and 16-element receive array for human cardiac metabolic imaging at 7T." 2017<br> The data consist of the models used for simulating electromagnetic fields, in CST Studio 2016 format, for the whole-body coil and the surface coil, and of the the phantom and anonnymised in vivo data, in Siemens DICOM format, acquired as described in the manuscript.</p>

opencc-by-4.0Oct 2017View details →
zenodo36/100

Photoreceptor glucose metabolism determines normal retinal vascular growth

<p>The neural cells and factors determining normal vascular growth are not well defined even though vision-threatening neovessel growth, a major cause of blindness in retinopathy of prematurity (ROP) (and diabetic retinopathy), is driven by delayed normal vascular growth.  We examined if hyperglycemia and low adiponectin (APN) levels delayed normal retinal vascularization, driven primarily by dysregulated photoreceptor metabolism.</p> <p>One part of the experiments was to use targeted quantitative proteomics to measure the expression of proteins with selected reaction monitoring.  We measured the enzymes in glycolysis, the Krebs cycle, and several addition mitochondrial proteins.</p> <p>We found that in a neonatal mouse model of postnatal hyperglycemia modeling early ROP, hyperglycemia caused photoreceptor dysfunction and delayed neurovascular maturation associated with changes in the APN pathway; recombinant mouse APN or APN receptor agonist adipoRon treatment normalized vascular growth. APN deficiency decreased retinal mitochondrial metabolic enzyme levels particularly in photoreceptors, suppressed retinal vascular development and decreased photoreceptor platelet-derived growth factor (Pdgfb). APN pathway activation reversed these effects. Blockade of mitochondrial respiration abolished adipoRon-induced Pdgfb increase in photoreceptors.  Photoreceptor-knockdown of Pdgfb delayed retinal vascular formation. Stimulation of the APN pathway might prevent hyperglycemia-associated retinal abnormalities andsuppress Phase I ROP in premature infants.</p>

opencc-by-4.0Nov 2017View details →
dryad36/100

The scaling of metabolic traits differs among larvae and juvenile colonies of scleractinian corals

<p>Body size profoundly affects organism fitness and ecosystem dynamics through the scaling of physiological traits. This study tests for variation in metabolic scaling and its potential drivers among corals differing in life history strategies and taxonomic identity. Data were compiled from published sources and augmented with empirical measurements of corals in Moorea, French Polynesia. The data compilation revealed metabolic isometry in broadcasted larvae, but size-independent metabolism in brooded larvae; empirical measures of <em>Pocillopora acuta</em> larvae also supported size-independent metabolism in brooded coral larvae. In contrast, for juvenile colonies (i.e., 1–4 cm diameter), metabolic scaling was isometric for <em>Pocillopora</em> spp. and negatively allometric for <em>Porites</em> spp. The scaling of biomass with surface area was isometric for <em>Pocillopora</em> spp., but positively allometric for <em>Porites</em> spp., suggesting the surface area:biomass ratio mediates metabolic scaling in these corals. The scaling of tissue biomass and metabolism was not affected by light treatment (i.e., either natural photoperiods or constant darkness) in both juvenile taxa. However, biomass was reduced by 9–15% in the juvenile corals from the light treatments and this coincided with higher metabolic scaling exponents, thus supporting the causal role of biomass in driving variation in scaling. This study shows that metabolic scaling is plastic in the early life stages of corals, with intrinsic differences between life history strategy (i.e., brooded and broadcasted larvae) and taxa (i.e., <em>Pocillopora </em>spp<em>. </em>and <em>Porites </em>spp<em>.</em>), and acquired differences attributed to changes in area-normalized biomass.</p>

opencc-zeroApr 2024View details →

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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.

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Allen Brain Atlas

Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.

allen-brain-atlas
neuroscienceopenDocumentation, web resources, and API references are available online.
Last verified 2026-04-30Open record

Annotated Behaviour and Observability Dataset (ABODe)

ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.

abode-home-cage
behavioral-neuroscienceopenThe DataShare record exposes download links for annotations, documentation, license text, and the zipped per-snippet data directory.
Last verified 2026-04-30Open record

DANDI Archive for NWB datasets

DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.

dandi-nwb
electrophysiologyopenPublished Dandiset metadata and archive endpoints are available through the production DANDI API.
Last verified 2026-04-30Open record

International Brain Laboratory public data

The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.

ibl
behavioral-neuroscienceopenPublic sessions can be searched and loaded from the IBL public data server through ONE.
Last verified 2026-04-29Open record

OpenNeuro

OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.

openneuro
neuroscienceopenPublished datasets are available on demand over the internet.
Last verified 2026-04-29Open record

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