Determination of 14C-labelled ketone bodies by liquid-scintillation counting.
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ABSTRACT:
SUBMITTER: Mayes PA
PROVIDER: S-EPMC1270233 | biostudies-other | 1967 Jan
REPOSITORIES: biostudies-other
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Project description:1. Inexpensive scintillation mixtures are described which enable the detection of as little as 40mumuc of (14)C in aqueous solution with an efficiency of counting of over 80%. 2. A rapid method for the counting of alkaline, acidic and neutral aqueous solutions of up to 1ml. volume is described. Ethanol or 2-ethoxyethanol is used as blending agent. 3. The scintillation counting of alkaline solutions is applied to the accurate determination of the specific activity of (14)C-labelled proteins from plant tissues. 4. Attention has been paid to the importance of a standardized washing procedure for the removal of all traces of radioactive material from glassware.
| S-EPMC1207196 | biostudies-other
Project description:An informal bilateral comparison of (14)C liquid scintillation (LS) counting at the National Research Council of Canada (NRC) and the National Institute of Standards and Technology (NIST) has been completed. Two solutions, one containing (14)C-labeled sodium benzoate and one containing (14)C-labeled n-hexadecane, were measured at both laboratories. Despite observed LS cocktail instabilities, the two laboratories achieved accord in their standardizations of both solutions. At the conclusion of the comparison, the beta spectrum used for efficiency calculations was identified as inadequate and the data were reanalyzed with different inputs, improving accord.
| S-EPMC4937459 | biostudies-literature
Project description:Labelled ketone bodies were produced readily from [U-(14)C]palmitate, [2-(14)C]palmitate and [1-(14)C]glycerol by sheep rumen-epithelial and liver tissues in vitro. On a tissue-nitrogen basis, both tissues had similar capacities for ketogenesis. Palmitate was a ketogenic substrate in both rumen-epithelial tissue and liver, and more of its (14)C appeared in ketone bodies than in the (14)CO(2) liberated. Glycerol was actively metabolized to ketone bodies, but more readily underwent complete oxidation to carbon dioxide; this complete oxidation was most pronounced in rumen-epithelial tissue from ketotic ewes. These experiments with labelled compounds confirm earlier observations that rumen-epithelial tissue, like liver, actively forms ketone bodies from long-chain fatty acids and show further that normal rumen-epithelial tissue can convert palmitate into ketone bodies as readily as into carbon dioxide. Free glycerol, which is metabolized only by liver tissue in non-ruminants, is also metabolized by rumen epithelium. The rumen epithelium thus has unique metabolic capacity among extrahepatic tissues.
| S-EPMC1198497 | biostudies-other
Project description:PurposeThe implementation of photon-counting detectors is widely expected to be the next breakthrough in X-ray computed tomography (CT) instrumentation. A small number of prototype scanners equipped with direct-conversion detectors based on room-temperature semiconductors, such as CdTe and CdZnTe (CZT), are currently installed at medical centers. Here, we investigate the feasibility of using silicon photomultiplier (SiPM)-based scintillation detectors in photon-counting computed tomography (PCCT) scanners, as a potential alternative to CdTe and CZT detectors.MethodsWe introduce a model that allows us to compute the expected energy resolution as well as the expected pulse shape and associated rate capability of SiPM-based PCCT detectors. The model takes into account SiPM saturation and optical crosstalk, because these phenomena may substantially affect the performance of SiPM-based PCCT detectors with sub-mm pixels. We present model validation experiments using a single-pixel detector consisting of a 0.9 × 0.9 × 1.0 mm3 LuAP:Ce scintillation crystal coupled to a 1 × 1 mm2 SiPM. We subsequently use the validated model to compute the expected performance of the fast scintillators LYSO:Ce, LuAP:Ce, and LaBr3 :Ce, coupled to currently available SiPMs, as well as to a more advanced SiPM prototype with improved dynamic range, for sub-mm pixel sizes.ResultsThe model was found to be in good agreement with the validation experiments, both with respect to energy resolution and pulse shape. It shows how saturation progressively degrades the energy resolution of detectors equipped with currently available SiPMs as the pixel size decreases. Moreover, the expected pulse duration is relatively long (~200 ns) with these SiPMs. However, when LuAP:Ce and LaBr3 :Ce are coupled to the more advanced SiPM prototype, the pulse duration improves to less than 60 ns, which is in the same order of magnitude as pulses from CdTe and CZT detectors. It follows that sufficient rate capability can be achieved with pixel sizes of 400 μm or smaller. Moreover, LaBr3 :Ce detectors can provide an energy resolution of 11.5%-13.5% at 60 keV, comparable to CdTe and CZT detectors.ConclusionsThis work provides first evidence that it may be feasible to develop SiPM-based scintillation detectors for PCCT that can compete with CdTe and CZT detectors in terms of energy resolution and rate capability.
| S-EPMC8596580 | biostudies-literature
Project description:The ketone body β-hydroxybutyrate is no longer viewed simply as a metabolic intermediate, as it regulates a broad range of physiological processes at cellular and systemic levels. Particularly, β-hydroxybutyrate functions as a stress response molecule and orchestrates an antioxidant defense program to maintain redox homeostasis in response to environmental and metabolic challenges, such as ischemia. This property of β-hydroxybutyrate might be key for the beneficial effect of calorie restriction on stress response and disease processes.
| S-EPMC6911969 | biostudies-literature
Project description:Diets characterized by increased blood levels of ketone bodies can protect the brain against a variety of acute and chronic neurological diseases. Moreover, ketone bodies are neuroprotective in many in vitro models of neurological injury. The underlying mechanisms remain unknown however. Recently, we have shown that ketone bodies do not only decrease neuronal injury and death but also protect long-term potentiation in acute hippocampal slices exposed to oxidative stress in the form of exogenous hydrogen peroxide. Elucidating the mechanisms behind the effects of ketone bodies on neuronal survival and function will undoubtedly lead to the development of novel neuroprotective treatments. Our aim is to determine acute changes in gene expression of CA1 pyramidal neurons exposed to various duration of the ketone bodies acetoacetate and beta-hydroxybutyrate. CA1 hippocampal pyramidal neurons exposed to oxidative stress do not display any long-term potention following burst stimulation of Schaffer collaterals. Incubation with the ketone bodies acetoacetate and beta-hydroxybutyrate for at least 20 min prior to hydrogen peroxide application restores long-term potentiation to control levels. We hypothesize that the neuroprotective effects of ketone bodies are mediated by changes in gene expression. Acute hippocampal slices (400 microns in thickness) were obtained from 4 week-old rats and exposed to acetoacetate and beta-hydroxybutyrate (1 mM each) for 1 h and 6 h. A control group was incubated in artificial cerebrospinal fluid only. After treatment, the hippocampal slices were used immediately for RNA isolation. Isolated RNA was sent for analysis. Each sample sent for analysis included tissue from 7 separate animals. Hybridization to an Affymetrix array is being performed 3 times for each experimental condition.
2008-06-15 | E-GEOD-7323 | biostudies-arrayexpress
Project description:BackgroundCancer Anorexia Cachexia Syndrome (CACS) is a distinct atrophy disease negatively influencing multiple aspects of clinical care and patient quality of life. Although it directly causes 20% of all cancer-related deaths, there are currently no model systems that encompass the entire multifaceted syndrome, nor are there any effective therapeutic treatments.MethodsA novel model of systemic metastasis was evaluated for the comprehensive CACS (metastasis, skeletal muscle and adipose tissue wasting, inflammation, anorexia, anemia, elevated protein breakdown, hypoalbuminemia, and metabolic derangement) in both males and females. Ex vivo skeletal muscle analysis was utilized to determine ubiquitin proteasome degradation pathway activation. A novel ketone diester (R/S 1,3-Butanediol Acetoacetate Diester) was assessed in multifaceted catabolic environments to determine anti-atrophy efficacy.ResultsHere, we show that the VM-M3 mouse model of systemic metastasis demonstrates a novel, immunocompetent, logistically feasible, repeatable phenotype with progressive tumor growth, spontaneous metastatic spread, and the full multifaceted CACS with sex dimorphisms across tissue wasting. We also demonstrate that the ubiquitin proteasome degradation pathway was significantly upregulated in association with reduced insulin-like growth factor-1/insulin and increased FOXO3a activation, but not tumor necrosis factor-α-induced nuclear factor-kappa B activation, driving skeletal muscle atrophy. Additionally, we show that R/S 1,3-Butanediol Acetoacetate Diester administration shifted systemic metabolism, attenuated tumor burden indices, reduced atrophy/catabolism and mitigated comorbid symptoms in both CACS and cancer-independent atrophy environments.ConclusionsOur findings suggest the ketone diester attenuates multifactorial CACS skeletal muscle atrophy and inflammation-induced catabolism, demonstrating anti-catabolic effects of ketone bodies in multifactorial atrophy.
| S-EPMC7432582 | biostudies-literature
Project description:A solution of 124I was standardized for activity by 4??(LS)-?(NaI) live-timed anticoincidence (LTAC) counting, with confirmatory measurements by triple-to-double coincidence ratio (TDCR) and CIEMAT-NIST efficiency tracing (CNET) liquid scintillation counting. The LTAC-based standard was shown to be in agreement (within k?=?1 uncertainties) with previous measurements at NIST and elsewhere. Calibration settings for radionuclide calibrators were determined and a discrepancy with literature values, partially due to a calibration methodology dependent upon an erroneous setting for 18F, was identified and explained.
| S-EPMC6839768 | biostudies-literature
Project description:The circadian system has endowed animals with the ability to anticipate recurring food availability at particular times of day. As daily food anticipation (FA) is independent of the suprachiasmatic nuclei, the central pacemaker of the circadian system, questions arise of where FA signals originate and what role components of the circadian clock might play. Here we show that liver-specific deletion of Per2 in mice abolishes FA, an effect that is rescued by viral overexpression of Per2 in the liver. RNA sequencing indicates that Per2 regulates ?-hydroxybutyrate (?OHB) production to induce FA leading to the conclusion that liver Per2 is important for this process. Unexpectedly, we show that FA originates in the liver and not in the brain. However, manifestation of FA involves processing of the liver-derived ?OHB signal in the brain, indicating that the food-entrainable oscillator is not located in a single tissue but is of systemic nature.
| S-EPMC4742855 | biostudies-literature
Project description:Diets characterized by increased blood levels of ketone bodies can protect the brain against a variety of acute and chronic neurological diseases. Moreover, ketone bodies are neuroprotective in many in vitro models of neurological injury. The underlying mechanisms remain unknown however. Recently, we have shown that ketone bodies do not only decrease neuronal injury and death but also protect long-term potentiation in acute hippocampal slices exposed to oxidative stress in the form of exogenous hydrogen peroxide. Elucidating the mechanisms behind the effects of ketone bodies on neuronal survival and function will undoubtedly lead to the development of novel neuroprotective treatments. Our aim is to determine acute changes in gene expression of CA1 pyramidal neurons exposed to various duration of the ketone bodies acetoacetate and beta-hydroxybutyrate. CA1 hippocampal pyramidal neurons exposed to oxidative stress do not display any long-term potention following burst stimulation of Schaffer collaterals. Incubation with the ketone bodies acetoacetate and beta-hydroxybutyrate for at least 20 min prior to hydrogen peroxide application restores long-term potentiation to control levels. We hypothesize that the neuroprotective effects of ketone bodies are mediated by changes in gene expression. Acute hippocampal slices (400 microns in thickness) were obtained from 4 week-old rats and exposed to acetoacetate and beta-hydroxybutyrate (1 mM each) for 1 h and 6 h. A control group was incubated in artificial cerebrospinal fluid only. After treatment, the hippocampal slices were used immediately for RNA isolation. Isolated RNA was sent for analysis. Each sample sent for analysis included tissue from 7 separate animals. Hybridization to an Affymetrix array is being performed 3 times for each experimental condition. Keywords: dose response
2007-03-20 | GSE7323 | GEO